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  1. Myocardial alterations due to free-radical generation

    SciTech Connect

    Burton, K.P.; McCord, J.M.; Ghai, G.

    1984-06-01

    Oxygen-derived free radicals have been proposed as general mediators of tissue injury in a variety of disease states. Recent interest has focused on the possibility that free radicals may be involved in ischemic myocardial damage. The purpose of this study was to evaluate the effects of superoxide and hydroxyl radicals on myocardial structure and function in an isolated perfused rabbit interventricular septal preparation. Superoxide was generated by adding purine (2.3 mM) and xanthine oxidase (0.01 U/ml) to the physiological solutions perfusing the septa. Hydroxyl radical generation was catalyzed by the addition of 2.4 ..mu..M Fe/sup 3 +/-loaded transferrin to the system. Exposure of normal septa to superoxide-generating solutions resulted in the development of structural alterations in the vascular endothelium including the development of vacuoles. Membranous cellular debris was evident in the extracellular space and within the vessels. Cardiac myocytes showed evidence of mild alterations. Exposure of septa to solutions capable of generating hydroxyl radicals resulted in more extensive and severe damage. Vascular endothelial cells showed evidence of vacuoles or blebs and edema. Severe swelling of mitochondria was evident in cardiac myocytes and vascular endothelial cells. In addition, myocytes often showed blebbing of the basement membrane. Normal septa exposed to superoxide showed no significant decrease in developed tension, whereas hydroxyl radical exposure resulted in a significant decrease in myocardial functions. Addition of superoxide dismutase to the solutions perfusing the septa protected against myocardial alterations. Thus oxygen-derived free radicals, when generated in the heart, are capable of causing significant myocardial injury.

  2. Myocardial infection due to Fusobacterium nucleatum.

    PubMed

    Storm, Jeremy C; Ford, Bradley A; Streit, Judy A

    2013-12-01

    Fusobacterium nucleatum is an anaerobic gram-negative bacillus, which inhabits the oropharynx, gastrointestinal tract, and female genital tract. Infections classically affect the head and neck. We report a patient with a myocardial mass due to F. nucleatum, initially thought to be a neoplasm, and discuss anaerobic cardiac infections.

  3. Myocardial infarction due to lightning strike.

    PubMed

    Karadas, Sevdegul; Vuruskan, Ertan; Dursun, Recep; Sincer, Isa; Gonullu, Hayriye; Akkaya, Emre

    2013-09-01

    Cardiac events due to lightning strike and their severity vary according to the strength of the electric current and the duration of exposure. The electrophysiological effects of lightning on the heart can result in ventricular fibrillation, asystole, QT prolongation, supraventricular tachycardia, and non-specific ST-T wave changes. In this report, a case of a patient who suffered myocardial infarction due to lightning strike is presented, which is a rare complication. PMID:24601203

  4. Myocardial infarction due to lightning strike.

    PubMed

    Karadas, Sevdegul; Vuruskan, Ertan; Dursun, Recep; Sincer, Isa; Gonullu, Hayriye; Akkaya, Emre

    2013-09-01

    Cardiac events due to lightning strike and their severity vary according to the strength of the electric current and the duration of exposure. The electrophysiological effects of lightning on the heart can result in ventricular fibrillation, asystole, QT prolongation, supraventricular tachycardia, and non-specific ST-T wave changes. In this report, a case of a patient who suffered myocardial infarction due to lightning strike is presented, which is a rare complication.

  5. A case of acute myocardial infarction due to coronary spasm in the myocardial bridge.

    PubMed

    Fujibayashi, Daisuke; Morino, Yoshihiro; Ikari, Yuji

    2008-07-01

    A 68-year-old Japanese man with acute inferior myocardial infarction underwent emergent coronary angiography which showed a myocardial bridge, but no coronary stenosis, at the infarctrelated artery. A spasm provocation test using intracoronary acetylcholine revealed a total occlusion due to severe spasm at the site of the myocardial bridge. Thus, the myocardial ischemia in this case was caused by the coronary spasm, but not by the limited flow due to the myocardial bridge. Although a beta-blocker is usually the appropriate drug, it should be avoided for coronary spasm. The spasm provocation test is useful to determine the type of medication needed for treatment.

  6. Myocardial failure with altered response to adrenaline in endotoxin shock

    PubMed Central

    Archer, L.T.; Black, M.R.; Hinshaw, L.B.

    1975-01-01

    1 There is a growing concensus that myocardial performance in the early stages of experimental endotoxic and septic shock is relatively normal; however, recent reports have identified an intermediate phase of shock when myocardial dysfunction is clearly apparent. 2 The mechanism of dysfunction has become a subject of intense investigation. A current view is that altered myocardial responsiveness to circulating catecholamines may play an important role in the dysfunction observed after endotoxin administration. The present studies, in which an isolated working heart preparation of the dog was used, were designed to test this hypothesis. This particular experimental preparation was selected to provide an adequate interpretation of results; cardiac output, afterload, and concentrations of adrenaline reaching the coronary vascular bed were controlled in all experiments. Responses to infusions of adrenaline were recorded in the `steady-state' condition. Control (non-shocked) heart responses to adrenaline were highly reproducible in terms of inotropic, chronotropic and coronary vascular behaviour. 3 Results from the study document myocardial dysfunction within 4-6 h following an LD70 endotoxin administration on the basis of increased left ventricular end diastolic pressure (LVEDP), decreased cardiac power and myocardial efficiency, and depressed negative and positive dP/dt parameters. 4 Findings suggest significantly altered responsiveness of the myocardium to infused adrenaline at rates of 1, 2, and 5 μg/min with concentrations between 10 and 1 ng/ml blood. LVEDP was elevated while calculated power and efficiency parameters remained significantly below control values during infusion of adrenaline in endotoxin-treated hearts. Depressions of responsiveness were interpreted to occur on the basis of failure to restore positive and negative dP/dt to normal values and depressed coronary blood flow responses during adrenaline administration. Increases in coronary flow were

  7. Cardiovascular collapse after myocardial infarction due to centipede bite.

    PubMed

    Üreyen, Çağin Mustafa; Arslan, Şakir; Baş, Cem Yunus

    2015-07-01

    Centipede bites have been reported to cause localized and/or systemic symptoms including local pain, erythema and edema, nausea and vomiting, palpitations, headache, lymphadenopathy, and rhabdomyolysis. However, acute myocardial infarction due to centipede envenomation is reported in only three cases in English medical literature.We present a case of 31-year-old male bitten by a golden colored centipede leading to myocardial infarction and cardiopulmonary arrest which is seen very rarely. The patient was admitted to emergency department with a swollen and painful right foot. However, typical chest pain became the major complaint and cardiopulmonary arrest developed while electrocardiography was being obtained. The patient was resuscitated successfully for 5 min and acute infero-posterolateral myocardial infarction was detected on electrocardiography.

  8. Cardiovascular collapse after myocardial infarction due to centipede bite.

    PubMed

    Üreyen, Çağin Mustafa; Arslan, Şakir; Baş, Cem Yunus

    2015-07-01

    Centipede bites have been reported to cause localized and/or systemic symptoms including local pain, erythema and edema, nausea and vomiting, palpitations, headache, lymphadenopathy, and rhabdomyolysis. However, acute myocardial infarction due to centipede envenomation is reported in only three cases in English medical literature.We present a case of 31-year-old male bitten by a golden colored centipede leading to myocardial infarction and cardiopulmonary arrest which is seen very rarely. The patient was admitted to emergency department with a swollen and painful right foot. However, typical chest pain became the major complaint and cardiopulmonary arrest developed while electrocardiography was being obtained. The patient was resuscitated successfully for 5 min and acute infero-posterolateral myocardial infarction was detected on electrocardiography. PMID:25994876

  9. Myocardial Bridging

    PubMed Central

    Yuan, Shi-Min

    2016-01-01

    Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results. PMID:27074276

  10. Nitrendipine binding in congestive heart failure due to myocardial infarction

    SciTech Connect

    Dixon, I.M.; Lee, S.L.; Dhalla, N.S. )

    1990-03-01

    Depressed cardiac pump function is the hallmark of congestive heart failure, and it is suspected that decreased influx of Ca2+ into the cardiac cell is responsible for depressed contractile function. Since Ca2+ channels in the sarcolemmal membrane are considered to be an important route for the entry of Ca2+, we examined the status of Ca2+ receptors/channels in failing rat hearts after myocardial infarction of the left ventricular free wall. For this purpose, the left coronary artery was ligated and hearts were examined 4, 8, and 16 weeks later; sham-operated animals served as controls. Hemodynamic assessment revealed decreased total mechanical energy (left ventricular systolic pressure x heart rate), increased left ventricular diastolic pressure, and decreased positive and negative dP/dt in experimental animals at 4, 8, and 16 weeks. Although accumulation of ascites in the abdominal cavity was evident at 4 weeks, other clinical signs of congestive heart failure in experimental rats were evident from the presence of lung congestion and cardiac dilatation at 8 and 16 weeks after induction of myocardial infarction. The density of Ca2+ receptors/channels in crude membranes, as assessed by (3H)nitrendipine binding assay, was found to be decreased in the uninfarcted experimental left ventricle at 8 and 16 weeks; however, no change in the affinity of nitrendipine was evident. A similar depression in the specific binding of another dihydropyridine compound, (3H)PN200-110, was also evident in failing hearts. Brain and skeletal muscle crude membrane preparations, unlike those of the right ventricle and liver, revealed a decrease in Ca2+ receptors/channels density in experimental animals at 16 weeks.

  11. Altered phosphate metabolism in myocardial infarction: P-31 MR spectroscopy

    SciTech Connect

    Bottomley, P.A.; Herfkens, R.J.; Smith, L.S.; Bashore, T.M.

    1987-12-01

    The high-energy myocardial phosphate metabolism of four patients with acute anterior myocardial infarction after coronary angioplasty and drug therapy was evaluated with cardiac-gated phosphorus magnetic resonance (MR) depth-resolved surface coil spectroscopy (DRESS) 5-9 days after the onset of symptoms. Significant reductions (about threefold) in the phosphocreatine (PCr) to inorganic phosphate (Pi) ratio and elevations in the Pi to adenosine triphosphate (ATP) ratio were observed in endocardially or transmurally derived MR spectra when compared with values from epicardially displaced spectra and values from seven healthy volunteers (P less than .05). High-energy phosphate metabolites and Pi ratios did not vary significantly during the cardiac cycle in healthy volunteers. However, contamination of Pi resonances by phosphomonoester components, including blood 2,3-diphosphoglycerate, precluded accurate spectral quantification of Pi and pH. The results indicate that localized P-31 MR spectroscopy may be used to directly assess cellular energy reserve in clinical myocardial infarction and to evaluate metabolic response to interventions.

  12. Altered Gene Expression Pattern in Peripheral Blood Mononuclear Cells in Patients with Acute Myocardial Infarction

    PubMed Central

    Kiliszek, Marek; Burzynska, Beata; Michalak, Marcin; Gora, Monika; Winkler, Aleksandra; Maciejak, Agata; Leszczynska, Agata; Gajda, Ewa; Kochanowski, Janusz; Opolski, Grzegorz

    2012-01-01

    Background Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. Methods and Results Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4–6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease, without history of myocardial infarction. Gene expression analysis was performed with Affymetrix Human Gene 1.0 ST microarrays and GCS3000 TG system. Lists of genes showing altered expression levels (fold change >1.5, p<0.05) were submitted to Ingenuity Pathway Analysis. Gene lists from each group were examined for canonical pathways and molecular and cellular functions. Comparing acute phase of MI with the same patients after 6 months (stable phase) and with control group we found 24 genes with changed expression. In canonical analysis three pathways were highlighted: signaling of PPAR (peroxisome proliferator-activated receptor), IL-10 and IL-6 (interleukin 10 and 6). Conclusions In the acute phase of STEMI, dozens of genes from several pathways linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability show altered expression. Up-regulation of SOCS3 and FAM20 genes in the first days of myocardial infarction is observed in the vast majority of patients. PMID:23185530

  13. Acute myocardial infarction due to marijuana smoking in a young man: guilty should not be underestimated.

    PubMed

    Velibey, Yalcin; Sahin, Sinan; Tanık, Ozan; Keskin, Muhammed; Bolca, Osman; Eren, Mehmet

    2015-08-01

    Marijuana (cannabis) is a frequently used recreational drug that potentially imposes serious health problems. We present a case of acute myocardial infarction with chronic total occlusion of left main coronary artery due to marijuana smoking in a 27-year-old man, which was not previously reported. This case illustrate that marijuana abuse can lead to serious cardiovascular events.

  14. Early and prolonged ECG alterations resembling a myocardial injury after severe amitriptyline poisoning.

    PubMed

    Berlot, G; Vergolini, A; Calderan, C

    2010-01-01

    Evidence of cardiovascular toxicity is present in the majority of tricyclic antidepressant overdoses. We report the case of a 63-year-old woman admitted to our department with a severe amitriptyline poisoning. The ECG at admission showed a pattern mimicking an acute anteroseptal subepicardial infarction. This pattern persisted for 11 days. Myocardial enzymes and echocardiographic findings never confirmed an ischemic event. At discharge, the ECG returned normal without cardiac or neurologic sequelae. Our experience suggest that after severe tricyclic antidepressant ingestion, ECG alterations resembling myocardial injury may occur early and last for a longer period than previously reported.

  15. Case of angina pectoris at rest and during effort due to coronary spasm and myocardial bridging

    PubMed Central

    Teragawa, Hiroki; Fujii, Yuichi; Ueda, Tomohiro; Murata, Daiki; Nomura, Shuichi

    2015-01-01

    We present a case of a 71-year-old male who had chest symptoms at rest and during effort. He had felt chest oppression during effort for 1 year, and his chest symptoms had recently worsened. One month before admission he felt chest squeezing at rest in the early morning. He presented at our institution to evaluate his chest symptoms. Electrocardiography and echocardiography failed to show any specific changes. Because of the possibility that his chest symptoms were due to myocardial ischemia, he was admitted to our institution for coronary angiography (CAG). An initial CAG showed mild atherosclerotic changes in the proximal segment of the left anterior descending coronary artery (LAD) and mid-segment of the left circumflex coronary artery. Subsequent spasm provocation testing using acetylcholine revealed a bilateral coronary vasospasm, which was relieved after the intracoronary infusion of nitroglycerin. Finally, a CAG showed myocardial bridging (MB) of the mid-distal segments of the LAD. Fractional flow reserve using the intravenous administration of adenosine triphosphate was positive at 0.77, which jumped up to 0.90 through the myocardial bridging segments when the pressure wire was pulled back. Thus, coronary vasospasm and MB might have contributed to his chest symptoms at rest and during effort. Interventional cardiologists should consider the presence of MB as a potential cause of myocardial ischemia. PMID:26131343

  16. Finite-Element Extrapolation of Myocardial Structure Alterations Across the Cardiac Cycle in Rats.

    PubMed

    David Gomez, Arnold; Bull, David A; Hsu, Edward W

    2015-10-01

    Myocardial microstructures are responsible for key aspects of cardiac mechanical function. Natural myocardial deformation across the cardiac cycle induces measurable structural alteration, which varies across disease states. Diffusion tensor magnetic resonance imaging (DT-MRI) has become the tool of choice for myocardial structural analysis. Yet, obtaining the comprehensive structural information of the whole organ, in 3D and time, for subject-specific examination is fundamentally limited by scan time. Therefore, subject-specific finite-element (FE) analysis of a group of rat hearts was implemented for extrapolating a set of initial DT-MRI to the rest of the cardiac cycle. The effect of material symmetry (isotropy, transverse isotropy, and orthotropy), structural input, and warping approach was observed by comparing simulated predictions against in vivo MRI displacement measurements and DT-MRI of an isolated heart preparation at relaxed, inflated, and contracture states. Overall, the results indicate that, while ventricular volume and circumferential strain are largely independent of the simulation strategy, structural alteration predictions are generally improved with the sophistication of the material model, which also enhances torsion and radial strain predictions. Moreover, whereas subject-specific transversely isotropic models produced the most accurate descriptions of fiber structural alterations, the orthotropic models best captured changes in sheet structure. These findings underscore the need for subject-specific input data, including structure, to extrapolate DT-MRI measurements across the cardiac cycle.

  17. Finite-Element Extrapolation of Myocardial Structure Alterations Across the Cardiac Cycle in Rats

    PubMed Central

    David Gomez, Arnold; Bull, David A.; Hsu, Edward W.

    2015-01-01

    Myocardial microstructures are responsible for key aspects of cardiac mechanical function. Natural myocardial deformation across the cardiac cycle induces measurable structural alteration, which varies across disease states. Diffusion tensor magnetic resonance imaging (DT-MRI) has become the tool of choice for myocardial structural analysis. Yet, obtaining the comprehensive structural information of the whole organ, in 3D and time, for subject-specific examination is fundamentally limited by scan time. Therefore, subject-specific finite-element (FE) analysis of a group of rat hearts was implemented for extrapolating a set of initial DT-MRI to the rest of the cardiac cycle. The effect of material symmetry (isotropy, transverse isotropy, and orthotropy), structural input, and warping approach was observed by comparing simulated predictions against in vivo MRI displacement measurements and DT-MRI of an isolated heart preparation at relaxed, inflated, and contracture states. Overall, the results indicate that, while ventricular volume and circumferential strain are largely independent of the simulation strategy, structural alteration predictions are generally improved with the sophistication of the material model, which also enhances torsion and radial strain predictions. Moreover, whereas subject-specific transversely isotropic models produced the most accurate descriptions of fiber structural alterations, the orthotropic models best captured changes in sheet structure. These findings underscore the need for subject-specific input data, including structure, to extrapolate DT-MRI measurements across the cardiac cycle. PMID:26299478

  18. Myocardial uptake of thallium and rubidium during alterations in perfusion and oxygenation in isolated rabbit hearts

    SciTech Connect

    Leppo, J.A.

    1987-05-01

    The comparative effects of altered cellular function and coronary perfusion on myocardial /sup 201/Tl and /sup 83/Rb uptake were evaluated in three groups of isolated rabbit hearts having isovolumic contractions. Paired-indication dilution experiments were performed with /sup 201/Tl, /sup 83/Rb, and /sup 111/In-labeled albumin as an intravascular reference marker. In Group A hearts (n = 12), isotope transport was determined during control, hypoxia, and ischemia. In Group B hearts (n = 8), isotope transport was measured at control flow and again at a 50% and 80% reduction. In Group C hearts (n = 8) only /sup 201/Tl uptake was determined at control and following coronary reperfusion. Myocardial /sup 201/Tl and /sup 83/Rb transport were not significantly different and were proportional to flow. Although all interventions caused significant hemodynamic alterations, neither tracer was affected by hypoxia at constant flow. Thallium-201 permeation, however, was transiently decreased immediately after coronary reperfusion. We conclude that myocardial uptake of /sup 201/Tl and /sup 83/Rb are similar and directly related to flow, but do not reflect hypoxia induced cellular dysfunction.

  19. Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus.

    PubMed

    Hardwick, Jean C; Ryan, Shannon E; Powers, Emily N; Southerland, E Marie; Ardell, Jeffrey L

    2015-07-15

    Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg(-1)·day(-1)), AT1 receptor antagonist (losartan, 3 mg·kg(-1)·day(-1)), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg(-1)·day(-1)) on remodeling of the guinea pig intrinsic cardiac plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the cardiac plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig cardiac plexus following MI is mediated, in part, by activation of both AT1 and AT2 receptors.

  20. Myocardial Reloading After Extracorporeal Membrane Oxygenation Alters Substrate Metabolism While Promoting Protein Synthesis

    PubMed Central

    Kajimoto, Masaki; O'Kelly Priddy, Colleen M.; Ledee, Dolena R.; Xu, Chun; Isern, Nancy; Olson, Aaron K.; Rosiers, Christine Des; Portman, Michael A.

    2013-01-01

    Background Extracorporeal membrane oxygenation (ECMO) unloads the heart, providing a bridge to recovery in children after myocardial stunning. ECMO also induces stress which can adversely affect the ability to reload or wean the heart from the circuit. Metabolic impairments induced by altered loading and/or stress conditions may impact weaning. However, cardiac substrate and amino acid requirements upon weaning are unknown. We assessed the hypothesis that ventricular reloading with ECMO modulates both substrate entry into the citric acid cycle (CAC) and myocardial protein synthesis. Methods and Results Sixteen immature piglets (7.8 to 15.6 kg) were separated into 2 groups based on ventricular loading status: 8‐hour ECMO (UNLOAD) and postwean from ECMO (RELOAD). We infused into the coronary artery [2‐13C]‐pyruvate as an oxidative substrate and [13C6]‐L‐leucine as an indicator for amino acid oxidation and protein synthesis. Upon RELOAD, each functional parameter, which were decreased substantially by ECMO, recovered to near‐baseline level with the exclusion of minimum dP/dt. Accordingly, myocardial oxygen consumption was also increased, indicating that overall mitochondrial metabolism was reestablished. At the metabolic level, when compared to UNLOAD, RELOAD altered the contribution of various substrates/pathways to tissue pyruvate formation, favoring exogenous pyruvate versus glycolysis, and acetyl‐CoA formation, shifting away from pyruvate decarboxylation to endogenous substrate, presumably fatty acids. Furthermore, there was also a significant increase of tissue concentrations for all CAC intermediates (≈80%), suggesting enhanced anaplerosis, and of fractional protein synthesis rates (>70%). Conclusions RELOAD alters both cytosolic and mitochondrial energy substrate metabolism, while favoring leucine incorporation into protein synthesis rather than oxidation in the CAC. Improved understanding of factors governing these metabolic perturbations may

  1. Percutaneous revascularization in acute myocardial infarction due to left main stem occlusion.

    PubMed

    Valeur, Nana; Gaster, Anne Louise; Saunamäki, Kari

    2005-04-01

    Following the encouraging results of trials testing the effect of primary percutaneous coronary intervention (PCI) more cases of left main arterial stenosis (LMS) as culprit lesions in acute myocardial infarction (AMI) are being handled. Not many cases of primary PCI on LMS have been published. We present 12 cases of primary PCI on LMS. Eighty-three percent of the patients presented with cardiogenic shock and only 42% were discharged alive. Due to the high rate of cardiogenic shock at presentation, PCI seems to be the treatment of choice, over coronary artery bypass grafting (CABG), although one might consider using PCI as a bridge over to CABG.

  2. Mechanical Chest Compressions in Prolonged Cardiac Arrest due to ST Elevation Myocardial Infarction Can Cause Myocardial Contusion.

    PubMed

    Stechovsky, Cyril; Hajek, Petr; Cipro, Simon; Veselka, Josef

    2016-09-01

    Acute coronary syndrome is a common cause of sudden cardiac death. We present a case report of a 60-year-old man without a history of coronary artery disease who presented with ST-elevation myocardial infarction. During transportation to the hospital, he developed ventricular fibrillation (VF) and later pulseless electrical activity. Chest compressions with LUCAS 2 (Medtronic, Minneapolis, MN) automated mechanical compression-decompression device were initiated. Coronary angiography showed total occlusion of the left main coronary artery and primary percutaneous coronary intervention (PCI) was performed. After the PCI, his heart started to generate effective contractions and LUCAS could be discontinued. Return of spontaneous circulation was achieved after 90 minutes of cardiac arrest. The patient died of cardiogenic shock 11 hours later. An autopsy revealed a transmural anterolateral myocardial infarction but also massive subepicardial hemorrhage and interstitial edema and hemorrhages on histologic samples from regions of the myocardium outside the infarction itself and also from the right ventricle. These lesions were concluded to be a myocardial contusion. The true incidence of myocardial contusion as a consequence of mechanical chest compressions is not known. We speculate that severe myocardial contusion might have influenced outcome of our patient. PMID:27574387

  3. Primary percutaneous coronary intervention for acute myocardial infarction in a pediatric patient with giant coronary aneurysm due to Kawasaki disease.

    PubMed

    Mongiovì, Maurizio; Alaimo, Annalisa; Vernuccio, Federica; Pieri, Daniele

    2014-01-01

    We report a case of acute myocardial infarction in an 8-year-old boy with a history of Kawasaki disease and giant coronary aneurysms in the right and left coronary arteries. We performed coronary angiography and percutaneous coronary intervention 4 hours after the onset of symptoms. This case suggests that primary percutaneous coronary intervention might be safe and effective in the long-term treatment of acute myocardial infarction due to coronary sequelae of Kawasaki.

  4. Myocardial infarction in mice alters sarcomeric function via post-translational protein modification.

    PubMed

    Avner, Benjamin S; Shioura, Krystyna M; Scruggs, Sarah B; Grachoff, Milana; Geenen, David L; Helseth, Donald L; Farjah, Mariam; Goldspink, Paul H; Solaro, R John

    2012-04-01

    Myocardial physiology in the aftermath of myocardial infarction (MI) before remodeling is an under-explored area of investigation. Here, we describe the effects of MI on the cardiac sarcomere with focus on the possible contributions of reactive oxygen species. We surgically induced MI in 6-7-month-old female CD1 mice by ligation of the left anterior descending coronary artery. Data were collected 3-4 days after MI or sham (SH) surgery. MI hearts demonstrated ventricular dilatation and systolic dysfunction upon echo cardiographic analysis. Sub-maximum Ca-activated tension in detergent-extracted fiber bundles from papillary muscles increased significantly in the preparations from MI hearts. Ca(2+) sensitivity increased after MI, whereas cooperativity of activation decreased. To assess myosin enzymatic integrity we measured splitting of Ca-ATP in myofibrillar preparations, which demonstrated a decline in Ca-ATPase activity of myofilament myosin. Biochemical analysis demonstrated post-translational modification of sarcomeric proteins. Phosphorylation of cardiac troponin I and myosin light chain 2 was reduced after MI in papillary samples, as measured using a phospho-specific stain. Tropomyosin was oxidized after MI, forming disulfide products detectable by diagonal non-reducing-reducing SDS-PAGE. Our analysis of myocardial protein oxidation post-MI also demonstrated increased S-glutathionylation. We functionally linked protein oxidation with sarcomere function by treating skinned fibers with the sulfhydryl reducing agent dithiothreitol, which reduced Ca(2+) sensitivity in MI, but not SH, samples. Our data indicate important structural and functional alterations to the cardiac sarcomere after MI, and the contribution of protein oxidation to this process.

  5. Ultrastructural alterations in allylamine cardiovascular toxicity. Late myocardial and vascular lesions.

    PubMed Central

    Boor, P. J.; Ferrans, V. J.

    1985-01-01

    The late myocardial and vascular ultrastructural changes in rat hearts following consumption of the cardiovascular toxin allylamine were studied. Rats were given 0.1% allylamine HCl in drinking water for 10-104 days. From 10 to 21 days, there was organization of acute myocardial necrosis by macrophages and scattered polymorphonuclear leukocytes with prominent interstitial-cell proliferation. Alterations at 21-104 days included extensive scarring with formation of dense mature collagen with scattered fibroblasts present, grossly evident left-ventricular aneurysm, and gross and microscopic changes similar to those observed in the secondary form of endocardial fibroelastosis. Areas of scar contained highly cellular foci of smooth-muscle cells, myofibroblasts, and abundant extracellular elastin. Cardiac myocytes frequently showed markedly disorganized myofilaments, bizarrely distorted mitochondria with condensed cristae, and other severe degenerative changes. Small vessels within and adjacent to scar showed proliferation of intimal smooth-muscle cells. Endothelial lesions or recent or organized thrombi were not seen. Focal endocardial metaplasia, consisting of both chondroid and osseous tissue, was found in areas of transmural scarring, or ventricular aneurysm. Chondrocytes had the overall nuclear and cellular morphology, abundant rough endoplasmic reticulum, and surrounding lacunae typical of mature fibrocartilage. In some areas, the collagen matrix was undergoing calcification with the typical cross-banded pattern of calcifying connective tissue. Osteocytes were located in a densely calcified bone matrix and displayed characteristic cellular extensions into surrounding canaliculi. These findings indicate a severe myocardial, small-vessel, and endocardial injury during the course of chronic allylamine intoxication. Images Figure 13 Figure 14 Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 Figure 11 Figure 12 Figure 15 Figure

  6. Varying Definitions for Periprocedural Myocardial Infarction Alter Event Rates and Prognostic Implications

    PubMed Central

    Idris, Hanan; Lo, Sidney; Shugman, Ibrahim M.; Saad, Yousef; Hopkins, Andrew P.; Mussap, Christian; Leung, Dominic; Thomas, Liza; Juergens, Craig P.; French, John K.

    2014-01-01

    Background Periprocedural myocardial infarction (PMI) has had several definitions in the last decade, including the Society for Cardiovascular Angiography and Interventions (SCAI) definition, that requires marked biomarker elevations congruent with surgical PMI criteria. Methods and Results The aim of this study was to examine the definition‐based frequencies of PMI and whether they influenced the reported association between PMI and increased rates of late death/ myocardial infarction (MI). We studied 742 patients; 492 (66%) had normal troponin T (TnT) levels and 250 (34%) had elevated, but stable or falling, TnT levels. PMI, using the 2007 and the 2012 universal definition, occurred in 172 (23.2%) and in 99 (13.3%) patients, respectively, whereas 19 (2.6%) met the SCAI PMI definition (P<0.0001). Among patients with PMI using the 2012 definition, occlusion of a side branch ≤1 mm occurred in 48 patients (48.5%) and was the most common angiographic finding for PMI. The rates of death/MI at 2 years in patients with, compared to those without, PMI was 14.7% versus 10.1% (P=0.087) based on the 2007 definition, 16.9% versus 10.3% (P=0.059) based on the 2012 definition, and 29.4% versus 10.7% (P=0.015) based on the SCAI definition. Conclusion In this study, PMI, according to the SCAI definition, was associated with more‐frequent late death/MI, with ≈20% of all patients, who had PMI using the 2007 universal MI definition, not having SCAI‐defined PMI. Categorizing these latter patients as SCAI‐defined no PMI did not alter the rate of death/MI among no‐PMI patients. PMID:25359403

  7. Predictive Factors of Hospital Mortality Due to Myocardial Infarction: A Multilevel Analysis of Iran's National Data

    PubMed Central

    Ahmadi, Ali; Soori, Hamid; Mehrabi, Yadollah; Etemad, Koorosh; Sajjadi, Homeira; Sadeghi, Mehraban

    2015-01-01

    Background: Regarding failure to establish the statistical presuppositions for analysis of the data by conventional approaches, hierarchical structure of the data as well as the effect of higher-level variables, this study was conducted to determine the factors independently associated with hospital mortality due to myocardial infarction (MI) in Iran using a multilevel analysis. Methods: This study was a national, hospital-based, and cross-sectional study. In this study, the data of 20750 new MI patients between April, 2012 and March, 2013 in Iran were used. The hospital mortality due to MI was considered as the dependent variable. The demographic data, clinical and behavioral risk factors at the individual level and environmental data were gathered. Multilevel logistic regression models with Stata software were used to analyze the data. Results: Within 1-year of study, the frequency (%) of hospital mortality within 30 days of admission was derived 2511 (12.1%) patients. The adjusted odds ratio (OR) of mortality with (95% confidence interval [CI]) was derived 2.07 (95% CI: 1.5–2.8) for right bundle branch block, 1.5 (95% CI: 1.3–1.7) for ST-segment elevation MI, 1.3 (95% CI: 1.1–1.4) for female gender, and 1.2 (95% CI: 1.1–1.3) for humidity, all of which were considered as risk factors of mortality. But, OR of mortality was 0.7 for precipitation (95% CI: 0.7–0.8) and 0.5 for angioplasty (95% CI: 0.4–0.6) were considered as protective factors of mortality. Conclusions: Individual risk factors had independent effects on the hospital mortality due to MI. Variables in the province level had no significant effect on the outcome of MI. Increasing access and quality to treatment could reduce the mortality due to MI. PMID:26730342

  8. Alterations in vasomotor control of coronary resistance vessels in remodelled myocardium of swine with a recent myocardial infarction.

    PubMed

    Duncker, Dirk J; de Beer, Vincent J; Merkus, Daphne

    2008-05-01

    The mechanism underlying the progressive deterioration of left ventricular (LV) dysfunction after myocardial infarction (MI) towards overt heart failure remains incompletely understood, but may involve impairments in coronary blood flow regulation within remodelled myocardium leading to intermittent myocardial ischemia. Blood flow to the remodelled myocardium is hampered as the coronary vasculature does not grow commensurate with the increase in LV mass and because extravascular compression of the coronary vasculature is increased. In addition to these factors, an increase in coronary vasomotor tone, secondary to neurohumoral activation and endothelial dysfunction, could also contribute to the impaired myocardial oxygen supply. Consequently, we explored, in a series of studies, the alterations in regulation of coronary resistance vessel tone in remodelled myocardium of swine with a 2 to 3-week-old MI. These studies indicate that myocardial oxygen balance is perturbed in remodelled myocardium, thereby forcing the myocardium to increase its oxygen extraction. These perturbations do not appear to be the result of blunted beta-adrenergic or endothelial NO-mediated coronary vasodilator influences, and are opposed by an increased vasodilator influence through opening of K(ATP) channels. Unexpectedly, we observed that despite increased circulating levels of noradrenaline, angiotensin II and endothelin-1, alpha-adrenergic tone remained negligible, while the coronary vasoconstrictor influences of endogenous endothelin and angiotensin II were virtually abolished. We conclude that, early after MI, perturbations in myocardial oxygen balance are observed in remodelled myocardium. However, adaptive alterations in coronary resistance vessel control, consisting of increased vasodilator influences in conjunction with blunted vasoconstrictor influences, act to minimize the impairments of myocardial oxygen balance.

  9. Myocardial cell damage and cardiovascular changes due to i.v. infusion of adrenochrome in rats.

    PubMed Central

    Singal, P. K.; Dhillon, K. S.; Beamish, R. E.; Kapur, N.; Dhalla, N. S.

    1982-01-01

    In vivo effects of adrenochrome (1-32 mg/kg), an oxidation product of catecholamines, on the heart ultrastructure, ECG and blood pressure were studied in rats over a period of 60 min following a single i.v. injection of the drug. One milligram of the drug had no influence on the myocardium or the cardiovascular system, whereas maximum changes in these parameters were recorded at 32 mg/kg of adrenochrome. The maximum structural damage, reached within 5-10 min, included marked swelling of mitochondria and sarcotubular system, intracellular and perinuclear oedema, hypercontraction of myofibrils and partial separation of the intercalated disc. Ultrastructural changes in the myocardium due to 4 and 8 mg of adrenochrome were not accompanied by any cardiovascular effects and the changes were fully reversed within 60 min of the injection of the drug. However, at 16 and 32 mg/kg of adrenochrome both heart rate and blood pressure were depressed within 5 min of drug administration. At these concentrations of adrenochrome arrhythmias, mainly due to premature ventricular contractions, were also noticed. Ultrastructural and cardiovascular changes seen at these higher concentrations of adrenochrome showed only a partial recovery. The data indicates that adrenochrome-induced ultrastructural changes in the heart are due to a direct myocardial effect of the drug which may not involve haemodynamic changes and the latter are most probably a consequence of this effect. However, the present study has not been able to rule out direct vascular effects at higher concentrations of adrenochrome. Images Fig. 2 Fig. 3 Fig. 4 Fig. 5 Fig. 6 Fig. 7 Fig. 8 Fig. 9 PMID:7073958

  10. Cardiac-Specific Overexpression of Catalase Attenuates Paraquat-Induced Myocardial Geometric and Contractile Alteration: Role of ER Stress

    PubMed Central

    Ge, We; Zhang, Yingmei; Han, Xuefeng; Ren, Jun

    2010-01-01

    Paraquat, a quarternary nitrogen herbicide, is a highly toxic prooxidant resulting in multi-organ failure including the heart via generation of reactive oxygen species although the underlying mechanism has not been well elucidated. This study examined the influence of cardiac-specific overexpression of catalase, an antioxidant detoxifying H2O2, on paraquat-induced myocardial geometric and functional alterations, with a focus on ER stress. FVB and catalase transgenic mice were administrated paraquat for 48 hrs. Myocardial geometry, contractile function, apoptosis, and ER stress were evaluated using echocardiography, edge-detection, caspase-3 activity and immunoblotting. Our results revealed that paraquat treatment significantly enlarged LV end-diastolic and systolic diameters, increased LV mass and resting myocyte length, reduced fractional shortening, cardiomyocyte peak shortening, maximal velocity of shortening/relengthening and prolonged relengthening duration in FVB group. While catalase transgene itself did not alter myocardial geometry and function, it mitigated or significantly attenuated paraquat-elicited myocardial geometric and functional changes. Paraquat promoted overt apoptosis and ER stress as evidenced by increased caspase-3 activity, apoptosis and ER stress markers including Bax, Bcl-2, GADD153, calregulin and phosphorylation of JNK, IRE1α and eIF2α, all were ablated by catalase transgene. Paraquat-induced cardiomyocyte dysfunction was mitigated by the ER stress inhibitor tauroursodeoxycholic acid. Moreover, the JNK inhibitor SP600125 reversed paraquat-induced ER stress as evidenced by enhanced GADD153 and IRE1α phosphorylation. Taken together, these data revealed that catalase may rescue paraquat-induced myocardial geometric and functional alteration possibly via alleviating JNK-mediated ER stress. PMID:20937379

  11. Hydrologic property alterations due to elevated temperatures at Yucca Mountain

    SciTech Connect

    Flint, A.L.; Nash, M.H.; Nash, M.S.

    1994-12-31

    Yucca Mountain is currently being evaluated as a potential site for a high level nuclear waste repository. The pre-emplacement hydrologic properties of the rock are important in determining the suitability of the site; however, post emplacement thermal loads and associated drying may permanently alter the character of the rock. A preliminary study was undertaken to determine the effects of elevated temperatures on hydrologic properties of the welded Topopah Spring member of the Paintbrush Tuff and a zeolitic, nonwelded tuff from the Tuffaceous Beds of Calico Hills. Rock outcrop samples were collected and dried in the laboratory at different temperatures (up to 400 degrees C). Hydrologic and physical properties -were tested before and after each of the drying cycles.

  12. Acute Myocardial Infarction Due to Spontaneous Dissection of the Right Coronary Artery in a Young Male

    SciTech Connect

    Papadopoulos, Dimitris P. Moyssakis, Ioannis; Perakis, Alexandros; Athanasiou, Andreas; Anagnostopoulou, Sophia; Benos, Ioannis; Votteas, Vassilios E.

    2004-09-15

    Spontaneous coronary artery dissection is a rare cause of acute myocardial infarction. We report a case of a 33-year-old male who presented with an acute inferior myocardial infarction. Coronary arteriography performed 3 hours after the episode revealed a dissection involving the middle segment of right coronary artery. Because of a spiral form of dissection and the TIMI 3 flow grade, our patient was treated medically and repeat coronary angiography 6 months later was decided.

  13. Prenatal methamphetamine differentially alters myocardial sensitivity to ischemic injury in male and female adult hearts.

    PubMed

    Rorabaugh, Boyd R; Seeley, Sarah L; Bui, Albert D; Sprague, Lisanne; D'Souza, Manoranjan S

    2016-02-15

    Methamphetamine is one of the most common illicit drugs abused during pregnancy. The neurological effects of prenatal methamphetamine are well known. However, few studies have investigated the potential effects of prenatal methamphetamine on adult cardiovascular function. Previous work demonstrated that prenatal cocaine exposure increases sensitivity of the adult heart to ischemic injury. Methamphetamine and cocaine have different mechanisms of action, but both drugs exert their effects by increasing dopaminergic and adrenergic receptor stimulation. Thus the goal of this study was to determine whether prenatal methamphetamine also worsens ischemic injury in the adult heart. Pregnant rats were injected with methamphetamine (5 mg·kg(-1)·day(-1)) or saline throughout pregnancy. When pups reached 8 wk of age, their hearts were subjected to ischemia and reperfusion by means of a Langendorff isolated heart system. Prenatal methamphetamine had no significant effect on infarct size, preischemic contractile function, or postischemic recovery of contractile function in male hearts. However, methamphetamine-treated female hearts exhibited significantly larger infarcts and significantly elevated end-diastolic pressure during recovery from ischemia. Methamphetamine significantly reduced protein kinase Cε expression and Akt phosphorylation in female hearts but had no effect on these cardioprotective proteins in male hearts. These data indicate that prenatal methamphetamine differentially affects male and female sensitivity to myocardial ischemic injury and alters cardioprotective signaling proteins in the adult heart.

  14. Intraventricular flow alterations due to dyssynchronous wall motion

    NASA Astrophysics Data System (ADS)

    Pope, Audrey M.; Lai, Hong Kuan; Samaee, Milad; Santhanakrishnan, Arvind

    2015-11-01

    Roughly 30% of patients with systolic heart failure suffer from left ventricular dyssynchrony (LVD), in which mechanical discoordination of the ventricle walls leads to poor hemodynamics and suboptimal cardiac function. There is currently no clear mechanistic understanding of how abnormalities in septal-lateral (SL) wall motion affects left ventricle (LV) function, which is needed to improve the treatment of LVD using cardiac resynchronization therapy. We use an experimental flow phantom with an LV physical model to study mechanistic effects of SL wall motion delay on LV function. To simulate mechanical LVD, two rigid shafts were coupled to two segments (apical and mid sections) along the septal wall of the LV model. Flow through the LV model was driven using a piston pump, and stepper motors coupled to the above shafts were used to locally perturb the septal wall segments relative to the pump motion. 2D PIV was used to examine the intraventricular flow through the LV physical model. Alterations to SL delay results in a reduction in the kinetic energy (KE) of the flow field compared to synchronous SL motion. The effect of varying SL motion delay from 0% (synchronous) to 100% (out-of-phase) on KE and viscous dissipation will be presented. This research was supported by the Oklahoma Center for Advancement of Science and Technology (HR14-022).

  15. Altered responsiveness to chemokines due to targeted disruption of SHIP

    PubMed Central

    Kim, Chang H.; Hangoc, Giao; Cooper, Scott; Helgason, Cheryl D.; Yew, Sandie; Humphries, R. Keith; Krystal, Gerald; Broxmeyer, Hal E.

    1999-01-01

    SHIP has been implicated in negative signaling in a number of hematopoietic cell types and is postulated to downregulate phosphatidylinositol-3-kinase– (PI-3K–) initiated events in diverse receptor signaling pathways. Because PI-3K is implicated in chemokine signaling, we investigated whether SHIP plays any role in cellular responses to chemokines. We found that a number of immature and mature hematopoietic cells from SHIP-deficient mice manifested enhanced directional migration (chemotaxis) in response to the chemokines stromal cell–derived factor-1 (SDF-1) and B-lymphocyte chemoattractant (BLC). SHIP–/– cells were also more active in calcium influx and actin polymerization in response to SDF-1. However, colony formation by SHIP-deficient hematopoietic progenitor cell (HPCs) was not inhibited by 13 myelosuppressive chemokines that normally inhibit proliferation of HPCs. These altered biologic activities of chemokines on SHIP-deficient cells are not caused by simple modulation of chemokine receptor expression in SHIP-deficient mice, implicating SHIP in the modulation of chemokine-induced signaling and downstream effects. J. Clin. Invest. 104:1751–1759 (1999). PMID:10606629

  16. Alteration in metabolic signature and lipid metabolism in patients with angina pectoris and myocardial infarction.

    PubMed

    Park, Ju Yeon; Lee, Sang-Hak; Shin, Min-Jeong; Hwang, Geum-Sook

    2015-01-01

    Lipid metabolites are indispensable regulators of physiological and pathological processes, including atherosclerosis and coronary artery disease (CAD). However, the complex changes in lipid metabolites and metabolism that occur in patients with these conditions are incompletely understood. We performed lipid profiling to identify alterations in lipid metabolism in patients with angina and myocardial infarction (MI). Global lipid profiling was applied to serum samples from patients with CAD (angina and MI) and age-, sex-, and body mass index-matched healthy subjects using ultra-performance liquid chromatography/quadruple time-of-flight mass spectrometry and multivariate statistical analysis. A multivariate analysis showed a clear separation between the patients with CAD and normal controls. Lysophosphatidylcholine (lysoPC) and lysophosphatidylethanolamine (lysoPE) species containing unsaturated fatty acids and free fatty acids were associated with an increased risk of CAD, whereas species of lysoPC and lyso-alkyl PC containing saturated fatty acids were associated with a decreased risk. Additionally, PC species containing palmitic acid, diacylglycerol, sphingomyelin, and ceramide were associated with an increased risk of MI, whereas PE-plasmalogen and phosphatidylinositol species were associated with a decreased risk. In MI patients, we found strong positive correlation between lipid metabolites related to the sphingolipid pathway, sphingomyelin, and ceramide and acute inflammatory markers (high-sensitivity C-reactive protein). The results of this study demonstrate altered signatures in lipid metabolism in patients with angina or MI. Lipidomic profiling could provide the information to identity the specific lipid metabolites under the presence of disturbed metabolic pathways in patients with CAD.

  17. Both enalapril and losartan attenuate sarcolemmal Na+-K+-ATPase remodeling in failing rat heart due to myocardial infarction.

    PubMed

    Guo, Xiaobing; Wang, Jingwei; Elimban, Vijayan; Dhalla, Naranjan S

    2008-04-01

    To investigate the mechanisms underlying the depressed sarcolemmal (SL) Na(+)-K(+)-ATPase activity in congestive heart failure (CHF), different isoforms and gene expression of Na(+)-K(+)-ATPase were examined in the failing left ventricle (LV) at 8 weeks after myocardial infarction (MI). In view of the increased activity of renin-angiotensin system (RAS) in CHF, these parameters were also studied after 5 weeks of treatment with enalapril (10 mg x kg-1 x day-1), an angiotensin-converting enzyme inhibitor, and losartan (20 mg.kg-1.day-1), an angiotensin II type 1 receptor antagonist, starting at 3 weeks after the coronary ligation in rats. The infarcted animals showed LV dysfunction and depressed SL Na(+)-K(+)-ATPase activity. Protein content and mRNA levels for Na(+)-K(+)-ATPase alpha2 isoform were decreased whereas those for Na(+)-K(+)-ATPase alpha3 isoform were increased in the failing LV. On the other hand, no significant changes were observed in protein content or mRNA levels for Na(+)-K(+)-ATPase alpha1 and beta1 isoforms. The treatment of infarcted animals with enalapril or losartan improved LV function and attenuated the depression in Na(+)-K(+)-ATPase alpha2 isoform as well as the increase in alpha3 isoform, at both the protein and mRNA levels; however, combination therapy with enalapril and losartan did not produce any additive effects. These results provide further evidence that CHF due to MI is associated with remodeling of SL membrane and suggest that the blockade of RAS plays an important role in preventing these alterations in the failing heart.

  18. Catecholamines and myocardial contractile function during hypodynamia and with an altered thyroid hormone balance

    NASA Technical Reports Server (NTRS)

    Pruss, G. M.; Kuznetsov, V. I.; Zhilinskaya, A. A.

    1980-01-01

    The dynamics of catecholamine content and myocardial contractile function during hypodynamia were studied in 109 white rats whose motor activity was severely restricted for up to 30 days. During the first five days myocardial catecholamine content, contractile function, and physical load tolerance decreased. Small doses of thyroidin counteracted this tendency. After 15 days, noradrenalin content and other indices approached normal levels and, after 30 days, were the same as control levels, although cardiac functional reserve was decreased. Thyroidin administration after 15 days had no noticeable effect. A detailed table shows changes in 17 indices of myocardial contractile function during hypodynamia.

  19. Pseudo-acute myocardial infarction due to transient apical ventricular dysfunction syndrome (Takotsubo syndrome)

    PubMed Central

    Maciel, Bruno Araújo; Cidrão, Alan Alves de Lima; Sousa, Ítalo Bruno dos Santos; Ferreira, José Adailson da Silva; Messias Neto, Valdevino Pedro

    2013-01-01

    Takotsubo syndrome is characterized by predominantly medial-apical transient left ventricular dysfunction, which is typically triggered by physical or emotional stress. The present article reports the case of a 61-year-old female patient presenting with dizziness, excessive sweating, and sudden state of ill feeling following an episode involving intense emotional stress. The physical examination and electrocardiogram were normal upon admission, but the troponin I and creatine kinase-MB concentrations were increased. Acute myocardial infarction without ST segment elevation was suspected, and coronary angiography was immediately performed, which showed severe diffuse left ventricular hypokinesia, medial-apical systolic ballooning, and a lack of significant coronary injury. The patient was referred to the intensive care unit and was successfully treated with supportive therapy. As this case shows, Takotsubo syndrome might simulate the clinical manifestations of acute myocardial infarction, and coronary angiography is necessary to distinguish between both myocardial infarction and myocardial infarction in the acute stage. The present patient progressed with spontaneous resolution of the ventricular dysfunction without any sequelae. PMID:23887762

  20. Coronary steal due to ruptured right coronary aneurysm causing myocardial infarction in a patient with systemic lupus erythematosus.

    PubMed

    Hirata, Kazuhito; Yagi, Nobuhito; Wake, Minoru; Takahashi, Takanori; Nakazato, Jun; Miyagi, Tadayoshi; Shimotakahara, Junichi

    2014-08-01

    A 34-year-old female with a history of systemic lupus erythematosus (SLE) developed an acute inferior myocardial infarction while hospitalized for methicillin-resistant Staphylococcus Aureus sepsis. An emergent coronary angiography revealed an ectatic proximal left coronary artery and a huge aneurysm (37 mm × 32 mm) in the mid-portion of the right coronary artery, which had ruptured into the right atrium. A "steal phenomenon" due to significant left to right shunt resulting from the ruptured aneurysm was the cause of the myocardial infarction. Infection of the wall of the aneurysm might have contributed to the growth and the rupture in the presence of a pre-existing coronary aneurysm.

  1. A case of acute myocardial infarction due to the use of cayenne pepper pills.

    PubMed

    Sayin, Muhammet Rasit; Karabag, Turgut; Dogan, Sait Mesut; Akpinar, Ibrahim; Aydin, Mustafa

    2012-04-01

    The use of weight loss pills containing cayenne pepper has ever been increasing. The main component of cayenne pepper pills is capsaicin. There are conflicting data about the effects of capsaicin on the cardiovascular system. In this paper, we present the case of a 41 year old male patient with no cardiovascular risk factors who took cayenne pepper pills to lose weight and developed acute myocardial infarction.

  2. Acute inferior myocardial infarction due to cannabis smoking in a young man.

    PubMed

    Kocabay, Gonenc; Yildiz, Mustafa; Duran, Nilufer Eksi; Ozkan, Mehmet

    2009-09-01

    Cannabis smoking, which has euphoric effects, is consistently increasing in Europe. Smoking cannabis is a rare trigger of acute myocardial infarction (MI) by inducing coronary artery spasm. Some cases who have thrombus formation in acute coronary artery and no serious atherosclerotic lesions have been reported in the literature. These cases had involved the left coronary artery. Although some cases were reported with MI after cannabis smoking, only two case reports with inferior MI after cannabis smoking were reported in the literature. The present report is of a young male patient who was affected by acute inferior MI half an hour after cannabis smoking. PMID:19436220

  3. ST segment elevation myocardial infarction due to slow coronary flow occurring after cannabis consumption.

    PubMed

    Karabulut, Ahmet; Cakmak, Mahmut

    2010-11-01

    Slow coronary flow (SCF) is an angiographic finding defined as the slow movement of contrast throughout the coronary lumen in the absence of epicardial coronary stenosis. It has been reported that SCF can on rare occasions cause ST elevated myocardial infarction (MI). Recent studies have shown that cannabis consumption can increase the risk of coronary heart disease and can trigger acute coronary syndromes, especially in young individuals without common risk factors. Here, we present a case of inferior MI in a patient who had consumed cannabis regularly over a long period and whose coronary angiography revealed SCF. PMID:21108208

  4. Acute Myocardial Infarction Following Right Coronary Artery Dissection due to Blunt Trauma

    PubMed Central

    Mubang, Ronnie N.; Hillman Terzian, W. T.; Cipolla, James; Keeney, Scott; Lukaszczyk, John J.; Stawicki, Stanislaw P.

    2016-01-01

    Despite the frequent occurrence of blunt chest trauma, associated cardiac injuries are relatively rare. The most common presentation of blunt cardiac injury is benign arrhythmia (e.g., sinus tachycardia), followed in decreasing frequency by increasingly severe arrhythmias and finally physically evident injuries to the heart muscle, the conducting system, cardiac valves, and/or coronary vessels. Here we present an unusual case of a patient who sustained a right coronary artery dissection and associated acute myocardial infarction following a motor vehicle crash. PMID:27293529

  5. Time dependent alterations of serum matrix metalloproteinase-1 and metalloproteinase-1 tissue inhibitor after successful reperfusion of acute myocardial infarction.

    PubMed Central

    Hirohata, S.; Kusachi, S.; Murakami, M.; Murakami, T.; Sano, I.; Watanabe, T.; Komatsubara, I.; Kondo, J.; Tsuji, T.

    1997-01-01

    OBJECTIVE: To test the hypothesis that changes in serum matrix metalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) after acute myocardial infarction reflect extracellular matrix remodelling and the infarct healing process. PATIENTS: 13 consecutive patients with their first acute myocardial infarction who underwent successful reperfusion. METHODS: Blood was sampled on the day of admission, and on days 2, 3, 4, 5, 7, 14, and 28. Serum MMP-1 and TIMP-1 were measured by one step sandwich enzyme immunoassay. Left ventricular volume indices were determined by left ventriculography performed four weeks after the infarct. RESULTS: Serum concentrations of both MMP-1 and TIMP-1 changed over time. The average serum MMP-1 was more than 1 SD below the mean control values during the initial four days, increased thereafter, reaching a peak concentration around day 14, and then returned to the middle control range. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum MMP-1 on day 5, when it began to rise, and for the magnitude of rise in MMP-1 on day 5 compared to admission. Serum TIMP-1 at admission was more than 1 SD below the mean control value, and increased gradually thereafter, reaching a peak on around day 14. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum TIMP-1 on days 5 and 7, and for the magnitude of rise in TIMP-1 on days 5 and 7 compared to admission. CONCLUSIONS: Both MMP-1 and TIMP-1 showed significant time dependent alteration after acute myocardial infarction. Thus MMP-1 and TIMP-1 may provide useful information in evaluating the healing process as it affects left ventricular remodelling after acute myocardial infarction. PMID:9391291

  6. Acute ST-elevation myocardial infarction due to septic embolism: a case report and review of management options.

    PubMed

    Singh, Maninder; Mishra, Abhishek; Kaluski, Edo

    2015-05-01

    Acute ST-elevation myocardial (STEMI) infarction due to septic embolism is rare and management strategies differ from those applied to atherothrombotic STEMI. A 70-year-old male with aortic valve endocarditis and persistent bacteremia developed acute inferior wall STEMI due to septic embolism. Due to inferior STEMI accompanied by hemodynamic instability, coronary angiography and primary PCI (stenting) to a totally occluded right coronary artery (RCA) was performed. Despite excellent immediate angiographic results and hemodynamic stabilization, repeat angiogram two weeks later showed mycotic aneurysms at the site of stent placement. Patient later suffered from intracranial hemorrhage and splenic infarct and had worsening aortic regurgitation, prompting surgical aortic valve replacement with bypass of the RCA. Despite aggressive medical, interventional and surgical management, he expired four weeks after the surgery. Selection of an optimal revascularization strategy in this scenario is unclear with a potential harm from standard therapies. We have reviewed prior reports and summarized results in a tabular form.

  7. Acute myocardial infarction due to coronary thrombosis caused by blunt chest trauma

    PubMed Central

    Treuth, Gregory M; Baibars, Motaz; Alraiyes, Abdul Hamid; Alraies, M Chadi

    2014-01-01

    A 65-year-old man presented to the emergency department following an anterior chest trauma. He had significant chest pain and chest X-ray was significant for revealed multiple rib fractures and negative. CT scan of the chest ruled out pulmonary embolism or aortic dissection. However, few hours later he developed hypotension requiring admission to medical intensive care unit and intravenous vasopressors. Further workup showed ST elevation myocardial infarction involving the anterior ECG leads. Emergent coronary angiography was performed with intervention to the mid-left anterior descending occlusion. Cardiogenic shock resolved and patient was discharged few days later. One-year follow-up with echocardiogram showed stable ischaemic cardiomyopathy with improved left ventricular ejection fraction to 50%. PMID:24769662

  8. Acute Myocardial Infarction in a Young Lady due to Vitamin B12 Deficiency Induced Hyperhomocysteinemia.

    PubMed

    Shamkani, Warkaa Al; Jafar, Nagham Saeed; Narayanan, Sunil Roy; Rajappan, Anil Kumar

    2015-01-01

    Hyper-homocysteinemia is a risk factor for coronary artery disease in young patients. A 32 years old female without any conventional risk factors except obesity presented with acute anterior wall myocardial infarction (MI). Her echocardiography showed anterior wall hypokinesia with moderate left ventricular dysfunction. Angiography showed tight stenosis of the proximal left anterior descending (LAD) and borderline lesion in left circumflex coronary artery (LCX). She underwent percutaneous coronary intervention (PCI) to LAD with good result. Her blood tests showed low vitamin B12, folate and serum iron levels and elevated serum homocysteine level. She was given folic acid and vitamin B12 and her homocysteine levels normalized. This case demonstrates that hyperhomocysteinemia caused by nutritional deficiency of vitamin co factors may lead to MI. Hyperhomocysteinemia should be considered in the evalauation of young people with MI, especially those without conventional risk factors.

  9. Acute Myocardial Infarction in a Young Lady due to Vitamin B12 Deficiency Induced Hyperhomocysteinemia

    PubMed Central

    Shamkani, Warkaa Al; Jafar, Nagham Saeed; Narayanan, Sunil Roy; Rajappan, Anil Kumar

    2015-01-01

    Hyper-homocysteinemia is a risk factor for coronary artery disease in young patients. A 32 years old female without any conventional risk factors except obesity presented with acute anterior wall myocardial infarction (MI). Her echocardiography showed anterior wall hypokinesia with moderate left ventricular dysfunction. Angiography showed tight stenosis of the proximal left anterior descending (LAD) and borderline lesion in left circumflex coronary artery (LCX). She underwent percutaneous coronary intervention (PCI) to LAD with good result. Her blood tests showed low vitamin B12, folate and serum iron levels and elevated serum homocysteine level. She was given folic acid and vitamin B12 and her homocysteine levels normalized. This case demonstrates that hyperhomocysteinemia caused by nutritional deficiency of vitamin co factors may lead to MI. Hyperhomocysteinemia should be considered in the evalauation of young people with MI, especially those without conventional risk factors. PMID:25838876

  10. [Cardiac Angiosarcoma with Acute Myocardial Infarction due to Tumor Embolism;Report of a Case].

    PubMed

    Date, Yusuke; Miyazu, Katsuyuki; Ikeda, Masahiro

    2016-09-01

    We report the case of a 28-year-old man with a rare angiosarcoma complicated by acute myocardial infarction secondary to tumor embolism. He was transported to our emergency unit because of sudden onset of chest pain. The echocardiography showed a 42×60 mm mass in the left ventricle, and the coronary angiography showed embolic occlusion of the proximal left anterior descending and circumflex arteries. Emergent surgical removal of the mass was attempted under cardiopulmonary bypass, concomitant with double coronary artery bypass grafting and mitral valve replacement with a mechanical prosthesis. However, complete tumor excision was impossible. The postoperative pathological examination revealed undifferentiated angiosarcoma. Twenty days after the operation, the patient suffered acute cerebral hemorrhage from a metastatic tumor in the brain. He died at 37 days after the initial cardiac surgery. PMID:27586319

  11. Myocardial Reloading after Extracorporeal Membrane Oxygenation Alters Substrate Metabolism While Promoting Protein Synthesis

    SciTech Connect

    Kajimoto, Masaki; Priddy, Colleen M.; Ledee, Dolena; Xu, Chun; Isern, Nancy G.; Olson, Aaron; Des Rosiers, Christine; Portman, Michael A.

    2013-08-19

    Extracorporeal membrane oxygenation (ECMO) unloads the heart providing a bridge to recovery in children after myocardial stunning. Mortality after ECMO remains high.Cardiac substrate and amino acid requirements upon weaning are unknown and may impact recovery. We assessed the hypothesis that ventricular reloading modulates both substrate entry into the citric acid cycle (CAC) and myocardial protein synthesis. Fourteen immature piglets (7.8-15.6 kg) were separated into 2 groups based on ventricular loading status: 8 hour-ECMO (UNLOAD) and post-wean from ECMO (RELOAD). We infused [2-13C]-pyruvate as an oxidative substrate and [13C6]-L-leucine, as a tracer of amino acid oxidation and protein synthesis into the coronary artery. RELOAD showed marked elevations in myocardial oxygen consumption above baseline and UNLOAD. Pyruvate uptake was markedly increased though RELOAD decreased pyruvate contribution to oxidative CAC metabolism.RELOAD also increased absolute concentrations of all CAC intermediates, while maintaining or increasing 13C-molar percent enrichment. RELOAD also significantly increased cardiac fractional protein synthesis rates by >70% over UNLOAD. Conclusions: RELOAD produced high energy metabolic requirement and rebound protein synthesis. Relative pyruvate decarboxylation decreased with RELOAD while promoting anaplerotic pyruvate carboxylation and amino acid incorporation into protein rather than to the CAC for oxidation. These perturbations may serve as therapeutic targets to improve contractile function after ECMO.

  12. The Frequency and Significance of Silent Myocardial Ischemia Due to Hyoscine Butylbromide Use in Peripheral Angiography

    SciTech Connect

    Maher, Richard; Phillips-Hughes, Jane; Banning, Adrian; Boardman, Philip

    1999-09-15

    Purpose: Hyoscine-N-butylbromide (HB) is an anticholinergic drug used in digital subtraction angiography of the aortoiliac region because it decreases bowel gas movement artifact. HB also causes an increase in heart rate. We investigated whether this could cause silent myocardial ischemia (SMI) in susceptible patients during peripheral angiography. Methods: Thirty-six patients undergoing peripheral angiography were randomized into two groups, with 17 patients receiving 20 mg HB intraarterially during the angiogram and 19 patients receiving no drug. All patients were fitted with a Holter monitor that recorded the electrocardiogram before, during, and after the angiogram. Heart rate trends and ST segments were then analyzed. Results: Patients given HB had a statistically significant rise in heart rate compared with the control group. Although the difference was not statistically significant, two (12%) patients receiving HB had procedural ST depression compared with none in the control group. Pre- and postprocedural episodes of ST depression were common, occurring in 41% of patients receiving HB and 37% of patients receiving no drug, and were associated with an increase in heart rate. Conclusion: The infrequent episodes of procedural SMI, potentially caused by the positive chronotropic effects of HB, are probably insignificant when compared with the high frequency of SMI episodes occurring outside the procedure.

  13. Alteration in the global and regional myocardial strain patterns in patients with inferior ST-elevation myocardial infarction prior to and after percutaneous coronary intervention.

    PubMed

    Song, Chen-Fang; Zhou, Qing; Guo, Rui-Qiang

    2014-01-01

    This study was designed to investigate the alteration on regional and global strains of left and right ventricle (LV, RV) in patients with inferior wall ST-elevation myocardial infarction (MI). Patients were examined prior to and 7 days after percutaneous coronary intervention (PCI) using speckle-tracking techniques. Fifty-nine patients (36 males and 23 females) and 60 healthy controls (40 males and 20 females) were enrolled in this study. LV strains were measured from three deformations including radial, longitudinal, and circumferential. RV strains were measured only from the longitudinal. Three types of LV global strains were significantly lower in patients than in controls, and LV global longitudinal and circumferential strains were moderately improved by PCI. The LV regional strains reduced significantly in most of the segments (87%) after inferior wall MI and over half of them (60%) were improved by PCI. The RV global longitudinal strains were significantly lower in patients than in controls, and they were moderately improved by PCI. In conclusion, the regional and global strains of LV and RV were reduced in patients with inferior wall MI, and PCI most markedly improved the global strains and regional strains of the infarct and adjacent myocardium in the apical and middle levels.

  14. [Ischemia-reperfusion myocardial injury].

    PubMed

    de Micheli, Alfredo; Chávez, Edmundo

    2003-01-01

    In this article, we present some considerations on the myocardial damage due to a deficit of oxygen supply. In fact, this damage properly constitutes a partial diastolic depolarization or injury, i.e., a moderate reduction of the rest transmembrane potential. This phenomenon is characteristic of the acute phase of the myocardial infarction syndrome and is responsible for the main electrical manifestations appearing in this phase: disorders of rhythm and conduction, as well as a reduced contractility of the involved myocardial fibers. All the mentioned phenomena are due to a defect of the myocardial energetic mechanisms, owing to the mitochondrial alterations in myocytes: early reduction of the nicotinamide adenine nucleotides, accumulation of calcium ("calcium overload") into mitochondria, and a drop in oxidative phosphorylation. These changes can present again, more exaggerated, in a following phase of evolution of the myocardial infarction due to myocardial reperfusion. Its severity is related to the duration of the initial ischemia period. Moreover, consequences of the oxidative stress can add producing cellular damage by liberation of reactive oxygen species. Oxidant stress causes also alterations in the mitochondrial DNA, i.e., mutations due to oxidation of nitrogenous bases. During the initial ischemia phase, as well as during reperfusion, metabolic therapy can be very useful as, for example, glucose-insulin-potassium solutions (G-I-K). These could act as scavengers of the free radicals derived from oxygen and avoid or reduce the myocardial damage due to reperfused myocytes. Metabolic drugs, as for example trimetazidine, antioxidants, etc, can also be used in the myocardial reperfusion phase.

  15. Acute myocardial infarction due to left main coronary artery disease in men and women: does ST-segment elevation matter?

    PubMed Central

    Gutkowski, Wojciech; Raczyński, Grzegorz; Janion-Sadowska, Agnieszka; Gierlotka, Marek; Poloński, Lech

    2015-01-01

    Introduction Gender-specific issues regarding ST-segment elevation (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) due to unprotected left main coronary artery (ULMCA) disease were not sufficiently studied. We assessed the value of STEMI/NSTEMI initial classification on the management of men and women with acute MI due to critical stenosis or occlusion of the ULMCA. Material and methods The study group consisted of 643 consecutive patients with acute MI with the ULMCA as the infarct-related artery. Data derive from an ongoing, nationwide, multicenter, prospective, observational registry. Results Isolated ULMCA disease was more frequent in women and multivessel disease was more frequent in men in the NSTEMI group. The incidence of cardiogenic shock or pulmonary edema and cardiac arrest was higher in the STEMI group. Totally occluded ULMCA was more frequent in the STEMI group. Although the majority of patients underwent percutaneous coronary intervention (PCI), it was less frequently used in NSTEMI women and NSTEMI men. Although in-hospital and long-term mortality rates were higher in the STEMI group, there were no gender-related differences within groups. The initial ST-segment elevation was an independent predictor of in-hospital (OR = 2.37, 95% CI: 1.14–4.91, p = 0.02) and 12-month (OR = 1.52, 95% CI: 1.01–2.27, p = 0.045) mortality. Conclusions There were no gender-related differences in the management within the STEMI or NSTEMI group. Although acute myocardial infarction due to ULMCA disease is associated with high mortality in both genders, STEMI was a negative prognostic factor of in-hospital and 12-month mortality. Despite poor baseline characteristics and clinical presentation in women, female gender itself did not influence mortality. PMID:26788080

  16. Sudden death of a child from myocardial infarction due to arteritis of the left coronary trunk.

    PubMed

    Takahashi, Shirushi; Takada, Aya; Saito, Kazuyuki; Hara, Masaaki; Yoneyama, Katsumi; Nakanishi, Hiroaki; Takahashi, Kei; Moriya, Takuya; Funayama, Masato

    2015-01-01

    An eight-year-old Japanese boy developed abdominal pain, followed by convulsion and loss of consciousness. He was taken to an emergency room but could not be resuscitated. At autopsy, the left main coronary trunk (LMT) demonstrated an increase in caliber with severe luminal narrowing, and the left anterior descending branch (LAD) subsequent to the LMT showed severe stenosis. Microscopically, the intima of the LMT demonstrated severe fibrosis and infiltration of lymphocytes and histiocytes suggesting vasculitis, and the small lumen was occupied by a fresh thrombus. The LAD showed significant intimal thickening with strong lymphocytic inflammation at the edge of the thickening. The left ventricle showed widespread myocardial infarction in the recovery stage. There were no findings of atherosclerosis, vasculitis or fibrocellular changes in the ascending aorta or intravisceral arteries other than the LMT and the LAD under investigation. The increase in the caliber of the LMT and the limitation of arteritis to the LMT and the subsequent branch suggested Kawasaki disease (KD), but it was atypical that the patient had no clinical history consistent with KD. The present case showed no findings suggesting classical polyarteritis nodosa (cPAN) at the acute or scar stage in the other vessels being investigated, and cPAN in childhood is rare compared to KD. A nonspecific inflammatory reaction (single organ vasculitis, SOV) was also considered as a possible cause, but it is difficult to determine whether the cause of the coronary stenosis in the present case was SOV because the sampling of arteries was insufficient. If forensic pathologists make unusual findings suggesting vasculitis at autopsy, the collection of a sufficient number of vessels of various sizes is warranted. PMID:25239164

  17. Pronounced alterations of cellular metabolism and structure due to hyper- or hypo-osmosis.

    PubMed

    Mao, Lei; Hartl, Daniela; Nolden, Tobias; Koppelstätter, Andrea; Klose, Joachim; Himmelbauer, Heinz; Zabel, Claus

    2008-09-01

    Cell volume alteration represents an important factor contributing to the pathology of late-onset diseases. Previously, it was reported that protein biosynthesis and degradation are inversely (trans) regulated during cell volume regulation. Upon cell shrinkage, protein biosynthesis was up-regulated and protein degradation down-regulated. Cell swelling showed opposite regulation. Recent evidence suggests a decrease of protein biodegradation activity in many neurodegenerative diseases and even during aging; both also show prominent cell shrinkage. To clarify the effect of cell volume regulation on the overall protein turnover dynamics, we investigated mouse embryonic stem cells under hyper- and hypotonic osmotic conditions using a 2-D gel based proteomics approach. These conditions cause cell swelling and shrinkage, respectively. Our results demonstrate that the adaption to altered osmotic conditions and therefore cell volume alterations affects a broad spectrum of cellular pathways, including stress response, cytoskeleton remodeling and importantly, cellular metabolism and protein degradation. Interestingly, protein synthesis and degradation appears to be cis-regulated (same direction) on a global level. Our findings also support the hypothesis that protein alterations due to osmotic stress contribute to the pathology of neurodegenerative diseases due to a 60% expression overlap with proteins found altered in Alzheimer's, Huntington's, or Parkinson's disease. Eighteen percent of the proteins altered are even shared with all three disorders. PMID:18646788

  18. Evidence Report: Risk of Crew Adverse Health Event Due to Altered Immune Response

    NASA Technical Reports Server (NTRS)

    Crucian, Brian; Sams, Clarence F.

    2013-01-01

    The Risk of Crew Adverse Health Event Due to Altered Immune Response is identified by the National Aeronautics and Space Administration (NASA) Human Research Program (HRP) as a recognized risk to human health and performance in space. The HRP Program Requirements Document (PRD) defines these risks. This Evidence Report provides a summary of the evidence that has been used to identify and characterize this risk. It is known that human immune function is altered in- and post-flight, but it is unclear at present if such alterations lead to increased susceptibility to disease. Reactivation of latent viruses has been documented in crewmembers, although this reactivation has not been directly correlated with immune changes or with observed diseases. As described in this report, further research is required to better characterize the relationships between altered immune response and susceptibility to disease during and after spaceflight. This is particularly important for future deep-space exploration missions.

  19. Interrelation between Alterations in Pulmonary Mechanics and hemodynamics in Acute Myocardial Infarction

    PubMed Central

    Interiano, Benjamin; Hyde, Richard W.; Hodges, Morrison; Yu, Paul N.

    1973-01-01

    Pulmonary mechanics were evaluated in 30 patients with acute myocardial infarction by measuring forced expiratory flow rates and total pulmonary resistance (RT) with the oscillometric method at the resonant frequency of the chest (6-8) cycle/s). During the first 3 days after infarction, forced expiratory volume (FEV) and forced mid-expiratory flow rate (FEF25-75%) were 69% and 60% of predicted values, respectively. 10 or more wk later these values were 95% and 91%. Initially, RT was 52% greater than predicted, but was only 4% greater 10 or more wk later. In 11 patients RT was measured at both resonant frequency and at 3 cycle/s. Five of these patients had no clinical signs of heart failure, but nine had abnormally high values of pulmonary artery pressure, “wedge” pressure and pulmonary extravascular water volume. All of these patients recovered. Initially, RT at resonance was 50% and RT at 3 cycle/s was 130% greater than predicted values. 2-3 wk later these figures were -3% and +6% of those predicted, respectively. At 10 wk or more, significant frequency dependence of RT had disappeared (RT at 3 cycle/s was 7% greater than RT at resonance). Isoproterenol inhalation in six patients caused no change in flow rates, RT at resonance, or RT at 3 cycle/s. RT at resonance and at 3 cycle/s, FEV, and FEF25-75% correlated significantly with the pulmonary vascular pressures. Patients with more marked arterial hypoxia and larger values for extravascular water volume had greater elevations of RT and depression of FEF25-75%, but linear correlations were not significant. Clinical signs of congestive heart failure significantly correlated with a fall in FEV and FEF25-75%, the development of frequency dependence of RT, and elevation of the pulmonary wedge pressure. The initial elevation of RT and low flow rates indicate a modest degree of airway obstruction in acute myocardial infarction. Lack of response to isoproterenol suggests that bronchial muscular constriction is not a

  20. Myocardial MiR-30 downregulation triggered by doxorubicin drives alterations in β-adrenergic signaling and enhances apoptosis.

    PubMed

    Roca-Alonso, L; Castellano, L; Mills, A; Dabrowska, A F; Sikkel, M B; Pellegrino, L; Jacob, J; Frampton, A E; Krell, J; Coombes, R C; Harding, S E; Lyon, A R; Stebbing, J

    2015-01-01

    The use of anthracyclines such as doxorubicin (DOX) has improved outcome in cancer patients, yet associated risks of cardiomyopathy have limited their clinical application. DOX-associated cardiotoxicity is frequently irreversible and typically progresses to heart failure (HF) but our understanding of molecular mechanisms underlying this and essential for development of cardioprotective strategies remains largely obscure. As microRNAs (miRNAs) have been shown to play potent regulatory roles in both cardiovascular disease and cancer, we investigated miRNA changes in DOX-induced HF and the alteration of cellular processes downstream. Myocardial miRNA profiling was performed after DOX-induced injury, either via acute application to isolated cardiomyocytes or via chronic exposure in vivo, and compared with miRNA profiles from remodeled hearts following myocardial infarction. The miR-30 family was downregulated in all three models. We describe here that miR-30 act regulating the β-adrenergic pathway, where preferential β1- and β2-adrenoceptor (β1AR and β2AR) direct inhibition is combined with Giα-2 targeting for fine-tuning. Importantly, we show that miR-30 also target the pro-apoptotic gene BNIP3L/NIX. In aggregate, we demonstrate that high miR-30 levels are protective against DOX toxicity and correlate this in turn with lower reactive oxygen species generation. In addition, we identify GATA-6 as a mediator of DOX-associated reductions in miR-30 expression. In conclusion, we describe that DOX causes acute and sustained miR-30 downregulation in cardiomyocytes via GATA-6. miR-30 overexpression protects cardiac cells from DOX-induced apoptosis, and its maintenance represents a potential cardioprotective and anti-tumorigenic strategy for anthracyclines. PMID:25950484

  1. Spontaneous alterations in left ventricular regional wall motion after acute myocardial infarction.

    PubMed

    Shen, W F; Cui, L Q; Wang, M H; Gong, L S; Lesbre, J P

    1990-12-01

    For assessing the relationship between the left ventricular (LV) wall motion abnormalities and the status of residual flow to the infarcted region, the extent of coronary artery disease and one-year outcome, 60 patients with a first transmural, Q-wave myocardial infarction (MI) underwent serial echocardiographic examinations. The abnormal wall motion (AWM) score was calculated, and the cardiac events (death, reinfarction, severe ventricular arrhythmia or congestive heart failure) after discharge were recorded. The AWM score of the infarcted area was higher in patients with total occlusion than in those with subtotal occlusion (anterior MI: 14.6 +/- 2.4 vs 7.2 +/- 2.1; inferior MI: 9.7 +/- 2.1 vs 5.1 +/-1.2, all P less than 0.01). Regional wall motion of the noninfarcted area was preserved in patients with single vessel disease but decreased in those with multivessel disease. In patients who developed cardiac events in follow-up period a higher AWM (16.4 +/- 3.7) was found than in those who did not (8.9 +/- 3.1, P less than 0.05). A score of greater than 13 had a strong prediction of cardiac events after acute MI, with a sensitivity of 81%, specificity of 94% and positive predictive accuracy of 88%. PMID:2127245

  2. Comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion

    SciTech Connect

    Huey, B.L.; Beller, G.A.; Kaiser, D.L.; Gibson, R.S.

    1988-11-01

    Forty consecutive patients with creatine kinase-MB confirmed myocardial infarction due to circumflex artery occlusion (Group 1) were prospectively evaluated and compared with 107 patients with infarction due to right coronary artery occlusion (Group 2) and 94 with left anterior descending artery occlusion (Group 3). All 241 patients underwent exercise thallium-201 scintigraphy, radionuclide ventriculography, 24 h Holter electrocardiographic (ECG) monitoring and coronary arteriography before hospital discharge and were followed up for 39 +/- 18 months. There were no significant differences among the three infarct groups in age, gender, number of risk factors, prevalence and type of prior infarction, Norris index, Killip class and frequency of in-hospital complications. Acute ST segment elevation was present in only 48% of patients in Group 1 versus 71 and 72% in Groups 2 and 3, respectively (p = 0.012), and 38% of patients with a circumflex artery-related infarct had no significant ST changes (that is, elevation or depression) on admission (versus 21 and 20% for patients in Groups 2 and 3, respectively) (p = 0.001). Abnormal R waves in lead V1 were more common in Group 1 than in Group 2 (p less than 0.003) as was ST elevation in leads I, aVL and V4 to V6 (p less than or equal to 0.048). These differences in ECG findings between Group 1 and 2 patients correlated with a significantly higher prevalence of posterior and lateral wall asynergy in the group with a circumflex artery-related infarct. Infarct size based on peak creatine kinase levels and multiple radionuclide variables was intermediate in Group 1 compared with that in Group 2 (smallest) and Group 3 (largest). During long-term follow-up, the probability of recurrent cardiac events was similar in the three infarct groups.

  3. Image reconstruction in higher dimensions: myocardial perfusion imaging of tracer dynamics with cardiac motion due to deformation and respiration

    NASA Astrophysics Data System (ADS)

    Shrestha, Uttam M.; Seo, Youngho; Botvinick, Elias H.; Gullberg, Grant T.

    2015-11-01

    Myocardial perfusion imaging (MPI) using slow rotating large field of view cameras requires spatiotemporal reconstruction of dynamically acquired data to capture the time variation of the radiotracer concentration. In vivo, MPI contains additional degrees of freedom involving unavoidable motion of the heart due to quasiperiodic beating and the effects of respiration, which can severely degrade the quality of the images. This work develops a technique for a single photon emission computed tomography (SPECT) that reconstructs the distribution of the radiotracer concentration in the myocardium using a tensor product of different sets of basis functions that approximately describe the spatiotemporal variation of the radiotracer concentration and the motion of the heart. In this study the temporal B-spline basis functions are chosen to reflect the dynamics of the radiotracer, while the intrinsic deformation and the extrinsic motion of the heart are described by a product of a discrete set of Gaussian basis functions. Reconstruction results are presented showing the dynamics of the tracer in the myocardium as it deforms due to cardiac beating, and is displaced due to respiratory motion. These results are compared with the conventional 4D-spatiotemporal reconstruction method that models only the temporal changes of the tracer activity. The higher dimensional reconstruction method proposed here improves bias, yet the signal-to-noise ratio (SNR) decreases slightly due to redistribution of the counts over the cardiac-respiratory gates. Additionally, there is a trade-off between the number of gates and the number of projections per gate to achieve high contrast images.

  4. Image Reconstruction in Higher Dimensions: Myocardial Perfusion Imaging of Tracer Dynamics with Cardiac Motion Due to Deformation and Respiration

    PubMed Central

    Shrestha, Uttam M.; Seo, Youngho; Botvinick, Elias H.; Gullberg, Grant T.

    2015-01-01

    Myocardial perfusion imaging (MPI) using slow rotating large field of view cameras requires spatiotemporal reconstruction of dynamically acquired data to capture the time variation of the radiotracer concentration. In vivo, MPI contains additional degrees of freedom involving unavoidable motion of the heart due to quasiperiodic beating and the effects of respiration, which can severely degrade the quality of the images. This work develops a technique for a single photon emission computed tomography (SPECT) that reconstructs the distribution of the radiotracer concentration in the myocardium using a tensor product of different sets of basis functions that approximately describe the spatiotemporal variation of the radiotracer concentration and the motion of the heart. In this study the temporal B-spline basis functions are chosen to reflect the dynamics of the radiotracer, while the intrinsic deformation and the extrinsic motion of the heart are described by a product of a discrete set of Gaussian basis functions. Reconstruction results are presented showing the dynamics of the tracer in the myocardium as it deforms due to cardiac beating, and is displaced due to respiratory motion. These results are compared with the conventional 4D-spatiotemporal reconstruction method that models only the temporal changes of the tracer activity. The higher dimensional reconstruction method proposed here improves bias, yet the signal-to-noise ratio (SNR) decreases due to redistribution of the counts over the cardiac-respiratory gates. However, there is a trade-off between the number of gates and the number of projections per gate to achieve high contrast images. PMID:26450115

  5. Image reconstruction in higher dimensions: myocardial perfusion imaging of tracer dynamics with cardiac motion due to deformation and respiration

    DOE PAGES

    Shrestha, Uttam M.; Seo, Youngho; Botvinick, Elias H.; Gullberg, Grant T.

    2015-10-09

    Myocardial perfusion imaging (MPI) using slow rotating large field of view cameras requires spatiotemporal reconstruction of dynamically acquired data to capture the time variation of the radiotracer concentration. In vivo, MPI contains additional degrees of freedom involving unavoidable motion of the heart due to quasiperiodic beating and the effects of respiration, which can severely degrade the quality of the images. This work develops a technique for a single photon emission computed tomography (SPECT) that reconstructs the distribution of the radiotracer concentration in the myocardium using a tensor product of different sets of basis functions that approximately describe the spatiotemporal variationmore » of the radiotracer concentration and the motion of the heart. In this study the temporal B-spline basis functions are chosen to reflect the dynamics of the radiotracer, while the intrinsic deformation and the extrinsic motion of the heart are described by a product of a discrete set of Gaussian basis functions. Reconstruction results are presented showing the dynamics of the tracer in the myocardium as it deforms due to cardiac beating, and is displaced due to respiratory motion. We find these results are compared with the conventional 4D-spatiotemporal reconstruction method that models only the temporal changes of the tracer activity. The higher dimensional reconstruction method proposed here improves bias, yet the signal-to-noise ratio (SNR) decreases slightly due to redistribution of the counts over the cardiac-respiratory gates. Additionally, there is a trade-off between the number of gates and the number of projections per gate to achieve high contrast images.« less

  6. Image reconstruction in higher dimensions: myocardial perfusion imaging of tracer dynamics with cardiac motion due to deformation and respiration

    SciTech Connect

    Shrestha, Uttam M.; Seo, Youngho; Botvinick, Elias H.; Gullberg, Grant T.

    2015-10-09

    Myocardial perfusion imaging (MPI) using slow rotating large field of view cameras requires spatiotemporal reconstruction of dynamically acquired data to capture the time variation of the radiotracer concentration. In vivo, MPI contains additional degrees of freedom involving unavoidable motion of the heart due to quasiperiodic beating and the effects of respiration, which can severely degrade the quality of the images. This work develops a technique for a single photon emission computed tomography (SPECT) that reconstructs the distribution of the radiotracer concentration in the myocardium using a tensor product of different sets of basis functions that approximately describe the spatiotemporal variation of the radiotracer concentration and the motion of the heart. In this study the temporal B-spline basis functions are chosen to reflect the dynamics of the radiotracer, while the intrinsic deformation and the extrinsic motion of the heart are described by a product of a discrete set of Gaussian basis functions. Reconstruction results are presented showing the dynamics of the tracer in the myocardium as it deforms due to cardiac beating, and is displaced due to respiratory motion. We find these results are compared with the conventional 4D-spatiotemporal reconstruction method that models only the temporal changes of the tracer activity. The higher dimensional reconstruction method proposed here improves bias, yet the signal-to-noise ratio (SNR) decreases slightly due to redistribution of the counts over the cardiac-respiratory gates. Additionally, there is a trade-off between the number of gates and the number of projections per gate to achieve high contrast images.

  7. Image reconstruction in higher dimensions: myocardial perfusion imaging of tracer dynamics with cardiac motion due to deformation and respiration.

    PubMed

    Shrestha, Uttam M; Seo, Youngho; Botvinick, Elias H; Gullberg, Grant T

    2015-11-01

    Myocardial perfusion imaging (MPI) using slow rotating large field of view cameras requires spatiotemporal reconstruction of dynamically acquired data to capture the time variation of the radiotracer concentration. In vivo, MPI contains additional degrees of freedom involving unavoidable motion of the heart due to quasiperiodic beating and the effects of respiration, which can severely degrade the quality of the images. This work develops a technique for a single photon emission computed tomography (SPECT) that reconstructs the distribution of the radiotracer concentration in the myocardium using a tensor product of different sets of basis functions that approximately describe the spatiotemporal variation of the radiotracer concentration and the motion of the heart. In this study the temporal B-spline basis functions are chosen to reflect the dynamics of the radiotracer, while the intrinsic deformation and the extrinsic motion of the heart are described by a product of a discrete set of Gaussian basis functions. Reconstruction results are presented showing the dynamics of the tracer in the myocardium as it deforms due to cardiac beating, and is displaced due to respiratory motion. These results are compared with the conventional 4D-spatiotemporal reconstruction method that models only the temporal changes of the tracer activity. The higher dimensional reconstruction method proposed here improves bias, yet the signal-to-noise ratio (SNR) decreases slightly due to redistribution of the counts over the cardiac-respiratory gates. Additionally, there is a trade-off between the number of gates and the number of projections per gate to achieve high contrast images. PMID:26450115

  8. Global-scale analysis of river flow alterations due to water withdrawals and reservoirs

    NASA Astrophysics Data System (ADS)

    Döll, P.; Fiedler, K.; Zhang, J.

    2009-12-01

    Global-scale information on natural river flows and anthropogenic river flow alterations is required to identify areas where aqueous ecosystems are expected to be strongly degraded. Such information can support the identification of environmental flow guidelines and a sustainable water management that balances the water demands of humans and ecosystems. This study presents the first global assessment of the anthropogenic alteration of river flow regimes, in particular of flow variability, by water withdrawals and dams/reservoirs. Six ecologically relevant flow indicators were quantified using an improved version of the global water model WaterGAP. WaterGAP simulated, with a spatial resolution of 0.5 degree, river discharge as affected by human water withdrawals and dams around the year 2000, as well as naturalized discharge without this type of human interference. Compared to naturalized conditions, long-term average global discharge into oceans and internal sinks has decreased by 2.7% due to water withdrawals, and by 0.8% due to dams. Mainly due to irrigation, long-term average river discharge and statistical low flow Q90 (monthly river discharge that is exceeded in 9 out of 10 months) have decreased by more than 10% on one sixth and one quarter of the global land area (excluding Antarctica and Greenland), respectively. Q90 has increased significantly on only 5% of the land area, downstream of reservoirs. Due to both water withdrawals and reservoirs, seasonal flow amplitude has decreased significantly on one sixth of the land area, while interannual variability has increased on one quarter of the land area mainly due to irrigation. It has decreased on only 8% of the land area, in areas downstream of reservoirs where consumptive water use is low. The impact of reservoirs is likely underestimated by our study as small reservoirs are not taken into account. Areas most affected by anthropogenic river flow alterations are the Western and Central USA, Mexico, the

  9. Global-scale analysis of river flow alterations due to water withdrawals and reservoirs

    NASA Astrophysics Data System (ADS)

    Döll, P.; Fiedler, K.; Zhang, J.

    2009-07-01

    Global-scale information on natural river flows and anthropogenic river flow alterations is required to identify areas where aqueous ecosystems are expected to be strongly degraded. Such information can support the identification of environmental flow guidelines and a sustainable water management that balances the water demands of humans and ecosystems. This study presents the first global assessment of the anthropogenic alteration of river flow regimes by water withdrawals and dams, focusing in particular on the change of flow variability. Six ecologically relevant flow indicators were quantified using an improved version of the global water model WaterGAP. WaterGAP simulated, with a spatial resolution of 0.5 degree, river discharge as affected by human water withdrawals and dams, as well as naturalized discharge without this type of human interference. Mainly due to irrigation, long-term average river discharge and statistical low flow Q90 (monthly river discharge that is exceeded in 9 out of 10 months) have decreased by more than 10% on one sixth and one quarter of the global land area (excluding Antarctica and Greenland), respectively. Q90 has increased significantly on only 5% of the land area, downstream of reservoirs. Due to both water withdrawals and dams, seasonal flow amplitude has decreased significantly on one sixth of the land area, while interannual variability has increased on one quarter of the land area mainly due to irrigation. It has decreased on only 8% of the land area, in areas with little consumptive water use that are downstream of dams. Areas most affected by anthropogenic river flow alterations are the western and central USA, Mexico, the western coast of South America, the Mediterranean rim, Southern Africa, the semi-arid and arid countries of the Near East and Western Asia, Pakistan and India, Northern China and the Australian Murray-Darling Basin, as well as some Arctic rivers. Due to a large number of uncertainties related e.g. to the

  10. Disordered myocardial Ca(2+) homeostasis results in substructural alterations that may promote occurrence of malignant arrhythmias.

    PubMed

    Tribulova, N; Knezl, V; Szeiffova Bacova, B; Egan Benova, T; Viczenczova, C; Gonçalvesova, E; Slezak, J

    2016-09-19

    We aimed to determine the impact of Ca(2+)-related disorders induced in intact animal hearts on ultrastructure of the cardiomyocytes prior to occurrence of severe arrhythmias. Three types of acute experiments were performed that are known to be accompanied by disturbances in Ca(2+) handling. Langedorff-perfused rat or guinea pig hearts subjected to K(+)-deficient perfusion to induce ventricular fibrillation (VF), burst atrial pacing to induce atrial fibrillation (AF) and open chest pig heart exposed to intramyocardial noradrenaline infusion to induce ventricular tachycardia (VT). Tissue samples for electron microscopic examination were taken during basal condition, prior and during occurrence of malignant arrhythmias. Cardiomyocyte alterations preceding occurrence of arrhythmias consisted of non-uniform sarcomere shortening, disruption of myofilaments and injury of mitochondria that most likely reflected cytosolic Ca(2+) disturbances and Ca(2+) overload. These disorders were linked with non-uniform pattern of neighboring cardiomyocytes and dissociation of adhesive junctions suggesting defects in cardiac cell-to-cell coupling. Our findings identified heterogeneously distributed high [Ca(2+)](i)-induced subcellular injury of the cardiomyocytes and their junctions as a common feature prior occurrence of VT, VF or AF. In conclusion, there is a link between Ca(2+)-related disorders in contractility and coupling of the cardiomyocytes pointing out a novel paradigm implicated in development of severe arrhythmias. PMID:27643936

  11. Percutaneous coronary intervention for acute myocardial infarction in a pediatric patient with coronary aneurysm and stenosis due to Kawasaki disease.

    PubMed

    Drossner, David M; Chappell, Clay; Rab, Tanveer; Kim, Dennis

    2012-06-01

    We report the case of an acutely ill 3-year-old female, with a previous medical history of Kawasaki disease, who presented to care with an acute myocardial infarction. We describe the coordinated therapies employed by pediatric and adult cardiologists aimed to establish coronary revascularization.

  12. Myocardial abscess complicating healed myocardial infarction.

    PubMed Central

    Weisz, S.; Young, D. G.

    1977-01-01

    An isolated myocardial abscess due to Bacteroides fragilis developed in the scar of a myocardial infarction. Fever, chills and signs of pericarditis were the main clinical features. Mild enteritis 1 week prior to the onset of symptoms related to the abscess was the most likely cause of the bacteremia. The diagnosis was established at thoracotomy, performed because of cardiac tamponade. Thirteen other cases of isolated bacterial myocardial abscess accompanying myocardial infarction have been reported, but all the infarctions were recent. Surgical resection for a suspected myocardial abscess should be considered in view of the high mortality, largely from cardiac rupture. Images FIG. 1 PMID:861868

  13. Hydraulic Property Alterations due to Wettability Induced Changes by Diesel Fuels

    NASA Astrophysics Data System (ADS)

    O'Carroll, Denis

    2013-04-01

    The remediation of non-aqueous phase liquid (NAPL) contaminated sites is impeded due to subsurface complexities, including wettability. Wettability quantifies which of two immiscible fluids preferentially coats a solid. At most contaminated sites water-wetting conditions are typically assumed despite mounting evidence that is not always the case. In this study, wettability was examined for two NAPL samples of contrasting origin: a fresh and a field sample. Wettability was assessed through (i) cyclical, 'cumulative elapsed contact time' intrinsic contact angle measurements, (ii) interface jar tests, and (iii) cyclical, pseudo-static capillary pressure-saturation curves. The work as a whole demonstrated that while the fresh diesel sample was consistently water-wet, the field diesel sample exhibited repeatable cycles of wettability reversal between water drainage and imbibition. And while wettability hysteresis increased with contact time for the field diesel, the occurrence of wettability reversal at each change of saturation direction was independent of contact time. Such behavior is not easily assessed by standard wettability indices. Moreover, it contrasts with the permanent wettability alteration observed for complex organics (e.g., coal tar) observed in most studies. It is hypothesized that the cyclical wettability reversal is related to cyclical changes in intermediate pore wettability due to sorption of surface active compounds (causing NAPL-wetting imbibition) and rupturing of the the soil grain water film (causing water-wet drainage). The wettability differences between the two NAPLs may be due to additives (i.e., a surfactant) in the original formulation and/or byproducts from subsurface weathering. These results support better characterization of site-specific wettability, improved model development and more realistic site conceptual models for improved remediation efforts.

  14. ST Segment Elevation Myocardial Infarction Due to Severe Ostial Left Main Stem Stenosis in a Patient with Syphilitic Aortitis.

    PubMed

    Predescu, L M; Zarma, L; Platon, P; Postu, M; Bucsa, A; Croitoru, M; Prodan, B; Chioncel, O; Deleanu, D

    2016-01-01

    Cardiovascular manifestations of tertiary syphilis infections are uncommon, but represent an important cause of mortality and morbidity. Syphilitic aortitis is characterized by aortic regurgitation, dilatation of ascending aorta and ostial coronary artery lesions. We report a case of 36 years old man admitted to our hospital for acute anterior ST segment elevation myocardial infarction complicated with cardiogenic shock (hypotension 75/50 mmHg). Transthoracic echocardiography revealed a dilated left ventricle with severe systolic dysfunction (ejection fraction = 25%), severe mitral regurgitation, moderate aortic regurgitation and mildly dilated ascending aorta. Coronary angiography showed a severe ostial lesion of left main coronary artery which was treated by urgent stent implantation and an intra-aortic contrapulsation balloon was implanted. Blood tests for syphilitic infection were positive. The patient was discharged with treatment including benzathine penicillin. In our case, we present an acute manifestation of a syphilitic ostial left main stenosis treated by primary percutaneous coronary intervention in acute myocardial infarction. Long term follow-up of the patient is crucial as a result of potential rapid in-stent restenosis caused by continuous infection of the ascending aorta. This case is particular because it shows that syphilitic aortitis can be diagnosed in acute settings, like ST segment elevation myocardial infarction.

  15. ST Segment Elevation Myocardial Infarction Due to Severe Ostial Left Main Stem Stenosis in a Patient with Syphilitic Aortitis.

    PubMed

    Predescu, L M; Zarma, L; Platon, P; Postu, M; Bucsa, A; Croitoru, M; Prodan, B; Chioncel, O; Deleanu, D

    2016-01-01

    Cardiovascular manifestations of tertiary syphilis infections are uncommon, but represent an important cause of mortality and morbidity. Syphilitic aortitis is characterized by aortic regurgitation, dilatation of ascending aorta and ostial coronary artery lesions. We report a case of 36 years old man admitted to our hospital for acute anterior ST segment elevation myocardial infarction complicated with cardiogenic shock (hypotension 75/50 mmHg). Transthoracic echocardiography revealed a dilated left ventricle with severe systolic dysfunction (ejection fraction = 25%), severe mitral regurgitation, moderate aortic regurgitation and mildly dilated ascending aorta. Coronary angiography showed a severe ostial lesion of left main coronary artery which was treated by urgent stent implantation and an intra-aortic contrapulsation balloon was implanted. Blood tests for syphilitic infection were positive. The patient was discharged with treatment including benzathine penicillin. In our case, we present an acute manifestation of a syphilitic ostial left main stenosis treated by primary percutaneous coronary intervention in acute myocardial infarction. Long term follow-up of the patient is crucial as a result of potential rapid in-stent restenosis caused by continuous infection of the ascending aorta. This case is particular because it shows that syphilitic aortitis can be diagnosed in acute settings, like ST segment elevation myocardial infarction. PMID:27141575

  16. Structural alterations of the coronary arterial wall are associated with myocardial flow heterogeneity in type 2 diabetes mellitus

    PubMed Central

    Schindler, Thomas H.; Facta, Alvaro D.; Prior, John O.; Cadenas, Jerson; Zhang, Xiao-Li; Li, Yanjie; Sayre, James; Goldin, Jonathan

    2016-01-01

    Purpose To determine the relationship between carotid intima–media thickness (IMT), coronary artery calcification (CAC), and myocardial blood flow (MBF) at rest and during vasomotor stress in type 2 diabetes mellitus (DM). Methods In 68 individuals, carotid IMT was measured using high-resolution vascular ultrasound, while the presence of CAC was determined with electron beam tomography (EBT). Global and regional MBF was determined in milliliters per gram per minute with 13N-ammonia and positron emission tomography (PET) at rest, during cold pressor testing (CPT), and during adenosine (ADO) stimulation. Results There was neither a relationship between carotid IMT and CAC (r=0.10, p=0.32) nor between carotid IMT and coronary circulatory function in response to CPT and during ADO (r=−0.18, p=0.25 and r=0.10, p=0.54, respectively). In 33 individuals, EBT detected CAC with a mean Agatston-derived calcium score of 44±18. There was a significant difference in regional MBFs between territories with and without CAC at rest and during ADO-stimulated hyperemia (0.69±0.24 vs. 0.74±0.23 and 1.82±0.50 vs. 1.95±0.51 ml/g/min; p≤0.05, respectively) and also during CPT in DM but less pronounced (0.81±0.24 vs. 0.83±0.23 ml/g/min; p=ns). The increase in CAC was paralleled with a progressive regional decrease in resting as well as in CPT- and ADO-related MBFs (r=−0.36, p≤0.014; r=−0.46, p≤0.007; and r=−0.33, p≤0.041, respectively). Conclusions The absence of any correlation between carotid IMT and coronary circulatory function in type 2 DM suggests different features and stages of early atherosclerosis in the peripheral and coronary circulation. PET-measured MBF heterogeneity at rest and during vasomotor stress may reflect downstream fluid dynamic effects of coronary artery disease (CAD)-related early structural alterations of the arterial wall. PMID:18704406

  17. Protection against Myocardial Ischemia-Reperfusion Injury at Onset of Type 2 Diabetes in Zucker Diabetic Fatty Rats Is Associated with Altered Glucose Oxidation

    PubMed Central

    Povlsen, Jonas Agerlund; Løfgren, Bo; Dalgas, Christian; Birkler, Rune Isak Dupont; Johannsen, Mogens; Støttrup, Nicolaj Brejnholt; Bøtker, Hans Erik

    2013-01-01

    Background Inhibition of glucose oxidation during initial reperfusion confers protection against ischemia-reperfusion (IR) injury in the heart. Mitochondrial metabolism is altered with progression of type 2 diabetes (T2DM). We hypothesized that the metabolic alterations present at onset of T2DM induce cardioprotection by metabolic shutdown during IR, and that chronic alterations seen in late T2DM cause increased IR injury. Methods Isolated perfused hearts from 6 (prediabetic), 12 (onset of T2DM) and 24 (late T2DM) weeks old male Zucker diabetic fatty rats (ZDF) and their age-matched heterozygote controls were subjected to 40 min ischemia/120 min reperfusion. IR injury was assessed by TTC-staining. Myocardial glucose metabolism was evaluated by glucose tracer kinetics (glucose uptake-, glycolysis- and glucose oxidation rates), myocardial microdialysis (metabolomics) and tissue glycogen measurements. Results T2DM altered the development in sensitivity towards IR injury compared to controls. At late diabetes ZDF hearts suffered increased damage, while injury was decreased at onset of T2DM. Coincident with cardioprotection, oxidation of exogenous glucose was decreased during the initial and normalized after 5 minutes of reperfusion. Metabolomic analysis of citric acid cycle intermediates demonstrated that cardioprotection was associated with a reversible shutdown of mitochondrial glucose metabolism during ischemia and early reperfusion at onset of but not at late type 2 diabetes. Conclusions The metabolic alterations of type 2 diabetes are associated with protection against IR injury at onset but detrimental effects in late diabetes mellitus consistent with progressive dysfunction of glucose oxidation. These findings may explain the variable efficacy of cardioprotective interventions in individuals with type 2 diabetes. PMID:23704975

  18. DETECTING STREAM INVERTEBRATE COMMUNITY ALTERATION DUE TO MID TO LOW LEVELS OF WATERSHED LANDSCAPE MODIFICATION

    EPA Science Inventory

    As part of an investigation into the effects of watershed landscape alteration on stream ecosystems, quantitative invertebrate samples were collected from riffles in 26 second and third order south shore Lake Superior streams. Nonmetric multidimensional scaling (NMDS) ordination ...

  19. Myocardial contractile depression from high-frequency vibration is not due to increased cross-bridge breakage.

    PubMed

    Campbell, K B; Wu, Y; Kirkpatrick, R D; Slinker, B K

    1998-04-01

    Experiments were conducted in 10 isolated rabbit hearts at 25 degrees C to test the hypothesis that vibration-induced depression of myocardial contractile function was the result of increased cross-bridge breakage. Small-amplitude sinusoidal changes in left ventricular volume were administered at frequencies of 25, 50, and 76.9 Hz. The resulting pressure response consisted of a depressive response [delta Pd(t), a sustained decrease in pressure that was not at the perturbation frequency] and an infrequency response [delta Pf(t), that part at the perturbation frequency]. delta Pd(t) represented the effects of contractile depression. A cross-bridge model was applied to delta Pf(t) to estimate cross-bridge cycling parameters. Responses were obtained during Ca2+ activation and during Sr2+ activation when the time course of pressure development was slowed by a factor of 3. delta Pd(t) was strongly affected by whether the responses were activated by Ca2+ or by Sr2+. In the Sr(2+)-activated state, delta Pd(t) declined while pressure was rising and relaxation rate decreased. During Ca2+ and Sr2+ activation, velocity of myofilament sliding was insignificant as a predictor of delta Pd(t) or, when it was significant, participated by reducing delta Pd(t) rather than contributing to its magnitude. Furthermore, there was no difference in cross-bridge cycling rate constants when the Ca(2+)-activated state was compared with the Sr(2+)-activated state. An increase in cross-bridge detachment rate constant with volume-induced change in cross-bridge distortion could not be detected. Finally, processes responsible for delta Pd(t) occurred at slower frequencies than those of cross-bridge detachment. Collectively, these results argue against a cross-bridge detachment basis for vibration-induced myocardial depression.

  20. Alterations in myocardial perfusion during exercise after isosorbide dinitrate infusion in patients with coronary disease: assessment by thallium-201 scintigraphy

    SciTech Connect

    Tono, I.; Satoh, S.; Kanaya, T.; Komatani, A.; Takahashi, K.; Tsuiki, K.; Yasui, S.

    1986-03-01

    We studied the effect of intravenous isosorbide dinitrate (ISDN) on myocardial perfusion of patients with coronary artery disease, by using exercise thallium-201 (TI-201) myocardial scintigraphy. A control study was conducted initially to assess regional myocardial perfusion rate. Left ventricular myocardium was divided into six parts: anterior, lateral, apical, inferior, posterior, and septal segments. The segmental myocardial perfusion was characterized according to TI-201 initial uptake index (IUI) of relative distribution and redistribution index (RDI) of TI-201 washout. The normal limit of IUI and RDI was established from the data of 17 persons with normal coronary arteries, and then the IUI less than or equal to 84% and the RDI greater than or equal to 1.12 was defined as abnormal. Based on IUI and RDI, each segment was characterized into three types: A type = IUI less than or equal to 84%, RDI greater than or equal to 1.12; B type = IUI less than or equal to 84%, RDI less than 1.12; and C type = IUI greater than 84%, RDI less than 1.12. ISDN was given as a dose of 0.1 mg/kg/hr, and then treadmill testing was repeated for the same duration of exercise time using the same protocol as in the control period. The segments of A type showed a significant improvement in IUI and RDI after receiving ISDN infusion, while the B and C type segments showed no change. It was also shown that the improvement of IUI and RDI of the A type segments was not as marked in multivessel disease as in cases of single-vessel disease.

  1. Metabolic programming due to alterations in nutrition in the immediate postnatal period.

    PubMed

    Patel, Mulchand S; Srinivasan, Malathi

    2010-03-01

    Altered nutritional experiences such as undernutrition, overnutrition, and modified milk formula in the immediate postnatal life via the phenomenon of metabolic programming have been identified as one of the components in the etiology of metabolic syndrome. We have developed a rat model in which an altered dietary experience in the form of a high-carbohydrate (HC) milk formula in the immediate postnatal life of rat pups results in chronic hyperinsulinemia and adult-onset obesity in these rats. The HC dietary modification causes functional alterations in pancreatic islets and the hypothalamus during the period of the dietary modification. These early adaptations in islets (supporting hyperinsulinemia) and the hypothalamus (supporting hyperphagia and increased body weight gain) persist in the postweaning period despite withdrawal of the HC milk formula at the time of weaning. In female rat pups receiving the HC milk formula, metabolic programming effects translate into an adverse (hyperinsulinemic, hyperleptinemic, and obese) intrauterine environment during pregnancy, causing spontaneous transfer of the maternal phenotype to the progeny (generational effect). Our results suggest that alterations in feeding practices for babies (early introduction of cereals, fruits, etc.) and babies born to obese/hyperinsulinemic mothers may be contributing factors for the obesity epidemic prevalent in developed and developing countries.

  2. Are Amygdalar Volume Alterations in Children with Tourette Syndrome Due to ADHD Comorbidity?

    ERIC Educational Resources Information Center

    Ludolph, Andrea G.; Pinkhardt, Elmar H.; van Elst, Ludger Tebartz; Libal, Gerhard; Ludolph, Albert C.; Fegert, Jorg M.; Kassubek, Jan

    2008-01-01

    Recent studies have shown that changes in the basal ganglia circuitry and limbic loops may play an important role both in Tourette syndrome (TS) and attention-deficit-hyperactivity disorder (ADHD). This study aimed to investigate in vivo possible morphological alterations of the amygdala as a key component of the limbic system. Amygdalar and total…

  3. Expression of phospholipase D isozymes in scar and viable tissue in congestive heart failure due to myocardial infarction.

    PubMed

    Dent, Melissa R; Singal, Tushi; Dhalla, Naranjan S; Tappia, Paramjit S

    2004-01-01

    The phospholipase D (PLD) associated with the cardiac sarcolemmal (SL) membrane hydrolyses phosphatidylcholine to produce phosphatidic acid, an important phospholipid signaling molecule known to influence cardiac function. The present study was undertaken to examine PLD isozyme mRNA expression, protein contents and activities in congestive heart failure (CHF) subsequent to myocardial infarction (MI). MI was induced in rats by occlusion of the left anterior descending coronary artery. At 8 weeks after the surgical procedure, hemodynamic assessment revealed that these experimental rats were at a moderate stage of CHF. Semi-quantitative reverse transcriptase-polymerase chain reaction revealed that PLD1 and PLD2 mRNA amounts were unchanged in viable left ventricular (LV) tissue of the failing heart. Furthermore, this technique demonstrated the presence of PLD1 and PLD2 mRNA in the scar tissue. While SL PLD1 and PLD2 protein contents were elevated in the viable LV tissue of the failing heart, SL PLD1 activity was significantly decreased, whereas SL PLD2 activity was significantly increased. On the other hand, although PLD1 protein was undetectable, PLD2 protein and activity were detected in the scar tissue. Our findings suggest that differential changes in PLD isozymes may contribute to the pathophysiology of CHF and may also be involved in the processes of scar remodeling. PMID:15601581

  4. Systemic and Cardiac Depletion of M2 Macrophage through CSF-1R Signaling Inhibition Alters Cardiac Function Post Myocardial Infarction.

    PubMed

    Leblond, Anne-Laure; Klinkert, Kerstin; Martin, Kenneth; Turner, Elizebeth C; Kumar, Arun H; Browne, Tara; Caplice, Noel M

    2015-01-01

    The heart hosts tissue resident macrophages which are capable of modulating cardiac inflammation and function by multiple mechanisms. At present, the consequences of phenotypic diversity in macrophages in the heart are incompletely understood. The contribution of cardiac M2-polarized macrophages to the resolution of inflammation and repair response following myocardial infarction remains to be fully defined. In this study, the role of M2 macrophages was investigated utilising a specific CSF-1 receptor signalling inhibition strategy to achieve their depletion. In mice, oral administration of GW2580, a CSF-1R kinase inhibitor, induced significant decreases in Gr1lo and F4/80hi monocyte populations in the circulation and the spleen. GW2580 administration also induced a significant depletion of M2 macrophages in the heart after 1 week treatment as well as a reduction of cardiac arginase1 and CD206 gene expression indicative of M2 macrophage activity. In a murine myocardial infarction model, reduced M2 macrophage content was associated with increased M1-related gene expression (IL-6 and IL-1β), and decreased M2-related gene expression (Arginase1 and CD206) in the heart of GW2580-treated animals versus vehicle-treated controls. M2 depletion was also associated with a loss in left ventricular contractile function, infarct enlargement, decreased collagen staining and increased inflammatory cell infiltration into the infarct zone, specifically neutrophils and M1 macrophages. Taken together, these data indicate that CSF-1R signalling is critical for maintaining cardiac tissue resident M2-polarized macrophage population, which is required for the resolution of inflammation post myocardial infarction and, in turn, for preservation of ventricular function.

  5. Myocardial deletion of transcription factor CHF1/Hey2 results in altered myocyte action potential and mild conduction system expansion but does not alter conduction system function or promote spontaneous arrhythmias.

    PubMed

    Hartman, Matthew E; Liu, Yonggang; Zhu, Wei-Zhong; Chien, Wei-Ming; Weldy, Chad S; Fishman, Glenn I; Laflamme, Michael A; Chin, Michael T

    2014-07-01

    CHF1/Hey2 is a Notch-responsive basic helix-loop-helix transcription factor involved in cardiac development. Common variants in Hey2 are associated with Brugada syndrome. We hypothesized that absence of CHF1/Hey2 would result in abnormal cellular electrical activity, altered cardiac conduction system (CCS) development, and increased arrhythmogenesis. We isolated neonatal CHF/Hey2-knockout (KO) cardiac myocytes and measured action potentials and ion channel subunit gene expression. We also crossed myocardial-specific CHF1/Hey2-KO mice with cardiac conduction system LacZ reporter mice and stained for conduction system tissue. We also performed ambulatory ECG monitoring for arrhythmias and heart rate variability. Neonatal cardiomyocytes from CHF1/Hey2-KO mice demonstrate a 50% reduction in action potential dV/dT, a 50-75% reduction in SCN5A, KCNJ2, and CACNA1C ion channel subunit gene expression, and an increase in delayed afterdepolarizations from 0/min to 12/min. CHF1/Hey2 cKO CCS-lacZ mice have a ∼3-fold increase in amount of CCS tissue. Ambulatory ECG monitoring showed no difference in cardiac conduction, arrhythmias, or heart rate variability. Wild-type cells or animals were used in all experiments. CHF1/Hey2 may contribute to Brugada syndrome by influencing the expression of SCN5A and formation of the cardiac conduction system, but its absence does not cause baseline conduction defects or arrhythmias in the adult mouse.-Hartman, M. E., Liu, Y., Zhu, W.-Z., Chien, W.-M., Weldy, C. S., Fishman, G. I., Laflamme, M. A., Chin, M. T. Myocardial deletion of transcription factor CHF1/Hey2 results in altered myocyte action potential and mild conduction system expansion but does not alter conduction system function or promote spontaneous arrhythmias.

  6. Alterations in lung clearance mechanisms due to single and repeated nitrogen dioxide exposures in the rabbit

    SciTech Connect

    Vollmuth, T.A.

    1986-01-01

    Tracheobronchial mucociliary clearance was assessed following single, two-hour exposures to either 0.3, 1.0, 3.0, or 10.0 ppm NO/sub 2/, or 14 daily two hour exposures to 0.3, 1.0, 3.0 ppm NO/sub 2/. No significant changes in the mean residence time of tracer particles in the tracheobronchial region were produced under any exposure condition, indicating no effect upon mucociliary clearance. Macrophage functional properties were examined in vitro at select times following single, two hour in vivo exposures to 1.0 and 10.0 ppm NO/sub 2/. Macrophage number and viability were not affected; however, significant dose-related differences in phagocytosis and mobility were observed. These changes were associated with altered in vivo alveolar clearance patterns. Additional studies examined the effects of in vitro exposure to nitrite and hydrogen ion, two known NO/sub 2/ reaction products in the lung, on macrophage phagocytosis. While hydrogen ion had no effect at the levels used, nitrate was shown to enhance phagocytosis. These results demonstrate that alveolar clearance and macrophage function are altered by short-term NO/sub 2/ exposure at realistic, environmental levels. These data also provide insight into the mechanisms of NO/sub 2/-induced alteration in lung clearance pathways.

  7. Risk of Crew Adverse Health Event Due to Altered Immune Response

    NASA Technical Reports Server (NTRS)

    Crucian, Brian; Kunz, Hawley; Sams, Clarence F.

    2015-01-01

    Determining the effect of space travel on the human immune system has proven to be extremely challenging. Limited opportunities for in-flight studies, varying mission durations, technical and logistical obstacles, small subject numbers, and a broad range of potential assays have contributed to this problem. Additionally, the inherent complexity of the immune system, with its vast array of cell populations, sub-populations, diverse regulatory molecules, and broad interactions with other physiological systems, makes determining precise variables to measure very difficult. There is also the challenge of determining the clinical significance of any observed immune alterations. Will such a change lead to disease, or is it a transient subclinical observation related to short-term stress? The effect of this problem may be observed by scanning publications associated with immunity and spaceflight, which began to appear during the 1970s. Although individually they are each valid studies, the comprehensive literature to date suffers from widely varying sampling methods and assay techniques, low subject counts, and sometimes a disparate focus on narrow aspects of immunity. The most clinically relevant data are derived from in-flight human studies, which have demonstrated altered cell-mediated immunity and reactivation of latent herpes viruses. Much more data are available from post-flight testing of humans, with clear evidence of altered cytokine production patterns, altered leukocyte distribution, continued latent viral reactivation, and evidence of dramatically altered virus-specific immunity. It is unknown if post-flight assessments relate to the in-flight condition or are a response to landing stress and readaptation. In-flight culture of cells has clearly demonstrated that immune cells are gravity-sensitive and display altered functional characteristics. It is unknown if these data are related to in vivo immune cell function or are an artifact of microgravity culture

  8. Alteration of interleaflet coupling due to compounds displaying rapid translocation in lipid membranes

    PubMed Central

    Reigada, Ramon

    2016-01-01

    The spatial coincidence of lipid domains at both layers of the cell membrane is expected to play an important role in many cellular functions. Competition between the surface interleaflet tension and a line hydrophobic mismatch penalty are conjectured to determine the transversal behavior of laterally heterogeneous lipid membranes. Here, by a combination of molecular dynamics simulations, a continuum field theory and kinetic equations, I demonstrate that the presence of small, rapidly translocating molecules residing in the lipid bilayer may alter its transversal behavior by favoring the spatial coincidence of similar lipid phases. PMID:27596355

  9. Alteration of interleaflet coupling due to compounds displaying rapid translocation in lipid membranes

    NASA Astrophysics Data System (ADS)

    Reigada, Ramon

    2016-09-01

    The spatial coincidence of lipid domains at both layers of the cell membrane is expected to play an important role in many cellular functions. Competition between the surface interleaflet tension and a line hydrophobic mismatch penalty are conjectured to determine the transversal behavior of laterally heterogeneous lipid membranes. Here, by a combination of molecular dynamics simulations, a continuum field theory and kinetic equations, I demonstrate that the presence of small, rapidly translocating molecules residing in the lipid bilayer may alter its transversal behavior by favoring the spatial coincidence of similar lipid phases.

  10. Alteration of interleaflet coupling due to compounds displaying rapid translocation in lipid membranes.

    PubMed

    Reigada, Ramon

    2016-01-01

    The spatial coincidence of lipid domains at both layers of the cell membrane is expected to play an important role in many cellular functions. Competition between the surface interleaflet tension and a line hydrophobic mismatch penalty are conjectured to determine the transversal behavior of laterally heterogeneous lipid membranes. Here, by a combination of molecular dynamics simulations, a continuum field theory and kinetic equations, I demonstrate that the presence of small, rapidly translocating molecules residing in the lipid bilayer may alter its transversal behavior by favoring the spatial coincidence of similar lipid phases. PMID:27596355

  11. Reciprocal white matter alterations due to 16p11.2 chromosomal deletions versus duplications.

    PubMed

    Chang, Yi Shin; Owen, Julia P; Pojman, Nicholas J; Thieu, Tony; Bukshpun, Polina; Wakahiro, Mari L J; Marco, Elysa J; Berman, Jeffrey I; Spiro, John E; Chung, Wendy K; Buckner, Randy L; Roberts, Timothy P L; Nagarajan, Srikantan S; Sherr, Elliott H; Mukherjee, Pratik

    2016-08-01

    Copy number variants at the 16p11.2 chromosomal locus are associated with several neuropsychiatric disorders, including autism, schizophrenia, bipolar disorder, attention-deficit hyperactivity disorder, and speech and language disorders. A gene dosage dependence has been suggested, with 16p11.2 deletion carriers demonstrating higher body mass index and head circumference, and 16p11.2 duplication carriers demonstrating lower body mass index and head circumference. Here, we use diffusion tensor imaging to elucidate this reciprocal relationship in white matter organization, showing widespread increases of fractional anisotropy throughout the supratentorial white matter in pediatric deletion carriers and, in contrast, extensive decreases of white matter fractional anisotropy in pediatric and adult duplication carriers. We find associations of these white matter alterations with cognitive and behavioral impairments. We further demonstrate the value of imaging metrics for characterizing the copy number variant phenotype by employing linear discriminant analysis to predict the gene dosage status of the study subjects. These results show an effect of 16p11.2 gene dosage on white matter microstructure, and further suggest that opposite changes in diffusion tensor imaging metrics can lead to similar cognitive and behavioral deficits. Given the large effect sizes found in this study, our results support the view that specific genetic variations are more strongly associated with specific brain alterations than are shared neuropsychiatric diagnoses. Hum Brain Mapp 37:2833-2848, 2016. © 2016 Wiley Periodicals, Inc.

  12. Reciprocal white matter alterations due to 16p11.2 chromosomal deletions versus duplications.

    PubMed

    Chang, Yi Shin; Owen, Julia P; Pojman, Nicholas J; Thieu, Tony; Bukshpun, Polina; Wakahiro, Mari L J; Marco, Elysa J; Berman, Jeffrey I; Spiro, John E; Chung, Wendy K; Buckner, Randy L; Roberts, Timothy P L; Nagarajan, Srikantan S; Sherr, Elliott H; Mukherjee, Pratik

    2016-08-01

    Copy number variants at the 16p11.2 chromosomal locus are associated with several neuropsychiatric disorders, including autism, schizophrenia, bipolar disorder, attention-deficit hyperactivity disorder, and speech and language disorders. A gene dosage dependence has been suggested, with 16p11.2 deletion carriers demonstrating higher body mass index and head circumference, and 16p11.2 duplication carriers demonstrating lower body mass index and head circumference. Here, we use diffusion tensor imaging to elucidate this reciprocal relationship in white matter organization, showing widespread increases of fractional anisotropy throughout the supratentorial white matter in pediatric deletion carriers and, in contrast, extensive decreases of white matter fractional anisotropy in pediatric and adult duplication carriers. We find associations of these white matter alterations with cognitive and behavioral impairments. We further demonstrate the value of imaging metrics for characterizing the copy number variant phenotype by employing linear discriminant analysis to predict the gene dosage status of the study subjects. These results show an effect of 16p11.2 gene dosage on white matter microstructure, and further suggest that opposite changes in diffusion tensor imaging metrics can lead to similar cognitive and behavioral deficits. Given the large effect sizes found in this study, our results support the view that specific genetic variations are more strongly associated with specific brain alterations than are shared neuropsychiatric diagnoses. Hum Brain Mapp 37:2833-2848, 2016. © 2016 Wiley Periodicals, Inc. PMID:27219475

  13. Degeneration of Dopaminergic Neurons Due to Metabolic Alterations and Parkinson’s Disease

    PubMed Central

    Song, Juhyun; Kim, Jongpil

    2016-01-01

    The rates of metabolic diseases, such as type 2 diabetes mellitus (T2DM), obesity, and cardiovascular disease (CVD), markedly increase with age. In recent years, studies have reported an association between metabolic changes and various pathophysiological mechanisms in the central nervous system (CNS) in patients with metabolic diseases. Oxidative stress and hyperglycemia in metabolic diseases lead to adverse neurophysiological phenomena, including neuronal loss, synaptic dysfunction, and improper insulin signaling, resulting in Parkinson’s disease (PD). In addition, several lines of evidence suggest that alterations of CNS environments by metabolic changes influence the dopamine neuronal loss, eventually affecting the pathogenesis of PD. Thus, we reviewed recent findings relating to degeneration of dopaminergic neurons during metabolic diseases. We highlight the fact that using a metabolic approach to manipulate degeneration of dopaminergic neurons can serve as a therapeutic strategy to attenuate pathology of PD. PMID:27065205

  14. Detection of time-varying harmonic amplitude alterations due to spectral interpolations between musical instrument tones.

    PubMed

    Horner, Andrew B; Beauchamp, James W; So, Richard H Y

    2009-01-01

    Gradated spectral interpolations between musical instrument tone pairs were used to investigate discrimination as a function of time-averaged spectral difference. All possible nonidentical pairs taken from a collection of eight musical instrument sounds consisting of bassoon, clarinet, flute, horn, oboe, saxophone, trumpet, and violin were tested. For each pair, several tones were generated with different balances between the primary and secondary instruments, where the balance was fixed across the duration of each tone. Among primary instruments it was found that changes to horn and bassoon [corrected] were most easily discriminable, while changes to saxophone and trumpet timbres were least discriminable. Among secondary instruments, the clarinet had the strongest effect on discrimination, whereas the bassoon had the least effect. For primary instruments, strong negative correlations were found between discrimination and their spectral incoherences, suggesting that the presence of dynamic spectral variations tends to increase the difficulty of detecting time-varying alterations such as spectral interpolation. PMID:19173434

  15. Detection of time-varying harmonic amplitude alterations due to spectral interpolations between musical instrument tones.

    PubMed

    Horner, Andrew B; Beauchamp, James W; So, Richard H Y

    2009-01-01

    Gradated spectral interpolations between musical instrument tone pairs were used to investigate discrimination as a function of time-averaged spectral difference. All possible nonidentical pairs taken from a collection of eight musical instrument sounds consisting of bassoon, clarinet, flute, horn, oboe, saxophone, trumpet, and violin were tested. For each pair, several tones were generated with different balances between the primary and secondary instruments, where the balance was fixed across the duration of each tone. Among primary instruments it was found that changes to horn and bassoon [corrected] were most easily discriminable, while changes to saxophone and trumpet timbres were least discriminable. Among secondary instruments, the clarinet had the strongest effect on discrimination, whereas the bassoon had the least effect. For primary instruments, strong negative correlations were found between discrimination and their spectral incoherences, suggesting that the presence of dynamic spectral variations tends to increase the difficulty of detecting time-varying alterations such as spectral interpolation.

  16. Pathological alterations due to motile Aeromonas infection in red swordtail fish (Xiphophorus helleri).

    PubMed

    Bunnajirakul, S; Pavasutthipaisit, S; Steinhagen, D

    2015-01-01

    A herd of red swordtail fish (Xiphophorus helleri) was reared in outdoor concrete ponds and suffered from occasional mortality. Moribund fishes showing abdominal dropsy and fin rots were sent for diagnosis. Gross necropsy findings showed enlargement of liver, spleen, and kidney in concurrence with congestion, and a severe accumulation of peritoneal fluid. Histopathological findings revealed an alteration of hepatocytes, with a severe diffuse accumulation of fat vacuoles in the cytoplasm. In the trunk kidney, severe accumulation of mononuclear cells together with cloudy swelling of the renal tubular epithelium was observed. From internal organs of the fish motile Aeromonas spp. were identified. The pathological findings might be associated with a long-term infection of affected fish fostered by common stressors such as improper feeding and poor pond environment condition (water temperature). Effective therapeutic measures comprised an advancement of keeping conditions and appropriate feeding to improve the health status in combination with the application of antibiotic substances. PMID:26527040

  17. Long-term prognosis of patients with acute myocardial infarction due to unprotected left main coronary artery disease: a single-centre experience over 14 years

    PubMed Central

    Xu, Li; Sun, Hao; Wang, Le-Feng; Yang, Xin-Chun; Li, Kui-Bao; Zhang, Da-Peng; Wang, Hong-Shi; Li, Wei-Ming

    2016-01-01

    INTRODUCTION Acute myocardial infarction (AMI) due to unprotected left main coronary artery (ULMCA) disease is clinically catastrophic although it has a low incidence. Studies on the long-term prognosis of these patients are rare. METHODS From January 1999 to September 2013, 55 patients whose infarct-related artery was the ULMCA were enrolled. Clinical, angiographic and interventional data was collected. Short-term and long-term clinical follow-up results as well as prognostic determinants during hospitalisation and follow-up were analysed. RESULTS Cardiogenic shock (CS) occurred in 30 (54.5%) patients. During hospitalisation, 22 (40.0%) patients died. Multivariate logistic regression analysis showed that CS (odds ratio [OR] 5.86; p = 0.03), collateral circulation of Grade 2 or 3 (OR 0.14; p = 0.02) and final flow of thrombolysis in myocardial infarction (TIMI) Grade 3 (OR 0.05; p = 0.03) correlated with death during hospitalisation. 33 patients survived to discharge; another seven patients died during the follow-up period of 44.6 ± 31.3 (median 60, range 0.67–117.00) months. The overall mortality rate was 52.7% (n = 29). Kaplan-Meier analysis showed that the total cumulative survival rate was 30.7%. Cox multivariate regression analysis showed that CS during hospitalisation was the only predictor of overall mortality (hazard ratio 4.07, 95% confidence interval 1.40–11.83; p = 0.01). CONCLUSION AMI caused by ULMCA lesions is complicated by high incidence of CS and mortality. CS, poor collateral blood flow and failure to restore final flow of TIMI Grade 3 correlated with death during hospitalisation. CS is the only predictor of long-term overall mortality. PMID:27439434

  18. Sap flow is Underestimated by Thermal Dissipation Sensors due to Alterations of Wood Anatomy

    NASA Astrophysics Data System (ADS)

    Marañón-Jiménez, S.; Wiedemann, A.; van den Bulcke, J.; Cuntz, M.; Rebmann, C.; Steppe, K.

    2014-12-01

    The thermal dissipation technique (TD) is one of the most commonly adopted methods for sap flow measurements. However, underestimations of up to 60% of the tree transpiration have been reported with this technique, although the causes are not certainly known. The insertion of TD sensors within the stems causes damage of the wood tissue and subsequent healing reactions, changing wood anatomy and likely the sap flow path. However, the anatomical changes in response to the insertion of sap flow sensors and the effects on the measured flow have not been assessed yet. In this study, we investigate the alteration of vessel anatomy on wounds formed around TD sensors. Our main objectives were to elucidate the anatomical causes of sap flow underestimation for ring-porous and diffuse-porous species, and relate these changes to sap flow underestimations. Successive sets of TD probes were installed in early, mid and end of the growing season in Fagus sylvatica (diffuse-porous) and Quercus petraea (ring-porous) trees. They were logged after the growing season and additional sets of sensors were installed in the logged stems with presumably no healing reaction. The wood tissue surrounding each sensor was then excised and analysed by X-ray computed microtomography (X-ray micro CT). This technique allowed the quantification of vessel anatomical characteristics and the reconstruction of the 3-D internal microstructure of the xylem vessels so that extension and shape of the altered area could be determined. Gels and tyloses clogged the conductive vessels around the sensors in both beech and oak. The extension of the affected area was larger for beech although these anatomical changes led to similar sap flow underestimations in both species. The higher vessel size in oak may explain this result and, therefore, larger sap flow underestimation per area of affected conductive tissue. The wound healing reaction likely occurred within the first weeks after sensor installation, which

  19. Spatial and Temporal Alterations on Carbon and Water Cycles Due to Grazing

    NASA Astrophysics Data System (ADS)

    Maksimowicz, M. M.; Brunsell, N. A.; Ham, J. M.

    2009-05-01

    Grasslands are vital in the carbon cycle, as large amounts of carbon are stored in the soils of the prairie. As climate change affects the carbon cycle, it is essential for the agricultural communities to understand the impacts of these changes on farming practices such as grazing and meat production. The objective of this study is to determine the effect of grazing on the carbon cycle by characterizing the surface boundary layer of both a grazed field and an ungrazed field. Data were collected from open path eddy covariance systems over Rannells Flint Hills Prairie Preserve in north-central Kansas, one over an ungrazed field and one over a grazed field. Cospectra of fluxes of CO2, heat, water, and momentum for July 2007 were compared to assess the size of eddies contributing energy to each field. For CO2, the cospectra for both the ungrazed and the ungrazed field were similar. For all of the other fluxes, lower frequency eddies contributed more energy in the grazed field than the ungrazed field. By using a footprint model, the contributing source areas were determined for fluxes from May through October of 2007. The grazed field had a larger distance of contribution in both stable and unstable atmospheric conditions. Implications of this study include the alterations on fields and impacts on the carbon and water cycles as a result of grazing.

  20. Golgi enlargement in Arf-depleted yeast cells is due to altered dynamics of cisternal maturation

    PubMed Central

    Bhave, Madhura; Papanikou, Effrosyni; Iyer, Prasanna; Pandya, Koushal; Jain, Bhawik Kumar; Ganguly, Abira; Sharma, Chandrakala; Pawar, Ketakee; Austin, Jotham; Day, Kasey J.; Rossanese, Olivia W.; Glick, Benjamin S.; Bhattacharyya, Dibyendu

    2014-01-01

    ABSTRACT Regulation of the size and abundance of membrane compartments is a fundamental cellular activity. In Saccharomyces cerevisiae, disruption of the ADP-ribosylation factor 1 (ARF1) gene yields larger and fewer Golgi cisternae by partially depleting the Arf GTPase. We observed a similar phenotype with a thermosensitive mutation in Nmt1, which myristoylates and activates Arf. Therefore, partial depletion of Arf is a convenient tool for dissecting mechanisms that regulate Golgi structure. We found that in arf1Δ cells, late Golgi structure is particularly abnormal, with the number of late Golgi cisternae being severely reduced. This effect can be explained by selective changes in cisternal maturation kinetics. The arf1Δ mutation causes early Golgi cisternae to mature more slowly and less frequently, but does not alter the maturation of late Golgi cisternae. These changes quantitatively explain why late Golgi cisternae are fewer in number and correspondingly larger. With a stacked Golgi, similar changes in maturation kinetics could be used by the cell to modulate the number of cisternae per stack. Thus, the rates of processes that transform a maturing compartment can determine compartmental size and copy number. PMID:24190882

  1. Alterations in myocardial metabolism and function at rest in stable angina pectoris: relations with the amount of exercise-induced thallium-201 perfusion defect

    SciTech Connect

    De Kock, M.; Melin, J.A.; Pouleur, H.; Rousseau, M.F.

    1986-01-01

    The relation between the amount of exercise-induced ischemia and alterations in left ventricular (LV) function and metabolism at rest was studied in 18 coronary patients with stable angina pectoris. An ischemic defect area score was computed from quantitative exercise thallium-201 (Tl-201) scintigraphy; this estimation of the amount of ischemic myocardium was used to classify the patients in group I (n = 8; score less than 15%, mean 6.7 +/- 2.5%) and II (n = 10; score greater than 15%; mean 27.2 +/- 8.9%). Hemodynamics and metabolism were studied in basal state. No patient had anginal pain during the study, and the extent of angiographic coronary artery disease (CAD) was comparable in the two groups. Heart rate, aortic pressure, coronary blood flow, and myocardial oxygen uptake were also similar in both groups. However, ejection fraction was reduced in group II (51 +/- 13 vs 63 +/- 5%; p less than 0.01) and LV relaxation was impaired as shown by the increase in time-constant of isovolumic pressure fall (55 +/- 16 vs 44 +/- 6 ms in group I; p less than 0.05); the LV end-diastolic pressure was also increased in group II (19 +/- 8 vs 10 +/- 4 mmHg in group l; p less than 0.05). Furthermore, in group II, myocardial lactate uptake was reduced (4 +/- 19 vs 30 +/- 29 mumole/min in group I; p less than 0.01) and the productions of alanine and glutamine were augmented (-7.5 +/- 4.4 vs -4.6 +/- 1.6 mumole/min in group I; p less than 0.05).

  2. The Asthenosphere Melting Regimes Alteration due to Changing Conditions of Upper Mantle

    NASA Astrophysics Data System (ADS)

    Perepechko, Y. V.; Sharapov, V. N.; Sorokin, K., Jr.

    2014-12-01

    Analyzed in the article are different asthenosphere magma generation regimes above the upper mantle hot spots as thermodynamic and geometric parameters of the upper mantle and the conditions on its boundaries vary. The two-layer mantle model is applied to consider the formation of decompression melting areas. The thickness of metasomatically altered lithospheric mantle is determined by the mantle substance rheology and the location of the upper boundary of asthenosphere. We also take into consideration the principal solid state phase transitions by using the mantle substance state equation. The sizes and distribution of hot spots as well as their maximal temperature were defined by the thermodynamic conditions of the perovskite transition existence. The numerical analysis results demonstrate the manifestation of three main mantle dynamics modes; the conditions necessary to form the partial melting zones are not reached; some melting areas with the 30 to 65 Ma existence time do occur; the melting areas that are formed exist permanently. The permanently existing asthenosphere zones are marked by quasiperiodical variation in thickness and the degree of melting. The typical temperatures of a hot spot sharing these modes are the 1740°С and 2020°С correspondingly. The originally presupposed heating degree and the temperature ratio of the upper mantle do influence the decompression melting degree substantially and - to a lesser extent - they influence the size of melting zones. The primary evolution of the second mode is described by the development of a complex system of asthenosphere zones that lead to the occurrence of additional convectional cells dividing the partial melting zone. The variation in the rheological properties of the mantle substance also contributes to the manifestation of the complex structure of asthenosphere zone. The work was made with support of the Russian Foundation for Basic Research grant #12-05-00625.

  3. Assessing Receiving Water Quality Impacts due to Flow Path Alteration in Residential Catchments, using the Stormwater and Wastewater Management Model

    NASA Astrophysics Data System (ADS)

    Wolosoff, S. E.; Duncan, J.; Endreny, T.

    2001-05-01

    The Croton water supply system, responsible for supplying approximately 10% of New York City's water, provides an opportunity for exploration into the impacts of significant terrestrial flow path alteration upon receiving water quality. Natural flow paths are altered during residential development in order to allow for construction at a given location, reductions in water table elevation in low lying areas and to provide drainage of increased overland flow volumes. Runoff conducted through an artificial drainage system, is prevented from being attenuated by the natural environment, thus the pollutant removal capacity inherent in most natural catchments is often limited to areas where flow paths are not altered by development. By contrasting the impacts of flow path alterations in two small catchments in the Croton system, with different densities of residential development, we can begin to identify appropriate limits to the re-routing of runoff in catchments draining into surface water supplies. The Stormwater and Wastewater Management Model (SWMM) will be used as a tool to predict the runoff quantity and quality generated from two small residential catchments and to simulate the potential benefits of changes to the existing drainage system design, which may improve water quality due to longer residence times.

  4. Myocardial ischemia due to compression of an unruptured thoracic aortic aneurysm in a patient with Marfan syndrome.

    PubMed

    Minami, Hiroya; Asada, Tatsuro; Gan, Kunio; Abe, Koichiro; Izumi, Satoshi

    2007-06-01

    We report a 33-year-old woman who had a 60-mm thoracic aneurysm of the ascending aorta with Marfan syndrome and effort angina due to compression of the right coronary artery (RCA) by the aneurysm. Surgery was performed using the Bentall procedure and a coronary artery bypass graft to the RCA. Postoperatively, coronary angiography showed that the coronary flow of the RCA was restored by removing the aneurysmal compression. The patient was discharged without angina on postoperative day 21. PMID:17642279

  5. Alterations in tissue glutathione and angiotensin converting enzyme due to inhalation of diesel engine exhaust

    SciTech Connect

    Chaudhari, A.; Dutta, S.

    1982-02-01

    Quantitative changes in reduced glutathione (GSH) and angiotensin converting enzyme (ACE) of lung and extrapulmonary tissues were determined following exposure of laboratory animals to diesel engine exhaust (DEE). Exposure of male rats and guinea pigs to DEE containing 750 ..mu..g particulates per cubic meter for 1 wk did not cause any changes in GSH levels of lung, liver, and heart compared to control values. Rats were then exposed for various time periods to 6 mg/m/sup 3/ DEE. Two weeks of exposure produced statistically significant increases of 21 and 7% in GSH levels of lung and liver, respectively, but no change in the heart. Following 4 wk of exposure, lung showed a 14% increase and heat an 11% increase in GSH level. Furthermore, rats exposed for 4 wk to DEE did not show any particular susceptibility toward the GSH-depleting effect of acetaminophen as compared to controls. A significant depletion (15%) of hepatic GSH was observed after 8 wk of exposure, while lung was still showing an increase of 18% in GSH and heart was unaffected. Time-dependent increases of 18 and 33% in serum ACE activity were noted after 4 and 8 wk of exposure. Pulmonary ACE activity did not decrease until after 8 wk, and then to a small extent (7%). The observed increases in GSH may have been related to the presence of NO/sub 2/ in the DEE. On the other hand, the depletion of hepatic GSH suggests production of electrophillic compounds due to an induction of metabolic activity of liver. The change in serum ACE activity may be due to time-requiring perturbations in the pulmonary endothelial cells.

  6. Experimental investigation of injectivity alteration due to salt precipitation during CO2 sequestration in saline aquifers

    NASA Astrophysics Data System (ADS)

    Jeddizahed, Javad; Rostami, Behzad

    2016-10-01

    Injection of CO2 into saline aquifers causes the geochemical reaction of rock-fluid and salt precipitation due to the evaporation of water as a physical process. Well injectivity is an important issue in carbon capture and storage (CCS) projects because large volumes of CO2 must be stored for a long time and salt precipitation can significantly reduce injectivity by reducing the permeability. The impact of salt precipitation on the injectivity must therefore be specified in order to maintain the security of CCS projects and enable them to perform at a high level of practicality. The objective of this work is to investigate the influence of the injection rate and brine salinity on injectivity reduction due to evaporation and salt precipitation. In this study, we injected supercritical CO2 into a sandstone rock sample fully saturated with NaCl brine to characterize the salt precipitation induced by the evaporation process. Evaporation is investigated by mass measurement of the water and vapor produced. The extension in time of salt precipitation and the precipitation profile are analyzed by drying rate measurement, Capillary number and Peclet number. The consequences of salt precipitation on injectivity are specified by permeability and relative permeability analysis. The results show that a high drying rate in the early stage of injection induces rapid salt precipitation. The level of salt precipitation increases with salinity, within a permeability reduction range of 21-66%, and decreases with the injection rate, within a permeability reduction range of 43-62%. The relative permeability of CO2 is affected by both the injection rate and salinity.

  7. Emergency revascularization procedures in patients with acute ST-elevation myocardial infarction due to acute total occlusion of unprotected left main coronary artery: a report of five cases.

    PubMed

    Aygül, Nazif; Aygül, Meryem Ulkü; Ozdemir, Kurtuluş; Altunkeser, Bülent Behlül

    2010-03-01

    Several studies have compared the efficacy of elective coronary artery stenting and coronary artery bypass grafting (CABG) in patients with unprotected left main coronary artery (ULMCA) disease. However, a definite reperfusion modality has yet to be established in ST-elevation myocardial infarction (STEMI) due to acute total occlusion of ULMCA, which has catastrophic clinical results. We presented five patients (3 males, 2 females; mean age 59 years; range 53 to 67 years) with acute anterior STEMI and angiographically documented acute total occlusion of ULMCA. On presentation, all the patients had chest pain and four patients were in cardiogenic shock. All the patients were taken to the catheterization room with minimum delay. Intra-aortic balloon counterpulsation was used during coronary angiography in all the patients. Three patients underwent PCI and, after balloon predilatation, bare-metal stents were implanted and TIMI III flow was achieved. One patient who had atrial fibrillation on admission died on the 14th day of hospitalization after PCI due to pump failure. After diagnostic coronary angiography, two patients were submitted to surgery for emergency CABG. They both died, one within two hours of admission during preparation of the surgical team, and the other on the third postoperative day. Both were in cardiogenic shock on admission.

  8. Alteration of pressure-volume characteristics due to different types of edema induction in isolated rabbit lungs.

    PubMed

    Seeger, W; Wolf, H R; Stähler, G; Neuhof, H

    1983-01-01

    In a model of isolated, ventilated and perfused rabbit lungs the influence of a fixed amount of edema (standardized at 7 g weight gain/kg body weight) on the pressure-volume characteristics of the isolated lungs was investigated. Periodical stimulation with A 23187 or A 23187 plus indomethacin or A 23187 plus indomethacin plus glutathione evokes an increase in vascular permeability with subsequent severe alterations of the pressure-volume characteristics, reflecting a disturbance in the alveolar surfactant system, which is more extensive the more rapidly the edema develops. The alterations caused this way are markedly more severe than those caused by the same amount of weight gain due to mechanically increased capillary filtration pressure. PMID:6410476

  9. Alteration of the oxygen-dependent reactivity of de novo Due Ferri proteins

    NASA Astrophysics Data System (ADS)

    Reig, Amanda J.; Pires, Marcos M.; Snyder, Rae Ana; Wu, Yibing; Jo, Hyunil; Kulp, Daniel W.; Butch, Susan E.; Calhoun, Jennifer R.; Szyperski, Thomas G.; Solomon, Edward I.; Degrado, William F.

    2012-11-01

    De novo proteins provide a unique opportunity to investigate the structure-function relationships of metalloproteins in a minimal, well-defined and controlled scaffold. Here, we describe the rational programming of function in a de novo designed di-iron carboxylate protein from the Due Ferri family. Originally created to catalyse the O2-dependent, two-electron oxidation of hydroquinones, the protein was reprogrammed to catalyse the selective N-hydroxylation of arylamines by remodelling the substrate access cavity and introducing a critical third His ligand to the metal-binding cavity. Additional second- and third-shell modifications were required to stabilize the His ligand in the core of the protein. These structural changes resulted in at least a 106-fold increase in the relative rate between the arylamine N-hydroxylation and hydroquinone oxidation reactions. This result highlights the potential for using de novo proteins as scaffolds for future investigations of the geometric and electronic factors that influence the catalytic tuning of di-iron active sites.

  10. Altering the O2-Dependent Reactivity of de novo Due Ferri Proteins

    PubMed Central

    Reig, Amanda J.; Pires, Marcos M.; Snyder, Rae Ana; Wu, Yibing; Jo, Hyunil; Kulp, Daniel W.; Butch, Susan E.; Calhoun, Jennifer R.; Szyperski, Thomas; Solomon, Edward I.; DeGrado, William F.

    2012-01-01

    De novo proteins provide a unique opportunity for investigating the structure-function relationships of metalloproteins in a minimal, well-defined, and controlled scaffold. Herein, we describe the rational programming of function in a de novo designed di-iron carboxylate protein from the due ferri family. Originally created to catalyze O2-dependent, two-electron oxidation of hydroquinones, the protein was reprogrammed to catalyze the selective N-hydroxylation of arylamines by remodeling the substrate access cavity and introducing a critical third His ligand to the metal binding cavity. Additional second-and third-shell modifications were required to stabilize the His ligand in the core of the protein. These changes resulted in at least a 106 –fold increase in the relative rates of the two reactions. This result highlights the potential for using de novo proteins as scaffolds for future investigations of geometric and electronic factors that influence the catalytic tuning of di-iron active sites. PMID:23089864

  11. Adaptation to altered balance conditions in unilateral amputees due to atherosclerosis: a randomized controlled study

    PubMed Central

    2011-01-01

    Background Amputation impairs the ability to balance. We examined adaptation strategies in balance following dysvascularity-induced unilateral tibial amputation in skilled prosthetic users (SPU) and first fitted amputees (FFA) (N = 28). Methods Excursions of center of pressure (COP) were determined during 20 s quiet standing using a stabilometry system with eyes-open on both legs or on the non-affected leg(s). Main measures: COP trajectories and time functions; distribution of reaction forces between the two legs; inclination angles obtained through second order regression analysis using stabilogram data. Results FFA vs SPU demonstrated 27.8% greater postural sway in bilateral stance (p = 0.0004). Postural sway area was smaller in FFA standing on the non-affected leg compared with SPU (p = 0.028). The slope of the regression line indicating postural stability was nearly identical in FFA and SPU and the direction of regression line was opposite for the left and right leg amputees. Conclusion Of the two adaptation strategies in balance, the first appears before amputation due to pain and fatigue in the affected leg. This strategy appears in the form of reduced postural sway while standing on the non-affected leg. The second adaptation occurs during rehabilitation and regular use of the prosthesis resulting in normal weightbearing associated with reduced postural sway on two legs and return to the normal postural stability on one leg. PMID:21619618

  12. The Kutta-Zhukovsky Lift Theorem revisited: Alteration due to the Viscous Wake

    NASA Astrophysics Data System (ADS)

    Schmitz, Sven

    2011-11-01

    The circulation theory of lift comprised in the classical Kutta-Zhukovsky Lift Theorem forms the foundation of modern aerodynamic wing theory. The theorem has been applied ever since in lifting-line models of aircraft and rotary wings. Reynolds numbers larger than one million support its validity, yet the effect of a viscous wake on a change in the functional relationship between lift and circulation is not taken into account in standard lifting-line analyses. A discrepancy in circulation of more than six percent in comparison to the classical Kutta-Zhukovsky Lift Theorem has been demonstrated by the author (Schmitz & Chattot, Computers & Fluids, 36) for moderately separated flow around a wind turbine airfoil by means of a control volume analysis governed by the Navier-Stokes equations. The present work extends the previous analysis to general three-dimensional flow around a lifting body. An analytical expression is presented that extends the classical Kutta-Zhukovsky Lift Theorem by adding terms to the theorem due to chord- and spanwise vorticity transport. An integrated solution for induced drag is given that has not been documented in previous literature on the subject. The generalized theorem will find future application and quantification in actuator-line methods used to predict wind farm wake interactions with Atmospheric Boundary Layer flow.

  13. Altered combustion characteristics of metallized energetics due to stable secondary material inclusion

    NASA Astrophysics Data System (ADS)

    Terry, Brandon C.

    Though metals and metalloids have been widely considered as reactive fuels, the ability to tune their ignition and combustion characteristics remains challenging. One means to accomplish this may be through low-level inclusion of secondary materials into the metallized fuel. While there are several potential methods to stably introduce secondary inclusion materials, this work focuses on the use of mechanical activation (MA) and metal alloys. Recent work has shown that low-level inclusion of fluoropolymers into aluminum particles can have a substantial effect on their combustion characteristics. The reflected shock ignition of mechanically activated aluminum/polytetrafluoroethylene (MA Al/PTFE) is compared to a physical mixture (PM) of Al/PTFE, neat spherical aluminum, and flake aluminum. It was found that the powders with higher specific surface areas ignited faster than the spherical particles of the same size, and had ignition delay times comparable to agglomerates of aluminum particles that were two orders of magnitude smaller in size. Flake aluminum powder had the same ignition delay as MA Al/PTFE, indicating that any initial aluminum/fluoropolymer reactions did not yield an earlier onset of aluminum oxidation. However, MA Al/PTFE did have a shorter total burn time. The PM of Al/PTFE powder had a shorter ignition delay than neat spherical aluminum due to the rapid decomposition of PTFE into reactive fluorocarbon compounds, but the subsequent fluorocarbon reactions also created a secondary luminosity profile that significantly increased the total burn time of the system. The explosive shock ignition of aluminum and aluminum-silicon eutectic alloy compacts was evaluated with and without polymer inclusions. A statistical analysis was completed, investigating the effects of: detonation train orientation (into or not into a hard surface); the high explosive driver; whether the metal/polymer system is mechanically activated; particle size; particle morphology

  14. An Altered Pattern of Myocardial Histopathological and Molecular Changes Underlies the Different Characteristics of Type-1 and Type-2 Diabetic Cardiac Dysfunction

    PubMed Central

    Radovits, Tamás; Korkmaz, Sevil; Mátyás, Csaba; Oláh, Attila; Páli, Szabolcs; Zubarevich, Alina; Gwanmesia, Patricia Neh; Li, Shiliang; Loganathan, Sivakkanan; Barnucz, Enikő; Merkely, Béla; Szabó, Gábor

    2015-01-01

    Increasing evidence suggests that both types of diabetes mellitus (DM) lead to cardiac structural and functional changes. In this study we investigated and compared functional characteristics and underlying subcellular pathological features in rat models of type-1 and type-2 diabetic cardiomyopathy. Type-1 DM was induced by streptozotocin. For type-2 DM, Zucker Diabetic Fatty (ZDF) rats were used. Left ventricular pressure-volume analysis was performed to assess cardiac function. Myocardial nitrotyrosine immunohistochemistry, TUNEL assay, hematoxylin-eosin, and Masson's trichrome staining were performed. mRNA and protein expression were quantified by qRT-PCR and Western blot. Marked systolic dysfunction in type-1 DM was associated with severe nitrooxidative stress, apoptosis, and fibrosis. These pathological features were less pronounced or absent, while cardiomyocyte hypertrophy was comparable in type-2 DM, which was associated with unaltered systolic function and increased diastolic stiffness. mRNA-expression of hypertrophy markers c-fos, c-jun, and β-MHC, as well as pro-apoptotic caspase-12, was elevated in type-1, while it remained unaltered or only slightly increased in type-2 DM. Expression of the profibrotic TGF-β1 was upregulated in type-1 and showed a decrease in type-2 DM. We compared type-1 and type-2 diabetic cardiomyopathy in standard rat models and described an altered pattern of key pathophysiological features in the diabetic heart and corresponding functional consequences. PMID:25629059

  15. Reverse and pseudo redistribution of thallium-201 in healed myocardial infarction and normal and negative thallium-201 washout in ischemia due to background oversubtraction

    SciTech Connect

    Lear, J.L.; Raff, U.; Jain, R.

    1988-09-15

    While the interpolative background subtraction used in quantitative planar thallium scanning can significantly overestimate the background overlying the heart, the effects of background oversubtraction on quantitative analysis have not been well defined. A mathematical model that relates myocardial washout determined using interpolative background subtraction to true myocardial washout is presented. The model was validated using phantoms and applied to myocardial and pulmonary thallium kinetic data in 100 patients, 85 with and 15 without coronary artery disease. The model showed that when using interpolative background subtraction, measured washout equals true washout in normally perfused myocardium; however, depending on the relation between myocardial and pulmonary thallium clearance, myocardial washout in ischemic regions and areas of infarction can be substantially over- or underestimated. Based on generally accepted quantitative criteria, this incorrect washout determination can at times lead to misdiagnosis of infarction as ischemia and ischemia as normally perfused tissue. It can also cause both ''reverse redistribution'' and ''pseudo redistribution'' of thallium in myocardial infarction in the absence of a physiologic basis.

  16. Reduced Mitochondrial Function in Human Huntington Disease Lymphoblasts is Not Due to Alterations in Cardiolipin Metabolism or Mitochondrial Supercomplex Assembly.

    PubMed

    Mejia, Edgard M; Chau, Sarah; Sparagna, Genevieve C; Sipione, Simonetta; Hatch, Grant M

    2016-05-01

    Huntington's Disease (HD) is an autosomal dominant disease that occurs as a result of expansion of the trinucleotide repeat CAG (glutamine) on the HTT gene. HD patients exhibit various forms of mitochondrial dysfunction within neurons and peripheral tissues. Cardiolipin (Ptd2Gro) is a polyglycerophospholipid found exclusively in mitochondria and is important for maintaining mitochondrial function. We examined if altered Ptd2Gro metabolism was involved in the mitochondrial dysfunction associated with HD. Mitochondrial basal respiration, spare respiratory capacity, ATP coupling efficiency and rate of glycolysis were markedly diminished in Epstein-Barr virus transformed HD lymphoblasts compared to controls (CTRL). Mitochondrial supercomplex formation and Complex I activity within these supercomplexes did not vary between HD patients with different length of CAG repeats and appeared unaltered compared to CTRL. In contrast, in vitro Complex I enzyme activity in mitochondrial enriched samples was reduced in HD lymphoblasts compared to CTRL. The total cellular pool size of Ptd2Gro and its synthesis/remodeling from [(3)H]acetate/[(14)C]oleate were unaltered in HD lymphoblasts compared to CTRL. In addition, the molecular species of Ptd2Gro were essentially unaltered in HD lymphoblasts compared to CTRL. We conclude that compared to CTRL lymphoblasts, HD lymphoblasts display impaired mitochondrial basal respiration, spare respiratory capacity, ATP coupling efficiency and rate of glycolysis with any pathological CAG repeat length, but this is not due to alterations in Ptd2Gro metabolism. We suggest that HD patient lymphoblasts may be a useful model to study defective energy metabolism that does not involve alterations in Ptd2Gro metabolism. PMID:26846325

  17. Pain hypersensitivity induced by paradoxical sleep deprivation is not due to altered binding to brain mu-opioid receptors.

    PubMed

    Nascimento, Danielle C; Andersen, Monica L; Hipólide, Débora Cristina; Nobrega, José N; Tufik, Sergio

    2007-03-28

    Previous studies have established a relationship between sleep disruption and pain, and it has been suggested that hyperalgesia induced by paradoxical sleep deprivation (PSD) could be due to a reduction of opioidergic neurotransmission in the brain. In the present study rats deprived of sleep for 96 h as well as rats allowed to recover for 24h after PSD and normal controls received vehicle or morphine (2.5, 5 and 10 mg/kg, i.p.) and were tested on a hot plate 1h later. Quantitative receptor autoradiography was used to map alterations in binding to brain mu-opioid receptors in separate groups. Results demonstrated that PSD induced a significant reduction in thermal pain threshold, as measured by paw withdrawal latencies. This effect did not return to baseline control values after 24h of sleep recovery. The usual analgesic effect of morphine was observed in the control group but not in PSD or rebound groups except at the highest dose (10 mg/kg). Binding of [3H]DAMGO to mu sites did not differ significantly among the three groups in any of the 33 brain regions examined. These results do not exclude the participation of the opioid system in PSD-induced pain hypersensitivity since sleep-deprived rats were clearly resistant to morphine. However, the fact no changes were seen in [3H]DAMGO binding indicates that mechanisms other than altered mu-opioid binding must be sought to explain the phenomenon.

  18. Modeling of the relationship between the environmental air pollution, clinical risk factors, and hospital mortality due to myocardial infarction in Isfahan, Iran

    PubMed Central

    Sadeghi, Mehraban; Ahmadi, Ali; Baradaran, Azar; Masoudipoor, Neda; Frouzandeh, Soleiman

    2015-01-01

    Background: This study aimed to determine the relationship between the environmental factor, clinical risk factors, and individual variables with mortality due to acute myocardial infarction (MI) in Isfahan. Materials and Methods: This cross-sectional study was performed between April 2012 and March 2013. The data on the patients’ mortality due to MI in Isfahan were obtained from the MI National Registry. The international classification system (ICD10: I21-I22) was used to diagnose MI. The air quality indicators and environmental variables were used to measure the air pollution. Multilevel logistic regression in the Stata software was used to determine the factors associated with mortality in patients and odds ratios (ORs) were calculated. Results: Six hundred eleven patients with MI were studied during 1-year. 444 (72.2%) patients were male and the rest were female. 4.7% of the patients died due to MI. The mean age at MI incidence was 62.2 ± 13 years. Of the air pollution parameters, PM10 had the maximum mean concentration (49.113 ppm), followed by NOX, NO, NO2, CO, SO2, and O3. The adjusted OR of mortality was derived 2.07 (95% CI: 1.5-2.85) for right bundle branch block, 1.5 (95% CI: 1.3-1.7) for ST-segment elevation MI, 1.84 (95% CI: 1.13-3) for age, 1.06 (95% CI: 1.01-1.20) for CO, 1.1 (95% CI: 1.03-1.30) for O3, and 1.04 (95% CI: 1.01-1.4) for SO2, all of which were considered as the risk factors of mortality. However, OR of mortality was 0.79 for precipitation (95% CI: 0.74-0.84) and 0.52 for angioplasty (95% CI: 0.4-0.68) were considered as protective factors of mortality. The individual characteristics including age, history of MI in the immediate family, hypertension, and diabetes were significantly associated with mortality from MI. The indices of air pollution including SO2, CO, O3, and environmental factors such as the precipitation and temperature were the determinants of mortality in patients with MI. Conclusion: With regards to the factors

  19. Gray matter alterations in visual cortex of patients with loss of central vision due to hereditary retinal dystrophies.

    PubMed

    Plank, Tina; Frolo, Jozef; Brandl-Rühle, Sabine; Renner, Agnes B; Hufendiek, Karsten; Helbig, Horst; Greenlee, Mark W

    2011-06-01

    In patients with central visual field scotomata a large part of visual cortex is not adequately stimulated. Over time this lack of input could lead to a reduction of gray matter in the affected cortical areas. We used Voxel Based Morphometry to investigate structural brain changes in patients with central scotomata due to hereditary retinal dystrophies and compared their results to those of normal sighted subjects. Additionally we correlated clinical and demographic characteristics like duration of disease, scotoma size, visual acuity, fixation stability and reading speed to the amount of gray matter in whole brain analyses within the patient group. We found a decrease in gray matter around the lesion projection zone in visual cortex of patients in comparison to controls. Gray matter loss along the posterior and middle portions of the calcarine sulcus is also correlated with scotoma size, indicating that indeed the lack of functional input provokes the gray matter alterations. In whole brain regression analyses within the patient group we found an additional cluster in the right superior and middle frontal gyri, slightly anterior to the frontal eye fields, where gray matter correlated positively with fixation stability. This could be regarded as a consequence of oculomotor learning.

  20. Loss of TLR3 aggravates CHIKV replication and pathology due to an altered virus-specific neutralizing antibody response

    PubMed Central

    Her, Zhisheng; Teng, Terk-Shin; Tan, Jeslin JL; Teo, Teck-Hui; Kam, Yiu-Wing; Lum, Fok-Moon; Lee, Wendy WL; Gabriel, Christelle; Melchiotti, Rossella; Andiappan, Anand K; Lulla, Valeria; Lulla, Aleksei; Win, Mar K; Chow, Angela; Biswas, Subhra K; Leo, Yee-Sin; Lecuit, Marc; Merits, Andres; Rénia, Laurent; Ng, Lisa FP

    2015-01-01

    RNA-sensing toll-like receptors (TLRs) mediate innate immunity and regulate anti-viral response. We show here that TLR3 regulates host immunity and the loss of TLR3 aggravates pathology in Chikungunya virus (CHIKV) infection. Susceptibility to CHIKV infection is markedly increased in human and mouse fibroblasts with defective TLR3 signaling. Up to 100-fold increase in CHIKV load was observed in Tlr3−/− mice, alongside increased virus dissemination and pro-inflammatory myeloid cells infiltration. Infection in bone marrow chimeric mice showed that TLR3-expressing hematopoietic cells are required for effective CHIKV clearance. CHIKV-specific antibodies from Tlr3−/− mice exhibited significantly lower in vitro neutralization capacity, due to altered virus-neutralizing epitope specificity. Finally, SNP genotyping analysis of CHIKF patients on TLR3 identified SNP rs6552950 to be associated with disease severity and CHIKV-specific neutralizing antibody response. These results demonstrate a key role for TLR3-mediated antibody response to CHIKV infection, virus replication and pathology, providing a basis for future development of immunotherapeutics in vaccine development. PMID:25452586

  1. Hydrogeochemical alteration of groundwater due to a CO2 injection test into a shallow aquifer in Northeast Germany

    NASA Astrophysics Data System (ADS)

    Dethlefsen, Frank; Peter, Anita; Hornbruch, Götz; Lamert, Hendrik; Garbe-Schönberg, Dieter; Beyer, Matthias; Dietrich, Peter; Dahmke, Andreas

    2014-05-01

    The accidental release of CO2 into potable aquifers, for instance as a consequence of a leakage out of a CO2 store site, can endanger drinking water resources due to the induced geochemical processes. A 10-day CO2 injection experiment into a shallow aquifer was carried out in Wittstock (Northeast Germany) in order to investigate the geochemical impact of a CO2 influx into such an aquifer and to test different monitoring methods. Information regarding the site investigation, the injection procedure monitoring setup, and first geochemical monitoring results are described in [1]. Apart from the utilization of the test results to evaluate monitoring approaches [2], further findings are presented on the evaluation of the geophysical monitoring [3], and the monitoring of stable carbon isotopes [4]. This part of the study focuses of the hydrogeochemical alteration of groundwater due to the CO2 injection test. As a consequence of the CO2 injection, major cations were released, i.e. concentrations increased, whereas major anion concentrations - beside bicarbonate - decreased, probably due to increased anion sorption capacity at variably charged exchange sites of minerals. Trace element concentrations increased as well significantly, whereas the relative concentration increase was far larger than the relative concentration increase of major cations. Furthermore, geochemical reactions show significant spatial heterogeneity, i.e. some elements such as Cr, Cu, Pb either increased in concentration or remained at stable concentrations with increasing TIC at different wells. Statistical analyses of regression coefficients confirm the different spatial reaction patterns at different wells. Concentration time series at single wells give evidence, that the trace element release is pH dependent, i.e. trace elements such as Zn, Ni, Co are released at pH of around 6.2-6.6, whereas other trace elements like As, Cd, Cu are released at pH of 5.6-6.4. [1] Peter, A., et al., Investigation of

  2. A bypass case due to an acute inferior myocardial infarction caused by vascular occlusion of the left subclavian artery and left anterior descending artery

    PubMed Central

    Altas, Yakup; Ulugg, Ali Veysel

    2016-01-01

    ST segment elevation is the most common electrocardiographic finding in acute myocardial infarction. ST elevation in chest leads generally represents left anterior descending artery occlusion, while elevation in DII and III, and aVF represents right coronary and circumflex artery occlusion. A female patient aged 66 years was admitted to our emergency service with ST elevation in leads DIII and aVF. A diagnosis of acute inferior myocardial infarction was made. The patient’s history included coronary artery bypass graft involving the left internal mammary artery to the left anterior descending coronary artery and aorta to the right coronary artery. The patient was taken to the cardiac catheterization laboratory for primary percutaneous coronary intervention and a lesion in the left anterior descending artery was identified. Additionally, the left subclavian artery was totally occluded. Following intervention to the lesion, the patient was discharged on day 4 of admission. PMID:27555777

  3. A bypass case due to an acute inferior myocardial infarction caused by vascular occlusion of the left subclavian artery and left anterior descending artery.

    PubMed

    Altas, Yakup; Ulugg, Ali Veysel

    2016-01-01

    ST segment elevation is the most common electrocardiographic finding in acute myocardial infarction. ST elevation in chest leads generally represents left anterior descending artery occlusion, while elevation in DII and III, and aVF represents right coronary and circumflex artery occlusion. A female patient aged 66 years was admitted to our emergency service with ST elevation in leads DIII and aVF. A diagnosis of acute inferior myocardial infarction was made. The patient's history included coronary artery bypass graft involving the left internal mammary artery to the left anterior descending coronary artery and aorta to the right coronary artery. The patient was taken to the cardiac catheterization laboratory for primary percutaneous coronary intervention and a lesion in the left anterior descending artery was identified. Additionally, the left subclavian artery was totally occluded. Following intervention to the lesion, the patient was discharged on day 4 of admission. PMID:27555777

  4. Fetal rat metabonome alteration by prenatal caffeine ingestion probably due to the increased circulatory glucocorticoid level and altered peripheral glucose and lipid metabolic pathways

    SciTech Connect

    Liu, Yansong; Xu, Dan; Feng, Jianghua; Kou, Hao; Liang, Gai; Yu, Hong; He, Xiaohua; Zhang, Baifang; Chen, Liaobin; Magdalou, Jacques; Wang, Hui

    2012-07-15

    The aims of this study were to clarify the metabonome alteration in fetal rats after prenatal caffeine ingestion and to explore the underlying mechanism pertaining to the increased fetal circulatory glucocorticoid (GC). Pregnant Wistar rats were daily intragastrically administered with different doses of caffeine (0, 20, 60 and 180 mg/kg) from gestational days (GD) 11 to 20. Metabonome of fetal plasma and amniotic fluid on GD20 were analyzed by {sup 1}H nuclear magnetic resonance-based metabonomics. Gene and protein expressions involved in the GC metabolism, glucose and lipid metabolic pathways in fetal liver and gastrocnemius were measured by real-time RT-PCR and immunohistochemistry. Fetal plasma metabonome were significantly altered by caffeine, which presents as the elevated α- and β‐glucose, reduced multiple lipid contents, varied apolipoprotein contents and increased levels of a number of amino acids. The metabonome of amniotic fluids showed a similar change as that in fetal plasma. Furthermore, the expressions of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD-2) were decreased, while the level of blood GC and the expressions of 11β-HSD-1 and glucocorticoid receptor (GR) were increased in fetal liver and gastrocnemius. Meanwhile, the expressions of insulin-like growth factor 1 (IGF-1), IGF-1 receptor and insulin receptor were decreased, while the expressions of adiponectin receptor 2, leptin receptors and AMP-activated protein kinase α2 were increased after caffeine treatment. Prenatal caffeine ingestion characteristically change the fetal metabonome, which is probably attributed to the alterations of glucose and lipid metabolic pathways induced by increased circulatory GC, activated GC metabolism and enhanced GR expression in peripheral metabolic tissues. -- Highlights: ► Prenatal caffeine ingestion altered the metabonome of IUGR fetal rats. ► Caffeine altered the glucose and lipid metabolic pathways of IUGR fetal rats. ► Prenatal caffeine

  5. Alteration of the Carbon and Nitrogen Isotopic Composition in the Martian Surface Rocks Due to Cosmic Ray Exposure

    NASA Technical Reports Server (NTRS)

    Pavlov, A. A.; Pavlov, A. K.; Ostryakov, V. M.; Vasilyev, G. I.; Mahaffy, P.; Steele, A.

    2014-01-01

    C-13/C-12 and N-15/N-14 isotopic ratios are pivotal for our understanding of the Martian carbon cycle, history of the Martian atmospheric escape, and origin of the organic compounds on Mars. Here we demonstrate that the carbon and nitrogen isotopic composition of the surface rocks on Mars can be significantly altered by the continuous exposure of Martian surface to cosmic rays. Cosmic rays can effectively produce C-13 and N-15 isotopes via spallation nuclear reactions on oxygen atoms in various Martian rocks. We calculate that in the top meter of the Martian rocks, the rates of production of both C-13 and N-15 due to galactic cosmic rays (GCRs) exposure can vary within 1.5-6 atoms/cm3/s depending on rocks' depth and chemical composition. We also find that the average solar cosmic rays can produce carbon and nitrogen isotopes at a rate comparable to GCRs in the top 5-10 cm of the Martian rocks. We demonstrate that if the total carbon content in a surface Martian rock is <10 ppm, then the "light," potentially "biological" C-13/C-12 ratio would be effectively erased by cosmic rays over 3.5 billion years of exposure. We found that for the rocks with relatively short exposure ages (e.g., 100 million years), cosmogenic changes in N-15/N-14 ratio are still very significant. We also show that a short exposure to cosmic rays of Allan Hills 84001 while on Mars can explain its high-temperature heavy nitrogen isotopic composition (N-15/N-14). Applications to Martian meteorites and the current Mars Science Laboratory mission are discussed.

  6. High-fat, low-carbohydrate diet alters myocardial oxidative stress and impairs recovery of cardiac function after ischemia and reperfusion in obese rats.

    PubMed

    Liu, Jian; Lloyd, Steven G

    2013-04-01

    Obesity is associated with elevated risk of heart disease. A solid understanding of the safety and potential adverse effects of high-fat, low-carbohydrate diet (HFLCD) similar to that used by humans for weight loss on the heart is crucial. High fat intake is known to promote increases in reactive oxygen species and mitochondrial damage. We hypothesized that there would be adverse effects of HFLCD on myocardial ischemia/reperfusion injury through enhancing oxidative stress injury and impairing mitochondrial biogenesis in a nongenetic, diet-induced rat model of obesity. To test the hypothesis, 250-g male Sprague-Dawley rats were fed an obesity-promoting diet for 7 weeks to induce obesity, then switched to HFLCD or a low-fat control diet for 2 weeks. Isolated hearts underwent global low flow ischemia for 60 minutes and reperfusion for 60 minutes. High-fat, low-carbohydrate diet resulted in greater weight gain and lower myocardial glycogen, plasma adiponectin, and insulin. Myocardial antioxidant gene transcript and protein expression of superoxide dismutase and catalase were reduced in HFLCD, along with increased oxidative gene NADPH oxidase-4 transcript and xanthine oxidase activity, and a 37% increase in nitrated protein (nitrotyrosine) in HFLCD hearts. The cardiac expression of key mitochondrial regulatory factors such as nuclear respiratory factor-1 and transcription factor A-mitochondrial were inhibited and myocardial mitochondrial DNA copy number decreased. The cardiac expression of adiponectin and its receptors was down-regulated in HFLCD. High-fat, low-carbohydrate diet impaired recovery of left ventricular rate-pressure product after ischemia/reperfusion and led to 3.5-fold increased injury as measured by lactate dehydrogenase release. In conclusion, HFLCD leads to increased ischemic myocardial injury and impaired recovery of function after reperfusion and was associated with attenuation of mitochondrial biogenesis and enhanced oxidative stress in obese rats

  7. Myocardial diseases of animals.

    PubMed Central

    Van Vleet, J. F.; Ferrans, V. J.

    1986-01-01

    In this review we have attempted a comprehensive compilation of the cardiac morphologic changes that occur in spontaneous and experimental myocardial diseases of animals. Our coverage addresses diseases of mammals and birds and includes these diseases found in both domesticated and wild animals. A similar review of the myocardial diseases in this broad range of animal species has not been attempted previously. We have summarized and illustrated the gross, microscopic, and ultrastructural alterations for these myocardial diseases; and, whenever possible, we have reviewed their biochemical pathogenesis. We have arranged the myocardial diseases for presentation and discussion according to an etiologic classification with seven categories. These include a group of idiopathic or primary cardiomyopathies recognized in man (hypertrophic, dilated, and restrictive types) and a large group of secondary cardiomyopathies with known causes, such as inherited tendency; nutritional deficiency; toxicity; physical injury and shock; endocrine disorders, and myocarditides of viral, bacterial, and protozoal causation. Considerable overlap exists between each of the etiologic groups in the spectrum of pathologic alterations seen in the myocardium. These include various degenerative changes, myocyte necrosis, and inflammatory lesions. However, some diseases show rather characteristic myocardial alterations such as vacuolar degeneration in anthracycline cardiotoxicity, myofibrillar lysis in furazolidone cardiotoxicity, calcification in calcinosis of mice, glycogen accumulation in the glycogenoses, lipofuscinosis in cattle, fatty degeneration in erucic acid cardiotoxicity, myofiber disarray in hypertrophic cardiomyopathy, and lymphocytic inflammation with inclusion bodies in canine parvoviral myocarditis. The myocardial diseases represent the largest group in the spectrum of spontaneous cardiac diseases of animals. Pericardial and endocardial diseases and congential cardiac diseases are

  8. The altered expression profile of microRNAs in cardiopulmonary bypass canine models and the effects of mir-499 on myocardial ischemic reperfusion injury

    PubMed Central

    2013-01-01

    Background MicroRNAs were enrolled in various cardiovascular disease especially ischemic heart diseases, but the microRNA changes during myocardial ischemia reperfusion injury underwent cardiopulmonary bypass are still unknown. This study screens the microRNA differences in CPB canines and evaluates the relationship of microRNAs with myocardial ischemia reperfusion injury. Methods 13 healthy canines received CPB with 60 minutes of aortic clamping and cardioplegic arrest, followed by 90 minutes reperfusion. Left ventricular myocardial samples, blood samples and hemodynamic data were taken at different time points. We performed microRNAs microarray experiments upon the left ventricle myocardium tissue of canines before CPB and after reperfusion for 90 minutes by pooling 3 tissue samples together and used qRT-PCR for confirmation. Results Statistically significant difference was found in mir-499 level before CPB and after reperfusion (T1 vs. T4, p = 0.041). We further examined the mir-499 levels by using qRT-PCR in all 13 canines at 4 different time points (T1 vs. T4, p = 0.029). Mir-499 expression was negatively correlated with cardiac troponin T (cTnT) and creatine kinase- MB (CK-MB) levels of canines in all time points samples (r = 0.469, p < 0.001 and r = 0.273, p = 0.050 respectively). Moreover, higher mir-499 expression level was associated with higher dP/dtmax at 25 minutes and 90 minutes after reperfusion. Conclusion Myocardial ischemic reperfusion injury with cardiopulmonary bypass results in declining level of mir-499 expression in left ventricle myocardium of canines, suggesting mir-499 would be a potential therapeutic target in cardiac protection during open heart surgery. PMID:23800236

  9. 5-Lipoxygenase facilitates healing after myocardial infarction.

    PubMed

    Blömer, Nadja; Pachel, Christina; Hofmann, Ulrich; Nordbeck, Peter; Bauer, Wolfgang; Mathes, Denise; Frey, Anna; Bayer, Barbara; Vogel, Benjamin; Ertl, Georg; Bauersachs, Johann; Frantz, Stefan

    2013-07-01

    Early healing after myocardial infarction (MI) is characterized by a strong inflammatory reaction. Most leukotrienes are pro-inflammatory and are therefore potential mediators of healing and remodeling after myocardial ischemia. The enzyme 5-lipoxygenase (5-LOX) has a key role in the transformation of arachidonic acid in leukotrienes. Thus, we tested the effect of 5-LOX on healing after MI. After chronic coronary artery ligation, early mortality was significantly increased in 5-LOX(-/-) when compared to matching wildtype (WT) mice due to left ventricular rupture. This effect could be reproduced in mice treated with the 5-LOX inhibitor Zileuton. A perfusion mismatch due to the vasoactive potential of leukotrienes is not responsible for left ventricular rupture since local blood flow assessed by magnetic resonance perfusion measurements was not different. However, after MI, there was an accentuation of the inflammatory reaction with an increase of pro-inflammatory macrophages. Yet, mortality was not changed in chimeric mice (WT vs. 5-LOX(-/-) bone marrow in 5-LOX(-/-) animals), indicating that an altered function of 5-LOX(-/-) inflammatory cells is not responsible for the phenotype. Collagen production and accumulation of fibroblasts were significantly reduced in 5-LOX(-/-) mice in vivo after MI. This might be due to an impaired migration of 5-LOX(-/-) fibroblasts, as shown in vitro to serum. In conclusion, a lack or inhibition of 5-LOX increases mortality after MI because of healing defects. This is not mediated by a change in local blood flow, but through an altered inflammation and/or fibroblast function.

  10. Myocardial infarction resulting from coronary artery dissection in an adolescent with Ehlers-Danlos syndrome type IV due to a type III collagen mutation.

    PubMed Central

    Adès, L. C.; Waltham, R. D.; Chiodo, A. A.; Bateman, J. F.

    1995-01-01

    Ehlers-Danlos syndrome encompasses a group of inherited disorders of connective tissue, some of which are characterised by abnormalities of collagen metabolism. The chromosomal location, identified genes and biochemical defects, inheritance pattern, and clinical features for the various known subtypes are outlined. Prenatal diagnosis is possible for types IV, VI, VIIA1, and VIIA2. An unusual presentation of type IV Ehlers-Danlos syndrome in a 16 year old boy with an anterior myocardial infarction resulting from dissection of the left anterior descending coronary artery is reported here. A clinical diagnosis of type IV Ehlers-Danlos syndrome was made subsequently and confirmed by the reduced production, impaired secretion, and abnormally slow electrophoretic migration of type III collagen, indicating an underlying mutation in the COL3A1 gene. This patient represents the first case of type IV Ehlers-Danlos syndrome with symptomatic coronary artery dissection. Images PMID:7546986

  11. [Myocardial infarction as a work accident in Polish Supreme Court decisions. Part II. Job contraindications due to an employee's state of health].

    PubMed

    Jurczyk, Agnieszka P; Berent, Jarosław; Markuszewski, Leszek; Szram, Stefan

    2003-01-01

    This paper presents the second part on opinions given by the Polish Supreme Court on the acceptance of myocardial infarction as work accident. This it can be seen that, in certain cases, the judgements of the Court are contradictory. For in some cases, an external cause is recognized in the act of permitting employees to work whose state of health would contraindicate the performance of their duties, while in others, the principle is accepted that work duties not considered harmful for healthy people cannot be deemed an external cause for people with health problems. An external cause according to the Supreme Court may also be the act of allowing an employee to work without a valid medical examination, or even by not conducting routine required work-related medical examinations on time.

  12. Myocardial ischemia due to a type IV dual LAD with the long LAD arising from the right sinus of valsalva: a case report and literature review.

    PubMed

    Gao, Xiangyu; Li, Hongwei; Chen, Hui

    2015-01-01

    We herein report the case of a 60-year-old man who presented with chest discomfort. Coronary angiography demonstrated that the short left anterior descending artery (LAD) arose from the left main coronary artery and the long LAD from the right coronary sinus of Valsalva, which was confirmed by 64-slice multidetector computed tomography coronary angiography. Single-photon emission computed tomography revealed a significant, almost irreversible degree of hypoperfusion in the anterior wall of the left ventricle, thus indicating that the short LAD was associated with myocardial ischemia and severe atherosclerotic lesions. Therefore, SPECT showed that the myocardium was largely necrotic, and we did not perform angioplasty for the short LAD. PMID:26466699

  13. Radiation damage of strontium iodide crystals due to irradiation by 137Cs gamma rays: A novel approach to altering nonproportionality

    NASA Astrophysics Data System (ADS)

    Caudel, David; McCurdy, Michael; Fleetwood, Daniel M.; Reed, Robert A.; Weller, Robert A.; Goodwin, Brandon; Rowe, Emmanuel; Buliga, Vladimir; Groza, Michael; Stassun, Keivan; Burger, Arnold

    2016-11-01

    Strontium iodide doped with europium (SrI2:Eu2+) is a new scintillator being developed for use in high-energy astrophysical detectors with excellent energy resolution. Nonproportionality is the primary limiting factor to improving its energy resolution, although the physics of nonproportionality is not yet fully understood. In the past few years, co-dopants have been used to alter nonproportionality. By irradiating a SrI2:Eu2+ sample with a 2255 Ci 137Cs source, we explore both the crystal's potential for space-based applications in a radiation environment and this new method of altering nonproportionality. At 6200 Gy irradiation, a drop of 7.8% at 700 nm and a drop of 14.1% at 450 nm were seen in the transmission spectrum. Nonproportionality was also reduced after irradiation, shifting from 87% to 101% of the theoretical light yield at 32.1 keV, while the 4.7 keV peak decreased 40% closer to its theoretical value. We propose a novel method of altering the nonproportionality of scintillators, using radiation-induced F-centers in place of co-dopants.

  14. Myocardial Bridge

    MedlinePlus

    ... artery. See also on this site: Ask a Texas Heart Institute Doctor: Search "myocardial bridge" Updated August ... comments. Terms of Use and Privacy Policy © Copyright Texas Heart Institute All rights reserved.

  15. Complex level alterations of the 2f (1)-f (2) distortion product due to hypoxia in the guinea pig.

    PubMed

    Olzowy, Bernhard; von Gleichenstein, Gregor; Canis, Martin; Plesnila, Nikolaus; Mees, Klaus

    2008-11-01

    It is controversially discussed inasmuch acute hearing disorders might originate from impaired cochlear circulation. Hypoxia-specific alterations of inner ear parameters measurable in patients with acute sensorineural hearing loss would therefore be of great interest. Aim of this study was to characterize hypoxia-related alterations of the 2f (1)-f (2) distortion product. Nine guinea pigs were anaesthetized by i.m. administration of Midazolam, Medetomidin and Fentanyl. For introduction of hypoxia, the spontaneously breathing animals were offered a gas mixture of N(2)O and O(2) containing either 21 or 12-13% O(2). Distortion product otoacoustic emissions (DPOAEs) were continuously monitored at f (2) = 16 kHz; f (2)/f (1) = 1, 2; DP-definition = 2f (1)-f (2); L (1) = 65 dB and L (2) = 55 dB, while inhaled oxygen was switched from 21 to 12-13% and back. Oxygen saturation (SaO(2)) was continuously monitored. Data from an hypoxic interval were only used for further data processing if DPOAE levels were stable before and after hypoxia. Six hypoxic intervals in five animals fulfilled the stability criterion. During the hypoxic interval with the highest measured SaO(2) (75%), no alterations of DPOAE levels were observed. During the remaining five hypoxic intervals, when SaO(2) ranged between 57 and 70%, DPOAE levels were on average lower with an increased standard deviation compared to mean pre-hypoxic levels. Mean decrease correlated with the decrease of SaO(2 )(r = 0.90, P = 0.014). Alterations followed a characteristic time course-when hypoxia was started, DPOAE levels exhibited a short increase before they decreased and remarkably destabilized. After re-oxygenation DPOAE levels showed a pronounced level decrease, while SaO(2) already had recovered to pre-hypoxic values. After reaching a minimum, DPOAE levels slowly recovered to pre-hypoxic values. The decrease of DPOAE levels during hypoxia and the post-hypoxic level alterations have similarly been described by other

  16. Bentonite alteration due to thermal-hydro-chemical processes during the early thermal period in a nuclear waste repository

    SciTech Connect

    Xu, T.; Senger, R.; Finsterle, S.

    2011-02-01

    After closure of an underground nuclear waste repository, the decay of radionuclides will raise temperature in the repository, and the bentonite buffer will resaturate by water inflow from the surrounding host rock. The perturbations from these thermal and hydrological processes are expected to dissipate within hundreds to a few thousand years. Here, we investigate coupled thermal-hydro-chemical processes and their effects on the short-term performance of a potential nuclear waste repository located in a clay formation. Using a simplified geometric configuration and abstracted hydraulic parameters of the clayey formation, we examine geochemical processes, coupled with thermo-hydrologic phenomena, and potential changes in porosity near the waste container during the early thermal period. The developed models were used for evaluating the mineral alterations and potential changes in porosity of the buffer, which can affect the repository performance. The results indicate that mineral alteration and associated changes in porosity induced by early thermal and hydrological processes are relatively small and are expected to not significantly affect flow and transport properties. Chlorite precipitation was obtained in all simulation cases. A maximum of one percent volume fraction of chlorite could be formed, whose process may reduce swelling and sorption capacity of bentonite clay, affecting the performance of the repository. llitisation process was not obtained from the present simulations.

  17. Alterations in the coupling functions between cortical and cardio-respiratory oscillations due to anaesthesia with propofol and sevoflurane

    PubMed Central

    Petkoski, Spase; Raeder, Johan; Smith, Andrew F.; McClintock, Peter V. E.; Stefanovska, Aneta

    2016-01-01

    The precise mechanisms underlying general anaesthesia pose important and still open questions. To address them, we have studied anaesthesia induced by the widely used (intravenous) propofol and (inhalational) sevoflurane anaesthetics, computing cross-frequency coupling functions between neuronal, cardiac and respiratory oscillations in order to determine their mutual interactions. The phase domain coupling function reveals the form of the function defining the mechanism of an interaction, as well as its coupling strength. Using a method based on dynamical Bayesian inference, we have thus identified and analysed the coupling functions for six relationships. By quantitative assessment of the forms and strengths of the couplings, we have revealed how these relationships are altered by anaesthesia, also showing that some of them are differently affected by propofol and sevoflurane. These findings, together with the novel coupling function analysis, offer a new direction in the assessment of general anaesthesia and neurophysiological interactions, in general. PMID:27045000

  18. Altered joint tribology in osteoarthritis: Reduced lubricin synthesis due to the inflammatory process. New horizons for therapeutic approaches.

    PubMed

    Szychlinska, M A; Leonardi, R; Al-Qahtani, M; Mobasheri, A; Musumeci, G

    2016-06-01

    Osteoarthritis (OA) is the most common form of joint disease. This review aimed to consolidate the current evidence that implicates the inflammatory process in the attenuation of synovial lubrication and joint tissue homeostasis in OA. Moreover, with these findings, we propose some evidence for novel therapeutic strategies for preventing and/or treating this complex disorder. The studies reviewed support that inflammatory mediators participate in the onset and progression of OA after joint injury. The flow of pro-inflammatory cytokines following an acute injury seems to be directly associated with altered lubricating ability in the joint tissue. The latter is associated with reduced level of lubricin, one of the major joint lubricants. Future research should focus on the development of new therapies that attenuate the inflammatory process and restore lubricin synthesis and function. This approach could support joint tribology and synovial lubrication leading to improved joint function and pain relief.

  19. Alterations in the coupling functions between cortical and cardio-respiratory oscillations due to anaesthesia with propofol and sevoflurane

    NASA Astrophysics Data System (ADS)

    Stankovski, Tomislav; Petkoski, Spase; Raeder, Johan; Smith, Andrew F.; McClintock, Peter V. E.; Stefanovska, Aneta

    2016-05-01

    The precise mechanisms underlying general anaesthesia pose important and still open questions. To address them, we have studied anaesthesia induced by the widely used (intravenous) propofol and (inhalational) sevoflurane anaesthetics, computing cross-frequency coupling functions between neuronal, cardiac and respiratory oscillations in order to determine their mutual interactions. The phase domain coupling function reveals the form of the function defining the mechanism of an interaction, as well as its coupling strength. Using a method based on dynamical Bayesian inference, we have thus identified and analysed the coupling functions for six relationships. By quantitative assessment of the forms and strengths of the couplings, we have revealed how these relationships are altered by anaesthesia, also showing that some of them are differently affected by propofol and sevoflurane. These findings, together with the novel coupling function analysis, offer a new direction in the assessment of general anaesthesia and neurophysiological interactions, in general.

  20. Altered joint tribology in osteoarthritis: Reduced lubricin synthesis due to the inflammatory process. New horizons for therapeutic approaches.

    PubMed

    Szychlinska, M A; Leonardi, R; Al-Qahtani, M; Mobasheri, A; Musumeci, G

    2016-06-01

    Osteoarthritis (OA) is the most common form of joint disease. This review aimed to consolidate the current evidence that implicates the inflammatory process in the attenuation of synovial lubrication and joint tissue homeostasis in OA. Moreover, with these findings, we propose some evidence for novel therapeutic strategies for preventing and/or treating this complex disorder. The studies reviewed support that inflammatory mediators participate in the onset and progression of OA after joint injury. The flow of pro-inflammatory cytokines following an acute injury seems to be directly associated with altered lubricating ability in the joint tissue. The latter is associated with reduced level of lubricin, one of the major joint lubricants. Future research should focus on the development of new therapies that attenuate the inflammatory process and restore lubricin synthesis and function. This approach could support joint tribology and synovial lubrication leading to improved joint function and pain relief. PMID:27118399

  1. Cellular Signature of SIL1 Depletion: Disease Pathogenesis due to Alterations in Protein Composition Beyond the ER Machinery.

    PubMed

    Roos, Andreas; Kollipara, Laxmikanth; Buchkremer, Stephan; Labisch, Thomas; Brauers, Eva; Gatz, Christian; Lentz, Chris; Gerardo-Nava, José; Weis, Joachim; Zahedi, René P

    2016-10-01

    SIL1 acts as nucleotide exchange factor for the endoplasmic reticulum chaperone BiP. Mutations of SIL1 cause Marinesco-Sjögren syndrome (MSS), a neurodegenerative disorder. Moreover, a particular function of SIL1 for etiopathology of amyotrophic lateral sclerosis (ALS) was highlighted, thus declaring the functional SIL1-BiP complex as a modifier for neurodegenerative disorders. Thereby, depletion of SIL1 was associated with an earlier manifestation and in strengthened disease progression in ALS. Owing to the absence of appropriate in vitro models, the precise cellular pathophysiological mechanisms leading to neurodegeneration in MSS and triggering the same in further disorders like ALS are still elusive. We found that SIL1 depletion in human embryonic kidney 293 (HEK293) cells led to structural changes of the endoplasmic reticulum (ER) including the nuclear envelope and mitochondrial degeneration that closely mimic pathological alterations in MSS and ALS. Functional studies revealed disturbed protein transport, cytotoxicity with reduced proliferation and viability, accompanied by activation of cellular defense mechanisms including the unfolded protein response, ER-associated degradation pathway, proteolysis, and expression of apoptotic and survival factors. Our data moreover indicated that proteins involved in cytoskeletal organization, vesicular transport, mitochondrial function, and neurological processes contribute to SIL1 pathophysiology. Altered protein expression upon SIL1 depletion in vitro could be confirmed in Sil1-deficient motoneurones for paradigmatic proteins belonging to different functional classes. Our results demonstrate that SIL1-depleted HEK293 cells are an appropriate model to identify proteins modulated by SIL1 expression level and contributing to neurodegeneration in MSS and further disorders like ALS. Thereby, our combined results point out that proteins beyond such involved ER-related protein processing are affected by SIL1 depletion.

  2. Darbepoetin alpha, a long-acting erythropoeitin derivate, does not alter LPS evoked myocardial depression and gene expression of Bax, Bcl-Xs, Bcl-XL, Bcl-2, and TNF-alpha.

    PubMed

    Brendt, Peter; Frey, Ulrich; Adamzik, Michael; Schäfer, Simon T; Peters, Jürgen

    2009-01-01

    Darbepoetin alpha (DA), a long-acting erythropoietin derivative stimulating erythropoiesis, can, by antiapoptotic effects, mitigate myocardial I/R injury. We tested the hypothesis that DA treatment improves left ventricular function (LV) in LPS evoked cardiomyopathy and alters gene expression of apoptosis-regulating proteins (Bcl-XL, Bcl-2, Bax, and Bcl-Xs) and TNF-alpha. In a prospective, controlled, randomized study in Lewis rats (n = 56; 8 groups), myocardial depression was evoked by LPS administration (serotype O127:B8; 10 mg/kg, i.p.). Darbepoetin alpha or vehicle was injected either 24 h before (pretreatment) or 2 h after LPS injection (treatment). Hearts were isolated 8 h after LPS injection, perfused (Krebs-Henseleit solution) in a Langendorff apparatus, and LV developed pressure and its derivatives were measured. For gene expression analysis, real-time polymerase chain reaction of LV specimen was performed. LPS decreased LV developed pressure (-64.6 +/- 7.9 mmHg) and its derivates by more than 60% in comparison to vehicle (P < 0,01), but this effect was not attenuated by DA pretreatment or DA treatment. LPS administration increased gene expression of Bcl-Xs, Bax, and TNF-alpha, but this was not altered by DA pretreatment. Furthermore, there was no effect on Bcl-Xl and Bcl-2 expression by DA alone. Whereas proapoptotic genes of the myocardium are up-regulated in LPS-induced cardiomyopathy, neither DA pretreatment nor treatment has significant effects on LV function or gene expression. This may suggest cardiac resistance to darbepoetin in LPS-mediated sepsis.

  3. Intracellular survival of Staphylococcus aureus due to alteration of cellular activity in arsenic and lead intoxicated mature Swiss albino mice.

    PubMed

    Bishayi, Biswadev; Sengupta, Mahuya

    2003-02-14

    The role of heavy metals like arsenic (As) and lead (Pb) as environmental toxicants is established. However, the exact mechanism of their effect on immunocompetent cell activity is not well known. Staphylococcus aureus is a virulent pathogen that has the ability to cause a variety of potentially life-threatening infections. The objective of our study was to demonstrate in an experimental mouse model of bacteremic S. aureus infection, bacterial clearance from blood and spleen in arsenic, lead treated and control group of mice. Bacterial density was measured in blood and spleen after 0, 24, 48 and 72 h post-infection. Our findings show a significant increase in bacterial load in blood (P<0.025 for arsenic and P<0.01 for lead) and delayed bacterial clearance by spleen in both arsenic (P<0.05) and lead (P<0.025) treated groups as compared to control, thus highlighting an immuno-compromised state following heavy metal exposure. To further elucidate immunomodulatory effects of both arsenic and lead, cell function studies were performed on splenic macrophages (M(phi)) isolated from lead and arsenic treated as well as control group of mice. Our findings show a decrease in cell adhesion property (P<0.005) of splenic M(phi)s from 2.9925+/-0.053 in control to 1.395+/-0.106 in arsenic and 0.8835+/-0.0106 in lead treated mice at 60 min. Morphologic alteration of the splenic M(phi)s showed an increase (As: P<0.05, Pb: P<0.0005) in both arsenic (6.876+/-0.3287%) and lead (16.55+/-1.051%) treated mice to control (2.649+/-1.238%) which may be responsible for the formers' reduced functional status. The chemotactic index, a measure of chemotactic migration of the macrophages toward immune serum, was 16.43+/-1.007 in control cell and was reduced (P<0.0005) to 4.19+/-0.393 in arsenic and 2.92+/-0.649 in lead treated mice at 60 min. These altered cell functions could probably explain the intracellular survival of S. aureus but such a causal relationship awaits further detailed

  4. Alterations in Magnetic Resonance Imaging T2 Relaxation Times of the Ovine Intervertebral Disc Due to Non-enzymatic Glycation

    PubMed Central

    Jazini, Ehsan; Sharan, Alok D; Morse, Lee Jae; Dyke, Jonathon P; Aronowitz, Eric A; Chen, Louis KH; Tang, Simon Y

    2011-01-01

    Study Design An in vitro study using ovine intervertebral discs to correlate the effects of advanced glycation end-products (AGEs) with disc hydration evaluated by magnetic resonance imaging (MRI). Objective To determine the relationship between the level of AGEs and tissue water content in intervertebral discs using T2 relaxation MRI. Summary of Background Data AGEs result from nonenzymatic glycation, and AGEs have been shown to accumulate in the IVD tissue with aging and degeneration. AGEs can alter biochemical properties, including the hydrophobicity of the extracellular matrix. Since one of the degenerative signs of the IVD is the reduced hydration, it was hypothesized that increased levels of tissue AGEs may contribute to disc hydration. T2 relaxation MRI has been shown to be sensitive to the hydration status of the disc, and may be valuable in detecting the changes in the IVD mediated by the increase of AGEs. Methods Thirty-eight IVDs were obtained from 4 ovine spines, and the annulus fibrosis (AF) and nucleus pulposus (NP) tissues were isolated from these discs. The tissues were incubated in either a ribosylation or control solution for up to 8 days to induce the formation of AGEs. These tissues were subsequently analyzed for tissue water content and concentration of AGEs. T2 relaxation times were obtained from these tissues after ribosylation. Results Ribosylation led to the increased accumulation of AGEs and reduced water content in both the AF and NP in a dose-dependent manner. When analyzed by MRI, ribosylation significantly altered the mean T2 relaxation times in the NP (p=0.001), but not in the AF (p=0.912). Furthermore, the mean T2 values in the NP significantly decreased with increasing periods of incubation time (p<0.001). Conclusion This study demonstrates that levels of AGEs in the IVD may affect the tissue water content. Moreover, these ribosylation-mediated changes in tissue hydration were detectable using T2 relaxation MRI. T2 relaxation MRI

  5. Reduced phototropism in pks mutants may be due to altered auxin-regulated gene expression or reduced lateral auxin transport.

    PubMed

    Kami, Chitose; Allenbach, Laure; Zourelidou, Melina; Ljung, Karin; Schütz, Frédéric; Isono, Erika; Watahiki, Masaaki K; Yamamoto, Kotaro T; Schwechheimer, Claus; Fankhauser, Christian

    2014-02-01

    Phototropism allows plants to orient their photosynthetic organs towards the light. In Arabidopsis, phototropins 1 and 2 sense directional blue light such that phot1 triggers phototropism in response to low fluence rates, while both phot1 and phot2 mediate this response under higher light conditions. Phototropism results from asymmetric growth in the hypocotyl elongation zone that depends on an auxin gradient across the embryonic stem. How phototropin activation leads to this growth response is still poorly understood. Members of the phytochrome kinase substrate (PKS) family may act early in this pathway, because PKS1, PKS2 and PKS4 are needed for a normal phototropic response and they associate with phot1 in vivo. Here we show that PKS proteins are needed both for phot1- and phot2-mediated phototropism. The phototropic response is conditioned by the developmental asymmetry of dicotyledonous seedlings, such that there is a faster growth reorientation when cotyledons face away from the light compared with seedlings whose cotyledons face the light. The molecular basis for this developmental effect on phototropism is unknown; here we show that PKS proteins play a role at the interface between development and phototropism. Moreover, we present evidence for a role of PKS genes in hypocotyl gravi-reorientation that is independent of photoreceptors. pks mutants have normal levels of auxin and normal polar auxin transport, however they show altered expression patterns of auxin marker genes. This situation suggests that PKS proteins are involved in auxin signaling and/or lateral auxin redistribution.

  6. Metabolic alterations due to caloric restriction and every other day feeding in normal and growth hormone receptor knockout mice.

    PubMed

    Westbrook, Reyhan; Bonkowski, Michael S; Arum, Oge; Strader, April D; Bartke, Andrzej

    2014-01-01

    Mutations causing decreased somatotrophic signaling are known to increase insulin sensitivity and extend life span in mammals. Caloric restriction and every other day (EOD) dietary regimens are associated with similar improvements to insulin signaling and longevity in normal mice; however, these interventions fail to increase insulin sensitivity or life span in growth hormone receptor knockout (GHRKO) mice. To investigate the interactions of the GHRKO mutation with caloric restriction and EOD dietary interventions, we measured changes in the metabolic parameters oxygen consumption (VO2) and respiratory quotient produced by either long-term caloric restriction or EOD in male GHRKO and normal mice. GHRKO mice had increased VO2, which was unaltered by diet. In normal mice, EOD diet caused a significant reduction in VO2 compared with ad libitum (AL) mice during fed and fasted conditions. In normal mice, caloric restriction increased both the range of VO2 and the difference in minimum VO2 between fed and fasted states, whereas EOD diet caused a relatively static VO2 pattern under fed and fasted states. No diet significantly altered the range of VO2 of GHRKO mice under fed conditions. This provides further evidence that longevity-conferring diets cause major metabolic changes in normal mice, but not in GHRKO mice. PMID:23833202

  7. 96 h LC50, behavioural alterations and histopathological effects due to wastewater toxicity in a freshwater fish Channa punctatus.

    PubMed

    Kaur, Rajbir; Dua, Anish

    2015-04-01

    The aim of the study was to evaluate the toxic impact of wastewater from sites 1 and 2 of Tung Dhab drain in the state of Punjab, India, on fish behaviour, morphology and gill histopathological biomarkers in comparison to control group. Static non-renewal tests were conducted for 96 h to determine LC50 of the wastewater for both sites using five concentrations (6.25-100%). Fish were regularly noticed for any deviation in behaviour and external morphology. Physico-chemical analysis of wastewater was done using standard methods recommended by APHA/AWWA/WEF (2005). Chronic toxicity tests were conducted for 15 and 30 days with sublethal concentrations of wastewater (50-90% of LC50) and gill histopathology was assessed. Wastewater near a paper mill was more toxic as observed from LC50 values of 72.45%. There was evident deterioration of water quality as the recorded values of some parameters were higher than the standard discharge limits. The test fish exhibited increased air gulping and surfacing, erratic movements initially and decreased opercular movements as the exposure period increased. Morphological observations include increased body colouration, mucus secretion, scale loss and haemorrhages on the skin and lower lip. Alterations in the gill histology such as complete lamellar fusion, epithelial lifting and intraepithelial oedema, haemorrhages, lamellar necrosis and aneurysm were noted in the test fish. Results demonstrate that the fish exposed to wastewater from both sites showed significantly greater change in gill organ index (IG) as compared to control fish for 15 and 30 days.

  8. Geomorphic Framework to assess changes to aquatic habitat due to flow regulation and channel and floodplain alteration, Cedar River, Washington

    USGS Publications Warehouse

    Gendaszek, Andrew S.; Magirl, Christopher S.; Czuba, Christiana R.; Konrad, Christopher P.; Little, Rand

    2010-01-01

    Flow regulation, bank armoring, and floodplain alteration since the early 20th century have contributed to significant changes in the hydrologic regime and geomorphic processes of the Cedar River in Washington State. The Cedar River originates in the Cascade Range, provides drinking water to the Seattle metropolitan area, and supports several populations of anadromous salmonids. Flow regulation currently has limited influence on the magnitude, duration, and timing of high-flow events, which affect the incubation of salmonids as well as the production and maintenance of their habitat. Unlike structural changes to the channel and floodplain, flow regulation may be modified in the short-term to improve the viability of salmon populations. An understanding of the effects of flow regulation on those populations must be discerned over a range of scales from individual floods that affect the size of individual year classes to decadal high flow regime that influences the amount and quality of channel and off-channel habitat available for spawning and rearing. We present estimates of reach-scale sediment budgets and changes to channel morphology derived from historical orthoimagery, specific gage analyses at four long-term streamflow-gaging stations to quantify trends in aggradation, and hydrologic statistics of the magnitude and duration of peak streamflows. These data suggest a gradient of channel types from unconfined, sediment-rich segments to confined, sediment-poor segments that are likely to have distinct responses to high flows. Particle-size distribution data and longitudinal water surface and streambed profiles for the 56 km downstream of Chester Morse Lake measured in 2010 show the spatial extent of preferred salmonid habitat along the Cedar River. These historical and current data constitute a geomorphic framework to help assess different river management scenarios for salmonid habitat and population viability. PDF version of a presentation on changes to aquatic

  9. Rapid initial dimensional changes in wooden panel paintings due to simulated climate-induced alterations monitored by digital coherent out-of-plane interferometry

    NASA Astrophysics Data System (ADS)

    Bernikola, E.; Nevin, A.; Tornari, V.

    2009-05-01

    Climate and environmental change may provoke constant microscopic dimensional alterations to organically composed works of art. The complexity of alterations obstructs the classification of destructive effects and sustainable strategies for preservation, and systematic investigation of change requires safe inspection tools, repeatable procedures and non-perturbing approaches. In this paper, a state-of-the-art description on the dimensional monitoring tools for the assessment of the effects of climate fluctuations in paintings is given. Rapid initial start-up reactions of alteration processes that may simulate endangered conditions, which may be encountered during transportation of works of art, are studied. The case of wooden panel paintings is considered here as panels are representative models of inhomogeneous organic construction. The effect of the surface movement of panel painting surfaces due to simulated changes in temperature and relative humidity is characteristic of structural deterioration and as such these effects are primarily monitored in the start-up of the reaction process. The environmentally-provoked spatial alteration is recorded in full-field surface coordinates using optical coherent out-of-plane digital interferometry in a geometry utilizing holographic speckle patterns. Results demonstrate the suitability of the method to follow the start-up simulated process in real time directly from the work of art and to follow the rate of reaction towards equilibrium. The effectiveness of the full surface assessment provided in real time is presented and provides significant advantages compared to alternative techniques which are based on fragmented solutions.

  10. Inhibition of tomato (Solanum lycopersicum L.) root growth by cyanamide is due to altered cell division, phytohormone balance and expansin gene expression.

    PubMed

    Soltys, Dorota; Rudzińska-Langwald, Anna; Gniazdowska, Agnieszka; Wiśniewska, Anita; Bogatek, Renata

    2012-11-01

    Cyanamide (CA) has been reported as a natural compound produced by hairy vetch (Vicia villosa Roth.) and it was shown also to be an allelochemical, responsible for strong allelopathic potential in this species. CA phytotoxicity has been demonstrated on various plant species, but to date little is known about its mode of action at cellular level. Treatment of tomato (Solanum lycopersicum L.) roots with CA (1.2 mM) resulted in inhibition of growth accompanied by alterations in cell division, and imbalance of plant hormone (ethylene and auxin) homeostasis. Moreover, the phytotoxic effect of CA was also manifested by modifications in expansin gene expression, especially in expansins responsible for cell wall remodeling after the cytokinesis (LeEXPA9, LeEXPA18). Based on these results the phytotoxic activity of CA on growth of roots of tomato seedlings is likely due to alterations associated with cell division.

  11. First evidence of protein profile alteration due to the main cocaine metabolite (benzoylecgonine) in a freshwater biological model.

    PubMed

    Binelli, A; Marisa, I; Fedorova, M; Hoffmann, R; Riva, C

    2013-09-15

    Illicit drugs represent not only a great social problem but are also considered an environmental problem because their use and, often, abuse release large amounts of parent compounds, and especially their metabolites, into freshwaters. One of the most commonly used drugs is cocaine, which is the second most prevalent drug in Europe (accounting for almost 30% of all cocaine users worldwide). Cocaine is rapidly metabolised in humans to benzoylecgonine (35-54%), ecgonine methyl ester (32-49%) and norcocaine (5%), which are eliminated in the urine and are only partially removed by wastewater treatment plants (WWTPs). Because no studies have previously been carried out to evaluate the possible risks due to cocaine and its metabolites in non-target organisms, we applied a multi-disciplinary approach to investigate the possible environmental risk related to benzoylecgonine (BE), the main metabolite of cocaine. Previous studies carried out by means of a biomarker suite and the redox-proteomic approach showed an imbalance of anti-oxidant enzyme activities and several genotoxic effects to be caused by environmental BE concentrations in the freshwater bivalve Zebra mussel (Dreissena polymorpha). This report presents the results obtained in the last step of this study, based on a proteomics analysis. We analysed the protein expression profile in the gills of Zebra mussels exposed to two different concentrations (0.5 and 1 μg/L) of BE for 14 days through 2-DE and mass spectrometry analysis (RP-UPLC ESI-LTQ-Orbitrap). Our results highlight significant changes in some proteins in gill cells whose functions are crucial for overall metabolism. In particular, we detected a probable effect of BE on calcium homeostasis and a consequent imbalance of oxidative stress, as verified for vertebrates.

  12. First evidence of protein profile alteration due to the main cocaine metabolite (benzoylecgonine) in a freshwater biological model.

    PubMed

    Binelli, A; Marisa, I; Fedorova, M; Hoffmann, R; Riva, C

    2013-09-15

    Illicit drugs represent not only a great social problem but are also considered an environmental problem because their use and, often, abuse release large amounts of parent compounds, and especially their metabolites, into freshwaters. One of the most commonly used drugs is cocaine, which is the second most prevalent drug in Europe (accounting for almost 30% of all cocaine users worldwide). Cocaine is rapidly metabolised in humans to benzoylecgonine (35-54%), ecgonine methyl ester (32-49%) and norcocaine (5%), which are eliminated in the urine and are only partially removed by wastewater treatment plants (WWTPs). Because no studies have previously been carried out to evaluate the possible risks due to cocaine and its metabolites in non-target organisms, we applied a multi-disciplinary approach to investigate the possible environmental risk related to benzoylecgonine (BE), the main metabolite of cocaine. Previous studies carried out by means of a biomarker suite and the redox-proteomic approach showed an imbalance of anti-oxidant enzyme activities and several genotoxic effects to be caused by environmental BE concentrations in the freshwater bivalve Zebra mussel (Dreissena polymorpha). This report presents the results obtained in the last step of this study, based on a proteomics analysis. We analysed the protein expression profile in the gills of Zebra mussels exposed to two different concentrations (0.5 and 1 μg/L) of BE for 14 days through 2-DE and mass spectrometry analysis (RP-UPLC ESI-LTQ-Orbitrap). Our results highlight significant changes in some proteins in gill cells whose functions are crucial for overall metabolism. In particular, we detected a probable effect of BE on calcium homeostasis and a consequent imbalance of oxidative stress, as verified for vertebrates. PMID:23838174

  13. Myocardial thallium-201 kinetics and regional flow alterations with 3 hours of coronary occlusion and either rapid reperfusion through a totally patent vessel or slow reperfusion through a critical stenosis

    SciTech Connect

    Granato, J.E.; Watson, D.D.; Flanagan, T.L.; Beller, G.A.

    1987-01-01

    Myocardial thallium-201 kinetics and regional blood flow alterations were examined in a canine model using 3 hours of coronary occlusion and different methods of reperfusion. Group I comprised 10 dogs undergoing a 3 hour left anterior descending artery occlusion and no reperfusion. Group II comprised seven dogs undergoing 3 hours of left anterior descending artery occlusion and rapid reperfusion through a totally patent vessel. Group III comprised 10 dogs undergoing 3 hours of left anterior descending artery occlusion and slow reperfusion through a residual stenosis. All dogs received 1.5 mCi of thallium-201 after 40 minutes of coronary occlusion. During occlusion and 2 hours of reperfusion, serial hemodynamic, blood flow and myocardial thallium-201 activity measurements were made. The relative thallium-201 gradient (normal zone minus ischemic zone activity when initial normal activity is expressed as 100%) during left anterior descending coronary occlusion was similar in all groups. Group I, 87 +/- 3%; Group II, 78 +/- 6%; Group III, 83 +/- 6% (p = NS). After 2 hours of either method of reperfusion, the final relative gradient had decreased to a similar level (Group II, 51 +/- 9%; Group III, 42 +/- 6%). These values were not significantly different from the final relative thallium-201 gradient seen in dogs undergoing a sustained 3 hour occlusion (Group I, 55 +/- 5%). After 2 hours of reperfusion, both methods of reflow were associated with similar degrees of ''no reflow.'' Transmural flows in the central ischemic zone were 89 +/- 10% of normal in Group II and 71 +/- 6% of normal in Group III after reperfusion, with both flows substantially higher than the relative thallium-201 activities in these dogs.

  14. Aspiration thrombectomy in a case of acute myocardial infarction due to coronary emboli in a patient with peripartum cardiomyopathy and mural thrombus.

    PubMed

    Abdulbaki, Abdulrahman; Kocherla, Cyrus; Modi, Kalgi

    2015-01-01

    Acute coronary syndrome (ACS) due to embolic phenomenon in the setting of peripartum cardiomyopathy (PPCM) and left ventricular mural thrombus is a rare occurrence. There have been two known cases described in medical literature. We present a unique case in which catheter-based aspiration thrombectomy was used to successfully treat a patient with ACS due to coronary emboli in the setting of PPCMand left ventricular mural thrombus. We believe this to be the first report of the use of aspiration thrombectomy in such a clinical case.

  15. 2013 Immune Risk Standing Review Panel Evidence Review for: The Risk of Crew Adverse Health Event Due to Altered Immune Response

    NASA Technical Reports Server (NTRS)

    Steinberg, Susan

    2014-01-01

    The 2013 Immune Risk Standing Review Panel (from here on referred to as the SRP) met for a site visit in Houston, TX on February 3-4, 2014. The SRP reviewed the new Evidence Report for the Risk of Crew Adverse Health Event Due to Altered Immune Response (from here on referred to as the 2013 Immune Evidence Report), as well as the Research Plan for this Risk that is in the current version of the Human Research Program’s (HRP) Integrated Research Plan (IRP).

  16. Altered myocardial perfusion in patients with angina pectoris or silent ischemia during exercise as assessed by quantitative thallium-201 single-photon emission computed tomography

    SciTech Connect

    Mahmarian, J.J.; Pratt, C.M.; Cocanougher, M.K.; Verani, M.S. )

    1990-10-01

    The extent of abnormally perfused myocardium was compared in patients with and without chest pain during treadmill exercise from a large, relatively low-risk consecutive patient population (n = 356) referred for quantitative thallium-201 single-photon emission computed tomography (SPECT). All patients had concurrent coronary angiography. Patients were excluded if they had prior coronary angioplasty or bypass surgery. Tomographic images were assessed visually and from computer-generated polar maps. Chest pain during exercise was as frequent in patients with normal coronary arteries (12%) as in those with significant (greater than 50% stenosis) coronary artery disease (CAD) (14%). In the 219 patients with significant CAD, silent ischemia was fivefold more common than symptomatic ischemia (83% versus 17%, p = 0.0001). However, there were no differences in the extent, severity, or distribution of coronary stenoses in patients with silent or symptomatic ischemia. Our major observation was that the extent of quantified SPECT perfusion defects was nearly identical in patients with (20.9 +/- 15.9%) and without (20.5 +/- 15.6%) exertional chest pain. The sensitivity for detecting the presence of CAD was significantly improved with quantitative SPECT compared with stress electrocardiography (87% versus 65%, p = 0.0001). Although scintigraphic and electrocardiographic evidence of exercise-induced ischemia were comparable in patients with chest pain (67% versus 73%, respectively; p = NS), SPECT was superior to stress electrocardiography for detecting silent myocardial ischemia. The majority of patients in this study with CAD who developed ischemia during exercise testing were asymptomatic, although they exhibited an angiographic profile and extent of abnormally perfused myocardium similar to those of patients with symptomatic ischemia.

  17. Protective effects of Labisia pumila var. alata on biochemical and histopathological alterations of cardiac muscle cells in isoproterenol-induced myocardial infarction rats.

    PubMed

    Dianita, Roza; Jantan, Ibrahim; Amran, Athirah Z; Jalil, Juriyati

    2015-01-01

    The study was designed to evaluate the cardioprotective effects of the standardized aqueous and 80% ethanol extracts of Labisia pumila var. alata (LPva) in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. The extracts were administered to Wistar rats orally for 28 days with three doses (100, 200 and 400 mg/kg of body weight) prior to ISO (85 mg/kg)-induced MI in two doses on day 29 and 30. The sera and hearts were collected for biochemical and histopathological analysis after the rats were sacrificed 48 h after the first induction. The main components of the extracts, gallic acid, alkylresorcinols and flavonoids were identified and quantitatively analyzed in the extracts by using a validated reversed phase HPLC method. The extracts showed significant protective effects as pretreated rats showed a significant dose-dependent decrease (p < 0.05) in cardiac enzyme activities, i.e., cardiac troponin I (cTnI), creatine kinase MB isoenzyme (CK-MB), lactate dehydrogenase (LDH), alanine transaminase (ALT) and aspartate transaminase (AST), when compared with ISO-control rats. There were significant rises (p < 0.05) in the activity of oxidase enzymes, i.e., glutathione peroxide (GPx), catalase (CAT) and superoxide dismutase (SOD) of the pretreated rats, when compared with ISO-control group. Histopathological examination showed an improvement in membrane cell integrity in pre-treated rats compared to untreated rats. The major components of LPva extracts can be used as their biomarkers and contributed to the cardioprotective effects against ISO-induced MI rats. PMID:25786162

  18. Silent myocardial ischemia.

    PubMed

    Gutterman, David D

    2009-05-01

    Although much progress has been made in reducing mortality from ischemic cardiovascular disease, this condition remains the leading cause of death throughout the world. This might in part be due to the fact that over half of patients have a catastrophic event (heart attack or sudden death) as their initial manifestation of coronary disease. Contributing to this statistic is the observation that the majority of myocardial ischemic episodes are silent, indicating an inability or failure to sense ischemic damage or stress on the heart. This review examines the clinical characteristics of silent myocardial ischemia, and explores mechanisms involved in the generation of angina pectoris. Possible mechanisms for the more common manifestation of injurious reductions in coronary flow; namely, silent ischemia, are also explored. A new theory for the mechanism of silent ischemia is proposed. Finally, the prognostic importance of silent ischemia and potential future directions for research are discussed.

  19. Assessment of the structural brain network reveals altered connectivity in children with unilateral cerebral palsy due to periventricular white matter lesions

    PubMed Central

    Pannek, Kerstin; Boyd, Roslyn N.; Fiori, Simona; Guzzetta, Andrea; Rose, Stephen E.

    2014-01-01

    in FA in unilateral CP, and that these alterations in FA are related to clinical function. Application of this connectome-based analysis to investigate alterations in connectivity following treatment may elucidate the neurological correlates of improved functioning due to intervention. PMID:25003031

  20. Feasibility of altering type A behavior pattern after myocardial infarction. Recurrent Coronary Prevention Project Study: methods, baseline results and preliminary findings.

    PubMed

    Friedman, M; Thoresen, C E; Gill, J J; Ulmer, D; Thompson, L; Powell, L; Price, V; Elek, S R; Rabin, D D; Breall, W S; Piaget, G; Dixon, T; Bourg, E; Levy, R A; Tasto, D L

    1982-07-01

    We studied 1035 consecutive postinfarction patients to determine the feasibility of altering type A behavior and the effect such alteration might have on subsequent rates of infarction and cardiovascular death. Approximately 300 subjects were enrolled in small groups and primarily received cardiologic counseling on the usually accepted coronary risk factors. Six hundred subjects received, in addition to cardiologic counseling, advice and instructions designed to diminish the intensity of their type A behavior. The remaining subjects, serving as controls, received no counseling, but were examined and interviewed annually, as were those who dropped out of counseling groups. More than 98% of the 1035 subjects exhibited moderate-to-severe type A behavior during a videotaped structured interview. After the first year of this 5-year study, the rates of infarction and cardiovascular death were lower (p less than 0.01 and p less than 0.05, respectively) among subjects who received both cardiologic and behavioral counseling than among the control subjects. The rate of nonfatal infarction was lower (p less than 0.05) among subjects who received behavioral counseling than among those who received only cardiologic counseling or those who dropped out of either counseling group. The circumstances that most often preceded recurrent infarction or cardiovascular death were emotional crisis, excess physical activity, ingestion of a single fatty meal or a combination of these phenomena. PMID:7083525

  1. Level alterations of the 2f (1)-f (2) distortion product due to hypoxia in the guinea pig depend on the stimulus frequency.

    PubMed

    Olzowy, Bernhard; von Gleichenstein, Gregor; Canis, Martin; Plesnila, Nikolaus; Strieth, Sebastian; Deppe, Christoph; Mees, Klaus

    2010-03-01

    Increased intracranial pressure (ICP) is known to affect the levels of distortion product otoacoustic emissions (DPOAEs) in a frequency-specific manner. DPOAEs might, therefore, be used for monitoring the ICP non-invasively. Hypoxia can also cause alterations of DPOAE levels, which can be distinguished from ICP-related changes only, when their characteristics, in particular frequency specificity, are known in detail. DPOAEs at f (2) = 2, 4, 8, 12 and 16 kHz and oxygen saturation (SaO(2)) were continuously monitored in nine spontaneously breathing guinea pigs, anaesthetized by i.m. administration of midazolam, medetomidin and fentanyl, during the respiration of a gas mixture of N(2)O and O(2) containing either 30% O(2) or 13% O(2). Fourteen hypoxic intervals in eight animals were included into final data analysis. Characteristic hypoxic level alterations with a level decrease and a remarkable level destabilization during hypoxia, and a pronounced reversible level decrease after reoxygenation were observed at the frequencies of 4, 8 and 16 kHz. At 2 and 12 kHz, the only reproducible effect of hypoxia was an increased fluctuation of the DPOAE level, which was significantly less pronounced compared with the other frequencies (P < 0.05 for 12 vs. 16 and 8 kHz and for 2 vs. 16 kHz). DPOAE level alterations due to hypoxia depend on the frequency in guinea pigs. Studies in human are warranted to improve non-invasive ICP monitoring with DPOAE by the detection of hypoxia-related changes. PMID:19629511

  2. Prediction of Altered Bile Acid Disposition Due to Inhibition of Multiple Transporters: An Integrated Approach Using Sandwich-Cultured Hepatocytes, Mechanistic Modeling, and Simulation.

    PubMed

    Guo, Cen; Yang, Kyunghee; Brouwer, Kenneth R; St Claire, Robert L; Brouwer, Kim L R

    2016-08-01

    Transporter-mediated alterations in bile acid disposition may have significant toxicological implications. Current methods to predict interactions are limited by the interplay of multiple transporters, absence of protein in the experimental system, and inaccurate estimates of inhibitor concentrations. An integrated approach was developed to predict altered bile acid disposition due to inhibition of multiple transporters using the model bile acid taurocholate (TCA). TCA pharmacokinetic parameters were estimated by mechanistic modeling using sandwich-cultured human hepatocyte data with protein in the medium. Uptake, basolateral efflux, and biliary clearance estimates were 0.63, 0.034, and 0.074 mL/min/g liver, respectively. Cellular total TCA concentrations (Ct,Cells) were selected as the model output based on sensitivity analysis. Monte Carlo simulations of TCA Ct,Cells in the presence of model inhibitors (telmisartan and bosentan) were performed using inhibition constants for TCA transporters and inhibitor concentrations, including cellular total inhibitor concentrations ([I]t,cell) or unbound concentrations, and cytosolic total or unbound concentrations. For telmisartan, the model prediction was accurate with an average fold error (AFE) of 0.99-1.0 when unbound inhibitor concentration ([I]u) was used; accuracy dropped when total inhibitor concentration ([I]t) was used. For bosentan, AFE was 1.2-1.3 using either [I]u or [I]t This difference was evaluated by sensitivity analysis of the cellular unbound fraction of inhibitor (fu,cell,inhibitor), which revealed higher sensitivity of fu,cell,inhibitor for predicting TCA Ct,Cells when inhibitors exhibited larger ([I]t,cell/IC50) values. In conclusion, this study demonstrated the applicability of a framework to predict hepatocellular bile acid concentrations due to drug-mediated inhibition of transporters using mechanistic modeling and cytosolic or cellular unbound concentrations. PMID:27233294

  3. Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Space flight

    NASA Technical Reports Server (NTRS)

    Bloomberg, Jacob J.; Reschke, Millard F.; Clement, Gilles R.; Mulavara, Ajitkumar P.; Taylor, Laura C..

    2015-01-01

    Control of vehicles and other complex systems is a high-level integrative function of the central nervous system (CNS). It requires well-functioning subsystem performance, including good visual acuity, eye-hand coordination, spatial and geographic orientation perception, and cognitive function. Evidence from space flight research demonstrates that the function of each of these subsystems is altered by removing gravity, a fundamental orientation reference, which is sensed by vestibular, proprioceptive, and haptic receptors and used by the CNS for spatial orientation, posture, navigation, and coordination of movements. The available evidence also shows that the degree of alteration of each subsystem depends on a number of crew- and mission-related factors. There is only limited operational evidence that these alterations cause functional impacts on mission-critical vehicle (or complex system) control capabilities. Furthermore, while much of the operational performance data collected during space flight has not been available for independent analysis, those that have been reviewed are somewhat equivocal owing to uncontrolled (and/or unmeasured) environmental and/or engineering factors. Whether this can be improved by further analysis of previously inaccessible operational data or by development of new operational research protocols remains to be seen. The true operational risks will be estimable only after we have filled the knowledge gaps and when we can accurately assess integrated performance in off-nominal operational settings (Paloski et al. 2008). Thus, our current understanding of the Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Space flight is limited primarily to extrapolation of scientific research findings, and, since there are limited ground-based analogs of the sensorimotor and vestibular changes associated with space flight, observation of their functional

  4. Myocardial Tagging With SSFP

    PubMed Central

    Herzka, Daniel A.; Guttman, Michael A.; McVeigh, Elliot R.

    2007-01-01

    This work presents the first implementation of myocardial tagging with refocused steady-state free precession (SSFP) and magnetization preparation. The combination of myocardial tagging (a noninvasive method for quantitative measurement of regional and global cardiac function) with the high tissue signal-to-noise ratio (SNR) obtained with SSFP is shown to yield improvements in terms of the myocardium–tag contrast-to-noise ratio (CNR) and tag persistence when compared to the current standard fast gradient-echo (FGRE) tagging protocol. Myocardium–tag CNR and tag persistence were studied using numerical simulations as well as phantom and human experiments. Both quantities were found to decrease with increasing imaging flip angle (α) due to an increased tag decay rate and a decrease in myocardial steady-state signal. However, higher α yielded better blood–myocardium contrast, indicating that optimal α is dependent on the application: higher α for better blood–myocardium boundary visualization, and lower α for better tag persistence. SSFP tagging provided the same myocardium–tag CNR as FGRE tagging when acquired at four times the bandwidth and better tag– and blood–myocardium CNRs than FGRE tagging when acquired at equal or twice the receiver bandwidth (RBW). The increased acquisition efficiency of SSFP allowed decreases in breath-hold duration, or increases in temporal resolution, as compared to FGRE. PMID:12541254

  5. Effect of eating on thallium myocardial imaging

    SciTech Connect

    Wilson, R.A.; Sullivan, P.J.; Okada, R.D.; Boucher, C.A.; Morris, C.; Pohost, G.M.; Strauss, H.W.

    1986-02-01

    To determine if eating between initial and delayed thallium images alters the appearance of the delayed thallium scan, a prospective study was performed; 184 subjects sent for routine thallium imaging were randomized into two groups, those who ate a meal high in carbohydrates between initial and delayed thallium myocardial images (n = 106), and those who fasted (n = 78). The /sup 201/Tl images were interpreted in blinded fashion for global myocardial and pulmonary clearance of /sup 201/Tl myocardial defects. The eating group had a significantly lower incidence of transient myocardial defects compared to the noneating group (7 percent vs 18 percent, respectively; p less than 0.05). The time between initial and delayed images and the incidence of exercise-induced ischemic ST-segment depression or pathologic Q waves on the electrocardiogram were not significantly different between the two groups. These data suggest that eating a high-carbohydrate meal between initial and delayed /sup 201/Tl images causes increased /sup 201/Tl myocardial clearance rates and may alter /sup 201/Tl myocardial redistribution over time.

  6. Triosephosphate isomerase deficiency: haemolytic anaemia, myopathy with altered mitochondria and mental retardation due to a new variant with accelerated enzyme catabolism and diminished specific activity.

    PubMed

    Eber, S W; Pekrun, A; Bardosi, A; Gahr, M; Krietsch, W K; Krüger, J; Matthei, R; Schröter, W

    1991-09-01

    A new triosephosphate isomerase (TPI) variant is described in an 8-year-old Turkish girl suffering from chronic haemolytic anaemia, myopathy and developmental retardation since early infancy. The enzyme activity profile revealed a generalized deficiency in erythrocytes, granulocytes, mononuclear blood cells, skeletal muscle tissue and cerebrospinal fluid. The concentration of enzyme substrate dihydroxyacetone phosphate was distinctly elevated. Biochemical examination showed accelerated enzyme deamidation, the first step in the normal catabolism of TPI during aging of the erythrocyte. The specific activity of the variant TPI, determined by antibody titration, was reduced to 61% of normal. Its heat stability was markedly decreased. Muscle biopsy and neuropsychological testing further clarified the pathogenesis of the disorder. A prevalent alteration of mitochondria similar to that seen in mitochondrial myopathy and an elevated amount of intracellular glycogen were found. The patient's retarded intellectual development was mainly due to impaired visual perception and sensory-motor co-ordination in addition to a lack of syllogistic reasoning. The findings indicate that the low TPI activity leads to a metabolic block of the glycolytic pathway and hence to a generalized impairment of cellular energy supply.

  7. Prognostic Significance of Imaging Myocardial Sympathetic Innervation.

    PubMed

    Malhotra, Saurabh; Fernandez, Stanley F; Fallavollita, James A; Canty, John M

    2015-08-01

    There has been a longstanding interest in understanding whether the presence of inhomogeneity in myocardial sympathetic innervation can predict patients at risk of sudden cardiac arrest from lethal ventricular arrhythmias. The advent of radiolabeled norepinephrine analogs has allowed this to be imaged in patients with ischemic and non-ischemic cardiomyopathy using single, photon emission computed tomography (SPECT) and positron emission tomography (PET). Several observational studies have demonstrated that globally elevated myocardial sympathetic tone (as reflected by reduced myocardial norepinephrine analog uptake) can predict composite cardiac end-points including total cardiovascular mortality. More recent studies have indicated that quantifying the extent of regional denervation can predict the risk of lethal ventricular arrhythmias and sudden cardiac death. This review will summarize our current understanding of the prognostic significance of altered myocardial sympathetic innervation. PMID:26087899

  8. Postmortem detection of inapparent myocardial infarction

    PubMed Central

    McVie, J. G.

    1970-01-01

    Two methods of detecting early inapparent myocardial infarcts have been studied and their value in diagnostic practice compared. The better method proved to be the determination of the potassium to sodium ratio (ionic ratio) which falls in infarcted tissue within minutes of the onset of anoxia. The second method was nitro blue tetrazolium staining of gross sections of myocardium which revealed any infarct older than three and a half hours. As staining is dependent upon enzyme activity, the latter method is disturbed by autolysis. It was shown, on the other hand, that the ionic ratio (K+/Na+) was not affected by autolysis and was therefore well suited to forensic practice. Sixteen non-infarcted control hearts, plus the nine from cases of sudden death due to causes other than myocardial infarction, all yielded high ionic ratios (K+/Na+), average 1·4, and stained normally with tetrazolium (the normal controls). Positive control was provided by 20 histologically proven infarcts of which the ionic ratios (K+/Na+) were all low (average 0·7). Histochemical staining with tetrazolium delineated infarcted areas in each case. In a series of 29 sudden deaths, a cause of death other than myocardial infarction was found at necropsy in nine, mentioned above as normal controls. The remaining 20 hearts were not infarcted histologically, but were shown to be infarcted by examination of the ionic ratios (K+/Na+). These ratios were low (average 0·8) including three borderline ratios. Confirmatory evidence of infarction included nitro blue tetrazolium staining which revealed infarcts in 10 of the 20 cases, and clinical and necropsy observations. The ionic ratio (K+/Na+) decreases as the age of the infarct increases for at least 24 hours. Thereafter as healing proceeds, the ratio gradually reverts to normal. Thus, previous infarction and replacement fibrosis do not significantly alter the ionic ratio (K+/Na+). Nor is it changed by left ventricular hypertrophy, the presence of

  9. [Percutaneous coronary intervention in myocardial infarction. Current concepts].

    PubMed

    García, Eulogio

    2005-05-01

    Percutaneous mechanical reperfusion during acute myocardial infarction with ST-segment elevation has proved to be the most effective way of quickly restoring adequate flow in the affected coronary artery. Randomized clinical trials have shown that percutaneous coronary intervention (PCI) is superior to thrombolysis. Initial fears about the use of stents in primary angioplasty vanished when clinical studies demonstrated that they gave better results than those obtained under optimal conditions with balloon angioplasty. The need to transfer patients to a cardiac catheterization laboratory for primary PCI does not decrease the efficacy of this form of treatment, which remains superior to immediate thrombolysis at the admitting hospital. Distal embolization can alter the situation by preventing myocardial reperfusion. Although there are many therapeutic strategies for managing thrombotic lesions, only early administration of glycoprotein IIb/IIIa inhibitors, direct stenting, and use of an X-Sizer device followed by stent implantation have been shown in randomized studies to lead to significant improvements in clinical or angiographic parameters. No technique has been shown to prevent damage due to myocardial reperfusion. However, it would be difficult to improve upon the good results achieved with PCI in the majority of patients. Rescue PCI is indicated when thrombolysis appears to have failed, especially when a catheterization laboratory is close by or when patients can be transferred early to a center with angioplasty facilities. For most cases of cardiogenic shock, PCI is the only therapeutic modality currently recommended.

  10. 2013 Immune Risk Standing Review Panel Research Plan Review for: The Risk of Crew Adverse Health Event Due to Altered Immune Response

    NASA Technical Reports Server (NTRS)

    Steinberg, Susan

    2014-01-01

    The 2013 Immune Risk Standing Review Panel (from here on referred to as the SRP) participated in a meeting with representatives from the Human Research Program (HRP) Human Health Countermeasures (HHC) Element and HRP management on February 3-4, 2014 in Houston, TX to review the updated Research Plan for the Risk of Crew Adverse Health Event Due to Altered Immune Response in the HRP Integrated Research Plan. The SRP is impressed with the work the immune discipline has done since the 2012 SRP review and agrees with the new wording of the Gaps, no longer questions, now statements. The SRP also likes the addition of adding targets for closing the Gaps, but it is not clear how they got to some of the interim stages (interval percentages). A major concern that the SRP has mentioned since the initial 2009 SRP meeting is that there is still not enough emphasis on the interdisciplinary aspect of the immune risk associated with other risks (i.e., nutrition, radiation, etc.). The SRP recommends that a "translational SRP" or advisory group be developed that is composed of members from all of the HRP SRPs. The SRP also thinks that the immune discipline should consider a more systems biology approach. Lastly, the SRP is concerned that the risks observed in research from low Earth orbit (LEO) missions may not accurately reflect all the risks of longer duration flight beyond LEO. Also, there does not seem to be a concern for immune responses that may occur when someone is in space longer than six months, for example, a Mars mission would take three years. The absence of disease in past and current flight scenarios does not mean the risk may not be there in future flight settings.

  11. Assessment of myocardial metabolic flexibility and work efficiency in human type 2 diabetes using 16-[18F]fluoro-4-thiapalmitate, a novel PET fatty acid tracer.

    PubMed

    Mather, K J; Hutchins, G D; Perry, K; Territo, W; Chisholm, R; Acton, A; Glick-Wilson, B; Considine, R V; Moberly, S; DeGrado, T R

    2016-03-15

    Altered myocardial fuel selection likely underlies cardiac disease risk in diabetes, affecting oxygen demand and myocardial metabolic flexibility. We investigated myocardial fuel selection and metabolic flexibility in human type 2 diabetes mellitus (T2DM), using positron emission tomography to measure rates of myocardial fatty acid oxidation {16-[(18)F]fluoro-4-thia-palmitate (FTP)} and myocardial perfusion and total oxidation ([(11)C]acetate). Participants underwent paired studies under fasting conditions, comparing 3-h insulin + glucose euglycemic clamp conditions (120 mU·m(-2)·min(-1)) to 3-h saline infusion. Lean controls (n = 10) were compared with glycemically controlled volunteers with T2DM (n = 8). Insulin augmented heart rate, blood pressure, and stroke index in both groups (all P < 0.01) and significantly increased myocardial oxygen consumption (P = 0.04) and perfusion (P = 0.01) in both groups. Insulin suppressed available nonesterified fatty acids (P < 0.0001), but fatty acid concentrations were higher in T2DM under both conditions (P < 0.001). Insulin-induced suppression of fatty acid oxidation was seen in both groups (P < 0.0001). However, fatty acid oxidation rates were higher under both conditions in T2DM (P = 0.003). Myocardial work efficiency was lower in T2DM (P = 0.006) and decreased in both groups with the insulin-induced increase in work and shift in fuel utilization (P = 0.01). Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. This is accompanied by reduced work efficiency, possibly due to greater oxygen consumption with fatty acid metabolism. These observations suggest that improved fatty acid suppression, or reductions in myocardial fatty acid uptake and retention, could be therapeutic targets to improve myocardial ischemia tolerance in T2DM.

  12. Assessment of myocardial metabolic flexibility and work efficiency in human type 2 diabetes using 16-[18F]fluoro-4-thiapalmitate, a novel PET fatty acid tracer.

    PubMed

    Mather, K J; Hutchins, G D; Perry, K; Territo, W; Chisholm, R; Acton, A; Glick-Wilson, B; Considine, R V; Moberly, S; DeGrado, T R

    2016-03-15

    Altered myocardial fuel selection likely underlies cardiac disease risk in diabetes, affecting oxygen demand and myocardial metabolic flexibility. We investigated myocardial fuel selection and metabolic flexibility in human type 2 diabetes mellitus (T2DM), using positron emission tomography to measure rates of myocardial fatty acid oxidation {16-[(18)F]fluoro-4-thia-palmitate (FTP)} and myocardial perfusion and total oxidation ([(11)C]acetate). Participants underwent paired studies under fasting conditions, comparing 3-h insulin + glucose euglycemic clamp conditions (120 mU·m(-2)·min(-1)) to 3-h saline infusion. Lean controls (n = 10) were compared with glycemically controlled volunteers with T2DM (n = 8). Insulin augmented heart rate, blood pressure, and stroke index in both groups (all P < 0.01) and significantly increased myocardial oxygen consumption (P = 0.04) and perfusion (P = 0.01) in both groups. Insulin suppressed available nonesterified fatty acids (P < 0.0001), but fatty acid concentrations were higher in T2DM under both conditions (P < 0.001). Insulin-induced suppression of fatty acid oxidation was seen in both groups (P < 0.0001). However, fatty acid oxidation rates were higher under both conditions in T2DM (P = 0.003). Myocardial work efficiency was lower in T2DM (P = 0.006) and decreased in both groups with the insulin-induced increase in work and shift in fuel utilization (P = 0.01). Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. This is accompanied by reduced work efficiency, possibly due to greater oxygen consumption with fatty acid metabolism. These observations suggest that improved fatty acid suppression, or reductions in myocardial fatty acid uptake and retention, could be therapeutic targets to improve myocardial ischemia tolerance in T2DM. PMID:26732686

  13. Myocardial imaging. Coxsackie myocarditis

    SciTech Connect

    Wells, R.G.; Ruskin, J.A.; Sty, J.R.

    1986-09-01

    A 3-week-old male neonate with heart failure associated with Coxsackie virus infection was imaged with Tc-99m PYP and TI-201. The abnormal imaging pattern suggested myocardial infarction. Autopsy findings indicated that the cause was myocardial necrosis secondary to an acute inflammatory process. Causes of abnormal myocardial uptake of Tc-99m PYP in pediatrics include infarction, myocarditis, cardiomyopathy, bacterial endocarditis, and trauma. Myocardial imaging cannot provide a specific cause diagnosis. Causes of myocardial infarction in pediatrics are listed in Table 1.

  14. A large pseudoaneurysm of the left cardiac ventricle in a 57-year-old patient after urgent coronary artery bypass grafting and surgical mitral valve replacement due to acute myocardial infarction.

    PubMed

    Wieczorek, Joanna; Mizia-Stec, Katarzyna; Rybicka-Musialik, Anna; Janusiewicz, Piotr; Malinowski, Marcin; Deja, Marek A

    2014-12-01

    We present a rare case of a left ventricular pseudoaneurysm in a patient after inferior wall myocardial infarction. The infarction was complicated with acute mitral insufficiency, pulmonary edema, and cardiogenic shock. Urgent surgical mitral valve replacement and coronary artery bypass grafting were performed. After several months, the patient was hospitalized again because of deterioration of exercise tolerance and symptoms of acute congestive heart failure. A large pseudoaneurysm of the left ventricle was recognized and successfully treated surgically. PMID:26336464

  15. A large pseudoaneurysm of the left cardiac ventricle in a 57-year-old patient after urgent coronary artery bypass grafting and surgical mitral valve replacement due to acute myocardial infarction

    PubMed Central

    Mizia-Stec, Katarzyna; Rybicka-Musialik, Anna; Janusiewicz, Piotr; Malinowski, Marcin; Deja, Marek A.

    2014-01-01

    We present a rare case of a left ventricular pseudoaneurysm in a patient after inferior wall myocardial infarction. The infarction was complicated with acute mitral insufficiency, pulmonary edema, and cardiogenic shock. Urgent surgical mitral valve replacement and coronary artery bypass grafting were performed. After several months, the patient was hospitalized again because of deterioration of exercise tolerance and symptoms of acute congestive heart failure. A large pseudoaneurysm of the left ventricle was recognized and successfully treated surgically. PMID:26336464

  16. Invasion of a semi-arid shrubland by annual grasses increases autotrophic and heterotrophic soil respiration rates due to altered soil moisture and temperature patterns

    NASA Astrophysics Data System (ADS)

    Mauritz, M.; Hale, I.; Lipson, D.

    2010-12-01

    Shrub <-> grassland conversions are a globally occurring phenomenon altering habitat structure, quality and nutrient cycling. Grasses and shrubs differ in their above and belowground biomass allocation, root architecture, phenology, litter quality and quantity. Conversion affects soil microbial communities, soil moisture and temperature and carbon (C) allocation patterns. However, the effect of conversion on C storage is regionally variable and there is no consistent direction of change. In Southern California invasion by annual grasses is a major threat to native shrub communities and it has been proposed that grass invasion increases NPP and ecosystem C storage (Wolkovich et al, 2009). In order to better understand how this shrub <-> grassland conversion changes ecosystem C storage it is important to understand the partitioning of soil respiration into autotrophic and heterotrophic components. Respiration was measured in plots under shrubs and grasses from February when it was cold and wet to July when it was hot and dry, capturing seasonal transitions in temperature and water availability. Roots were excluded under shrubs and grasses with root exclusion cores to quantify heterotrophic respiration. Using total soil respiration (Rt) = autotrophic respiration (root) (Ra)+ heterotrophic respiration (microbial) (Rh) the components contributing to total soil respiration can be evaluated. Respiration, soil moisture and temperature were measured daily at four hour intervals using Licor 8100 automated chamber measurements. Throughout the measurement period, Rt under grasses exceeded Rt under shrubs. Higher Rt levels under grasses were mainly due to higher Ra in grasses rather than changes in Rh. On average grass Ra was almost double shrub Ra. Higher grass respiration levels are partially explained by differences in soil moisture and temperature between shrubs and grasses. Respiration rates responded similarly to seasonal transitions regardless of treatment although Ra

  17. Myocardial Factor Revisited: The Importance of Myocardial Fibrosis in Adults with Congenital Heart Disease

    PubMed Central

    Broberg, Craig S.; Burchill, Luke J.

    2015-01-01

    Pioneers in congenital heart surgery observed that exercise capacity did not return to normal levels despite successful surgical repair, leading some to cite a “myocardial factor” playing a role. They conjectured that residual alterations in myocardial function would be significant for patients’ long-term outlook. In fulfillment of their early observations, today’s adult congenital heart disease (ACHD) population shows well-recognized features of heart failure, even among patients without clear residual anatomic or hemodynamic abnormalities, demonstrating the vital role of the myocardium in their morbidity and mortality. Whereas the ‘myocardial factor’ was an elusive concept in the early history of congenital heart care, we now have imaging techniques to detect and quantify one such factor – myocardial fibrosis. Understanding the importance of myocardial fibrosis as a final common pathway in a variety of congenital lesions provides a framework for both the study and treatment of clinical heart failure in this context. While typical heart failure pharmacology should reduce or attenuate fibrogenesis, efforts to show meaningful improvements with standard pharmacotherapy in ACHD repeatedly fall short. This paper considers the importance of myocardial fibrosis and function, the current body of evidence for myocardial fibrosis in ACHD, and its implications for research and treatment. PMID:25897907

  18. A collagen α2(I) mutation impairs healing after experimental myocardial infarction.

    PubMed

    Hofmann, Ulrich; Bonz, Andreas; Frantz, Stefan; Hu, Kai; Waller, Christiane; Roemer, Katrin; Wolf, Jürgen; Gattenlöhner, Stefan; Bauersachs, Johann; Ertl, Georg

    2012-01-01

    Collagen breakdown and de novo synthesis are important processes during early wound healing after myocardial infarction (MI). We tested the hypothesis that collagen I, the main constituent of the extracellular matrix, affects wound healing after MI. The osteogenesis imperfecta mouse (OIM), lacking procollagen-α2(I) expression, represents a model of the type III form of the disease in humans. Homozygous (OIM/OIM), heterozygous (OIM/WT), and wild-type (WT/WT) mice were subjected to a permanent myocardial infarction protocol or sham surgery. Baseline functional and geometrical parameters determined by echocardiography did not differ between genotypes. After MI but not after sham surgery, OIM/OIM animals exhibited significantly increased mortality, due to early ventricular rupture between day 3 and 7. Echocardiography at day 1 demonstrated increased left ventricular dilation in OIM/OIM animals. Less collagen I mRNA within the infarct area was found in OIM/OIM animals. At 2 days after MI, MMP-9 expression in the infarct border zone was higher in OIM/OIM than in WT/WT animals. Increased granulocyte infiltration into the infarct border zone occurred in OIM/OIM animals. Neither granulocyte depletion nor MMP inhibition reduced mortality in OIM/OIM animals. In this murine model, deficiency of collagen I leads to a myocardial wound-healing defect. Both structural alterations within pre-existing collagen matrix and impaired collagen de novo expression contribute to a high rate of early myocardial rupture after MI.

  19. Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Space Flight

    NASA Technical Reports Server (NTRS)

    Bloomberg, Jacob J.; Reschke, Millard F.; Clément, Gilles R.; Mulavara, Ajitkumar P.; Taylor, Laura C.

    2016-01-01

    We examine the various dimensions of the Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Space flight by reviewing the research and operational evidence demonstrating sensorimotor performance decrements during and after space flight. These sensorimotor performance decrements might affect vehicle and complex system control, including decreased visual acuity, eye-hand coordination, spatial and geographic orientation perception, and cognitive function. Sensorimotor performance decrements might also affect the ability to egress and walk away from the vehicle in case of an emergency or an extravehicular activity on a planetary surface. We also review the countermeasures that have been tested, including medication, prevention techniques and training exercises, physical rehabilitation, and mechanical devices. Furthermore, we identify the current knowledge and mitigation gaps that must be filled through further research and/or data mining efforts before the risk can be fully mitigated. We conclude that the true operational risks associated with the impacts of adaptive sensorimotor changes on mobility and crew abilities to control vehicles and other complex systems will only be estimable after the gaps have been filled and we have been able to accurately assess integrated performance in off-nominal operational settings. A large body of sensorimotor research data obtained from space flight experiments over the past half-century demonstrates significant decrements in oculomotor control, eye-hand coordination, spatial orientation, posture\\locomotor control and cognition during space flight missions. While these changes are most severe during and after G-transitions, the most crucial time for many critical operational tasks (e.g., landing and egress), only limited information is available to assess the operational impacts of these changes. Some of the operational observations are

  20. Does cancer start in the womb? altered mammary gland development and predisposition to breast cancer due to in utero exposure to endocrine disruptors.

    PubMed

    Soto, Ana M; Brisken, Cathrin; Schaeberle, Cheryl; Sonnenschein, Carlos

    2013-06-01

    We are now witnessing a resurgence of theories of development and carcinogenesis in which the environment is again being accepted as a major player in phenotype determination. Perturbations in the fetal environment predispose an individual to disease that only becomes apparent in adulthood. For example, gestational exposure to diethylstilbestrol resulted in clear cell carcinoma of the vagina and breast cancer. In this review the effects of the endocrine disruptor bisphenol-A (BPA) on mammary development and tumorigenesis in rodents is used as a paradigmatic example of how altered prenatal mammary development may lead to breast cancer in humans who are also widely exposed to it through plastic goods, food and drink packaging, and thermal paper receipts. Changes in the stroma and its extracellular matrix led to altered ductal morphogenesis. Additionally, gestational and lactational exposure to BPA increased the sensitivity of rats and mice to mammotropic hormones during puberty and beyond, thus suggesting a plausible explanation for the increased incidence of breast cancer.

  1. [Myocardial viability, its importance for the therapeutic decision].

    PubMed

    Alexánderson, Erick; Ricalde, Alejandro; Meave, Aloha

    2005-01-01

    Myocardial viability detection is essential in patients with history of myocardial infarction whom develop ventricular dysfunction. Its detection influences the therapeutic decisions and the prognosis. Medical therapy in patients with ventricular dysfunction due to myocardial infarction and myocardial viability has been associated with higher morbidity and mortality rates than revascularization therapy, as well as improvements in the systolic function. Several imaging techniques used in the recognition of myocardial viability are available; these techniques are based on the assessment of the ventricular motion posterior to inotropic agents stimulation or on the demonstration of metabolic activity at the dysfunctional regions. In this study, some important aspects of each technique are reviewed, doing special emphasis in the utility of the Positron Emission Tomography (PET) which has been considered as the "gold standard" in the detection of myocardial viability. PMID:15909735

  2. Myocardial mechanics in cardiomyopathies.

    PubMed

    Modesto, Karen; Sengupta, Partho P

    2014-01-01

    Cardiomyopathies are a heterogeneous group of diseases that can be phenotypically recognized by specific patterns of ventricular morphology and function. The authors summarize recent clinical observations that mechanistically link the multidirectional components of left ventricular (LV) deformation with morphological phenotypes of cardiomyopathies for offering key insights into the transmural heterogeneity of myocardial function. Subendocardial dysfunction predominantly alters LV longitudinal shortening, lengthening and suction performance and contributes to the phenotypic patterns of heart failure (HF) with preserved ejection fraction (EF) seen with hypertrophic and restrictive patterns of cardiomyopathy. On the other hand, a more progressive transmural disease results in reduction of LV circumferential and twist mechanics leading to the phenotypic pattern of dilated cardiomyopathy and the clinical syndrome of HF with reduced (EF). A proper characterization of LV transmural mechanics, energetics, and space-time distributions of pressure and shear stress may allow recognition of early functional changes that can forecast progression or reversal of LV remodeling. Furthermore, the interactions between LV muscle and fluid mechanics hold the promise for offering newer mechanistic insights and tracking impact of novel therapies.

  3. Alterations of physiology and gene expression due to long-term magnesium-deficiency differ between leaves and roots of Citrus reticulata.

    PubMed

    Jin, Xiao-Lin; Ma, Cui-Lan; Yang, Lin-Tong; Chen, Li-Song

    2016-07-01

    Seedlings of Ponkan (Citrus reticulata) were irrigated with nutrient solution containing 0 (Mg-deficiency) or 1mM MgSO4 (control) every two day for 16 weeks. Thereafter, we examined magnesium (Mg)-deficiency-induced changes in leaf and root gas exchange, total soluble proteins and gene expression. Mg-deficiency lowered leaf CO2 assimilation, and increased leaf dark respiration. However, Mg-deficient roots had lower respiration. Total soluble protein level was not significantly altered by Mg-deficiency in roots, but was lower in Mg-deficient leaves than in controls. Using cDNA-AFLP, we obtained 70 and 71 differentially expressed genes from leaves and roots. These genes mainly functioned in signal transduction, stress response, carbohydrate and energy metabolism, cell transport, cell wall and cytoskeleton metabolism, nucleic acid, and protein metabolisms. Lipid metabolism (Ca(2+) signals)-related Mg-deficiency-responsive genes were isolated only from roots (leaves). Although little difference existed in the number of Mg-deficiency-responsive genes between them both, most of these genes only presented in Mg-deficient leaves or roots, and only four genes were shared by them both. Our data clearly demonstrated that Mg-deficiency-induced alterations of physiology and gene expression greatly differed between leaves and roots. In addition, we focused our discussion on the causes for photosynthetic decline in Mg-deficient leaves and the responses of roots to Mg-deficiency. PMID:27163764

  4. Transient myocardial bridging of the left anterior descending coronary artery in acute inferior myocardial infarction.

    PubMed

    Kilic, Harun; Akdemir, Ramazan; Bicer, Asuman; Dogan, Mehmet

    2009-01-24

    We observed transient myocardial bridging of left anterior descending coronary artery (LAD) in 18.75% (12 of the total 64) of the patients during acute inferior myocardial infarction (MI). Myocardial bridging occurred only in the acute phase of inferior MI and not in the chronic phase. In the acute phase of inferior MI, compensatory hypercontraction of the anterior wall is assumed to occur in response to the decrease in the movement of the infarct-related walls. In the chronic phase, disappearance of the myocardial bridging observed due to the resolution of compensatory anterior wall hypercontraction, as a result of the reperfusion of infarct-related coronary artery. Most of the myocardial bridges seen in autopsy series are not seen angiographically. Variation at angiography may in part be attributable to small and thin bridges causing little compression. Adrenergic stimulation or afterload reduction by nitroglycerin facilitates diagnosis of myocardial bridging by increasing coronary compression. Both of these conditions are almost always present in acute MI. We concluded that transient myocardial bridging of LAD can be observed in some patients with acute inferior MI during acute stage. PMID:17920712

  5. Potential alteration of fjordal circulation due to a large floating structure—Numerical investigation with application to Hood Canal basin in Puget Sound

    SciTech Connect

    Khangaonkar, Tarang; Wang, Taiping

    2013-01-02

    Circulation in typical fjords is characterized by a shallow brackish layer at the surface over a deep long and narrow saltwater column. This surface layer is responsible for the outflow of water from the fjord, is easily disrupted by external forces, such as wind, and is influenced by freshwater inflow. In this paper, we postulate that the stability of fjordal circulation may also be vulnerable to impacts from anthropogenic alterations, such as floating structures, that could constrict the mixing and transport in the upper layers of the water column. The potential for alteration of circulation in Hood Canal, a silled-fjord located inside Puget Sound, Washington, has been examined. Using classical analytical treatments along the lines formulated by Hansen and Rattray [1965], Rattray [1967], Dyer [1973] and more recently, MacCready [2004], we develop a solution applicable to a range of estuary classifications varying from a partially mixed estuary regime to classical fjord conditions. Both estuary types exist in the Puget Sound system, and we compare our analytical solution with observed data. The analysis is based on an exponential variation of eddy viscosity with depth, and it has been extended further with modifications of the free surface boundary conditions to develop a solution representing the presence of a floating bridge at the estuary/fjord entrance. The model results show that tidally averaged mean circulation under the influence of such a constraint could reduce by as much as 30 to 50 percent. The overall water quality of fjords and narrow estuaries is dependent on net circulation and flushing. A potential decrease in residual flow or a corresponding increase in residence time of this magnitude merits further study.

  6. Shifts in the climate space of temperate cyprinid fishes due to climate change are coupled with altered body sizes and growth rates.

    PubMed

    Ruiz-Navarro, Ana; Gillingham, Phillipa K; Britton, J Robert

    2016-09-01

    Predictions of species responses to climate change often focus on distribution shifts, although responses can also include shifts in body sizes and population demographics. Here, shifts in the distributional ranges ('climate space'), body sizes (as maximum theoretical body sizes, L∞) and growth rates (as rate at which L∞ is reached, K) were predicted for five fishes of the Cyprinidae family in a temperate region over eight climate change projections. Great Britain was the model area, and the model species were Rutilus rutilus, Leuciscus leuciscus, Squalius cephalus, Gobio gobio and Abramis brama. Ensemble models predicted that the species' climate spaces would shift in all modelled projections, with the most drastic changes occurring under high emissions; all range centroids shifted in a north-westerly direction. Predicted climate space expanded for R. rutilus and A. brama, contracted for S. cephalus, and for L. leuciscus and G. gobio, expanded under low-emission scenarios but contracted under high emissions, suggesting the presence of some climate-distribution thresholds. For R. rutilus, A. brama, S. cephalus and G. gobio, shifts in their climate space were coupled with predicted shifts to significantly smaller maximum body sizes and/or faster growth rates, aligning strongly to aspects of temperature-body size theory. These predicted shifts in L∞ and K had considerable consequences for size-at-age per species, suggesting substantial alterations in population age structures and abundances. Thus, when predicting climate change outcomes for species, outputs that couple shifts in climate space with altered body sizes and growth rates provide considerable insights into the population and community consequences, especially for species that cannot easily track their thermal niches.

  7. [The evolution of hospital mortality due to acute myocardial infarct in the first 2 GISSI studies. Participants in the GISSI 1 and GISSI 2 studies. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico].

    PubMed

    Mauri, F; De Vita, C; Staszewsky, L; Piantadosi, F R; Bosi, S; Mantini, L; Matta, F; Negrini, M; Valente, S; Martini L [corrected to Mantini, L

    1994-12-01

    During the short while of 5 years, between 1984 and 1985, two large clinical trials have been performed in Italy concerning fibrinolytic therapy in Acute Myocardial Infarction: GISSI 1 and GISSI 2. They made possible to evaluate the evolution of demographic and clinical features, the in-hospital mortality rate, and the causes of death of a huge number of patients admitted to CCU throughout the whole country. Out of 31,826 patients with acute myocardial infarction admitted to 176 CCU participating to the GISSI 1 16.9% were 75 years old and 24.7% were females; 21.8% and 26.4% were the percentages in the 38,086 patients admitted to the 223 CCU participating in the GISSI 2. Despite the higher prevalence of the two demographic characteristic with the worse prognosis, the in-hospital mortality rates were respectively 12.2% in the GISSI 1 and 10.0% in the GISSI 2 studies, with a statistically significant decrease (RR 0.84; C.L. 0.80-0.88). The significant decrease in the in-hospital mortality concerns also the patients populations selected according to the same criteria of inclusion in the two trials (within 6 hours from the onset of symptoms and with only ST elevation at the ECG of admission) and to the treatment with fibrinolytic drug (SK or rtPA). As a matter of fact 468 patients died of the 4,696 (10.0%) treated with SK in the GISSI 1 against 1,092 patients of 12,381 (8.8%) enrolled in the GISSI 2 and treated with SK or rtPA (RR 0.87; L.C. 0.78-0.98). The reduction of in-hospital mortality may be explained by some differences in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

  8. Identification of Temporal and Region-Specific Myocardial Gene Expression Patterns in Response to Infarction in Swine

    PubMed Central

    Nonell, Lara; Puigdecanet, Eulàlia; Astier, Laura; Solé, Francesc; Bayes-Genis, Antoni

    2013-01-01

    Molecular mechanisms associated with pathophysiological changes in ventricular remodelling due to myocardial infarction (MI) remain poorly understood. We analyzed changes in gene expression by microarray technology in porcine myocardial tissue at 1, 4, and 6 weeks post-MI. MI was induced by coronary artery ligation in 9 female pigs (30–40 kg). Animals were randomly sacrificed at 1, 4, or 6 weeks post-MI (n = 3 per group) and 3 healthy animals were also included as control group. Total RNA from myocardial samples was hybridized to GeneChip® Porcine Genome Arrays. Functional analysis was obtained with the Ingenuity Pathway Analysis (IPA) online tool. Validation of microarray data was performed by quantitative real-time PCR (qRT-PCR). More than 8,000 different probe sets showed altered expression in the remodelling myocardium at 1, 4, or 6 weeks post-MI. Ninety-seven percent of altered transcripts were detected in the infarct core and 255 probe sets were differentially expressed in the remote myocardium. Functional analysis revealed 28 genes de-regulated in the remote myocardial region in at least one of the three temporal analyzed stages, including genes associated with heart failure (HF), systemic sclerosis and coronary artery disease. In the infarct core tissue, eight major time-dependent gene expression patterns were recognized among 4,221 probe sets commonly altered over time. Altered gene expression of ACVR2B, BID, BMP2, BMPR1A, LMNA, NFKBIA, SMAD1, TGFB3, TNFRSF1A, and TP53 were further validated. The clustering of similar expression patterns for gene products with related function revealed molecular footprints, some of them described for the first time, which elucidate changes in biological processes at different stages after MI. PMID:23372767

  9. Combretastatin A4 disodium phosphate-induced myocardial injury.

    PubMed

    Tochinai, Ryota; Nagata, Yuriko; Ando, Minoru; Hata, Chie; Suzuki, Tomo; Asakawa, Naoyuki; Yoshizawa, Kazuhiko; Uchida, Kazumi; Kado, Shoichi; Kobayashi, Toshihide; Kaneko, Kimiyuki; Kuwahara, Masayoshi

    2016-07-01

    Histopathological and electrocardiographic features of myocardial lesions induced by combretastatin A4 disodium phosphate (CA4DP) were evaluated, and the relation between myocardial lesions and vascular changes and the direct toxic effect of CA4DP on cardiomyocytes were discussed. We induced myocardial lesions by administration of CA4DP to rats and evaluated myocardial damage by histopathologic examination and electrocardiography. We evaluated blood pressure (BP) of CA4DP-treated rats and effects of CA4DP on cellular impedance-based contractility of human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs). The results revealed multifocal myocardial necrosis with a predilection for the interventricular septum and subendocardial regions of the apex of the left ventricular wall, injury of capillaries, morphological change of the ST junction, and QT interval prolongation. The histopathological profile of myocardial lesions suggested that CA4DP induced a lack of myocardial blood flow. CA4DP increased the diastolic BP and showed direct effects on hiPS-CMs. These results suggest that CA4DP induces dysfunction of small arteries and capillaries and has direct toxicity in cardiomyocytes. Therefore, it is thought that CA4DP induced capillary and myocardial injury due to collapse of the microcirculation in the myocardium. Moreover, the direct toxic effect of CA4DP on cardiomyocytes induced myocardial lesions in a coordinated manner. PMID:27559241

  10. Myocardial Bridging: An Up-to-Date Review.

    PubMed

    Lee, Michael S; Chen, Cheng-Han

    2015-11-01

    Myocardial bridging is a congenital anomaly in which a segment of a coronary artery takes a "tunneled" intramuscular course under a "bridge" of overlying myocardium. This causes vessel compression in systole, resulting in hemodynamic changes that may be associated with angina, myocardial ischemia, acute coronary syndrome, left ventricular dysfunction, arrhythmias, and even sudden cardiac death. While described on autopsy for centuries, technological advances such as coronary computed tomography angiography and intravascular ultrasound have contributed greatly to our understanding of the anatomic, hemodynamic, and pathophysiological consequences of systolic compression. Atherosclerosis preferentially develops immediately proximal to the bridged segment, likely due to alterations in shear stress, while the compressed segment itself is often spared. First-line therapy of symptomatic bridging remains medical treatment with beta-blockers and non-dihydropyridine calcium-channel blockers, and nitrates are contraindicated. Surgical myotomy, intracoronary stenting, and coronary artery bypass graft surgery have been used for refractory symptoms, but long-term outcomes remain uncertain. Further research is required to better define the patient population that would derive the greatest benefit from surgical and percutaneous intervention.

  11. Myocardial Bridging: An Up-to-Date Review

    PubMed Central

    Lee, Michael S.; Chen, Cheng-Han

    2016-01-01

    Myocardial bridging is a congenital anomaly in which a segment of a coronary artery takes a “tunneled” intramuscular course under a “bridge” of overlying myocardium. This causes vessel compression in systole, resulting in hemodynamic changes that may be associated with angina, myocardial ischemia, acute coronary syndrome, left ventricular dysfunction, arrhythmias, and even sudden cardiac death. While described on autopsy for centuries, technological advances such as coronary computed tomography angiography and intravascular ultrasound have contributed greatly to our understanding of the anatomic, hemodynamic, and pathophysiological consequences of systolic compression. Atherosclerosis preferentially develops immediately proximal to the bridged segment, likely due to alterations in shear stress, while the compressed segment itself is often spared. First-line therapy of symptomatic bridging remains medical treatment with beta-blockers and non-dihydropyridine calcium-channel blockers, and nitrates are contraindicated. Surgical myotomy, intracoronary stenting, and coronary artery bypass graft surgery have been used for refractory symptoms, but long-term outcomes remain uncertain. Further research is required to better define the patient population that would derive the greatest benefit from surgical and percutaneous intervention. PMID:25999138

  12. Adventitial Alterations Are the Main Features in Pulmonary Artery Remodeling due to Long-Term Chronic Intermittent Hypobaric Hypoxia in Rats

    PubMed Central

    Brito, Julio; Siques, Patricia; Arribas, Silvia M.; López de Pablo, Angel L.; González, M. Carmen; Naveas, Nelson; Flores, Karen; León-Velarde, Fabiola; Pulido, Ruth; Ordenes, Stefany; López, M. Rosario

    2015-01-01

    Long-term chronic intermittent exposure to altitude hypoxia is a labor phenomenon requiring further research. Using a rat model, we examined whether this type of exposure differed from chronic exposure in terms of pulmonary artery remodeling and other features. Rats were subjected to chronic hypoxia (CH, n = 9) and long-term intermittent hypoxia (CIH2x2; 2 days of hypoxia/2 days of normoxia, n = 10) in a chamber (428 Torr, 4,600 m of altitude) for 46 days and compared to rats under normoxia (NX, n = 10). Body weight, hematocrit, and right ventricle ratio were measured. Pulmonary artery remodeling was assessed using confocal microscopy of tissues stained with a nuclear dye (DAPI) and CD11b antibody. Both hypoxic conditions exhibited increased hematocrit and hypertrophy of the right ventricle, tunica adventitia, and tunica media, with no changes in lumen size. The medial hypertrophy area (larger in CH) depicted a significant increase in smooth muscle cell number. Additionally, CIH2x2 increased the adventitial hypertrophy area, with an increased cellularity and a larger prevalence of clustered inflammatory cells. In conclusion, CIH2x2 elicits milder effects on pulmonary artery medial layer muscularization and subsequent right ventricular hypertrophy than CH. However, CIH2x2 induces greater and characteristic alterations of the adventitial layer. PMID:25738150

  13. Impaired Protofibril Formation in Fibrinogen γN308K Is Due to Altered D:D and "A:a" Interactions

    SciTech Connect

    Bowley, S.; Okumura, N; Lord, S

    2009-01-01

    'A:a' knob-hole interactions and D:D interfacial interactions are important for fibrin polymerization. Previous studies with recombinant ?N308K fibrinogen, a substitution at the D:D interface, showed impaired polymerization. We examined the molecular basis for this loss of function by solving the crystal structure of ?N308K fragment D. In contrast to previous fragment D crystals, the ?N308K crystals belonged to a tetragonal space group with an unusually long unit cell (a = b = 95 Angstroms, c = 448.3 Angstroms). Alignment of the normal and ?N308K structures showed the global structure of the variant was not changed and the knob 'A' peptide GPRP was bound as usual to hole 'a'. The substitution introduced an elongated positively charged patch in the D:D region. The structure showed novel, symmetric D:D crystal contacts between ?N308K molecules, indicating the normal asymmetric D:D interface in fibrin would be unstable in this variant. We examined GPRP binding to ?N308K in solution by plasmin protection assay. The results showed weaker peptide binding, suggesting that 'A:a' interactions were altered. We examined fibrin network structures by scanning electron microscopy and found the variant fibers were thicker and more heterogeneous than normal fibers. Considered together, our structural and biochemical studies indicate both 'A:a' and D:D interactions are weaker. We conclude that stable protofibrils cannot assemble from ?N308K monomers, leading to impaired polymerization.

  14. Excitatory synapses are stronger in the hippocampus of Rett syndrome mice due to altered synaptic trafficking of AMPA-type glutamate receptors

    PubMed Central

    Li, Wei; Xu, Xin

    2016-01-01

    Deficits in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cognitive impairments in neurodevelopmental disorders associated with intellectual disability and autism. Using the methyl-CpG-binding protein 2 (Mecp2) knockout (KO) mouse model of Rett syndrome, we show that naïve excitatory synapses onto hippocampal pyramidal neurons of symptomatic mice have all of the hallmarks of potentiated synapses. Stronger Mecp2 KO synapses failed to undergo LTP after either theta-burst afferent stimulation or pairing afferent stimulation with postsynaptic depolarization. On the other hand, basal synaptic strength and LTP were not affected in slices from younger presymptomatic Mecp2 KO mice. Furthermore, spine synapses in pyramidal neurons from symptomatic Mecp2 KO are larger and do not grow in size or incorporate GluA1 subunits after electrical or chemical LTP. Our data suggest that LTP is occluded in Mecp2 KO mice by already potentiated synapses. The higher surface levels of GluA1-containing receptors are consistent with altered expression levels of proteins involved in AMPA receptor trafficking, suggesting previously unidentified targets for therapeutic intervention for Rett syndrome and other MECP2-related disorders. PMID:26929363

  15. Bioenergetic Insufficiencies Due to Metabolic Alterations Regulated by the Inhibitory Receptor PD-1 Are an Early Driver of CD8(+) T Cell Exhaustion.

    PubMed

    Bengsch, Bertram; Johnson, Andy L; Kurachi, Makoto; Odorizzi, Pamela M; Pauken, Kristen E; Attanasio, John; Stelekati, Erietta; McLane, Laura M; Paley, Michael A; Delgoffe, Greg M; Wherry, E John

    2016-08-16

    Dynamic reprogramming of metabolism is essential for T cell effector function and memory formation. However, the regulation of metabolism in exhausted CD8(+) T (Tex) cells is poorly understood. We found that during the first week of chronic lymphocytic choriomeningitis virus (LCMV) infection, before severe dysfunction develops, virus-specific CD8(+) T cells were already unable to match the bioenergetics of effector T cells generated during acute infection. Suppression of T cell bioenergetics involved restricted glucose uptake and use, despite persisting mechanistic target of rapamycin (mTOR) signaling and upregulation of many anabolic pathways. PD-1 regulated early glycolytic and mitochondrial alterations and repressed transcriptional coactivator PGC-1α. Improving bioenergetics by overexpression of PGC-1α enhanced function in developing Tex cells. Therapeutic reinvigoration by anti-PD-L1 reprogrammed metabolism in a subset of Tex cells. These data highlight a key metabolic control event early in exhaustion and suggest that manipulating glycolytic and mitochondrial metabolism might enhance checkpoint blockade outcomes. PMID:27496729

  16. Adventitial alterations are the main features in pulmonary artery remodeling due to long-term chronic intermittent hypobaric hypoxia in rats.

    PubMed

    Brito, Julio; Siques, Patricia; Arribas, Silvia M; López de Pablo, Angel L; González, M Carmen; Naveas, Nelson; Arriaza, Karem; Flores, Karen; León-Velarde, Fabiola; Pulido, Ruth; Ordenes, Stefany; López, M Rosario

    2015-01-01

    Long-term chronic intermittent exposure to altitude hypoxia is a labor phenomenon requiring further research. Using a rat model, we examined whether this type of exposure differed from chronic exposure in terms of pulmonary artery remodeling and other features. Rats were subjected to chronic hypoxia (CH, n = 9) and long-term intermittent hypoxia (CIH2x2; 2 days of hypoxia/2 days of normoxia, n = 10) in a chamber (428 Torr, 4,600 m of altitude) for 46 days and compared to rats under normoxia (NX, n = 10). Body weight, hematocrit, and right ventricle ratio were measured. Pulmonary artery remodeling was assessed using confocal microscopy of tissues stained with a nuclear dye (DAPI) and CD11b antibody. Both hypoxic conditions exhibited increased hematocrit and hypertrophy of the right ventricle, tunica adventitia, and tunica media, with no changes in lumen size. The medial hypertrophy area (larger in CH) depicted a significant increase in smooth muscle cell number. Additionally, CIH2x2 increased the adventitial hypertrophy area, with an increased cellularity and a larger prevalence of clustered inflammatory cells. In conclusion, CIH2x2 elicits milder effects on pulmonary artery medial layer muscularization and subsequent right ventricular hypertrophy than CH. However, CIH2x2 induces greater and characteristic alterations of the adventitial layer.

  17. Excitatory synapses are stronger in the hippocampus of Rett syndrome mice due to altered synaptic trafficking of AMPA-type glutamate receptors.

    PubMed

    Li, Wei; Xu, Xin; Pozzo-Miller, Lucas

    2016-03-15

    Deficits in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cognitive impairments in neurodevelopmental disorders associated with intellectual disability and autism. Using the methyl-CpG-binding protein 2 (Mecp2) knockout (KO) mouse model of Rett syndrome, we show that naïve excitatory synapses onto hippocampal pyramidal neurons of symptomatic mice have all of the hallmarks of potentiated synapses. Stronger Mecp2 KO synapses failed to undergo LTP after either theta-burst afferent stimulation or pairing afferent stimulation with postsynaptic depolarization. On the other hand, basal synaptic strength and LTP were not affected in slices from younger presymptomatic Mecp2 KO mice. Furthermore, spine synapses in pyramidal neurons from symptomatic Mecp2 KO are larger and do not grow in size or incorporate GluA1 subunits after electrical or chemical LTP. Our data suggest that LTP is occluded in Mecp2 KO mice by already potentiated synapses. The higher surface levels of GluA1-containing receptors are consistent with altered expression levels of proteins involved in AMPA receptor trafficking, suggesting previously unidentified targets for therapeutic intervention for Rett syndrome and other MECP2-related disorders.

  18. Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure.

    PubMed

    Shah, Sanjiv J; Aistrup, Gary L; Gupta, Deepak K; O'Toole, Matthew J; Nahhas, Amanda F; Schuster, Daniel; Chirayil, Nimi; Bassi, Nikhil; Ramakrishna, Satvik; Beussink, Lauren; Misener, Sol; Kane, Bonnie; Wang, David; Randolph, Blake; Ito, Aiko; Wu, Megan; Akintilo, Lisa; Mongkolrattanothai, Thitipong; Reddy, Mahendra; Kumar, Manvinder; Arora, Rishi; Ng, Jason; Wasserstrom, J Andrew

    2014-01-01

    Although the development of abnormal myocardial mechanics represents a key step during the transition from hypertension to overt heart failure (HF), the underlying ultrastructural and cellular basis of abnormal myocardial mechanics remains unclear. We therefore investigated how changes in transverse (T)-tubule organization and the resulting altered intracellular Ca(2+) cycling in large cell populations underlie the development of abnormal myocardial mechanics in a model of chronic hypertension. Hearts from spontaneously hypertensive rats (SHRs; n = 72) were studied at different ages and stages of hypertensive heart disease and early HF and were compared with age-matched control (Wistar-Kyoto) rats (n = 34). Echocardiography, including tissue Doppler and speckle-tracking analysis, was performed just before euthanization, after which T-tubule organization and Ca(2+) transients were studied using confocal microscopy. In SHRs, abnormalities in myocardial mechanics occurred early in response to hypertension, before the development of overt systolic dysfunction and HF. Reduced longitudinal, circumferential, and radial strain as well as reduced tissue Doppler early diastolic tissue velocities occurred in concert with T-tubule disorganization and impaired Ca(2+) cycling, all of which preceded the development of cardiac fibrosis. The time to peak of intracellular Ca(2+) transients was slowed due to T-tubule disruption, providing a link between declining cell ultrastructure and abnormal myocardial mechanics. In conclusion, subclinical abnormalities in myocardial mechanics occur early in response to hypertension and coincide with the development of T-tubule disorganization and impaired intracellular Ca(2+) cycling. These changes occur before the development of significant cardiac fibrosis and precede the development of overt cardiac dysfunction and HF.

  19. Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation

    PubMed Central

    Che, Xia; Wang, Xin; Zhang, Junyan; Peng, Chengfeng; Zhen, Yilan; Shao, Xu; Zhang, Gongliang; Dong, Liuyi

    2016-01-01

    Purpose: The aim of this study was to explore the cardioprotective effect of vitexin on chronic myocardial ischemia/reperfusion injury in rats and potential mechanisms. Methods: A chronic myocardial ischemia/reperfusion injury model was established by ligating left anterior descending coronary for 60 minutes, and followed by reperfusion for 14 days. After 2 weeks ischemia/reperfusion, cardiac function was measured to assess myocardial injury. The level of ST segment was recorded in different periods by electrocardiograph. The change of left ventricular function and myocardial reaction degree of fibrosis of heart was investigated by hematoxylin and eosin (HE) staining and Sirius red staining. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. The blood samples were collected to measure the levels of MDA, the activities of SOD and NADPH in serum. Epac1, Rap1, Bax and Bcl-2 were examined by using Western Blotting. Results: Vitexin exerted significant protective effect on chronic myocardial ischemia/reperfusion injury, improved obviously left ventricular diastolic function and reduced myocardial reactive fibrosis degree in rats of myocardial ischemia. Medium and high-dose vitexin groups presented a significant decrease in Bax, Epac1 and Rap1 production and increase in Bcl-2 compared to the I/R group. It may be related to preventing myocardial cells from apoptosis, improving myocardial diastolic function and inhibiting lipid peroxidation. Conclusions: Vitexin is a cardioprotective herb, which may be a promising useful complementary and alternative medicine for patients with coronary heart disease.

  20. Inter-laboratory comparison of human renal proximal tubule (HK-2) transcriptome alterations due to Cyclosporine A exposure and medium exhaustion.

    PubMed

    Jennings, Paul; Aydin, Sonia; Bennett, Jason; McBride, Rachael; Weiland, Christina; Tuite, Niamh; Gruber, Leonhard N; Perco, Paul; Gaora, Peadar O; Ellinger-Ziegelbauer, Heidrun; Ahr, Hans-Juergen; Kooten, Cees Van; Daha, Mohamed R; Prieto, Pilar; Ryan, Michael P; Pfaller, Walter; McMorrow, Tara

    2009-04-01

    There is an acknowledged need to promote and further develop in vitro techniques in order to achieve the goal of improved risk assessment of chemicals and pharmaceuticals to humans. The EU 6th framework project "PREDICTOMICS" was established in order to contribute to the further development of in vitro toxicology, with a particular focus on emerging techniques including toxicogenomics. DNA microarray technology is being used more frequently in the in vitro field, however, only very few studies have assessed the reproducibility of this technique with respect to in vitro toxicology. To this end we conducted an interlaboratory comparison to test the reproducibility of transcriptomic changes induced by the immunosuppressive agent, Cyclosporine A (CsA) on the human renal proximal tubular cell line, HK-2 cell. Four European laboratories took part in this study. Under standardised conditions, each laboratory treated HK-2 cells with 5microM CsA for 12 and 48h. RNA was isolated and hybridised to Affymetrix HGU-133 plus two arrays at three different sites. Analysis of the transcription profiles demonstrated that one laboratory clustered away from the other laboratories, potentially due to an inclusion of a trypsinisation step by this laboratory. Once the genes responsible for this separate clustering were removed all laboratories showed similar expression profiles. There was a major impact of time since feed, due to medium exhaustion in the 48h arrays compared to the 12h arrays, regardless of CsA treatment. Biological processes including general vesicle transport, amino acid metabolism, amino acid transport and amino acid biosynthesis were over-represented due to time since feed, while cell cycle, DNA replication, mitosis and DNA metabolism were under-represented. CsA responsive genes were involved in cell cycle, the p53 pathway and Wnt signaling. Additionally there was an overlap of differentially expressed genes due to CsA and medium exhaustion which is most likely due to

  1. Noninvasive measurement of regional myocardial glucose metabolism by positron emission computed tomography. [Dogs

    SciTech Connect

    Schelbert, H.R.; Phelps, M.E.

    1980-06-01

    While the results of regional myocardial glucose metabolism measurements using positron emission computed tomography (/sup 13/N-ammonia) are promising, their utility and value remains to be determined in man. If this technique can be applied to patients with acute myocardial ischemia or infarction it may permit delineation of regional myocardial segments with altered, yet still active metabolism. Further, it may become possible to evaluate the effects of interventions designed to salvage reversibly injured myocardium by this technique.

  2. Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats.

    PubMed

    Roguski, Emily E; Sharp, Burt M; Chen, Hao; Matta, Shannon G

    2014-03-01

    In adult rats, we have shown full-gestational exposure to nicotine and ethanol (Nic + EtOH) augmented nicotine self-administration (SA) (increased nicotine intake) compared to pair-fed (PF) offspring. Therefore, we hypothesized that full-gestational exposure to Nic + EtOH disrupts control of dopaminergic (DA) circuitry by ventral tegmental area (VTA) NMDA receptors, augmenting nicotine SA and DA release in nucleus accumbens (NAcc) of adolescents. Both NAcc DA and VTA glutamate release were hyper-responsive to intra-VTA NMDA in Nic + EtOH offspring versus PF (p = 0.03 and 0.02, respectively). Similarly, DA release was more responsive to i.v. nicotine in Nic + EtOH offspring (p = 0.02). Local DL-2-Amino-5-phosphonopentanoic acid sodium salt (AP5) (NMDA receptor antagonist) infusion into the VTA inhibited nicotine-stimulated DA release in Nic + EtOH and PF offspring. Nicotine SA was augmented in adolescent Nic + EtOH versus PF offspring (p = 0.000001). Daily VTA microinjections of AP5 reduced nicotine SA by Nic + EtOH offspring, without affecting PF (p = 0.000032). Indeed, nicotine SA in Nic + EtOH offspring receiving AP5 was not different from PF offspring. Both VTA mRNA transcripts and NMDA receptor subunit proteins were not altered in Nic + EtOH offspring. In summary, adolescent offspring exposed to gestational Nic + EtOH show markedly increased vulnerability to become dependent on nicotine. This reflects the enhanced function of a subpopulation of VTA NMDA receptors that confer greater nicotine-induced DA release in NAcc. We hypothesized that concurrent gestational exposure to nicotine and ethanol would disrupt the control of VTA dopaminergic circuitry by NMDA receptors. Resulting in the augmented nicotine self-administration (SA) in adolescent offspring.

  3. A geomorphic framework to assess changes to aquatic habitat due to flow regulation and channel and floodplain alteration of the Cedar River, Washington

    NASA Astrophysics Data System (ADS)

    Gendaszek, A. S.; Magirl, C. S.; Barnas, C. R.; Konrad, C. P.; Little, R.

    2010-12-01

    Flow regulation, bank armoring, and floodplain alteration since the early 20th century have contributed to significant changes in the hydrologic regime and geomorphic processes of the Cedar River in Washington State. The Cedar River originates in the Cascade Range, provides drinking water to the Seattle metropolitan area, and supports several populations of anadromous salmonids. Flow regulation currently has limited influence on the magnitude, duration, and timing of high-flow events, which affect the incubation of salmonids as well as the production and maintenance of their habitat. Unlike structural changes to the channel and floodplain, flow regulation may be modified in the short-term to improve the viability of salmon populations. An understanding of the effects of flow regulation on those populations must be discerned over a range of scales from individual floods that affect the size of individual year classes to decadal high flow regime that influences the amount and quality of channel and off-channel habitat available for spawning and rearing. We present estimates of reach-scale sediment budgets and changes to channel morphology derived from historical orthoimagery, specific gage analyses at four long-term streamflow-gaging stations to quantify trends in aggradation, and hydrologic statistics of the magnitude and duration of peak streamflows. These data suggest a gradient of channel types from unconfined, sediment-rich segments to confined, sediment-poor segments that are likely to have distinct responses to high flows. Particle-size distribution data and longitudinal water surface and streambed profiles for the 56 km downstream of Chester Morse Lake measured in 2010 show the spatial extent of preferred salmonid habitat along the Cedar River. These historical and current data constitute a geomorphic framework to help assess different river management scenarios for salmonid habitat and population viability.

  4. Gsα activity is reduced in erythrocyte membranes of patients with psedohypoparathyroidism due to epigenetic alterations at the GNAS locus.

    PubMed

    Zazo, Celia; Thiele, Susanne; Martín, Cesar; Fernandez-Rebollo, Eduardo; Martinez-Indart, Lorea; Werner, Ralf; Garin, Intza; Hiort, Olaf; Perez de Nanclares, Guiomar

    2011-08-01

    In pseudohypoparathyroidism (PHP), PTH resistance results from impairment of signal transduction of G protein-coupled receptors caused by a deficiency of the Gsα-cAMP signaling cascade due to diminished Gsα activity in maternally imprinted tissues. In PHP-Ia, inactivating mutations of the GNAS gene lead to haploinsufficiency in some tissues with biallelic expression, so in addition to PHP, Albright's hereditary osteodystrophy (AHO) is also present. In PHP-Ib, caused by methylation defects at the GNAS locus, diminished Gsα activity was thought to be limited to maternally imprinted tissues, such as the renal proximal tubule and the thyroid, leading to a lack of AHO. Recently, we demonstrated methylation defects in patients with AHO signs, indicating a connection between epigenetic changes and AHO. Our objective was to determine Gsα activity in erythrocyte membranes in patients with epigenetic defects at the GNAS locus compared to normal controls and patients with inactivating GNAS mutations. Gsα activity and expression, mutation of the GNAS locus, and methylation status were studied in patients with PHP and mild signs of AHO (PHP-Ia: 12; PHP-Ib: 17, of which 8 had some features of AHO). Then, we statistically compared the Gsα activity of the different PHP subtypes. Patients with methylation defects at the GNAS locus show a significant decrease in erythrocyte Gsα activity compared to normal controls (PHP-Ib versus controls, p < .001). This was significantly lower in patients with AHO signs (PHP-Ib + mild-AHO versus PHP-Ib, p < .05). Our research shows that PHP-Ia and PHP-Ib classification is not only overlapped genetically, as reported, but also in terms of Gsα activity. Reduced expression of GNAS due to methylation defects could downregulate Gsα activity in other tissues beyond those described and could also be causative of AHO.

  5. Altered pathogenicity of a tl/CH/LDT3/03 genotype infectious bronchitis coronavirus due to natural recombination in the 5'- 17kb region of the genome.

    PubMed

    Han, Zongxi; Zhang, Tingting; Xu, Qianqian; Gao, Mengying; Chen, Yuqiu; Wang, Qiuling; Zhao, Yan; Shao, Yuhao; Li, Huixin; Kong, Xiangang; Liu, Shengwang

    2016-02-01

    An infectious bronchitis coronavirus, designated as ck/CH/LGX/130530, was isolated from an IBV strain H120-vaccinated chicken in this study. Analysis of the S1 gene showed that isolate ck/CH/LGX/130530 was a tl/CH/LDT3/03-like virus, with a nucleotide sequence similarity of 99%. However, a complete genomic sequence analysis showed that ck/CH/LGX/130530 was more closely related to a Massachusetts type strain (95% similarity to strain H120) than to the tl/CH/LDT3/03 strain (86%), suggesting that recombination might have occurred during the origin of the virus. A SimPlot analysis of the complete genomic sequence confirmed this hypothesis, and it showed that isolate ck/CH/LGX/130530 emerged from a recombination event between parental IBV H120 strain and pathogenic tl/CH/LDT3/03-like virus. The results obtained from the pairwise comparison and nucleotide similarity showed that the recombination breakpoint was located in the nsp14 gene at nucleotides 17055-17083. In line with the high S1 gene sequence similarity, the ck/CH/LGX/130530 isolate was serotypically close to that of the tl/CH/LDT3/03 strain (73% antigenic relatedness). Furthermore, vaccination with the LDT3-A vaccine, which was derived from the tl/CH/LDT3/03 strain by serial passaging in chicken eggs, provided good protection against challenge with the tl/CH/LDT3/03 strain, in contrast to the poor protection offered with the H120 vaccine. Interestingly, isolate ck/CH/LGX/130530 exhibited low pathogenicity toward specific-pathogen-free chickens compared with the nephropathogenic tl/CH/LDT3/03 strain, which was likely due to natural recombination in the 5' 17-kb region of the genome. Our results also indicate that the replicase gene of IBV isolate ck/CH/LGX/130530 is associated with viral pathogenicity.

  6. An uncommon cause of myocardial ischemia after coronary artery bypass grafting: "the dangerous drainage".

    PubMed

    Beiras-Fernandez, Andres; Möhnle, Patrick; Kopf, Carsten; Vicol, Calin; Kur, Felix; Reichart, Bruno

    2011-06-01

    The most common causes of myocardial ischemia and myocardial infarction early after coronary artery bypass grafting surgery are early graft occlusion/thrombosis or occlusion/ thrombosis of coronary arteries due to advanced coronary heart disease. We describe a case of postoperative myocardial ischemia due to an uncommon and quickly reversible cause: mechanical compression of a vein graft by a 19F flexible silicone mediastinal drainage tube.

  7. Multiplane Transesophageal Echocardiography with Dobutamine in Patients with Biventricular Inferior Myocardial Infarction.

    PubMed

    Espinola-Zavaleta, Nilda; Vargas-Barrón, Jesús; Romero-Cárdenas, Angel; Bialostozky, David; Alexanderson, Erick; Martinez-Sanchez, Carlos; Peña-Duque, Marco; Keirns, Candace; Rijlaarsdam, María; Lupi-Herrera, Eulo

    1998-02-01

    The purpose of this study was to evaluate the alterations of ventricular wall movement in patients with acute posteroinferior myocardial infarction with extension to right cavities with multiplane transesophageal echocardiography (TEE), as well as the utility of dobutamine with this technique to analyze myocardial viability. Nine men with a mean age of 51 years fulfilled the inclusion criteria. Myocardial TEE was performed in all the men 72 hours after the acute event with long- and short-axis transgastric images of both ventricles under basal conditions and with dobutamine infusions of 5 and 10 µg/kg per minute. Results were compared with myocardial perfusion findings obtained with Tc-99m Sestamibi SPECT. Left ventricular myocardial viability was demonstrated in 28 of 45 altered segments with dobutamine stress myocardial TEE and Tc-99m Sestamibi SPECT. Right ventricular myocardial viability was identified in 27 of 30 altered segments with dobutamine stress myocardial TEE in transgastric short and long axes, and with Tc-99m Sestamibi SPECT in 23 of 25 segments only in short-axis images. Multiplane TEE provided excellent image resolution and better definition of endocardial and epicardial borders, which facilitated detailed evaluation of ventricular segmental wall movement. Infusion of low doses of dobutamine made it possible to identify viable tissue in both ventricles, and results were comparable to those of nuclear medicine.

  8. Inhalation of decomposed chlorodifluoromethane (freon-22) and myocardial infarction.

    PubMed

    Sjögren, Bengt; Gunnare, Sara; Sandler, Håkan

    2002-06-01

    After exposure to decomposed chlorodifluoromethane (freon-22), a 65-year-old man developed respiratory symptoms such as cough, blood-stained sputum, and increasing dyspnea. Three weeks later, his family doctor diagnosed infectious bronchitis. Another week later he died due to myocardial infarction. The discussion focuses on an inflammatory process caused by the inhalation of decomposed freon and its possible association with myocardial infarction.

  9. Protective effect of taurine on myocardial antioxidant status in isoprenaline-induced myocardial infarction in rats.

    PubMed

    Shiny, K S; Kumar, S Hari Senthil; Farvin, K H Sabeena; Anandan, R; Devadasan, K

    2005-10-01

    We have examined the protective effect of taurine on the myocardial antioxidant defense system in isoprenaline (isoproterenol)-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Levels of diagnostic marker enzymes in plasma, lipid peroxides and reduced glutathione, and the activity of glutathione-dependent antioxidant enzymes and anti-peroxidative enzymes in the heart tissue were determined. Intraperitoneal administration of taurine significantly prevented the isoprenaline-induced increases in the levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatine phosphokinase in the plasma of rats. Taurine exerted an antioxidant effect against isoprenaline-induced myocardial infarction by preventing the accumulation of lipid peroxides and by maintaining the level of reduced glutathione and the activity of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase at near normality. The results indicated that the cardioprotective potential of taurine was probably due to the increase of the activity of the free radical enzymes, or to a counteraction of free radicals by its antioxidant nature, or to a strengthening of myocardial membrane by its membrane stabilizing property.

  10. Depression after myocardial infarction.

    PubMed

    Ziegelstein, R C

    2001-01-01

    Depression is an independent risk factor for increased postmyocardial infarction morbidity and mortality, even after controlling for the extent of coronary artery disease, infarct size, and the severity of left ventricular dysfunction. This risk factor takes on added significance when one considers that almost half of patients recovering from a myocardial infarction have major or minor depression and that major depression alone occurs in about one in five of these individuals. Despite the well-documented risk of depression, questions remain about the mechanism of the relationship between mood disturbance and adverse outcome. The link may be explained by an association with lower levels of social support, poor adherence to recommended medical therapy and lifestyle changes intended to reduce the risk of subsequent cardiac events, disturbances in autonomic tone, enhanced platelet activation and aggregation, and systemic immune activation. Unfortunately, questions about the pathophysiologic mechanism of depression in this setting are paralleled by uncertainties about the optimal treatment of depression for patients recovering from a myocardial infarction and by a lack of knowledge about whether treating depression lowers the associated increased mortality risk. Ongoing research studies will help to determine the benefits of psychosocial interventions and of antidepressant therapy for patients soon after myocardial infarction. Although the identification of depression as a risk factor may by itself be a reason to incorporate a comprehensive psychological evaluation into the routine care of patients with myocardial infarction, this practice should certainly become standard if studies show that treating depression reduces the increased mortality risk of these patients.

  11. Obesity does not Lead to Imbalance Between Myocardial Phospholamban Phosphorylation and Dephosphorylation

    PubMed Central

    Freire, Paula Paccielli; Alves, Carlos Augusto Barnabe; de Deus, Adriana Fernandes; Leopoldo, Ana Paula Lima; Leopoldo, André Soares; da Silva, Danielle Cristina Tomaz; de Tomasi, Loreta Casquel; Campos, Dijon Henrique Salomé; Cicogna, Antonio Carlos

    2014-01-01

    Background The activation of the beta-adrenergic system promotes G protein stimulation that, via cyclic adenosine monophosphate (cAMP), alters the structure of protein kinase A (PKA) and leads to phospholamban (PLB) phosphorylation. This protein participates in the system that controls intracellular calcium in muscle cells, and it is the primary regulator of sarcoplasmic reticulum calcium pump activity. In obesity, the beta-adrenergic system is activated by the influence of increased leptin, therefore, resulting in higher myocardial phospholamban phosphorylation via cAMP-PKA. Objective To investigate the involvement of proteins which regulate the degree of PLB phosphorylation due to beta-adrenergic activation in obesity. In the present study, we hypothesized that there is an imbalance between phospholamban phosphorylation and dephosphorylation, with prevalence of protein phosphorylation. Methods Male Wistar rats were randomly distributed into two groups: control (n = 14), fed with normocaloric diet; and obese (n = 13), fed with a cycle of four unsaturated high-fat diets. Obesity was determined by the adiposity index, and protein expressions of phosphatase 1 (PP-1), PKA, PLB, phosphorylated phospholamban at serine16 (PPLB-Ser16) were assessed by Western blot. Results Obesity caused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia and did not alter the protein expression of PKA, PP-1, PLB, PPLB-Ser16. Conclusion Obesity does not promote an imbalance between myocardial PLB phosphorylation and dephosphorylation via beta-adrenergic system. PMID:25120084

  12. Studies the alterations of biochemical and mineral contents in bone tissue of mus musculus due to aluminum toxicity and the protective action of desferrioxamine and deferiprone by FTIR, ICP-OES, SEM and XRD techniques

    NASA Astrophysics Data System (ADS)

    Sivakumar, S.; Khatiwada, Chandra Prasad; Sivasubramanian, J.

    The present study has attempt to analyze the changes in the biochemical and mineral contents of aluminum intoxicated bone and determine the protective action of desferrioxamine (DFO) and deferiprone (DFP) by using Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), inductively coupled plasma optical emission spectroscopy (ICP-OES), and scanning electron microscopy (SEM) techniques for four groups of animals such as control (Group I), aluminum intoxicated (Group II), Al + DFP (Group III) and Al + DFO + DFP (Group IV) treated groups respectively. The FTIR spectra of the aluminum intoxicated bone showed significant alteration in the biochemical constituents. The bands ratio at I1400/I877 significantly decreased from control to aluminum, but enhanced it by Al + DFP to Al + DFO + DFP treated bone tissue for treatments of 16 weeks. This result suggests that DFO and DFP are the carbonate inhibitor, recovered from chronic growth of bone diseases and pathologies. The alteration of proteins profile indicated by Amide I and Amide II, where peak area values decreased from control to aluminum respectively, but enhanced by treated with DFP (p.o.) and DFO + DFP (i.p.) respectively. The XRD analysis showed a decrease in crystallinity due to aluminum toxicity. Further, the Ca, Mg, and P contents of the aluminum exposed bone were less than those of the control group, and enhanced by treatments with DFO and DFP. The concentrations of trace elements were found by ICP-OES. Therefore, present study suggests that due to aluminum toxicity severe loss of bone minerals, decrease in the biochemical constituents and changes in the surface morphology.

  13. Bovine myocardial epithelial inclusions.

    PubMed

    Baker, D C; Schmidt, S P; Langheinrich, K A; Cannon, L; Smart, R A

    1993-01-01

    Light microscopic, histochemical, immunohistochemical, and ultrastructural methods were used to examine myocardial epithelial masses in the hearts of ten cattle. The tissues consisted of paraffin-embedded or formalin-fixed samples from eight hearts that were being inspected in slaughter houses and from two hearts from calves that died of septicemia. The ages of the cattle ranged from 4 days to 12 years; the breeds were unspecified for all but one Hereford female and the two Holstein calves; and there were three males, four females, and three steers. The masses in these cases were compared with similar appearing lesions found in other animal species. The lesions in the bovine hearts were single to multiple, well circumscribed, found in the left ventricle wall, and composed of squamous to cuboidal epithelial cells that formed tubular, ductular, and acinar structures with lumens that were void or filled with amorphous protein globules. Electron microscopic examination revealed epithelial cells that had sparse apical microvilli, tight apical intercellular junctions, perinuclear bundles of filaments, and rare cilia. Almost half of the bovine epithelial masses (4/9) had occasional diastase-resistant periodic acid-Schiff-positive granules in their cytoplasm, and few had hyaluronidase-resistant alcian blue-positive granules (2/9) or colloidal iron-positive granules (1/9). All myocardial masses had abundant collagen surrounding the tubular and acinar structures, and 2/9 had elastin fibers as well. None of the myocardial masses had Churukian-Schenk or Fontana Masson's silver staining granules in epithelial cells. Immunohistochemically, all bovine myocardial tumors stained positively for cytokeratin (8/8), and occasional masses stained positively for vimentin (3/8) or carcinoembryonic antigen (3/8). None of the masses stained positively for desmin. The myocardial epithelial tumors most likely represent endodermal rests of tissue misplaced during organogenesis.

  14. Perioperative Assessment of Myocardial Deformation

    PubMed Central

    Duncan, Andra E.; Alfirevic, Andrej; Sessler, Daniel I.; Popovic, Zoran B.; Thomas, James D.

    2014-01-01

    Evaluation of left ventricular performance improves risk assessment and guides anesthetic decisions. However, the most common echocardiographic measure of myocardial function, the left ventricular ejection fraction (LVEF), has important limitations. LVEF is limited by subjective interpretation which reduces accuracy and reproducibility, and LVEF assesses global function without characterizing regional myocardial abnormalities. An alternative objective echocardiographic measure of myocardial function is thus needed. Myocardial deformation analysis, which performs quantitative assessment of global and regional myocardial function, may be useful for perioperative care of surgical patients. Myocardial deformation analysis evaluates left ventricular mechanics by quantifying strain and strain rate. Strain describes percent change in myocardial length in the longitudinal (from base to apex) and circumferential (encircling the short-axis of the ventricle) direction and change in thickness in the radial direction. Segmental strain describes regional myocardial function. Strain is a negative number when the ventricle shortens longitudinally or circumferentially and is positive with radial thickening. Reference values for normal longitudinal strain from a recent meta-analysis using transthoracic echocardiography are (mean ± SD) −19.7 ± 0.4%, while radial and circumferential strain are 47.3 ± 1.9 and −23.3 ± 0.7%, respectively. The speed of myocardial deformation is also important and is characterized by strain rate. Longitudinal systolic strain rate in healthy subjects averages −1.10 ± 0.16 sec−1. Assessment of myocardial deformation requires consideration of both strain (change in deformation), which correlates with LVEF, and strain rate (speed of deformation), which correlates with rate of rise of left ventricular pressure (dP/dt). Myocardial deformation analysis also evaluates ventricular relaxation, twist, and untwist, providing new and noninvasive methods to

  15. Acute myocardial infarction and sudden death in Sioux Indians.

    PubMed Central

    Hrabovsky, S L; Welty, T K; Coulehan, J L

    1989-01-01

    While some Indian tribes have low rates of acute myocardial infarction, Northern Plains Indians, including the Sioux, have rates of morbidity and mortality from acute myocardial infarction higher than those reported for the United States population in general. In a review of diagnosed cases of acute myocardial infarction over a 3-year period in 2 hospitals serving predominantly Sioux Indians, 8% of cases were found misclassified, and 22% failed to meet rigorous diagnostic criteria, although the patients did indeed have ischemic heart disease. Patients had high frequencies of complications and risk factors and a fatality rate of 16% within a month of admission. Sudden deaths likely due to ischemic heart disease but in persons not diagnosed as having acute myocardial infarction by chart review occurred 3 times more frequently than deaths occurring within a month of clinical diagnosis. PMID:2735047

  16. The Influence of Diabetes Mellitus in Myocardial Ischemic Preconditioning

    PubMed Central

    Rezende, Paulo Cury; Rahmi, Rosa Maria

    2016-01-01

    Ischemic preconditioning (IP) is a powerful mechanism of protection discovered in the heart in which ischemia paradoxically protects the myocardium against other ischemic insults. Many factors such as diseases and medications may influence IP expression. Although diabetes poses higher cardiovascular risk, the physiopathology underlying this condition is uncertain. Moreover, although diabetes is believed to alter intracellular pathways related to myocardial protective mechanisms, it is still controversial whether diabetes may interfere with ischemic preconditioning and whether this might influence clinical outcomes. This review article looks at published reports with animal models and humans that tried to evaluate the possible influence of diabetes in myocardial ischemic preconditioning.

  17. The Influence of Diabetes Mellitus in Myocardial Ischemic Preconditioning

    PubMed Central

    Rezende, Paulo Cury; Rahmi, Rosa Maria

    2016-01-01

    Ischemic preconditioning (IP) is a powerful mechanism of protection discovered in the heart in which ischemia paradoxically protects the myocardium against other ischemic insults. Many factors such as diseases and medications may influence IP expression. Although diabetes poses higher cardiovascular risk, the physiopathology underlying this condition is uncertain. Moreover, although diabetes is believed to alter intracellular pathways related to myocardial protective mechanisms, it is still controversial whether diabetes may interfere with ischemic preconditioning and whether this might influence clinical outcomes. This review article looks at published reports with animal models and humans that tried to evaluate the possible influence of diabetes in myocardial ischemic preconditioning. PMID:27656659

  18. Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation

    PubMed Central

    Che, Xia; Wang, Xin; Zhang, Junyan; Peng, Chengfeng; Zhen, Yilan; Shao, Xu; Zhang, Gongliang; Dong, Liuyi

    2016-01-01

    Purpose: The aim of this study was to explore the cardioprotective effect of vitexin on chronic myocardial ischemia/reperfusion injury in rats and potential mechanisms. Methods: A chronic myocardial ischemia/reperfusion injury model was established by ligating left anterior descending coronary for 60 minutes, and followed by reperfusion for 14 days. After 2 weeks ischemia/reperfusion, cardiac function was measured to assess myocardial injury. The level of ST segment was recorded in different periods by electrocardiograph. The change of left ventricular function and myocardial reaction degree of fibrosis of heart was investigated by hematoxylin and eosin (HE) staining and Sirius red staining. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. The blood samples were collected to measure the levels of MDA, the activities of SOD and NADPH in serum. Epac1, Rap1, Bax and Bcl-2 were examined by using Western Blotting. Results: Vitexin exerted significant protective effect on chronic myocardial ischemia/reperfusion injury, improved obviously left ventricular diastolic function and reduced myocardial reactive fibrosis degree in rats of myocardial ischemia. Medium and high-dose vitexin groups presented a significant decrease in Bax, Epac1 and Rap1 production and increase in Bcl-2 compared to the I/R group. It may be related to preventing myocardial cells from apoptosis, improving myocardial diastolic function and inhibiting lipid peroxidation. Conclusions: Vitexin is a cardioprotective herb, which may be a promising useful complementary and alternative medicine for patients with coronary heart disease. PMID:27648122

  19. Myocardial apoptosis and SIDS.

    PubMed

    Grasmeyer, Sarah; Madea, Burkhard

    2015-01-01

    Apoptosis mediates cardiac damage in severe forms of myocarditis. In fatal myocarditis, large amounts of cardiomyocytes show apoptotic DNA fragmentation, while in human controls, few apoptotic cardiomyocytes are found. In the present study the frequency of apoptosis in 88 SIDS cases (category 1b according to the San Diego Classification) and 15 control cases was investigated. In every case myocardial samples from 8 standard locations were collected. Detection of apoptotic cardiomyocytes was performed by TUNEL method. Furthermore the myocardial tissue was stained with HE and immunohistochemical methods (LCA, CD68, CD45-R0). More than 90% of the slides did not contain apoptotic cardiomyocytes at all. The detection rate of apoptotic cardiomyocytes was almost equal in control group (26.7%) and SIDS group (23.86%). A quantification of apoptotic cardiomyocytes per mm(2) revealed no significant difference between both groups either. Altogether there is no evidence for a higher rate of apoptosis in SIDS.

  20. Myocardial gene therapy

    NASA Astrophysics Data System (ADS)

    Isner, Jeffrey M.

    2002-01-01

    Gene therapy is proving likely to be a viable alternative to conventional therapies in coronary artery disease and heart failure. Phase 1 clinical trials indicate high levels of safety and clinical benefits with gene therapy using angiogenic growth factors in myocardial ischaemia. Although gene therapy for heart failure is still at the pre-clinical stage, experimental data indicate that therapeutic angiogenesis using short-term gene expression may elicit functional improvement in affected individuals.

  1. Matrix metalloproteinases: drug targets for myocardial infarction

    PubMed Central

    Yabluchanskiy, Andriy; Li, Yaojun; Chilton, Robert J.; Lindsey, Merry L.

    2013-01-01

    Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide. Rapid advances in the treatment of acute MI have significantly improved short-term outcomes in patient, due in large part to successes in preventing myocardial cell death and limiting infarct area during the time of ischemia and subsequent reperfusion. Matrix metalloproteases (MMPs) play key roles in post-MI cardiac remodeling and in the development of adverse outcomes. This review highlights the importance of MMPs in the injury and remodeling response of the left ventricle and also discusses their potential as therapeutic targets Additional pre-clinical and clinical research is needed to further investigate and understand the cardioprotective effects of MMPs inhibitors. PMID:23316962

  2. Perioperative myocardial infarction in patients undergoing myocardial revascularization surgery

    PubMed Central

    Pretto, Pericles; Martins, Gerez Fernandes; Biscaro, Andressa; Kruczan, Dany David; Jessen, Barbara

    2015-01-01

    Introduction Perioperative myocardial infarction adversely affects the prognosis of patients undergoing coronary artery bypass graft and its diagnosis was hampered by numerous difficulties, because the pathophysiology is different from the traditional instability atherosclerotic and the clinical difficulty to be characterized. Objective To identify the frequency of perioperative myocardial infarction and its outcome in patients undergoing coronary artery bypass graft. Methods Retrospective cohort study performed in a tertiary hospital specialized in cardiology, from May 01, 2011 to April 30, 2012, which included all records containing coronary artery bypass graft records. To confirm the diagnosis of perioperative myocardial infarction criteria, the Third Universal Definition of Myocardial Infarction was used. Results We analyzed 116 cases. Perioperative myocardial infarction was diagnosed in 28 patients (24.1%). Number of grafts and use and cardiopulmonary bypass time were associated with this diagnosis and the mean age was significantly higher in this group. The diagnostic criteria elevated troponin I, which was positive in 99.1% of cases regardless of diagnosis of perioperative myocardial infarction. No significant difference was found between length of hospital stay and intensive care unit in patients with and without this complication, however patients with perioperative myocardial infarction progressed with worse left ventricular function and more death cases. Conclusion The frequency of perioperative myocardial infarction found in this study was considered high and as a consequence the same observed average higher troponin I, more cases of worsening left ventricular function and death. PMID:25859867

  3. Cardioprotection against experimental myocardial ischemic injury using cornin

    PubMed Central

    Xu, Y.; Xu, Y.; Luan, H.; Jiang, Y.; Tian, X.; Zhang, S.

    2016-01-01

    Phosphorylated-cyclic adenosine monophosphate response element-binding protein (Phospho-CREB) has an important role in the pathogenesis of myocardial ischemia. We isolated the iridoid glycoside cornin from the fruit of Verbena officinalis L, investigated its effects against myocardial ischemia and reperfusion (I/R) injury in vivo, and elucidated its potential mechanism in vitro. Effects of cornin on cell viability, as well as expression of phospho-CREB and phospho-Akt in hypoxic H9c2 cells in vitro, and myocardial I/R injury in vivo, were investigated. Cornin attenuated hypoxia-induced cytotoxicity significantly in H9c2 cells in a concentration-dependent manner. Treatment of H9c2 cells with cornin (10 µM) blocked the reduction of expression of phospho-CREB and phospho-Akt in a hypoxic condition. Treatment of rats with cornin (30 mg/kg, iv) protected them from myocardial I/R injury as indicated by a decrease in infarct volume, improvement in hemodynamics, and reduction of severity of myocardial damage. Cornin treatment also attenuated the reduction of expression of phospho-CREB and phospho-Akt in ischemic myocardial tissue. These data suggest that cornin exerts protective effects due to an increase in expression of phospho-CREB and phospho-Akt. PMID:26871971

  4. Cardioprotection against experimental myocardial ischemic injury using cornin.

    PubMed

    Xu, Y; Xu, Y; Luan, H; Jiang, Y; Tian, X; Zhang, S

    2016-02-01

    Phosphorylated-cyclic adenosine monophosphate response element-binding protein (Phospho-CREB) has an important role in the pathogenesis of myocardial ischemia. We isolated the iridoid glycoside cornin from the fruit of Verbena officinalis L, investigated its effects against myocardial ischemia and reperfusion (I/R) injury in vivo, and elucidated its potential mechanism in vitro. Effects of cornin on cell viability, as well as expression of phospho-CREB and phospho-Akt in hypoxic H9c2 cells in vitro, and myocardial I/R injury in vivo, were investigated. Cornin attenuated hypoxia-induced cytotoxicity significantly in H9c2 cells in a concentration-dependent manner. Treatment of H9c2 cells with cornin (10 µM) blocked the reduction of expression of phospho-CREB and phospho-Akt in a hypoxic condition. Treatment of rats with cornin (30 mg/kg, iv) protected them from myocardial I/R injury as indicated by a decrease in infarct volume, improvement in hemodynamics, and reduction of severity of myocardial damage. Cornin treatment also attenuated the reduction of expression of phospho-CREB and phospho-Akt in ischemic myocardial tissue. These data suggest that cornin exerts protective effects due to an increase in expression of phospho-CREB and phospho-Akt.

  5. Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction

    PubMed Central

    Hall, A R; Burke, N; Dongworth, R K; Kalkhoran, S B; Dyson, A; Vicencio, J M; Dorn II, G W; Yellon, D M; Hausenloy, D J

    2016-01-01

    Mitochondria alter their shape by undergoing cycles of fusion and fission. Changes in mitochondrial morphology impact on the cellular response to stress, and their interactions with other organelles such as the sarcoplasmic reticulum (SR). Inhibiting mitochondrial fission can protect the heart against acute ischemia/reperfusion (I/R) injury. However, the role of the mitochondrial fusion proteins, Mfn1 and Mfn2, in the response of the adult heart to acute I/R injury is not clear, and is investigated in this study. To determine the effect of combined Mfn1/Mfn2 ablation on the susceptibility to acute myocardial I/R injury, cardiac-specific ablation of both Mfn1 and Mfn2 (DKO) was initiated in mice aged 4–6 weeks, leading to knockout of both these proteins in 8–10-week-old animals. This resulted in fragmented mitochondria (electron microscopy), decreased mitochondrial respiratory function (respirometry), and impaired myocardial contractile function (echocardiography). In DKO mice subjected to in vivo regional myocardial ischemia (30 min) followed by 24 h reperfusion, myocardial infarct size (IS, expressed as a % of the area-at-risk) was reduced by 46% compared with wild-type (WT) hearts. In addition, mitochondria from DKO animals had decreased MPTP opening susceptibility (assessed by Ca2+-induced mitochondrial swelling), compared with WT hearts. Mfn2 is a key mediator of mitochondrial/SR tethering, and accordingly, the loss of Mfn2 in DKO hearts reduced the number of interactions measured between these organelles (quantified by proximal ligation assay), attenuated mitochondrial calcium overload (Rhod2 confocal microscopy), and decreased reactive oxygen species production (DCF confocal microscopy) in response to acute I/R injury. No differences in isolated mitochondrial ROS emissions (Amplex Red) were detected in response to Ca2+ and Antimycin A, further implicating disruption of mitochondria/SR tethering as the protective mechanism. In summary, despite apparent

  6. Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction.

    PubMed

    Hall, A R; Burke, N; Dongworth, R K; Kalkhoran, S B; Dyson, A; Vicencio, J M; Dorn Ii, G W; Yellon, D M; Hausenloy, D J

    2016-01-01

    Mitochondria alter their shape by undergoing cycles of fusion and fission. Changes in mitochondrial morphology impact on the cellular response to stress, and their interactions with other organelles such as the sarcoplasmic reticulum (SR). Inhibiting mitochondrial fission can protect the heart against acute ischemia/reperfusion (I/R) injury. However, the role of the mitochondrial fusion proteins, Mfn1 and Mfn2, in the response of the adult heart to acute I/R injury is not clear, and is investigated in this study. To determine the effect of combined Mfn1/Mfn2 ablation on the susceptibility to acute myocardial I/R injury, cardiac-specific ablation of both Mfn1 and Mfn2 (DKO) was initiated in mice aged 4-6 weeks, leading to knockout of both these proteins in 8-10-week-old animals. This resulted in fragmented mitochondria (electron microscopy), decreased mitochondrial respiratory function (respirometry), and impaired myocardial contractile function (echocardiography). In DKO mice subjected to in vivo regional myocardial ischemia (30 min) followed by 24 h reperfusion, myocardial infarct size (IS, expressed as a % of the area-at-risk) was reduced by 46% compared with wild-type (WT) hearts. In addition, mitochondria from DKO animals had decreased MPTP opening susceptibility (assessed by Ca(2+)-induced mitochondrial swelling), compared with WT hearts. Mfn2 is a key mediator of mitochondrial/SR tethering, and accordingly, the loss of Mfn2 in DKO hearts reduced the number of interactions measured between these organelles (quantified by proximal ligation assay), attenuated mitochondrial calcium overload (Rhod2 confocal microscopy), and decreased reactive oxygen species production (DCF confocal microscopy) in response to acute I/R injury. No differences in isolated mitochondrial ROS emissions (Amplex Red) were detected in response to Ca(2+) and Antimycin A, further implicating disruption of mitochondria/SR tethering as the protective mechanism. In summary, despite apparent

  7. Noninvasive estimation of regional myocardial oxygen consumption by positron emission tomography with carbon-11 acetate in patients with myocardial infarction

    SciTech Connect

    Walsh, M.N.; Geltman, E.M.; Brown, M.A.; Henes, C.G.; Weinheimer, C.J.; Sobel, B.E.; Bergmann, S.R. )

    1989-11-01

    We previously demonstrated in experimental studies that myocardial oxygen consumption (MVO2) can be estimated noninvasively with positron emission tomography (PET) from analysis of the myocardial turnover rate constant (k) after administration of carbon-11 (11C) acetate. To determine regional k in healthy human subjects and to estimate alterations in MVO2 accompanying myocardial ischemia, we administered (11C)acetate to five healthy human volunteers and to six patients with myocardial infarction. Extraction of (11C)acetate by the myocardium was avid and clearance from the blood-pool rapid yielding myocardial images of excellent quality. Regional k was homogeneous in myocardium of healthy volunteers (coefficient variation = 11%). In patients, k in regions remote from the area of infarction was not different from values in myocardium of healthy human volunteers (0.061 +/- 0.025 compared with 0.057 +/- 0.008 min-1). In contrast, MVO2 in the center of the infarct region was only 6% of that in remote regions (p less than 0.01). In four patients studied within 48 hr of infarction and again more than seven days after the acute event, regional k and MVO2 did not change. The approach developed should facilitate evaluation of the efficacy of interventions designed to enhance recovery of jeopardized myocardium and permit estimation of regional MVO2 and metabolic reserve underlying cardiac disease of diverse etiologies.

  8. Primary ST changes. Diagnostic aid in paced patients with acute myocardial infarction.

    PubMed Central

    Niremberg, V; Amikam, S; Roguin, N; Pelled, B; Riss, E

    1977-01-01

    In 34 out of 36 patients with apical right ventricular endocardial pacing, primary ischaemic ST alterations were observed during the early stage of acute myocardial infarction. These ST changes, indicating acute injury, were detected in the paced beats in inferior and in anterior infarct. The primary ST changes were consistent only during the early stages of acute myocardial infarction and were not detected when the electrode tip was not in the apex of the right ventricle. It is suggested that the primary ST changes should be used to diagnose acute myocardial infarction in paced patients. Images PMID:861092

  9. Using biomaterials to improve the efficacy of cell therapy following acute myocardial infarction.

    PubMed

    Traverse, Jay H

    2012-02-01

    Cardiovascular cell therapy has the potential to improve left ventricular (LV) function and alter the course of adverse LV remodeling following acute myocardial infarction (AMI). However, current therapy using autologous intracoronary bone marrow mononuclear cells results in only minimal recovery of LV function. A major impediment appears to be limited retention and engraftment of the transplanted cells, in part due to loss of the extracellular matrix (ECM) following AMI that can lead to apoptosis of the delivered cells through the mechanism of anoikis. Recent pre-clinical studies suggest that the delivery of ECM surrogates to the infarct zone following AMI significantly improves LV function through multiple mechanisms. The use of ECM surrogates in conjunction with stem cell administration may represent a new paradigm for cardiac repair following AMI. This review discusses the potential use of biologically based ECM surrogates in the clinical setting following STEMI.

  10. Impact of high-fat, low-carbohydrate diet on myocardial substrate oxidation, insulin sensitivity, and cardiac function after ischemia-reperfusion.

    PubMed

    Liu, Jian; Wang, Peipei; Douglas, Samuel L; Tate, Joshua M; Sham, Simon; Lloyd, Steven G

    2016-07-01

    High-fat, low-carbohydrate Diet (HFLCD) impairs the myocardial response to ischemia-reperfusion, but the underlying mechanisms remain elusive. We sought to determine the magnitude of diet-induced alterations in intrinsic properties of the myocardium (including insulin sensitivity and substrate oxidation) and circulating substrate and insulin differences resulting from diet, leading to this impaired response. Rats were fed HFLCD (60% kcal from fat/30% protein/10% carbohydrate) or control diet (CONT) (16%/19%/65%) for 2 wk. Isolated hearts underwent global low-flow ischemia followed by reperfusion (I/R). Carbon-13 NMR spectroscopy was used to determine myocardial substrate TCA cycle entry. Myocardial insulin sensitivity was assessed as dose-response of Akt phosphorylation. There was a significant effect of HFLCD and I/R with both these factors leading to an increase in free fatty acid (FFA) oxidation and a decrease in carbohydrate or ketone oxidation. Following I/R, HFLCD led to decreased ketone and increased FFA oxidation; the recovery of left ventricular (LV) function was decreased in HFLCD and was negatively correlated with FFA oxidation and positively associated with ketone oxidation. HFLCD also resulted in reduced insulin sensitivity. Under physiologic ranges, there were no direct effects of buffer insulin and ketone levels on oxidation of any substrate and recovery of cardiac function after I/R. An insulin-ketone interaction exists for myocardial substrate oxidation characteristics. We conclude that the impaired recovery of function after ischemia-reperfusion with HFLCD is largely due to intrinsic diet effects on myocardial properties, rather than to diet effect on circulating insulin or substrate levels.

  11. Carbon monoxide pollution impairs myocardial perfusion reserve: implication of coronary endothelial dysfunction.

    PubMed

    Meyer, G; Boissiere, J; Tanguy, S; Rugale, C; Gayrard, S; Jover, B; Obert, P; Reboul, C

    2011-12-01

    Chronic exposure to simulated urban CO pollution is reported to be associated with cardiac dysfunction. Despite the potential implication of myocardial perfusion alteration in the pathophysiology of CO pollution, the underlying mechanisms remain today still unknown. Therefore, the aim of this work was to evaluate the effects of prolonged exposure to simulated urban CO pollution on the regulation of myocardial perfusion. Cardiac hemodynamics and myocardial perfusion were assessed under basal conditions and during the infusion of a β-Adrenergic agonist. The effects of CO exposure on capillary density, coronary endothelium-dependent vasodilatation, eNOS expression and eNOS uncoupling were also evaluated. Our main results were that prolonged CO exposure was associated with a blunted myocardial perfusion response to a physiological stress responsible for an altered contractile reserve. The impairment of myocardial perfusion reserve was not accounted for a reduced capillary density but rather by an alteration in coronary endothelium-dependent vasorelaxation (-45% of maximal relaxation to ACh). In addition, though chronic CO exposure did not change eNOS expression, it significantly increased eNOS uncoupling. Therefore, the present work underlines the fact that chronic CO exposure, at levels found in urban air pollution, is associated with reduced myocardial perfusion reserve. This phenomenon is explained at the coronary-vessel level by deleterious effects of CO exposure on the endothelium NO-dependent vasorelaxation via eNOS uncoupling.

  12. Myocardial fibre calcification.

    PubMed Central

    McClure, J; Pieterse, A S; Pounder, D J; Smith, P S

    1981-01-01

    Three cases of myocardial fibre calcification found at post-mortem examination are described. In one case there was antemortem hypercalcaemia and hyperphosphataemia and the case was clearly an example of metastatic calcification. In the other two cases there was ischaemic myocardial necrosis and calcification was seen in fibres which were not overtly necrotic, but which were both in proximity to (the majority) and remote from the necrotic zones. Since renal failure with hyperphosphataemia was present in both cases, these were considered to be examples of augmented (by the hyperphosphataemia) dystrophic calcification. The histological, histochemical and ultrastructural features were identical in the three cases. Hydroxyapatite formation was observed initially in mitochondria, followed by spillage of crystals into the cytosol and ultimately into the interstitium. It is suggested that the fundamental lesion is a dysfunction of the fibre membrane; the similarity of this reaction with the calcification seen in skeletal muscle fibres in various myopathies is noted and a unifying hypothesis of the mechanism of skeletal and cardiac muscle fibre calcification is thereby suggested. Images PMID:7309897

  13. Valsartan after myocardial infarction.

    PubMed

    Güleç, Sadi

    2014-12-01

    One of the important problems of the patients undergoing acute myocardial infarction (MI) is early development of heart failure. It has been revealed in various studies that renin-angiotensin-aldosterone system (RAAS) has a significant role in this process. The studies conducted with angiotensin converting enzyme (ACE) inhibitors have resulted in decreased mortality rate. Another RAAS blocker which was discovered about ten years later than other ACE inhibitors in historical process is angiotensin receptor blockers (ARB) inhibiting the efficiency of angiotensin 2 by binding to angiotensin 1 receptor. Valsartan is one of the molecules of this group, which has higher number of large-scale randomized clinical studies. In this review, following presentation of a general overview on heart failure after acute MI, the efficiency of ARBs in this patient group will be discussed. This discussion will mostly emphasize the construction, outcomes and clinical importance of VALIANT (VALsartan In Acute myocardial iNfarcTion), which is the study on valsartan after acute MI heart failure. PMID:25604205

  14. Trauma induced myocardial infarction.

    PubMed

    Lolay, Georges A; Abdel-Latif, Ahmed K

    2016-01-15

    Chest Trauma in athletes is a common health problem. However, myocardial infarction secondary to coronary dissection in the setting of blunt chest trauma is extremely rare. We report a case of acute inferior wall myocardial infarction following blunt chest trauma. A 32-year-old male with no relevant medical problems was transferred to our medical center for retrosternal chest pain after being elbowed in the chest during a soccer game. Few seconds later, he started experiencing sharp retrosternal chest pain that was severe to that point where he called the emergency medical service. Upon arrival to the trauma department patient was still complaining of chest pain. ECG demonstrated ST segment elevation in the inferior leads with reciprocal changes in the lateral leads all consistent with active ischemia. After rolling out aortic dissection, patient was loaded with ASA, ticagerlor, heparin and was emergently taken to the cardiac catheterization lab. Coronary angiography demonstrated 100% thrombotic occlusion in the distal right coronary artery with TIMI 0 flow distally. After thrombus aspiration, a focal dissection was noted on the angiogram that was successfully stented. Two days after admission patient was discharged home. Echocardiography prior to discharge showed inferior wall akinesis, normal right ventricular systolic function and normal overall ejection fraction.

  15. Mass spectrometry for the measurement of intramyocardial gas tensions: methodology and application to the study of myocardial ischemia.

    PubMed

    Khuri, S F; O'Riordan, J; Flaherty, J T; Brawley, R K; Donahoo, J S; Gott, V L

    1975-01-01

    The methodology for use of the mass spectrometer for the measurement of intramyocardial gas tensions in the canine preparation is described. Baseling studies were carried out initially in 36 animals, and control levels for myocardial oxygen tension and myocardial carbon dioxide tension were 19 mm Hg (S.D. 6 mm Hg) and 43 mm Hg (S.D. 10 mm Hg), respectively. Myocardial oxygen tension was not altered significantly by varying the arterial oxygen tension between 65 and 300 mm Hg. However, myocardial carbon dioxide tension increased linearly with increased arterial carbon dioxide tension. In 15 dogs placed on total cardiopulmonary bypass, a perfusion pressure 40-60 mm lower than the control mean arterial pressure resulted in myocardial ischemia with a decrease in myocardial oxygen tension and an increase in myocardial carbon dioxide tension. A subsequent increase in perfusion pressure to control levels resulted in resolution of ischemia and return of myocardial oxygen and carbon dioxide tensions to their control level. In another series of open-chest dogs on cardiopulmonary bypass, a proximal constriction applied to the left coronary circumflex artery resulted in a marked decrease in myocardial oxygen tensions and a marked increase in myocardial carbon dioxide tensions in the region supplied by the constricted vessel. In yet another series of open-chest dogs, it was found that incremental decreases in coronary flow established by constriction of the circumflex artery resulted in an exponential increase in both myocardial carbon dioxide tensions and ST-segment elevation as determined by a 25-gauge multi-contact plunge electrode placed in the posterior left ventricular wall. It appears that mass spectrometry techniques for evaluating myocardial ischemia have several advantages over myocardial biopsy techniques for assay of ATP and lactate, and also over the technique of coronary sinus lactate determination. PMID:1209001

  16. Computational Modeling of the Effects of Myocardial Infarction on Left Ventricular Hemodynamics

    NASA Astrophysics Data System (ADS)

    Vedula, Vijay; Seo, Jung Hee; Mittal, Rajat; Fortini, Stefania; Querzoli, Giorgio

    2012-11-01

    Most in-vivo and modeling studies on myocardial infarction and ischemia have been directed towards understanding the left ventricular wall mechanics including stress-strain behavior, end systolic pressure-volume correlations, ejection fraction and stroke work. Fewer studies have focused on the alterations in the intraventricular blood flow behavior due to local infarctions. Changes in the motion of the endocardium can cause local circulation and stagnation regions; these increase the blood cell residence time in the left ventricle and may eventually be implicated in thrombus formation. In the present study, we investigate the effects of myocardial infarction on the ventricular hemodynamics in simple models of the left ventricle using an immersed-boundary flow solver. Apart from the Eulerian flow features such as vorticity and velocity flow fields, pressure distribution, shear stress, viscous dissipation and pump work, we also examine the Lagrangian dynamics of the flow to gain insights into the effect of flow dynamics on thrombus formation. The study is preceded by a comprehensive validation study which is based on an in-vitro experimental model of the left ventricle and this study is also described. This research is supported by the U.S. National Science Foundation through (NSF) CDI-Type II grant IOS-1124804. Computational resources for some of the simulations were also provided in part through the NSF grant NSF-OCI-108849.

  17. ECG phenomena: pseudopreexcitation and repolarization disturbances resembling ST-elevation myocardial infarction caused by an intraatrial rhabdomyoma in a newborn.

    PubMed

    Paech, Christian; Gebauer, Roman Antonin

    2014-01-01

    As is known from other reports, a rhabdomyoma or tumor metastasis may alter intracardiac electrical conduction, producing electrical phenomena like pseudopreexcitation or repolarization disturbances resembling ST-elevation myocardial infarction or Brugada's syndrome. We present a newborn with a giant atrial rhabdomyoma and additionally multiple ventricular rhabdomyomas. He presented with several electrocardiogram (ECG) phenomena due to tumor-caused atrial depolarization and repolarization disturbances. Except from the cardiac tumors, the physical status was within normal range. Initial ECG showed a rapid atrial tachycardia with a ventricular rate of 230 bpm, which was terminated by electrical cardioversion. Afterwards, the ECG showed atrial rhythm with frequent atrial premature contractions and deformation of the PR interval with large, broad P waves and loss of discret PR segment, imposing as pseudopreexcitation. The following QRS complex was normal, with seemingly abnormal ventricular repolarization resembeling ST-elevation myocardial infarction. The atrial tumor was resected with consequent vast atrial reconstruction using patch plastic. The ventricular tumors were left without manipulation. After surgery, pseudopreexcitation and repolarization abnormalities vanished entirely and an alternans between sinus rhythm and ectopic atrial rhythm was present. These phenomena were supposably caused by isolated atrial depolarization disturbances due to tumor-caused heterogenous endocardial activation. The seemingly abnormal ventricular repolarization is probably due to repolarization of the atrial mass, superimposed on the ventricular repolarization. Recognizably, the QRS complex before and after surgical resection of the rhabdomyoma is identical, underlining the atrial origin of the repolarization abnormalities before surgery.

  18. 2015 Sensorimotor Risk Standing Review Panel Evidence and Status Review For: the Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Spaceflight

    NASA Technical Reports Server (NTRS)

    Steinberg, Susan

    2015-01-01

    The 2015 Sensorimotor Risk Standing Review Panel (from here on referred to as the SRP) participated in a WebEx/teleconference with members of the Human Health Countermeasures (HHC) Element, representatives from the Human Research Program (HRP), NASA Headquarters, and NASA Research and Education Support Services (NRESS) on December 17, 2015 (list of participants is in Section VI of this report). The SRP reviewed the new Evidence Report for the Risk of Impaired Control of Spacecraft/Associated Systems and Decreased Mobility Due to Vestibular/Sensorimotor Alterations Associated with Spaceflight (from here on referred to as the 2015 Sensorimotor Evidence Report), and also received a status review of the Risk. The opening section of the 2015 Sensorimotor Evidence Report provides written descriptions of various incidents that have occurred during space missions. In most of these incidents, the main underlying contributing factors are not easy to identify unambiguously. For example, in section 1.9, a number of falls occurred while astronauts were walking on the moon. It is not clear to the SRP, however, why they fell. It is only possible to extrapolate from likely specific psychophysical or physiological abnormalities, but how these abnormalities were determined, and how they were directly responsible for the falls is unclear to the SRP. Section 2.1.2 on proprioception is very interesting, but the functional significance of the abnormalities detected is not clear. The SRP sees this as a problem throughout the report: a mapping between the component abnormalities identified and the holistic behaviors that are most relevant, for example, controlling the vehicle, and locomotion during egress, is generally lacking. The SRP thinks the cognitive section is too strongly focused on vestibular functioning. The SRP questions the notion that the main cognitive effects are mainly attributable to reversible vestibular changes induced by spaceflight. The SRP thinks that there can also

  19. Acute myocardial infarction complicating subarachnoid haemorrhage

    PubMed Central

    van der Velden, L.B.J.; Otterspoor, L.C.; Schultze Kool, L.J.; Biessels, G.J.; Verheugt, F.W.A.

    2009-01-01

    An acute myocardial infarction is a rare complication of a subarachnoid haemorrhage. The combination of these two conditions imposes important treatment dilemmas. We describe two patients with this combination of life-threatening conditions. Patient 1 was treated with emergency percutaneous coronary intervention followed by clipping of the anterior communicating artery aneurysm. Six months after discharge the patient's memory and orientation had almost completely recovered. Patient 2 was treated with aspirin until coiling of the aneurysm could be performed. After successful coiling low-molecular-weight heparin was added. One week later the patient died due to a free wall rupture. (Neth Heart J 2009;17:284-7.19789696) PMID:19789696

  20. Myocardial perfusion as assessed by thallium-201 scintigraphy during the discontinuation of mechanical ventilation in ventilator-dependent patients

    SciTech Connect

    Hurford, W.E.; Lynch, K.E.; Strauss, H.W.; Lowenstein, E.; Zapol, W.M. )

    1991-06-01

    Patients who cannot be separated from mechanical ventilation (MV) after an episode of acute respiratory failure often have coexisting coronary artery disease. The authors hypothesized that increased left ventricular (LV) wall stress during periods of spontaneous ventilation (SV) could alter myocardial perfusion in these patients. Using thallium-201 (201TI) myocardial scintigraphy, the authors studied the occurrence of myocardial perfusion abnormalities during periods of SV in 15 MV-dependent patients (nine women, six men; aged 71 {plus minus} 7 yr, mean {plus minus} SD). Fourteen of these patients were studied once with 201TI myocardial scintigraphy during intermittent mechanical ventilation (IMV) and again on another day, after at least 10 min of SV through a T-piece. One patient was studied during SV only. Thirteen of 14 of the patients (93%) studied during MV had abnormal patterns of initial myocardial 201TI uptake, but only 1 patient demonstrated redistribution of 201TI on delayed images. The remainder of the abnormalities observed during MV were fixed defects. SV produced significant alterations of myocardial 201TI distribution or transient LV dilation, or both, in 7 of the 15 patients (47%). Four patients demonstrated new regional decreases of LV myocardial thallium concentration with redistribution of the isotope on delayed images. The patient studied only during SV also had myocardial 201TI defects with redistribution. Five patients (3 also having areas of 201TI redistribution) had transient LV dilation during SV.

  1. Acute myocardial infarction and myocardial ischemia-reperfusion injury: a comparison.

    PubMed

    Hashmi, Satwat; Al-Salam, Suhail

    2015-01-01

    Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia. Myocardial reperfusion is the restoration of coronary blood flow after a period of coronary occlusion. Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). Standard histologic, immunohistochemical and Elisa techniques were used to study the histopathologic, oxidative, apoptotic and inflammatory changes in MI and IR. The IL-6 levels in the LV of the MI group were significantly raised as compared to the IR group (P=0.0008). Plasma IL-6 was also significantly increased in the MI group as compared to the IR group (P=0.031). MI model was also associated with increase in the neutrophil polymorphs number in the infarction related myocardium as compared to the re-perfused myocardium. A significant increase in troponin I level in the MI group as compared to the IR group is also seen (P=0.0001). Our IR model showed enhanced pro-apoptotic mediators like cleaved caspase-3 (P=0.005) and cytochrome c in the myocardium as compared to the MI model. In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis.

  2. Acute myocardial infarction in young adults: causes and management

    PubMed Central

    Osula, S; Bell, G; Hornung, R

    2002-01-01

    The case report in this review illustrates an acute myocardial infarction in a young adult probably due to arterial thrombosis that can be attributed to a hypercoagulable state resulting from the nephrotic syndrome. Although rare, acute myocardial infarction should be considered in young adults presenting with chest pain. A detailed clinical history may help to identify the aetiology, and guide subsequent management, but diagnostic coronary angiography is essential. Careful risk factor modification and treatment of the underlying cause should reduce the incidence of recurrent cardiac events. PMID:11796868

  3. [Painless anterior acute myocardial infarction in a transplanted heart].

    PubMed

    Poyet, R; Capilla, E; Tortat, A V; Brocq, F X; Pons, F; Kerebel, S; Jego, C; Cellarier, G R

    2015-11-01

    Cardiac allograft vasculopathy is the major determinant of long-term survival in patients after heart transplantation. Clinical presentations are congestive heart failure, ventricular arrhythmias and sudden cardiac death. Acute coronary syndrome is a rare presentation of cardiac allograft vasculopathy due to myocardial denervation. We present the case of a 31-year-old patient, who had undergone heart transplantation 6 months earlier and who developed a painless anterior myocardial infarction revealed by syncope. He was successfully treated by percutaneous coronary intervention with drug eluting stent implantation. PMID:26472502

  4. Nitroglycerin Use in Myocardial Infarction Patients: Risks and Benefits

    PubMed Central

    Ferreira, Julio C.B.; Mochly-Rosen, Daria

    2012-01-01

    Acute myocardial infarction and its sequelae are leading causes of morbidity and mortality worldwide. Nitroglycerin remains a first-line treatment for angina pectoris and acute myocardial infarction. Nitroglycerin achieves its benefit by giving rise to nitric oxide, which causes vasodilation and increases blood flow to the myocardium. However, continuous delivery of nitroglycerin results in tolerance, limiting the use of this drug. Nitroglycerin tolerance is due, at least in part, to inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts nitroglycerin to the vasodilator, nitric oxide. We have recently found that, in addition to nitroglycerin’s effect on the vasculature, sustained treatment with nitroglycerin negatively affects cardiomyocyte viability following ischemia, thus resulting in increased infarct size in a myocardial infarction model in animals. Co-administration of Alda-1, an activator of ALDH2, with nitroglycerin improves metabolism of reactive aldehyde adducts and prevents the nitroglycerin-induced increase in cardiac dysfunction following myocardial infarction. In this review, we describe the molecular mechanisms associated with the benefits and risks of nitroglycerin administration in myocardial infarction. (167 of 200). PMID:22040938

  5. Stem cell therapy after myocardial infarction: ready for clinical application?

    PubMed

    Engelmann, Markus G; Franz, Wolfgang M

    2006-10-01

    The discovery of stem cells capable of generating angiogenic or contractile cells and structures might offer new treatment options for patients suffering from heart disease. In particular, embryonic stem cells are considered to have great potential for regenerative medicine and tissue engineering. Studies suggest that delivery or mobilization of stem and progenitor cells might improve tissue perfusion and contractile performance of the damaged heart; however, the underlying mechanisms are poorly understood. Fusion or trans-differentiation into cardiomyocytes or vascular cells are considered rare events of cellular engraftment, and adult stem cells are now considered as 'regenerator cells', acting via paracrine effects of cytokines, or by activation of resident stent cells, thereby supporting the myocardial healing mechanisms after injury. Administration of autologous hematopoietic stem cells or mobilization of endogenous stem cells has been shown to be safe after myocardial infarction or cardiomyopathies, whereas skeletal myoblasts are considered to be hazardous due to the occurrence of life-threatening arrhythmias. This review focuses on the use of adult human stem cells for treating myocardial infarction and cardiomyopathy, and discusses recent preliminary efficacy data, which suggest that 'regenerator cells' might have the potential to improve myocardial perfusion and contractile performance in patients suffering from myocardial infarction, severe ischemic heart disease and chronic heart failure. PMID:17078382

  6. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction

    PubMed Central

    Hritani, Abdulwahab; Antoun, Patrick

    2016-01-01

    Weight loss is one of the most researched and marketed topics in American society. Dietary regimens, medications that claim to boost the metabolism, and the constant pressure to fit into society all play a role in our patient's choices regarding new dietary products. One of the products that are well known to suppress appetite and cause weight loss is amphetamines. While these medications suppress appetite, most people are not aware of the detrimental side effects of amphetamines, including hypertension, tachycardia, arrhythmias, and in certain instances acute myocardial infarction. Here we present the uncommon entity of an acute myocardial infarction due to chronic use of an amphetamine containing dietary supplement in conjunction with an exercise regimen. Our case brings to light further awareness regarding use of amphetamines. Clinicians should have a high index of suspicion of use of these substances when young patients with no risk factors for coronary artery disease present with acute arrhythmias, heart failure, and myocardial infarctions. PMID:27516911

  7. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction.

    PubMed

    Perez-Downes, Julio; Hritani, Abdulwahab; Baldeo, Candice; Antoun, Patrick

    2016-01-01

    Weight loss is one of the most researched and marketed topics in American society. Dietary regimens, medications that claim to boost the metabolism, and the constant pressure to fit into society all play a role in our patient's choices regarding new dietary products. One of the products that are well known to suppress appetite and cause weight loss is amphetamines. While these medications suppress appetite, most people are not aware of the detrimental side effects of amphetamines, including hypertension, tachycardia, arrhythmias, and in certain instances acute myocardial infarction. Here we present the uncommon entity of an acute myocardial infarction due to chronic use of an amphetamine containing dietary supplement in conjunction with an exercise regimen. Our case brings to light further awareness regarding use of amphetamines. Clinicians should have a high index of suspicion of use of these substances when young patients with no risk factors for coronary artery disease present with acute arrhythmias, heart failure, and myocardial infarctions. PMID:27516911

  8. [A comprehensive analysis of incidence of myocardial infarction in Vladikavkaz depending on solar and geomagnetic activity].

    PubMed

    Botoeva, N K; Khetarugova, l G; Rapoport, S I

    2013-01-01

    The data on myocardial infarction morbidity in Vladikavkaz for 2007-2010 were analysed with reference to solar and geomagnetic activity. Time series of morbidity in men and women were constructed and their seasonal constituent was distinguished. It was found that the number of myocardial infarctions increases on day with enhanced geomagnetic activity especially among subjects aged 50-69 years. Regression analysis of the relationship between the number of sunspots and myocardial infarctions yielded the equation of piecewise linear regression showing that 42% of the cases were due to the changes in the number of sunspots. Medium strength negative correlation was found between the number of myocardial infarctions and the recurrence index of Bz-component of the interplanetary magnetic field. It suggests an important role of chaotic dynamics of external factors in the development of myocardial infarction. PMID:25696947

  9. Bronchogenic Carcinoma with Cardiac Invasion Simulating Acute Myocardial Infarction

    PubMed Central

    Das, Anirban; Das, Sibes K.; Pandit, Sudipta; Karmakar, Rathindra Nath

    2016-01-01

    Cardiac metastases in bronchogenic carcinoma may occur due to retrograde lymphatic spread or by hematogenous dissemination of tumour cells, but direct invasion of heart by adjacent malignant lung mass is very uncommon. Pericardium is frequently involved in direct cardiac invasion by adjacent lung cancer. Pericardial effusion, pericarditis, and tamponade are common and life threatening presentation in such cases. But direct invasion of myocardium and endocardium is very uncommon. Left atrial endocardium is most commonly involved in such cases due to anatomical contiguity with pulmonary hilum through pulmonary veins, and in most cases left atrial involvement is asymptomatic. But myocardial compression and invasion by adjacent lung mass may result in myocardial ischemia and may present with retrosternal, oppressive chest pain which clinically may simulate with the acute myocardial infarction (AMI). As a result, it leads to misdiagnosis and delayed diagnosis of lung cancer. Here we report a case of non-small-cell carcinoma of right lung which was presented with asymptomatic invasion in left atrium and retrosternal chest pain simulating AMI due to myocardial compression by adjacent lung mass, in a seventy-four-year-old male smoker. PMID:27042370

  10. Myocardial Salvaging Effects of Berberine in Experimental Diabetes Co-Existing with Myocardial Infarction

    PubMed Central

    Borde, Manjusha K.; Mohanty, Ipseeta Ray; Maheshwari, Ujwala; Deshmukh, Y.A.

    2016-01-01

    Introduction Berberine, an isoquinoline alkaloid isolated from the Berberis aristata, has been shown to display a wide array of pharmacological activities (hypoglycaemic and hypolipidemic). Aim The present study was designed to investigate whether these pharmacological properties translate into the cardioprotective effects of Berberine in the setting of diabetes mellitus. Materials and Methods Necessary approval from the Institutional Animal Ethics Committee was taken for the study. Experimental diabetes was produced with single dose of Streptozotocin (STZ): 45mg/kg ip and myocardial infarction was induced by administering Isoproterenol (ISP): 85mg/kg, sc to rats on 35th & 36th day. After the confirmation of diabetes on 7th day (>200mg/dl), Berberine (100 mg/kg) was administered orally to experimental rats from day 8 and continued for 30 days thereafter. Various anti-diabetic (Glucose, HbA1c), cardioprotective (CPK-MB), metabolic (lipid profile), safety {liver function (SGPT, kidney function (Creatinine)} and histopathological indices of injury were evaluated in Healthy Control, Diabetic Control and Berberine treated groups. Results Administration of STZ-ISP resulted in a significant decrease in body weight (p<0.001), diabetic changes (increase in blood glucose, HbA1c), cardiac injury (leakage of myocardial CPK-MB), altered lipid profile, SGPT, creatinine levels (p<0.001) in the diabetic control group rats as compared to healthy control. Berberine treatment demonstrated significant antidiabetic as well as myocardial salvaging effects as indicated by restoration of blood glucose, HbA1c and CPK-MB levels (p<0.001) compared to diabetic control group. In addition, Berberine favourably modulated the lipid parameters (total cholesterol, triglycerides, HDL, LDL). Subsequent to ISP challenge, histopathological assessment of heart, pancreas and biochemical indices of injury confirmed the cardioprotective effects of Berberine in setting of diabetes. In addition, Berberine

  11. Postmortem mRNA Expression Patterns in Left Ventricular Myocardial Tissues and Their Implications for Forensic Diagnosis of Sudden Cardiac Death

    PubMed Central

    Son, Gi Hoon; Park, Seong Hwan; Kim, Yunmi; Kim, Ji Yeon; Kim, Jin Wook; Chung, Sooyoung; Kim, Yu-Hoon; Kim, Hyun; Hwang, Juck-Joon; Seo, Joong-Seok

    2014-01-01

    Sudden cardiac death (SCD), which is primarily caused by lethal heart disorders resulting in structural and arrhythmogenic abnormalities, is one of the prevalent modes of death in most developed countries. Myocardial ischemia, mainly due to coronary artery disease, is the most common type of heart disease leading to SCD. However, postmortem diagnosis of SCD is frequently complicated by obscure histological evidence. Here, we show that certain mRNA species, namely those encoding hemoglobin A1/2 and B (Hba1/2 and Hbb, respectively) as well as pyruvate dehydrogenase kinase 4 (Pdk4), exhibit distinct postmortem expression patterns in the left ventricular free wall of SCD subjects when compared with their expression patterns in the corresponding tissues from control subjects with non-cardiac causes of death. Hba1/2 and Hbb mRNA expression levels were higher in ischemic SCD cases with acute myocardial infarction or ischemic heart disease without recent infarction, and even in cardiac death subjects without apparent pathological signs of heart injuries, than control subjects. By contrast, Pdk4 mRNA was expressed at lower levels in SCD subjects. In conclusion, we found that altered myocardial Hba1/2, Hbb, and Pdk4 mRNA expression patterns can be employed as molecular signatures of fatal cardiac dysfunction to forensically implicate SCD as the primary cause of death. PMID:24642708

  12. Lidocaine Enhances Contractile Function of Ischemic Myocardial Regions in Mouse Model of Sustained Myocardial Ischemia

    PubMed Central

    Kania, Gabriela; Osto, Elena; Jakob, Philipp; Krasniqi, Nazmi; Beck-Schimmer, Beatrice; Blyszczuk, Przemyslaw; Eriksson, Urs

    2016-01-01

    Rationale Perioperative myocardial ischemia is common in high-risk patients. The use of interventional revascularisation or even thrombolysis is limited in this patient subset due to exceedingly high bleeding risks. Blockade of voltage-gated sodium channels (VGSC) with lidocaine had been suggested to reduce infarct size and cardiomyocyte cell death in ischemia/reperfusion models. However, the impact of lidocaine on cardiac function during sustained ischemia still remains unclear. Methods Sustained myocardial ischemia was induced by ligation of the left anterior descending artery in 12–16 weeks old male BALB/c mice. Subcutaneous lidocaine (30 mg/kg) was used to block VGSC. Cardiac function was quantified at baseline and at 72h by conventional and speckle-tracking based echocardiography to allow high-sensitivity in vivo phenotyping. Infarct size and cardiomyocyte cell death were assessed post mortem histologically and indirectly using troponin measurements. Results Ischemia strongly impaired both, global systolic and diastolic function, which were partially rescued in lidocaine treated in mice. No differences regarding infarct size and cardiomyocyte cell death were observed. Mechanistically, and as shown with speckle-tracking analysis, lidocaine specifically improves residual contractility in the ischemic but not in the remote, non-ischemic myocardium. Conclusion VGSC blockade with lidocaine rescues function of ischemic myocardium as a potential bridging to revascularisation in the setting of perioperative myocardial ischemia. PMID:27140425

  13. Rat myocardial protein degradation.

    PubMed

    Steer, J H; Hopkins, B E

    1981-07-01

    1. Myocardial protein degradation rates were determined by following tyrosine release from rat isolated left hemi-atria in vitro. 2. After two 20 min preincubations the rate of tyrosine release from hemi-atria was constant for 4 h. 3. Skeletal muscle protein degradation was determined by following tyrosine release from rat isolated hemi-diaphragm (Fulks, Li & Goldberg, 1975). 4. Insulin (10(-7) M) inhibited tyrosine release from hemi-atria and hemi-diaphragm to a similar extent. A 48 h fast increased tyrosine release rate from hemi-diaphragm and decreased tyrosine release rate from hemi-atria. Hemi-diaphragm tyrosine release was inhibited by 15 mmol/l D-glucose but a variety of concentrations of D-glucose (0, 5, 15 mmol/l) had no effect on tyrosine release from hemi-atria. Five times the normal plasma levels of the branched-chain amino acids leucine, isoleucine and valine had no effect on tyrosine release from either hemi-atria or hemi-diaphragm.

  14. Acute inferior myocardial infarction in a patient with a prosthetic aortic valve and high international normalized ratio

    PubMed Central

    Sari, Ibrahim; Delil, Kenan; Ileri, Cigdem; Samadov, Fuad

    2014-01-01

    ST elevation acute myocardial infarction in patients with a mechanical prosthetic valve is rare and usually due to inadequate anticoagulation. We present a case of acute inferior myocardial infarction in a patient with a prosthetic aortic valve and high international normalized ratio, which has not been reported previously. PMID:24799934

  15. Myocardial tissue phase mapping reveals impaired myocardial tissue velocities in obesity.

    PubMed

    Rider, Oliver J; Ajufo, Ezimamaka; Ali, Mohammed K; Petersen, Steffen E; Nethononda, Richard; Francis, Jane M; Neubauer, Stefan

    2015-02-01

    Although obesity is linked to heart failure on a population level, not all obese subjects develop cardiac failure. As a result, identifying obese subjects with subclinical changes in myocardial velocities may enable earlier detection of those susceptible to developing overt heart failure. As echocardiography is limited in obesity due to limited acoustic window, we used phase contrast magnetic resonance imaging to assess myocardial velocities in obese and normal weight subjects. Normal weight (BMI 23 ± 3; n = 40) and obese subjects (BMI 37 ± 7; n = 59) without identifiable cardiovascular risk factors underwent MRI (1.5 Tesla) to determine left ventricular myocardial velocities using phase contrast tissue phase mapping. Systolic function was not different between normal and obese subjects (LVEF 67 ± 5 vs 68 ± 4, p = 0.22). However, obesity was associated with significantly impaired peak radial and longitudinal diastolic myocardial velocity (by 13 and 19 % respectively, both p < 0.001). In addition time-to-peak longitudinal diastolic velocity was delayed in obesity (by 39 ms, p < 0.001). In addition, peak longitudinal diastolic strain was 20 % lower in obesity (p = 0.015) and time-to-peak longitudinal diastolic strain rate significantly delayed in obesity (by 92 ms, p < 0.001).Although peak radial systolic velocity was similar between obese and normal weight subjects (p = 0.14) peak longitudinal systolic velocity was 7 % lower in the obese cohort (p = 0.02). In obesity without co-morbidities, tissue phase mapping has shown subclinical changes in systolic and diastolic function. Given the link between obesity and heart failure, early detection of changes may become clinically important to prevent disease progression.

  16. Myocardial perfusion imaging for detection of silent myocardial ischemia

    SciTech Connect

    Beller, G.A.

    1988-04-21

    Despite the widespread use of the exercise stress test in diagnosing asymptomatic myocardial ischemia, exercise radionuclide imaging remains useful for detecting silent ischemia in numerous patient populations, including those who are totally asymptomatic, those who have chronic stable angina, those who have recovered from an episode of unstable angina or an uncomplicated myocardial infarction, and those who have undergone angioplasty or received thrombolytic therapy. Studies show that thallium scintigraphy is more sensitive than exercise electrocardiography in detecting ischemia, i.e., in part, because perfusion defects occur more frequently than ST depression and before angina in the ischemic cascade. Thallium-201 scintigraphy can be performed to differentiate a true- from a false-positive exercise electrocardiographic test in patients with exercise-induced ST depression and no angina. The development of technetium-labeled isonitriles may improve the accuracy of myocardial perfusion imaging. 11 references.

  17. Myocardial contrast echo effect: the dilemma of coronary blood flow and volume.

    PubMed

    Rovai, D; DeMaria, A N; L'Abbate, A

    1995-07-01

    Despite the useful information provided by myocardial contrast echocardiography, the meaning of myocardial contrast intensity remains elusive. This review is meant to define the contribution of physical and biologic factors in producing myocardial contrast and to elucidate the relative roles of coronary blood flow and intramyocardial blood volume in determining contrast effect. The main physical factors influencing the contrast echo effect include the properties of microbubbles as scattering elements (mainly their radius, compressibility, stability and concentration), electronic signal processing, instrument setting and contrast-induced signal attenuation. The effect of these factors can be limited by an appropriate experimental or clinical setup. Biologic factors are less easily controllable, and changes in coronary blood flow and alterations in myocardial blood volume appear to be the main determinants of myocardial contrast intensity. Moreover, these factors influence contrast intensity in opposite directions. Both the area under the time-intensity curve and the mean transit time of myocardial contrast are inversely related to coronary blood flow but directly related to myocardial vascularity and blood volume. Therefore, an increase in coronary flow not accompanied by an increase in myocardial vascularity and volume is accompanied by a decrease in the area under the curve and mean transit time of contrast. Conversely, an increase in coronary flow mediated by augmented myocardial vascularity and volume will produce an increase in the area under the curve and mean transit time. A better understanding of the physical and biologic determinants of contrast echo intensity will be fundamental in the clinical application of new agents and technologies. PMID:7797739

  18. Recombinant human neuregulin-1β is protective against radiation-induced myocardial cell injury.

    PubMed

    Zhou, Qiang; Hu, Wenbing; Fei, Xinxiong; Huang, Xuqun; Chen, Xi; Zhao, Deqing; Huang, Jun; Jiang, Lan; Wang, Gangsheng

    2016-07-01

    The aim of the present study was to investigate the role of recombinant human neuregulin-1β (rhNRG-1β) in the repair of the radiation-induced damage of myocardial cells and the underlying mechanism. Rats were divided into the radiotherapy alone group, the rhNRG-1β group (radiotherapy with rhNRG‑1β treatment) and the Herceptin group (radiotherapy with Herceptin treatment), and their myocardial cells were analyzed. The morphology of the myocardial cells was observed under an optical microscope, and the expression of γ‑H2AX and p53 was analyzed using immunohistochemistry and western blot analysis. Damage to the myocardial cells was identified in the three groups following radiation treatment, which was identified by cell swelling and altered morphology. The integrated optical density values of γ‑H2AX in the radiotherapy alone, rhNRG‑1β and Herceptin groups were 50.96±5.548, 27.63±10.61 and 76.12±2.084, respectively. The OD of the radiotherapy alone group was significantly higher than that of the rhNRG‑1β treated group (P<0.0001), and the value of the Herceptin group was significantly higher than that of the radiotherapy alone group (P<0.0001). The p53 level in the rhNRG‑1β group was less than that of the radiotherapy alone group (P<0.001), and was higher in the Herceptin group compared with the radiotherapy alone group (P<0.0001). Thus, rhNRG‑1β can ameliorate radiotherapy-induced myocardial cell injury, predominantly by enhancing myocardial cell DNA repair, inhibiting cell apoptosis and improving myocardial function. The results of this study in myocardial cells suggest that patients with thoracic cancer may benefit from treatment with rhNRG‑1β for the repair of the radiation-induced damage of myocardial cells. PMID:27150576

  19. MYOCARDIAL AKT: THE OMNIPRESENT NEXUS

    PubMed Central

    Sussman, Mark A.; Völkers, Mirko; Fischer, Kimberlee; Bailey, Brandi; Cottage, Christopher T.; Din, Shabana; Gude, Natalie; Avitabile, Daniele; Alvarez, Roberto; Sundararaman, Balaji; Quijada, Pearl; Mason, Matt; Konstandin, Mathias H.; Malhowski, Amy; Cheng, Zhaokang; Khan, Mohsin; McGregor, Michael

    2013-01-01

    One of the greatest examples of integrated signal transduction is revealed by examination of effects mediated by AKT kinase in myocardial biology. Positioned at the intersection of multiple afferent and efferent signals, AKT exemplifies a molecular sensing node that coordinates dynamic responses of the cell in literally every aspect of biological responses. The balanced and nuanced nature of homeostatic signaling is particularly essential within the myocardial context, where regulation of survival, energy production, contractility, and response to pathological stress all flow through the nexus of AKT activation or repression. Equally important, the loss of regulated AKT activity is primarily the cause or consequence of pathological conditions leading to remodeling of the heart and eventual decompensation. This review presents an overview compendium of the complex world of myocardial AKT biology gleaned from more than a decade of research. Summarization of the widespread influence that AKT exerts upon myocardial responses leaves no doubt that the participation of AKT in molecular signaling will need to be reckoned with as a seemingly omnipresent regulator of myocardial molecular biological responses. PMID:21742795

  20. How reliable is myocardial imaging in the diagnosis of acute myocardial infarction

    SciTech Connect

    Willerson, J.T.

    1983-01-01

    Myocardial scintigraphic techniques available presently allow a sensitive and relatively specific diagnosis of acute myocardial infarction when they are used correctly, although every technique has definite limitations. Small myocardial infarcts (less than 3 gm.) may be missed, and there are temporal limitations in the usefulness of the scintigraphic techniques. The development of tomographic methodology that may be used with single-photon radionuclide emitters (including technetium and /sup 201/Tl will allow the detection of relatively small abnormalities in myocardial perfusion and regions of myocardial infarction and will help to provide a more objective interpretation of the myocardial scintigrams. The use of overlay techniques allowing simultaneous assessment of myocardial perfusion, infarct-avid imaging, and radionuclide ventriculograms will provide insight into the relevant aspects of the extent of myocardial damage, the relationship of damage to myocardial perfusion, and the functional impact of myocardial infarction on ventricular performance.

  1. Myocardial Infarction: Symptoms and Treatments.

    PubMed

    Lu, Lei; Liu, Min; Sun, RongRong; Zheng, Yi; Zhang, Peiying

    2015-07-01

    Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include, taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and loosing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. In this article the causes, symptoms and treatments of MI are described. PMID:25638347

  2. Myocardial Infarction: Symptoms and Treatments.

    PubMed

    Lu, Lei; Liu, Min; Sun, RongRong; Zheng, Yi; Zhang, Peiying

    2015-07-01

    Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include, taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and loosing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. In this article the causes, symptoms and treatments of MI are described.

  3. Multifunctional MR monitoring of the healing process after myocardial infarction.

    PubMed

    Bönner, Florian; Jacoby, Christoph; Temme, Sebastian; Borg, Nadine; Ding, Zhaoping; Schrader, Jürgen; Flögel, Ulrich

    2014-01-01

    Healing of the myocardium after infarction comprises a variety of local adaptive processes which contribute to the functional outcome after the insult. Therefore, we aimed to establish a setting for concomitant assessment of regional alterations in contractile function, morphology, and immunological state to gain prognostic information on cardiac recovery after infarction. For this, mice were subjected to myocardial ischemia/reperfusion (I/R) and monitored for 28 days by cine MRI, T2 mapping, late gadolinium enhancement (LGE), and (19)F MRI. T2 values were calculated from gated multi-echo sequences. (19)F-loaded nanoparticles were injected intravenously for labelling circulating monocytes and making them detectable by (19)F MRI. In-house developed software was used for regional analysis of cine loops, T2 maps, LGE, and (19)F images to correlate local wall movement, tissue damage as well as monocyte recruitment over up to 200 sectors covering the left ventricle. This enabled us to evaluate simultaneously zonal cardiac necrosis, oedema, and inflammation patterns together with sectional fractional shortening (FS) and global myocardial function. Oedema, indicated by a rise in T2, showed a slightly better correlation with FS than LGE. Regional T2 values increased from 19 ms to above 30 ms after I/R. In the course of the healing process oedema resolved within 28 days, while myocardial function recovered. Infiltrating monocytes could be quantitatively tracked by (19)F MRI, as validated by flow cytometry. Furthermore, (19)F MRI proved to yield valuable insight on the outcome of myocardial infarction in a transgenic mouse model. In conclusion, our approach permits a comprehensive surveillance of key processes involved in myocardial healing providing independent and complementary information for individual prognosis. PMID:25098936

  4. Multifunctional MR monitoring of the healing process after myocardial infarction.

    PubMed

    Bönner, Florian; Jacoby, Christoph; Temme, Sebastian; Borg, Nadine; Ding, Zhaoping; Schrader, Jürgen; Flögel, Ulrich

    2014-01-01

    Healing of the myocardium after infarction comprises a variety of local adaptive processes which contribute to the functional outcome after the insult. Therefore, we aimed to establish a setting for concomitant assessment of regional alterations in contractile function, morphology, and immunological state to gain prognostic information on cardiac recovery after infarction. For this, mice were subjected to myocardial ischemia/reperfusion (I/R) and monitored for 28 days by cine MRI, T2 mapping, late gadolinium enhancement (LGE), and (19)F MRI. T2 values were calculated from gated multi-echo sequences. (19)F-loaded nanoparticles were injected intravenously for labelling circulating monocytes and making them detectable by (19)F MRI. In-house developed software was used for regional analysis of cine loops, T2 maps, LGE, and (19)F images to correlate local wall movement, tissue damage as well as monocyte recruitment over up to 200 sectors covering the left ventricle. This enabled us to evaluate simultaneously zonal cardiac necrosis, oedema, and inflammation patterns together with sectional fractional shortening (FS) and global myocardial function. Oedema, indicated by a rise in T2, showed a slightly better correlation with FS than LGE. Regional T2 values increased from 19 ms to above 30 ms after I/R. In the course of the healing process oedema resolved within 28 days, while myocardial function recovered. Infiltrating monocytes could be quantitatively tracked by (19)F MRI, as validated by flow cytometry. Furthermore, (19)F MRI proved to yield valuable insight on the outcome of myocardial infarction in a transgenic mouse model. In conclusion, our approach permits a comprehensive surveillance of key processes involved in myocardial healing providing independent and complementary information for individual prognosis.

  5. Identifying Early Changes in Myocardial Microstructure in Hypertensive Heart Disease

    PubMed Central

    Hiremath, Pranoti; Bauer, Michael; Aguirre, Aaron D.; Cheng, Hui-Wen; Unno, Kazumasa; Patel, Ravi B.; Harvey, Bethany W.; Chang, Wei-Ting; Groarke, John D.; Liao, Ronglih; Cheng, Susan

    2014-01-01

    The transition from healthy myocardium to hypertensive heart disease is characterized by a series of poorly understood changes in myocardial tissue microstructure. Incremental alterations in the orientation and integrity of myocardial fibers can be assessed using advanced ultrasonic image analysis. We used a modified algorithm to investigate left ventricular myocardial microstructure based on analysis of the reflection intensity at the myocardial-pericardial interface on B-mode echocardiographic images. We evaluated the extent to which the novel algorithm can differentiate between normal myocardium and hypertensive heart disease in humans as well as in a mouse model of afterload resistance. The algorithm significantly differentiated between individuals with uncomplicated essential hypertension (N = 30) and healthy controls (N = 28), even after adjusting for age and sex (P = 0.025). There was a trend in higher relative wall thickness in hypertensive individuals compared to controls (P = 0.08), but no difference between groups in left ventricular mass (P = 0.98) or total wall thickness (P = 0.37). In mice, algorithm measurements (P = 0.026) compared with left ventricular mass (P = 0.053) more clearly differentiated between animal groups that underwent fixed aortic banding, temporary aortic banding, or sham procedure, on echocardiography at 7 weeks after surgery. Based on sonographic signal intensity analysis, a novel imaging algorithm provides an accessible, non-invasive measure that appears to differentiate normal left ventricular microstructure from myocardium exposed to chronic afterload stress. The algorithm may represent a particularly sensitive measure of the myocardial changes that occur early in the course of disease progression. PMID:24831515

  6. Myocardial contusion caused by a baseball.

    PubMed

    Morikawa, M; Hirose, K; Mori, T; Kusukawa, J; Tomioka, N; Watanabe, Y

    1996-10-01

    Myocardial contusion is a rare type of sports injury. We report a case of myocardial contusion caused by a baseball. In this patient, arrhythmias were induced by an exercise test 1 week after injury. That patients with myocardial contusion but without arrhythmias at rest need to be treated carefully is emphasized.

  7. Myocardial Mapping With Cardiac Magnetic Resonance: The Diagnostic Value of Novel Sequences.

    PubMed

    Sanz, Javier; LaRocca, Gina; Mirelis, Jesús G

    2016-09-01

    Cardiac magnetic resonance has evolved into a crucial modality for the evaluation of cardiomyopathy due to its ability to characterize myocardial structure and function. In the last few years, interest has increased in the potential of "mapping" techniques that provide direct and objective quantification of myocardial properties such as T1, T2, and T2* times. These approaches enable the detection of abnormalities that affect the myocardium in a diffuse fashion and/or may be too subtle for visual recognition. This article reviews the current state of myocardial T1 and T2-mapping in both health and disease. PMID:27450946

  8. Morphological aspects of myocardial bridges.

    PubMed

    Lujinović, Almira; Kulenović, Amela; Kapur, Eldan; Gojak, Refet

    2013-11-01

    Although some myocardial bridges can be asymptomatic, their presence often causes coronary disease either through direct compression of the "tunnel" segment or through stimulation and accelerated development of atherosclerosis in the segment proximally to the myocardial bridge. The studied material contained 30 human hearts received from the Department of Anatomy. The hearts were preserved 3 to 5 days in 10% formalin solution. Thereafter, the fatty tissue was removed and arterial blood vessels prepared by careful dissection with special reference to the presence of the myocardial bridges. Length and thickness of the bridges were measured by the precise electronic caliper. The angle between the myocardial bridge fibre axis and other axis of the crossed blood vessel was measured by a goniometer. The presence of the bridges was confirmed in 53.33% of the researched material, most frequently (43.33%) above the anterior interventricular branch. The mean length of the bridges was 14.64 ± 9.03 mm and the mean thickness was 1.23 ± 1.32 mm. Myocardial bridge fibres pass over the descending blood vessel at the angle of 10-90 degrees. The results obtained on a limited sample suggest that the muscular index of myocardial bridge is the highest for bridges located on RIA, but that the difference is not significant in relation to bridges located on other branches. The results obtained suggest that bridges located on other branches, not only those on RIA, could have a great contractive power and, consequently, a great compressive force, which would be exerted on the wall of a crossed blood vessel.

  9. Morin protects heart from beta-adrenergic-stimulated myocardial infarction: an electrocardiographic, biochemical, and histological study in rats.

    PubMed

    Pogula, Bharath Kumar; Maharajan, Mari Kannan; Oddepalli, Divya Rekha; Boini, Lavanya; Arella, Mounika; Sabarimuthu, Darlin Quine

    2012-09-01

    In recent years, polyphenols have attracted considerable attention as agents that protect cells or molecules from oxidative myocardial injury. The aim of the study was to prove the cardioprotective benefits of the flavonoid morin in isoproterenol-induced myocardial infarcted rats. Male Wistar rats are treated orally with morin (10 and 20 mg/kg) daily for a period of 21 days. After 21 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days to induce myocardial infarction. Electrocardiographical abnormalities and biomarkers were measured in normal and experimental rats. Isoproterenol-induced myocardial infarcted rats showed significant (p<0.05) increase in the levels of cardiac markers. Pretreatment with morin regulated the abnormalities in electrocardiograph and biomarkers. The lipid peroxidation products were increased and indicated the increased lipid peroxidation in isoproterenol-induced myocardial infarcted rats. The rats pretreated with morin significantly reduced lipid peroxidation. The altered lipid metabolism was observed in isoproterenol-induced myocardial infarcted rats and in pretreatment with morin-regulated lipid metabolism. Histopathological study evidenced that the pretreatment with morin inhibited myocardial damage. The results of this study proved the protective effect of morin as pretreatment and are rational to understand the beneficial effects of morin on cardioprotection against myocardial injury. Based on the results, the cardioprotective ability of morin on human beings can be studied in the future.

  10. Acute myocardial infarction in rats.

    PubMed

    Wu, Yewen; Yin, Xing; Wijaya, Cori; Huang, Ming-He; McConnell, Bradley K

    2011-01-01

    With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular diseases. Animal models that mimic human cardiac disease, such as myocardial infarction (MI) and ischemia-reperfusion (IR) that induces heart failure as well as pressure-overload (transverse aortic constriction) that induces cardiac hypertrophy and heart failure (Goldman and Tarnavski), are useful models to study cardiovascular disease. In particular, myocardial ischemia (MI) is a leading cause for cardiovascular morbidity and mortality despite controlling certain risk factors such as arteriosclerosis and treatments via surgical intervention (Thygesen). Furthermore, an acute loss of the myocardium following myocardial ischemia (MI) results in increased loading conditions that induces ventricular remodeling of the infarcted border zone and the remote non-infarcted myocardium. Myocyte apoptosis, necrosis and the resultant increased hemodynamic load activate multiple biochemical intracellular signaling that initiates LV dilatation, hypertrophy, ventricular shape distortion, and collagen scar formation. This pathological remodeling and failure to normalize the increased wall stresses results in progressive dilatation, recruitment of the border zone myocardium into the scar, and eventually deterioration in myocardial contractile function (i.e. heart failure). The progression of LV dysfunction and heart failure in rats is similar to that observed in patients who sustain a large myocardial infarction, survive and subsequently develops heart failure (Goldman). The acute myocardial infarction (AMI) model in rats has been used to mimic human cardiovascular disease; specifically used to study cardiac signaling mechanisms associated with heart failure as well as to assess the contribution of therapeutic strategies for the treatment of heart failure. The method described in this report is the rat model of acute myocardial

  11. Myocardial tissue engineering using electrospun nanofiber composites

    PubMed Central

    Kim, Pyung-Hwan; Cho, Je-Yoel

    2016-01-01

    Emerging trends for cardiac tissue engineering are focused on increasing the biocompatibility and tissue regeneration ability of artificial heart tissue by incorporating various cell sources and bioactive molecules. Although primary cardiomyocytes can be successfully implanted, clinical applications are restricted due to their low survival rates and poor proliferation. To develop successful cardiovascular tissue regeneration systems, new technologies must be introduced to improve myocardial regeneration. Electrospinning is a simple, versatile technique for fabricating nanofibers. Here, we discuss various biodegradable polymers (natural, synthetic, and combinatorial polymers) that can be used for fiber fabrication. We also describe a series of fiber modification methods that can increase cell survival, proliferation, and migration and provide supporting mechanical properties by mimicking micro-environment structures, such as the extracellular matrix (ECM). In addition, the applications and types of nanofiber-based scaffolds for myocardial regeneration are described. Finally, fusion research methods combined with stem cells and scaffolds to improve biocompatibility are discussed. [BMB Reports 2016; 49(1): 26-36] PMID:26497579

  12. Thallium-201 myocardial scintigraphy in acute myocardial infarction and ischemia

    SciTech Connect

    Wackers, F.J.

    1982-04-01

    Thallium-201 scintigraphy provides a sensitive and reliable method of detecting acute myocardial infarction and ischemia when imaging is performed with understanding of the temporal characteristics and accuracy of the technique. The results of scintigraphy are related to the time interval between onset of symptoms and time of imaging. During the first 6 hr after chest pain almost all patients with acute myocardial infarction and approximately 50% of the patients with unstable angina will demonstrate /sup 201/TI pefusion defects. Delayed imaging at 2-4 hr will permit distinction between ischemia and infarction. In patients with acute myocardial infarction, the size of the perfusion defect accurately reflects the extent of the infarcted and/or jeopardized myocardium, which may be used for prognostic stratification. In view of the characteristics of /sup 201/TI scintigraphy, the most practical application of this technique is in patients in whom myocardial infarction has to be ruled out, and for early recognition of patients at high risk for complications.

  13. Influence of microvascular dysfunction on regional myocardial deformation post-acute myocardial infarction: insights from a novel angiographic index for assessing myocardial tissue-level reperfusion.

    PubMed

    He, Ben; Ding, Song; Qiao, Zhiqing; Gao, Lincheng; Wang, Wei; Ge, Heng; Shen, Xuedong; Pu, Jun

    2016-05-01

    To investigate the impact of microvascular dysfunction assessed by angiography on myocardial deformation assessed by two-dimensional speckle-tracking echocardiography in ST-segment elevation myocardial infarction (STEMI). A total of 121 STEMI patients who received primary percutaneous coronary intervention were included. Thrombolysis in myocardial infarction, Myocardial Perfusion Frame Count (TMPFC), a novel angiographic method to assess myocardial perfusion, was used to evaluate microvascular dysfunction. Two-dimensional speckle-tracking echocardiography was performed at 3-7 days after reperfusion. The infarction related regional longitudinal (RLS) strains as well as circumferential (RCS) and radial (RRS) ones, along with global longitudinal, circumferential (GCS), and radial (GRS) strains were measured. Patients with microvascular dysfunction had decreased peak amplitude of RLS (p = 0.012), RCS (p < 0.001), RRS (p = 0.012) at the regional level and decreased peak amplitude of GCS (p = 0.005), GRS (p = 0.012) at the global level. The RCS to RLS and RCS to RRS ratios were significantly different between patients without than with microvascular dysfunction (1.28 ± 0.31 vs. 1.07 ± 0.47, p = 0.027 and 0.69 ± 0.33 vs. 0.56 ± 0.28, p = 0.047). Receiver operator characteristics curves identified a cutoff value of 94 frames for TMPFC to differentiate between normal and abnormal wall motion score index in the sub-acute phase of STEMI (AUC = 0.72; p < 0.001). In the sub-acute phase of STEMI, the presence of microvascular dysfunction in infarcted tissue relates to reduced global and regional myocardial deformation. RCS alterations were more significant than RLS and RRS between patients with than without microvascular dysfunction. TMPFC was useful to predict left ventricular systolic dysfunction in the sub-acute phase of STEMI.

  14. Attention Alters Perceived Attractiveness.

    PubMed

    Störmer, Viola S; Alvarez, George A

    2016-04-01

    Can attention alter the impression of a face? Previous studies showed that attention modulates the appearance of lower-level visual features. For instance, attention can make a simple stimulus appear to have higher contrast than it actually does. We tested whether attention can also alter the perception of a higher-order property-namely, facial attractiveness. We asked participants to judge the relative attractiveness of two faces after summoning their attention to one of the faces using a briefly presented visual cue. Across trials, participants judged the attended face to be more attractive than the same face when it was unattended. This effect was not due to decision or response biases, but rather was due to changes in perceptual processing of the faces. These results show that attention alters perceived facial attractiveness, and broadly demonstrate that attention can influence higher-level perception and may affect people's initial impressions of one another. PMID:26966228

  15. Myocardial contusion following nonfatal blunt chest trauma

    SciTech Connect

    Kumar, S.A.; Puri, V.K.; Mittal, V.K.; Cortez, J.

    1983-04-01

    Currently available diagnostic techniques for myocardial contusion following blunt chest trauma were evaluated. We investigated 30 patients prospectively over a period of 1 year for the presence of myocardial contusion. Among the 30 patients, eight were found to have myocardial contusion on the basis of abnormal electrocardiograms, elevated creatine phosphokinase MB fraction (CPK-MB), and positive myocardial scan. Myocardial scan was positive in seven of eight patients (87.5%). CPK-MB fraction was elevated in four of eight patients (50%). Definitive electrocardiographic changes were seen in only two of eight patients (25%). It appears that myocardial scan using technetium pyrophosphate and CPK-MB fraction determinations are the most reliable aids in diagnosis of myocardial contusion following blunt chest trauma.

  16. Over-expression of catalase in myeloid cells confers acute protection following myocardial infarction.

    PubMed

    Cabigas, E Bernadette; Somasuntharam, Inthirai; Brown, Milton E; Che, Pao Lin; Pendergrass, Karl D; Chiang, Bryce; Taylor, W Robert; Davis, Michael E

    2014-05-21

    Cardiovascular disease is the leading cause of death in the United States and new treatment options are greatly needed. Oxidative stress is increased following myocardial infarction and levels of antioxidants decrease, causing imbalance that leads to dysfunction. Therapy involving catalase, the endogenous scavenger of hydrogen peroxide (H2O2), has been met with mixed results. When over-expressed in cardiomyocytes from birth, catalase improves function following injury. When expressed in the same cells in an inducible manner, catalase showed a time-dependent response with no acute benefit, but a chronic benefit due to altered remodeling. In myeloid cells, catalase over-expression reduced angiogenesis during hindlimb ischemia and prevented monocyte migration. In the present study, due to the large inflammatory response following infarction, we examined myeloid-specific catalase over-expression on post-infarct healing. We found a significant increase in catalase levels following infarction that led to a decrease in H2O2 levels, leading to improved acute function. This increase in function could be attributed to reduced infarct size and improved angiogenesis. Despite these initial improvements, there was no improvement in chronic function, likely due to increased fibrosis. These data combined with what has been previously shown underscore the need for temporal, cell-specific catalase delivery as a potential therapeutic option.

  17. Myocardial iron metabolism in the regulation of cardiovascular diseases in rats.

    PubMed

    Zhao, Na; Sun, Zhidan; Mao, Yuying; Hang, Pengzhou; Jiang, Xing; Sun, Lihua; Zhao, Jinlong; Du, Zhimin

    2010-01-01

    The iron homeostasis plays an important role in cardiac function. To understand how it acts in diabetic and ischemic myocardial injury, we studied the myocardial iron metabolism in diabetic and myocardial ischemic rats. Diabetic rats were induced by intraperitoneal injection of streptozocin (STZ) after intragastric administration of a high-fat diet while the ischemic rat hearts were subjected to coronary artery ligation for 0.5, 1, 6, 12 or 24 h, respectively. In STZ-induced diabetic rats, the contents of serum and myocardial iron were found elevated obviously accompany with the decrease of hepatic iron determined by the flame emission atomic absorption spectroscopy. The levels of superoxide dismutase (SOD), malonaldehyde (MDA) and serum ferritin were increased in diabetic rats. Moreover, protein level of divalent metal transporter 1 (DMT1) was decreased while that for transferrin receptor (TfR) and metal transporter protein 1 (MTP1) was increased. In contrast, no alteration of iron concentration was observed in the ischemic rats. The expression of DMT1, TfR and MTP1 has not changed after infraction. The findings suggested that diabetes mellitus (DM) induced the iron overload in the myocardium, at least in part by up-regulation of TfR. Meanwhile, down-regulation of DMT1 and up-regulation of MTP1 were induced to alleviate the excessive iron in the myocardium. However, myocardial infraction (MI) has not broken the balance of myocardial iron. In conclusion, the iron homeostasis reacts differently in DM and MI. PMID:20511703

  18. Relaxin protects against myocardial injury caused by ischemia and reperfusion in rat heart.

    PubMed Central

    Bani, D.; Masini, E.; Bello, M. G.; Bigazzi, M.; Sacchi, T. B.

    1998-01-01

    Myocardial injury caused by ischemia and reperfusion comes from multiple pathogenic events, including endothelial damage, neutrophil extravasation into tissue, platelet and mast cell activation, and peroxidation of cell membrane lipids, which are followed by myocardial cell alterations resulting eventually in cell necrosis. The current study was designed to test the possible cardioprotective effect of the hormone relaxin, which has been found to cause coronary vessel dilation and to inhibit platelet and mast cell activation. Ischemia (for 30 minutes) was induced in rat hearts in vivo by ligature of the left anterior descending coronary artery; reperfusion (for 60 minutes or less if the rats died before this predetermined time) was induced by removal of the ligature. Relaxin (100 ng) was given intravenously 30 minutes before ischemia. The results obtained showed that relaxin strongly reduces 1) the extension of the myocardial areas affected by ischemia-reperfusion-induced damage, 2) ventricular arrhythmias, 3) mortality, 4) myocardial neutrophil number, 5) myeloperoxidase activity, a marker of neutrophil accumulation, 6) production of malonyldialdehyde, an end product of lipid peroxidation, 7) mast cell granule release, 8) calcium overload, and 9) morphological signs of myocardial cell injury. This study shows that relaxin can be regarded as an agent with a marked cardioprotective action against ischemia-reperfusion-induced myocardial injury. Images Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 PMID:9588905

  19. Seasonal pattern in admissions and mortality from acute myocardial infarction in elderly patients in Isfahan, Iran

    PubMed Central

    Mohammadian-Hafshejani, Abdollah; Sarrafzadegan, Nizal; Hosseini, Shidokht; Baradaran, Hamid Reza; Roohafza, Hamidreza; Sadeghi, Masoumeh; Asadi-Lari, Mohsen

    2014-01-01

    BACKGROUND Seasonal variation in admissions and mortality due to acute myocardial infarction has been observed in different countries. Since there are scarce reports about this variation in Iran, this study was carried out to determine the existence of seasonal rhythms in hospital admissions for acute myocardial infarction, and in mortality due to acute myocardial infarction (AMI) in elderly patients in Isfahan city. METHODS This prospective hospital-based study included a total of 3990 consecutive patients with acute myocardial infarction admitted to 13 hospitals from January 2002 to December 2007. Seasonal variations were analyzed with the Kaplan-Meier table, log rank test, and Cox regression model. RESULTS There was a statistically significant relationship between the occurrence of heart disease based on season and type of acute myocardial infarction anatomical (P < 0.001). The relationship between the occurrence of death and season and type of AMI according to International Classification of Diseases code 10 (ICD) was also observed and it was statistically significant (P = 0.026). Hazard ratio for death from acute myocardial infarction were 0.96 [Confidence interval of 95% (95% CI) = 0.78-1.18], 0.9 (95%CI = 0.73-1.11), and 1.04 (95%CI = 0.85-1.26) during spring, summer, and winter, respectively. CONCLUSION There is seasonal variation in hospital admission and mortality due to AMI; however, after adjusting in the model only gender and age were significant predictor factors. PMID:24963314

  20. Myocardial revascularization in Jehovah Witnesses.

    PubMed

    Seifert, P E; Auer, J E; Hohensee, P

    1989-04-01

    The refusal of certain patients to accept blood transfusions need not be a deterrent to surgery. We report on nine Jehovah's Witnesses who over a one-year period underwent myocardial revascularization without significant blood loss or decrease in hematocrit values. PMID:2786287

  1. [Myocardial infarction in young population].

    PubMed

    Shklovskii, B L; Prokhorchik, A A; Koltunov, A N; Lishchuk, A N; Ryzhman, N N; Ivanov, A V; Navaznov, V V; Baksheev, V I

    2015-03-01

    Description of clinical observation and literature review. Myocardial infarction in patients younger than 45 years is rare, but it is an important clinical, organizational and psychological problem. A case of myocardial infarction in 19-years old patient, who suffered since 6 years from kidney disease, is described. Transmural left-ventricular myocardial infarction has developed on the background of chronic glomerulonephritis, excessive exercise, and traditional risk factors for cardiovascular disease. Coronary venous bypass with the benefit-pleasing outcome is performed. When analysing the literature, the authors emphasize that in comparison with elderly patients, young people have different profiles of risk factors, clinical manfestations and prognosis of myocardial infarction. It is emphasized that kidney chronic disease, regardless the stage, worsen short-term and long-term outcomes of cardiovascular disease. Early stabilization is possible under the condition of risk stratification and-early revascularization, which leads to better clinical outcomes. Particular attention should be given to a comprehensive assessment, it prognostic criteria, risk factor modification, secondary prevention of major and associated diseases, clinical- and -dynamic observation, including patients with asymptomatic course of the disease.

  2. Spousal Adjustment to Myocardial Infarction.

    ERIC Educational Resources Information Center

    Ziglar, Elisa J.

    This paper reviews the literature on the stresses and coping strategies of spouses of patients with myocardial infarction (MI). It attempts to identify specific problem areas of adjustment for the spouse and to explore the effects of spousal adjustment on patient recovery. Chapter one provides an overview of the importance in examining the…

  3. Myocardial infarction following sternal surgery.

    PubMed Central

    Aggarwal, R. K.; Morrison, W. L.

    1996-01-01

    We report a case of myocardial infarction in a 32-year-old man undergoing sternal surgery. Thrombotic occlusion of the right coronary artery with no underlying atheromatous disease was demonstrated angiographically and successfully treated with intracoronary thrombolysis. Images Figure 1 Figure 2 PMID:8796219

  4. Assessment, significance and mechanism of ventricular electrical instability after myocardial infarction.

    PubMed

    Richards, David A B; Denniss, A Robert

    2007-06-01

    The mechanism of reentrant tachycardia was established nearly a century ago, but the relationships between myocardial infarction and predisposition to sudden death were not unravelled until much later. In the latter half of the twentieth century many studies sought to ascertain what variables were predictive of death following myocardial infarction. Approximately one half of all deaths during the year following myocardial infarction are sudden and due to ventricular tachycardia (VT) or ventricular fibrillation (VF). We aimed to utilise non-invasive signal-averaging, along with programmed electrical stimulation of the heart, to determine whether one could predict spontaneous ventricular tachycardia and sudden death late after myocardial infarction. The sensitivity of ventricular electrical instablility (inducible ventricular tachycardia or fibrillation) as a predictor of instantaneous death or spontaneous VT was 86%, and the specificity was 83%. When other variables (delayed ventricular activation at signal-averaging, ejection fraction at gated heart pool scan, ventricular ectopic activity at ambulatory monitoring and exercise testing) were taken into account, inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden cardiac death after myocardial infarction. The Westmead studies of Uther et al. in the decade or so from 1980 established programmed stimulation as the best predictor of sudden death after myocardial infarction. Subsequent studies by others have demonstrated a survival advantage of defibrillator implantation in patients with low ejection fraction (and inducible ventricular tachycardia) after myocardial infarction. PMID:17446130

  5. Myocardial metabolism during hypoxia: Maintained lactate oxidation during increased glycolysis

    SciTech Connect

    Mazer, C.D.; Stanley, W.C.; Hickey, R.F.; Neese, R.A.; Cason, B.A.; Demas, K.A.; Wisneski, J.A.; Gertz, E.W. )

    1990-09-01

    In the intact animal, myocardial lactate utilization and oxidation during hypoxia are not well understood. Nine dogs were chronically instrumented with flow probes on the left anterior descending coronary artery and with a coronary sinus sampling catheter. ({sup 14}C)lactate and ({sup 13}C)glucose tracers, or ({sup 13}C)lactate and ({sup 14}C)glucose were administered to quantitate lactate and glucose oxidation, lactate conversion to glucose, and simultaneous lactate extraction and release. The animals were anesthetized and exposed to 90 minutes of severe hypoxia (PO2 = 25 +/- 4 torr). Hypoxia resulted in significant increases in heart rate, cardiac output and myocardial blood flow, but no significant change in myocardial oxygen consumption. The arterial/coronary sinus differences for glucose and lactate did not change from normoxia to hypoxia; however, the rate of glucose uptake increased significantly due to the increase in myocardial blood flow. Tracer-measured lactate extraction did not decrease with hypoxia, despite a 250% increase in lactate release. During hypoxia, 90% +/- 4% of the extracted {sup 14}C-lactate was accounted for by the appearance of {sup 14}CO{sub 2} in the coronary sinus, compared with 88% +/- 4% during normoxia. Thus, in addition to the expected increase in glucose uptake and lactate production, we observed an increase in lactate oxidation during hypoxia.

  6. Antioxidant enzymes attenuate myocardial stunning in the conscious dog

    SciTech Connect

    Triana, J.F.; Unisa, A.; Bolli, R. )

    1990-02-26

    Several studies have shown that postischemic myocardial dysfunction (myocardial stunning) is attenuated by antioxidants, implying a pathogenetic role of oxy-radicals in this phenomenon. However, since all these studies have been performed in open-chest preparations, artifacts due to anesthesia, trauma, and other nonphysiologic conditions cannot be excluded. Accordingly, chronically instrumented dogs underwent a 15-minute occlusion (o) of the left anterior descending artery followed by reperfusion. Dogs received i.v. either saline or superoxide dismutase (SOD) plus catalase (CAT) (16,000 U/kg and 55,000 U/kg, respectively, over 1 hour starting 15 minutes before O). Regional myocardial function was assessed as systolic wall thickening (WTh) using a pulsed Doppler probe. WTh after reperfusion was significantly greater in treated dogs, and this difference could not be ascribed to differences in collateral flow or hemodynamics. The authors conclude that SOD plus catalase attenuate myocardial stunning in the conscious dog, indicating that oxy-radicals play a pathogenetic role in this phenomenon under physiologic conditions.

  7. Hemorrhagic shock impairs myocardial cell volume regulation and membrane integrity in dogs

    SciTech Connect

    Horton, J.W.

    1987-06-01

    An in vitro myocardial slice technique was used to quantitate alterations in cell volume regulation and membrane integrity after 2 h or hemorrhagic shock. After in vitro incubation in Krebs-Ringer-phosphate medium containing trace (/sup 14/C)inulin, values (ml H/sub 2/O/g dry wt) for control nonshocked myocardial slices were 4.03 /plus minus/ 0.11 (SE) for total water, 2.16 /plus minus/ 0.07 for inulin impermeable space, and 1.76 /plus minus/ 0.15 for inulin diffusible space. Shocked myocardial slices showed impaired response to cold incubation. After 2 h of in vivo shock, total tissue water, inulin diffusible space, and inulin impermeable space increased significantly for subendocardium, whereas changes in subepicardium parameters were minimal. Shock-induced cellular swelling was accompanied by an increased total tissue sodium, but no change in tissue potassium. Calcium entry blockade in vivo significantly reduced subendocardial total tissue water as compared with shock-untreated dogs. In addition, calcium entry blockade reduced shock-induced increases in inulin diffusible space. In vitro myocardial slice studies confirm alterations in subendocardial membrane integrity after 2 h of in vivo hemorrhagic shock. Shock-induced abnormalities in myocardial cell volume regulation are reduced by calcium entry blockade in vivo.

  8. Myocardial Energy Substrate Metabolism in Heart Failure : from Pathways to Therapeutic Targets.

    PubMed

    Fukushima, Arata; Milner, Kenneth; Gupta, Abhishek; Lopaschuk, Gary D

    2015-01-01

    Despite recent advances in therapy, heart failure remains a major cause of mortality and morbidity and is a growing healthcare burden worldwide. Alterations in myocardial energy substrate metabolism are a hallmark of heart failure, and are associated with an energy deficit in the failing heart. Previous studies have shown that a metabolic shift from mitochondrial oxidative metabolism to glycolysis, as well as an uncoupling between glycolysis and glucose oxidation, plays a crucial role in the development of cardiac inefficiency and functional impairment in heart failure. Therefore, optimizing energy substrate utilization, particularly by increasing mitochondrial glucose oxidation, can be a potentially promising approach to decrease the severity of heart failure by improving mechanical cardiac efficiency. One approach to stimulating myocardial glucose oxidation is to inhibit fatty acid oxidation. This review will overview the physiological regulation of both myocardial fatty acid and glucose oxidation in the heart, and will discuss what alterations in myocardial energy substrate metabolism occur in the failing heart. Furthermore, lysine acetylation has been recently identified as a novel post-translational pathway by which mitochondrial enzymes involved in all aspects of cardiac energy metabolism can be regulated. Thus, we will also discuss the effect of acetylation of metabolic enzymes on myocardial energy substrate preference in the settings of heart failure. Finally, we will focus on pharmacological interventions that target enzymes involved in fatty acid uptake, fatty acid oxidation, transcriptional regulation of fatty acid oxidation, and glucose oxidation to treat heart failure. PMID:26166604

  9. Myocardial Energy Substrate Metabolism in Heart Failure : from Pathways to Therapeutic Targets.

    PubMed

    Fukushima, Arata; Milner, Kenneth; Gupta, Abhishek; Lopaschuk, Gary D

    2015-01-01

    Despite recent advances in therapy, heart failure remains a major cause of mortality and morbidity and is a growing healthcare burden worldwide. Alterations in myocardial energy substrate metabolism are a hallmark of heart failure, and are associated with an energy deficit in the failing heart. Previous studies have shown that a metabolic shift from mitochondrial oxidative metabolism to glycolysis, as well as an uncoupling between glycolysis and glucose oxidation, plays a crucial role in the development of cardiac inefficiency and functional impairment in heart failure. Therefore, optimizing energy substrate utilization, particularly by increasing mitochondrial glucose oxidation, can be a potentially promising approach to decrease the severity of heart failure by improving mechanical cardiac efficiency. One approach to stimulating myocardial glucose oxidation is to inhibit fatty acid oxidation. This review will overview the physiological regulation of both myocardial fatty acid and glucose oxidation in the heart, and will discuss what alterations in myocardial energy substrate metabolism occur in the failing heart. Furthermore, lysine acetylation has been recently identified as a novel post-translational pathway by which mitochondrial enzymes involved in all aspects of cardiac energy metabolism can be regulated. Thus, we will also discuss the effect of acetylation of metabolic enzymes on myocardial energy substrate preference in the settings of heart failure. Finally, we will focus on pharmacological interventions that target enzymes involved in fatty acid uptake, fatty acid oxidation, transcriptional regulation of fatty acid oxidation, and glucose oxidation to treat heart failure.

  10. Biochemical Markers of Myocardial Damage

    PubMed Central

    2016-01-01

    Heart diseases, especially coronary artery diseases (CAD), are the leading causes of morbidity and mortality in developed countries. Effective therapy is available to ensure patient survival and to prevent long term sequelae after an acute ischemic event caused by CAD, but appropriate therapy requires rapid and accurate diagnosis. Research into the pathology of CAD have demonstrated the usefulness of measuring concentrations of chemicals released from the injured cardiac muscle can aid the diagnosis of diseases caused by myocardial ischemia. Since the mid-1950s successively better biochemical markers have been described in research publications and applied for the clinical diagnosis of acute ischemic myocardial injury. Aspartate aminotransferase of the 1950s was replaced by other cytosolic enzymes such as lactate dehydrogenase, creatine kinase and their isoenzymes that exhibited better cardiac specificity. With the availability of immunoassays, other muscle proteins, that had no enzymatic activity, were also added to the diagnostic arsenal but their limited tissue specificity and sensitivity lead to suboptimal diagnostic performance. After the discovery that cardiac troponins I and T have the desired specificity, they have replaced the cytosolic enzymes in the role of diagnosing myocardial ischemia and infarction. The use of the troponins provided new knowledge that led to revision and redefinition of ischemic myocardial injury as well as the introduction of biochemicals for estimation of the probability of future ischemic myocardial events. These markers, known as cardiac risk markers, evolved from the diagnostic markers such as CK-MB or troponins, but markers of inflammation also belong to these groups of diagnostic chemicals. This review article presents a brief summary of the most significant developments in the field of biochemical markers of cardiac injury and summarizes the most recent significant recommendations regarding the use of the cardiac markers in

  11. Myocardial disarray. A critical review.

    PubMed Central

    Becker, A E; Caruso, G

    1982-01-01

    Myocardial disarray or disorganisation is at present a contentious topic, not least because its value as a clinical marker for hypertrophic cardiomyopathy has changed considerably over the years. Initially observed as one of the features of asymmetric septal hypertrophy, disarray has since been promoted as its pathognomonic histological feature, regarded by some observers as the morphological manifestation of a genetically transmitted myocardial defect. Recently, however, it has become evident that myocardial disarray is not limited to hypertrophic cardiomyopathy, but is encountered in hearts with both congenital and acquired conditions, and is also observed in normal hearts. The specificity of disarray for hypertrophic cardiomyopathy is thus seriously questioned. Latterly, it has been suggested that disarray, judged from through-and-through sections of the ventricular midseptum is a highly specific and sensitive marker of hypertrophic cardiomyopathy when considered in quantitative rather than qualitative fashion. The present study sets out to answer the question whether disarray could be the histological expression of the normal but intricate fibre architecture of the heart, a consideration also initiated by debatable definitions of normality and abnormality of myocardial histology. Gross fibre dissections in five normal hearts showed that many sites occurred in which disarray was a natural phenomenon. In five more hearts it was found that the plane of section of a tissue block might profoundly influence the histology. In fact, tissue cubicles sampled from different faces showed a change in histology in the vast majority. Thus the diagnostic significance of myocardial disarray as a marker of hypertrophic cardiomyopathy in the clinical setting almost vanishes; a change in orientation of a tissue section may actually turn "normality" into "disarray". Images PMID:7044398

  12. Biochemical Markers of Myocardial Damage.

    PubMed

    Bodor, Geza S

    2016-04-01

    Heart diseases, especially coronary artery diseases (CAD), are the leading causes of morbidity and mortality in developed countries. Effective therapy is available to ensure patient survival and to prevent long term sequelae after an acute ischemic event caused by CAD, but appropriate therapy requires rapid and accurate diagnosis. Research into the pathology of CAD have demonstrated the usefulness of measuring concentrations of chemicals released from the injured cardiac muscle can aid the diagnosis of diseases caused by myocardial ischemia. Since the mid-1950s successively better biochemical markers have been described in research publications and applied for the clinical diagnosis of acute ischemic myocardial injury. Aspartate aminotransferase of the 1950s was replaced by other cytosolic enzymes such as lactate dehydrogenase, creatine kinase and their isoenzymes that exhibited better cardiac specificity. With the availability of immunoassays, other muscle proteins, that had no enzymatic activity, were also added to the diagnostic arsenal but their limited tissue specificity and sensitivity lead to suboptimal diagnostic performance. After the discovery that cardiac troponins I and T have the desired specificity, they have replaced the cytosolic enzymes in the role of diagnosing myocardial ischemia and infarction. The use of the troponins provided new knowledge that led to revision and redefinition of ischemic myocardial injury as well as the introduction of biochemicals for estimation of the probability of future ischemic myocardial events. These markers, known as cardiac risk markers, evolved from the diagnostic markers such as CK-MB or troponins, but markers of inflammation also belong to these groups of diagnostic chemicals. This review article presents a brief summary of the most significant developments in the field of biochemical markers of cardiac injury and summarizes the most recent significant recommendations regarding the use of the cardiac markers in

  13. [Mechanisms of delayed myocardial enhancement and value of MR and CT contrast materials in the evaluation of myocardial viability].

    PubMed

    Jacquier, A; Revel, D; Croisille, P; Gaubert, J Y; Saeed, M

    2010-01-01

    The purpose of this article is to present a brief theoretical review of the models characterizing delayed myocardial enhancement applicable to both MR and CT imaging, review the different characteristics of commercially available gadolinium-based and iodinated contrast materials, and summarize the literature on the potential value of dedicated MR imaging contrast currently in development for the diagnosis of myocardial viability. The intensity of myocardial enhancement following infarction is related to two factors: expansion of the interstitial volume (15+/-2% in normal myocardium and 80+/-3% within necrosis) secondary to cell necrosis and perfusion abnormalities due to the absence of revascularization or lesions to the microcirculation. A kinetic model of contrast material properties within myocardium could be constructed from Kety's equation with regards to enhancement within the different myocardial tissues (viable myocardium, necrotic myocardium, fibrosis, no-reflow zones, stunned or hibernating myocardium). This model can be applied to both CT and MR since clinically available contrast agents are extracellular, inert and kinetically comparable. The development of dedicated contrast agents for viability and necrosis or molecular contrast agents open new horizons for preclinical research. PMID:20814358

  14. Recovery of regional myocardial dysfunction after successful coronary angioplasty early after a non-Q wave myocardial infarction

    SciTech Connect

    Suryapranata, H.; Serruys, P.W.; Beatt, K.; De Feyter, P.J.; van den Brand, M.; Roelandt, J. )

    1990-08-01

    More aggressive therapy has been suggested for patients who have a non-Q wave myocardial infarction (MI) because of the frequency of subsequent unstable angina, recurrent MI, and high mortality rate compared to patients with Q wave MI. The present study was undertaken to investigate the effect of coronary angioplasty on regional myocardial function of the infarct zone in patients with angina early after a non-Q wave MI. The study population consisted of 36 patients undergoing successful coronary angioplasty within 30 days of a non-Q wave MI, in whom sequential left ventricular angiograms of adequate quality were obtained before the initial procedure and at follow-up angiography. The global ejection fraction increased significantly from 60 +/- 9% to 67 +/- 6% (p = 0.0003). This significant increase in the global ejection fraction was primarily due to a significant improvement in the regional myocardial function of the infarct zone. The results of the present study show not only that ischemic attacks early after a non-Q wave MI may lead to prolonged regional myocardial dysfunction but more important that this depressed myocardium has the potential to achieve normal contraction after successful coronary angioplasty.

  15. Myocardial Tissue Remodeling in Adolescent Obesity

    PubMed Central

    Shah, Ravi V.; Abbasi, Siddique A.; Neilan, Tomas G.; Hulten, Edward; Coelho‐Filho, Otavio; Hoppin, Alison; Levitsky, Lynne; de Ferranti, Sarah; Rhodes, Erinn T.; Traum, Avram; Goodman, Elizabeth; Feng, Henry; Heydari, Bobak; Harris, William S.; Hoefner, Daniel M.; McConnell, Joseph P.; Seethamraju, Ravi; Rickers, Carsten; Kwong, Raymond Y.; Jerosch‐Herold, Michael

    2013-01-01

    Background Childhood obesity is a significant risk factor for cardiovascular disease in adulthood. Although ventricular remodeling has been reported in obese youth, early tissue‐level markers within the myocardium that precede organ‐level alterations have not been described. Methods and Results We studied 21 obese adolescents (mean age, 17.7±2.6 years; mean body mass index [BMI], 41.9±9.5 kg/m2, including 11 patients with type 2 diabetes [T2D]) and 12 healthy volunteers (age, 15.1±4.5 years; BMI, 20.1±3.5 kg/m2) using biomarkers of cardiometabolic risk and cardiac magnetic resonance imaging (CMR) to phenotype cardiac structure, function, and interstitial matrix remodeling by standard techniques. Although left ventricular ejection fraction and left atrial volumes were similar in healthy volunteers and obese patients (and within normal body size‐adjusted limits), interstitial matrix expansion by CMR extracellular volume fraction (ECV) was significantly different between healthy volunteers (median, 0.264; interquartile range [IQR], 0.253 to 0.271), obese adolescents without T2D (median, 0.328; IQR, 0.278 to 0.345), and obese adolescents with T2D (median, 0.376; IQR, 0.336 to 0.407; P=0.0001). ECV was associated with BMI for the entire population (r=0.58, P<0.001) and with high‐sensitivity C‐reactive protein (r=0.47, P<0.05), serum triglycerides (r=0.51, P<0.05), and hemoglobin A1c (r=0.76, P<0.0001) in the obese stratum. Conclusions Obese adolescents (particularly those with T2D) have subclinical alterations in myocardial tissue architecture associated with inflammation and insulin resistance. These alterations precede significant left ventricular hypertrophy or decreased cardiac function. PMID:23963758

  16. Myocardial mechanics in aortic and mitral valvular regurgitation: the concept of instantaneous impedance as a determinant of the performance of the intact heart

    PubMed Central

    Urschel, Charles W.; Covell, James W.; Sonnenblick, Edmund H.; Ross, John; Braunwald, Eugene

    1968-01-01

    The effects on myocardial mechanics of acute, artificial aortic and mitral regurgitation were studied in the dog to determine the manner in which the changes in load induced by valvular regurgitation alter ventricular performance. With mitral and aortic regurgitant volumes of approximately the same magnitude as the forward stroke volume, immediate increases occurred in total stroke volume, left ventricular enddiastolic pressure, and peak ejection velocity, whereas contractility remained unchanged. Although calculated myocardial fiber tension rose, the rate of decline of tension during ejection was accelerated with regurgitation due to the more rapid decrease in ventricular size. Average tension therefore decreased relative to average pressure. As a consequence of the increased fiber length and this unloading, contractile element velocity, work, and power were increased. Despite unchanged contractility of the myocardium, the ejection fraction rose with both aortic and mitral regurgitation. When regurgitant beats were compared with control beats at a constant end-diastolic volume, ventricular stroke volume, work, power, and ejection fraction, as well as contractile element velocity, work, and power consistently increased. Thus, reduction of instantaneous impedance to ejection allowed the ventricle to empty further, reducing ventricular wall tension with a resultant increase in the velocity of shortening. External energy output was increased despite unchanged contractility and diastolic fiber length. It is concluded that the impedance to ejection and myocardial fiber tension during ejection govern the velocity and extent of contractile element shortening, and hence affect stroke volume, peak aortic flow rate, and ejection fraction. The alterations of ventricular function accompanying valvular regurgitation can be explained by an evaluation of the effects of these lesions on the instantaneous impedance to left ventricular ejection. Images PMID:5641623

  17. Caffeine reduces myocardial blood flow during exercise.

    PubMed

    Higgins, John P; Babu, Kavita M

    2013-08-01

    Caffeine consumption has been receiving increased interest from both the medical and lay press, especially given the increased amounts now available in energy products. Acute ingestion of caffeine usually increases cardiac work; however, caffeine impairs the expected proportional increase in myocardial blood flow to match this increased work of the heart, most notably during exercise. This appears to be mainly due to caffeine's effect on blocking adenosine-induced vasodilatation in the coronary arteries in normal healthy subjects. This review summarizes the available medical literature specifically relating to pure caffeine tablet ingestion and reduced exercise coronary blood flow, and suggests possible mechanisms. Further studies are needed to evaluate this effect for other common caffeine-delivery systems, including coffee, energy beverages, and energy gels, which are often used for exercise performance enhancement, especially in teenagers and young athletes.

  18. Regenerating functional heart tissue for myocardial repair

    PubMed Central

    Alcon, Andre; Bozkulak, Esra Cagavi; Qyang, Yibing

    2012-01-01

    Heart disease is one of the leading causes of death worldwide and the number of patients with the disease is likely to grow with the continual decline in health for most of the developed world. Heart transplantation is one of the only treatment options for heart failure due to an acute myocardial infarction, but limited donor supply and organ rejection limit its widespread use. Cellular cardiomyoplasty, or cellular implantation, combined with various tissue-engineering methods aims to regenerate functional heart tissue. This review highlights the numerous cell sources that have been used to regenerate the heart as well as cover the wide range of tissue-engineering strategies that have been devised to optimize the delivery of these cells. It will probably be a long time before an effective regenerative therapy can make a serious impact at the bedside. PMID:22388688

  19. Acute myocardial infarction in the obstetric patient.

    PubMed

    Firoz, Tabassum; Magee, Laura A

    2012-06-01

    Acute myocardial infraction (AMI) in the obstetric patient is a rare event, although the incidence is rising due to advancing maternal age and pre-existing cardiac risk factors and medical co-morbidities. While atherosclerotic disease is the leading cause of AMI, coronary artery dissection is an important consideration in pregnancy and in the postpartum period. The physiological changes of pregnancy as well as pregnancy-specific risk factors can predispose the obstetric patient to AMI. Diagnosis of AMI can be challenging as symptoms may be atypical. Furthermore, diagnostic tests must be interpreted in the context of pregnancy. While the overall management of the obstetric patient with AMI is similar to that outside of pregnancy, drug therapy requires modification as some medications may be contraindicated in pregnancy and breastfeeding. There is limited information about prognosis and risk stratification but it is anticipated that future studies will address this issue.

  20. Caffeine reduces myocardial blood flow during exercise.

    PubMed

    Higgins, John P; Babu, Kavita M

    2013-08-01

    Caffeine consumption has been receiving increased interest from both the medical and lay press, especially given the increased amounts now available in energy products. Acute ingestion of caffeine usually increases cardiac work; however, caffeine impairs the expected proportional increase in myocardial blood flow to match this increased work of the heart, most notably during exercise. This appears to be mainly due to caffeine's effect on blocking adenosine-induced vasodilatation in the coronary arteries in normal healthy subjects. This review summarizes the available medical literature specifically relating to pure caffeine tablet ingestion and reduced exercise coronary blood flow, and suggests possible mechanisms. Further studies are needed to evaluate this effect for other common caffeine-delivery systems, including coffee, energy beverages, and energy gels, which are often used for exercise performance enhancement, especially in teenagers and young athletes. PMID:23764265

  1. Urinary Amino Acid Alterations in 3-Year-Old Children with Neurodevelopmental Effects due to Perinatal Dioxin Exposure in Vietnam: A Nested Case-Control Study for Neurobiomarker Discovery

    PubMed Central

    Nishijo, Muneko; Tai, Pham The; Anh, Nguyen Thi Nguyet; Nghi, Tran Ngoc; Nakagawa, Hideaki; Van Luong, Hoang; Anh, Tran Hai; Morikawa, Yuko; Waseda, Tomoo; Kido, Teruhiko; Nishijo, Hisao

    2015-01-01

    In our previous study of 3-year-old children in a dioxin contamination hot spot in Vietnam, the high total dioxin toxic equivalent (TEQ-PCDDs/Fs)-exposed group during the perinatal period displayed lower Bayley III neurodevelopmental scores, whereas the high 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-exposed group displayed increased autistic traits. In autistic children, urinary amino acid profiles have revealed metabolic alterations in the amino acids that serve as neurotransmitters in the developing brain. Therefore, our present study aimed to investigate the use of alterations in urinary amino acid excretion as biomarkers of dioxin exposure-induced neurodevelopmental deficits in highly exposed 3-year-old children in Vietnam. A nested case-control study of urinary analyses was performed for 26 children who were selected from 111 3-year-old children whose perinatal dioxin exposure levels and neurodevelopmental status were examined in follow-up surveys conducted in a dioxin contaminated hot spot. We compared urinary amino acid levels between the following 4 groups: (1) a high TEQ-PCDDs/Fs and high TCDD-exposed group; (2) a high TEQ-PCDDs/Fs but low TCDD-exposed group; (3) a low TEQ-PCDDs/Fs exposed and poorly developed group; and (4) a low TEQ-PCDDs/Fs exposed and well-developed group. Urinary levels of histidine and tryptophan were significantly decreased in the high TEQ-PCDDs/Fs and high TCDD group, as well as in the high TEQ-PCDDs/Fs but low TCDD group, compared with the low TEQ-PCDDs/Fs and well-developed group. However, the ratio of histidine to glycine was significantly lower only in the high TEQ-PCDDs/Fs and high TCDD group. Furthermore, urinary histidine levels and the ratio of histidine to glycine were significantly correlated with neurodevelopmental scores, particularly for language and fine motor skills. These results indicate that urinary histidine is specifically associated with dioxin exposure-induced neurodevelopmental deficits, suggesting that

  2. Myocardial viability in patients with chronic coronary artery disease and previous myocardial infarction: comparison of myocardial contrast echocardiography and myocardial perfusion scintigraphy.

    PubMed

    Vernon, S; Kaul, S; Powers, E R; Camarano, G; Gimple, L W; Ragosta, M

    1997-11-01

    The aim of this study was to compare perfusion patterns on myocardial contrast echocardiography with those on myocardial perfusion scintigraphy for the assessment of myocardial viability in patients with previous myocardial infarction. Accordingly, perfusion scores with the two techniques were compared in 91 ventricular regions in 21 patients with previous (>6 weeks old) myocardial infarction. Complete concordance between the two techniques was found in 63 (69%) regions; 25 (27%) regions were discordant by only 1 grade, and complete discordance (2 grades) was found in only 3 (3%) regions. A kappa statistic of 0.65 indicated good concordance between the two techniques. Although the scores on both techniques demonstrated a relation with the wall motion score, the correlation between the myocardial contrast echocardiography and wall motion scores was closer (r = -0.63 vs r = -0.50, p = 0.05). It is concluded that myocardial contrast echocardiography provides similar information regarding myocardial viability as myocardial perfusion scintigraphy in patients with coronary artery disease and previous myocardial infarction.

  3. In vivo induction of antioxidant response and oxidative stress associated with genotoxicity and histopathological alteration in two commercial fish species due to heavy metals exposure in northern India (Kali) river.

    PubMed

    Fatima, Mahino; Usmani, Nazura; Firdaus, Fakiha; Zafeer, Mohammad Faraz; Ahmad, Shafeeque; Akhtar, Kafil; Dawar Husain, S M; Ahmad, Mir Hilal; Anis, Ehraz; Mobarak Hossain, M

    2015-01-01

    Heavy metals can significantly bioaccumulate in fish tissues. The step wise mechanism of heavy metal toxicities on fish health is still limited. The present study assessed the tissue-specific antioxidant response and oxidative stress biomarkers of commercially important fish species namely, Channa striatus and Heteropneustes fossilis inhabiting Kali River of northern India where heavy-metal load is beyond the World Health Organisation - maximum permissible limits. Heavy metals chromium (Cr), nickel (Ni), lead (Pb) and cadmium (Cd) were elevated in both fish species compared to recommended values of the Federal Environmental Protection Agency (FEPA), 1999 for edible fishes. Reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CATA) activities in all tissues (brachial, neural, renal and hepatic) were altered. Cellular lipid and protein compromisation in both fishes induced by heavy metals was determined by lipid peroxidation (LPO) and protein carbonylation (PC) assays. Micronucleus (MN) test of erythrocytes and comet assay of liver cells confirmed genotoxicity. Histopathology of the liver, kidney and brain of affected fishes was distorted significantly with its reference fishes thereby affecting the quality and quantity of these fish stocks. This raises a serious concern as these fishes are consumed by the local population which would ultimately affect human health. PMID:26191657

  4. In vivo induction of antioxidant response and oxidative stress associated with genotoxicity and histopathological alteration in two commercial fish species due to heavy metals exposure in northern India (Kali) river.

    PubMed

    Fatima, Mahino; Usmani, Nazura; Firdaus, Fakiha; Zafeer, Mohammad Faraz; Ahmad, Shafeeque; Akhtar, Kafil; Dawar Husain, S M; Ahmad, Mir Hilal; Anis, Ehraz; Mobarak Hossain, M

    2015-01-01

    Heavy metals can significantly bioaccumulate in fish tissues. The step wise mechanism of heavy metal toxicities on fish health is still limited. The present study assessed the tissue-specific antioxidant response and oxidative stress biomarkers of commercially important fish species namely, Channa striatus and Heteropneustes fossilis inhabiting Kali River of northern India where heavy-metal load is beyond the World Health Organisation - maximum permissible limits. Heavy metals chromium (Cr), nickel (Ni), lead (Pb) and cadmium (Cd) were elevated in both fish species compared to recommended values of the Federal Environmental Protection Agency (FEPA), 1999 for edible fishes. Reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CATA) activities in all tissues (brachial, neural, renal and hepatic) were altered. Cellular lipid and protein compromisation in both fishes induced by heavy metals was determined by lipid peroxidation (LPO) and protein carbonylation (PC) assays. Micronucleus (MN) test of erythrocytes and comet assay of liver cells confirmed genotoxicity. Histopathology of the liver, kidney and brain of affected fishes was distorted significantly with its reference fishes thereby affecting the quality and quantity of these fish stocks. This raises a serious concern as these fishes are consumed by the local population which would ultimately affect human health.

  5. [Perioperative myocardial ischemia in patients with peripheral arterial occlusive diseases].

    PubMed

    Rapp, H J; Buselmeier, P; Gasteiger, P; Hoberg, E; Striebel, J P

    1990-04-01

    Patients with peripheral vascular disease (PVD) often have coronary artery disease (CAD) which means an increased risk during anesthesia. The prevalence of CAD is nearly 50% among such patients. Owing to claudication, diagnostic stress tests can rarely be performed in PVD patients. In order to evaluate the frequency of transient perioperative myocardial ischemia, Holter monitoring was performed in 30 consecutive PVD patients with ASA II-III and AVK scale (Fontaine) II-IV who were undergoing femoropopliteal bypass surgery. Patients who had left bundle branch block and left ventricular hypertrophy or were taking digitalis medication were excluded from Holter monitoring. The ST-segment analysis of the frequency modulated recordings (n = 19) revealed episodes of myocardial ischemia in 26% of the patients. Most (75%) of the episodes occurred preoperatively, and 25%, during or after the anesthesia or during preparation for it. Risk factors for CAD were more often found in patients with ST segment alterations than in patients without ST segment deviations, even though the preoperative antianginal medication administered was comparable in the two subgroups. It is concluded that in a considerable subset of PVD patients silent myocardial ischemia occurs, which can be related to the different perioperative intervals by means of ST segment analyses of Holter recordings. The ST segment may allow a better insight into the cardiac state of PVD patients. Further studies are necessary in larger populations to test our suspicion.

  6. Chasing myocardial outcomes: perioperative myocardial infarction and cardiac troponin.

    PubMed

    Royo, Marc B; Fleisher, Lee A

    2016-02-01

    Perioperative myocardial infarction represents the most common cardiovascular complication following non-cardiac surgery, but frequently presents without the usual clinical signs and symptoms consistent with acute coronary syndrome. Given the silent nature of this event, a clinician's reliance on risk stratification tools and cardiac specific biomarkers to assist in the identification of at-risk individuals is heightened in the perioperative setting. Although cardiac troponin elevations following non-cardiac surgery have been consistently linked to increased mortality, uncertainty remains over how to clinically intervene to prevent harm. This decision is further complicated by the increasing sensitivity of the newest generation of cardiac biomarker immunoassays. In this narrative review, the growing body of evidence surrounding cardiac troponin elevations in the perioperative setting, how the evidence has been integrated into recent clinical practice guidelines, and its implications for the detection of perioperative myocardial infarction are discussed. PMID:26634279

  7. Electrotonic remodeling following myocardial infarction in dogs susceptible and resistant to sudden cardiac death.

    PubMed

    Del Rio, Carlos L; McConnell, Patrick I; Kukielka, Monica; Dzwonczyk, Roger; Clymer, Bradley D; Howie, Michael B; Billman, George E

    2008-02-01

    Passive electrical remodeling following myocardial infarction (MI) is well established. These changes can alter electrotonic loading and trigger the remodeling of repolarization currents, a potential mechanism for ventricular fibrillation (VF). However, little is known about the role of passive electrical markers as tools to identify VF susceptibility post-MI. This study investigated electrotonic remodeling in the post-MI ventricle, as measured by myocardial electrical impedance (MEI), in animals prone to and resistant to VF. MI was induced in dogs by a two-stage left anterior descending (LAD) coronary artery ligation. Before infarction, MEI electrodes were placed in remote (left circumflex, LCX) and infarcted (LAD) myocardium. MEI was measured in awake animals 1, 2, 7, and 21 days post-MI. Subsequently, VF susceptibility was tested by a 2-min LCX occlusion during exercise; 12 animals developed VF (susceptible, S) and 12 did not (resistant, R). The healing infarct had lower MEI than the normal myocardium. This difference was stable by day 2 post-MI (287 +/- 32 Omega vs. 425 +/- 62 Omega, P < 0.05). Significant differences were observed between resistant and susceptible animals 7 days post-MI; susceptible dogs had a wider electrotonic gradient between remote and infarcted myocardium (R: 89 +/- 60 Omega vs. S: 180 +/- 37 Omega). This difference increased over time in susceptible animals (252 +/- 53 Omega at 21 days) due to post-MI impedance changes on the remote myocardium. These data suggest that early electrotonic changes post-MI could be used to assess later arrhythmia susceptibility. In addition, passive-electrical changes could be a mechanism driving active-electrical remodeling post-MI, thereby facilitating the induction of arrhythmias.

  8. [Myocardial infarction caused by exertion].

    PubMed

    Bernard, F; Weber, S

    1997-01-01

    Myocardial infarction is the main cause of sudden death during physical exercise, particularly in subjects over 40 and may even occur in high-performance young athletes. Sports and physical activity have a beneficial effect in preventing cardiovascular diseases, but certain rules of prudence must be followed to avoid the risk of a severe coronary event. Myocardial infarction always occurs in particularly susceptible subjects with several risk factors, predominantly smoking, hypercholesterolemia, family history of atherosclerosis. Dietary factors, either before, during or after the exercise, are always found. Distribution of coronary lesions differs with age. Before 40 years, the coronary network is normal in 40% of the cases. The infarction is partially explained by platelet hyperaggregahility and coronary spasms at exercise or in the post-exercise period.

  9. Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential.

    PubMed

    Heymans, Stephane; González, Arantxa; Pizard, Anne; Papageorgiou, Anna P; López-Andrés, Natalia; Jaisser, Frédéric; Thum, Thomas; Zannad, Faiez; Díez, Javier

    2015-08-01

    Myocardial fibrosis is the result of excessive fibrillar collagen synthesis and deposition without reciprocally balanced degradation. It causes cardiac dysfunction, arrhythmias, and ischaemia, and thereby determines the clinical course and outcome of cardiac patients even when adequately treated. Therefore, further research is needed to identify and better understand the factors that trigger and maintain the myocardial fibrotic response against different injuries in a variety of cardiac diseases. Here, we will focus on the following major areas of research: molecules that stimulate the differentiation of fibroblasts into myofibroblasts and subsequently alter collagen turnover (e.g. cardiotrophin-1, galectin-3, NADPH oxidases, and neutrophil gelatinase-associated lipocalin), microRNA-induced alterations of collagen gene expression, and matricellular protein- and lysyl oxidase-mediated alterations of collagen cross-linking and deposition.

  10. Myocardialization of the cardiac outflow tract

    NASA Technical Reports Server (NTRS)

    van den Hoff, M. J.; Moorman, A. F.; Ruijter, J. M.; Lamers, W. H.; Bennington, R. W.; Markwald, R. R.; Wessels, A.

    1999-01-01

    During development, the single-circuited cardiac tube transforms into a double-circuited four-chambered heart by a complex process of remodeling, differential growth, and septation. In this process the endocardial cushion tissues of the atrioventricular junction and outflow tract (OFT) play a crucial role as they contribute to the mesenchymal components of the developing septa and valves in the developing heart. After fusion, the endocardial ridges in the proximal portion of the OFT initially form a mesenchymal outlet septum. In the adult heart, however, this outlet septum is basically a muscular structure. Hence, the mesenchyme of the proximal outlet septum has to be replaced by cardiomyocytes. We have dubbed this process "myocardialization." Our immunohistochemical analysis of staged chicken hearts demonstrates that myocardialization takes place by ingrowth of existing myocardium into the mesenchymal outlet septum. Compared to other events in cardiac septation, it is a relatively late process, being initialized around stage H/H28 and being basically completed around stage H/H38. To unravel the molecular mechanisms that are responsible for the induction and regulation of myocardialization, an in vitro culture system in which myocardialization could be mimicked and manipulated was developed. Using this in vitro myocardialization assay it was observed that under the standard culture conditions (i) whole OFT explants from stage H/H20 and younger did not spontaneously myocardialize the collagen matrix, (ii) explants from stage H/H21 and older spontaneously formed extensive myocardial networks, (iii) the myocardium of the OFT could be induced to myocardialize and was therefore "myocardialization-competent" at all stages tested (H/H16-30), (iv) myocardialization was induced by factors produced by, most likely, the nonmyocardial component of the outflow tract, (v) at none of the embryonic stages analyzed was ventricular myocardium myocardialization-competent, and finally

  11. Pharmacology of myocardial calcium-handling.

    PubMed

    Vogler, Julia; Eckardt, Lars

    2012-07-01

    Disturbed myocardial calcium (Ca(+)) handling is one of the pathophysiologic hallmarks of cardiovascular diseases such as congestive heart failure, cardiac hypertrophy, and certain types of tachyarrhythmias. Pharmacologic treatment of these diseases thus focuses on restoring myocardial Ca(2+) homeostasis by interacting with Ca(2+)-dependent signaling pathways. In this article, we review the currently used pharmacologic agents that are able to restore or maintain myocardial Ca(2+) homeostasis and their mechanism of action as well as emerging new substances.

  12. Tombstoning ST-Elevation Myocardial Infarction

    PubMed Central

    Balci, Bahattin

    2009-01-01

    Tombstoning ST elevation myocardial infarction can be described as a STEMI characterized by tombstoning ST-segment elevation. This myocardial infarction is associated with extensive myocardial damage, reduced left ventricle function, serious hospital complications and poor prognosis. Tombstoning ECG pattern is a notion beyond morphological difference and is associated with more serious clinical results. Despite the presence of a few reports on tombstoning ST elevation, there is no report which reviews STEMI demonstrating this electrocardiographic pattern. PMID:21037844

  13. Echocardiographic assessment of myocardial strain.

    PubMed

    Gorcsan, John; Tanaka, Hidekazu

    2011-09-27

    Echocardiographic strain imaging, also known as deformation imaging, has been developed as a means to objectively quantify regional myocardial function. First introduced as post-processing of tissue Doppler imaging velocity converted to strain and strain rate, strain imaging has more recently also been derived from digital speckle tracking analysis. Strain imaging has been used to gain greater understanding into the pathophysiology of cardiac ischemia and infarction, primary diseases of the myocardium, and the effects of valvular disease on myocardial function, and to advance our understanding of diastolic function. Strain imaging has also been used to quantify abnormalities in the timing of mechanical activation for heart failure patients undergoing cardiac resynchronization pacing therapy. Further advances, such as 3-dimensional speckle tracking strain imaging, have emerged to provide even greater insight. Strain imaging has become established as a robust research tool and has great potential to play many roles in routine clinical practice to advance the care of the cardiovascular patient. This perspective reviews the physiology of myocardial strain, the technical features of strain imaging using tissue Doppler imaging and speckle tracking, their strengths and weaknesses, and the state-of-the-art present and potential future clinical applications.

  14. Myocardial Infarction in the Elderly

    PubMed Central

    Carro, Amelia; Kaski, Juan Carlos

    2011-01-01

    Advances in pharmacological treatment and effective early myocardial revascularization have –in recent years- led to improved clinical outcomes in patients with acute myocardial infarction (AMI). However, it has been suggested that compared to younger subjects, elderly AMI patients are less likely to receive evidence-based treatment, including myocardial revascularization therapy. Several reasons have been postulated to explain this trend, including uncertainty regarding the true benefits of the interventions commonly used in this setting as well as increased risk mainly associated with comorbidities. The diagnosis, management, and post-hospitalization care of elderly patients presenting with an acute coronary syndrome pose many difficulties at present. A complex interplay of variables such as comorbidities, functional and socioeconomic status, side effects associated with multiple drug administration, and individual biologic variability, all contribute to creating a complex clinical scenario. In this complex setting, clinicians are often required to extrapolate evidence-based results obtained in cardiovascular trials from which older patients are often, implicitly or explicitly, excluded. This article reviews current recommendations regarding management of AMI in the elderly. PMID:22396870

  15. Cocaine, a risk factor for myocardial infarction.

    PubMed

    Galasko, G I

    1997-06-01

    Cocaine usage goes back thousands of years, to the times of the Incas. Over the past 20 years, its use has increased dramatically, especially in America, and adverse cardiovascular reactions to the drug have begun to be reported. The first report of myocardial infarction temporally related to the recreational use of cocaine appeared in 1982. Since then, myocardial infarction has become recognized as the drug's most common cardiovascular consequence, with over 250 cases now documented in the literature. This review discusses the history of cocaine use, its pharmacology, the possible pathological mechanisms underlying the pathogenesis of myocardial ischaemia and infarction, and current ideas on the management of cocaine-induced myocardial infarction.

  16. Comparison of stress-only vs. stress/rest with technetium-99m methoxyisobutylisonitrile myocardial perfusion imaging.

    PubMed

    Worsley, D F; Fung, A Y; Coupland, D B; Rexworthy, C G; Sexsmith, G P; Lentle, B C

    1992-01-01

    Unlike conventional thallium-201 myocardial imaging, technetium-99m methoxyisobutylisonitrile (MIBI) requires separate stress and rest injections. We prospectively studied 148 consecutive patients referred for myocardial perfusion studies to determine the diagnostic value of rest images once normal exercise or dipyridamole tomographic images had been obtained. In patients referred with no history of previous myocardial infarction in whom the diagnosis of coronary artery disease was suspected, 45 of 109 (41%) patients had normal stress tomographic images. Obtaining rest images did not alter the final interpretation in any of these cases. From this we infer that in patients with normal images after exercise or dipyridamole administration and no past history of myocardial infarction, 99mTc-MIBI rest images are not required. This provides several advantages including increased speed of diagnosis, decreased patient radiation exposure, improved cost efficiency and decreased demand on tomographic camera time.

  17. Green tea extract given before regional myocardial ischemia-reperfusion in rats improves myocardial contractility by attenuating calcium overload.

    PubMed

    Liou, Ying-Ming; Hsieh, Shih-Rong; Wu, Tsu-Juey; Chen, Jan-Yow

    2010-11-01

    There is evidence for a negative correlation between green tea consumption and cardiovascular diseases. The aim of the present study was to examine whether green tea extract (GTE) given before regional myocardial ischemia could improve depression of myocardial contractility by preventing cytosolic Ca(2+) overload. Regional ischemia-reperfusion (IR) was induced in rats by ligating the left anterior descending branch for 20 min, then releasing the ligature. Ligation induced ventricular arrhythmias in rats without GTE pretreatment, but decreased arrhythmogenesis was seen in rats pretreated 30 min earlier with GTE (400 mg/kg). During reperfusion, arrhythmias only occurred during the initial 5 min, and GTE pretreatment had no effect. After overnight recovery, serum cTnI levels were greatly increased in control post-IR rats but only slightly elevated in GTE-pretreated post-IR rats. Myocardial contractility measured by echocardiography was still depressed after 3 days in control post-IR rats, but not in GTE-pretreated post-IR rats. No myocardial ischemic injury was seen in post-IR rats with or without GTE pretreatment. Using freshly isolated single heart myocytes, GTE was found to attenuate the post-IR injury-associated cytosolic Ca(2+) overload and modulate changes in the levels and distribution of myofibril, adherens junction, and gap junction proteins. In summary, GTE pretreatment protects cardiomyocytes from IR injury by preventing cytosolic Ca(2+) overload, myofibril disruption, and alterations in adherens and gap junction protein expression and distribution. PMID:20922441

  18. Simultaneously Presented Acute Ischemic Stroke and Non-ST Elevation Myocardial Infarction in a Patient with Paroxysmal Atrial Fibrillation

    PubMed Central

    Kim, Hack-Lyoung; Seo, Jae-Bin; Chung, Woo-Young; Zo, Joo-Hee; Kim, Myung-A

    2013-01-01

    Although atrial fibrillation is the most frequent cause of embolic stroke, coronary embolism from atrial fibrillation is a very rare cause of acute myocardial infarction. Therefore, simultaneously presented acute ischemic stroke and acute myocardial infarction due to atrial fibrillation in the same patient has not been documented. The present report describes the case of a 58-year-old man with paroxysmal atrial fibrillation who initially presented with a large cerebral infarction due to embolic occlusion of the left middle cerebral artery. Four hours after the diagnosis of cerebral embolism, he was subsequently diagnosed with acute myocardial infarction due to concurrent coronary embolism. He underwent successful coronary revascularization with a drug-eluting stent. The possibility of combined coronary embolism as a rare etiology should be kept in mind when a patient with acute embolic stroke presents, especially when there is evidence of acute myocardial infarction. PMID:24363753

  19. Regional Myocardial Substrate Uptake in Hypertensive Rats: A Quantitative Autoradiographic Measurement

    NASA Astrophysics Data System (ADS)

    Yonekura, Yoshiharu; Bertrand Brill, A.; Som, Prantika; Yamamoto, Kazutaka; Srivastava, Suresh C.; Iwai, Junichi; Elmaleh, David R.; Livni, Eli; Strauss, H. William; Goodman, Mark M.; Knapp, Furn F.

    1985-03-01

    Severe hypertension causes global and regional changes in myocardial perfusion and substrate utilization. Regional perfusion and fatty acid utilization were evaluated by dual-tracer autoradiography in normotensive and hypertensive rats of the Dahl strain. The regional distributions of perfusion and fatty acid utilization were homogeneous in normotensive rats. Severe hypertension was associated with a homogeneous pattern of regional perfusion, but fatty acid utilization was focally decreased in the free wall of the left ventricle. The decrease in fatty acid uptake was associated with a concomitant increase in glucose utilization. These findings suggest that severe hypertension is associated with uniform myocardial perfusion and focal alterations in the substrates used for the performance of myocardial work.

  20. EMPOWERING ADULT STEM CELLS FOR MYOCARDIAL REGENERATION

    PubMed Central

    Mohsin, Sadia; Siddiqi, Sailay; Collins, Brett; Sussman, Mark A.

    2012-01-01

    Treatment strategies for heart failure remain a high priority for ongoing research due to the profound unmet need in clinical disease coupled with lack of significant translational progress. The underlying issue is the same whether the cause is acute damage, chronic stress from disease, or aging: progressive loss of functional cardiomyocytes and diminished hemodynamic output. To stave off cardiomyocyte losses, a number of strategic approaches have been embraced in recent years involving both molecular and cellular approaches to augment myocardial structure and performance. Resultant excitement surrounding regenerative medicine in the heart has been tempered by realizations that reparative processes in the heart are insufficient to restore damaged myocardium to normal functional capacity and that cellular cardiomyoplasty is hampered by poor survival, proliferation, engraftment and differentiation of the donated population. To overcome these limitations, a combination of molecular and cellular approaches needs to be adopted involving use of genetic engineering to enhance resistance to cell death and increase regenerative capacity. This review will highlight biological properties of approached to potentiate stem cell-mediated regeneration to promote enhanced myocardial regeneration, persistence of donated cells, and long lasting tissue repair. Optimizing cell delivery and harnessing the power of survival signaling cascades for ex vivo genetic modification of stem cells prior to reintroduction into the patient will be critical to enhance the efficacy of cellular cardiomyoplasty. Once this goal is achieved, then cell-based therapy has great promise for treatment of heart failure to combat the loss of cardiac structure and function associated with acute damage, chronic disease or aging. PMID:22158649

  1. Multimodality imaging in the assessment of myocardial viability

    PubMed Central

    Partington, Sara L.; Kwong, Raymond Y.

    2014-01-01

    The prevalence of heart failure due to coronary artery disease continues to increase, and it portends a worse prognosis than non-ischemic cardiomyopathy. Revascularization improves prognosis in these high-risk patients who have evidence of viability; therefore, optimal assessment of myocardial viability remains essential. Multiple imaging modalities exist for differentiating viable myocardium from scar in territories with contractile dysfunction. Given the multiple modalities available, choosing the best modality for a specific patient can be a daunting task. In this review, the physiology of myocardial hibernation and stunning will be reviewed. All the current methods available for assessing viability including echocardiography, cardiac magnetic resonance imaging, nuclear imaging with single photon emission tomography and positron emission tomography imaging and cardiac computed tomography will be reviewed. The effectiveness of the various techniques will be compared, and the limitations of the current literature will be discussed. PMID:21069458

  2. Polycythemia vera presenting as acute myocardial infarction: An unusual presentation

    PubMed Central

    Bahbahani, Hussain; Aljenaee, Khaled; Bella, Abdelhaleem

    2014-01-01

    Acute myocardial infarction (AMI) is usually seen in the setting of atherosclerosis and its associated risk factors. Myocardial infarction in the young poses a particular challenge, as the disease is less likely, due to atherosclerosis. We report the case of a 37-year-old female patient who presented with ST segment elevation anterolateral AMI. The only abnormality on routine blood investigation was raised hemoglobin and hematocrit. After further testing, she was diagnosed according to the World Health Organization (WHO) criteria with polycythemia vera. This case illustrates the importance of recognizing polycythemia vera as an important cause of thrombosis, which can present initially as AMI, and to emphasize the early recognition of the disease in order to initiate appropriate management strategies. PMID:25544823

  3. Automatic Characterization of Myocardial Perfusion in Contrast Enhanced MRI

    NASA Astrophysics Data System (ADS)

    Positano, Vincenzo; Santarelli, Maria Filomena; Landini, Luigi

    2003-12-01

    The use of contrast medium in cardiac MRI allows joining the high-resolution anatomical information provided by standard magnetic resonance with functional information obtained by means of the perfusion of contrast agent in myocardial tissues. The current approach to perfusion MRI characterization is the qualitative one, based on visual inspection of images. Moving to quantitative analysis requires extraction of numerical indices of myocardium perfusion by analysis of time/intensity curves related to the area of interest. The main problem in quantitative image sequence analysis is the heart movement, mainly due to patient respiration. We propose an automatic procedure based on image registration, segmentation of the myocardium, and extraction and analysis of time/intensity curves. The procedure requires a minimal user interaction, is robust with respect to the user input, and allows effective characterization of myocardial perfusion. The algorithm was tested on cardiac MR images acquired from voluntaries and in clinical routine.

  4. Usefulness of MRI to demonstrate the mechanisms of myocardial ischemia in hypertrophic cardiomyopathy with myocardial bridge.

    PubMed

    Thomson, Vivien; Botnar, Rene; Croisille, Pierre

    2007-01-01

    We present a case of symptomatic primary hypertrophic cardiomyopathy (HCM) associated with myocardial bridging of the left anterior descending (LAD) artery and suspected ischemia that could be related either to LAD artery compression or to microvascular perfusion abnormalities. MRI demonstrated the morphological appearance of myocardial hypertrophy, and coronary MR angiography evidenced the myocardial bridge and its functional consequences with stress MR perfusion. In conclusion, as a non-invasive comprehensive imaging technique, MRI should be considered in identifying the mechanisms of myocardial ischemia in HCM with myocardial bridge. PMID:16888385

  5. Intestinal Microbial Metabolites Are Linked to Severity of Myocardial Infarction in Rats.

    PubMed

    Lam, Vy; Su, Jidong; Hsu, Anna; Gross, Garrett J; Salzman, Nita H; Baker, John E

    2016-01-01

    Intestinal microbiota determine severity of myocardial infarction in rats. We determined whether low molecular weight metabolites derived from intestinal microbiota and transported to the systemic circulation are linked to severity of myocardial infarction. Plasma from rats treated for seven days with the non-absorbed antibiotic vancomycin or a mixture of streptomycin, neomycin, polymyxin B and bacitracin was analyzed using mass spectrometry-based metabolite profiling platforms. Antibiotic-induced changes in the abundance of individual groups of intestinal microbiota dramatically altered the host's metabolism. Hierarchical clustering of dissimilarities separated the levels of 284 identified metabolites from treated vs. untreated rats; 193 were altered by the antibiotic treatments with a tendency towards decreased metabolite levels. Catabolism of the aromatic amino acids phenylalanine, tryptophan and tyrosine was the most affected pathway comprising 33 affected metabolites. Both antibiotic treatments decreased the severity of an induced myocardial infarction in vivo by 27% and 29%, respectively. We then determined whether microbial metabolites of the amino acids phenylalanine, tryptophan and tyrosine were linked to decreased severity of myocardial infarction. Vancomycin-treated rats were administered amino acid metabolites prior to ischemia/reperfusion studies. Oral or intravenous pretreatment of rats with these amino acid metabolites abolished the decrease in infarct size conferred by vancomycin. Inhibition of JAK-2 (AG-490, 10 μM), Src kinase (PP1, 20 μM), Akt/PI3 kinase (Wortmannin, 100 nM), p44/42 MAPK (PD98059, 10 μM), p38 MAPK (SB203580, 10 μM), or KATP channels (glibenclamide, 3 μM) abolished cardioprotection by vancomycin, indicating microbial metabolites are interacting with cell surface receptors to transduce their signals through Src kinase, cell survival pathways and KATP channels. These inhibitors have no effect on myocardial infarct size in

  6. Paricalcitol attenuates lipopolysaccharide-induced myocardial inflammation by regulating the NF-κB signaling pathway

    PubMed Central

    LEE, AE SIN; JUNG, YU JIN; THANH, TÙNG NGUYỄN; LEE, SIK; KIM, WON; KANG, KYUNG PYO; PARK, SUNG KWANG

    2016-01-01

    Vitamin D deficiency is associated with an increased risk of cardiovascular disease, diabetes, colon and breast cancer, infectious diseases and allergies. Vascular alterations are an important pathophysiological mechanism of sepsis. Experimental data suggest that paricalcitol, a vitamin D2 analogue, exerts beneficial effects on renal inflammation and fibrosis. In the present study, we aimed to investigate the effects of paricalcitol on lipopolysaccharide (LPS)-induced myocardial inflammation and to elucidate the underlying mechanisms. We used primary cultured human umbilical vein endothelial cells for in vitro experiments, in which stimulation with tumor necrosis factor (TNF)-α was used to induce endothelial cell inflammation. For in vivo experiments, myocardial inflammation was induced by an intraperitoneal injection of 15 mg/kg LPS into C57BL6 mice pre-treated with or without 0.2 µg/kg paricalcitol. Treatment with paricalcitol suppressed the TNF-α-induced increase in the protein expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and fractalkine in endothelial cells. Treatment with paricalcitol also decreased the TNF-α-induced nuclear factor (NF)-κB binding activity. In a mouse model of LPS-induced myocardial inflammation, pre-treatment with paricalcitol prevented the LPS-induced increase in the expression of myocardial ICAM-1, phosphorylated p65 and myocardial TNF-α. Pre-treatment with paricalcitol also alleviated endotoxemia-induced microvascular leakage in the myocardium. The findings of our study suggest that paricalcitol exerts a protective effect against LPS-induced myocardial inflammation by regulating the expression of cell adhesion molecules and TNF-α, and by improving myocardial permeability. PMID:26954764

  7. Paricalcitol attenuates lipopolysaccharide-induced myocardial inflammation by regulating the NF-κB signaling pathway.

    PubMed

    Lee, Ae Sin; Jung, Yu Jin; Thanh, Tùng Nguyễn; Lee, Sik; Kim, Won; Kang, Kyung Pyo; Park, Sung Kwang

    2016-04-01

    Vitamin D deficiency is associated with an increased risk of cardiovascular disease, diabetes, colon and breast cancer, infectious diseases and allergies. Vascular alterations are an important pathophysiological mechanism of sepsis. Experimental data suggest that paricalcitol, a vitamin D2 analogue, exerts beneficial effects on renal inflammation and fibrosis. In the present study, we aimed to investigate the effects of paricalcitol on lipopolysaccharide (LPS)-induced myocardial inflammation and to elucidate the underlying mechanisms. We used primary cultured human umbilical vein endothelial cells for in vitro experiments, in which stimulation with tumor necrosis factor (TNF)-α was used to induce endothelial cell inflammation. For in vivo experiments, myocardial inflammation was induced by an intraperitoneal injection of 15 mg/kg LPS into C57BL6 mice pre-treated with or without 0.2 µg/kg paricalcitol. Treatment with paricalcitol suppressed the TNF-α-induced increase in the protein expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and fractalkine in endothelial cells. Treatment with paricalcitol also decreased the TNF-α-induced nuclear factor (NF)-κB binding activity. In a mouse model of LPS-induced myocardial inflammation, pre-treatment with paricalcitol prevented the LPS-induced increase in the expression of myocardial ICAM-1, phosphorylated p65 and myocardial TNF-α. Pre-treatment with paricalcitol also alleviated endotoxemia‑induced microvascular leakage in the myocardium. The findings of our study suggest that paricalcitol exerts a protective effect against LPS-induced myocardial inflammation by regulating the expression of cell adhesion molecules and TNF-α, and by improving myocardial permeability. PMID:26954764

  8. Myocardial dysfunction and cardiovascular disease in type 2 diabetes.

    PubMed

    Ofstad, Anne Pernille

    2016-07-01

    Type 2 diabetes mellitus (T2DM) is strongly associated with increased risk of myocardial dysfunction and cardiovascular disease (CVD), two separate conditions which often co-exist and influence each other's course. The prevalence of myocardial dysfunction may be as high as 75% in T2DM populations but is often overlooked due to the initial asymptomatic nature of the disease, complicating co-morbidities such as coronary artery disease (CAD) and obesity, and the lack of consensus on diagnostic criteria. More sensitive echocardiographic applications are furthermore needed to improve detection of early subclinical changes in myocardial function which do not affect conventional echocardiographic parameters. The pathophysiology of the diabetic myocardial dysfunction is not fully elucidated, but involves hyperglycemia and high levels of free fatty acids. It evolves over several years and increases the risk of developing overt HF, and is suggested to at least in part account for the worse outcome seen in T2DM individuals after cardiac events. CAD and stroke are the most frequent CV manifestations among T2DM patients and relate to a large degree to the accelerated atherosclerosis driven by inflammation. Diagnosing CAD is challenging due to the lower sensitivity inherent in the diagnostic tests and there is thus a need for new biomarkers to improve prediction and detection of CAD. It seems that a multi-factorial approach (i.e. targeting several CV risk factors simultaneously) is superior to a strict glucose lowering strategy in reducing risk for macrovascular events, and recent research may even support an effect also on HF outcomes. PMID:27071642

  9. Possible mechanisms of C-reactive protein mediated acute myocardial infarction.

    PubMed

    Fordjour, Patrick Asare; Wang, Yadong; Shi, Yang; Agyemang, Kojo; Akinyi, Mary; Zhang, Qiang; Fan, Guanwei

    2015-08-01

    Myocardial infarction is a relevant cardiovascular event worldwide for morbidity and mortality. It has been theorized that acute myocardial infarctions (AMIs) and other acute coronary events that are precipitated by atherosclerosis are due to arterial blockage from fat deposits. It is now known, however, that atherosclerosis involves more than just lipids. Inflammation has also been studied extensively to play a substantial role in myocardial infarction. There have been debates and conflicting reports over the past few years about the value of assessing levels of C-reactive protein and other biomarkers of inflammation for the prediction of cardiovascular events. Several studies have shown that CRP is not only an inflammatory marker, but also involved in the pathogenesis of myocardial infarction. Studies have linked atherogenesis and rupture of atherosclerotic lesion to endothelial dysfunction. CRP directly inhibits endothelial cell nitric oxide (NO) production via destabilizing endothelial NO synthase (eNOS). Decreased NO release causes CRP mediated inhibition of angiogenesis, stimulating endothelial cell apoptosis. CRP can also activate the complement system through the classical pathway. Complement activation plays an important role in mediating monocyte and neutrophil recruitment in an injured myocardium and may therefore lead to increase in infarct size. This article discusses the possible roles of CRP in complement activation, endothelial dysfunction and its impact on the development of myocardial infarction. We also reviewed the possible therapeutic approaches to myocardial infarction.

  10. Altered fingerprints: analysis and detection.

    PubMed

    Yoon, Soweon; Feng, Jianjiang; Jain, Anil K

    2012-03-01

    The widespread deployment of Automated Fingerprint Identification Systems (AFIS) in law enforcement and border control applications has heightened the need for ensuring that these systems are not compromised. While several issues related to fingerprint system security have been investigated, including the use of fake fingerprints for masquerading identity, the problem of fingerprint alteration or obfuscation has received very little attention. Fingerprint obfuscation refers to the deliberate alteration of the fingerprint pattern by an individual for the purpose of masking his identity. Several cases of fingerprint obfuscation have been reported in the press. Fingerprint image quality assessment software (e.g., NFIQ) cannot always detect altered fingerprints since the implicit image quality due to alteration may not change significantly. The main contributions of this paper are: 1) compiling case studies of incidents where individuals were found to have altered their fingerprints for circumventing AFIS, 2) investigating the impact of fingerprint alteration on the accuracy of a commercial fingerprint matcher, 3) classifying the alterations into three major categories and suggesting possible countermeasures, 4) developing a technique to automatically detect altered fingerprints based on analyzing orientation field and minutiae distribution, and 5) evaluating the proposed technique and the NFIQ algorithm on a large database of altered fingerprints provided by a law enforcement agency. Experimental results show the feasibility of the proposed approach in detecting altered fingerprints and highlight the need to further pursue this problem.

  11. Altered fingerprints: analysis and detection.

    PubMed

    Yoon, Soweon; Feng, Jianjiang; Jain, Anil K

    2012-03-01

    The widespread deployment of Automated Fingerprint Identification Systems (AFIS) in law enforcement and border control applications has heightened the need for ensuring that these systems are not compromised. While several issues related to fingerprint system security have been investigated, including the use of fake fingerprints for masquerading identity, the problem of fingerprint alteration or obfuscation has received very little attention. Fingerprint obfuscation refers to the deliberate alteration of the fingerprint pattern by an individual for the purpose of masking his identity. Several cases of fingerprint obfuscation have been reported in the press. Fingerprint image quality assessment software (e.g., NFIQ) cannot always detect altered fingerprints since the implicit image quality due to alteration may not change significantly. The main contributions of this paper are: 1) compiling case studies of incidents where individuals were found to have altered their fingerprints for circumventing AFIS, 2) investigating the impact of fingerprint alteration on the accuracy of a commercial fingerprint matcher, 3) classifying the alterations into three major categories and suggesting possible countermeasures, 4) developing a technique to automatically detect altered fingerprints based on analyzing orientation field and minutiae distribution, and 5) evaluating the proposed technique and the NFIQ algorithm on a large database of altered fingerprints provided by a law enforcement agency. Experimental results show the feasibility of the proposed approach in detecting altered fingerprints and highlight the need to further pursue this problem. PMID:21808092

  12. Do antioxidant vitamins reduce infarct size following acute myocardial ischemia/reperfusion?

    PubMed

    Bellows, S D; Hale, S L; Simkhovich, B Z; Kay, G L; Kloner, R A

    1995-02-01

    There is controversy concerning the ability of antioxidant vitamins to reduce myocardial infarct size. We sought to determine whether a brief prophylactic treatment of vitamin C or vitamin C plus Trolox (a water-soluble form of vitamin E) could reduce myocardial infarct size in an experimental model. We used an anesthetized open-chest rabbit model in which a branch of the circumflex coronary artery was ligated for 30 minutes followed by 4 hours of reperfusion. Experiments were performed in a randomized and blinded fashion. An IV injection of normal saline pH balanced to 7.4 (control group n = 15), vitamin C (150 mg/kg, n = 14), or vitamin C plus Trolox (150 mg/kg plus 100 mg/kg, respectively, n = 15) was administered prior to coronary occlusion. Collateral blood flow during coronary occlusion was measured by radioactive microspheres, myocardial risk zone (AR) was assessed by blue dye injection, and myocardial infarct size (AN) was assessed by triphenyltetrazolium chloride staining. All rabbits received comparable ischemic insult: Collateral blood flow and AR were similar among all three groups. Infarct size, measured as a percent of AR, did not differ significantly among the controls (21%), vitamin C (29%), or the vitamin C plus Trolox (18%) groups. Therefore, in this ischemia/reperfusion model, antioxidant vitamins did not alter myocardial infarct size. PMID:7540423

  13. Cardiac Remodeling, Adaptations and Associated Myocardial Mechanics in Hypertensive Heart Diseases

    PubMed Central

    Lai, Yau-Huei; Lo, Chi-In; Wu, Yih-Jer; Hung, Chung-Lieh; Yeh, Hung-I

    2013-01-01

    Hypertension is the leading cause of heart failure and cardiovascular comorbidities in developed countries. Left ventricular structural/functional alterations such as concentric remodeling or hypertrophy have been extensively studied in hypertensive heart diseases. Furthermore, it is also well-recognized that diastolic function actually deteriorates in hypertensive subjects prior to overt heart failure. Novel imaging modality techniques such as myocardial deformation have allowed for early detection of regional/global myocardial contractile dysfunction. Myocardial deformation, which can be quantified by measuring the systolic strain and strain rate in three different directions (longitudinal, circumferential and radial), has facilitated new insights into the understanding of cardiac systolic mechanics in subjects with early stage myocardial damage. Previous studies had shown that longitudinal function remains the most sensitive parameter in identifying hypertension-related myocardial dysfunction, particularly for those patients who had developed LV hypertrophy. Instead, preserved or enhanced short-axis function, when presented as circumferential or radial strains, may remain relatively preserved or enhanced in order to compensate for longitudinal functional decline. In this manner, global cardiac pumping in terms of ejection fraction may remain relatively unchanged. The early recognition of subclinical systolic dysfunction and associated mechanical compensation in the context of hypertension is crucial, which potentially helps to identify a disease stage that is still responsive to therapeutic intervention. PMID:27122686

  14. Untargeted metabolic profiling reveals potential biomarkers in myocardial infarction and its application.

    PubMed

    Yao, Hong; Shi, Peiying; Zhang, Ling; Fan, Xiaohui; Shao, Qing; Cheng, Yiyu

    2010-06-01

    Although some important biomarkers for myocardial injury have been identified, there still lacks a systematic view of the development and progression of myocardial infarction, including enzymatic regulation, metabolite levels, fluxes, etc., which are pivotal to elucidate the physiological mechanism of disease. Here we present an untargeted analytical approach based on gas chromatography coupled with mass spectrometry (GC-MS) to map the temporal metabolic profilings in blood sera of myocardial infarction rat model prepared by left coronary artery ligation. Using XCMS software (http://metlin.scripps.edu/download/), data processing was simplified greatly. We identified the changes in circulating levels of 24 metabolites during the myocardial ischemia. By combination of previous proteomic results, it gives rise to a new insight view of energy metabolism changes referring to anaerobic glycolysis, citric acid cycle, fatty acid beta-oxidation, and some amino acids metabolism. With these altered metabolism pathways as possible drug targets, we validated a role for the presented metabonomic profiling in the systematic understanding of the action mechanism of component-complex medicine herbs, such as Radix Ophiopogonis, a widely-used anti-myocardial ischemia herbal medicine in Asia.

  15. Myocardial contusion in patients with blunt chest trauma as evaluated by thallium 201 myocardial scintigraphy

    SciTech Connect

    Bodin, L.; Rouby, J.J.; Viars, P.

    1988-07-01

    Fifty five patients suffering from blunt chest trauma were studied to assess the diagnosis of myocardial contusion using thallium 201 myocardial scintigraphy. Thirty-eight patients had consistent scintigraphic defects and were considered to have a myocardial contusion. All patients with scintigraphic defects had paroxysmal arrhythmias and/or ECG abnormalities. Of 38 patients, 32 had localized ST-T segment abnormalities; 29, ST-T segment abnormalities suggesting involvement of the same cardiac area as scintigraphic defects; 21, echocardiographic abnormalities. Sixteen patients had segmental hypokinesia involving the same cardiac area as the scintigraphic defects. Fifteen patients had clinical signs suggestive of myocardial contusion and scintigraphic defects. Almost 70 percent of patients with blunt chest trauma had scintigraphic defects related to areas of myocardial contusion. When thallium 201 myocardial scintigraphy directly showed myocardial lesion, two-dimensional echocardiography and standard ECG detected related functional consequences of cardiac trauma.

  16. Myocardial infarct associated with a partial thickness left atrial tear in a dog with mitral insufficiency.

    PubMed

    Sleeper, Meg M; Maczuzak, Meredith E; Bender, Susan J

    2015-09-01

    A 10-year-old male neutered cavalier King Charles Spaniel with a 1-year history of degenerative mitral valve disease presented for dyspnea and severe weakness. He was diagnosed with congestive heart failure, systolic dysfunction, presumptive myocardial infarction and a left atrial thrombus based on thoracic radiographs, electrocardiogram and echocardiographic findings. Clinical signs also suggested right foreleg embolism. The dog was euthanized due to the grave prognosis and a postmortem evaluation was performed. The postmortem examination confirmed myocardial infarction and was thought to be due to embolic showering from the thrombus attached to a partial thickness left atrial endocardial tear. PMID:26263842

  17. Apoptosis in myocardial ischaemia and infarction.

    PubMed

    Krijnen, P A J; Nijmeijer, R; Meijer, C J L M; Visser, C A; Hack, C E; Niessen, H W M

    2002-11-01

    Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in animals.

  18. Myocardial perfusion SPECT in a case of retropulmonary looping of left coronary artery in a baby after arterial switch surgery

    PubMed Central

    Padma, Subramanyam; Sundaram, Palaniswamy Shanmuga

    2014-01-01

    Pediatric myocardial perfusion imaging (MPI) is not a routine investigation in an Indian setting due to under referrals and logistic problems. However, MPI is a frequently performed and established modality of investigation in adults for the identification of myocardial ischemia and viability. We report myocardial perfusion scintigraphy in a case of retropulmonary looping of left coronary artery in a baby after arterial switch surgery. Adenosine stress MPI revealed a large infarct involving anterior segment with moderate reversible ischemia of the lateral left ventricular segment. Coronary angiogram later confirmed left main coronary artery ostial occlusion with retrograde collateral supply from dilated right coronary artery. PMID:24761067

  19. Myocardial protection with mild hypothermia.

    PubMed

    Tissier, Renaud; Ghaleh, Bijan; Cohen, Michael V; Downey, James M; Berdeaux, Alain

    2012-05-01

    Mild hypothermia, 32-35° C, is very potent at reducing myocardial infarct size in rabbits, dogs, sheep, pigs, and rats. The benefit is directly related to reduction in normothermic ischaemic time, supporting the relevance of early and rapid cooling. The cardioprotective effect of mild hypothermia is not limited to its recognized reduction of infarct size, but also results in conservation of post-ischaemic contractile function, prevention of no-reflow or microvascular obstruction, and ultimately attenuation of left ventricular remodelling. The mechanism of the anti-infarct effect does not appear to be related to diminished energy utilization and metabolic preservation, but rather to survival signalling that involves either the extracellular signal-regulated kinases and/or the Akt/phosphoinositide 3-kinase/mammalian target of rapamycin pathways. Initial clinical trials of hypothermia in patients with ST-segment elevation myocardial infarction were disappointing, probably because cooling was too slow to shorten normothermic ischaemic time appreciably. New approaches to more rapid cooling have recently been described and may soon be available for clinical use. Alternatively, it may be possible to pharmacologically mimic the protection provided by cooling soon after the onset of ischaemia with an activator of mild hypothermia signalling, e.g. extracellular signal-regulated kinase activator, that could be given by emergency medical personnel. Finally, the protection afforded by cooling can be added to that of pre- and post-conditioning because their mechanisms differ. Thus, myocardial salvage might be greatly increased by rapidly cooling patients as soon as possible and then giving a pharmacological post-conditioning agent immediately prior to reperfusion. PMID:22131353

  20. [ST myocardial infarction with spontaneous coronary reperfusion].

    PubMed

    Uriel, Nir; Moravsky, Gil; Blatt, Alex; Vered, Zvi; Krakover, Ricardo; Kaluski, Edo

    2006-05-01

    ST elevation myocardial infarction continues to be a major medical problem even in the beginning of the 21st century. Treatment guidelines for these patients are based on multiple randomized clinical trials. In order to minimize myocardial damage, early patency of the infarct relating artery must be accomplished. This is the major difference in the treatment strategy between ST elevation myocardial infarction and other acute coronary syndromes. Primary percutaneous coronary intervention and fibrinolysis are the two treatment modalities for achieving myocardial reperfusion. The subgroup of ST elevation myocardial infarction with spontaneous coronary artery reperfusion carries a more favorable prognosis. This review addresses the clinical characteristics, natural history, prognosis and treatment strategies for this group, with special emphasis on the optimal timing for revascularization, and the role of glycoprotein IIb/IIIa inhibitors.

  1. Risk stratification after myocardial infarction. Clinical overview

    SciTech Connect

    O'Rourke, R.A. )

    1991-09-01

    Many patients with an acute myocardial infarction can be stratified into subgroups that are at high risk for morbidity and mortality on the basis of clinical characteristics that indicate recurrent myocardial ischemia, persistent left ventricular dysfunction, and/or recurrent cardiac arrhythmias. In patients with uncomplicated myocardial infarction the assessment of symptoms, physical findings, and ECG changes during predischarge exercise testing often identifies patients at increased risk for further cardiac events. Because of the suboptimum sensitivity and specificity of the exercise ECG for detecting myocardial ischemia, myocardial perfusion imaging with 201Tl and/or assessment of global and segmental ventricular function by two-dimensional echocardiography or radionuclide cineangiography during or immediately after exercise are often added to the predischarge risk stratification.

  2. Macrophage Roles Following Myocardial Infarction

    PubMed Central

    Lambert, Jessica M.; Lopez, Elizabeth F.; Lindsey, Merry L.

    2010-01-01

    Following myocardial infarction (MI), circulating blood monocytes respond to chemotactic factors, migrate into the infarcted myocardium, and differentiate into macrophages. At the injury site, macrophages remove necrotic cardiac myocytes and apoptotic neutrophils; secrete cytokines, chemokines, and growth factors; and modulate phases of the angiogenic response. As such, the macrophage is a primary responder cell type that is involved in the regulation of post-MI wound healing at multiple levels. This review summarizes what is currently known about macrophage functions post-MI and borrows literature from other injury and inflammatory models to speculate on additional roles. Basic science and clinical avenues that remain to be explored are also discussed. PMID:18656272

  3. Solar activity and myocardial infarction.

    PubMed

    Szczeklik, E; Mergentaler, J; Kotlarek-Haus, S; Kuliszkiewicz-Janus, M; Kucharczyk, J; Janus, W

    1983-01-01

    The correlation between the incidence of myocardial infarction, sudden cardiac death, the solar activity and geomagnetism in the period 1969-1976 was studied, basing on Wrocław hospitals material registered according to WHO standards; sudden death was assumed when a person died within 24 hours after the onset of the disease. The highest number of infarctions and sudden deaths was detected for 1975, which coincided with the lowest solar activity, and the lowest one for the years 1969-1970 coinciding with the highest solar activity. Such an inverse, statistically significant correlation was not found to exist between the studied biological phenomena and geomagnetism. PMID:6851574

  4. New Trends in Radionuclide Myocardial Perfusion Imaging

    PubMed Central

    Hung, Guang-Uei; Wang, Yuh-Feng; Su, Hung-Yi; Hsieh, Te-Chun; Ko, Chi-Lun; Yen, Ruoh-Fang

    2016-01-01

    Radionuclide myocardial perfusion imaging (MPI) with single photon emission computed tomography (SPECT) has been widely used clinically as one of the major functional imaging modalities for patients with coronary artery disease (CAD) for decades. Ample evidence has supported the use of MPI as a useful and important tool in the diagnosis, risk stratification and treatment planning for CAD. Although popular in the United States, MPI has become the most frequently used imaging modality among all nuclear medicine tests in Taiwan. However, it should be acknowledged that MPI SPECT does have its limitations. These include false-positive results due to certain artifacts, false-negative due to balanced ischemia, complexity and adverse reaction arising from current pharmacological stressors, time consuming nature of the imaging procedure, no blood flow quantitation and relatively high radiation exposure. The purpose of this article was to review the recent trends in nuclear cardiology, including the utilization of positron emission tomography (PET) for MPI, new stressor, new SPECT camera with higher resolution and higher sensitivity, dynamic SPECT protocol for blood flow quantitation, new software of phase analysis for evaluation of LV dyssynchrony, and measures utilized for reducing radiation exposure of MPI. PMID:27122946

  5. Sum of effects of myocardial ischemia followed by electrically induced tachycardia on myocardial function

    PubMed Central

    Díez, José Luis; Hernándiz, Amparo; Cosín-Aguilar, Juan; Aguilar, Amparo; Portolés, Manuel

    2013-01-01

    Background The alteration of contractile function after tachyarrhythmia ceases is influenced by the type of prior ischemia (acute coronary syndrome or ischemia inherent in a coronary revascularization procedure). We aimed to analyze cardiac dysfunction in an acute experimental model of supraphysiological heart rate preceded by different durations and types of ischemia. Material/Methods Twenty-four pigs were included in: (S1) series of ventricular pacing; (S2, A and B) series with 10 or 20 min, respectively, of coronary occlusion previous to ventricular pacing; S3 with 20 brief, repeated ischemia/reperfusion processes prior to ventricular pacing and; (S4) control series. Overall cardiac function parameters and regional myocardial contractility at the apex and base of the left ventricle were recorded, as were oxidative stress markers (glutathione and lipid peroxide serum levels). Left ventricular pacing at 60% over baseline heart rate was performed for 2 h followed by 1 h of recovery. Results High ventricular pacing rates preceded by short, repeated periods of coronary ischemia/reperfusion resulted in worse impairment of overall cardiac and regional function that continued to be altered 1 h after tachycardia ceased. There was significant reduction of stroke volume (26.9±5.3 basal vs. 16±6.2 ml; p<0.05), LVP; dP/dt and LAD flow (13.1±1.5 basal vs. 8.4±1.6 ml/min; p<0.05); the base contractility remained altered when recovering compared to baseline (base SF: 5.6±2.8 vs. 2.2±0.7%; p<0.05); and LPO levels were higher than less aggressive series at the end of recovery. Conclusions Ischemia and tachycardia accumulate their effects, with increased cardiac involvement depending on the type of ischemia. PMID:23722244

  6. Myocardial Perfusion: Characteristics of Distal Intramyocardial Arteriolar Trees.

    PubMed

    Zamir, Mair; Vercnocke, Andrew J; Edwards, Phillip K; Anderson, Jill L; Jorgensen, Steven M; Ritman, Erik L

    2015-11-01

    A combination of experimental, theoretical, and imaging methodologies is used to examine the hierarchical structure and function of intramyocardial arteriolar trees in porcine hearts to provide a window onto a region of myocardial microvasculature which has been difficult to fully explore so far. A total of 66 microvascular trees from 6 isolated myocardial specimens were analyzed, with a cumulative number of 2438 arteriolar branches greater than or equal to 40 μm lumen diameter. The distribution of flow rates within each tree was derived from an assumed power law relationship for that tree between the diameter of vessel segments and flow rates that are consistent with that power law and subject to conservation of mass along hierarchical structure of the tree. The results indicate that the power law index increases at levels of arteriolar vasculature closer to the capillary level, consistent with a concomitant decrease in shear stress acting on endothelial tissue. These results resolve a long standing predicament which could not be resolved previously because of lack of data about the 3D, interconnected, arterioles. In the context of myocardial perfusion, the results indicate that the coefficient of variation of flow rate in pre-capillary distal arterioles is high, suggesting that heterogeneity of flow rate in these arterioles is not entirely random but may be due at least in part to active control.

  7. Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema.

    PubMed

    Desai, Ketaki V; Laine, Glen A; Stewart, Randolph H; Cox, Charles S; Quick, Christopher M; Allen, Steven J; Fischer, Uwe M

    2008-06-01

    Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures. PMID:18375722

  8. Direct Evidence that Myocardial Insulin Resistance following Myocardial Ischemia Contributes to Post-Ischemic Heart Failure.

    PubMed

    Fu, Feng; Zhao, Kun; Li, Jia; Xu, Jie; Zhang, Yuan; Liu, Chengfeng; Yang, Weidong; Gao, Chao; Li, Jun; Zhang, Haifeng; Li, Yan; Cui, Qin; Wang, Haichang; Tao, Ling; Wang, Jing; Quon, Michael J; Gao, Feng

    2015-12-14

    A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its association with HF are inadequately investigated. This study aims to determine the role of myocardial insulin resistance in ischemic HF and its underlying mechanisms. Male Sprague-Dawley rats subjected to myocardial infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk post-MI. Of note, myocardial insulin sensitivity was decreased as early as 1 wk after MI, which was accompanied by increased production of myocardial TNF-α. Overexpression of TNF-α in heart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI. Treatment of rats with a specific TNF-α inhibitor improved myocardial insulin signaling post-MI. Insulin treatment given immediately following MI suppressed myocardial TNF-α production and improved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling. Moreover, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with controls. In conclusion, MI induces myocardial insulin resistance (without systemic insulin resistance) mediated partly by ischemia-induced myocardial TNF-α overproduction and promotes the development of HF. Our findings underscore the direct and essential role of myocardial insulin signaling in protection against post-ischemic HF.

  9. Nifedipine and thallium-201 myocardial perfusion in progressive systemic sclerosis

    SciTech Connect

    Kahan, A.; Devaux, J.Y.; Amor, B.; Menkes, C.J.; Weber, S.; Nitenberg, A.; Venot, A.; Guerin, F.; Degeorges, M.; Roucayrol, J.C.

    1986-05-29

    Heart disease in patients with progressive systemic sclerosis may be due in part to myocardial ischemia caused by a disturbance of the coronary microcirculation. To determine whether abnormalities of myocardial perfusion in this disorder are potentially reversible, we evaluated the effect of the coronary vasodilator nifedipine on myocardial perfusion assessed by thallium-201 scanning in 20 patients. Thallium-201 single-photon-emission computerized tomography was performed under control conditions and 90 minutes after 20 mg of oral nifedipine. The mean (+/- SD) number of left ventricular segments with perfusion defects decreased from 5.3 +/- 2.0 to 3.3 +/- 2.2 after nifedipine (P = 0.0003). Perfusion abnormalities were quantified by a perfusion score (0 to 2.0) assigned to each left ventricular segment and by a global perfusion score (0 to 18) for the entire left ventricle. The mean perfusion score in segments with resting defects increased from 0.97 +/- 0.24 to 1.26 +/- 0.44 after nifedipine (P less than 0.00001). The mean global perfusion score increased from 11.2 +/- 1.7 to 12.8 +/- 2.4 after nifedipine (P = 0.003). The global perfusion score increased by at least 2.0 in 10 patients and decreased by at least 2.0 in only 1. These observations reveal short-term improvement in thallium-201 myocardial perfusion with nifedipine in patients with progressive systemic sclerosis. The results are consistent with a potentially reversible abnormality of coronary vasomotion in this disorder, but the long-term therapeutic effects of nifedipine remain to be determined.

  10. Magnetic resonance imaging of myocardial injury and ventricular torsion after marathon running.

    PubMed

    Hanssen, Henner; Keithahn, Alexandra; Hertel, Gernot; Drexel, Verena; Stern, Heiko; Schuster, Tibor; Lorang, Dan; Beer, Ambros J; Schmidt-Trucksäss, Arno; Nickel, Thomas; Weis, Michael; Botnar, Rene; Schwaiger, Markus; Halle, Martin

    2011-02-01

    Recent reports provide indirect evidence of myocardial injury and ventricular dysfunction after prolonged exercise. However, existing data is conflicting and lacks direct verification of functional myocardial alterations by CMR [cardiac MR (magnetic resonance)]. The present study sought to examine structural myocardial damage and modification of LV (left ventricular) wall motion by CMR imaging directly after a marathon. Analysis of cTnT (cardiac troponin T) and NT-proBNP (N-terminal pro-brain natriuretic peptide) serum levels, echocardiography [pulsed-wave and TD (tissue Doppler)] and CMR were performed before and after amateur marathon races in 28 healthy males aged 41 ± 5 years. CMR included LGE (late gadolinium enhancement) and myocardial tagging to assess myocardial injury and ventricular motion patterns. Echocardiography indicated alterations of diastolic filling [decrease in E/A (early transmitral diastolic filling velocity/late transmitral diastolic filling velocity) ratio and E' (tissue Doppler early transmitral diastolic filling velocity)] postmarathon. All participants had a significant increase in NT-proBNP and/or cTnT levels. However, we found no evidence of LV LGE. MR tagging demonstrated unaltered radial shortening, circumferential and longitudinal strain. Myocardial rotation analysis, however, revealed an increase of maximal torsion by 18.3% (13.1 ± 3.8 to 15.5 ± 3.6 °; P=0.002) and maximal torsion velocity by 35% (6.8 ± 1.6 to 9.2 ± 2.5 °·s-1; P<0.001). Apical rotation velocity during diastolic filling was increased by 1.23 ± 0.33 °·s-1 after marathon (P<0.001) in a multivariate analysis adjusted for heart rate, whereas peak untwist rate showed no relevant changes. Although marathon running leads to a transient increase of cardiac biomarkers, no detectable myocardial necrosis was observed as evidenced by LGE MRI (MR imaging). Endurance exercise induces an augmented systolic wringing motion of the myocardium and increased diastolic filling

  11. Circadian influences on myocardial infarction

    PubMed Central

    Virag, Jitka A. I.; Lust, Robert M.

    2014-01-01

    Components of circadian rhythm maintenance, or “clock genes,” are endogenous entrainable oscillations of about 24 h that regulate biological processes and are found in the suprachaismatic nucleus (SCN) and many peripheral tissues, including the heart. They are influenced by external cues, or Zeitgebers, such as light and heat, and can influence such diverse phenomena as cytokine expression immune cells, metabolic activity of cardiac myocytes, and vasodilator regulation by vascular endothelial cells. While it is known that the central master clock in the SCN synchronizes peripheral physiologic rhythms, the mechanisms by which the information is transmitted are complex and may include hormonal, metabolic, and neuronal inputs. Whether circadian patterns are causally related to the observed periodicity of events, or whether they are simply epi-phenomena is not well established, but a few studies suggest that the circadian effects likely are real in their impact on myocardial infarct incidence. Cycle disturbances may be harbingers of predisposition and subsequent response to acute and chronic cardiac injury, and identifying the complex interactions of circadian rhythms and myocardial infarction may provide insights into possible preventative and therapeutic strategies for susceptible populations. PMID:25400588

  12. [Acute myocardial infarction during sport].

    PubMed

    Fujiwara, M; Asakuma, S; Nakamura, K; Nakamura, T; Yasutomi, N; Iwasaki, T

    1995-10-01

    Thirty patients with acute myocardial infarction which occurred during sport were investigated to identify the type of sport, prodromata, situations at the onset of disease, habit of exercise, preceding medical evaluation, coronary risk factors, and coronary angiographic findings. Infarction occurred during golf in 12 patients, bowling in 4, gateball in 4, jogging or running in 5, baseball in 2, and tennis or table tennis in 3. The majority of the patients were playing ball games. Twenty-seven patients were men (90%) and 3 were women (10%). All patients had played the same kind of sport for several years. Twenty-four patients had one or more coronary risk factors, and especially 18 patients smoked cigarettes. Nine patients had experienced anterior chest pain but only two patients had received medical evaluation. Coronary angiography was performed in 25 patients (83.3%), revealing single-vessel disease in 14, two-vessel disease in 6, three-vessel disease in 4, and disease of all left main coronary trunks in 1. The acute episode of infarction occurred mainly in spring or fall. Many patients with acute myocardial infarction occurring during sport participate in sports of low or moderate dynamic and low static exercises which are generally regarded safe. Many patients had enjoyed their sports regularly for a long time. Though many patients had coronary risk factors, only a few had received a medical check before their heart attack.

  13. Altered heart proteome in fructose-fed Fisher 344 rats exposed to bisphenol A.

    PubMed

    Ljunggren, S A; Iggland, M; Rönn, M; Lind, L; Lind, P M; Karlsson, H

    2016-03-10

    Bisphenol A (BPA), is an artificial estrogen initially produced for medical purposes but is today widely used in polycarbonate plastics and epoxy resins. Exposure-related reproductive disorders have been found, but recently it has also been suggested that BPA may be involved in obesity, diabetes, myocardial hypertrophy and myocardial infarction in humans. To mimic a modern lifestyle, female rats were fed with fructose or fructose plus BPA (0.25mg/L drinking water). The myocardial left ventricle proteome of water controls, fructose-fed and fructose-fed plus BPA supplemented rats was explored. The proteome was investigated using nano-liquid chromatography tandem mass spectrometry and two-dimensional gel electrophoresis followed by matrix assisted laser desorption/ionization mass spectrometry identification. In total, 41 proteins were significantly altered by BPA exposure compared to water or fructose controls. Principal component analysis and cellular process enrichment analysis of altered proteins suggested increased fatty acid transport and oxidation, increased ROS generation and altered structural integrity of the myocardial left ventricle in the fructose-fed BPA-exposed rats, indicating unfavorable effects on the myocardium. In conclusion, BPA exposure in the rats induces major alterations in the myocardial proteome.

  14. Altered heart proteome in fructose-fed Fisher 344 rats exposed to bisphenol A.

    PubMed

    Ljunggren, S A; Iggland, M; Rönn, M; Lind, L; Lind, P M; Karlsson, H

    2016-03-10

    Bisphenol A (BPA), is an artificial estrogen initially produced for medical purposes but is today widely used in polycarbonate plastics and epoxy resins. Exposure-related reproductive disorders have been found, but recently it has also been suggested that BPA may be involved in obesity, diabetes, myocardial hypertrophy and myocardial infarction in humans. To mimic a modern lifestyle, female rats were fed with fructose or fructose plus BPA (0.25mg/L drinking water). The myocardial left ventricle proteome of water controls, fructose-fed and fructose-fed plus BPA supplemented rats was explored. The proteome was investigated using nano-liquid chromatography tandem mass spectrometry and two-dimensional gel electrophoresis followed by matrix assisted laser desorption/ionization mass spectrometry identification. In total, 41 proteins were significantly altered by BPA exposure compared to water or fructose controls. Principal component analysis and cellular process enrichment analysis of altered proteins suggested increased fatty acid transport and oxidation, increased ROS generation and altered structural integrity of the myocardial left ventricle in the fructose-fed BPA-exposed rats, indicating unfavorable effects on the myocardium. In conclusion, BPA exposure in the rats induces major alterations in the myocardial proteome. PMID:26930160

  15. Electromechanical and structural alterations in the aging rabbit heart and aorta

    PubMed Central

    Cooper, Leroy L.; Odening, Katja E.; Hwang, Min-Sig; Chaves, Leonard; Schofield, Lorraine; Taylor, Chantel A.; Gemignani, Anthony S.; Mitchell, Gary F.; Forder, John R.; Choi, Bum-Rak

    2012-01-01

    Aging increases the risk for arrhythmias and sudden cardiac death (SCD). We aimed at elucidating aging-related electrical, functional, and structural changes in the heart and vasculature that account for this heightened arrhythmogenic risk. Young (5–9 mo) and old (3.5–6 yr) female New Zealand White (NZW) rabbits were subjected to in vivo hemodynamic, electrophysiological, and echocardiographic studies as well as ex vivo optical mapping, high-field magnetic resonance imaging (MRI), and histochemical experiments. Aging increased aortic stiffness (baseline pulse wave velocity: young, 3.54 ± 0.36 vs. old, 4.35 ± 0.28 m/s, P < 0.002) and diastolic (end diastolic pressure-volume relations: 3.28 ± 0.5 vs. 4.95 ± 1.5 mmHg/ml, P < 0.05) and systolic (end systolic pressure-volume relations: 20.56 ± 4.2 vs. 33.14 ± 8.4 mmHg/ml, P < 0.01) myocardial elastances in old rabbits. Electrophysiological and optical mapping studies revealed age-related slowing of ventricular and His-Purkinje conduction (His-to-ventricle interval: 23 ± 2.5 vs. 31.9 ± 2.9 ms, P < 0.0001), altered conduction anisotropy, and a greater inducibility of ventricular fibrillation (VF, 3/12 vs. 7/9, P < 0.05) in old rabbits. Histochemical studies confirmed an aging-related increased fibrosis in the ventricles. MRI showed a deterioration of the free-running Purkinje fiber network in ventricular and septal walls in old hearts as well as aging-related alterations of the myofibrillar orientation and myocardial sheet structure that may account for this slowed conduction velocity. Aging leads to parallel stiffening of the aorta and the heart, including an increase in systolic stiffness and contractility and diastolic stiffness. Increasingly, anisotropic conduction velocity due to fibrosis and altered myofibrillar orientation and myocardial sheet structure may contribute to the pathogenesis of VF in old hearts. The aging rabbit model represents a useful tool for elucidating age-related changes that

  16. Alterations in bone forming cells due to reduced weight bearing

    NASA Technical Reports Server (NTRS)

    Doty, S. B.; Morey-Holton, E.

    1984-01-01

    A reduction in new bone formation occurred as a result of space flight (Cosmos 1129) and in the suspended animal model of Morey-Holton (1979, 1980). The results indicate that alkaline phosphatase activity of the bone-forming cells is also reduced under these conditions, and the cells in the diaphysis are more affected than those in the metaphyseal region. In addition, these cells show (1) reduced proline incorporation into bone matrix, and (2) increased intracellular lysosomal activity. A change in the cytoskeleton could be the common factor in explaining these results. This suggestion is futher supported by the previous observations that colchicine injections result in decreased osteoblastic function.

  17. Anatomical alterations due to polyploidy in cassava, Manihot esculenta Crantz.

    PubMed

    Nassar, Nagib M A; Graciano-Ribeiro, D; Fernandes, S D C; Araujo, P C

    2008-01-01

    Information on anatomical structure is needed by breeders working on improvement for drought tolerance. For studying the effect of polyploidy on cassava anatomy and its significance to tolerance to drought, we induced a polyploidy type of a selected clone (UnB 530) by applying an aqueous solution of 0.2% colchicine on lateral buds for a period of 12 h. The stem identified as tetraploid was propagated to produce the whole plant. Free-hand cross-sections of the median portion between stem internodes were made. They were clarified using 50% sodium hypochlorite solution, stained with 1% safranin-alcian blue, passed through an ethanol series and butyl acetate and mounted in synthetic resin. The tetraploid type showed more prismatic and druse crystals in the cortical parenchyma, and its pericycle fibers had thicker walls. The secondary xylem of tetraploid types was wider than diploid ones, having thinner walls and less starch. PMID:18551393

  18. Mechanism of hearing disturbance due to alteration in atmospheric pressure.

    PubMed

    Kitahara, M; Kodama, A; Ozawa, H; Izukura, H

    1994-01-01

    We used a soundproof pressure chamber to examine how the changes in atmospheric pressure as experienced in daily life reduces bone conduction in a total of 48 normal adults. The subjects were given special ear plugs that connected external auditory canal to the pressure gauge and a small pump located outside the chamber, and were instructed not to swallow, to avoid active opening of the Eustachian tube. The chamber pressure was increased (or decreased) to +/- 500 mmH2O at a rate of 33 mmH2O/s. Then pressure in the external auditory canal was increased (or decreased) gradually after the chamber pressure had reached +/- 500 mmH2O, to equilibrate the pressure across the ear drum. Bone conduction did not recover the level before increase (or decrease) in the chamber pressure. We conclude that at least a minor part of the deterioration in bone conduction after changes in the chamber pressure was caused by displacement of the round window membrane.

  19. Alterations in gray matter volume due to unilateral hearing loss

    PubMed Central

    Wang, Xingchao; Xu, Pengfei; Li, Peng; Wang, Zhenmin; Zhao, Fu; Gao, Zhixian; Xu, Lei; Luo, Yue-jia; Fan, Jin; Liu, Pinan

    2016-01-01

    Although extensive research on neural plasticity resulting from hearing deprivation has been conducted, the direct influence of compromised audition on the auditory cortex and the potential impact of long durations of incomplete sensory stimulation on the adult cortex are still not fully understood. In this study, using voxel-based morphometry, we evaluated gray matter (GM) volume changes that may be associated with reduced hearing ability and the duration of hearing impairment in 42 unilateral hearing loss (UHL) patients with acoustic neuromas compared to 24 normal controls. We found significant GM volume increases in the somatosensory and motor systems and GM volume decreases in the auditory (i.e., Heschl’s gyrus) and visual systems (i.e., the calcarine cortex) in UHL patients. The GM volume decreases in the primary auditory cortex (i.e., superior temporal gyrus and Heschl’s gyrus) correlated with reduced hearing ability. Meanwhile, the GM volume decreases in structures involving high-level cognitive control functions (i.e., dorsolateral prefrontal cortex and anterior cingulate cortex) correlated positively with hearing loss duration. Our findings demonstrated that the severity and duration of UHL may contribute to the dissociated morphology of auditory and high-level neural structures, providing insight into the brain’s plasticity related to chronic, persistent partial sensory loss. PMID:27174521

  20. Alterations of Cloud Microphysics Due to Cloud Processed CCN

    NASA Astrophysics Data System (ADS)

    Hudson, J. G.; Tabor, S. S.; Noble, S. R., Jr.

    2015-12-01

    High-resolution CCN spectra have revealed bimodality (Hudson et al. 2015) similar to aerosol size spectra (e.g., Hoppel et al. 1985). Bimodality is caused by chemical and physical cloud processes that increase mass or hygroscopicity of only CCN that produced activated cloud droplets. Bimodality is categorized by relative CCN concentrations (NCCN) within the two modes, Nu-Np; i.e., NCCN within the higher critical supersaturation, Sc, mode that did not undergo cloud processing minus NCCN within the lower Sc mode that was cloud processed. Lower, especially negative, Nu-Np designates greater processing. The table shows regressions between Nu-Np and characteristics of clouds nearest the CCN measurements. ICE-T MASE parameter R SL R SL Nc 0.17 93.24 -0.26 98.65 MD -0.31 99.69 0.33 99.78 σ -0.27 99.04 0.48 100.00 Ld -0.31 99.61 0.38 99.96 Table. Correlation coefficients, R, and one-tailed significance levels in percent, SL, for Nu-Np with microphysics of the clouds closest to each CCN measurement, 75 ICE-T and 74 MASE cases. Nc is cloud droplet concentration, MD is cloud droplet mean diameter, σ is standard deviation of cloud droplet spectra, Ldis drizzle drop LWC. Two aircraft field campaigns, Ice in Clouds Experiment-Tropical (ICE-T) and Marine Stratus/Stratocumulus Experiment (MASE) show opposite R signs because coalescence dominated cloud processing in low altitude ICE-T cumuli whereas chemical transformations predominated in MASE low altitude polluted stratus. Coalescence reduces Nc and NCCN, which thus increases MD, and σ, which promote Ld. Chemical transformations, e.g., SO2 to SO4, increase CCN hygroscopicity, thus reducing Sc, but not affecting Nc or NCCN. Lower Sc CCN are capable of producing greater Nc in subsequent cloud cycles, which leads to lower MD and σ which reduce Ld (figure). These observations are consistent with cloud droplet growth models for the higher vertical wind (W) of cumuli and lower W of stratus. Coalescence thus reduces the indirect aerosol effect (IAE) with a positive feedback that further enhances coalescence and drizzle. Chemical cloud processing enhances both components of IAE; 1st IAE by greater droplet surface area, 2ndIAE by suppressing drizzle and thus increasing cloudiness. Hoppel, Fitzgerald and Larson: JGR 90, 2365-79 Hudson, Noble and Tabor: JGRA 120, 3436-52

  1. The Munich Triathlon Heart Study: ventricular function, myocardial velocities, and two-dimensional strain in healthy children before and after endurance stress.

    PubMed

    Hauser, Michael; Petzuch, Kurt; Kühn, Andreas; Schön, Patrick; Elmenhorst, Julia; Schönfelder, Martin; Oberhoffer, Renate; Vogt, Manfred O

    2013-03-01

    Intense exercise has been shown to have negative effects on systolic and diastolic ventricular function in adults. Very little is known about the normal reaction of the growing heart to endurance stress. For this study, 26 healthy children (18 males) with a mean age of 12.61 years (range, 7.92-16.42 years) took part in an age-adapted triathlon circuit. The athletes were investigated by two-dimensional (2D) echocardiographic/speckle tracking, M-mode, pulse-wave Doppler, color Doppler, and color-coded tissue Doppler at 2-4 weeks before and immediately after the race. After the competition, cardiac output increased, mediated by an increase in heart rate and not by an elevated preload, according the Frank-Starling mechanism. Two-dimensional speckle tracking showed a reduced longitudinal strain in the right and left ventricles and additionally reduced circumferential strain in the left ventricle. The late diastolic inflow velocities were increased in both ventricles, indicating reduced diastolic function due to an impairment of myocardial relaxation. Immediately after endurance exercise, systolic and diastolic functions were attenuated in children and adolescents. In contrast to adult studies, this study could show a heart rate-mediated increase in cardiac output. The sequelae of these alterations are unclear, and the growing heart especially may be more susceptible to myocardial damage caused by intense endurance stress.

  2. Use of thallium 201 myocardial imaging to exclude myocardial infarction after dissection in congenital coarctation of the aorta

    SciTech Connect

    Halon, D.A.; Weiss, A.T.; Tzivoni, D.; Atlan, H.; Gotsman, M.S.

    1981-10-01

    The use of a mobile gamma camera with thallium 201 myocardial imaging is described to exclude myocardial infarction in a patient admitted to the coronary care unit in shock and with clinical, enzyme, and ECG changes consistent with infarction. The patient suffered from acute aortic dissection associated with congenital coarctation of the aorta. The myocardial scan excluded transmural myocardial injury.

  3. Cardioplegia and myocardial preservation during cardiopulmonary bypass.

    PubMed

    Engelman, R M; Levitsky, S; O'Donoghue, M J; Auvil, J

    1978-09-01

    A standard experimental protocol was developed to explore the role of hypothermia and potassium cardioplegia in myocardial preservation during 120 minutes of ischemic arrest followed by 30 minutes of reperfusion. Seven different experimental groups of six animals each were evaluated using an in-vivo pig heart preparation. Hypothermic arrest without cardioplegia and cardioplegic arrest at normothermia were each compared to hypothermic cardioplegia. In addition, the use of an asanguineous hypothermic coronary perfusate without cardioplegia was compared to both multidose cardioplegia and single-dose cardioplegia followed by the same asanguineous perfusate. The parameters measured included: myocardial contractility and compliance, myocardial blood flow, endocardial/epicardial blood flow ratio, and electron microscopic studies. Myocardial preservation was inadequate with hypothermic arrest alone (without cardioplegia; and with cardioplegia at normothermia. In both experimental groups, myocardial contractility and compliance were so depressed that the) could not be accurately measured following ischemia and reperfusion while coronary blood flow remained significantly elevated. Preservation was improved but still inadequate following myocardial washout with a normokalemic or hypokalemic perfusate and following single dose cardioplegia plus myocardial washout. In the latter four groups, contractility ranged from 42 to 78% of control, and there was a decrease in compliance of 16 to 78%. Adequate preservation was found only after hypothermia and multidose potassium (35 mEq/L) cardioplegia. In this group, contractility was 129 +/- 13% of control and compliance increased by 21 +/- 24% compared to that of the control.

  4. Electrocardiograms Corresponding to the Development of Myocardial Infarction in Anesthetized WHHLMI Rabbits (Oryctolagus cuniculus), an Animal Model for Familial Hypercholesterolemia

    PubMed Central

    Kobayashi, Tsutomu; Ito, Takashi; Yamada, Satoshi; Kuniyoshi, Nobue; Shiomi, Masashi

    2012-01-01

    The aim of this study was to determine whether features indicative of myocardial ischemia occur in the electrocardiograms (ECG) in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits, an animal model for human familial hypercholesterolemia. ECG were recorded in 110 anesthetized WHHLMI rabbits (age, 10 to 39 mo) by using unipolar and bipolar limb leads with or without chest leads. We noted the following electrocardiographic changes: T wave inversion (37.4%), ST segment depression (31.8%), deep Q wave (16.3%), reduced R wave amplitude (7.3%), ST segment elevation (2.7%), and high T wave (1.8%). These ECG changes resembled those in human patients with coronary heart disease. Histopathologic examination revealed that the left ventricular wall showed acute myocardial lesions, including loss of cross-striations, vacuolar degeneration, coagulation necrosis of cardiac myocytes, and edema between myofibrils, in addition to chronic myocardial lesions such as myocardial fibrosis. The coronary arteries that caused these ECG changes were severely stenosed due to atherosclerotic lesions. Ischemic ECG changes corresponded to the locations of the myocardial lesions. Normal ECG waveforms were similar between WHHLMI rabbits and humans, in contrast to the large differences between rabbits and mice or rats. In conclusion, ischemic ECG changes in WHHLMI rabbits reflect the location of myocardial lesions, making this model useful for studying coronary heart disease. PMID:23114045

  5. Electrocardiograms corresponding to the development of myocardial infarction in anesthetized WHHLMI rabbits (Oryctolagus cuniculus), an animal model for familial hypercholesterolemia.

    PubMed

    Kobayashi, Tsutomu; Ito, Takashi; Yamada, Satoshi; Kuniyoshi, Nobue; Shiomi, Masashi

    2012-10-01

    The aim of this study was to determine whether features indicative of myocardial ischemia occur in the electrocardiograms (ECG) in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits, an animal model for human familial hypercholesterolemia. ECG were recorded in 110 anesthetized WHHLMI rabbits (age, 10 to 39 mo) by using unipolar and bipolar limb leads with or without chest leads. We noted the following electrocardiographic changes: T wave inversion (37.4%), ST segment depression (31.8%), deep Q wave (16.3%), reduced R wave amplitude (7.3%), ST segment elevation (2.7%), and high T wave (1.8%). These ECG changes resembled those in human patients with coronary heart disease. Histopathologic examination revealed that the left ventricular wall showed acute myocardial lesions, including loss of cross-striations, vacuolar degeneration, coagulation necrosis of cardiac myocytes, and edema between myofibrils, in addition to chronic myocardial lesions such as myocardial fibrosis. The coronary arteries that caused these ECG changes were severely stenosed due to atherosclerotic lesions. Ischemic ECG changes corresponded to the locations of the myocardial lesions. Normal ECG waveforms were similar between WHHLMI rabbits and humans, in contrast to the large differences between rabbits and mice or rats. In conclusion, ischemic ECG changes in WHHLMI rabbits reflect the location of myocardial lesions, making this model useful for studying coronary heart disease. PMID:23114045

  6. Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers

    ClinicalTrials.gov

    2016-01-25

    Acute Myocardial Infarction (AMI); Acute Coronary Syndrome (ACS); ST Elevation (STEMI) Myocardial Infarction; Ischemic Reperfusion Injury; Non-ST Elevation (NSTEMI) Myocardial Infarction; Angina, Unstable

  7. Serum nickle estimation in acute myocardial infarction.

    PubMed

    Narang, N K; Goyal, R K; Gupta, A K; Balwani, S

    1989-11-01

    Serum nickle was estimated by atomic absorption spectrometer in 20 healthy controls and in 25 cases of acute myocardial infarction at 12 hourly intervals upto 48 hours, after the onset of chest pain. The mean serum nickel was 0.27 micrograms/dl in healthy controls and 0.40,050,049 and 0.30 micrograms/dl in patients of acute myocardial infarction. The serum nickel values were significantly (P less than 0.001) raised upto 36 hours in acute myocardial infarction when compared with controls.

  8. Nanog expression in heart tissues induced by acute myocardial infarction.

    PubMed

    Luo, Huanhuan; Li, Qiong; Pramanik, Jogen; Luo, Jiankai; Guo, Zhikun

    2014-10-01

    Nanog is a potential stem cell marker and is considered a regeneration factor during tissue repair. In the present study, we investigated expression patterns of nanog in the rat heart after acute myocardial infarction by semi-quantitative RT-PCR, immunohistochemistry and Western blot analyses. Our results show that nanog at both mRNA and protein levels is positively expressed in myocardial cells, fibroblasts and small round cells in different myocardial zones at different stages after myocardial infarction, showing a spatio-temporal and dynamic change. After myocardial infarction, the nanog expression in fibroblasts and small round cells in the infarcted zone (IZ) is much stronger than that in the margin zone (MZ) and remote infarcted zone (RIZ). From day 7 after myocardial infarction, the fibroblasts and small cells strongly expressed nanog protein in the IZ, and a few myocardial cells in the MZ and the RIZ and the numbers of nanog-positive fibroblasts and small cells reached the highest peak at 21 days after myocardial infarction, but in this period the number of nanog-positive myocardial cells decreased gradually. At 28 days after myocardial infarction, the numbers of all nanog-positive cells decreased into a low level. Therefore, our data suggest that all myocardial cells, fibroblasts and small round cells are involved in myocardial reconstruction after cardiac infarction. The nanog-positive myocardial cells may respond to early myocardial repair, and the nanog-positive fibroblasts and small round cells are the main source for myocardial reconstruction after cardiac infarction.

  9. Isoproterenol-induced myocardial fibrosis in relation to myocyte necrosis

    SciTech Connect

    Benjamin, I.J.; Jalil, J.E.; Tan, L.B.; Cho, K.; Weber, K.T.; Clark, W.A. )

    1989-09-01

    Treatment of rats with the beta-adrenergic agonist isoproterenol results in cardiac hypertrophy, myocyte necrosis, and interstitial cell fibrosis. Our objectives in this study have been to examine whether hypertrophy and fibrosis occur in a compensatory and reparative response to myocyte loss or whether either process may be occurring independently of myocyte loss and thus be a reactive response to adrenergic hormone stimulation. We have examined this question by evaluating each of these responses in rats treated with different doses and forms of isoproterenol administration. Myocyte necrosis was evaluated using in vivo labeling with monoclonal antimyosin for identification of myocytes with permeable sarcolemma, which was indicative of irreversible injury. Myocardial fibrosis was evaluated by morphometric point counting of Gomori-stained tissue sections and by assessment of the stimulation of fibroblast proliferation by determination of increased levels of DNA synthesis. Stimulation of fibroblast DNA synthesis was determined from DNA specific radioactivities and radioautography after pulse labeling with (3H)thymidine. The evidence provided by this study suggests that the degree and timing of myocardial hypertrophy does not follow the course of myocyte loss and, thus, appears to be either a response to altered cardiac loading or a reactive response to beta-adrenergic hormone stimulation rather than a compensation for myocyte loss. Myocardial fibrosis, on the other hand, appears to be more closely related to myocyte necrosis with respect to collagen accumulation in the same areas of the heart, its dose-response relation to the amount of isoproterenol administered, and the timing of increased DNA synthesis, or fibroblast proliferation, after myocyte loss.

  10. Haemodynamic profile of acebutolol in acute myocardial infarction.

    PubMed

    Wan, S H; Seah, C S; Teh, L B; Letchmana, K

    1980-10-01

    This paper evaluates the haemodynamics of intravenous Acebutolol (SECTRAL) (0.5 mgm/Kgm) in the acute phase of myocardial infarction uncomplicated by hypertension, cardiac failure or conduction abnormalities. Nineteen observations were made on 15 consecutive patients. Haemodynamic parameters were recorded just before, and at 15 and 30 min after injections, using Swan-Ganz Catheter-Thermister and Edslab Cardiac Output Computer (9520) in the Intensive Care Unit. All patients survived; none had extension of infarction. The Heart Rate dropped by 9 +/- 1% (+/- SEM) (from 90.2 +/- 4.0 to 81.6 +/- 3.1 per min, P less than 0.001) but systolic and mean Blood Pressures were not significantly altered. Pulmonary Capillary Pressure was elevated by 2.5 +/- 6% (from 11.6 +/- 0.8 to 14.4 +/- 0.9 mmHg P less than 0.001) but cardiac failure hardly ever developed clinically. The mean Pulmonary Arterial Pressure rose by 10 +/- 2% (P less than 0.005) while the Right Atrial mean increased from 6.0 +/- 1.0 to 8.3 +/- 1.3 mm Hg (P less than 0.005). Although the Cardiac Index was depressed by 11 +/- 2% (from 3.0 +/- 0.1 to 2.7 +/- 0.1 L/min/M2; P less than 0.001), the Stroke Index remained virtually unaffected. Myocardial oxygen consumption per min as reflected by Heart Rate x BP product declined by 12 +/- 2% (P less than 0.001), while the Stroke Work Index was lowered by 9 +/- 3% (P less than 0.005). The haemodynamic profile indicates that intravenous Acebutolol in uncomplicated infarcts is well tolerated, and that it could be employed with advantage to manipulate determinants of myocardial oxygen consumption through reduction of Heart Rate Pressure product and Stroke Work Index.

  11. Adaptation of myocardial blood flow to increased metabolic demand is not dependent on endothelial vasodilators in the rat heart.

    PubMed Central

    Tiefenbacher, C. P.; Tillmanns, H.; Niroomand, F.; Zimmermann, R.; Kübler, W.

    1997-01-01

    OBJECTIVE: To investigate the role of endothelial vasodilating factors in adaptation of myocardial blood flow to increased metabolic demands. DESIGN: Alterations in the effects of endothelium dependent (acetylcholine) and independent (sodium nitroprusside) vasodilators and the beta 1 receptor agonist dobutamine were studied after inhibition of endothelium derived relaxing factor (EDRF) with L-NG-nitro-arginine methyl ester (L-NAME), prostanoid synthesis with indomethacin, and ATP sensitive potassium channels with glibenclamide. EXPERIMENTAL ANIMALS: Female Wistar rats, in situ perfused heart. MAIN OUTCOME MEASURES: Myocardial blood flow (H2 clearance); systolic fractional thickening (pulsed Doppler); mean arterial blood pressure. RESULTS: L-NAME reduced myocardial blood flow by 58 (12)% (mean (SD), P < 0.001) and systolic thickening fraction (FT) by 36 (9)% (P < 0.05). These effects were significantly reversed by administration of L-arginine but not D-arginine. Pretreatment with L-NAME inhibited the increase in myocardial blood flow caused by acetylcholine (control: +42 (9)%; L-NAME: -29 (7)%, P < 0.001) but did not affect the increase in myocardial blood flow caused by sodium nitroprusside (control: +44 (5)%; L-NAME: +34 (10)%, NS). Pretreatment with L-NAME did not change the effect of dobutamine on myocardial blood flow (+61 (3)%) and FT (+32 (8)%) compared with baseline values (P < 0.001). Neither pretreatment with indomethacin nor with glibenclamide reduced the dobutamine induced increase in myocardial blood flow. CONCLUSIONS: Inhibition of EDRF, prostanoid synthesis, and ATP sensitive potassium channels did not reduce the vasodilator reserve during increased metabolic demands induced by beta 1 adrenergic stimulation. Therefore, adaptation of myocardial blood flow to increased metabolic demands is independent of endothelial relaxing factors in the rat heart. PMID:9068398

  12. Effect of beam hardening on transmural myocardial perfusion quantification in myocardial CT imaging

    NASA Astrophysics Data System (ADS)

    Fahmi, Rachid; Eck, Brendan L.; Levi, Jacob; Fares, Anas; Wu, Hao; Vembar, Mani; Dhanantwari, Amar; Bezerra, Hiram G.; Wilson, David L.

    2016-03-01

    The detection of subendocardial ischemia exhibiting an abnormal transmural perfusion gradient (TPG) may help identify ischemic conditions due to micro-vascular dysfunction. We evaluated the effect of beam hardening (BH) artifacts on TPG quantification using myocardial CT perfusion (CTP). We used a prototype spectral detector CT scanner (Philips Healthcare) to acquire dynamic myocardial CTP scans in a porcine ischemia model with partial occlusion of the left anterior descending (LAD) coronary artery guided by pressure wire-derived fractional flow reserve (FFR) measurements. Conventional 120 kVp and 70 keV projection-based mono-energetic images were reconstructed from the same projection data and used to compute myocardial blood flow (MBF) using the Johnson-Wilson model. Under moderate LAD occlusion (FFR~0.7), we used three 5 mm short axis slices and divided the myocardium into three LAD segments and three remote segments. For each slice and each segment, we characterized TPG as the mean "endo-to-epi" transmural flow ratio (TFR). BH-induced hypoenhancement on the ischemic anterior wall at 120 kVp resulted in significantly lower mean TFR value as compared to the 70 keV TFR value (0.29+/-0.01 vs. 0.55+/-0.01 p<1e-05). No significant difference was measured between 120 kVp and 70 keV mean TFR values on segments moderately affected or unaffected by BH. In the entire ischemic LAD territory, 120 kVp mean endocardial flow was significantly reduced as compared to mean epicardial flow (15.80+/-10.98 vs. 40.85+/-23.44 ml/min/100g; p<1e-04). At 70 keV, BH was effectively minimized resulting in mean endocardial MBF of 40.85+/-15.3407 ml/min/100g vs. 74.09+/-5.07 ml/min/100g (p=0.0054) in the epicardium. We also found that BH artifact in the conventional 120 kVp images resulted in falsely reduced MBF measurements even under non-ischemic conditions.

  13. Effects of heart rate on myocardial thallium-201 uptake and clearance

    SciTech Connect

    Nordrehaug, J.E.; Danielsen, R.; Vik-Mo, H. )

    1989-12-01

    The effects of heart rate on the myocardial uptake and clearance of {sup 201}Tl were studied prospectively in seven healthy men, mean age 43 +/- 7 (s.d.) yr. Initial and delayed (3 hr) thallium images were obtained in three views after three bicycle exercise tests: to maximal, 80% and 60% of predicted maximal heart rate. The mean of three views initial myocardial {sup 201}Tl uptake was higher at maximal than at both 80% and 60% of predicted maximal heart rate, being 81% (p less than 0.01) and 60% (p less than 0.01) of maximal activity, respectively. The myocardial activity in the delayed images was identical. There was a linear relationship between heart rate and the initial myocardial activity, r = 0.86 (p less than 0.001). The mean (range) {sup 201}Tl clearance was 58% (51-65), 47% (34-56), and 34% (22-49) (all differences p less than 0.01), respectively. Concordance among the three individual views in estimating clearance was best for the highest exercise level. There was a linear relationship between heart rate and clearance, r = 0.80 (p less than 0.001). Clearance was altered by only 1.67 x 10%/heart bpm (0.024 hr/heart beat). Clearance in the liver, spleen and lungs increased at submaximal exercise levels. Thus, a linear relationship between heart rate and clearance is the result of changes in the initial exercise myocardial {sup 201}Tl activity. Submaximal exercise may reduce reproducibility of clearance estimation, and the change of myocardial clearance with heart rate seems less than previously suggested.

  14. Oxygen surrounding the heart during ischemic conservation determines the myocardial injury during reperfusion.

    PubMed

    Feng, Yansheng; Bopassa, Jean Chrisostome

    2015-01-01

    There is discrepancy regarding the duration of reperfusion required using 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) staining to assess myocardial infarction in an isolated, perfused heart model. Several investigators prefer long-term reperfusion (120 minutes) to determine myocardial injury, while others have used a shorter duration (30-40 minutes). We investigated whether oxygen surrounding the myocardium during ischemia plays a critical role in the installation of myocardial infarction during reperfusion. Mice hearts were perfused with a Langendorff apparatus using Krebs Henseleit (KH) buffer oxygenated with 95% O2 plus 5% CO2 at 37°C. Hearts were either immersed in KH or suspended in air during 18 minutes of global ischemia in a normothermic, water-jacketed chamber. Hearts then were reperfused for 40, 60, or 90 minutes. We found that hearts immersed in KH had decreased recovery of function and increased myocardial infarct size, reaching a steady-state level after 40 minutes of reperfusion. In contrast, hearts suspended in air approached steady-state after 90 minutes of reperfusion. Thus, mitochondrial reactive oxygen species (ROS) production was much lower in air-maintained hearts than in KH-immersed hearts. To investigate whether an increase in oxygen surrounding the myocardium during ischemia might cause further damage, we bubbled the KH solution with nitrogen (KH+N2) rather than oxygen (KH+O2). With this alteration, recovery of cardiac function was improved and myocardial infarct size and mitochondrial ROS production were reduced compared with hearts immersed in KH+O2. In conclusion, short-term (40 minutes) reperfusion is sufficient to reach steady-state myocardial infarct size when hearts are immersed in physiologic solution during ischemia; however, a longer duration of reperfusion (90 minutes) is required if hearts are suspended in air. Thus, oxygen surrounding the heart during ischemia determines the extent of myocardium injury during reperfusion

  15. Oxygen surrounding the heart during ischemic conservation determines the myocardial injury during reperfusion.

    PubMed

    Feng, Yansheng; Bopassa, Jean Chrisostome

    2015-01-01

    There is discrepancy regarding the duration of reperfusion required using 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) staining to assess myocardial infarction in an isolated, perfused heart model. Several investigators prefer long-term reperfusion (120 minutes) to determine myocardial injury, while others have used a shorter duration (30-40 minutes). We investigated whether oxygen surrounding the myocardium during ischemia plays a critical role in the installation of myocardial infarction during reperfusion. Mice hearts were perfused with a Langendorff apparatus using Krebs Henseleit (KH) buffer oxygenated with 95% O2 plus 5% CO2 at 37°C. Hearts were either immersed in KH or suspended in air during 18 minutes of global ischemia in a normothermic, water-jacketed chamber. Hearts then were reperfused for 40, 60, or 90 minutes. We found that hearts immersed in KH had decreased recovery of function and increased myocardial infarct size, reaching a steady-state level after 40 minutes of reperfusion. In contrast, hearts suspended in air approached steady-state after 90 minutes of reperfusion. Thus, mitochondrial reactive oxygen species (ROS) production was much lower in air-maintained hearts than in KH-immersed hearts. To investigate whether an increase in oxygen surrounding the myocardium during ischemia might cause further damage, we bubbled the KH solution with nitrogen (KH+N2) rather than oxygen (KH+O2). With this alteration, recovery of cardiac function was improved and myocardial infarct size and mitochondrial ROS production were reduced compared with hearts immersed in KH+O2. In conclusion, short-term (40 minutes) reperfusion is sufficient to reach steady-state myocardial infarct size when hearts are immersed in physiologic solution during ischemia; however, a longer duration of reperfusion (90 minutes) is required if hearts are suspended in air. Thus, oxygen surrounding the heart during ischemia determines the extent of myocardium injury during reperfusion.

  16. Association between Myocardial Triglyceride Content and Cardiac Function in Healthy Subjects and Endurance Athletes

    PubMed Central

    Sai, Eiryu; Shimada, Kazunori; Yokoyama, Takayuki; Sato, Shuji; Miyazaki, Tetsuro; Hiki, Makoto; Tamura, Yoshifumi; Aoki, Shigeki; Watada, Hirotaka; Kawamori, Ryuzo; Daida, Hiroyuki

    2013-01-01

    Ectopic fat accumulation plays important roles in various metabolic disorders and cardiovascular diseases. Recent studies reported that myocardial triglyceride (TG) content measured by proton magnetic resonance spectroscopy (1H-MRS) is associated with aging, diabetes mellitus, and cardiac dysfunction. However, myocardial TG content in athletes has not yet been investigated. We performed 1H-MRS and cardiac magnetic resonance imaging in 10 male endurance athletes and 15 healthy male controls. Serum markers and other clinical parameters including arterial stiffness were measured. Cardiopulmonary exercise testing was also performed. There were no significant differences in clinical characteristics including age, anthropometric parameters, blood test results, or arterial stiffness between the two groups. Peak oxygen uptakes, end–diastolic volume (EDV), end–systolic volume (ESV), left ventricular (LV) mass, peak ejection rates and peak filling rates were significantly higher in the athlete group than in the control group (all P<0.02). Myocardial TG content was significantly lower in the athlete group than in the control group (0.60±0.20 vs. 0.89±0.41%, P<0.05). Myocardial TG content was negatively correlated with EDV (r = −0.47), ESV (r = −0.64), LV mass (r = −0.44), and epicardial fat volume (r = 0.47) (all P<0.05). In conclusion, lower levels of myocardial TG content were observed in endurance athletes and were associated with morphological changes related to physiological LV alteration in athletes, suggesting that metabolic imaging for measurement of myocardial TG content by 1H-MRS may be a useful technique for noninvasively assessing the “athlete’s heart”. PMID:23613879

  17. Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness

    NASA Technical Reports Server (NTRS)

    Harris, Todd S.; Baicu, Catalin F.; Conrad, Chester H.; Koide, Masaaki; Buckley, J. Michael; Barnes, Mary; Cooper, George 4th; Zile, Michael R.

    2002-01-01

    Recent studies have suggested that pressure overload hypertrophy (POH) alters the viscoelastic properties of individual cardiocytes when studied in isolation. However, whether these changes in cardiocyte properties contribute causally to changes in the material properties of the cardiac muscle as a whole is unknown. Accordingly, a selective, isolated, acute change in cardiocyte constitutive properties was imposed in an in vitro system capable of measuring the resultant effect on the material properties of the composite cardiac muscle. POH caused an increase in both myocardial elastic stiffness, from 20.5 +/- 1.3 to 28.4 +/- 1.8, and viscous damping, from 15.2 +/- 1.1 to 19.8 +/- 1.5 s (normal vs. POH, P < 0.05), respectively. Recent studies have shown that cardiocyte constitutive properties could be acutely altered by depolymerizing the microtubules with colchicine. Colchicine caused a significant decrease in the viscous damping in POH muscles (19.8 +/- 1.5 s at baseline vs. 14.7 +/- 1.3 s after colchicine, P < 0.05). Therefore, myocardial material properties can be altered by selectively changing the constitutive properties of one element within this muscle tissue, the cardiocyte. Changes in the constitutive properties of the cardiocytes themselves contribute to the abnormalities in myocardial stiffness and viscosity that develop during POH.

  18. Myocardial macronutrient transporter adaptations in the adult pregestational female intrauterine and postnatal growth-restricted offspring

    PubMed Central

    Abbasi, Afshan; Thamotharan, Manikkavasagar; Shin, Bo-Chul; Jordan, Maria C.; Roos, Kenneth P.; Stahl, Andreas

    2012-01-01

    Associations between exponential childhood growth superimposed on low birth weight and adult onset cardiovascular disease with glucose intolerance/type 2 diabetes mellitus exist in epidemiological investigations. To determine the metabolic adaptations that guard against myocardial failure on subsequent exposure to hypoxia, we compared with controls (CON), the effect of intrauterine (IUGR), postnatal (PNGR), and intrauterine and postnatal (IPGR) calorie and growth restriction (n = 6/group) on myocardial macronutrient transporter (fatty acid and glucose) -mediated uptake in pregestational young female adult rat offspring. A higher myocardial FAT/CD36 protein expression in IUGR, PNGR, and IPGR, with higher FATP1 in IUGR, FATP6 in PNGR, FABP-c in PNGR and IPGR, and no change in GLUT4 of all groups was observed. These adaptive macronutrient transporter protein changes were associated with no change in myocardial [3H]bromopalmitate accumulation but a diminution in 2-deoxy-[14C]glucose uptake. Examination of the sarcolemmal subfraction revealed higher basal concentrations of FAT/CD36 in PNGR and FATP1 and GLUT4 in IUGR, PNGR, and IPGR vs. CON. Exogenous insulin uniformly further enhanced sarcolemmal association of these macronutrient transporter proteins above that of basal, with the exception of insulin resistance of FATP1 and GLUT4 in IUGR and FAT/CD36 in PNGR. The basal sarcolemmal macronutrient transporter adaptations proved protective against subsequent chronic hypoxic exposure (7 days) only in IUGR and PNGR, with notable deterioration in IPGR and CON of the echocardiographic ejection fraction. We conclude that the IUGR and PNGR pregestational adult female offspring displayed a resistance to insulin-induced translocation of FATP1, GLUT4, or FAT/CD36 to the myocardial sarcolemma due to preexistent higher basal concentrations. This basal adaptation of myocardial macronutrient transporters ensured adequate fatty acid uptake, thereby proving protective against chronic

  19. Small Bowel Obstruction Mimicking Acute ST-Elevation Myocardial Infarction

    PubMed Central

    Chang, Nai-Lun; Shulik, Oleg; DePasquale, Joseph; Shamoon, Fayez

    2015-01-01

    We present a case of a 42-year-old female who presented to our institution with a small bowel obstruction and had emergent surgical decompression. Thirteen days postoperatively, the patient became tachycardic and had worsening epigastric pain. Electrocardiogram showed significant ST-segment elevations in leads II, III, aVF, and V3–V6, suggesting the possibility of acute inferolateral myocardial infarction. Subsequent workup revealed the cause of the ST-elevations to be due to recurrent small bowel obstruction. Although intra-abdominal causes of ST-elevation have been reported, our case may be the first to be associated with small bowel obstruction. PMID:25838963

  20. Noncompaction and embolic myocardial infarction: the importance of oral anticoagulation.

    PubMed

    Pulignano, Giovanni; Tinti, Maria Denitza; Tolone, Stefano; Musto, Carmine; De Lio, Lucia; Pino, Paolo Giuseppe; Minardi, Giovanni; Violini, Roberto; Uguccioni, Massimo

    2015-01-01

    Left ventricular noncompaction (LVNC) is characterized by left ventricular (LV) hypertrabeculations and is associated with heart failure, arrhythmias and embolism. We report the case of a 67-year-old LVNC patient, under oral anticoagulation (OAC) therapy for apical thrombosis. After she discontinued OAC, the thrombus involved almost the whole of the left ventricle; in a few months her condition worsened, requiring hospitalization, and despite heparin infusion she experienced myocardial infarction (MI), caused by embolic occlusion of the left anterior descending artery. Although infrequent as a complication of LVNC, and usually attributable to microvascular dysfunction, in this case MI seems due to coronary thromboembolism from dislodged thrombotic material in the left ventricle.

  1. Lay Public's Knowledge and Decisions in Response to Symptoms of Acute Myocardial Infarction

    ERIC Educational Resources Information Center

    Cytryn, Kayla N.; Yoskowitz, Nicole A.; Cimino, James J.; Patel, Vimla L.

    2009-01-01

    Despite public health initiatives targeting rapid action in response to symptoms of myocardial infarction (MI), people continue to delay in going to a hospital when experiencing these symptoms due to lack of recognition as cardiac-related. The objective of this research was to characterize lay individuals' knowledge of symptoms of acute myocardial…

  2. Myocardial infarction in young adults

    PubMed Central

    Egred, M; Viswanathan, G; Davis, G

    2005-01-01

    Although myocardial infarction (MI) mainly occurs in patients older than 45, young men or women can suffer MI. Fortunately, its incidence is not common in patients younger than 45 years. However, the disease carries a significant morbidity, psychological effects, and financial constraints for the person and the family when it occurs at a young age. The causes of MI among patients aged less than 45 can be divided into four groups: (1) atheromatous coronary artery disease; (2) non-atheromatous coronary artery disease; (2) hyper-coagulable states; (4) MI related to substance misuse. There is a considerable overlap between all the groups. This article reviews the literature and highlights the practical issues involved in the management of young adults with MI. PMID:16344295

  3. Myocyte repolarization modulates myocardial function in aging dogs.

    PubMed

    Sorrentino, Andrea; Signore, Sergio; Qanud, Khaled; Borghetti, Giulia; Meo, Marianna; Cannata, Antonio; Zhou, Yu; Wybieralska, Ewa; Luciani, Marco; Kannappan, Ramaswamy; Zhang, Eric; Matsuda, Alex; Webster, Andrew; Cimini, Maria; Kertowidjojo, Elizabeth; D'Alessandro, David A; Wunimenghe, Oriyanhan; Michler, Robert E; Royer, Christopher; Goichberg, Polina; Leri, Annarosa; Barrett, Edward G; Anversa, Piero; Hintze, Thomas H; Rota, Marcello

    2016-04-01

    Studies of myocardial aging are complex and the mechanisms involved in the deterioration of ventricular performance and decreased functional reserve of the old heart remain to be properly defined. We have studied a colony of beagle dogs from 3 to 14 yr of age kept under a highly regulated environment to define the effects of aging on the myocardium. Ventricular, myocardial, and myocyte function, together with anatomical and structural properties of the organ and cardiomyocytes, were evaluated. Ventricular hypertrophy was not observed with aging and the structural composition of the myocardium was modestly affected. Alterations in the myocyte compartment were identified in aged dogs, and these factors negatively interfere with the contractile reserve typical of the young heart. The duration of the action potential is prolonged in old cardiomyocytes contributing to the slower electrical recovery of the myocardium. Also, the remodeled repolarization of cardiomyocytes with aging provides inotropic support to the senescent muscle but compromises its contractile reserve, rendering the old heart ineffective under conditions of high hemodynamic demand. The defects in the electrical and mechanical properties of cardiomyocytes with aging suggest that this cell population is an important determinant of the cardiac senescent phenotype. Collectively, the delayed electrical repolarization of aging cardiomyocytes may be viewed as a critical variable of the aging myopathy and its propensity to evolve into ventricular decompensation under stressful conditions.

  4. Cardiac oxidative stress and inflammatory cytokines response after myocardial infarction.

    PubMed

    Neri, Margherita; Fineschi, Vittorio; Di Paolo, Marco; Pomara, Cristoforo; Riezzo, Irene; Turillazzi, Emanuela; Cerretani, Daniela

    2015-01-01

    Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protection. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-α (Tumor Necrosis Factor α), IL-1β (Interleukin- 1β) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.

  5. Successful treatment of a young woman with acute complicated myocardial infarction

    PubMed Central

    Serpytis, Pranas; Kibarskis, Aleksandras; Katkus, Rimgaudas; Samalavicius, Robertas; Glaveskaite, Sigita; Rackauskas, Gediminas

    2013-01-01

    Therapeutic hypothermia is method used to improve the neurological status of patients who are at risk of ischaemia after myocardial infarction. We report a case of a 28-year-old woman who suffered acute myocardial infarction complicated by ventricular fibrillation. The patient was successfully resuscitated. Invasive and non-invasive medical treatment was applied including therapeutic hypothermia. Success was achieved due to adequate public reaction, fast transportation, blood vessel revascularization and application of therapeutic hypothermia. The patient was successfully discharged after one week of treatment, and just minor changes in heart function were present. PMID:24570755

  6. [Stem cell perspectives in myocardial infarctions].

    PubMed

    Aceves, José Luis; Archundia, Abel; Díaz, Guillermo; Páez, Araceli; Masso, Felipe; Alvarado, Martha; López, Manuel; Aceves, Rocío; Ixcamparij, Carlos; Puente, Adriana; Vilchis, Rafael; Montaño, Luis Felipe

    2005-01-01

    Myocardial infarction is the leading cause of congestive heart failure and death in industrializated countries. The cellular cardiomyoplasty has emerged as an alternative treatment in the regeneration of infarted myocardial tissue. In animals' models, different cellular lines such as cardiomyocites, skeletal myoblasts, embryonic stem cells and adult mesenchymal stem cells have been used, resulting in an improvement in ventricular function and decrease in amount of infarcted tissue. The first three cells lines have disvantages as they are allogenics and are difficult to obtain. The adult mesenchymal stem cells are autologous and can be obtained throught the aspiration of bone marrow or from peripherical circulation, after stimulating with cytokines (G-CSF). The implantation in humans with recent and old myocardial infarction have shown improvements similar to those shown in animal models. These findings encourage the continued investigation in the mechanism of cellular differentiation and implantation methods in infarcted myocardial tissue.

  7. Physiology and pharmacology of myocardial preconditioning.

    PubMed

    Raphael, Jacob

    2010-03-01

    Perioperative myocardial ischemia and infarction are not only major sources of morbidity and mortality in patients undergoing surgery but also important causes of prolonged hospital stay and resource utilization. Ischemic and pharmacological preconditioning and postconditioning have been known for more than two decades to provide protection against myocardial ischemia and reperfusion and limit myocardial infarct size in many experimental animal models, as well as in clinical studies (1-3). This paper will review the physiology and pharmacology of ischemic and drug-induced preconditioning and postconditioning of the myocardium with special emphasis on the mechanisms by which volatile anesthetics provide myocardial protection. Insights gained from animal and clinical studies will be presented and reviewed and recommendations for the use of perioperative anesthetics and medications will be given.

  8. Exosomes and cardiac repair after myocardial infarction.

    PubMed

    Sahoo, Susmita; Losordo, Douglas W

    2014-01-17

    Myocardial infarction is a leading cause of death among all cardiovascular diseases. The analysis of molecular mechanisms by which the ischemic myocardium initiates repair and remodeling indicates that secreted soluble factors are key players in communication to local and distant tissues, such as bone marrow. Recently, actively secreted membrane vesicles, including exosomes, are being recognized as new candidates with important roles in intercellular and tissue-level communication. In this review, we critically examine the emerging role of exosomes in local and distant microcommunication mechanisms after myocardial infarction. A comprehensive understanding of the role of exosomes in cardiac repair after myocardial infarction could bridge a major gap in knowledge of the repair mechanism after myocardial injury.

  9. Effect of Diltiazem on Coronary Artery Flow and Myocardial Perfusion in Patients With Isolated Coronary Artery Ectasia and Either Stable Angina Pectoris or Positive Myocardial Ischemic Stress Test.

    PubMed

    Ozcan, Ozgur Ulas; Atmaca, Yusuf; Goksuluk, Huseyin; Akbulut, Irem Muge; Ozyuncu, Nil; Ersoy, Nedret; Erol, Cetin

    2015-10-15

    Isolated coronary artery ectasia (CAE) may be associated with stable or unstable coronary events despite the absence of epicardial coronary stenosis. Impaired coronary flow dynamics and myocardial perfusion have been demonstrated in stable patients with ectatic coronary arteries. We aimed to assess whether epicardial flow and tissue-level perfusion would be improved by diltiazem in myocardial regions subtended by the ectatic coronary arteries in patients with isolated CAE. A total of 60 patients with isolated CAE were identified of 9,780 patients who underwent elective coronary angiography. Patients were randomized to 5 mg of intracoronary diltiazem or saline. Coronary blood flow of the microvascular network was assessed using myocardial blush grade (MBG) technique. The thrombolysis in myocardial infarction (TIMI) flow grade and TIMI frame count (TFC) were used to assess epicardial coronary flow. MBG (from 2.4 to 2.6, p = 0.02), TIMI flow grades (from 2.4 to 2.8, p <0.001), and TFC (from 35 to 26, p <0.001) were significantly improved after diltiazem, whereas no significant change was noticed after saline (from 2.4 to 2.4, p = 0.86 for MBG; from 2.3 to 2.3, p = 0.71 for TIMI flow grade; and from 35 to 33, p = 0.43 for TFC). Diltiazem provided amelioration of the altered coronary flow dynamics, which was suggested as the pathophysiological influence of CAE. In conclusion, the favorable effects of the diltiazem on myocardial perfusion were observed at both epicardial and tissue levels.

  10. The effect of tadalafil on the time to exercise-induced myocardial ischaemia in subjects with coronary artery disease

    PubMed Central

    Patterson, Dean; Kloner, Robert; Effron, Mark; Emmick, Jeffrey; Bedding, Alun; Warner, Margaret; Mitchell, Malcolm; Braat, Simon; MacDonald, Thomas

    2005-01-01

    Objective To investigate the effect of tadalafil on the time to exercise-induced myocardial ischaemia in subjects with coronary artery disease (CAD). Background CAD and erectile dysfunction (ED) share similar risk factors. It is important to know the cardiovascular effects of tadalafil in patients with CAD during physical exertion that is comparable with sexual activity. Methods A randomized, placebo-controlled, double-blind, two-period, crossover study comparing the effects of tadalafil 10 mg and placebo on the time to exercise treadmill test (ETT)-induced myocardial ischaemia in subjects with stable CAD (n = 23; age range: 53–75 years, all exhibited ST-segment depression >1.5 mm at screening ETT at >5METS). Haemodynamic responses to sublingual nitroglycerin (NTG) were assessed before and after ETT. Results Compared with placebo, tadalafil did not significantly affect the time to ETT-induced ischaemia (13 min/31 s vs. 13 min/36 s, respectively). Before exercise, NTG evoked decreases in sitting systolic blood pressure (SBP) that were significantly greater when subjects received tadalafil compared with placebo, and after exercise, more subjects experienced a decrease in SBP <85 mmHg in response to NTG after taking tadalafil vs. placebo. When subjects received tadalafil compared with placebo, SBP was lower at rest (−7 mmHg; −12,-2), during ETT (−10 mmHg; −16, −3), and after ETT (−13 mmHg; −19, −7). Conclusion Tadalafil did not significantly alter the time to ETT-induced ischaemia compared with placebo in subjects with CAD. Tadalafil reduced resting and exercise SBP. Due to the potential for hypotension, the concomitant use of nitrates and tadalafil is contraindicated. PMID:16236035

  11. High-fat, low-carbohydrate diet promotes arrhythmic death and increases myocardial ischemia-reperfusion injury in rats

    PubMed Central

    Liu, Jian; Wang, Peipei; Zou, Luyun; Qu, Jing; Litovsky, Silvio; Umeda, Patrick; Zhou, Lufang; Chatham, John; Marsh, Susan A.; Dell'Italia, Louis J.

    2014-01-01

    High-fat, low-carbohydrate diets (HFLCD) are often eaten by humans for a variety of reasons, but the effects of such diets on the heart are incompletely understood. We evaluated the impact of HFLCD on myocardial ischemia/reperfusion (I/R) using an in vivo model of left anterior descending coronary artery ligation. Sprague-Dawley rats (300 g) were fed HFLCD (60% calories fat, 30% protein, 10% carbohydrate) or control (CONT; 16% fat, 19% protein, 65% carbohydrate) diet for 2 wk and then underwent open chest I/R. At baseline (preischemia), diet did not affect left ventricular (LV) systolic and diastolic function. Oil red O staining revealed presence of lipid in the heart with HFLCD but not in CONT. Following I/R, recovery of LV function was decreased in HFLCD. HFLCD hearts exhibited decreased ATP synthase and increased uncoupling protein-3 gene and protein expression. HFLCD downregulated mitochondrial fusion proteins and upregulated fission proteins and store-operated Ca2+ channel proteins. HFLCD led to increased death during I/R; 6 of 22 CONT rats and 16 of 26 HFLCD rats died due to ventricular arrhythmias and hemodynamic shock. In surviving rats, HFLCD led to larger infarct size. We concluded that in vivo HFLCD does not affect nonischemic LV function but leads to greater myocardial injury during I/R, with increased risk of death by pump failure and ventricular arrhythmias, which might be associated with altered cardiac energetics, mitochondrial fission/fusion dynamics, and store-operated Ca2+ channel expression. PMID:24929857

  12. High-fat, low-carbohydrate diet promotes arrhythmic death and increases myocardial ischemia-reperfusion injury in rats.

    PubMed

    Liu, Jian; Wang, Peipei; Zou, Luyun; Qu, Jing; Litovsky, Silvio; Umeda, Patrick; Zhou, Lufang; Chatham, John; Marsh, Susan A; Dell'Italia, Louis J; Lloyd, Steven G

    2014-08-15

    High-fat, low-carbohydrate diets (HFLCD) are often eaten by humans for a variety of reasons, but the effects of such diets on the heart are incompletely understood. We evaluated the impact of HFLCD on myocardial ischemia/reperfusion (I/R) using an in vivo model of left anterior descending coronary artery ligation. Sprague-Dawley rats (300 g) were fed HFLCD (60% calories fat, 30% protein, 10% carbohydrate) or control (CONT; 16% fat, 19% protein, 65% carbohydrate) diet for 2 wk and then underwent open chest I/R. At baseline (preischemia), diet did not affect left ventricular (LV) systolic and diastolic function. Oil red O staining revealed presence of lipid in the heart with HFLCD but not in CONT. Following I/R, recovery of LV function was decreased in HFLCD. HFLCD hearts exhibited decreased ATP synthase and increased uncoupling protein-3 gene and protein expression. HFLCD downregulated mitochondrial fusion proteins and upregulated fission proteins and store-operated Ca(2+) channel proteins. HFLCD led to increased death during I/R; 6 of 22 CONT rats and 16 of 26 HFLCD rats died due to ventricular arrhythmias and hemodynamic shock. In surviving rats, HFLCD led to larger infarct size. We concluded that in vivo HFLCD does not affect nonischemic LV function but leads to greater myocardial injury during I/R, with increased risk of death by pump failure and ventricular arrhythmias, which might be associated with altered cardiac energetics, mitochondrial fission/fusion dynamics, and store-operated Ca(2+) channel expression.

  13. [The latest treatments for myocardial infarction].

    PubMed

    Leclercq, Florence

    2015-03-01

    Ischemic heart disease and its main complication, myocardial infarction, remain the leading cause of death after the age of forty in developed countries. Myocardial infarction is the consequence of a sudden obstruction of a coronary artery by a thrombus. Thrombolysis and coronary angioplasty are the two emergency coronary artery revascularisation techniques. A medication-based treatment and adapted lifestyle aim to prevent repeat infarction. PMID:26040139

  14. Tachycardia induced myocardial dysfunction. A reversible phenomenon?

    PubMed Central

    McLaran, C J; Gersh, B J; Sugrue, D D; Hammill, S C; Seward, J B; Holmes, D R

    1985-01-01

    Four patients with myocardial dysfunction related to tachycardia underwent electrophysiological studies, which showed a re-entrant supraventricular tachycardia using an accessory atrioventricular connexion. Serial assessment of left ventricular function by echocardiography before and after control of the tachycardia indicated a variable degree of reversibility. Endomyocardial biopsy in two patients detected non-specific histological changes. Because of the possible role of ischaemia in this condition effective control of prolonged tachycardia is needed to prevent deterioration of myocardial function. Images PMID:3970789

  15. Improved exercise myocardial perfusion during lidoflazine therapy

    SciTech Connect

    Shapiro, W.; Narahara, K.A.; Park, J.

    1983-11-01

    Lidoflazine is a synthetic drug with calcium-channel blocking effects. In a study of 6 patients with severe classic angina pectoris, single-blind administration of lidoflazine was associated with improved myocardial perfusion during exercise as determined by thallium-201 stress scintigraphy. These studies demonstrate that lidoflazine therapy is associated with relief of angina, an increased physical work capacity, and improved regional myocardial perfusion during exercise.

  16. Acute myocardial ischemia and reperfusion: MR imaging with albumin-Gd-DTPA

    SciTech Connect

    Schmiedl, U.; Sievers, R.E.; Brasch, R.C.; Wolfe, C.L.; Chew, W.M.; Ogan, M.D.; Engeseth, H.; Lipton, M.J.; Moseley, M.E.

    1989-02-01

    The utility of a macromolecular, intravascular contrast agent, albumin-gadolinium diethylenetriaminepentaacetic acid (DTPA), for the differentiation of acutely ischemic and reperfused myocardium on magnetic resonance (MR) images was investigated. Regional, reversible myocardial ischemia was produced in rats and confirmed. After reperfusion, flow to the compromised myocardial segment returned to baseline. Normal myocardium could not be differentiated from ischemic myocardium on nonenhanced MR images (n = 12). After 5 minutes of myocardial ischemia and after administration of albumin-Gd-DTPA, the ischemic zone involving the free wall of the left ventricle was characterized by the absence of significant enhancement. Normal myocardium appeared homogeneously enhanced (by 145%). This pattern persisted for up to 1 hour of myocardial ischemia. In six rats that underwent myocardial reperfusion after 5 minutes of ischemia, the normal and reperfused myocardium became isointense. Radiotracer studies with albumin-Gd-153-DTPA confirmed the decreased distribution of contrast agent to the ischemic myocardium, possibly due to decreased blood pool or a blocked primary delivery system in the ischemic myocardium.

  17. Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension.

    PubMed

    Egan Benova, T; Szeiffova Bacova, B; Viczenczova, C; Diez, E; Barancik, M; Tribulova, N

    2016-09-19

    Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of life-threatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that down-regulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.

  18. Myocardial perfusion of infarcted and normal myocardium in propofol-anesthetized minipigs using (82)Rubidium PET.

    PubMed

    Rasmussen, Thomas; Follin, Bjarke; Kastrup, Jens; Christensen, Thomas Emil; Hammelev, Karsten Pharao; Kjær, Andreas; Hasbak, Philip

    2016-06-01

    Cardiac Rubidium-82 ((82)Rb) positron-emission-tomography (PET) is a good method for quantification of myocardial blood flow in man. Quantification of myocardial blood flow in animals to evaluate new treatment strategies or to understand underlying disease is also of great interest but raises some challenges. Animals, which have been anesthetized during PET acquisition, might react differently to used stress medications, and therefore difficulties might exist while evaluating the resulting PET images using standard software packages from commercial vendors optimized for human hearts. Furthermore propofol, used for anesthesia, can influence myocardial perfusion and coronary flow reserve due to its vasorelaxant effect, and interactions might exist between propofol and used stress agents, potentially affecting the result of the examination. We present cardiac (82)Rb-PET studies performed in propofol-anesthetized minipigs with normal and infarcted myocardium stressed with both adenosine and dipyridamole. Despite the mentioned challenges, we were able to trace the small minipig heart with software designed for human cardiac PET and to achieve blood flow measurements comparable with results in humans with both adenosine and dipyridamole. We found dipyridamole to be a superior stress agent for this experimental setup. Finally, we were able to clearly identify the myocardial perfusion defect after an induced myocardial infarction. PMID:26931633

  19. Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension.

    PubMed

    Egan Benova, T; Szeiffova Bacova, B; Viczenczova, C; Diez, E; Barancik, M; Tribulova, N

    2016-09-19

    Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of life-threatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that down-regulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension. PMID:27643938

  20. Cardiac Motion Analysis Using High-Speed Video Images in a Rat Model for Myocardial Infarction

    NASA Astrophysics Data System (ADS)

    Ishii, Idaku; Okuda, Toshikazu; Nie, Yuman; Takaki, Takeshi; Orito, Kensuke; Tanaka, Akane; Matsuda, Hiroshi

    In this study, we performed a cardiac motion analysis by using 1000-frames per second (fps) stereo images to capture the three-dimensional motion of small color markers in a rat heart. This method of recording cardiac motion could quantify the rate of change in the myocardial area, which indicated localized myocardial activity of rhythmic expansion and contraction. We analyzed the three-dimensional motion distributions in a rat model for myocardial infarction, in which the heart rate was 4 times/s or more. In the analysis, we spatiotemporally quantified the characteristic cardiac motion in ischemic heart diseases and found that infarction due to ischemia in the rat heart was spread around the left ventricle.

  1. Intravenous methylphenidate: an unusual way to provoke ST-elevation myocardial infarction.

    PubMed

    Hay, Emile; Shklovski, Vitaly; Blaer, Yossef; Shlakhover, Vladimir; Katz, Amos

    2015-02-01

    Acute ST-T elevation is a sign of myocardial ischemia or infarction usually due to coronary artery atherosclerosis or coronary spasm. Coronary spasm may be spontaneous or can occur as a result of a drug that causes arterial spam. Ritalin, Novartis Pharmaceut. Corporation, USA (methylphenidate hydrochloride), a dopamine reuptake inhibitor,is an oral drug used to treat attention-deficit/hyperactivity disorder and narcolepsy. Sudden deaths, stroke, and myocardial infarction have been reported in adults taking stimulant drugs at usual dose for attention-deficit/hyperactivity disorder [1]. This drug is not supplied as solution for injection [2]. We report here, what we believe to be, the first case report of a 40-year-old male patient who was admitted for acute chest pain and ST-elevation myocardial infarction after intravenous self-injection of Ritalin. His coronary angiogram demonstrated nonobstructive coronary disease.

  2. Assessment of myocardial perfusion in patients after the arterial switch operation

    SciTech Connect

    Vogel, M.; Smallhorn, J.F.; Gilday, D.; Benson, L.N.; Ash, J.; Williams, W.G.; Freedom, R.M. )

    1991-02-01

    In 21 patients who had undergone the arterial switch operation, the adequacy of myocardial perfusion was evaluated by thallium-201 computed scintigraphy 2.6 +/- 2 (0.3-7) yr after surgery. Fourteen patients had undergone the arterial switch procedure after pulmonary artery banding and seven as a primary repair. Isoproterenol stress increased the heart rate by at least 55%. Tomographic imaging was performed at peak stress and 3 hr later in the reperfusion phase. Nine patients had perfusion defects. The perfusion defects were located at the left ventricular apex in four (with extension to the inferolateral wall in one), left ventricular anterolateral wall in two, ventricular septum in one, left ventricular inferior wall in one, and right ventricular free wall in one. Some of these defects could be due to myocardial damage at the time of surgery, but these results also raise concern about long-term adequacy of myocardial perfusion following the arterial switch procedure.

  3. Relationship between myocardial bridging and coronary arteriosclerosis.

    PubMed

    Sun, Jian Ling; Huang, Wei Min; Guo, Ji Hong; Li, Xiao Ying; Ma, Xian Lin; Wang, Chong Yu

    2013-04-01

    The objective of the study was to explore the prevalence and characteristics of myocardial bridging in patients who underwent coronary angiography and to also evaluate the correlation between bridged coronary segments and atherosclerosis. For this purpose, clinical materials of 1,500 patients who had received coronary angiography were retrospectively analyzed. The location and length of the myocardial bridge were recorded as well as the extent and location of coronary artery stenosis was described. Segments proximal and distal to the bridging were evaluated for coronary arteriosclerosis as were the remaining coronary segments. We found that myocardial bridging was present in 179 (11.9 %) patients. Bridges were frequently (84.9 %) localized in the mid-distal segment of the left anterior descending (LAD) artery. Myocardial bridging was not considered a significant risk factor for coronary atherosclerosis (odds ratio 0.58) compared with traditional cardiovascular risk factors. The incidence of coronary arteriosclerosis in the distal segments was significantly less affected than the proximal segments (P < 0.01). It was, therefore, concluded that myocardial bridging frequently localized in the mid-distal segment of the LAD artery. The presence of myocardial bridging promotes proximal atherosclerosis but it is not an additional risk factor for coronary atherosclerosis. PMID:23076634

  4. A somatic component to myocardial infarction.

    PubMed Central

    Nicholas, A S; DeBias, D A; Ehrenfeuchter, W; England, K M; England, R W; Greene, C H; Heilig, D; Kirschbaum, M

    1985-01-01

    Sixty two patients were randomised to be seen by osteopathic physicians for palpation of the thoracic paravertebral soft tissue, T1-T8. Twenty five patients had clinically confirmed acute myocardial infarction. Of the remainder, 22 without known cardiovascular disease served as controls and 15 were placed in an excluded group because of diagnosed cardiovascular disease other than myocardial infarction. Observations were described in predetermined standard terminology. The control group was found to have a low incidence of palpable changes throughout the thoracic dorsum, and these changes were uniformly distributed from T1 to T8. Examination of the group with myocardial infarction disclosed a significantly higher incidence of soft tissue changes (increased firmness, warmth, ropiness, oedematous changes, heavy musculature), confined almost entirely to the upper four thoracic levels. The 15 patients who were excluded from the experimental group because they had various cardiovascular diseases other than myocardial infarction also showed significantly different changes on palpation compared with the group with myocardial infarction. These findings suggest that myocardial infarction is accompanied by characteristic paravertebral soft tissue changes which are readily detected by palpation. PMID:3926040

  5. Novel adjunctive treatments of myocardial infarction

    PubMed Central

    Schmidt, Michael Rahbek; Pryds, Kasper; Bøtker, Hans Erik

    2014-01-01

    Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic and pharmacological conditioning, but despite decades of research, the translation into clinical effects has been challenging. Recently published clinical studies, however, prompt optimism as novel techniques allow for improved clinical applicability. Cyclosporine A, the GLP-1 analogue exenatide and rapid cooling by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary surgery and percutaneous coronary intervention. The discovery that RIC can be performed noninvasively using a blood pressure cuff on the upper arm to induce brief episodes of limb ischemia and reperfusion has facilitated the translation of RIC into the clinical arena. This review focus on novel advances in adjunctive therapies in relation to acute and elective coronary procedures. PMID:24976915

  6. Computational modeling of acute myocardial infarction.

    PubMed

    Sáez, P; Kuhl, E

    2016-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size. PMID:26583449

  7. Sensitive Troponin Assay and the Classification of Myocardial Infarction

    PubMed Central

    Shah, Anoop S.V.; McAllister, David A.; Mills, Rosamund; Lee, Kuan Ken; Churchhouse, Antonia M.D.; Fleming, Kathryn M.; Layden, Elizabeth; Anand, Atul; Fersia, Omar; Joshi, Nikhil V.; Walker, Simon; Jaffe, Allan S.; Fox, Keith A.A.; Newby, David E.; Mills, Nicholas L.

    2015-01-01

    Background Lowering the diagnostic threshold for troponin is controversial because it may disproportionately increase the diagnosis of myocardial infarction in patients without acute coronary syndrome. We assessed the impact of lowering the diagnostic threshold of troponin on the incidence, management, and outcome of patients with type 2 myocardial infarction or myocardial injury. Methods Consecutive patients with elevated plasma troponin I concentrations (≥50 ng/L; n = 2929) were classified with type 1 (50%) myocardial infarction, type 2 myocardial infarction or myocardial injury (48%), and type 3 to 5 myocardial infarction (2%) before and after lowering the diagnostic threshold from 200 to 50 ng/L with a sensitive assay. Event-free survival from death and recurrent myocardial infarction was recorded at 1 year. Results Lowering the threshold increased the diagnosis of type 2 myocardial infarction or myocardial injury more than type 1 myocardial infarction (672 vs 257 additional patients, P < .001). Patients with myocardial injury or type 2 myocardial infarction were at higher risk of death compared with those with type 1 myocardial infarction (37% vs 16%; relative risk [RR], 2.31; 95% confidence interval [CI], 1.98-2.69) but had fewer recurrent myocardial infarctions (4% vs 12%; RR, 0.35; 95% CI, 0.26-0.49). In patients with troponin concentrations 50 to 199 ng/L, lowering the diagnostic threshold was associated with increased healthcare resource use (P < .05) that reduced recurrent myocardial infarction and death for patients with type 1 myocardial infarction (31% vs 20%; RR, 0.64; 95% CI, 0.41-0.99), but not type 2 myocardial infarction or myocardial injury (36% vs 33%; RR, 0.93; 95% CI, 0.75-1.15). Conclusions After implementation of a sensitive troponin assay, the incidence of type 2 myocardial infarction or myocardial injury disproportionately increased and is now as frequent as type 1 myocardial infarction. Outcomes of patients with type 2 myocardial

  8. Myocardial infarction caused by myocardial bridging in a male adolescent athlete.

    PubMed

    Zhu, Cheng-Gang; Liu, Jun; Liu, Wei-Dong; Xu, Yan-Lu; Wu, Na-Qiong; Guo, Yuan-Lin; Tang, Yi-Da; Jiang, Li-Xin; Li, Jian-Jun

    2012-02-01

    Myocardial bridging is a common congenital abnormality of a coronary artery, and is usually thought to be a benign anatomical variant. Although rare, previous studies have reported that patients with myocardial bridging may suffer from myocardial ischemia, myocardial infarction (MI), arrhythmias and even sudden death. Here we report the case of an 18-year-old adolescent athlete with myocardial bridging resulting in MI. Coronary angiography revealed 80% luminal narrowing by systolic compression in the proximal and mid segments of the left anterior descending coronary artery, which returned to normal during diastole. We considered that heavy sports might be a potential trigger for his MI attack. Therefore, special attention should be paid to this kind of athlete, especially if adolescent.

  9. Incidence of acute myocardial infarction in patients with exercise-induced silent myocardial ischemia

    SciTech Connect

    Assey, M.E.; Walters, G.L.; Hendrix, G.H.; Carabello, B.A.; Usher, B.W.; Spann, J.F. Jr.

    1987-03-01

    Fifty-five patients with angiographically proved coronary artery disease (CAD) underwent Bruce protocol exercise stress testing with thallium-201 imaging. Twenty-seven patients (group I) showed myocardial hypoperfusion without angina pectoris during stress, which normalized at rest, and 28 patients (group II) had a similar pattern of reversible myocardial hypoperfusion but also had angina during stress. Patients were followed for at least 30 months. Six patients in group I had an acute myocardial infarction (AMI), 3 of whom died, and only 1 patient in group II had an AMI (p = 0.05), and did not die. Silent myocardial ischemia uncovered during exercise stress thallium testing may predispose to subsequent AMI. The presence of silent myocardial ischemia identified in this manner is of prognostic value, independent of angiographic variables such as extent of CAD and left ventricular ejection fraction.

  10. Radionuclide imaging of myocardial perfusion and viability in assessment of acute myocardial infarction

    SciTech Connect

    Berman, D.S.; Kiat, H.; Maddahi, J.; Shah, P.K.

    1989-07-18

    Technical advances in radionuclide imaging have important implications for the management of patients with acute myocardial infarction. Single-photon emission computerized tomography with thallium 201 (TI-201) offers greater accuracy than planar imaging in detecting, localizing and sizing myocardial perfusion defects. Use of single-photon emission computerized tomography with TI-201 should allow for a more accurate assessment of prognosis after myocardial infarction. A new radiopharmaceutical, technetium 99-m methoxyisobutyl isonitrile, provides a number of advantages over TI-201, including higher quality images, lack of redistribution, and the ability to assess first-pass ventricular function. Applications of TI-201 and technetium 99-m methoxyisobutyl isonitrile include assessment of arterial patency and myocardial salvage immediately after thrombolytic therapy, detection of resting ischemia after thrombolytic therapy, targeting of subsets of patients for further intervention, and predischarge assessment to predict the future course of patients after an acute myocardial infarction.

  11. Protection against myocardial ischemia-reperfusion injury in clinical practice.

    PubMed

    Garcia-Dorado, David; Rodríguez-Sinovas, Antonio; Ruiz-Meana, Marisol; Inserte, Javier

    2014-05-01

    Even when reperfusion therapy is applied as early as possible, survival and quality of life are compromised in a considerable number of patients with ST-segment elevation acute myocardial infarction. Some cell death following transient coronary occlusion occurs during reperfusion, due to poor handling of calcium in the sarcoplasmic reticulum-mitochondria system, calpain activation, oxidative stress, and mitochondrial failure, all promoted by rapid normalization of intracellular pH. Various clinical trials have shown that infarct size can be limited by nonpharmacological strategies--such as ischemic postconditioning and remote ischemic conditioning--or by drugs--such as cyclosporine, insulin, glucagon-like peptide-1 agonists, beta-blockers, or stimulation of cyclic guanosine monophosphate synthesis. However, some clinical studies have yielded negative results, largely due to a lack of consistent preclinical data or a poor design, especially delayed administration. Large-scale clinical trials are therefore necessary, particularly those with primary clinical variables and combined therapies that consider age, sex, and comorbidities, to convert protection against reperfusion injury into a standard treatment for patients with ST-segment elevation acute myocardial infarction. PMID:24774733

  12. Protection against myocardial ischemia-reperfusion injury in clinical practice.

    PubMed

    Garcia-Dorado, David; Rodríguez-Sinovas, Antonio; Ruiz-Meana, Marisol; Inserte, Javier

    2014-05-01

    Even when reperfusion therapy is applied as early as possible, survival and quality of life are compromised in a considerable number of patients with ST-segment elevation acute myocardial infarction. Some cell death following transient coronary occlusion occurs during reperfusion, due to poor handling of calcium in the sarcoplasmic reticulum-mitochondria system, calpain activation, oxidative stress, and mitochondrial failure, all promoted by rapid normalization of intracellular pH. Various clinical trials have shown that infarct size can be limited by nonpharmacological strategies--such as ischemic postconditioning and remote ischemic conditioning--or by drugs--such as cyclosporine, insulin, glucagon-like peptide-1 agonists, beta-blockers, or stimulation of cyclic guanosine monophosphate synthesis. However, some clinical studies have yielded negative results, largely due to a lack of consistent preclinical data or a poor design, especially delayed administration. Large-scale clinical trials are therefore necessary, particularly those with primary clinical variables and combined therapies that consider age, sex, and comorbidities, to convert protection against reperfusion injury into a standard treatment for patients with ST-segment elevation acute myocardial infarction.

  13. [Characteristics of therapy of acute myocardial infarction in diabetes].

    PubMed

    Motz, W; Kerner, W

    2012-05-01

    Therapy of acute myocardial infarction (STEMI and NSTEMI) in diabetics does not principally differ from that of non-diabetic patients. Due to the higher mortality in diabetics reperfusion measures, such as direct percutaneous coronary intervention (PCI), should be rapidly performed. An intensive drug treatment with thrombocyte aggregation inhibitors, angiotensin-converting enzyme (ACE) inhibitors and beta-receptor blocking agents must be carried out according to the current guidelines. An important factor is the high risk of renal failure due to the contrast dye administered during PCI in the presence of pre-existing diabetic kidney damage which should be limited to 100 ml if possible. Direct PCI should be limited to the infarcted vessel. After stabilization a comprehensive strategy to cure coronary artery disease, whether with PCI or coronary artery bypass graft (CABG) should be finalized. If severe coronary 3-vessel disease is present, CABG should be favored in diabetic patients. After surviving an acute myocardial infarction differentiated metabolic monitoring is mandatory.

  14. [Occupational stress and myocardial infarction].

    PubMed

    Consoli, Silla M

    2015-01-01

    Besides the best-known role of depressed mood, occupational stress deserves to be taken as a coronary risk factor. There are two basic models to define occupational stress: Karasek's model (high job psychological demands associated with low decision latitude, or even low social support at work) and Siegrist's model (imbalance between efforts and rewards received). The combination of the two models better reflects the coronary risk than each model alone. Occupational stress appears both as a risk factor and a prognostic factor after the occurrence of myocardial infarction. The relevance of the models is best in men or in younger age subjects. In women, role conflicts (occupational/domestic), the existence of excessive "intrinsic" efforts (job over investment) and association with marital stress provide more specific information. Burnout, particularly among health professionals, and bullying at work are also linked to cardiovascular risk. Occupational stress is a collective indicator of health at work, valuable to the employer. At an individual level, it can lead to therapeutic preventive approaches. PMID:26150284

  15. Echocardiographic assessment of myocardial ischemia

    PubMed Central

    Dworrak, Birgit; Sanchis-Gomar, Fabian; Lucia, Alejandro; Buck, Thomas; Erbel, Raimund

    2016-01-01

    Over the last 60 years, echocardiography has emerged as a dominant and indispensable technique for the detection and assessment of coronary heart disease (CHD). In this review, we will describe and discuss this powerful tool of cardiology, especially in the hands of an experienced user, with a focus on myocardial ischemia. Technical development is still on-going, and various new ultrasound techniques have been established in the field of echocardiography in the last several years, including tissue Doppler imaging (TDI), contrast echocardiography, three-dimensional echocardiography (3DE), and speckle tracking echocardiography (i.e., strain/strain rate-echocardiography). High-end equipment with harmonic imaging, high frame rates and the opportunity to adjust mechanical indices has improved imaging quality. Like all new techniques, these techniques must first be subjected to comprehensive scientific assessment, and appropriate training that accounts for physical and physiological limits should be provided. These limits will constantly be redefined as echocardiographic techniques continue to change, which will present new challenges for the further development of ultrasound technology. PMID:27500160

  16. [Occupational stress and myocardial infarction].

    PubMed

    Consoli, Silla M

    2015-01-01

    Besides the best-known role of depressed mood, occupational stress deserves to be taken as a coronary risk factor. There are two basic models to define occupational stress: Karasek's model (high job psychological demands associated with low decision latitude, or even low social support at work) and Siegrist's model (imbalance between efforts and rewards received). The combination of the two models better reflects the coronary risk than each model alone. Occupational stress appears both as a risk factor and a prognostic factor after the occurrence of myocardial infarction. The relevance of the models is best in men or in younger age subjects. In women, role conflicts (occupational/domestic), the existence of excessive "intrinsic" efforts (job over investment) and association with marital stress provide more specific information. Burnout, particularly among health professionals, and bullying at work are also linked to cardiovascular risk. Occupational stress is a collective indicator of health at work, valuable to the employer. At an individual level, it can lead to therapeutic preventive approaches.

  17. Pediatric myocardial protection: an overview.

    PubMed

    Allen, B S; Barth, M J; Ilbawi, M N

    2001-01-01

    This article describes the experimental infrastructure and subsequent successful clinical application of a comprehensive bypass and cardioplegic strategy that limits intraoperative injury and improves postoperative outcomes in pediatric patients. The infant heart is at high risk of damage from poor protection because of preoperative hypertrophy, cyanosis, and ischemia. The background factors of vulnerability to damage caused by cyanosis and ischemia are discussed, together with studies of the infrastructure of strategies to use normoxia versus hyperoxia as bypass starts, white blood cell filtration, warm induction and reperfusion with substrate enhancements, multidose blood cardioplegia, and an integrated approach to allow ischemia only when vision is needed in pediatric surgeries. Data on cardioplegic management, including reducing calcium, increasing magnesium, and reducing perfusion pressure are shown, as used during this technique. These principles were applied to a consecutive series of 567 patients at the Heart Institute for Children and University of Illinois hospital over a 2-year period. Included also were 72 patients with hypoplastic left heart over a 4-year period with this myocardial management strategy. Application of these concepts may improve the safety of protection in infant hearts. PMID:11309728

  18. Molecular genetics of myocardial infarction

    PubMed Central

    Ichihara, Sahoko; Nishida, Tamotsu

    2008-01-01

    Abstract Myocardial infarction (MI) is an important clinical problem because of its large contribution to mortality. The main causal and treatable risk factors for MI include hypertension, hypercholesterolemia or dyslipidemia, diabetes mellitus, and smoking. In addition to these risk factors, recent studies have shown the importance of genetic factors and interactions between multiple genes and environmental factors. Disease prevention is an important strategy for reducing the overall burden of MI, with the identification of markers for disease risk being key both for risk prediction and for potential intervention to lower the chance of future events. Although genetic linkage analyses of families and sib-pairs as well as candidate gene and genome-wide association studies have implicated several loci and candidate genes in predisposition to coronary heart disease (CHD) or MI, the genes that contribute to genetic susceptibility to these conditions remain to be identified definitively. In this review, we summarize both candidate loci for CHD or MI identified by linkage analyses and candidate genes examined by association studies. We also review in more detail studies that have revealed the association with MI or CHD of polymorphisms in MTHFR, LPL, and APOE by the candidate gene approach and those in LTA and at chromosomal region 9p21.3 by genome-wide scans. Such studies may provide insight into the function of implicated genes as well as into the role of genetic factors in the development of CHD and MI. PMID:18704761

  19. Echocardiographic assessment of myocardial ischemia.

    PubMed

    Leischik, Roman; Dworrak, Birgit; Sanchis-Gomar, Fabian; Lucia, Alejandro; Buck, Thomas; Erbel, Raimund

    2016-07-01

    Over the last 60 years, echocardiography has emerged as a dominant and indispensable technique for the detection and assessment of coronary heart disease (CHD). In this review, we will describe and discuss this powerful tool of cardiology, especially in the hands of an experienced user, with a focus on myocardial ischemia. Technical development is still on-going, and various new ultrasound techniques have been established in the field of echocardiography in the last several years, including tissue Doppler imaging (TDI), contrast echocardiography, three-dimensional echocardiography (3DE), and speckle tracking echocardiography (i.e., strain/strain rate-echocardiography). High-end equipment with harmonic imaging, high frame rates and the opportunity to adjust mechanical indices has improved imaging quality. Like all new techniques, these techniques must first be subjected to comprehensive scientific assessment, and appropriate training that accounts for physical and physiological limits should be provided. These limits will constantly be redefined as echocardiographic techniques continue to change, which will present new challenges for the further development of ultrasound technology. PMID:27500160

  20. [Holiday effect in myocardial infarct].

    PubMed

    Otto, W; Hempel, W E; Goebel, H; Erkens, R

    1975-03-15

    Aimed measures of the organisation of the combat against infarction demand also the observation of temporary frequencies. On the basis of the evaluation of certificates of death of the month December of the years 1969 to 1973 of the GDR with differentiation according to so-called prehospital dead (persons who died at home and on the way to the hospital) and patients who died in the hospital with high significance an unwarrantedly high prehospital mortality during the period from Christmas to the end of the year (25th to 31st December) was established compared with the preceding week (18th to 24th December). Since in contrast to this the hospital cases and the cases "on the way" do not show any significant differences main tasks for the beginning of improvements concerning health policy may be deduced, all the more since the so-called holiday effect, expressed by a high home/clinic-relation of patients who died of myocardial infarction, could be restricted to 6 counties of the GDR on account of the analysis of further localities. From the results the tendency of a retrogression of the holiday effect is to be read off in the course of years. In the discussion an explantation of this peculiarity is attempted, and practicable conclusions for the removal and thus for the improvement the infarct situation are formulated.

  1. Regional myocardial contractile function: multiparametric strain mapping.

    PubMed

    Cupps, Brian P; Taggar, Ajay K; Reynolds, Lina M; Lawton, Jennifer S; Pasque, Michael K

    2010-06-01

    Magnetic resonance imaging (MRI) with tissue tagging enables the quantification of multiple strain indices that can be combined through normalization into a single multiparametric index of regional myocardial contractile function. The aim of this study was to test the ability of multiparametric strain analysis to quantify regional differences in contractile function in an ovine model of myocardial injury. Regional variance in myocardial contractile function was induced in eight sheep by the ligation of the blood supply to the anterior and apical left ventricular (LV) myocardial walls. LV systolic strain was obtained from tissue tagged MRI images. A normal strain database (n=50) defines all parameters of systolic strain and allows normalization of regional function at 15,300 LV points by calculation of a z-score. Multiparametric systolic strain z-scores were therefore determined for 15,300 points in each injured sheep left ventricle. Multiparametric z-scores were found to vary significantly by region (P<0.001). z-Scores in regions remote to the infarct were found to be significantly smaller than those in the regions most likely to include infarcted myocardium. In this pre-clinical evaluation of MRI-based multiparametric strain analysis, it accurately quantified and visually defined regional differences in myocardial contractile function.

  2. Myocardial perfusion imaging with dual energy CT.

    PubMed

    Jin, Kwang Nam; De Cecco, Carlo N; Caruso, Damiano; Tesche, Christian; Spandorfer, Adam; Varga-Szemes, Akos; Schoepf, U Joseph

    2016-10-01

    Dual-energy CT (DECT) enables simultaneous use of two different tube voltages, thus different x-ray absorption characteristics are acquired in the same anatomic location with two different X-ray spectra. The various DECT techniques allow material decomposition and mapping of the iodine distribution within the myocardium. Static dual-energy myocardial perfusion imaging (sCTMPI) using pharmacological stress agents demonstrate myocardial ischemia by single snapshot images of myocardial iodine distribution. sCTMPI gives incremental values to coronary artery stenosis detected on coronary CT angiography (CCTA) by showing consequent reversible or fixed myocardial perfusion defects. The comprehensive acquisition of CCTA and sCTMPI offers extensive morphological and functional evaluation of coronary artery disease. Recent studies have revealed that dual-energy sCTMPI shows promising diagnostic accuracy for the detection of hemodynamically significant coronary artery disease compared to single-photon emission computed tomography, invasive coronary angiography, and cardiac MRI. The aim of this review is to present currently available DECT techniques for static myocardial perfusion imaging and recent clinical applications and ongoing investigations.

  3. Cardiac BMIPP imaging in acute myocardial infarction.

    PubMed

    Nakata, T; Hashimoto, A; Eguchi, M

    1999-02-01

    Fatty acid metabolism functions as a major energy-producing system under aerobic conditions, but it is impaired immediately after myocardial ischaemia. This imaging can provide intracellular information which cannot be obtained by angiographical, perfusional or functional analysis. 123I-BMIPP and perfusion imagings in patients with acute myocardial infarction have demonstrated three different correlations between myocardial perfusion and fatty acid metabolism: concordant defects of perfusion and BMIPP which represent scar or non-viable tissue; lower BMIPP uptake relative to perfusion (perfusion-BMIPP mismatch) which implicates metabolically damaged, often dysynergic, but viable myocardium; and equivalently normal uptakes of perfusion and BMIPP in completely salvaged myocardium. Identification of these perfusion-metabolism correlations contributes to the detection of ischaemia-related myocardial injury in viable and non-viable myocardium, to the prediction of post-ischaemic or post-interventional functional recovery and to the identification of patients who have myocardium at ischaemic risk. Further clinical investigations might reveal more clearly the pathophysiological and prognostic implications of cardiac BMIPP imaging in patients with acute myocardial infarction.

  4. Myocardial protection by simple systemic hypothermia without aortic occlusion.

    PubMed

    Susilo, A W; Rocher, A; Mohan, R; van der Laarse, A

    1990-01-01

    Systemic hypothermia at 25 degrees-28 degrees C without chemical cardioplegia was used in 908 patients undergoing coronary artery bypass grafting. Local coronary artery flow was interrupted only during grafting of a distal anastomosis. Systemic perfusion pressure was maintained at 80-100 mmHg, hematocrit at 20%-25%, and pCO2 and pH were monitored during hypothermia according to the alpha-stat principle, while the left ventricle was vented routinely. Proximal anastomoses were performed just before extracorporeal circulation was started by only partially occluding the ascending aorta. Preoperatively 61.9% of the patients had had a myocardial infarction, and 44% had unstable angina. In 14% a severe lesion of the main stem of the left coronary artery was present. Left ventricular function was moderately depressed in 25% and severely depressed in 8% of the patients. Forty-eight patients (5.3%) were aged 70 years or older. The mean number of grafts placed per patient was 3.3. Perioperative myocardial infarction occurred in 3%. Death due to left ventricular failure occurred in 0.4%. No left ventricular assist devices were needed; an intra-aortic balloon pump was used in 1%; positive inotropic support was required in 3.8% of the patients. These results indicate that systemic hypothermia alone provides safe myocardial protection and in certain cases may be the method of choice, particularly if aortic cross clamping or administration of cardioplegic solution is contraindicated. In addition, this method provides rapid revascularization of a severely ischemic zone, as present after unsuccessful PTCA procedures.

  5. The iron-regulatory peptide hepcidin is upregulated in the ischemic and in the remote myocardium after myocardial infarction.

    PubMed

    Simonis, Gregor; Mueller, Katrin; Schwarz, Peggy; Wiedemann, Stephan; Adler, Guido; Strasser, Ruth H; Kulaksiz, Hasan

    2010-09-01

    Recent evidence suggests that iron metabolism contributes to the ischemic damage after myocardial infarction. Hepcidin, a recently discovered peptide hormone, regulates iron uptake and metabolism, protecting the body from iron overload. In this study we analyzed the regulation of hepcidin in the heart and blood of rats after myocardial infarction. To induce a myocardial infarction in the rats, left anterior descending coronary artery ligation was performed. After 1-24h, biopsies from the ischemic and the non-ischemic myocardium were taken. In these biopsies, the mRNA levels and the protein expression of hepcidin were analyzed by quantitative RT-PCR and immunoblot analysis, respectively. In parallel, the serum levels of prohepcidin were measured by ELISA. Six hours after myocardial infarction, the hepcidin mRNA expression was temporally upregulated in the ischemic and in the non-ischemic myocardium. The upregulation was specific for hepcidin, since other iron-related genes (hemojuvelin, IREG-1) remained unchanged. Furthermore, the alteration of the hepcidin protein expression in the ischemic area was connected to the level of hepcidin in the serum of the infarcted rats, where hepcidin also raised up. Angiotensin receptor blockade with candesartan did not influence the mRNA regulation of hepcidin. Together, these data show a particular upregulation of the iron-regulatory peptide hepcidin in the ischemic and the non-ischemic myocardium after myocardial infarction. It is speculated that upregulation of hepcidin may reduce iron toxicity and thus infarct size expansion in an infarcted heart.

  6. Quantitative assessment of myocardial strain with displacement encoding with stimulated echoes MRI in patients with coronary artery disease.

    PubMed

    Miyagi, Hideki; Nagata, Motonori; Kitagawa, Kakuya; Kato, Shingo; Takase, Shinichi; Sigfridsson, Andreas; Ishida, Masaki; Dohi, Kaoru; Ito, Masaaki; Sakuma, Hajime

    2013-12-01

    To determine the diagnostic performance and reproducibility of strain assessment with displacement encoding with stimulated echoes (DENSE) cardiovascular magnetic resonance (CMR) in identifying contractile abnormalities in myocardial segments with late gadolinium enhancement (LGE). DENSE CMR was obtained on short-axis planes of the left ventricle (LV) in 24 patients with suspected coronary artery disease. e1 and e2 strains of LV wall were quantified. Cine MRI was acquired to determine percent systolic wall thickening (%SWT), followed by (LGE) CMR. The diagnostic performance of e1, e2 and %SWT for predicting the presence of LGE was evaluated by receiver operating characteristics (ROC) analysis. Myocardial scar on LGE CMR was observed in 91 (24 %) of 384 segments. The area under ROC curve for predicting the segments with LGE was 0.874 by e1, 0.916 by e2 and 0.828 by %SWT (p = 0.001 between e2 and %SWT). Excellent inter-observer reproducibility was found for strain [Intraclass correlation coefficient (ICC) = 0.962 for e1, 0.955 for e2] as compared with %SWT (ICC = 0.790). DENSE CMR can be performed as a part of routine CMR study and allows for quantification of myocardial strain with high inter-observer reproducibility. Myocardial strain, especially e2 is useful in detecting altered abnormal systolic contraction in the segments with myocardial scar.

  7. Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

    PubMed Central

    de Matos Soeiro, Alexandre; Ruppert, Aline D; Canzian, Mauro; Capelozzi, Vera L; Serrano, Carlos V

    2012-01-01

    OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has

  8. Alterations in carbohydrate metabolism and its regulation in PPARalpha null mouse hearts

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Although a shift from fatty acids (FAs) to carbohydrates (CHOs) is considered beneficial for the diseased heart, it is unclear why subjects with FA beta-oxidation defects are prone to cardiac decompensation under stress conditions. The present study investigated potential alterations in the myocardi...

  9. Aortocoronary graft flow and reactive hyperaemia in relation to postoperative myocardial infarction.

    PubMed Central

    Skotnicki, S; Vonk, J; Sleegers, T; Dercksen, S; Linssen, G; Lacquet, L; Kuijpers, P

    1976-01-01

    Blood flow through aortocoronary venous grafts and its response to a brief period of arterial occlusion--reactive hyperaemia--were studied in relation to the development of postoperative myocardial infarction. In 40 patients with intractable angina due to obstructive coronary artery disease, 72 aortocoronary venous grafts were constructed. In 18% of the grafts there was no response to the flow to temporary occlusion, due to absence of reactive hyperaemia. In the remaining grafts the flow increased from 17% to 26%. In 17-5% of the patients postoperative myocardial infarction was diagnosed. No relation could be established between this control flow through aortocoronary grafts and postoperative myocardial infarction. A significant difference was found in the magnitude of the reactive hyperaemia following occlusion of the graft between patients who developed myocardial infarction (13-0%) and those who did not (26-8%). Some of our observations suggest that the myocardium is in a state of reactive hyperaemia after coronary surgery. With certain technical precautions the flow changes caused by reactive hyperaemia can be used as an indicator of the result to be expected from bypass surgery. PMID:781900

  10. Panic attack triggering myocardial ischemia documented by myocardial perfusion imaging study. A case report

    PubMed Central

    2012-01-01

    Background Chest pain, a key element in the investigation of coronary artery disease is often regarded as a benign prognosis when present in panic attacks. However, panic disorder has been suggested as an independent risk factor for long-term prognosis of cardiovascular diseases and a trigger of acute myocardial infarction. Objective Faced with the extreme importance in differentiate from ischemic to non-ischemic chest pain, we report a case of panic attack induced by inhalation of 35% carbon dioxide triggering myocardial ischemia, documented by myocardial perfusion imaging study. Discussion Panic attack is undoubtedly a strong component of mental stress. Patients with coronary artery disease may present myocardial ischemia in mental stress response by two ways: an increase in coronary vasomotor tone or a sympathetic hyperactivity leading to a rise in myocardial oxygen consumption. Coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. Possibly the carbon dioxide challenge test could trigger myocardial ischemia by the same mechanisms. Conclusion The use of mental stress has been suggested as an alternative method for myocardial ischemia investigation. Based on translational medicine objectives the use of CO2 challenge followed by Sestamibi SPECT could be a useful method to allow improved application of research-based knowledge to the medical field, specifically at the interface of PD and cardiovascular disease. PMID:22999016

  11. Role of myocardial perfusion imaging in evaluating thrombolytic therapy for acute myocardial infarction

    SciTech Connect

    Beller, G.A.

    1987-03-01

    Myocardial thallium-201 scintigraphy is being increasingly employed as a method for assessing the efficacy of coronary reperfusion in acute myocardial infarction. New thallium uptake after intracoronary tracer administration after successful recanalization indicates that nutrient blood flow has been successfully restored. One may also presume that some myocardial salvage occurred if thallium administered in this manner is transported intracellularly by myocytes with intact sarcolemmal membranes. However, if one injects thallium by way of the intracoronary route immediately after reperfusion, the initial uptake of thallium in reperfused myocardium may predominantly represent hyperemic flow and regional thallium counts measured may not be proportional to the mass of viable myocytes. When thallium is injected intravenously during the occlusion phase the degree of redistribution after thrombolysis is proportional to the degree of flow restoration and myocardial viability. When thallium is injected for the first time intravenously immediately after reperfusion, an overestimation of myocardial salvage may occur because of excess thallium uptake in the infarct zone consequent to significant hyperemia. Another approach to myocardial thallium scintigraphy in patients undergoing thrombolytic therapy is to administer two separate intravenous injections before and 24 hours or later after treatment. Finally, patients with acute myocardial infarction who receive intravenous thrombolytic therapy are candidates for predischarge exercise thallium-201 scintigraphy for risk stratification and detection of residual ischemia.

  12. Spontaneous changes in /sup 201/Tl myocardial perfusion imaging after myocardial infarction

    SciTech Connect

    Buda, A.J.; Dubbin, J.D.; MacDonald, I.L.; Strauss, H.D.; Orr, S.A.; Meindok, H.

    1982-12-01

    To examine regional myocardial perfusion after myocardial infarction, 26 patients underwent exercise electrocardiographic testing with /sup 201/Tl myocardial perfusion imaging 3 weeks and 3 months after infarction. At 3 weeks, 9 of 26 patients (35%) had myocardial ischemia by exercise electrocardiographic testing, whereas 18 of 26 (69%) had ischemia by /sup 201/Tl imaging. The /sup 201/Tl scintigrams were scored by dividing each image, in 3 views, into 5 segments, using a 5-point scoring scheme. The exercise /sup 201/Tl score was 44.3 +/- 1.2 and increased to 47.3 +/- 1.2 in the redistribution study (p less than 0.001). Three months after infarction, although there was a significantly greater rate-pressure product which would predict a larger ischemic defect and a decrease in the stress /sup 201/Tl score, the stress score was improved (48.3 +/- 1.1, p less than 0.001). The redistribution score was similar, that is, 48.9 +/- 1.0. The improvement in /sup 201/Tl myocardial perfusion was associated with a loss of stress-induced ischemia in 8 patients (30%). These results indicate that spontaneous improvements in /sup 201/Tl myocardial perfusion imaging may occur after myocardial infarction.

  13. Temperature, air pollution, and mortality from myocardial infarction in São Paulo, Brazil.

    PubMed

    Sharovsky, R; César, L A M; Ramires, J A F

    2004-11-01

    An increase in daily mortality from myocardial infarction has been observed in association with meteorological factors and air pollution in several cities in the world, mainly in the northern hemisphere. The objective of the present study was to analyze the independent effects of environmental variables on daily counts of death from myocardial infarction in a subtropical region in South America. We used the robust Poisson regression to investigate associations between weather (temperature, humidity and barometric pressure), air pollution (sulfur dioxide, carbon monoxide, and inhalable particulate), and the daily death counts attributed to myocardial infarction in the city of São Paulo in Brazil, where 12,007 fatal events were observed from 1996 to 1998. The model was adjusted in a linear fashion for relative humidity and day-of-week, while nonparametric smoothing factors were used for seasonal trend and temperature. We found a significant association of daily temperature with deaths due to myocardial infarction (P < 0.001), with the lowest mortality being observed at temperatures between 21.6 and 22.6 degrees C. Relative humidity appeared to exert a protective effect. Sulfur dioxide concentrations correlated linearly with myocardial infarction deaths, increasing the number of fatal events by 3.4% (relative risk of 1.03; 95% confidence interval = 1.02-1.05) for each 10 microg/m(3) increase. In conclusion, this study provides evidence of important associations between daily temperature and air pollution and mortality from myocardial infarction in a subtropical region, even after a comprehensive control for confounding factors.

  14. Myocardial perfusion and contraction in acute ischemia and chronic ischemic heart disease.

    PubMed

    Canty, John M; Suzuki, Gen

    2012-04-01

    A large body of evidence has demonstrated that there is a close coupling between regional myocardial perfusion and contractile function. When ischemia is mild, this can result in the development of a new balance between supply and energy utilization that allows the heart to adapt for a period of hours over which myocardial viability can be maintained, a phenomenon known as "short-term hibernation". Upon reperfusion after reversible ischemia, regional myocardial function remains depressed. The "stunned myocardium" recovers spontaneously over a period of hours to days. The situation in myocardium subjected to chronic repetitive ischemia is more complex. Chronic dysfunction can initially reflect repetitive stunning with insufficient time for the heart to recover between episodes of spontaneous ischemia. As the frequency and/or severity of ischemia increases, the heart undergoes a series of adaptations which downregulate metabolism to maintain myocyte viability at the expense of contractile function. The resulting "hibernating myocardium" develops regional myocyte cellular hypertrophy as a compensatory response to ischemia-induced apoptosis along with a series of molecular adaptations that while regional, are similar to global changes found in advanced heart failure. As a result, flow-function relations become independently affected by tissue remodeling and interventions that stimulate myocyte regeneration. Similarly, chronic vascular remodeling may alter flow regulation in a fashion that increases myocardial vulnerability to ischemia. Here we review our current understanding of myocardial flow-function relations during acute ischemia in normal myocardium and highlight newly identified complexities in their interpretation in viable chronically dysfunctional myocardium with myocyte cellular and molecular remodeling. This article is part of a Special Issue entitled "Coronary Blood Flow".

  15. Association of stroke and myocardial infarction in children.

    PubMed

    Nakashima, M; Takashima, S; Hashimoto, K; Shiraishi, M

    1982-02-01

    A 9-year-old boy with cerebrovascular accident (CVA) and old myocardial infarction with mural thrombi is reported. The cause of the myocardial infarction was congenital coronary artery fistula originating from the left coronary artery and emptying into the right atrium. Although a common cause of strokes in adults, myocardial infarction has infrequently been reported as the source of emboli in children.

  16. In vivo characterization of myocardial infarction using fluorescence and diffuse reflectance spectroscopy

    NASA Astrophysics Data System (ADS)

    Ti, Yalin; Chen, Poching; Lin, Wei-Chiang

    2010-05-01

    We explore the feasibility of using combined fluorescence and diffuse reflectance spectroscopy to characterize a myocardial infarct at different developing stages. An animal study is conducted using rats with surgically induced myocaridal infarction (MI). In vivo fluorescence spectra at 337-nm excitation and diffuse reflectance between 400 and 900 nm are measured from the heart. Spectral acquisition is performed: 1. for normal heart tissue; 2. for the area immediately surrounding the infarct; and 3. for the infarcted tissue itself, one, two, three, and four weeks into MI development. Histological and statistical analyses are used to identify unique pathohistological features and spectral alterations associated with the investigated regions. The main alterations (p<0.05) in diffuse reflectance spectra are identified primarily between 450 and 600 nm. The dominant fluorescence alterations are increases in peak fluorescence intensity at 400 and 460 nm. The extent of these spectral alterations is related to the duration of the infarction. The findings of this study support the concept that optical spectroscopy could be useful as a tool to noninvasively determine the in vivo pathophysiological features of a myocardial infarct and its surrounding tissue, thereby providing real-time feedback to surgeons during various surgical interventions for MI.

  17. [The perioperative myocardial infarction - an interdisciplinary task].

    PubMed

    Karatolios, Konstantinos; Rolfes, Caroline; Wulf, Hinnerk; Schieffer, Bernhard

    2016-09-01

    Cardiovascular complications, particularly perioperative myocardial infarction (PMI), are major contributors to mortaliyt after noncardiac surgery. PMI often occurs unnoticed without symptoms or ECG changes. Despite ist silent presentation, PMI is associated with increased mortality. The combination of high associated mortality and diagnostic challenges mandates increased awareness of PMI. Perioperative myocardial infarction may result from plaque rupture (PMI type I) or be caused by a myocardial supply-demand imbalance of oxygen without plaque rupture (PMI type II). Most PMIs occur within the first 3 days after surgery, highlighting the need for clinical monitoring in order to allow fast diagnosis and initiation of appropriate therapy. Measurement of cardiac troponin and 12-lead ECG are the diagnostic cornerstone. Therapy of PMI represents a challenge for physicians and requires a collaboration of surgeons, anesthesiologists and cardiologists. PMID:27631445

  18. Winter weather conditions and myocardial infarctions.

    PubMed

    Ohlson, C G; Bodin, L; Bryngelsson, I L; Helsing, M; Malmberg, L

    1991-03-01

    The daily number of cases of myocardial infarctions admitted to a hospital in middle Sweden over three winter seasons 1984-87 was correlated to the weather conditions on a day-to-day basis. The study encompassed 634 days and all cases younger than 70 years, living within the catchment area, in all 382 subjects. Information on temperature, wind force, precipitation and atmospheric pressure was obtained from the Swedish Institute of Meteorology and Hydrology. A low number of myocardial infarctions was seen on Saturdays and Sundays with a mild wind chill factor and on days with moderate snowfall and high atmospheric pressure. A high number was observed for workdays, especially Mondays, as day of diagnosis. Heterogeneity of the study population and a misclassification of the time relationships between dates of diagnosis and weather changes may have caused an underestimation of the impact of weather conditions. However, weather conditions do not seem to be a major triggering factor of myocardial infarctions in Sweden.

  19. Action of acetylstrophanthidin on experimental myocardial infarction.

    NASA Technical Reports Server (NTRS)

    Nola, G. T.; Pope, S. E.; Harrison, D. C.

    1972-01-01

    An experimental animal model with acute myocardial infarction of a size insufficient to produce profound heart failure or shock was used to study the effects of acute infarction on digitalis tolerance and the hemodynamic changes produced by moderate and large doses of acetylstrophanthidin. With acute myocardial infarction, digitalis toxic arrhythmias could be precipitated with significantly lower doses of digitalis than in animals without myocardial infarction. There was no precise correlation between the size of infarction and the toxic dose of glycoside. Coronary artery ligation produced a stable but relatively depressed circulatory state, as evidenced by lowered cardiac output and stroke volume and elevated systemic vascular resistance and left atrial mean pressure. When digitalis was infused, the following significant changes were observed at nontoxic doses: (1) elevation of aortic and left ventricular pressures; (2) further decline in cardiac output; and (3) decreased left atrial mean pressure.

  20. Myocardial disarray in Noonan syndrome

    PubMed Central

    Burch, Michael; Mann, Jessica M; Sharland, Michael; Shinebourne, Elliot A; Patton, Michael A; McKenna, William J

    1992-01-01

    Objective—To characterise the histopathology of the left ventricular hypertrophy commonly associated with Noonan syndrome by assessing the extent of myocyte disarray and therefore to define one aspect of the relation between this disease and idiopathic hypertrophic cardiomyopathy. Design—Blinded histological analysis. Setting—Hospital medical school. Patients—Six hearts of children with the Noonan phenotype and isolated ventricular hypertrophy were compared with age and sex matched controls. Methods—Histological analysis was performed with an image analyser under light microscopy. Representative sections from the entire left ventricular free wall were examined. Results were expressed as the percentage of fields showing disarray related to the number of fields evaluated: 100 fields were examined for each patient. Results—In the patients with Noonan syndrome myocardial disarray was present in the ventricular septum in 24 (5·7)% (mean (SD)) of fields and in the free wall in 22·2 (6·8)%. In the controls disarray was present in the septum in 3·8 (2·3)% of fields and in the free wall in 2·4 (2·8)%. In both regions the extent of disarray was significantly greater in patients with Noonan syndrome (p < 0·0005; 95% confidence interval 14 to 26·3 for the septum: p < 0·005, 95% confidence interval 11·4 to 28·2 for the free wall). Conclusions—The ventricular hypertrophy associated with Noonan syndrome is histologically similar to hypertrophic cardiomyopathy but whether the two diseases are the expression of the same genetic defect remains to be determined. PMID:1467053

  1. Asymptomatic myocardial ischemia following cold provocation

    SciTech Connect

    Shea, M.J.; Deanfield, J.E.; deLandsheere, C.M.; Wilson, R.A.; Kensett, M.; Selwyn, A.P.

    1987-09-01

    Cold is thought to provoke angina in patients with coronary disease either by an increase in myocardial demand or an increase in coronary vascular resistance. We investigated and compared the effects of cold pressor stimulation and symptom-limited supine bicycle exercise on regional myocardial perfusion in 35 patients with stable angina and coronary disease and in 10 normal subjects. Regional myocardial perfusion was assessed with positron emission tomography and rubidium-82. Following cold pressor stimulation 24 of 35 patients demonstrated significant abnormalities of regional myocardial perfusion with reduced cation uptake in affected regions of myocardium: 52 +/- 9 to 43 +/- 9 (p less than 0.001 vs normal subjects). Among these 24 patients only nine developed ST depression and only seven had angina. In contrast, 29 of 35 patients underwent supine exercise, and abnormal regional myocardial perfusion occurred in all 29, with a reduction in cation intake from 48 +/- 10 to 43 +/- 14 (p less than 0.001 vs normal subjects). Angina was present in 27 of 29 and ST depression in 25 of 29. Although the absolute decrease in cation uptake was somewhat greater following cold as opposed to exercise, the peak heart rate after cold was significantly lower than that after exercise (82 +/- 12 vs 108 +/- 16 bpm, p less than 0.05). Peak systolic blood pressures after cold and exercise were similar (159 +/- 24 vs 158 +/- 28). Thus, cold produces much more frequent asymptomatic disturbances of regional myocardial perfusion in patients with stable angina and coronary disease than is suggested by pain or ECG changes.

  2. Abnormal Myocardial Strain Indices in Children Receiving Anthracycline Chemotherapy.

    PubMed

    Pignatelli, Ricardo H; Ghazi, Payam; Reddy, S Chandra-Bose; Thompson, Patrick; Cui, Qiqiong; Castro, Jacqueline; Okcu, Mehmet F; Jefferies, John Lynn

    2015-12-01

    Anthracycline chemotherapy (AC) is associated with impaired left ventricular (LV) systolic function. LV ejection fraction (EF %) obtained by two-dimensional echocardiography is the current gold standard for detection and monitoring of LV systolic function. However, dependence on LVEF has been shown to be unreliable due to its inherent limitations. Speckle tracking echocardiography (STE) measures myocardial strain and is a sensitive method to detect LV systolic dysfunction with demonstrated utility in such detection in adult and pediatric cohort studies. Compare myocardial strain indices derived by STE with LVEF to detect ACT-induced LV systolic dysfunction. Prospective, cross-sectional measurements of LV myocardial strain indices derived from STE with LVEF. Pediatric cohort of 25 patients (pts): 17 females, eight males with a mean age 9.8 ± 5.8 years, who received anthracyclines (AC); median cumulative dose ≥150 ± 124.4 mg/m(2), range 60-450 mg/m(2) showing normal LV end-diastolic diameter (mm) and normal LVEF (≥55 %) underwent STE to obtain LV myocardial strain indices: strain and strain rate. The inter- and intraobserver variability for the strain indices was 5 %. Fifteen of 25 pts (60 %) showed abnormal global longitudinal peak systolic strain (GLPSS) and 19/25 pts (76 %) showed abnormal peak circumferential strain (PCS) compared to age-matched controls (p = 0.005). In contrast, no significant differences was observed in either indices with the dose of AC. Likewise, no significant changes in the systolic or diastolic strain rate were noted with the dose of AC (r (2) = 0.0076 for peak E, r (2) = 0.072 for peak A, p = NS). GLPSS and PCS were diminished and, however, correlated poorly with the cumulative dose of AC. These observations indicate an early onset of LV systolic dysfunction by the strain indices in pts who continue to show a normal LVEF implying presence of occult LV systolic dysfunction. These novel strain indices may assist in

  3. Intestinal Microbial Metabolites Are Linked to Severity of Myocardial Infarction in Rats

    PubMed Central

    Lam, Vy; Su, Jidong; Hsu, Anna; Gross, Garrett J.; Salzman, Nita H.

    2016-01-01

    Intestinal microbiota determine severity of myocardial infarction in rats. We determined whether low molecular weight metabolites derived from intestinal microbiota and transported to the systemic circulation are linked to severity of myocardial infarction. Plasma from rats treated for seven days with the non-absorbed antibiotic vancomycin or a mixture of streptomycin, neomycin, polymyxin B and bacitracin was analyzed using mass spectrometry-based metabolite profiling platforms. Antibiotic-induced changes in the abundance of individual groups of intestinal microbiota dramatically altered the host’s metabolism. Hierarchical clustering of dissimilarities separated the levels of 284 identified metabolites from treated vs. untreated rats; 193 were altered by the antibiotic treatments with a tendency towards decreased metabolite levels. Catabolism of the aromatic amino acids phenylalanine, tryptophan and tyrosine was the most affected pathway comprising 33 affected metabolites. Both antibiotic treatments decreased the severity of an induced myocardial infarction in vivo by 27% and 29%, respectively. We then determined whether microbial metabolites of the amino acids phenylalanine, tryptophan and tyrosine were linked to decreased severity of myocardial infarction. Vancomycin-treated rats were administered amino acid metabolites prior to ischemia/reperfusion studies. Oral or intravenous pretreatment of rats with these amino acid metabolites abolished the decrease in infarct size conferred by vancomycin. Inhibition of JAK-2 (AG-490, 10 μM), Src kinase (PP1, 20 μM), Akt/PI3 kinase (Wortmannin, 100 nM), p44/42 MAPK (PD98059, 10 μM), p38 MAPK (SB203580, 10 μM), or KATP channels (glibenclamide, 3 μM) abolished cardioprotection by vancomycin, indicating microbial metabolites are interacting with cell surface receptors to transduce their signals through Src kinase, cell survival pathways and KATP channels. These inhibitors have no effect on myocardial infarct size in

  4. The role of CD36 in the regulation of myocardial lipid metabolism.

    PubMed

    Kim, Ty T; Dyck, Jason R B

    2016-10-01

    Since the heart has one of the highest energy requirements of all organs in the body, it requires a constant and plentiful supply of fuel to function properly. Mitochondrial oxidation of lipids provides a major source of ATP for the heart, and the cellular processes that regulate lipid uptake and utilization are important contributors to maintaining proper myocardial energetic status. Although numerous proteins are coordinately regulated in order to ensure proper fatty acid utilization in the cardiomyocyte, a key first step in this process is the entry of fatty acids into the cell. An important protein involved in the transport of fatty acids into the cardiomyocyte is the plasma membrane-associated protein known as fatty acid translocase (FAT; also known as CD36). While multiple proteins are involved in facilitating fatty acid uptake in the heart, CD36 accounts for approximately 50-70% of the total fatty acid taken up in cardiomyocytes. As such, myocardial metabolism of fatty acids may depend upon proper CD36 function. Consistent with this, changes in CD36 levels/function have been implicated in the alteration of myocardial metabolism in the pathophysiology of certain cardiovascular diseases. As such, a better understanding of the role and function of CD36 in the heart may provide important insights for the development of new treatments for specific cardiovascular diseases. Herein, we review the role of CD36 in myocardial lipid metabolism in the healthy heart and describe how CD36-mediated alterations in lipid metabolism may contribute to cardiovascular disease. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk. PMID:26995462

  5. Recurrent myocardial infarction with patent coronary arteries.

    PubMed Central

    Haywood, L. J.; Khan, A. H.; Bornheimer, J.; Finck, E.; Tatter, D.

    1997-01-01

    Two separate episodes of severe chest pain occurred several years apart in a 25-year-old male patient with typical clinical findings of acute myocardial infarction with each episode. Cardiac catheterization following the second infarction confirmed the presence of myocardial dysfunction with apical akinesis and dyskinesis. Both coronary arteries were radiologically patent; however, there was evidence of probable recanalization of the right coronary artery. Several months later, the patient developed flank pain, hematuria, progressive renal failure, and cardiac decompensation, and died with intractable arrhythmias. At autopsy, a large apical mitral thrombosis was found and was the presumptive source of multiple systemic emboli. Images Figure 3 Figure 4 PMID:9195802

  6. Visualizing myocardial function using HARP MRI

    NASA Astrophysics Data System (ADS)

    Osman, Nael F.; Prince, Jerry L.

    2000-06-01

    Harmonic phase magnetic resonance imaging (HARP) is a new technique for measuring the motion of the left ventricle of the heart. HARP uses magnetic resonance tagging, Fourier filtering and special processing algorithms to calculate key indices of myocardial motion including Eulerian and Lagrangian strain. This paper presents several new methods for visualizing myocardial motion based on HARP. Quantities that are computed and visualized include motion grids, velocity fields, strain rates, pathlines, tracked Eulerian strain, and contraction angle. The computations are fast and fully automated and have the potential for clinical application.

  7. Altered States of Consciousness and Alcohol.

    ERIC Educational Resources Information Center

    Jones, Ben Morgan; And Others

    This document contains the reports of research at a symposium on "Altered States of Consciousness and Alcohol." The participants primarily agreed that alcohol induces an altered state of consciousness similar to other drugs, but that this phenomenon has not been explicitly stated due to the current interest in newer and more novel drugs. The…

  8. Myocardial Cell Pattern on Piezoelectric Nanofiber Mats for Energy Harvesting

    NASA Astrophysics Data System (ADS)

    Liu, X.; Wang, X.; Zhao, H.; Du, Y.

    2014-11-01

    The paper presents in vitro contractile myocardial cell pattern on piezoelectric nanofiber mats with applications in energy harvesting. The cell-based energy harvester consists of myocardial cell sheet and a PDMS substrate with a PVDF nanofiber mat on. Experimentally, cultured on specifically distributed nanofiber mats, neonatal rat ventricular cardiomyocytes are characterized with the related morphology and contraction. Previously, we have come up with the concept of energy harvesting from heart beating using piezoelectric material. A bio-hybrid energy harvester combined living cardiomyocytes, PDMS polymer substrate and piezoelectric PVDF film with the electrical output of peak current 87.5nA and peak voltage 92.3mV. However, the thickness of the cardiomyocyte cultured on a two-dimensional substrate is much less than that of the piezoelectric film. The Micro Contact Printing (μCP) method used in cell pattern on the PDMS thin film has tough requirement for the film surface. As such, in this paper we fabricated nanofiber-constructed PDMS thin film to realize cell pattern due to PVDF nanofibers with better piezoelectricity and microstructures of nanofiber mats guiding cell distribution. Living cardiomyocytes patterned on those distributed piezoelectric nanofibers with the result of the same distribution as the nanofiber pattern.

  9. Current Stem Cell Delivery Methods for Myocardial Repair

    PubMed Central

    Sheng, Calvin C.; Zhou, Li; Hao, Jijun

    2013-01-01

    Heart failure commonly results from an irreparable damage due to cardiovascular diseases (CVDs), the leading cause of morbidity and mortality in the United States. In recent years, the rapid advancements in stem cell research have garnered much praise for paving the way to novel therapies in reversing myocardial injuries. Cell types currently investigated for cellular delivery include embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), and adult stem cell lineages such as skeletal myoblasts, bone-marrow-derived stem cells (BMSCs), mesenchymal stem cells (MSCs), and cardiac stem cells (CSCs). To engraft these cells into patients' damaged myocardium, a variety of approaches (intramyocardial, transendocardial, transcoronary, venous, intravenous, intracoronary artery and retrograde venous administrations and bioengineered tissue transplantation) have been developed and explored. In this paper, we will discuss the pros and cons of these delivery modalities, the current state of their therapeutic potentials, and a multifaceted evaluation of their reported clinical feasibility, safety, and efficacy. While the issues of optimal delivery approach, the best progenitor stem cell type, the most effective dose, and timing of administration remain to be addressed, we are highly optimistic that stem cell therapy will provide a clinically viable option for myocardial regeneration. PMID:23509740

  10. Imaging of cocaine-induced global and regional myocardial ischemia

    SciTech Connect

    Oster, Z.H.; Som, P.; Wang, G.J.; Weber, D.A. )

    1991-08-01

    Severe and often fatal cardiac complications have been reported in cocaine users with narrowed coronary arteries caused by atherosclerosis as well as in young adults with normal coronaries. The authors have found that in normal dogs cocaine induces severe temporary hypoperfusion of the left ventricle as indicated by a significantly lower 201Tl concentration compared to the baseline state. The most significant decrease in uptake occurred 5 min after injection and was more pronounced in the septal and apical segments. Following intravenous administration of cocaine, instead of gradual disappearance of 201Tl from the left ventricle, there was continuous increase in 201Tl concentration in the left ventricle. These imaging experiments indicate that the deleterious effects of cocaine on the heart are probably due to spasm of the coronaries and decreased myocardial perfusion. Since spasm of the large subpericardial vessels does not seem to explain the magnitude of the increased coronary resistance and decreased coronary flow after cocaine as described in the literature, it is suggested that microvascular spasm of smaller vessels plays a major role in the temporary decrease in perfusion. The data may also suggest that severe temporary myocardial ischemia is probably the initiating factor for the cardiac complications induced by cocaine.

  11. Current stem cell delivery methods for myocardial repair.

    PubMed

    Sheng, Calvin C; Zhou, Li; Hao, Jijun

    2013-01-01

    Heart failure commonly results from an irreparable damage due to cardiovascular diseases (CVDs), the leading cause of morbidity and mortality in the United States. In recent years, the rapid advancements in stem cell research have garnered much praise for paving the way to novel therapies in reversing myocardial injuries. Cell types currently investigated for cellular delivery include embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), and adult stem cell lineages such as skeletal myoblasts, bone-marrow-derived stem cells (BMSCs), mesenchymal stem cells (MSCs), and cardiac stem cells (CSCs). To engraft these cells into patients' damaged myocardium, a variety of approaches (intramyocardial, transendocardial, transcoronary, venous, intravenous, intracoronary artery and retrograde venous administrations and bioengineered tissue transplantation) have been developed and explored. In this paper, we will discuss the pros and cons of these delivery modalities, the current state of their therapeutic potentials, and a multifaceted evaluation of their reported clinical feasibility, safety, and efficacy. While the issues of optimal delivery approach, the best progenitor stem cell type, the most effective dose, and timing of administration remain to be addressed, we are highly optimistic that stem cell therapy will provide a clinically viable option for myocardial regeneration.

  12. Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?

    PubMed

    Conraads, Viviane M; Vrints, Christiaan J; Rodrigus, Inez E; Hoymans, Vicky Y; Van Craenenbroeck, Emeline M; Bosmans, Johan; Claeys, Marc J; Van Herck, Paul; Linke, Axel; Schuler, Gerhard; Adams, Volker

    2010-03-01

    Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently (<2 weeks) infarcted regions (MI), compared with patients undergoing coronary artery bypass surgery, with normal systolic function and without previous infarction (control or Con). Left ventricular myocardial biopsies were obtained from the contralateral normal zone in MI (n = 14) patients and from the Con (n = 12) group. MuRF-1/MAFbx expression was assessed using RT-PCR and Western blot (WB). In addition, the myocardial expression of TNF-alpha was measured (RT-PCR) and troponin I, beta-myosin and phosphorylated Akt/Akt (pAkt/Akt) were quantified (WB). MuRF1 and MAFbx expression (mRNA and protein level) were significantly reduced in biopsies from MI patients. TNF-alpha was significantly higher in MI and exhibited a negative correlation with MuRF1 and MAFbx. The expression of troponin I and cardiomyocyte size were increased in MI in comparison to Con, whereas beta-myosin expression was not altered. When compared with Con, pAkt/Akt was elevated. The results of the present study suggest that the atrogenes MuRF1/MAFbx are involved in regulating the hypertrophic response, characteristic of the early post-infarction remodeling phase. Reduced expression of MuRF1 and MAFbx in the myocardium might permit hypertrophy, which is supported by the elevation of troponin I. A regulatory role of TNF-alpha needs to be confirmed in further experiments. PMID:19859778

  13. Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?

    PubMed

    Conraads, Viviane M; Vrints, Christiaan J; Rodrigus, Inez E; Hoymans, Vicky Y; Van Craenenbroeck, Emeline M; Bosmans, Johan; Claeys, Marc J; Van Herck, Paul; Linke, Axel; Schuler, Gerhard; Adams, Volker

    2010-03-01

    Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently (<2 weeks) infarcted regions (MI), compared with patients undergoing coronary artery bypass surgery, with normal systolic function and without previous infarction (control or Con). Left ventricular myocardial biopsies were obtained from the contralateral normal zone in MI (n = 14) patients and from the Con (n = 12) group. MuRF-1/MAFbx expression was assessed using RT-PCR and Western blot (WB). In addition, the myocardial expression of TNF-alpha was measured (RT-PCR) and troponin I, beta-myosin and phosphorylated Akt/Akt (pAkt/Akt) were quantified (WB). MuRF1 and MAFbx expression (mRNA and protein level) were significantly reduced in biopsies from MI patients. TNF-alpha was significantly higher in MI and exhibited a negative correlation with MuRF1 and MAFbx. The expression of troponin I and cardiomyocyte size were increased in MI in comparison to Con, whereas beta-myosin expression was not altered. When compared with Con, pAkt/Akt was elevated. The results of the present study suggest that the atrogenes MuRF1/MAFbx are involved in regulating the hypertrophic response, characteristic of the early post-infarction remodeling phase. Reduced expression of MuRF1 and MAFbx in the myocardium might permit hypertrophy, which is supported by the elevation of troponin I. A regulatory role of TNF-alpha needs to be confirmed in further experiments.

  14. Stimulating Myocardial Regeneration with Periostin Peptide in Large Mammals Improves Function Post-Myocardial Infarction but Increases Myocardial Fibrosis

    PubMed Central

    Ladage, Dennis; Yaniz-Galende, Elisa; Rapti, Kleopatra; Ishikawa, Kiyotake; Tilemann, Lisa; Shapiro, Scott; Takewa, Yoshiaki; Muller-Ehmsen, Jochen; Schwarz, Martin; Garcia, Mario J.; Sanz, Javier; Hajjar, Roger J.; Kawase, Yoshiaki

    2013-01-01

    Aims Mammalian myocardium has a finite but limited capacity to regenerate. Experimentally stimulating proliferation of cardiomyocytes with extracellular regeneration factors like periostin enhances cardiac repair in rodents. The aim of this study was to develop a safe method for delivering regeneration factors to the heart and to test the functional and structural effects of periostin peptide treatment in a large animal model of myocardial infarction (MI). Methods and Results We developed a controlled release system to deliver recombinant periostin peptide into the pericardial space. A single application of this method was performed two days after experimental MI in swine. Animals were randomly assigned to receive either saline or periostin peptide. Experimental groups were compared at baseline, day 2, 1 month and 3 months. Treatment with periostin peptide increased the EF from 31% to 41% and decreased by 22% the infarct size within 12 weeks. Periostin peptide-treated animals had newly formed myocardium strips within the infarct scar, leading to locally improved myocardial function. In addition the capillary density was increased in animals receiving periostin. However, periostin peptide treatment increased myocardial fibrosis in the remote region at one week and 12 weeks post-treatment. Conclusion Our study shows that myocardial regeneration through targeted peptides is possible. However, in the case of periostin the effects on cardiac fibrosis may limit its clinical application as a viable therapeutic strategy. PMID:23700403

  15. Oxidative stress and myocardial injury in the diabetic heart

    PubMed Central

    Ansley, David M.; Wang, Baohua

    2013-01-01

    Reactive oxygen or nitrogen species play an integral role in both myocardial injury and repair. This dichotomy is differentiated at the level of species type, amount, duration of free radical generated. Homeostatic mechanisms designed to prevent free radical generation in the first instance, scavenge, or enzymatically convert them to less toxic forms and water, play crucial roles in maintenance of cellular structure and function. The outcome between functional recovery and dysfunction is dependent upon the inherent ability of these homeostatic antioxidant defenses to withstand acute free radical generation, in the order of seconds to minutes. Alternatively, pre-existent antioxidant capacity (from intracellular and extracellular sources) may regulate the degree of free radical generation. This converts reactive oxygen and nitrogen species to the role of second messenger involved in cell signalling. The adaptive capacity of the cell is altered by the balance between death or survival signal converging at the level of the mitochondria, with distinct pathophysiologic consequences that extends the period of injury from hours to days and weeks. Hyperglycemia, hyperlipidemia, and insulin resistance enhance oxidative stress in diabetic myocardium that cannot adapt to ischemia reperfusion. Altered glucose flux, mitochondrial derangements and nitric oxide synthase uncoupling in the presence of decreased antioxidant defense and impaired prosurvival cell signalling may render the diabetic myocardium more vulnerable to injury, remodelling and heart failure. PMID:23011912

  16. Assessment of Myocardial Fibrosis with Cardiac Magnetic Resonance

    PubMed Central

    Nathan, Mewton; Ying, Liu Chia; Pierre, Croisille; David, Bluemke; João, Lima

    2011-01-01

    Diffuse interstitial or replacement myocardial fibrosis are common features of a broad variety of cardiomyopathies. Myocardial fibrosis leads to impaired cardiac diastolic and systolic function and is related to adverse cardiovascular events. Cardiac magnetic resonance (CMR) may uniquely characterize the extent of replacement fibrosis and may have prognostic value in various cardiomyopathies. Myocardial T1 mapping is an emerging technique that could improve CMR’s diagnostic accuracy especially for interstitial diffuse myocardial fibrosis. As such, CMR could be integrated in the monitoring and the therapeutic management of a large number of patients. This review summarizes the advantages and limitations of CMR for the assessment of myocardial fibrosis. PMID:21329834

  17. Assessment of myocardial fibrosis with cardiovascular magnetic resonance.

    PubMed

    Mewton, Nathan; Liu, Chia Ying; Croisille, Pierre; Bluemke, David; Lima, João A C

    2011-02-22

    Diffuse interstitial or replacement myocardial fibrosis is a common feature of a broad variety of cardiomyopathies. Myocardial fibrosis leads to impaired cardiac diastolic and systolic function and is related to adverse cardiovascular events. Cardiovascular magnetic resonance (CMR) may uniquely characterize the extent of replacement fibrosis and may have prognostic value in various cardiomyopathies. Myocardial longitudinal relaxation time mapping is an emerging technique that could improve CMR's diagnostic accuracy, especially for interstitial diffuse myocardial fibrosis. As such, CMR could be integrated in the monitoring and therapeutic management of a large number of patients. This review summarizes the advantages and limitations of CMR for the assessment of myocardial fibrosis. PMID:21329834

  18. Global myocardial strain assessment by different imaging modalities to predict outcomes after ST-elevation myocardial infarction: A systematic review

    PubMed Central

    Shetye, Abhishek; Nazir, Sheraz A; Squire, Iain B; McCann, Gerald P

    2015-01-01

    AIM: To conduct a systematic review relating myocardial strain assessed by different imaging modalities for prognostication following ST-elevation myocardial infarction (STEMI). METHODS: An online literature search was performed in PubMed and OVID® electronic databases to identify any studies that assessed global myocardial strain parameters using speckle-tracking echocardiography (STE) and/or cardiac magnetic resonance imaging (CMR) techniques [either myocardial tagging or feature tracking (FT) software] in an acute STEMI cohort (days 0-14 post-event) to predict prognosis [either development of major adverse cardiac events (MACE)] or adverse left ventricular (LV) remodelling at follow-up (≥ 6 mo for MACE, ≥ 3 mo for remodelling). Search was restricted to studies within the last 20 years. All studies that matched the pre-defined search criteria were reviewed and their results interpreted. Due to considerable heterogeneity between studies, meta-analysis was not performed. RESULTS: A total of seven studies (n = 7) were identified that matched the search criteria. All studies used STE to evaluate strain parameters - five (n = 5) assessed global longitudinal strain (GLS) (n = 5), one assessed GLS rate (GLS-R) (n = 1) and one assessed both (n = 1). Three studies showed that GLS independently predicted the development of adverse LV remodelling by multivariate analysis - odds ratio between 1.19 (CI: 1.04-1.37, P < 0.05) and 10 (CI: 6.7-14, P < 0.001) depending on the study. Four studies showed that GLS predicted the development of MACE - hazard ratio (HR) between 1.1 (CI: 1-1.1, P = 0.006) and 2.34 (1.10-4.97, P < 0.05). One paper found that GLS-R could significantly predict MACE - HR 18 (10-35, P < 0.001) - whilst another showed it did not. GLS < -10.85% had sensitivity/specificity of 89.7%/91% respectively for predicting the development of remodelling whilst GLS < -13% could predict the development of MACE with sensitivity/specificity of 100%/89% respectively. No

  19. [Effect of wall thickness of left ventricle on 201Tl myocardial SPECT images: myocardial phantom study].

    PubMed

    Koto, M; Namura, H; Kawase, O; Yamasaki, K; Kono, M

    1996-07-01

    201Tl myocardial SPECT is known for better sensitivity, specificity, and accuracy than planar images in detecting coronary artery disease and diagnosing myocardial viability. SPECT images are also superior to planar images in diagnostic sensitivity and anatomical orientation. However, as limitation of the spatial resolution of the machine, we often encounter poor SPECT plower image quality in patients with decreased wall thickness. To test the accuracy of SPECT images in patients with marked thinning of the left ventricular wall, as occurs in dilated cardiomyopathy, we performed a experimental study using myocardial phantom with 7 mm wall thickness. Tomographic image of the phantom images were rather heterogeneous, though no artificial defect was located. Dilated cardiomyopathy is thought to be characterized by patchy defects in the left ventricle. Careful attention should be given to elucidating myocardial perfusion in patients with a thin left ventricle wall, as there are technical limitations in addition to clinical features.

  20. 32 CFR 310.33 - New and altered record systems.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... alterations. (ii) Increases in numbers of individuals due to normal growth are not considered alterations... significantly the scope of population covered (for example, expansion of a system of records covering a...

  1. Relationship between post-cardiac arrest myocardial oxidative stress and myocardial dysfunction in the rat

    PubMed Central

    2014-01-01

    Background Reperfusion after resuscitation from cardiac arrest (CA) is an event that increases reactive oxygen species production leading to oxidative stress. More specifically, myocardial oxidative stress may play a role in the severity of post-CA myocardial dysfunction. This study investigated the relationship between myocardial oxidative stress and post-CA myocardial injury and dysfunction in a rat model of CA and cardiopulmonary resuscitation (CPR). Ventricular fibrillation was induced in 26 rats and was untreated for 6 min. CPR, including mechanical chest compression, ventilation, and epinephrine, was then initiated and continued for additional 6 min prior to defibrillations. Resuscitated animals were sacrificed at two h (n = 9), 4 h (n = 6) and 72 h (n = 8) following resuscitation, and plasma collected for assessment of: high sensitivity cardiac troponin T (hs-cTnT), as marker of myocardial injury; isoprostanes (IsoP), as marker of lipid peroxidation; and 8-hydroxyguanosine (8-OHG), as marker of DNA oxidative damage. Hearts were also harvested for measurement of tissue IsoP and 8-OHG. Myocardial function was assessed by echocardiography at the corresponding time points. Additional 8 rats were not subjected to CA and served as baseline controls. Results Compared to baseline, left ventricular ejection fraction (LVEF) was reduced at 2 and 4 h following resuscitation (p < 0.01), while it was similar at 72 h. Inversely, plasma hs-cTnT increased, compared to baseline, at 2 and 4 h post-CA (p < 0.01), and then recovered at 72 h. Similarly, plasma and myocardial tissue IsoP and 8-OHG levels increased at 2 and 4 h post-resuscitation (p < 0.01 vs. baseline), while returned to baseline 72 h later. Myocardial IsoP were directly related to hs-cTnT levels (r = 0.760, p < 0.01) and inversely related to LVEF (r = -0.770, p < 0.01). Myocardial 8-OHG were also directly related to hs-cTnT levels (r = 0.409, p < 0.05) and

  2. Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.

    PubMed

    Shimkunas, Rafael; Makwana, Om; Spaulding, Kimberly; Bazargan, Mona; Khazalpour, Michael; Takaba, Kiyoaki; Soleimani, Mehrdad; Myagmar, Bat-Erdene; Lovett, David H; Simpson, Paul C; Ratcliffe, Mark B; Baker, Anthony J

    2014-10-15

    After myocardial infarction, a poorly contracting nonischemic border zone forms adjacent to the infarct. The cause of border zone dysfunction is unclear. The goal of this study was to determine the myofilament mechanisms involved in postinfarction border zone dysfunction. Two weeks after anteroapical infarction of sheep hearts, we studied in vitro isometric and isotonic contractions of demembranated myocardium from the infarct border zone and a zone remote from the infarct. Maximal force development (Fmax) of the border zone myocardium was reduced by 31 ± 2% versus the remote zone myocardium (n = 6/group, P < 0.0001). Decreased border zone Fmax was not due to a reduced content of contractile material, as assessed histologically, and from myosin content. Furthermore, decreased border zone Fmax did not involve altered cross-bridge kinetics, as assessed by muscle shortening velocity and force development kinetics. Decreased border zone Fmax was associated with decreased cross-bridge formation, as assessed from muscle stiffness in the absence of ATP where cross-bridge formation should be maximized (rigor stiffness was reduced 34 ± 6%, n = 5, P = 0.011 vs. the remote zone). Furthermore, the border zone myocardium had significantly reduced phosphorylation of myosin essential light chain (ELC; 41 ± 10%, n = 4, P < 0.05). However, for animals treated with doxycycline, an inhibitor of matrix metalloproteinases, rigor stiffness and ELC phosphorylation were not reduced in the border zone myocardium, suggesting that doxycycline had a protective effect. In conclusion, myofilament dysfunction contributes to postinfarction border zone dysfunction, myofilament dysfunction involves impaired cross-bridge formation and decreased ELC phosphorylation, and matrix metalloproteinase inhibition may be beneficial for limiting postinfarct border zone dysfunction.

  3. Myocardial Ischemia: Lack of Coronary Blood Flow or Myocardial Oxygen Supply/Demand Imbalance?

    PubMed

    Heusch, Gerd

    2016-07-01

    Regional myocardial blood flow and contractile function in ischemic myocardium are well matched, and there is no evidence for an oxygen supply/demand imbalance. Thus, myocardial ischemia is lack of coronary blood flow with electric, functional, metabolic, and structural consequences for the myocardium. All therapeutic interventions must aim to improve blood flow to ischemic myocardium as much and as quickly as possible. PMID:27390331

  4. Association of fragmented QRS complex with myocardial reperfusion in acute ST-elevated myocardial infarction.

    PubMed

    Erdem, Fatma Hizal; Tavil, Yusuf; Yazici, Hüseyin; Aygül, Nazif; Abaci, Adnan; Boyaci, Bülent

    2013-01-01

    In this study, we aimed to evaluate the relationship between TIMI myocardial perfusion (TMP) grade, as an indicator of myocardial reperfusion, and fragmented QRS (fQRS) in standard 12-lead electrocardiogram. Also, we evaluate fQRS is an additional indicator of myocardial reperfusion. One hundred patients admitted with first STEMI to Coronary Intensive Care Unit and who were used thrombolytic therapy was included in this retrospective study. Standard 12-lead electrocardiogram records of patients simultaneous with coronary angiography (second day) were assessed and analysed for the presence of fQRS. Also, coronary angiography images were analyzed to identify the infarct related artery, TIMI grade of infarct related artery and TMP grade of infarct related artery. The patients with fQRS demonstrated a significantly lower TMP grade, TIMI grade and ejection fraction compared with the non-fQRS patients (P = 0.004, P = 0.003, P = 0.02 respectively). The patients with inadequate myocardial reperfusion demonstrated a significantly higher fQRS compared with the adequate myocardial reperfusion patients. (56.9% versus 23.5%, P = 0.002 respectively). On correlation analysis, there was a significant negative correlation between fQRS and left ventricular ejection fraction (r = -232, P = 0.02) TMP grade and adequate myocardial reperfusion (TMP 3) showed significant negative correlation with fQRS (r = -0.370, P = 0.000; r = -0.318, P = 0.001 respectively). Presence of fragmented QRS in STEMI patients was associated with inadequate myocardial reperfusion and it can be used as a simple, noninvasive parameter to evaluate myocardial reperfusion.

  5. Relation of impaired Thrombolysis In Myocardial Infarction myocardial perfusion grades to residual thrombus following the restoration of epicardial patency in ST-elevation myocardial infarction.

    PubMed

    Kirtane, Ajay J; Weisbord, Aaron; Karmpaliotis, Dimitrios; Murphy, Sabina A; Giugliano, Robert P; Cannon, Christopher P; Antman, Elliott M; Ohman, E Magnus; Roe, Matthew T; Braunwald, Eugene; Gibson, C Michael

    2005-01-15

    Clinical and angiographic data were analyzed from 929 patients who had ST-elevation myocardial infarction and open epicardial arteries after fibrinolytic therapy. Residual angiographically evident thrombus was associated with more frequent Thrombolysis In Myocardial Infarction (TIMI) grade 2 flow (33.6% vs 26.8%, p = 0.03), higher corrected TIMI frame counts (34 vs 31 frames, p = 0.0003), and lower TIMI myocardial perfusion grades (43.0% vs 32.0% TIMI myocardial perfusion grades 0/1, p = 0.001) among all patients and among patients who had TIMI grade 3 flow (33.5% vs 26.0% TIMI myocardial perfusion grades 0/1, p = 0.043). In multivariate analyses, angiographically evident thrombus was associated with higher corrected TIMI frame counts and worsened myocardial perfusion independent of clinical and angiographic covariates, including TIMI grade 3 flow.

  6. Role of lymphocytes in myocardial injury, healing, and remodeling after myocardial infarction.

    PubMed

    Hofmann, Ulrich; Frantz, Stefan

    2015-01-16

    A large body of evidence produced during decades of research indicates that myocardial injury activates innate immunity. On the one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial infarction (MI). On the other hand, innate immunity activation contributes to myocardial healing, as exemplified by monocytes' central role in the formation of a stable scar and protection against intraventricular thrombi after acute infarction. Although innate leukocytes can recognize a wide array of self-antigens via pattern recognition receptors, adaptive immunity activation requires highly specific cooperation between antigen-presenting cells and distinct antigen-specific receptors on lymphocytes. We have only recently begun to examine lymphocyte activation's relationship to adaptive immunity and significance in the context of ischemic myocardial injury. There is some experimental evidence that CD4(+) T-cells contribute to ischemia-reperfusion injury. Several studies have shown that CD4(+) T-cells, especially CD4(+) T-regulatory cells, improve wound healing after MI, whereas depleting B-cells is beneficial post MI. That T-cell activation after MI is induced by T-cell receptor signaling implicates autoantigens that have not yet been identified in this context. Also, the significance of lymphocytes in humans post MI remains unclear, primarily as a result of methodology. This review summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk with innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeling after myocardial infarction.

  7. Myocardial ischemic protection in natural mammalian hibernation.

    PubMed

    Yan, Lin; Kudej, Raymond K; Vatner, Dorothy E; Vatner, Stephen F

    2015-03-01

    Hibernating myocardium is an important clinical syndrome protecting the heart with chronic myocardial ischemia, named for its assumed resemblance to hibernating mammals in winter. However, the effects of myocardial ischemic protection have never been studied in true mammalian hibernation, which is a unique strategy for surviving extreme winter environmental stress. The goal of this investigation was to test the hypothesis that ischemic stress may also be protected in woodchucks as they hibernate in winter. Myocardial infarction was induced by coronary occlusion followed by reperfusion in naturally hibernating woodchucks in winter with and without hibernation and in summer, when not hibernating. The ischemic area at risk was similar among groups. Myocardial infarction was significantly less in woodchucks in winter, whether hibernating or not, compared with summer, and was similar to that resulting after ischemic preconditioning. Whereas several genes were up or downregulated in both hibernating woodchuck and with ischemic preconditioning, one mechanism was unique to hibernation, i.e., activation of cAMP-response element binding protein (CREB). When CREB was upregulated in summer, it induced protection similar to that observed in the woodchuck heart in winter. The cardioprotection in hibernation was also mediated by endothelial nitric oxide synthase, rather than inducible nitric oxide synthase. Thus, the hibernating woodchuck heart is a novel model to study cardioprotection for two major reasons: (1) powerful cardioprotection occurs naturally in winter months in the absence of any preconditioning stimuli, and (2) it resembles ischemic preconditioning, but with novel mechanisms, making this model potentially useful for clinical translation.

  8. Myocardial ischemic protection in natural mammalian hibernation.

    PubMed

    Yan, Lin; Kudej, Raymond K; Vatner, Dorothy E; Vatner, Stephen F

    2015-03-01

    Hibernating myocardium is an important clinical syndrome protecting the heart with chronic myocardial ischemia, named for its assumed resemblance to hibernating mammals in winter. However, the effects of myocardial ischemic protection have never been studied in true mammalian hibernation, which is a unique strategy for surviving extreme winter environmental stress. The goal of this investigation was to test the hypothesis that ischemic stress may also be protected in woodchucks as they hibernate in winter. Myocardial infarction was induced by coronary occlusion followed by reperfusion in naturally hibernating woodchucks in winter with and without hibernation and in summer, when not hibernating. The ischemic area at risk was similar among groups. Myocardial infarction was significantly less in woodchucks in winter, whether hibernating or not, compared with summer, and was similar to that resulting after ischemic preconditioning. Whereas several genes were up or downregulated in both hibernating woodchuck and with ischemic preconditioning, one mechanism was unique to hibernation, i.e., activation of cAMP-response element binding protein (CREB). When CREB was upregulated in summer, it induced protection similar to that observed in the woodchuck heart in winter. The cardioprotection in hibernation was also mediated by endothelial nitric oxide synthase, rather than inducible nitric oxide synthase. Thus, the hibernating woodchuck heart is a novel model to study cardioprotection for two major reasons: (1) powerful cardioprotection occurs naturally in winter months in the absence of any preconditioning stimuli, and (2) it resembles ischemic preconditioning, but with novel mechanisms, making this model potentially useful for clinical translation. PMID:25613166

  9. Rehabilitation of Patients Following Myocardial Infarction.

    ERIC Educational Resources Information Center

    Blumenthal, James A.; Emery, Charles F.

    1988-01-01

    Examines three behavioral strategies in cardiac rehabilitation (CR) for formal treatment for physical and psychosocial sequelae of myocardial infarction (MI): exercise therapy, Type A modification, and nonspecific psychological therapies. Concludes CR improves the quality of life among post-MI patients, but does not prolong life or significantly…

  10. Decreased selenium levels in acute myocardial infarction

    SciTech Connect

    Kok, F.J.; Hofman, A.; Witteman, J.C.M.; de Bruijn, A.M.; Kruyssen, D.H.C.M.; de Bruin, M.; Valkenburg, H.A. )

    1989-02-24

    To study the association between selenium status and the risk of myocardial infarction, the authors compared plasma, erythrocyte, and toenail selenium levels and the activity of erythrocyte glutathione peroxidase among 84 patients with acute myocardial infarction and 84 population controls. Mean concentrations of all selenium measurements were lower in cases than controls. The differences were statistically significant, except for the plasma selenium level. A positive trend in the risk of acute myocardial infarction from high to low toenail selenium levels was observed, which persisted after adjustment for other risk factors for myocardial infarction. In contrast, erythrocyte glutathione peroxidase activity was significantly higher in cases than controls. Because toenail selenium level reflects blood levels up to one year before sampling, these findings suggest that a low selenium status was present before the infarction and, thus, may be of etiologic relevance. The higher glutathione peroxidase activity in the cases may be interpreted as a defense against increased oxidant stress either preceding or following the acute event.

  11. Circadian rhythms in myocardial metabolism and function

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Circadian rhythms in myocardial function and dysfunction are firmly established in both animal models and humans. For example, the incidence of arrhythmias and sudden cardiac death increases when organisms awaken. Such observations have classically been explained by circadian rhythms in neurohumoral...

  12. [Myocardial infarction after conduction electrical weapon shock].

    PubMed

    Ben Ahmed, H; Bouzouita, K; Selmi, K; Chelli, M; Mokaddem, A; Ben Ameur, Y; Boujnah, M R

    2013-04-01

    Controversy persists over the safety of conducted electrical weapons, which are increasingly used by law enforcement agencies around the world. We report a case of 33-year-old man who had an acute inferior myocardial infarction after he was shot in the chest with an electrical weapon.

  13. Cardiac MRI evaluation of myocardial disease.

    PubMed

    Captur, Gabriella; Manisty, Charlotte; Moon, James C

    2016-09-15

    Cardiovascular magnetic resonance (CMR) is a key imaging technique for cardiac phenotyping with a major clinical role. It can assess advanced aspects of cardiac structure and function, scar burden and other myocardial tissue characteristics but there is new information that can now be derived. This can fill many of the gaps in our knowledge with the potential to change thinking, disease classifications and definitions as well as patient care. Established techniques such as the late gadolinium enhancement technique are now embedded in clinical care. New techniques are coming through. Myocardial tissue characterisation techniques, particularly myocardial mapping can precisely measure tissue magnetisation-T1, T2, T2* and also the extracellular volume. These change in disease. Key biological pathways are now open for scrutiny including focal fibrosis (scar) and diffuse fibrosis, inflammation, metabolism and infiltration. Other new areas to engage in where major insights are growing include detailed assessments of myocardial mechanics and performance, spectroscopy and hyperpolarised CMR. In spite of the advances, challenges remain, particularly surrounding utilisation, technical development to improve accuracy, reproducibility and deliverability, and the role of multidisciplinary research to understand the detailed pathological basis of the MR signal changes. Collectively, these new developments are galvanising CMR uptake and having a major translational impact on healthcare globally and it is steadily becoming key imaging tool. PMID:27354273

  14. A framework to measure myocardial extracellular volume fraction using dual-phase low dose CT images

    SciTech Connect

    Liu, Yixun; Summers, Ronald M.; Yao, Jianhua; Liu, Songtao; Sibley, Christopher T.; Bluemke, David A.; Nacif, Marcelo S.

    2013-10-15

    Purpose: Myocardial extracellular volume fraction (ECVF) is a surrogate imaging biomarker of diffuse myocardial fibrosis, a hallmark of pathologic ventricular remodeling. Low dose cardiac CT is emerging as a promising modality to detect diffuse interstitial myocardial fibrosis due to its fast acquisition and low radiation; however, the insufficient contrast in the low dose CT images poses great challenge to measure ECVF from the image. Methods: To deal with this difficulty, the authors present a complete ECVF measurement framework including a point-guided myocardial modeling, a deformable model-based myocardium segmentation, nonrigid registration of pre- and post-CT, and ECVF calculation. Results: The proposed method was evaluated on 20 patients by two observers. Compared to the manually delineated reference segmentations, the accuracy of our segmentation in terms of true positive volume fraction (TPVF), false positive volume fraction (FPVF), and average surface distance (ASD), were 92.18% ± 3.52%, 0.31% ± 0.10%, 0.69 ± 0.14 mm, respectively. The interobserver variability measured by concordance correlation coefficient regarding TPVF, FPVF, and ASD were 0.95, 0.90, 0.94, respectively, demonstrating excellent agreement. Bland-Altman method showed 95% limits of agreement between ECVF at CT and ECVF at MR. Conclusions: The proposed framework demonstrates its efficiency, accuracy, and noninvasiveness in ECVF measurement and dramatically advances the ECVF at cardiac CT toward its clinical use.

  15. Prediction of coronary plaque location on arteries having myocardial bridge, using finite element models.

    PubMed

    Nikolić, Dalibor; Radović, Miloš; Aleksandrić, Srđan; Tomašević, Miloje; Filipović, Nenad

    2014-11-01

    This study was performed to evaluate the influences of the myocardial bridges on the plaque initializations and progression in the coronary arteries. The wall structure is changed due to the plaque presence, which could be the reason for multiple heart malfunctions. Using simplified parametric finite element model (FE model) of the coronary artery having myocardial bridge and analyzing different mechanical parameters from blood circulation through the artery (wall shear stress, oscillatory shear index, residence time), we investigated the prediction of "the best" position for plaque progression. We chose six patients from the angiography records and used data from DICOM images to generate FE models with our software tools for FE preprocessing, solving and post-processing. We found a good correlation between real positions of the plaque and the ones that we predicted to develop at the proximal part of the myocardial bridges with wall shear stress, oscillatory shear index and residence time. This computer model could be additional predictive tool for everyday clinical examination of the patient with myocardial bridge. PMID:25139775

  16. Effect of myocardial anisotropy on the torso current flow patterns, potentials and magnetic fields.

    PubMed

    Ramon, C; Wang, Y; Haueisen, J; Schimpf, P; Jaruvatanadilok, S; Ishimaru, A

    2000-05-01

    The effects of myocardial anisotropy on the torso current flow patterns, voltage and the magnetic field were examined using an anatomically realistic torso model of an adult male subject. A finite element model of the torso was built with 19 major tissue types identified. The myocardial fibre orientation in the heart wall was included with a voxel resolution of 0.078 x 0.078 x 0.3 cm. The fibre orientations from the canine heart which are available in the literature were mapped to our adult male subject's human heart using deformable mapping techniques. The current and potential distribution in the whole torso were computed using an idealized dipolar source of +/-1.0 V in the middle of the septum of the heart wall as a boundary condition. An adaptive finite element solver was used. Two cases were studied. In one case the myocardium was isotropic and in the other it was anisotropic. It was found that the current density distribution shows a very noticeable difference between the isotropic and anisotropic myocardium. The resultant magnetic field in front of the torso was computed using the Biot-Savart law. It was found that the magnetic field profile was slightly affected by the myocardial anisotropy. The potential on the torso surface also shows noticeable changes due to the myocardial anisotropy. PMID:10843096

  17. [Altered states of consciousness].

    PubMed

    Gora, E P

    2005-01-01

    The review of modern ideas concerning the altered states of consciousness is presented in this article. Various methods of entry into the altered states of consciousness are looked over. It is shown that the altered states of consciousness are insufficiently known, but important aspects of human being existence. The role of investigation of the altered states of consciousness for the creation of integrative scientific conception base is discussed.

  18. [Altered states of consciousness].

    PubMed

    Gora, E P

    2005-01-01

    The review of modern ideas concerning the altered states of consciousness is presented in this article. Various methods of entry into the altered states of consciousness are looked over. It is shown that the altered states of consciousness are insufficiently known, but important aspects of human being existence. The role of investigation of the altered states of consciousness for the creation of integrative scientific conception base is discussed. PMID:15810684

  19. The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited

    PubMed Central

    Kurian, Gino A.; Rajagopal, Rashmi; Vedantham, Srinivasan; Rajesh, Mohanraj

    2016-01-01

    Oxidative and reductive stress are dual dynamic phases experienced by the cells undergoing adaptation towards endogenous or exogenous noxious stimulus. The former arises due to the imbalance between the reactive oxygen species production and antioxidant defenses, while the latter is due to the aberrant increase in the reducing equivalents. Mitochondrial malfunction is the common denominator arising from the aberrant functioning of the rheostat that maintains the homeostasis between oxidative and reductive stress. Recent experimental evidences suggest that the maladaptation during oxidative stress could play a pivotal role in the pathophysiology of major cardiovascular diseases such as myocardial infraction, atherosclerosis, and diabetic cardiovascular complications. In this review we have discussed the role of oxidative and reductive stress pathways in the pathogenesis of myocardial ischemia/reperfusion injury and diabetic cardiomyopathy (DCM). Furthermore, we have provided impetus for the development of subcellular organelle targeted antioxidant drug therapy for thwarting the deterioration of the failing myocardium in the aforementioned cardiovascular conditions. PMID:27313825

  20. The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited.

    PubMed

    Kurian, Gino A; Rajagopal, Rashmi; Vedantham, Srinivasan; Rajesh, Mohanraj

    2016-01-01

    Oxidative and reductive stress are dual dynamic phases experienced by the cells undergoing adaptation towards endogenous or exogenous noxious stimulus. The former arises due to the imbalance between the reactive oxygen species production and antioxidant defenses, while the latter is due to the aberrant increase in the reducing equivalents. Mitochondrial malfunction is the common denominator arising from the aberrant functioning of the rheostat that maintains the homeostasis between oxidative and reductive stress. Recent experimental evidences suggest that the maladaptation during oxidative stress could play a pivotal role in the pathophysiology of major cardiovascular diseases such as myocardial infraction, atherosclerosis, and diabetic cardiovascular complications. In this review we have discussed the role of oxidative and reductive stress pathways in the pathogenesis of myocardial ischemia/reperfusion injury and diabetic cardiomyopathy (DCM). Furthermore, we have provided impetus for the development of subcellular organelle targeted antioxidant drug therapy for thwarting the deterioration of the failing myocardium in the aforementioned cardiovascular conditions. PMID:27313825

  1. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    PubMed Central

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Vesey, Alex T; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L; Fletcher, Alison M; van Beek, Edwin J R; Rudd, James H F; Fox, Keith A A; Dweck, Marc R; Newby, David E

    2015-01-01

    Background Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans. Methods and Results Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non–ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI. Conclusions The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization

  2. Compatibility of Astragalus and Salvia extract inhibits myocardial fibrosis and ventricular remodeling by regulation of protein kinase D1 protein

    PubMed Central

    Mao, Bingyu; Nuan, Liu; Yang, Lei; Zeng, Xiaotao

    2015-01-01

    Aims: This study is to determine the effect of astragalus and salvia extract on the alteration of myocardium in a rat model of myocardial infarction. Methods: A total of 40 male Sprague-Dawley rats were randomly divided into the sham-operated group, the control group, the Astragalus group, the Salvia group, and the compatibility of Astragalus and Salvia and group. The cardiac functions were determined at 8 weeks after treatment. Hematoxylin-eosin staining was performed to observe the morphology and arrangement of cardiomyocytes. Masson’s trichrome staining was performed to investigate the distribution of myocardial interstitial collagen. Immunohistochemical staining was performed to determine the expression ofprotein kinase D1 in myocardial tissues. Results: In the sham-operated group, the Astragalus group, the Salvia group, and the compatibility of Astragalus and Salvia group, the left ventricular systolic pressure and the maximum rate of left ventricular pressure were significantly increased while the left ventricular end diastolic pressure were significantly decreased when compared with those in the control group (P < 0.05). Normal morphology and arrangement of cardiomyocytes were maintained in the compatibility of Astragalus and Salvia group. Contents of collagen fibers in myocardial tissues were decreased in the compatibility of Astragalus and Salvia group (P < 0.05). Expression levels of protein kinase D1 were significantly decreased in cardiomyocytes of the compatibility of Astragalus and Salvia group. Conclusions: Compatibility of Astragalus and Salvia extract may inhibit myocardial fibrosis and ventricular remodeling by regulation of protein kinase D1 protein in a rat model of myocardial infarction. PMID:26064267

  3. Control of intraopera