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Sample records for pentadecanoic acid myocardial

  1. Diagnosis of myocardial involvement in patients with systemic myopathies with 15-(p-(I-123)iodophenyl) pentadecanoic acid (IPPA) SPECT

    SciTech Connect

    Kropp, J.; Briele, B.; Smekal, A.V.; Hotze, A.L.; Biersack, H.J.; Koehler, U.; Zierz, St. ); Knapp, F.F. )

    1992-01-01

    Involvement of the myocardium in non-infectious myopathies presents in most cases as systolic dysfunction or a disturbed cardiac rhythm. We are interested in exploring how often cardiac involvement can be evaluated with various diagnostic techniques in patients with proven myopathy. We investigated 41 patients with myopathies of various etiology, including mitochondrial and congenital myopathies, Curshmann-Steinert disease, muscular dystrophy, and others. Myopathy was proven by muscular biopsy usually from the bicep. Fatty acid imaging was performed with 15-(p-(I-123)iodophenyl)pentadecanoic acid (IP-PA) and sequential SPECT-scintigraphy with a 180 deg. rotation starting at the 45 deg. RAO position. 190 MBq were injected at the maximal stage of a submaximal exercise. Filtered backprojection and reorientation of the slices were achieved by standard techniques. The quantitative comparison of the oblique slices (bulls-eye technique) of the SPECT-studies revealed turnover-rates as a qualitative measure of {beta}-oxidation. Serum levels of lactate (L), pyruvate (P), glucose (G) and triglycerides (TG) were measured at rest and stress. Ventricular function was investigated by radionuclide ventriculography (MUGA) at rest and under stress with Tc-99m labeled red blood cells. In addition, ECG, 24 hour-ECG, and echocardiography were also performed with standard techniques.

  2. Diagnosis of myocardial involvement in patients with systemic myopathies with 15-(p-[I-123]iodophenyl) pentadecanoic acid (IPPA) SPECT

    SciTech Connect

    Kropp, J.; Briele, B.; Smekal, A.V.; Hotze, A.L.; Biersack, H.J.; Koehler, U.; Zierz, St.; Knapp, F.F.

    1992-03-01

    Involvement of the myocardium in non-infectious myopathies presents in most cases as systolic dysfunction or a disturbed cardiac rhythm. We are interested in exploring how often cardiac involvement can be evaluated with various diagnostic techniques in patients with proven myopathy. We investigated 41 patients with myopathies of various etiology, including mitochondrial and congenital myopathies, Curshmann-Steinert disease, muscular dystrophy, and others. Myopathy was proven by muscular biopsy usually from the bicep. Fatty acid imaging was performed with 15-(p-[I-123]iodophenyl)pentadecanoic acid (IP-PA) and sequential SPECT-scintigraphy with a 180 deg. rotation starting at the 45 deg. RAO position. 190 MBq were injected at the maximal stage of a submaximal exercise. Filtered backprojection and reorientation of the slices were achieved by standard techniques. The quantitative comparison of the oblique slices (bulls-eye technique) of the SPECT-studies revealed turnover-rates as a qualitative measure of {beta}-oxidation. Serum levels of lactate (L), pyruvate (P), glucose (G) and triglycerides (TG) were measured at rest and stress. Ventricular function was investigated by radionuclide ventriculography (MUGA) at rest and under stress with Tc-99m labeled red blood cells. In addition, ECG, 24 hour-ECG, and echocardiography were also performed with standard techniques.

  3. The comparison of 2-18F-2-deoxyglucose and 15-(ortho-123I-phenyl)-pentadecanoic acid uptake in persisting defects on thallium-201 tomography in myocardial infarction

    SciTech Connect

    Henrich, M.M.; Vester, E.; von der Lohe, E.; Herzog, H.; Simon, H.; Kuikka, J.T.; Feinendegen, L.E. )

    1991-07-01

    The myocardial uptake of glucose and fatty acids into 201Tl redistribution defects were studied in 32 patients with myocardial infarction by tomography using 2-18F-2-deoxyglucose (FDG) and 15-(ortho-123I-phenyl)-pentadecanoic acid (oPPA). A total of 1153 segments were analyzed, 408 (35%) of which showed a persistent thallium-defect in stress-redistribution images. Of the segments with a decreased 201Tl uptake in these redistribution tomograms, 50.5% had a decreased uptake of both FDG and oPPA; in 21.8% FDG as well as oPPA uptake was within normal range. Normal FDG uptake but decreased oPPA uptake was detected in 17.4%, whereas 10.3% of the segments had normal oPPA uptake but decreased FDG uptake (chi-square test, p less than 0.001). A significant correlation of FDG and oPPA uptake (r = 0.51) was found in the segments with persistent 201Tl defect. Thus, a substantial fraction of persistent thallium-defects after healed myocardial infarction exhibit FDG as well as oPPA uptake, probably due to residual fatty acid metabolism in partially ischemic regions.

  4. Plasma phospholipid pentadecanoic acid, EPA, and DHA, and the frequency of dairy and fish product intake in young children

    PubMed Central

    Lund-Blix, Nicolai A.; Rønningen, Kjersti S.; Bøås, Håkon; Tapia, German; Andersen, Lene F.

    2016-01-01

    Background There is a lack of studies comparing dietary assessment methods with the biomarkers of fatty acids in children. Objective The objective was to evaluate the suitability of a food frequency questionnaire (FFQ) to rank young children according to their intake of dairy and fish products by comparing food frequency estimates to the plasma phospholipid fatty acids pentadecanoic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Design Cross-sectional data for the present study were derived from the prospective cohort ‘Environmental Triggers of Type 1 Diabetes Study’. Infants were recruited from the Norwegian general population during 2001–2007. One hundred and ten (age 3–10 years) children had sufficient volumes of plasma and FFQ filled in within 2 months from blood sampling and were included in this evaluation study. The quantitative determination of plasma phospholipid fatty acids was done by fatty acid methyl ester analysis. The association between the frequency of dairy and fish product intake and the plasma phospholipid fatty acids was assessed by a Spearman correlation analysis and by investigating whether participants were classified into the same quartiles of distribution. Results Significant correlations were found between pentadecanoic acid and the intake frequency of total dairy products (r=0.29), total fat dairy products (r=0.39), and cheese products (r=0.36). EPA and DHA were significantly correlated with the intake frequency of oily fish (r=0.26 and 0.37, respectively) and cod liver/fish oil supplements (r=0.47 for EPA and r=0.50 DHA). To a large extent, the FFQ was able to classify individuals into the same quartile as the relevant fatty acid biomarker. Conclusions The present study suggests that, when using the plasma phospholipid fatty acids pentadecanoic acid, EPA, and DHA as biomarkers, the FFQ used in young children showed a moderate capability to rank the intake frequency of dairy products with a high-fat content

  5. Potential organ or tumor imaging agents. 32. A triglyceride ester of p-iodophenyl pentadecanoic acid as a potential hepatic imaging agent.

    PubMed

    Schwendner, S W; Weichert, J P; Longino, M A; Gross, M D; Counsell, R E

    1992-08-01

    A triglyceride analog, glycerol-2-palmitoyl-1,3-di-15-(p-iodophenyl)pentadecanoate (DPPG) was synthesized and radiolabeled for evaluation as a potential functional liver scintigraphic agent. Uptake of DPPG was compared in normal, diabetic, tumor-bearing and heparin pretreated rats, revealing differences in uptake and clearance of radioactivity, correlating with hepatic lipase activity of these groups. Similar results were observed by gamma-camera scintigraphy. Comparing the uptake of DPPG with that of its fatty acid component, 15-(p-iodophenyl)pentadecanoic acid (IPPA), revealed that the peak uptake of IPPA in the liver was about half that of DPPG. Based upon these findings, DPPG warrants further study as a hepatic radiodiagnostic agent. PMID:1522018

  6. Serum pentadecanoic acid (15:0), a short-term marker of dairy food intake, is inversely associated with incident type 2 diabetes and its underlying disorders123

    PubMed Central

    Santaren, Ingrid D; Watkins, Steven M; Liese, Angela D; Wagenknecht, Lynne E; Rewers, Marian J; Haffner, Steven M; Lorenzo, Carlos

    2014-01-01

    Background: Growing evidence suggests that dairy consumption is associated with lower type 2 diabetes risk. However, observational studies have reported inconsistent results, and few have examined dairy's association with the underlying disorders of insulin resistance and β-cell dysfunction. Objective: We investigated the association of the dairy fatty acid biomarkers pentadecanoic acid (15:0) and trans-palmitoleic acid (trans 16:1n−7) with type 2 diabetes traits by evaluating 1) prospective associations with incident diabetes after 5 y of follow-up and 2) cross-sectional associations with directly measured insulin resistance and β-cell dysfunction. Design: The study analyzed 659 adults without diabetes at baseline from the triethnic multicenter Insulin Resistance Atherosclerosis Study (IRAS). Diabetes status was assessed by using oral-glucose-tolerance tests. Frequently sampled intravenous-glucose-tolerance tests measured insulin sensitivity (SI) and β-cell function [disposition index (DI)]. Serum fatty acids were quantified by using gas chromatography. Logistic and linear regression models were adjusted for demographic, lifestyle, and dietary variables. Results: Serum 15:0 was a significant biomarker for total dairy intake in the IRAS cohort. It was associated with a decreased incident diabetes risk (OR: 0.73, P = 0.02) and was positively associated with log SI (β: 0.84, P = 0.03) and log DI (β: 2.21, P = 0.02) in fully adjusted models. trans 16:1n−7 was a marker of total partially hydrogenated dietary fat intake and was not associated with outcomes in fully adjusted models. Conclusions: Serum 15:0, a marker of short-term intake of this fatty acid, was inversely associated with diabetes risk in this multiethnic cohort. This study may contribute to future recommendations regarding the benefits of dairy products on type 2 diabetes risk. PMID:25411288

  7. Normal values for nuclear cardiology: Japanese databases for myocardial perfusion, fatty acid and sympathetic imaging and left ventricular function.

    PubMed

    Nakajima, Kenichi

    2010-04-01

    Myocardial normal databases for stress myocardial perfusion study have been created by the Japanese Society of Nuclear Medicine Working Group. The databases comprised gender-, camera rotation range- and radiopharmaceutical-specific data-sets from multiple institutions, and normal database files were created for installation in common nuclear cardiology software. Based on the electrocardiography-gated single-photon emission computed tomography (SPECT), left ventricular function, including ventricular volumes, systolic and diastolic functions and systolic wall thickening were also analyzed. Normal databases for fatty acid imaging using (123)I-beta-methyl-iodophenyl-pentadecanoic acid and sympathetic imaging using (123)I-meta-iodobenzylguanidine were also examined. This review provides lists and overviews of normal values for myocardial SPECT and ventricular function in a Japanese population. The population-specific approach is a key factor for proper diagnostic and prognostic evaluation. PMID:20108130

  8. Normal values for nuclear cardiology: Japanese databases for myocardial perfusion, fatty acid and sympathetic imaging and left ventricular function

    PubMed Central

    2010-01-01

    Myocardial normal databases for stress myocardial perfusion study have been created by the Japanese Society of Nuclear Medicine Working Group. The databases comprised gender-, camera rotation range- and radiopharmaceutical-specific data-sets from multiple institutions, and normal database files were created for installation in common nuclear cardiology software. Based on the electrocardiography-gated single-photon emission computed tomography (SPECT), left ventricular function, including ventricular volumes, systolic and diastolic functions and systolic wall thickening were also analyzed. Normal databases for fatty acid imaging using 123I-beta-methyl-iodophenyl-pentadecanoic acid and sympathetic imaging using 123I-meta-iodobenzylguanidine were also examined. This review provides lists and overviews of normal values for myocardial SPECT and ventricular function in a Japanese population. The population-specific approach is a key factor for proper diagnostic and prognostic evaluation. PMID:20108130

  9. Tracer kinetics of 15-(ortho-123/131I-phenyl)-pentadecanoic acid (oPPA) and 15-(para-123/131I-phenyl)-pentadecanoic acid (pPPA) in animals and man

    SciTech Connect

    Kaiser, K.P.; Geuting, B.; Grossmann, K.; Vester, E.; Loesse, B.A.; Antar, M.A.; Machulla, H.J.; Feinendegen, L.E. )

    1990-10-01

    The human myocardium retains oPPA as opposed to pPPA. Therefore turnover of oPPA was compared with that of pPPA in rat hearts and in man, the latter by using substrates double-labeled with 123/131I and 14C. Moreover, substrate binding to coenzyme-A was tested in vitro. In rats, oPPA remained mainly in the pool of free fatty acids, as opposed to pPPA, which was metabolized by mitochondrial beta-oxidation. Binding to coenzyme-A at maximum was 62% for oPPA, 81% for pPPA and 90% for palmitic acid. In man, after i.v. and intracoronary injection of double-labeled oPPA, the two radionuclides reappeared together in venous blood and in coronary sinus respectively, in an unchanged ratio but at a significantly lower rate than with pPPA. It can be concluded that oPPA is bound to coenzyme-A and is retained in the cytosolic lipid pool, while pPPA is metabolized by mitochondrial beta-oxidation. A dual-tracer application of oPPA and pPPA has the potential of being a specific probe for the function of the carnitine shuttle.

  10. Imaging of myocardial fatty acid oxidation.

    PubMed

    Mather, Kieren J; DeGrado, Timothy R

    2016-10-01

    Myocardial fuel selection is a key feature of the health and function of the heart, with clear links between myocardial function and fuel selection and important impacts of fuel selection on ischemia tolerance. Radiopharmaceuticals provide uniquely valuable tools for in vivo, non-invasive assessment of these aspects of cardiac function and metabolism. Here we review the landscape of imaging probes developed to provide non-invasive assessment of myocardial fatty acid oxidation (MFAO). Also, we review the state of current knowledge that myocardial fatty acid imaging has helped establish of static and dynamic fuel selection that characterizes cardiac and cardiometabolic disease and the interplay between fuel selection and various aspects of cardiac function. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk. PMID:26923433

  11. Quantitation of myocardial fatty acid metabolism using PET

    SciTech Connect

    Bergmann, S.R.; Weinheimer, C.J.; Markham, J.; Herrero, P.

    1996-10-01

    Abnormalities of fatty acid metabolism in the heart presage contractile dysfunction and arrhythmias. This study was performed to determine whether myocardial fatty acid metabolism could be quantified noninvasively using PET and 1-{sup 11}C-palmitate. Anesthetized dogs were studied during control conditions; during administration of dobutamine; after oxfenicine; and during infusion of glucose. Dynamic PET data after administration of 1-{sup 11}C-palmitate were fitted to a four-compartment mathematical model. Modeled rates of palmitate utilization correlated closely with directly measured myocardial palmitate and total long-chain fatty acid utilization (r = 0.93 and 0.96, respectively, p < 0.001 for each) over a wide range of arterial fatty acid levels and altered patterns of myocardial substrate use (fatty acid extraction fraction ranging from 1% to 56%, glucose extraction fraction from 1% to 16% and myocardial fatty acid utilization from 1 to 484 nmole/g/min). The percent of fatty acid undergoing oxidation could also be measured. The results demonstrate the ability to quantify myocardial fatty acid utilization with PET. The approach is readily applicable for the determination of fatty acid metabolism noninvasively in patients. 37 refs., 5 figs., 4 tabs.

  12. [Usefulness of 201Tl/123I-BMIPP myocardial SPECT to evaluate myocardial viability and area at risk in acute myocardial infarction--comparison with 201Tl/99mTc-PYP dual SPECT].

    PubMed

    Isobe, N; Toyama, T; Hoshizaki, H; Oshima, S; Taniguchi, K

    1997-04-01

    To evaluate the area at risk and the myocardial viability of acute myocardial infarction (AMI), we compared rest 123I-beta-methyl iodophenyl pentadecanoic acid (123I-BMIPP) and 201Tl myocardial SPECT with 201Tl/99mTc-PYP dual SPECT (D-SPECT) in 65 patients (mean age 64 +/- 11 years) with AMI. D-SPECT was performed in 3 to 5 days, 123I-BMIPP myocardial SPECT in 5 to 7 days, and left ventriculography on 1 month after onset of AMI. Furthermore, 201Tl/123I-BMIPP myocardial SPECT and left ventriculography were performed on 4 months after onset of AMI. The area which showed the reduced 123I-BMIPP uptake was larger than that showed the accumulation of 99mTc-PYP. The improvement of regional wall motion on 4 months after onset of AMI tended to be more closely correlated with the existence of discrepancy zone between 201Tl and 123I-BMIPP uptake than that of overlap zone between 201Tl and 99mTc-PYP uptake in acute period. We conclude that 201Tl/123I-BMIPP myocardial SPECT is more useful to evaluate the area at risk and myocardial viability of AMI than D-SPECT. PMID:9183144

  13. Double-nuclide study of the myocardium using 201Tl and 123I-labeled fatty acids in non-ischemic myocardial diseases.

    PubMed

    Knapp, W H; Vyska, K; Machulla, H J; Notohamiprodjo, G; Schmidt, U; Knust, E J; Gleichmann, U

    1988-06-01

    Metabolic impairment and perfusion abnormalities are known to occur in hypertensive heart disease (HHD) and in cardiomyopathies. Free fatty acid (FFA) extraction is severely inhibited in a number of pathobiochemical reactions. This parameter was assessed using the radiolabeled FFA analogue 123I-(p-iodo-phenyl-)-pentadecanoic acid (IPPA) and 201Tl as perfusion marker, both of them injected at maximal physical workload. The regional extraction fraction of IPPA (IPPA-EF) was estimated by relating the regional IPPA and 201Tl uptake to each other. In HHD (normal coronary arteries) with posterior wall thickness less than or equal to 12 mm IPPA-EF was 77 +/- 18% (SD) in septum and 92 +/- 17% in the posterolateral wall (N = 13), with thickness of greater than 12 mm 60 +/- 23% in septum and 61 +/- 20% in the posterolateral wall (N = 8) when compared with IPPA-EF in normal subjects (= 100%, N = 9). In hypertrophic cardiomyopathy (HCM) IPPA-EF averaged 51 +/- 20% in septum and 87 +/- 10% in the posterolateral wall (N = 11). In these patient groups no systematic regional changes in 201TI uptake were observed. In dilated cardiomyopathy (DCM) both IPPA-EF and 201Tl uptake showed distinct regional variations and a great interindividual variability with a mean IPPA-EF reduction of 12% (N = 9). Thus, IPPA uptake in primarily non-ischemic myocardial disease may already be compromised when 201Tl uptake is unchanged. The double-nuclide method for IPPA-EF determination allows to eliminate the influence of flow in FFA imaging and enhances the potential of scintigraphy in the differential diagnosis of HHD versus coronary artery disease. PMID:3405780

  14. Myocardial imaging and metabolic studies with (17-/sup 123/I)iodoheptadecanoic acid

    SciTech Connect

    Freundlieb, C.; Hoeck, A.; Vyska, K.; Feinendegen, L.E.; Machulla, H.J.; Stoecklin, G.

    1980-11-01

    After intravenous administration of the stearic acid analogue (17-/sup 123/I)iodoheptadecanoic acid (I-123 HA), myocardial metabolism was studied in ten normal individuals, eight patients with coronary artery disease and three patients with congestive heart failure. High-quality images were obtained in sequential scintigraphy of I-123 metabolically bound in myocardial tissue. Infarcted zones as well as ischemic regions are indicated by reduced tracer uptake. Iodine-123 in the blood pool and interstitial space consists mainly of radioiodide that is liberated by fatty-acid metabolism and was corrected for. Using the proposed correction not only are the images improved but the uptake and elimination of the I-123 in the myocardial cells can be followed. The average disappearance half-time of I-123 HA from the myocardium of normal persons was 24 +- 4.7 min. In patients with coronary artery disease significant differences between myocardial regions were observed.

  15. The Cardioprotective Effects of Citric Acid and L-Malic Acid on Myocardial Ischemia/Reperfusion Injury

    PubMed Central

    Tang, Xilan; Liu, Jianxun; Dong, Wei; Li, Peng; Li, Lei; Lin, Chengren; Zheng, Yongqiu; Hou, Jincai; Li, Dan

    2013-01-01

    Organic acids in Chinese herbs, the long-neglected components, have been reported to possess antioxidant, anti-inflammatory, and antiplatelet aggregation activities; thus they may have potentially protective effect on ischemic heart disease. Therefore, this study aims to investigate the protective effects of two organic acids, that is, citric acid and L-malic acid, which are the main components of Fructus Choerospondiatis, on myocardial ischemia/reperfusion injury and the underlying mechanisms. In in vivo rat model of myocardial ischemia/reperfusion injury, we found that treatments with citric acid and L-malic acid significantly reduced myocardial infarct size, serum levels of TNF-α, and platelet aggregation. In vitro experiments revealed that both citric acid and L-malic acid significantly reduced LDH release, decreased apoptotic rate, downregulated the expression of cleaved caspase-3, and upregulated the expression of phosphorylated Akt in primary neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation injury. These results suggest that both citric acid and L-malic acid have protective effects on myocardial ischemia/reperfusion injury; the underlying mechanism may be related to their anti-inflammatory, antiplatelet aggregation and direct cardiomyocyte protective effects. These results also demonstrate that organic acids, besides flavonoids, may also be the major active ingredient of Fructus Choerospondiatis responsible for its cardioprotective effects and should be attached great importance in the therapy of ischemic heart disease. PMID:23737849

  16. Direct imaging of myocardial ischemia: a potential new paradigm in nuclear cardiovascular imaging.

    PubMed

    Jain, Diwakar; He, Zuo-Xiang

    2008-01-01

    Myocardial perfusion imaging has been in clinical use for over 30 years, serving as an effective, reliable, and relatively simple tool for diagnosis, risk stratification, and long-term follow-up of patients with suspected or known coronary artery disease. However, a unique strength of nuclear imaging is its ability to provide tools for imaging biochemical and metabolic processes and receptor and transporter functions at molecular and cellular levels in intact organisms under a wide variety of physiologic conditions. Despite their high resolution and technical sophistication, other imaging modalities currently do not have this capability. Metabolic imaging techniques using radiolabeled free fatty acid and glucose analogs provide a unique ability to image myocardial ischemia directly in patients with known or suspected coronary artery disease. These techniques can potentially overcome some of the limitations of currently used stress-rest perfusion imaging and also provide a unique opportunity to detect and image an episode of ischemia in the preceding hours even in the absence of other markers of ongoing myocardial ischemia. We describe recent studies using fluorine 18-labeled deoxyglucose and iodine 123 beta-methyl-p-iodophenyl-pentadecanoic acid for imaging myocardial ischemia. PMID:18761264

  17. Superiority of zinc complex of acetylsalicylic acid to acetylsalicylic acid in preventing postischemic myocardial dysfunction.

    PubMed

    Korkmaz, Sevil; Atmanli, Ayhan; Li, Shiliang; Radovits, Tamás; Hegedűs, Peter; Barnucz, Enikő; Hirschberg, Kristóf; Loganathan, Sivakkanan; Yoshikawa, Yutaka; Yasui, Hiroyuki; Karck, Matthias; Szabó, Gábor

    2015-09-01

    The pathophysiology of ischemic myocardial injury involves cellular events, reactive oxygen species, and an inflammatory reaction cascade. The zinc complex of acetylsalicylic acid (Zn(ASA)2) has been found to possess higher anti-inflammatory and lower ulcerogenic activities than acetylsalicylic acid (ASA). Herein, we studied the effects of both ASA and Zn(ASA)2 against acute myocardial ischemia. Rats were pretreated with ASA (75 mg/kg) or Zn(ASA)2 (100 mg/kg) orally for five consecutive days. Isoproterenol (85 mg/kg, subcutaneously [s.c.]) was applied to produce myocardial infarction. After 17-22 h, animals were anesthetized with sodium pentobarbital (60 mg/kg, intraperitoneally [i.p.]) and both electrical and mechanical parameters of cardiac function were evaluated in vivo. Myocardial histological and gene expression analyses were performed. In isoproterenol-treated rats, Zn(ASA)2 treatment normalized significantly impaired left-ventricular contractility index (Emax 2.6 ± 0.7 mmHg/µL vs. 4.6 ± 0.5 mmHg/µL, P < 0.05), increased stroke volume (30 ± 3 µL vs. 50 ± 6 µL, P < 0.05), decreased systemic vascular resistance (7.2 ± 0.7 mmHg/min/mL vs. 4.2 ± 0.5 mmHg/min/mL, P < 0.05) and reduced inflammatory infiltrate into the myocardial tissues. ECG revealed a restoration of elevated ST-segment (0.21 ± 0.03 mV vs. 0.09 ± 0.02 mV, P < 0.05) and prolonged QT-interval (79.2 ± 3.2 ms vs. 69.5 ± 2.5 ms, P < 0.05) by Zn(ASA)2. ASA treatment did not result in an improvement of these parameters. Additionally, Zn(ASA)2 significantly increased the mRNA-expression of superoxide dismutase 1 (+73 ± 15%), glutathione peroxidase 4 (+44 ± 12%), and transforming growth factor (TGF)-β1 (+102 ± 22%). In conclusion, our data demonstrate that oral administration of zinc and ASA in the form of bis(aspirinato)zinc(II) complex is superior to ASA in preventing electrical

  18. [Interesting PYP, 201Tl, MIBG, AM and BMIPP myocardial SPECT images in a patient under successful reperfusion therapy].

    PubMed

    Tanaka, T; Aizawa, T; Katou, K; Ogasawara, K; Kirigaya, H; Okamoto, K; Hosoi, H; Oota, A

    1992-06-01

    Various types of radiopharmacons such as 201Tl, 99mTc-pyrophosphate(PYP), 123I-metaiodobenzyl-guanidine(MIBG), 111In-antimyosin Fab (AM) and 123I-beta-methyl iodophenyl pentadecanoic acid (BMIPP) were applied to a patient under successful reperfusion therapy. In the patient, elevated serum enzyme activity region in the subacute phase. Ten months after the ischemic event, AM uptake was noted at the region which maintained contractility. Two years after the ischemic event, depressed BMIPP uptake and delayed washout were noted at the apical region and the basal anteroseptal region. From these findings, the following conclusions were reached. Depressed 201Tl uptake was noted in the salvaged jeopardized myocardium. The lesions noted in the MIBG images showed depressed myocardial norepenephrine activity. This suggested that depressed sympathetic nervous function caused by severe ischemia persisted long after both myocardial perfusion and myocardial contractility had been restored. From abnormal AM uptake in the contractile myocardium myocardial cell damage, which permitted AM uptake, was persistent ten months after the ischemic event. Depressed BMIPP uptake and delayed washout suggested that abnormal fatty acid metabolism caused by severe ischemia was persistent. Severe ischemia caused various types of pathological states in the myocardium and radioisotope image was useful for studying these states. PMID:1535723

  19. Improvement of myocardial ischemic dysfunction with dichloroacetic acid: experimental study by repeated ischemia in dogs.

    PubMed

    Okuda, K; Nohara, R; Fujita, M; Tamaki, N; Konishi, J; Sasayama, S

    1995-12-01

    We investigated metabolic factors related to the recovery of myocardial function during ischemia and after reperfusion using dichloroacetic acid (DCA) in canine models with repeated 10-min regional ischemia and reperfusion. Administration of 100 mg/kg DCA, which activates pyruvate dehydrogenase, improved regional wall motion significantly as compared with the nontreated controls (p < 0.05). The mechanism was studied by determining changes in myocardial levels of pH, glucose, lactate, and nonesterified fatty acids (NEFA). Glucose extraction was increased significantly during ischemia and reperfusion by the pretreatment of DCA (p < 0.01). the calculated contribution of glucose to myocardial oxidative metabolism during ischemia and reperfusion was greater than that of NEFA and lactate in case of DCA treatment. The uptake of [99mTc]pyrophosphate (PYP), which reflects myocardial injury, was also significantly suppressed by DCA (p < 0.01). pH was not affected by an infusion of DCA. These findings suggest that the activation of glucose metabolism by DCA, which is impaired and reduced during ischemia and reperfusion, may be responsible for the improved myocardial function after reperfusion. PMID:8606539

  20. Plasma fatty acids, oxylipins, and risk of myocardial infarction: the Singapore Chinese health study

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Objective: We aimed to examine the prospective association between plasma fatty acids (FAs), oxylipins and risk of acute myocardial infarction (AMI) in a Singapore Chinese population. Methods: A nested case-control study with 744 incident AMI cases and 744 matched controls aged 47-83 years was condu...

  1. Synthesis of 15-(p-iodophenyl)-6-tellurapentadecanoic acid: a new myocardial imaging agent

    SciTech Connect

    Goodman, M.M.; Knapp, F.F. Jr.

    1982-07-16

    1-Cl-9-(p-iodophenyl)nonane was coupled with sodium (methylvaleryl) telluride to produce methyl-15-(p-iodophenyl)-6-tellurapentadecanoate in 90% yield. Hydrolysis produced the title compound. /sup 1/HNMR and chromatographic analysis substantiated the structure. This method can be used in the synthesis of other fatty acid analogues. The compound has been prepared with iodine 125 and 131 labels. These agents showed prolonged myocardial retention in rats with little in vivo deiodination.

  2. [Antithrombotic therapy after myocardial infarction: arguments for the use of acetylsalicylic acid and coumarin derivatives].

    PubMed

    Waskowsky, W M; Brouwer, A; Verheugt, F W A

    2005-01-01

    Patients who survived myocardial infarction and who are being treated with the current optimal therapy (antithrombotics, statins and beta-blockers), have a 10-20% chance of death, re-infarction and stroke within in the first year. A possible explanation for this could be an increased activation and generation ofthrombin for at least 6 months following the cardiovascular event preceding preventative therapy. Acetylsalicylic acid and clopidogrel do not affect activation by thrombin of the platelet aggregation and the clotting cascade. The additional use of cumarin derivatives could therefore reduce the chance of recurring thrombotic events, and subsequently improve prognosis. Since the nineteen-nineties several randomised trials have been conducted to study the clinical relevance ofcumarin derivatives both with and without acetylsalicylic acid, in patients who had had a myocardial infarction. The conclusions of these studies were not unambiguous. If the international normalized ratio (INR) was kept > 2 for a long period, by means of frequent check-ups and effective dosage adjustment, the chance of death, recurrent myocardial infarction or stroke was 30-50% lower than when acetylsalicylic acid only was used. The risk of bleeding was raised by 2-4 times, but there were no life-threatening episodes of bleeding. In view of the recent development of anticoagulant agents, for which monitoring seems to be becoming unnecessary, identification of patients who would benefit most from a combined antithrombotic strategy is warranted. PMID:15688836

  3. Myocardial metabolism of pantothenic acid in chronically diabetic rats.

    PubMed

    Beinlich, C J; Naumovitz, R D; Song, W O; Neely, J R

    1990-03-01

    Transport and metabolism of [3H]pantothenic acid ([3H]Pa) was investigated in hearts from control and streptozotocin-induced diabetic rats. In isolated perfused hearts from control animals, the transport of [3H]Pa was linear over 3 h of perfusion when 11 mM glucose was the only exogenous substrate. The in vitro transport of [3H]Pa by hearts from 48-h diabetic rats was reduced by 65% compared to controls and was linear over 2 h of perfusion with no further accumulation of Pa during the third hour. The defect in transport observed in vitro could be corrected by in vivo treatment with 4 U Lente insulin/day for 2 days. In vitro addition of insulin in the presence of 11 mM glucose or 11 mM glucose plus 1.2 mM palmitate had no effect on [3H]Pa transport in hearts from 48-h diabetic rats during 3 h of perfusion. Accumulation of [3H]Pa was not inhibited by inclusion of 0.7 mM amino acids, 1 mM carnitine, 50 microM mersalic acid or 1 mM panthenol, pantoyllactone or pantoyltaurine. Uptake was inhibited by 1 mM nonanoic, octanoic or heptanoic acid, 0.1 mM biotin or 0.25 mM probenecid, suggesting a requirement for the terminal carboxyl group for transport. Transport of pantothenic acid was reduced in hearts from diabetic rats within 24 h of injection of streptozotocin. In vitro accumulation of [3H]Pa decreased to 10% of control 1 week after streptozotocin injection and then remained at 30% of the control value over 10 weeks.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2141362

  4. Serum Fatty Acids, Traditional Risk Factors, and Comorbidity as Related to Myocardial Injury in an Elderly Population with Acute Myocardial Infarction

    PubMed Central

    Seljeflot, Ingebjørg; Schmidt, Erik B.; Myhre, Peder; Tveit, Arnljot; Arnesen, Harald

    2016-01-01

    Background. Epidemiological and randomized clinical trials indicate that marine polyunsaturated n-3 fatty acids (n-3 PUFAs) may have cardioprotective effects. Aim. Evaluate the associations between serum fatty acid profile, traditional risk factors, the presence of cardiovascular diseases (CVD), and peak Troponin T (TnT) levels in elderly patients with an acute myocardial infarction (AMI). Materials and Methods. Patients (n = 299) consecutively included in the ongoing Omega-3 fatty acids in elderly patients with myocardial infarction (OMEMI) trial were investigated. Peak TnT was registered during the hospital stay. Serum fatty acid analysis was performed 2–8 weeks later. Results. No significant correlations between peak TnT levels and any of the n-3 PUFAs were observed. However, patients with a history of atrial fibrillation had significantly lower docosahexaenoic acid levels than patients without. Significantly lower peak TnT levels were observed in patients with a history of hyperlipidemia, angina, MI, atrial fibrillation, intermittent claudication, and previous revascularization (all p < 0.02). Conclusions. In an elderly population with AMI, no association between individual serum fatty acids and estimated myocardial infarct size could be demonstrated. However, a history of hyperlipidemia and the presence of CVD were associated with lower peak TnT levels, possibly because of treatment with cardioprotective medications. PMID:26989512

  5. Serum Fatty Acids, Traditional Risk Factors, and Comorbidity as Related to Myocardial Injury in an Elderly Population with Acute Myocardial Infarction.

    PubMed

    Laake, Kristian; Seljeflot, Ingebjørg; Schmidt, Erik B; Myhre, Peder; Tveit, Arnljot; Arnesen, Harald; Solheim, Svein

    2016-01-01

    Background. Epidemiological and randomized clinical trials indicate that marine polyunsaturated n-3 fatty acids (n-3 PUFAs) may have cardioprotective effects. Aim. Evaluate the associations between serum fatty acid profile, traditional risk factors, the presence of cardiovascular diseases (CVD), and peak Troponin T (TnT) levels in elderly patients with an acute myocardial infarction (AMI). Materials and Methods. Patients (n = 299) consecutively included in the ongoing Omega-3 fatty acids in elderly patients with myocardial infarction (OMEMI) trial were investigated. Peak TnT was registered during the hospital stay. Serum fatty acid analysis was performed 2-8 weeks later. Results. No significant correlations between peak TnT levels and any of the n-3 PUFAs were observed. However, patients with a history of atrial fibrillation had significantly lower docosahexaenoic acid levels than patients without. Significantly lower peak TnT levels were observed in patients with a history of hyperlipidemia, angina, MI, atrial fibrillation, intermittent claudication, and previous revascularization (all p < 0.02). Conclusions. In an elderly population with AMI, no association between individual serum fatty acids and estimated myocardial infarct size could be demonstrated. However, a history of hyperlipidemia and the presence of CVD were associated with lower peak TnT levels, possibly because of treatment with cardioprotective medications. PMID:26989512

  6. Myocardial Infarct Imaging of Antibodies to Canine Cardiac Myosin with Indium-111-Diethylenetriamine Pentaacetic Acid

    NASA Astrophysics Data System (ADS)

    Khaw, Ban An; Fallon, John T.; Strauss, H. William; Haber, Edgar

    1980-07-01

    Antibodies, by virtue of marked selectivity and affinity, may lend themselves to identification of structures of unique antigenic specificity in vivo. In experimental myocardial infarction in dogs, F(ab')2 fragments of antibodies to cardiac myosin that had been labeled with iodine-131 were shown to localize within the lesion. Because the energy characteristics of iodine isotopes are not ideal for imaging with a gamma camera, a new method for labeling antibody fragments with divalent or polyvalent radionuclides was developed. A bifunctional chelating agent, diethylenetriamine pentaacetic acid was covalently coupled, by an amide bond, to Fab fragments of antibodies to canine cardiac myosin. A stable chelate was then formed with indium-111, a nuclide that has appropriate half-life and energy characteristics for gamma imaging. Antibodies treated in this way retain their antigen-binding activity and are useful in locating myocardial infarcts in vivo.

  7. Effect of doxorubicin on (at-I-131) heptadecanoic acid myocardial scintigraphy and echocardiography in dogs

    SciTech Connect

    Styles, C.B.; Noujaim, A.A.; Jugdutt, B.I.; Sykes, T.R.; Bain, G.O.; Shnitka, T.L.; Hooper, H.R.

    1983-11-01

    The effects of serial treatment with doxorubicin on dynamic myocardidal scintigraphy with (at-I-131) heptadecanoic acid (I-131 HA), and on global left-ventricular function determined echocardiographically, were studied in a group of nine mongrel dogs. Total extractable myocaridal lipid was compared postmortem between a group of control dogs and doxorubicin-treated dogs. A significant and then progressive fall in global LV function was observed at a cumulative doxorubicin dose of 4 mg/kg. A significant increase in the myocaridal t/sub 1/2/ of the I-131 HA was observed only at a higher cumulative dose, 10 mg/kg. No significant alteration in total extractable myocardial lipids was observed between control dogs and those treated with doxorubicin. The findings suggest that the changes leading to an alteration of myocardial dynamic imaging with I-131 HA are not the initiating factor in doxorubicin cardiotoxicity.

  8. Myocardial infarct imaging of antibodies to canine cardiac myosin with indium-111-diethylenetriamine pentaacetic acid.

    PubMed

    Khaw, B A; Fallon, F T; Strauss, H W; Haber, E

    1980-07-11

    Antibodies, by virtue of marked selectivity and affinity, may lend themselves to identification of structures of unique antigenic specificity in vivo. In experimental myocardial infarction in dogs, F(ab')2 fragments of antibodies to cardiac myosin that had been labeled with iodine-131 were shown to localize within the lesion. Because the energy characteristics of iodine isotopes are not ideal for imaging with a gamma camera, a new method for labeling antibody fragments with divalent or polyvalent radionuclides was developed. A bifunctional chelating agent, diethylenetriamine pentaacetic acid was covalently coupled, by an amide bond, to Fab fragments of antibodies to canine cardiac myosin. A stable chelate was then formed with indium-111, a nuclide that has appropriate half-life and energy characteristics for gamma imaging. Antibodies treated in this way retain their antigen-binding activity and are useful in locating myocardial infarcts in vivo. PMID:7384803

  9. New radioiodinated methyl-branched fatty acids for cardiac studies

    SciTech Connect

    Knapp, F.F. Jr.; Ambrose, K.R.; Goodman, M.M.

    1985-01-01

    The effects of 3-methyl-substitution on the heart retention and metabolism of 3-R,S-methyl-(BMIPP) and 3,3-dimethyl-(DMIPP) analogues of 15-(p-iodophenyl)-pentadecanoic acid (IPP) have been studied in rats. Methyl-substitution considerably increased the myocardial half-time values in fasted rats: IPP, 5 to 10 min; BMIPP, 30 to 45 min; DMIPP, 6 to 7 h. Because of the observed differences in the relative myocardial uptake and retention of these agents, an evaluation of the subcellular distribution profiles and the distribution of radioactivity within various lipid pools extracted from cell components was performed. Studies with DMIPP in fasted rats have shown high levels of the free fatty acid and only slow conversion to triglycerides. These data are in contrast to the rapid clearance of the straight chain IPP analogue and rapid incorporation into triglycerides. These data suggest that the prolonged myocardial retention observed with DMIPP in vivo may result from inhibition of US -oxidation. Subcellular distribution studies have shown predominate association of DMIPP and BMIPP with the mitochondrial and microsomal fractions, while IPP was primarily found in the cytoplasm. Because of the unique ''trapping'' properties and the high heart:blood ratios, ( STI)DMIPP should be useful for evaluation of aberrations in regional myocardial uptake. 7 refs., 9 figs., 1 tab.

  10. Protective effects of p-nitro caffeic acid phenethyl ester on acute myocardial ischemia-reperfusion injury in rats

    PubMed Central

    DU, QIN; HAO, CHUNZHI; GOU, JING; LI, XIAOLI; ZOU, KAILI; HE, XIAOYAN; LI, ZHUBO

    2016-01-01

    Myocardial ischemia-reperfusion (IR) causes widespread cardiomyocyte dysfunction, including apoptosis and necrosis. The present study aimed to investigate the possible cardioprotective effects of p-nitro caffeic acid phenethyl ester (CAPE-NO2) on myocardial IR-induced injury in vivo. To generate a rat model of myocardial IR, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion for 2 h. The rats were administered either the sham treatment (the sham and IR control groups) or the therapeutic agents [the caffeic acid phenethyl ester (CAPE) and CAPE-NO2 groups] 10 min prior to the occlusion. Myocardial IR-induced injury is characterized by: A significant increase in the levels of myocardial enzymes, including creatine kinase, lactate dehydrogenase and aspartate transaminase; a marked increase in intercellular adhesion molecule 1 expression levels, lipid peroxidation products and inflammatory mediators; and a significant decrease in myocardial antioxidants, including catalase, total superoxide dismutase and glutathione peroxidase. In the present study, pretreatment with CAPE-NO2 significantly ameliorated these changes, and decreased the infarct size, as compared with the IR control group (10.32±3.8 vs. 35.65±5.4%). Furthermore, western blotting demonstrated that pretreatment with CAPE-NO2 downregulated the myocardial IR-induced protein expression levels of B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), cleaved caspase-3, P38 and the Bax/Bcl-2 ratio. CAPE-NO2 also upregulated the myocardial IR-induced expression levels of Bcl-2, phosphoinositide-3-kinase, phosphorylated Akt and mammalian target of rapamycin. In conclusion, the results of the present study indicated that CAPE-NO2 demonstrated improved cardioprotective effects, as compared with CAPE; therefore, CAPE-NO2 may represent a novel approach to pharmacological cardioprotection. PMID:27073461

  11. TXNIP regulates myocardial fatty acid oxidation via miR-33a signaling.

    PubMed

    Chen, Junqin; Young, Martin E; Chatham, John C; Crossman, David K; Dell'Italia, Louis J; Shalev, Anath

    2016-07-01

    Myocardial fatty acid β-oxidation is critical for the maintenance of energy homeostasis and contractile function in the heart, but its regulation is still not fully understood. While thioredoxin-interacting protein (TXNIP) has recently been implicated in cardiac metabolism and mitochondrial function, its effects on β-oxidation have remained unexplored. Using a new cardiomyocyte-specific TXNIP knockout mouse and working heart perfusion studies, as well as loss- and gain-of-function experiments in rat H9C2 and human AC16 cardiomyocytes, we discovered that TXNIP deficiency promotes myocardial β-oxidation via signaling through a specific microRNA, miR-33a. TXNIP deficiency leads to increased binding of nuclear factor Y (NFYA) to the sterol regulatory element binding protein 2 (SREBP2) promoter, resulting in transcriptional inhibition of SREBP2 and its intronic miR-33a. This allows for increased translation of the miR-33a target genes and β-oxidation-promoting enzymes, carnitine octanoyl transferase (CROT), carnitine palmitoyl transferase 1 (CPT1), hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase-β (HADHB), and AMPKα and is associated with an increase in phospho-AMPKα and phosphorylation/inactivation of acetyl-CoA-carboxylase. Thus, we have identified a novel TXNIP-NFYA-SREBP2/miR-33a-AMPKα/CROT/CPT1/HADHB pathway that is conserved in mouse, rat, and human cardiomyocytes and regulates myocardial β-oxidation. PMID:27199118

  12. The room temperature structures of anhydrous zinc(II) hexanoate and pentadecanoate

    NASA Astrophysics Data System (ADS)

    Taylor, Richard A.; Ellis, Henry A.; Maragh, Paul T.; White, Nicole A. S.

    2006-04-01

    The room temperature structures of anhydrous zinc (II) hexanoate and pentadecanoate have been studied using infrared spectroscopy, X-ray diffraction and polarizing light microscopy. Lattice parameters from single crystal X-ray and powder diffraction data, for short chain length hexanoate, are compared to validate the powder method which is then used, in conjunction with density and other molecular calculations to determine the structure of the longer chain length pentadecanoate. The compounds are isostructural; in that, each zinc atom is tetrahedrally coordinated to oxygen atoms of four different carboxylate groups and each ligand forms a bidentate bridge with two tetrahedral zinc atoms in a syn-anti arrangement. Bonding is unsymmetrical around the zinc atom. For both compounds, hydrocarbon chains, in the fully extended all-trans configuration, are tilted at an average angle between 58 and 61° to the planes containing zinc ions, though, in the case of the hexanoate, a bilayer arrangement of hydrocarbon chains within a lamella is indicated. The arrangement of the chains within the bilayer is regular with a similar side chain interaction for all the hydrocarbon moieties. For the longer chain length compound, an interdigitated bilayer arrangement of chains within a lamella is proposed. For this, an alternating head-to-tail arrangement within the layers between zinc atoms is indicated from the X-ray data. Nevertheless, both compounds crystallize within a monoclinic unit cell with P1 c1 symmetry, at least for the hexanoate, with the chains arranged in a two dimensional network along the ac plane within the unit cell.

  13. Ascorbic acid improves embryonic cardiomyoblast cell survival and promotes vascularization in potential myocardial grafts in vivo.

    PubMed

    Martinez, Eliana C; Wang, Jing; Gan, Shu Uin; Singh, Rajeev; Lee, Chuen Neng; Kofidis, Theo

    2010-04-01

    Organ restoration via cell therapy and tissue transplantation is limited by impaired graft survival. We tested the hypothesis that ascorbic acid (AA) reduces cell death in myocardial grafts both in vitro and in vivo and introduced a new model of autologous graft vascularization for later transplantation. Luciferase (Fluc)- and green fluorescent protein (GFP)-expressing H9C2 cardiomyoblasts were seeded in gelatin scaffolds to form myocardial artificial grafts (MAGs). MAGs were supplemented with AA (5 or 50 mumol/L) or plain growth medium. Bioluminescence imaging showed increased cell photon emission from day 1 to 5 in grafts supplemented with 5 mumol/L (p < 0.001) and 50 mumol/L (p < 0.01) AA. The amount of apoptotic cells in plain MAGs was significantly higher than in AA-enriched grafts. In our in vitro model, AA also enhanced H9C2 cell myogenic differentiation. For in vivo studies, MAGs containing H9C2-GFP-Fluc cells and enriched with AA (n = 10) or phosphate-buffered saline (n = 10) were implanted in the renal pouch of Wistar rats. At day 6, postimplantation bioluminescence signals decreased by 74% of baseline in plain MAGs versus 36% in AA-enriched MAGs (p < 0.0001). AA grafts contained significantly higher amounts of blood vessels, GFP(+) donor cells, and endothelial cells. In this study, we identified AA as a potent supplement that improves cardiomyoblast survival and promotes neovascularization in bioartificial grafts. PMID:19908964

  14. 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

  15. Altered myocardial metabolic adaptation to increased fatty acid availability in cardiomyocyte-specific CLOCK mutant mice.

    PubMed

    Peliciari-Garcia, Rodrigo A; Goel, Mehak; Aristorenas, Jonathan A; Shah, Krishna; He, Lan; Yang, Qinglin; Shalev, Anath; Bailey, Shannon M; Prabhu, Sumanth D; Chatham, John C; Gamble, Karen L; Young, Martin E

    2016-10-01

    A mismatch between fatty acid availability and utilization leads to cellular/organ dysfunction during cardiometabolic disease states (e.g., obesity, diabetes mellitus). This can precipitate cardiac dysfunction. The heart adapts to increased fatty acid availability at transcriptional, translational, post-translational and metabolic levels, thereby attenuating cardiomyopathy development. We have previously reported that the cardiomyocyte circadian clock regulates transcriptional responsiveness of the heart to acute increases in fatty acid availability (e.g., short-term fasting). The purpose of the present study was to investigate whether the cardiomyocyte circadian clock plays a role in adaptation of the heart to chronic elevations in fatty acid availability. Fatty acid availability was increased in cardiomyocyte-specific CLOCK mutant (CCM) and wild-type (WT) littermate mice for 9weeks in time-of-day-independent (streptozotocin (STZ) induced diabetes) and dependent (high fat diet meal feeding) manners. Indices of myocardial metabolic adaptation (e.g., substrate reliance perturbations) to STZ-induced diabetes and high fat meal feeding were found to be dependent on genotype. Various transcriptional and post-translational mechanisms were investigated, revealing that Cte1 mRNA induction in the heart during STZ-induced diabetes is attenuated in CCM hearts. At the functional level, time-of-day-dependent high fat meal feeding tended to influence cardiac function to a greater extent in WT versus CCM mice. Collectively, these data suggest that CLOCK (a circadian clock component) is important for metabolic adaption of the heart to prolonged elevations in fatty acid availability. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk. PMID:26721420

  16. Distribution of carbon flux within fatty acid utilization during myocardial ischemia and reperfusion

    SciTech Connect

    Nellis, S.H.; Liedtke, A.J.; Renstrom, B. )

    1991-09-01

    Twenty-nine intact, working pig hearts were extracorporeally perfused and divided into two study groups (16 Aerobic and 13 Ischemic/Reflow hearts). Step function, equilibrium labeling with (14C)palmitate was used to develop uptake and washout curves of radioactive fatty acid products contained in coronary effluent during either aerobic perfusion or reperfusion after ischemia (60% reduction in left anterior descending coronary flow for 30 minutes). Left anterior descending control flows were slightly overperfused in Aerobic hearts (18% higher than in Ischemic/Reflow hearts); otherwise, circumflex and right coronary flows, left ventricular pressure, and serum fatty acids and blood sugar levels were comparable between groups. As expected in Ischemic/Reflow hearts, recovery of regional systolic shortening and myocardial oxygen consumption in reperfusion was only modestly impaired (-20% and -19%, respectively, not significant and p less than 0.011 compared with preischemic values, not significant from Aerobic hearts). The only significant metabolized product to be released from labeled fatty acid utilization in either group was 14CO2. A smaller fatty acid pool also was measured and accounted for by that contained in the coronary intravascular volume. The authors could determine no significant back diffusion of fatty acids from myocardium in either perfusion condition. Uptake time constants of the early phase of 14CO2 production also were virtually identical in both groups (19.9 {plus minus} 3.2 versus 16.7 {plus minus} 3.2 minutes in Aerobic and Ischemic/Reflow hearts, respectively) and strongly correlated with hemodynamics as described by heart rate. In washout studies, tissue radioactivity in the aqueous soluble and fatty acid pools declined in both study groups, and counts in complex lipids and cholesterol/cholesteryl esters remained steady, whereas those in triacylglycerols varied.

  17. Detection and Assessment Using Positron Emission Tomography of Genetically Determined Defects in Myocardial Fatty Acid Utilization. Final report, 8/1/93-6/30/97

    SciTech Connect

    Bergmann, Steven R.

    2000-04-09

    An approach using positron emission tomography (PET) was developed, validated and used to measure myocardial fatty acid metabolism in patients with inherited forms of heart failure. Abnormalities were correlated with the severity of the clinical illness. The approach developed was also shown to identify abnormalities in myocardial fatty acid metabolism in some patients with acquired forms of heart failure. The PET technique thus permits identification of abnormal fatty acid metabolism and provides an approach to evaluate the efficacy of interventional strategies.

  18. Pharmacological Postconditioning with Lactic Acid and Hydrogen Rich Saline Alleviates Myocardial Reperfusion Injury in Rats

    PubMed Central

    Zhang, Guoming; Gao, Song; Li, Xiaoyan; Zhang, Lulu; Tan, Hong; Xu, Lin; Chen, Yaoyu; Geng, Yongjian; Lin, Yanliang; Aertker, Benjamin; Sun, Yuanyuan

    2015-01-01

    This study investigated whether pharmacological postconditioning with lactic acid and hydrogen rich saline can provide benefits similar to that of mechanical postconditioning. To our knowledge, this is the first therapeutic study to investigate the co-administration of lactic acid and hydrogen. SD rats were randomly divided into 6 groups: Sham, R/I, M-Post, Lac, Hyd, and Lac + Hyd. The left coronary artery was occluded for 45 min. Blood was withdrawn from the right atrium to measure pH. The rats were sacrificed at different time points to measure mitochondrial absorbance, infarct size, serum markers and apoptotic index. Rats in Lac + Hyd group had similar blood pH and ROS levels when compared to the M-Post group. Additionally, the infarct area was reduced to the same extent in Lac + Hyd and M-Post groups with a similar trends observed for serum markers of myocardial injury and apoptotic index. Although the level of P-ERK in Lac + Hyd group was lower, P-p38/JNK, TNFα, Caspase-8, mitochondrial absorbance and Cyt-c were all similar in Lac + Hyd and M-Post groups. The Lac and Hyd groups were able to partially mimic this protective role. These data suggested that pharmacological postconditioning with lactic acid and hydrogen rich saline nearly replicates the benefits of mechanical postconditioning. PMID:25928542

  19. Plasma fatty acids, oxylipins, and risk of myocardial infarction: the Singapore Chinese Health Study.

    PubMed

    Sun, Ye; Koh, Hiromi W L; Choi, Hyungwon; Koh, Woon-Puay; Yuan, Jian-Min; Newman, John W; Su, Jin; Fang, Jinling; Ong, Choon Nam; van Dam, Rob M

    2016-07-01

    We aimed to examine the prospective association between plasma FAs, oxylipins, and risk of acute myocardial infarction (AMI) in a Singapore Chinese population. A nested case-control study with 744 incident AMI cases and 744 matched controls aged 47-83 years was conducted within the Singapore Chinese Health Study. Nineteen plasma FAs and 12 oxylipins were quantified using MS. These were grouped into 12 FA clusters and 5 oxylipin clusters using hierarchical clustering, and their associations with AMI risk were assessed. Long-chain n-3 FAs [odds ratio (OR) = 0.67 per SD increase, 95% confidence interval (CI): 0.53-0.84, P < 0.001] and stearic acid (OR = 0.65, 95% CI: 0.44-0.97, P = 0.03) were inversely associated with AMI risk, whereas arachidonic acid (AA) was positively associated with AMI risk (OR = 1.25, 95% CI: 1.03-1.52, P = 0.02) in the multivariable model with adjustment for other FAs. Further adjustment for oxylipins did not substantially change these associations. An inverse association was observed between AA-derived oxylipin, thromboxane (TX)B2, and AMI risk (OR = 0.81, 95% CI: 0.71-0.93, P = 0.003). Circulating long-chain n-3 FAs and stearic acid were associated with a lower and AA was associated with a higher AMI risk in this Chinese population. The association between the oxylipin TXB2 and AMI requires further research. PMID:27371261

  20. /sup 13/N-labeled L-amino acids for in vivo assessment of local myocardial metabolism

    SciTech Connect

    Baumgartner, F.J.; Barrio, J.R.; Henze, E.; Schelbert, H.R.; MacDonald, N.S.; Phelps, M.E.; Kuhl, D.E.

    1981-06-01

    The hot cell synthesis of sterile, pyrogen-free /sup 13/N-labeled L-amino acids was accomplished by employing the appropriate immobilized enzymes on a CNBr-activated Sepharose support and using remote, semiautomated systems. The syntheses were completed 6-12 min after cyclotron production of (/sup 13/N)ammonia. Myocardial time-activity curves after intracoronary injection of /sup 13/N-labeled L-amino acids in dogs were triexponential in both normal and ischemic myocardium. Higher retention of /sup 13/N activity was observed in ischemic segments. Positron computed tomography imaging also showed increased uptake of /sup 13/N-labeled L-glutamate and L-alanine in ischemic segments compared with normal myocardium when blood flow corrections were made. Myocardial transaminases are primarily responsible for the observed retention fractions. It suggests the participation of the carbon skeletons of these amino acids in the Krebs cycle.

  1. Serum complements and heart fatty acid binding protein in Bangladeshi patients with acute myocardial infarction

    PubMed Central

    Akhtar, Nayareen; Taher, Abu; Rahman, Rezwanur; Chowdhury, Ashesh Kumar

    2012-01-01

    The complement system is activated following acute myocardial infarction (AMI). Heart fatty acid binding protein (H-FABP) is a sensitive early biomarker of myocardial necrosis that can be used to confirm or exclude a diagnosis of AMI and to monitor recurrent infarction. This study was designed to detect changes in C3, C4 and H-FABP after AMI. Forty patients with AMI and a control group of 40 apparently healthy people were included. Selections were based on inclusion and exclusion criteria. The baseline characteristics were not significantly different between the groups. Patients’ blood samples were collected within 12 h of admission. Significant increases in C3 (AMI group 1.4260+0.04, healthy group 1.26040+0.04; p<0.05), C4 (AMI group 0.29305±0.013, healthy group 0.20860±0.012; p<0.05) and H-FABP (AMI group 12.3±1.69, healthy group 0.16±0.057; p<0.001) were seen in patients with AMI. The correlation between serum C3 and body mass index (BMI, r=0.33; p<0.05), serum C4 and BMI(r=0.313; p<0.05), serum C3 and total cholesterol high density lipoprotein (HDL, r=0.32; p<0.05), serum C4 and HbA1C (r=0.335; p<0.05) and serum C3 and troponin I (r= 0.325p<0.05) was found to be significant. But the correlation between serum C3 and waist:hip ratio (p=0.56), serum C4 and waist:hip ratio (p=0.83), serum C4 and total cholesterol HDL (p=0.993), serum C3 and HbA1C (p=0.440), serum C3 and random blood sugar (p=0.563), serum C4 and random blood sugar (p=0.828) and serum C4 and troponin I (p=0.373) was not significant. The significant complement activation detected in the plasma of patients with AMI indicated that complement plays a part in the pathogenesis of myocardial infarction. A significant increase of H-FABP improves the diagnosis of AMI.

  2. Targeting Amino Acid Metabolism for Molecular Imaging of Inflammation Early After Myocardial Infarction

    PubMed Central

    Thackeray, James T.; Bankstahl, Jens P.; Wang, Yong; Wollert, Kai C.; Bengel, Frank M.

    2016-01-01

    Acute tissue inflammation after myocardial infarction influences healing and remodeling and has been identified as a target for novel therapies. Molecular imaging holds promise for guidance of such therapies. The amino acid 11C-methionine is a clinically approved agent which is thought to accumulate in macrophages, but not in healthy myocytes. We assessed the suitability of positron emission tomography (PET) with 11C-methionine for imaging post-MI inflammation, from cell to mouse to man. Uptake assays demonstrated 7-fold higher 11C-methionine uptake by polarized pro-inflammatory M1 macrophages over anti-inflammatory M2 subtypes (p<0.001). C57Bl/6 mice (n=27) underwent coronary artery ligation or no surgery. Serial 11C-methionine PET was performed 3, 5 and 7d later. MI mice exhibited a perfusion defect in 32-50% of the left ventricle (LV). PET detected increased 11C-methionine accumulation in the infarct territory at 3d (5.9±0.9%ID/g vs 4.7±0.9 in remote myocardium, and 2.6±0.5 in healthy mice; p<0.05 and <0.01 respectively), which declined by d7 post-MI (4.3±0.6 in infarct, 3.4±0.8 in remote; p=0.03 vs 3d, p=0.08 vs healthy). Increased 11C-methionine uptake was associated with macrophage infiltration of damaged myocardium. Treatment with anti-integrin antibodies (anti-CD11a, -CD11b, -CD49d; 100µg) lowered macrophage content by 56% and 11C-methionine uptake by 46% at 3d post-MI. A patient study at 3d after ST-elevation MI and early reperfusion confirmed elevated 11C-methionine uptake in the hypoperfused myocardial region. Targeting of elevated amino acid metabolism in pro-inflammatory M1 macrophages enables PET imaging-derived demarcation of tissue inflammation after MI. 11C-methionine-based molecular imaging may assist in the translation of novel image-guided, inflammation-targeted regenerative therapies. PMID:27570549

  3. Targeting Amino Acid Metabolism for Molecular Imaging of Inflammation Early After Myocardial Infarction.

    PubMed

    Thackeray, James T; Bankstahl, Jens P; Wang, Yong; Wollert, Kai C; Bengel, Frank M

    2016-01-01

    Acute tissue inflammation after myocardial infarction influences healing and remodeling and has been identified as a target for novel therapies. Molecular imaging holds promise for guidance of such therapies. The amino acid (11)C-methionine is a clinically approved agent which is thought to accumulate in macrophages, but not in healthy myocytes. We assessed the suitability of positron emission tomography (PET) with (11)C-methionine for imaging post-MI inflammation, from cell to mouse to man. Uptake assays demonstrated 7-fold higher (11)C-methionine uptake by polarized pro-inflammatory M1 macrophages over anti-inflammatory M2 subtypes (p<0.001). C57Bl/6 mice (n=27) underwent coronary artery ligation or no surgery. Serial (11)C-methionine PET was performed 3, 5 and 7d later. MI mice exhibited a perfusion defect in 32-50% of the left ventricle (LV). PET detected increased (11)C-methionine accumulation in the infarct territory at 3d (5.9±0.9%ID/g vs 4.7±0.9 in remote myocardium, and 2.6±0.5 in healthy mice; p<0.05 and <0.01 respectively), which declined by d7 post-MI (4.3±0.6 in infarct, 3.4±0.8 in remote; p=0.03 vs 3d, p=0.08 vs healthy). Increased (11)C-methionine uptake was associated with macrophage infiltration of damaged myocardium. Treatment with anti-integrin antibodies (anti-CD11a, -CD11b, -CD49d; 100µg) lowered macrophage content by 56% and (11)C-methionine uptake by 46% at 3d post-MI. A patient study at 3d after ST-elevation MI and early reperfusion confirmed elevated (11)C-methionine uptake in the hypoperfused myocardial region. Targeting of elevated amino acid metabolism in pro-inflammatory M1 macrophages enables PET imaging-derived demarcation of tissue inflammation after MI. (11)C-methionine-based molecular imaging may assist in the translation of novel image-guided, inflammation-targeted regenerative therapies. PMID:27570549

  4. Conjugated linoleic acid and nitrite attenuate mitochondrial dysfunction during myocardial ischemia.

    PubMed

    Van Hoose, Patrick M; Kelm, Natia Qipshidze; Piell, Kellianne M; Cole, Marsha P

    2016-08-01

    Cardiovascular health is influenced by dietary composition and the western diet is composed of varying types/amounts of fat. Conjugated linoleic acid (cLA) is an abundant dietary unsaturated fatty acid associated with health benefits but its biological signaling is not well understood. Nitrite is enriched in vegetables within the diet and can impact signaling of unsaturated fatty acids; however, its role on cLA signaling is not well understood. Elucidating how nitrite may impact the biological signaling of cLA is important due to the dietary consumption of both cLA and nitrite in the western diet. Since co-administration of cLA and nitrite results in cardioprotection during myocardial infarction (MI), it was hypothesized that cLA and nitrite may affect cardiac mitochondrial respiratory function and complex activity in MI. C57BL/6J mice were treated with cLA and nitrite for either 10 or 13days, where MI was induced on day 3. Following treatment, respiration and complex activity were measured. Among the major findings of this study, cLA treatment (10days) decreases state 3 respiration in vivo. Following MI, nitrite alone and in combination with cLA attenuates increased state 3 respiration and decreases hydrogen peroxide levels. Further, nitrite and cLA co-treatment attenuates increased complex III activity after MI. These results suggest that cLA, nitrite and the combination significantly alter cardiac mitochondrial respiratory and electron transport chain activity in vivo and following MI. Overall, the daily consumption of cLA and nitrite in the diet can have diverse cardiovascular implications, some of which occur at the mitochondrial level. PMID:27156147

  5. Influence of revascularization on myocardial perfusion, metabolism and function evaluated with I-123-IPPA

    SciTech Connect

    Kropp, J.; Krois, M.; Eichhorn, B.; Feske, W.; Likungu, J.; Kirchhoff, P.J.; Luederitz, B.; Biersack, H.J.; Knapp, F.F. Jr.

    1993-10-01

    Patients with coronary artery disease (CAD) were investigated with sequential SPECT-scintigraphy after administration of 200 MBq of 15-(p-[I-123]iodophenyl)pentadecanoic acid (IPPA) at peak submaximal exercise. Twenty patients underwent coronary angioplasty (PTCA) from which 14 had control coronary arteriography (CA) and left ventricular cineventriculography (LVCV). Nineteen pts underwent bypass graft surgery (ACB) and stress sonagraphy. Semi-quantification of uptake (Up related to perfusion) and turnover (Tr) was obtained by segmental comparison of oblique slices. About 90% of the reperfused myocardial segments in the PTCA-group and 76% in the ACB-group showed an improvement of uptake after therapy (RUp). Of these, 50% and 66% exhibited increased turnover (RTr) after PTCA or ACB. Pathologic RTr was highly correlated with regional wall motion abnormalities after therapy in both groups. In the ACB-group presence of improvement of RTr was correlated with improved RWM at rest and stress. IPPA-studies show potential to provide information about changes of perfusion and metabolism after reperfusion and IPPA-turnover is a good predictor of the pattern of contractile function.

  6. Cardiac RNAi therapy using RAGE siRNA/deoxycholic acid-modified polyethylenimine complexes for myocardial infarction.

    PubMed

    Hong, Jueun; Ku, Sook Hee; Lee, Min Sang; Jeong, Ji Hoon; Mok, Hyejung; Choi, Donghoon; Kim, Sun Hwa

    2014-08-01

    Inflammatory response in myocardial ischemia-reperfusion injury plays a critical role in ventricular remodeling. To avoid deleterious effects of overwhelming inflammation, we blocked the expression of receptor for advanced glycation end-products (RAGE), a key mediator of the local and systemic inflammatory responses, via RNAi mechanism. Herein, a facial amphipathic deoxycholic acid-modified low molecular weight polyethylenimine (DA-PEI) was used as a siRNA delivery carrier to myocardium. The DA-PEI conjugate formed a stable complex with siRNA via electrostatic and hydrophobic interactions. The siRAGE/DA-PEI formulation having negligible toxicity could enhance intracellular delivery efficiency and successfully suppress RAGE expression both in vitro and in vivo. Furthermore, the cardiac administration of siRAGE/DA-PEI reduced apoptosis and inflammatory cytokine release, subsequently led to attenuation of left ventricular remodeling in rat myocardial infarction model. The potential therapeutic effects of RAGE gene silencing on myocardial ischemia-reperfusion injury may suggest that the siRAGE/DA-PEI delivery system can be considered as a promising strategy for treating myocardial infarction. PMID:24917027

  7. Metabolomic profiles of myocardial ischemia under treatment with salvianolic acid B

    PubMed Central

    2012-01-01

    Background Radix Salvia miltiorrhiza (Danshen) has been used as a principal herb in treating cardiovascular diseases in Chinese medicine. Salvianolic acid B (SA-B), a water-soluble active component of Danshen, was found to have anti-myocardial ischemia (anti-MI) effect. This study aims to investigate mechanisms of SA-B on MI. Methods Five conventional Western medicines (isosorbide dinitrate, verapamil, propranolol, captopril and trimethazine) with different mechanisms for treating cardiovascular diseases were selected as positive references to compare with SA-B in changing of the metabolomic profiles in MI rats under treatment. Potential mechanisms of SA-B were further investigated in H9C2 cell line. Results The metabolomic profiles between SA-B- and propranolol-treated MI rats were similar, since there was a big overlap between the two groups in the PLS-DA score plot. Finally, it was demonstrated that SA-B exhibited a protective effect on MI mainly by decreasing the concentration of cyclic adenosine monophosphate (cAMP) and Ca2+ and inhibiting protein kinase A (PKA). Conclusion SA-B and propanolol exhibited similar metabolomic profiles, indicating that the two drugs might have a similar mechanism. PMID:22409910

  8. Induction of a reversible cardiac lipidosis by a dietary long-chain fatty acid (erucic acid). Relationship to lipid accumulation in border zones of myocardial infarcts.

    PubMed Central

    Chien, K. R.; Bellary, A.; Nicar, M.; Mukherjee, A.; Buja, L. M.

    1983-01-01

    Previous studies have demonstrated that cardiac myocytes in the border zone of acute myocardial infarction become markedly overloaded with neutral lipid during the transition from reversible to irreversible injury. To examine directly the role of these changes in neutral lipid metabolism in the development of irreversible cellular injury and associated increases in tissue Ca2+ content, the authors fed rats large amounts of a fatty acid (erucic acid) that is poorly oxidized by the heart and that subsequently accumulates as neutral lipid. Rats fed a high erucic acid (C22:1) diet in the form of 20% rapeseed oil for 3-5 days had a fourfold increase in triglyceride (49.5 +/- 3.8 SEM mg/g wet wt versus 13.6 +/- 13, n = 4) and a 60% increase in long-chain acyl CoA content (166.0 +/- 21.9 versus 91.5 +/- 9.0 nM/g wet wt, n = 4), compared with controls. However, there was no change in long-chain acyl carnitine or total phospholipid content. Histochemical studies showed accumulation of numerous lipid droplets in the myocytes, and electron microscopy revealed localization of lipid vesicles in direct contact with mitochondria, thus mimicking the lipid-laden cells in the border zone regions of acute myocardial infarcts. The acute lipidosis was reversible with either continued feeding of erucic acid for several weeks or conversion to a normal diet. It was not associated with an increased tissue Ca2+ content, nor with cell necrosis. However, continued erucic acid intake for 3 months was associated with focal myocardial degeneration and loss of myocytes. These results suggest that acute increases in neutral lipids, as found in the border zone of acute myocardial infarction, may not be the cause of progression to irreversible damage during acute myocardial injury, but that the persistent presence of similar lipid material over months may result in focal myocardial degeneration. Images Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 PMID:6859230

  9. Role of Cardiac Myocytes Heart Fatty Acid Binding Protein Depletion (H-FABP) in Early Myocardial Infarction in Human Heart (Autopsy Study)

    PubMed Central

    Shabaiek, Amany; Ismael, Nour El-Hoda; Elsheikh, Samar; Amin, Hebat Allah

    2016-01-01

    BACKGROUND: Many immunohistochemical markers have been used in the postmortem detection of early myocardial infarction. AIM: In the present study we examined the role of Heart-type fatty acid binding protein (H-FABP), in the detection of early myocardial infarction. MATERIAL AND METHODS: We obtained samples from 40 human autopsy hearts with/without histopathological signs of ischemia. RESULTS: All cases of definite and probable myocardial infarction showed a well-defined area of H-FABP depletion. All of the control cases showed strong H-FABP expression, except two markedly autolysed myocardial samples that showed affected antigenicity. CONCLUSION: Thus, we suggest H-FABP as being one of the valuable tools facing the problem of postmortem detection of early myocardial infarction/ischemia, but not in autolysis.

  10. Acetyl salicylic acid protected against heat stress damage in chicken myocardial cells and may associate with induced Hsp27 expression.

    PubMed

    Wu, Di; Xu, Jiao; Song, Erbao; Tang, Shu; Zhang, Xiaohui; Kemper, N; Hartung, J; Bao, Endong

    2015-07-01

    We investigated whether acetyl salicylic acid (ASA) protects chicken myocardial cells from heat stress-mediated damage in vivo and whether the induction of Hsp27 expression is connected with this function. Pathological changes, damage-related enzyme levels, and Hsp27 expression were studied in chickens following heat stress (40 ± 1 °C for 0, 1, 2, 3, 5, 7, 10, 15, or 24 h, respectively) with or without ASA administration (1 mg/kg BW, 2 h prior). Appearance of pathological lesions such as degenerations and karyopyknosis as well as the myocardial damage-related enzyme activation indicated that heat stress causes considerable injury to the myocardial cells in vivo. Myocardial cell injury was most serious in chickens exposed to heat stress without prior ASA administration; meanwhile, ASA pretreatment acted protective function against high temperature-induced injury. Hsp27 expression was induced under all experimental conditions but was one-fold higher in the ASA-pretreated animals (0.3138 ± 0.0340 ng/mL) than in untreated animals (0.1437 ± 0.0476 ng/mL) 1 h after heat stress exposure, and such an increase was sustained over the length of the experiment. Our findings indicate that pretreatment with ASA protects chicken myocardial cells from acute heat stress in vivo with almost no obvious side effects, and this protection may involve an enhancement of Hsp27 expression. However, the detailed mechanisms underlying this effect require further investigation. PMID:25956131

  11. Blood risk factor metabolites associated with heart disease and myocardial fatty acids in copper-deficient male and female rats

    SciTech Connect

    Fields, M.; Lewis, C.; Beal, T. ); Berlin, E.; Kliman, P.G.; Peters, R.C. )

    1989-07-01

    Intact and castrated males and intact and ovariectomized female rats were fed a copper-deficient diet in order to establish whether the protection provided in females against cardiovascular pathology and mortality is due to endogenous sex hormones, and different levels of blood lipids and/or myocardial fatty acids. Seventy-three male and female rats were assigned to a copper-deficient diet (0.6 {mu}g of copper/g diet) containing 62% fructose for 8 weeks. Twelve of the male rats underwent castration and 12 of the females were ovariectomized. All animals exhibited high levels of plasma cholesterol, triglycerides, and uric acid, which were neither affected by the sex of the rat nor by the surgical treatment. The composition of fatty acids of the myocardium was similar in males and females. Except for those animals that were sacrificed by us, all other male rats died of heart pathology. In contrast, none of the female rats exhibited heart pathology and none died of the deficiency. It is suggested that heart pathology and mortality in copper deficiency are sex related and not due to high levels of plasma cholesterol, triglycerides, and uric acid or to differences in myocardial fatty acid composition.

  12. [Acetylsalicylic acid for the prevention of primary myocardial infarction and ischemic stroke].

    PubMed

    Samorodskaya, I V; Bolotova, E V; Boytsov, S A

    2015-01-01

    There is evidence that acetylsalicylic acid (ASA) is effective in preventing events in a number of cardiovascular diseases. However, there is a number of unresolved problems concerning the efficiency and suitability of its use as an agent for the prevention of cardiovascular events (CVEs) (myocardial infarction (Ml) and/or ischemic stroke (IS) and/or death) in subjects without any clinical manifestations and/or diagnosed coronary heart disease (primary prevention of CVEs). The aim of the review is to compare the current recommendations of, professional communities for the.use of ASA as an agent for the primary prevention of CVEs, to analyze cohort studies and meta-analyses that are not included in the above recommendations (2013-2014), and to consider particular issues on ASA administration (resistance to ASA; barriers to its preventive use). The analysis performed suggests that there is no convincing evidence that it is reasonable to use ASA as a population-wide prevention strategy. The studies and meta-analyses often show conflicting data, which is likely to be associated with the clinical features of population groups included in the studies, with the presence or absence of ASA resistance and motivation for therapy. According to the current clinical recommendations, the results of studies and meta-analysis, and expert's opinions, deciding whether it is expedient to use ASA as an agent for the prevention of primary MI and/or IS and death from atherosclerostic vascular events should be based on the assessment of an individual's risks for the above disorders, which are related to a risk for hemorrhages due to ASA intake. PMID:26591559

  13. Measurement of Myocardial Fatty Acid Esterification Using [1-11C]Palmitate and PET: Comparison with Direct Measurements of Myocardial Triglyceride Synthesis

    PubMed Central

    Coggan, Andrew R.; Kisrieva-Ware, Zulfia; Dence, Carmen S.; Eisenbeis, Paul; Gropler, Robert J.; Herrero, Pilar

    2010-01-01

    The purpose of the present study was to assess the accuracy of non-invasive estimates of the rate of myocardial fatty acid esterification (MFAE) obtained using positron emission tomography (PET). Methods Sixteen dogs were studied after an overnight fast (FAST), during a euglycemic hyperinsulinemic clamp (CLAMP), or during infusion of Intralipid (IL) or IL plus dobutamine (IL/DOB) (n=4/group). The rate of MFAE was quantified using a bolus injection of [1-11C]palmitate and compartmental modeling as described by Bergmann et al.3 and compared to the rate of triglyceride (TG) synthesis measured directly using a continuous infusion of [1-13C]palmitate and tissue sampling. Results Across groups, mean plasma free fatty acid (FFA) concentration varied ~20-fold, with this variation in FFA availability accompanied by a ~20-fold range in directly-measured TG synthesis (i.e., from 7±1 nmol/min/g in CLAMP to 128±75 nmol/min/g in IL). PET-based estimates of MFAE varied to a similar degree (i.e., from 22±9 nmol/min/g in CLAMP to 543±551 nmol/min/g in IL), and were significantly correlated with TG synthesis (i.e., R=0.77, P<0.001). MFAE, however, was 3- to 4-fold higher than TG synthesis in FAST, CLAMP, and IL, but comparable when cardiac work was increased in IL/DOB, suggesting that MFAE reflects, in part, the incorporation of label into amino acids via TCA cycle exchange reactions (e.g., α-ketoglutarate ↔ glutamate) as well as the synthesis of TG and other lipids. Conclusions Changes in the rate of MFAE as determined using PET and the compartmental model of Bergmann et al.3 parallel changes in the rate of TG synthesis, at least in the basal state. Although such measurements are not as robust as rates of myocardial FFA uptake and oxidation as estimated by the model, this method should still be useful for quantifying acute changes in FFA storage by the heart in various pathophysiological states. PMID:19479313

  14. [Separate evaluation of beta-methyl fatty acid uptake and perfusion in rat myocardium].

    PubMed

    Taniguchi, M; Bunkou, H; Nakajima, K; Taki, J; Muramori, A; Matsunari, I; Nambu, I; Shiirei, Y; Tonami, N; Hisada, K

    1989-12-01

    The kinetics and distribution of I-125 beta-methyl iodophenyl pentadecanoic acid (BMIPP) in rat's heart were studied for separate evaluation of perfusion and metabolism. Tl-201 and BMIPP were simultaneously injected. The experimental groups consisted of control (C), glucose (G) and sodium lactate loaded group (L). In C, myocardial uptake at 5 minutes after BMIPP injection was 3.60% ID/g and remained constant up to 60 minutes. The myocardium/lung ratio (2.44) and the myocardium/muscle ratio (4.55) of BMIPP were almost equal to those of Tl-201. But myocardium/liver ratio was low (1.31). In G, myocardial uptake of BMIPP (1.94 +/- 0.36% ID/g) and g-BMIPP/Tl (0.31 +/- 0.03) at 15 minutes after injection were significantly decreased (p less than 0.001) than those of C (3.16 +/- 0.18% ID/g and 0.48 +/- 0.05). In L. myocardial perfusion was decreased and g-BMIPP/Tl (0.73 +/- 0.14) was significantly higher (p less than 0.01) than those of C. Coefficient of variance of the density within a myocardium, and the ratio of inner to outer layer of myocardium (I/O ratio) were calculated from autoradiogram by videodensitometry. The myocardial distribution of BMIPP was more inhomogeneous, and the I/O ratio was lower than that of Tl-201, although these were not specific for metabolic interventions. In conclusion BMIPP is suitable for SPECT imaging and dual nuclide imaging by BMIPP and Tl-201 will provide informations about myocardial fatty acid metabolism and perfusion. PMID:2622083

  15. Protective effect of the combinations of glycyrrhizic, ferulic and cinnamic acid pretreatment on myocardial ischemia-reperfusion injury in rats

    PubMed Central

    GAO, YUQIN; HAO, JIPING; ZHANG, HONGKAO; QIAN, GUOQIANG; JIANG, RENWANG; HU, JING; WANG, JIANING; LEI, ZHANG; ZHAO, GUOPING

    2015-01-01

    The aim of this study was to find an effective drug cocktail pretreatment to protect myocardial tissue of the heart from ischemia-reperfusion (I/R) injury. The mechanisms underlying the effects of the drug cocktail were subsequently explored in order to expand the application of Dang-gui-si-ni-tang (DGSN), a Traditional Chinese Medicine. The active components of DGSN in the serum following oral administration were investigated using high-performance liquid chromatography. The activity of superoxide dismutase (SOD) and malondialdehyde (MDA) levels were then analyzed to show the effect of the active components in the treatment of myocardial I/R injury. An L16 (44) orthogonal experiment was utilized to determine the most effective cocktail mix and the mechanism underlying the effect of this mix on myocardial I/R injury was investigated. It was observed that FCG, a mixture of glycyrrhizic (50 mg/kg), cinnamic (200 mg/kg) and ferulic (300 mg/kg) acid, was the optimal drug cocktail present in DGSN. This was absorbed into the blood following oral administration and was shown to decrease MDA levels and increase the activity of SOD. In conclusion, the findings suggest that FCG, a combination of active ingredients in the DGSN decoction, can be absorbed into the blood and protect the myocardium from I/R injury. PMID:25574212

  16. Effects of a New Glutamic Acid Derivative on Myocardial Contractility of Stressed Animals under Conditions of Nitric Oxide Synthesis Blockade.

    PubMed

    Tyurenkov, I N; Perfilova, V N; Sadikova, N V; Berestovitskaya, V M; Vasil'eva, O S

    2015-07-01

    Glufimet (glutamic acid derivative) in a dose of 28.7 mg/kg limited the reduction of the cardiac functional reserve in animals subjected to 24-h stress under conditions of nonselective NO synthase blockade with L-NAME (10 mg/kg). Adrenoreactivity and increased afterload tests showed that the increment of myocardial contraction/relaxation rates, left-ventricular pressure, and HR were significantly higher in glufimet-treated stressed animals with NO synthesis blockade than in animals which received no glufimet. The efficiency of glufimet was higher than that of phenibut (the reference drug). PMID:26205724

  17. Dietary Phenolic Acids of Macrotyloma uniflorum (Horse Gram) Protect the Rat Heart Against Isoproterenol-Induced Myocardial Infarction.

    PubMed

    Panda, Vandana; Laddha, Ankit; Nandave, Mukesh; Srinath, Sudhamani

    2016-07-01

    The present study investigates the cardioprotective activity of the Macrotyloma uniflorum seed extract (MUSE) and its phenolic acids (p-coumaric acid and ferulic acid) in isoproterenol (ISO)-induced myocardial infarction in rats. The previously mentioned phenolic acids were isolated and quantified from MUSE by HPLC. Pretreatment of gemfibrozil (reference standard), MUSE (250 and 500 mg/kg) and the phenolic acids for 30 days to rats treated with ISO (85 mg/kg) on the last 2 days resulted in a significant attenuation of the ISO-elevated levels of serum marker enzymes (aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase MB), total cholesterol, triglycerides, uric acid, C-reactive protein and malondialdehyde and a restoration of the levels of the ISO-depleted marker enzymes, reduced glutathione and the antioxidant enzymes-superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in heart. Restoration of the ISO-altered electrocardiogram pattern and haemodynamic parameters (left ventricular end diastolic pressure, heart rate, systolic, diastolic and mean arterial pressure) was also brought about by treatment with MUSE and the phenolic acids. It may be concluded that MUSE treatment to ISO-challenged rats exhibits a significant cardioprotective effect probably because of the potent antioxidant activity of its phenolic acids that salvage the myocardium from the deleterious effects of ISO. Copyright © 2016 John Wiley & Sons, Ltd. PMID:27091200

  18. Effects of Polyunsaturated Fatty Acid Treatment on Postdischarge Outcomes After Acute Myocardial Infarction.

    PubMed

    Greene, Stephen J; Temporelli, Pier Luigi; Campia, Umberto; Vaduganathan, Muthiah; Degli Esposti, Luca; Buda, Stefano; Veronesi, Chiara; Butler, Javed; Nodari, Savina

    2016-02-01

    Clinical trials studying the efficacy of n-3 polyunsaturated fatty acids (PUFA) in reducing adverse events after acute myocardial infarction (AMI) have yielded conflicting results, and data regarding the influence of n-3 PUFA treatment after AMI in routine clinical practice are scarce. We conducted a retrospective observational cohort study including patients from 5 Italian Local Health Units who were discharged from the hospital with a primary diagnosis of AMI from January 1, 2010, to December 31, 2011. Using unique patient identifiers, patients were linked across governmental hospital discharge, medication prescription, and mortality databases and followed for 12-months post-index discharge. Patient characteristics and risk of all-cause mortality and repeat AMI were compared by n-3 PUFA prescription after discharge (for outcome analyses, defined as ≥ 2 prescriptions) at a presumed dose of 1 g/day. Overall, 11,269 patients met inclusion criteria, of which 2,425 patients (21.5%) were prescribed n-3 PUFA during follow-up. Patients treated with n-3 PUFA tended to be younger, men, and carry a diagnosis of diabetes and were more likely to be receiving guideline-recommended post-AMI medical therapy, including β blockers, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, statins, and antiplatelet therapy (all p <0.001). After adjusting for patient characteristics and concurrent therapies, n-3 PUFA treatment was associated with reduced all-cause mortality (hazard ratio 0.76, 95% CI 0.59 to 0.97) and recurrent AMI (hazard ratio 0.65, 95% CI 0.49 to 0.87) through 12-month follow-up. In conclusion, in this large, contemporary, observational study of "real-world" Italian patients hospitalized for AMI, the use of n-3 PUFA was independently associated with a robust reduction in all-cause mortality and recurrent AMI. These data support further randomized controlled trials with n-3 PUFA therapy in the post-AMI setting. PMID:26708689

  19. Seven-Day Caloric and Saturated Fat Restriction Increases Myocardial Dietary Fatty Acid Partitioning in Impaired Glucose-Tolerant Subjects.

    PubMed

    Noll, Christophe; Kunach, Margaret; Frisch, Frédérique; Bouffard, Lucie; Dubreuil, Stéphanie; Jean-Denis, Farrah; Phoenix, Serge; Cunnane, Stephen C; Guérin, Brigitte; Turcotte, Eric E; Carpentier, André C

    2015-11-01

    Subjects with impaired glucose tolerance (IGT) have increased myocardial partitioning of dietary fatty acids (DFAs) with left ventricular dysfunction, both of which are improved by modest weight loss over 1 year induced by lifestyle changes. Here, we determined the effects of a 7-day hypocaloric diet (-500 kcal/day) low in saturated fat (<7% of energy) (LOWCAL study) versus isocaloric with the usual amount saturated fat (∼10% of energy) diet (ISOCAL) on DFA metabolism in subjects with IGT. Organ-specific DFA partitioning and cardiac and hepatic DFA fractional uptake rates were measured in 15 IGT subjects (7 males/8 females) using the oral 14(R,S)-[18F]-fluoro-6-thia-heptadecanoic acid positron emission tomography method after 7 days of an ISOCAL diet versus a LOWCAL diet using a randomized crossover design. The LOWCAL diet led to reductions in weight and postprandial insulin area under the curve. Myocardial DFA partitioning over 6 h was increased after the LOWCAL diet (2.3 ± 0.1 vs. 1.9 ± 0.2 mean standard uptake value, P < 0.04). However, the early (90-120 min) myocardial DFA fractional uptake was unchanged after the LOWCAL diet (0.055 ± 0.025 vs. 0.046 ± 0.009 min(-1), P = 0.7). Liver DFA partitioning was unchanged, but liver fractional uptake of DFA tended to be increased. Very short-term caloric and saturated fat dietary restrictions do not lead to the same changes in organ-specific DFA metabolism as those associated with weight loss in subjects with IGT. PMID:26224886

  20. Caffeoylquinic Acid Derivatives Extract of Erigeron multiradiatus Alleviated Acute Myocardial Ischemia Reperfusion Injury in Rats through Inhibiting NF-KappaB and JNK Activations.

    PubMed

    Zhang, Zhifeng; Liu, Yuan; Ren, Xuecong; Zhou, Hua; Wang, Kaishun; Zhang, Hao; Luo, Pei

    2016-01-01

    Erigeron multiradiatus (Lindl.) Benth. has been used in Tibet folk medicine to treat various inflammatory diseases. The aim of this study was to investigate antimyocardial ischemia and reperfusion (I/R) injury effect of caffeoylquinic acids derivatives of E. multiradiatus (AE) in vivo and to explain underling mechanism. AE was prepared using the whole plant of E. multiradiatus and contents of 6 caffeoylquinic acids determined through HPLC analysis. Myocardial I/R was induced by left anterior descending coronary artery occlusion for 30 minutes followed by 24 hours of reperfusion in rats. AE administration (10, 20, and 40 mg/kg) inhibited I/R-induced injury as indicated by decreasing myocardial infarct size, reducing of CK and LDH activities, and preventing ST-segment depression in dose-dependent manner. AE decreased cardiac tissue levels of proinflammatory factors TNF-α and IL-6 and attenuated leukocytes infiltration. AE was further demonstrated to significantly inhibit I-κB degradation, nuclear translocation of p-65 and phosphorylation of JNK. Our results suggested that cardioprotective effect of AE could be due to suppressing myocardial inflammatory response and blocking NF-κB and JNK activation pathway. Thus, caffeoylquinic acids might be the active compounds in E. multiradiatus on myocardial ischemia and be a potential natural drug for treating myocardial I/R injury. PMID:27516722

  1. Caffeoylquinic Acid Derivatives Extract of Erigeron multiradiatus Alleviated Acute Myocardial Ischemia Reperfusion Injury in Rats through Inhibiting NF-KappaB and JNK Activations

    PubMed Central

    Liu, Yuan; Ren, Xuecong; Wang, Kaishun; Zhang, Hao

    2016-01-01

    Erigeron multiradiatus (Lindl.) Benth. has been used in Tibet folk medicine to treat various inflammatory diseases. The aim of this study was to investigate antimyocardial ischemia and reperfusion (I/R) injury effect of caffeoylquinic acids derivatives of E. multiradiatus (AE) in vivo and to explain underling mechanism. AE was prepared using the whole plant of E. multiradiatus and contents of 6 caffeoylquinic acids determined through HPLC analysis. Myocardial I/R was induced by left anterior descending coronary artery occlusion for 30 minutes followed by 24 hours of reperfusion in rats. AE administration (10, 20, and 40 mg/kg) inhibited I/R-induced injury as indicated by decreasing myocardial infarct size, reducing of CK and LDH activities, and preventing ST-segment depression in dose-dependent manner. AE decreased cardiac tissue levels of proinflammatory factors TNF-α and IL-6 and attenuated leukocytes infiltration. AE was further demonstrated to significantly inhibit I-κB degradation, nuclear translocation of p-65 and phosphorylation of JNK. Our results suggested that cardioprotective effect of AE could be due to suppressing myocardial inflammatory response and blocking NF-κB and JNK activation pathway. Thus, caffeoylquinic acids might be the active compounds in E. multiradiatus on myocardial ischemia and be a potential natural drug for treating myocardial I/R injury. PMID:27516722

  2. Evaluation of myocardial metabolism, with /sup 13/N- and /sup 11/C-labeled amino acids and positron computed tomography

    SciTech Connect

    Henze, E.; Schelbert, H.R.; Barrio, J.R.; Egbert, J.E.; Hansen, H.W.; MacDonald, N.S.; Phelps, M.E.

    1982-08-01

    To evaluate the utility of labeled L-amino acids (AA) for imaging regional myocardial AA metabolism by positron computed tomography (PCT), the myocardial uptake and clearance of Ala,* Glu, Gln, Asp, Leu tagged with /sup 13/N, and of /sup 11/C-tagged Asp, and oxaloacetate (Oxal), were examined in 44 experiments at control, during ischemia, and after transaminase inhibition. The myocardial time-activity curves recorded after intracoronary tracer injection had two clearance phases (an early and a late) for all /sup 13/N AA, and three (early, intermediate, late) for the two /sup 11/C compounds, with significantly different clearance half-times of 18.7 +/- 8.0 (s.d.) sec for the early phase, 141.7 +/- 56.5 sec for the intermediate, and 61.2 +/- 43.5 min for the late phase. The residual fractions ranged from 0.07 to 0.23 in normal myocardium, and consistently increased with ischemia by 0.01-0.07 for /sup 13/N-labeled Ala, Glu, Asp, and Leu, but not for /sup 13/N Gln and /sup 11/C compounds. Transaminase inhibition shortened the half-times of the late phases of /sup 13/N-labeled Ala, Glu, Asp, and Leu; had no effect on t1/2 of /sup 13/N Gln and /sup 11/C Oxal; and resulted in a loss of /sup 11/C CO/sub 2/ production and of the intermediate phase for /sup 11/C Asp. On the PCT images, /sup 13/N activity from labeled Ala and Glu was not decreased in an ischemic segment despite a significant flow reduction, as demonstrated by /sup 13/N NH/sub 3/ imaging and labeled microspheres. From the results, a three-compartment tracer kinetic model is proposed for the noninvasive quantification of Krebscycle activity, protein synthesis, and metabolic derangements related to ischemia.

  3. MSC-based VEGF gene therapy in rat myocardial infarction model using facial amphipathic bile acid-conjugated polyethyleneimine.

    PubMed

    Moon, Hyung-Ho; Joo, Min Kyung; Mok, Hyejung; Lee, Minhyung; Hwang, Ki-Chul; Kim, Sung Wan; Jeong, Ji Hoon; Choi, Donghoon; Kim, Sun Hwa

    2014-02-01

    Mesenchymal stem cells (MSCs) have attracted much attention in regenerative medicine owing to their apparent usefulness as multi-potent replacement cells. The potential of MSC therapy can be further improved by transforming MSCs with therapeutic genes that maximize the efficacy of gene therapy and their own therapeutic ability. Since most conventional transfection methodologies have shown marginal success in delivering exogenous genes into primary cultured cells, efficient gene transfer into primary MSCs is a prerequisite for the development of MSC-based gene therapy strategies to achieve repair and regeneration of damaged tissues. Herein, facially amphipathic bile acid-modified polyethyleneimine (BA-PEI) conjugates were synthesized and used to transfer hypoxia-inducible vascular endothelial growth factor gene (pHI-VEGF) in MSCs for the treatment of rat myocardial infarction. Under the optimized transfection conditions, the BA-PEI conjugates significantly increased the VEGF protein expression levels in rat MSCs, compared with traditional transfection methods such as Lipofectamine™ and branched-PEI (25 kDa). Furthermore, the prepared pHI-VEGF-engineered MSCs (VEGF-MSCs) resulted in improved cell viability, particularly during severe hypoxic exposure in vitro. The transplantation of MSCs genetically modified to overexpress VEGF by BA-PEI enhanced the capillary formation in the infarction region and eventually attenuated left ventricular remodeling after myocardial infarction in rats. This study demonstrates the applicability of the BA-PEI conjugates for the efficient transfection of therapeutic genes into MSCs and the feasibility of using the genetically engineered MSCs in regenerative medicine for myocardial infarction. PMID:24280192

  4. Different effects of interventions suppressing free fatty acid metabolism on myocardial ischemia.

    PubMed

    Kahles, H; Hellige, G; Hunnemann, D H; Junggeburth, J; Kochsiek, K

    1984-06-01

    We studied the effects of different metabolic interventions, which stimulate oxidative myocardial carbohydrate metabolism, on ischemic stress during repeated coronary occlusions of three minutes in open-chest dog hearts. Increase of glucose concentration in plasma and decrease of peripheral lipolysis by glucose-insulin-potassium (n = 6) had no substantial beneficial effects on myocardial damage indicated by hemodynamic, electrocardiographic, and metabolic parameters. Infusion of lactate and pyruvate (10 mM, n = 6) was detrimental. Only activation of pyruvate dehydrogenase by dichloroacetate (n = 6) without influence on plasma osmolality reduced epicardial ST-segment elevations (-42%) and myocardial release of potassium (-36%), phosphate (-58%), and lactate (-39%). Elevations of plasma osmolalities by 10 and 20 mOsm with the metabolically inert mannitol increased ECG changes, functional loss and release of potassium, phosphate, and lactate during ischemia in our model. It is suggested, that the oxygen-saving potency of metabolic interventions can exert univocal beneficial effects in experimental and in clinical conditions only when systemic hyperosmolality and hypervolemia are avoided. PMID:6430618

  5. Synthesis and biological evaluation of (E)-19-iodo-3,3-dimethyl-18-nonadecenoic acid, a new dimethyl-branched long-chain fatty acid to evaluate regional myocardial fatty acid uptake

    SciTech Connect

    Goodman, M.M.; Ambrose, K.R.; Neff, K.H.; Knapp, F.F. Jr.

    1986-01-01

    The synthetic method for the preparation of (E)-19-iodo-3,3-dimethyl-18-nonadecenoic acid (DMIVN) involved introduction of substituents into the 2- and 5-positions of a thiophene ring followed by sulfur extrusion of a 2,5-dialkyl thiophene derivative to provide a key 3,3-dimethyl-branched fatty acid intermediate, 17-iodo-3,3-dimethylheptadecanoic acid. Myocardial subcellular distribution studies of the /sup 125/I-labeled DMIVN in fasted rats showed a higher association of radioactivity with the microsomes when compared to the results obtained with the 19-carbon straight chain analogue. With the nonfasted rats the distribution profiles of the two analogues showed differences that seemed to correlate with the differences in myocardial retention that fasting and feeding can induce. 5 refs., 3 figs., 2 tabs.

  6. Myocardial accumulation of iodinated beta-methyl-branched fatty acid analogue, iodine-125-15-(p-iodophenyl)-3-(R,S)methylpentadecanoic acid (BMIPP), in relation to ATP concentration

    SciTech Connect

    Fujibayashi, Y.; Yonekura, Y.; Takemura, Y.; Wada, K.; Matsumoto, K.; Tamaki, N.; Yamamoto, K.; Konishi, J.; Yokoyama, A. )

    1990-11-01

    To clarify the relationship between the myocardial accumulation of {sup 125}I-15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) and intracellular adenosine-5'-triphosphate (ATP) content, the effect of 2,4-dinitrophenol (DNP, an electron transport uncoupler) on myocardial BMIPP accumulation was studied, in comparison with that of thallium-201-chloride ({sup 201}Tl-Cl). In the mouse myocardium, DNP decreased the intracellular ATP and ADP levels, without affecting either acyl-CoA synthetase activity or the level of CoA-SH. Following treatment with DNP, decreases in myocardial BMIPP accumulation correlated well with those of ATP, while {sup 201}Tl-Cl showed slightly increased accumulation in the myocardium. Thus, in some diseases, BMIPP may be useful in evaluating myocardial ATP levels.

  7. Association of serum uric acid level with mortality and morbidity of patients with acute ST-elevation myocardial infarction

    PubMed Central

    Hajizadeh, Reza; Ghaffari, Samad; Salehi, Rezvanieh; Mazani, Sarvin; Aghavali, Sharmin

    2016-01-01

    Introduction: Investigating the clinical impact of serum uric acid (UA) and its lowering agents on the complications and mortality of acute ST-elevation myocardial infarction (STEMI) can open a new era in STEMI treatment. The aim of this study was to evaluate the effect of on admission serum UA level on the mortality and morbidity of patients admitted with STEMI. Methods: A number of 608 patients with STEMI were enrolled in this study from December 21, 2012 until February 19, 2014. Patients were followed for 20 months. Male to female ratio was 2.53, and the mean age of patients was 62.6±13.4. The relationship between the level of UA and patients’ mortality and morbidity, left ventricular ejection fraction (LVEF), atrial and ventricular arrhythmia was analyzed. Results: Patients with high serum UA level had higher Killip class after STEMI (P=0.001). Mean LVEF was measured to be 39.5±9.6 in normal UA group and 34.6±11.6 in high UA group (P=0.001). In comparison with normal UA group, high UA group had significantly higher cTnI (2.68±0.09 vs 4.09±0.42, respectively, P=0.001), increased blood pressure (P=0.009), and higher atrial fibrillation (AF) occurrence (P=0.03), but no association was seen between ventricular tachycardia and serum UA level. Short term and midterm mortality were not different in two groups (P=0.44 and 0.31, respectively). Conclusion: In the current study, high serum UA level in patients with acute myocardial infarction (MI) was not associated with higher in-hospital or midterm mortality, but it was associated with lower LVEF, higher Killip class, elevated cTnI, creatinine, triglyceride, and higher AF. PMID:27489597

  8. Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction

    PubMed Central

    ZHANG, DUODUO; ZHANG, YAN; ZHAO, CHUNYAN; ZHANG, WENJIE; SHAO, GUOGUANG; ZHANG, HONG

    2016-01-01

    Lysophosphatidic acid (LPA) is an intermediate product of membrane phospholipid metabolism. Recently, LPA has gained attention for its involvement in the pathological processes of certain cardiovascular diseases. The aim of the present study was to clarify the association between the effect of LPA and the immune inflammatory response, and to investigate the effects of LPA on the protein expression levels of connexin 43 during myocardial infarction. Surface electrocardiograms of myocardial infarction rats and isolated rat heart tissue samples were obtained in order to determine the effect of LPA on the incidence of arrhythmia in rats that exhibited changes in immune status. The results demonstrated that the incidence of arrhythmia decreased when the rat immune systems were suppressed, and the incidence of arrhythmia increased when the rat immune systems were enhanced. The concentration levels of tumor necrosis factor (TNF)-α were determined by ELISA, and the results demonstrated that LPA induced T lymphocyte synthesis and TNF-α release. Using a patch-clamp technique, LPA was shown to increase the current amplitude of the voltage-dependent potassium channels (Kv) and calcium-activated potassium channels (KCa) in Jurkat T cells. The protein expression of connexin 43 (Cx43) was determined by immunohistochemical staining. The results indicated that LPA caused the degradation of Cx43 and decreased the expression of Cx43. This effect was associated with the immune status of the rats. There was a further decrease in Cx43 expression in the rats of the immune-enhanced group. To the best of our knowledge, these results provide the first evidence that LPA causes arrhythmia through the regulation of immune inflammatory cells and the decrease of Cx43 protein expression. The present study provided an experimental basis for the treatment of arrhythmia and may guide clinical care. PMID:27168781

  9. Global analysis of myocardial peptides containing cysteines with irreversible sulfinic and sulfonic acid post-translational modifications.

    PubMed

    Paulech, Jana; Liddy, Kiersten A; Engholm-Keller, Kasper; White, Melanie Y; Cordwell, Stuart J

    2015-03-01

    Cysteine (Cys) oxidation is a crucial post-translational modification (PTM) associated with redox signaling and oxidative stress. As Cys is highly reactive to oxidants it forms a range of post-translational modifications, some that are biologically reversible (e.g. disulfides, Cys sulfenic acid) and others (Cys sulfinic [Cys-SO2H] and sulfonic [Cys-SO3H] acids) that are considered "irreversible." We developed an enrichment method to isolate Cys-SO2H/SO3H-containing peptides from complex tissue lysates that is compatible with tandem mass spectrometry (MS/MS). The acidity of these post-translational modification (pKa Cys-SO3H < 0) creates a unique charge distribution when localized on tryptic peptides at acidic pH that can be utilized for their purification. The method is based on electrostatic repulsion of Cys-SO2H/SO3H-containing peptides from cationic resins (i.e. "negative" selection) followed by "positive" selection using hydrophilic interaction liquid chromatography. Modification of strong cation exchange protocols decreased the complexity of initial flowthrough fractions by allowing for hydrophobic retention of neutral peptides. Coupling of strong cation exchange and hydrophilic interaction liquid chromatography allowed for increased enrichment of Cys-SO2H/SO3H (up to 80%) from other modified peptides. We identified 181 Cys-SO2H/SO3H sites from rat myocardial tissue subjected to physiologically relevant concentrations of H2O2 (<100 μm) or to ischemia/reperfusion (I/R) injury via Langendorff perfusion. I/R significantly increased Cys-SO2H/SO3H-modified peptides from proteins involved in energy utilization and contractility, as well as those involved in oxidative damage and repair. PMID:25561502

  10. THYROID HORMONE REVERSES AGING-INDUCED MYOCARDIAL FATTY ACID OXIDATION DEFECTS AND IMPROVES THE RESPONSE TO ACUTELY INCREASED AFTERLOAD

    SciTech Connect

    Ledee, Dolena; Portman, Michael A.; Kajimoto, Masaki; Isern, Nancy G.; Olson, Aaron

    2013-06-07

    Background: Subclinical hypothyroidism occurs during aging in humans and mice and may contribute to development of heart failure. Aging also impairs myocardial fatty acid oxidation, causing increased reliance on flux through pyruvate dehydrogenase (PDH) to maintain function. We hypothesize that the metabolic changes in aged hearts make them less tolerant to acutely increased work and that thyroid hormone reverses these defects. Methods: Studies were performed on young (Young, 4-6 months) and aged (Old, 22-24 months) C57/BL6 mice at standard (50 mmHg) and high afterload (80 mmHg). Another aged group received thyroid hormone for 3 weeks (Old-TH, high afterload only). Function was measured in isolated working hearts along with substrate fractional contributions (Fc) to the citric acid cycle (CAC) using perfusate with 13C labeled lactate, pyruvate, glucose and unlabeled palmitate and insulin. Results: Cardiac function was similar between Young and Old mice at standard afterload. Palmitate Fc was reduced but no individual carbohydrate contributions differed. CAC and individual substrate fluxes decreased in aged. At high afterload, -dP/dT was decreased in Old versus Young. Similar to low afterload, palmitate Fc was decreased in Old. Thyroid hormone reversed aging-induced changes in palmitate Fc and flux while significantly improving cardiac function. Conclusion: The aged heart shows diminished ability to increase cardiac work due to substrate limitations, primarily impaired fatty acid oxidation. The heart accommodates slightly by increasing efficiency through oxidation of carbohydrate substrates. Thyroid hormone supplementation in aged mice significantly improves cardiac function potentially through restoration of fatty acid oxidation.

  11. Fatty acid desaturase gene variants, cardiovascular risk factors, and myocardial infarction in the costa rica study

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Genetic variation in fatty acid desaturases (FADS) has previously been linked to long-chain polyunsaturated fatty acids (PUFAs) in adipose tissue and cardiovascular risk. The goal of our study was to test associations between six common FADS polymorphisms (rs174556, rs3834458, rs174570, rs2524299, r...

  12. [Protective effects of 11,12-epoxyeicosatrienoic acid preconditioning and postconditioning on myocardial ischemia/reperfusion injury in rats].

    PubMed

    Wang, Yan-Xia; Lu, Ling-Qiao; Wang, Xiao-Yan; Mu, Jing; Zeng, Xiang-Jun; Zhang, Li-Ke; Tang, Chao-Shu; Hao, Gang

    2008-02-25

    To explore the effects of 11,12-epoxyeicosatrienoic acid (11,12-EET) preconditioning and postconditioning on myocardial ischemia/reperfusion (IR) injury in rats, the IR injury model was built by stopping perfusion for 40 min followed by reperfusion for 30 min, and the changes of mitochondrial functions, myocardial metabolism and function were measured. Langendorff-perfused isolated rat hearts were divided into 4 groups: control group, persistently perfused with Krebs-Henseleit (K-H) fluid for 100 min; IR group, stopped perfusion for 40 min followed by reperfusion for 30 min; Pre-EET group, preconditioned with 6.24×10(-9) mol/L 11,12-EET for 5 min twice before subjected to ischemia; Post-EET group, postconditioned with 6.24×10(-9) mol/L 11,12-EET for 30 s twice before reperfusion. The computer-based electrophysiological recording system was used to measure the changes of maximal rate of the pressure increase in contract phase (+dp/dt(max)), maximal rate of the pressure decrease in diastole phase of heart (-dp/dt(max)), left ventricular end-diastolic pressure (LVEDP) and difference of left ventricular pressure (DLVP). The activities of lactate dehydrogenase (LDH) in effluent, Ca(2+)-ATPase, Na(+)-K(+)-ATPase and succinate dehydrogenase (SDH) in mitochondria were measured with colorimetry method; superoxide dismutase (SOD) activity was measured with hydroxylamine method and malondialdehyde (MDA) content in myocardial tissues was measured with TBA method. The results showed that: (1) Compared with that in the control group, the myocardial functions, the values of SOD, SDH and Na(+)-K(+)-ATPase were decreased in IR group (P<0.05); the values of LDH, MDA and Ca(2+)-ATPase were increased (P<0.05) in IR group. (2) Compared with that in IR group, the values of SDH and Na(+)-K(+)-ATPase were increased (P<0.05) and the value of Ca(2+)-ATPase was decreased (P<0.05) in both Pre-EET and Post-EET groups. But no significant differences were detected between Pre-EET and Post

  13. Aging Impairs Myocardial Fatty Acid and Ketone Oxidation and Modifies Cardiac Functional and Metabolic Responses to Insulin in Mice

    SciTech Connect

    Hyyti, Outi M.; Ledee, Dolena; Ning, Xue-Han; Ge, Ming; Portman, Michael A.

    2010-07-02

    Aging presumably initiates shifts in substrate oxidation mediated in part by changes in insulin sensitivity. Similar shifts occur with cardiac hypertrophy and may contribute to contractile dysfunction. We tested the hypothesis that aging modifies substrate utilization and alters insulin sensitivity in mouse heart when provided multiple substrates. In vivo cardiac function was measured with microtipped pressure transducers in the left ventricle from control (4–6 mo) and aged (22–24 mo) mice. Cardiac function was also measured in isolated working hearts along with substrate and anaplerotic fractional contributions to the citric acid cycle (CAC) by using perfusate containing 13C-labeled free fatty acids (FFA), acetoacetate, lactate, and unlabeled glucose. Stroke volume and cardiac output were diminished in aged mice in vivo, but pressure development was preserved. Systolic and diastolic functions were maintained in aged isolated hearts. Insulin prompted an increase in systolic function in aged hearts, resulting in an increase in cardiac efficiency. FFA and ketone flux were present but were markedly impaired in aged hearts. These changes in myocardial substrate utilization corresponded to alterations in circulating lipids, thyroid hormone, and reductions in protein expression for peroxisome proliferator-activated receptor (PPAR)α and pyruvate dehydrogenase kinase (PDK)4. Insulin further suppressed FFA oxidation in the aged. Insulin stimulation of anaplerosis in control hearts was absent in the aged. The aged heart shows metabolic plasticity by accessing multiple substrates to maintain function. However, fatty acid oxidation capacity is limited. Impaired insulin-stimulated anaplerosis may contribute to elevated cardiac efficiency, but may also limit response to acute stress through depletion of CAC intermediates.

  14. Cardiac Per2 Functions as Novel Link between Fatty Acid Metabolism and Myocardial Inflammation during Ischemia and Reperfusion Injury of the Heart

    PubMed Central

    Bonney, Stephanie; Kominsky, Doug; Brodsky, Kelley; Eltzschig, Holger; Walker, Lori; Eckle, Tobias

    2013-01-01

    Disruption of peripheral circadian rhyme pathways dominantly leads to metabolic disorders. Studies on circadian rhythm proteins in the heart indicated a role for Clock or Per2 in cardiac metabolism. In contrast to Clock−/−, Per2−/− mice have larger infarct sizes with deficient lactate production during myocardial ischemia. To test the hypothesis that cardiac Per2 represents an important regulator of cardiac metabolism during myocardial ischemia, we measured lactate during reperfusion in Per1−/−, Per2−/− or wildtype mice. As lactate measurements in whole blood indicated an exclusive role of Per2 in controlling lactate production during myocardial ischemia, we next performed gene array studies using various ischemia-reperfusion protocols comparing wildtype and Per2−/− mice. Surprisingly, high-throughput gene array analysis revealed dominantly lipid metabolism as the differentially regulated pathway in wildtype mice when compared to Per2−/−. In all ischemia-reperfusion protocols used, the enzyme enoyl-CoA hydratase, which is essential in fatty acid beta-oxidation, was regulated in wildtype animals only. Studies using nuclear magnet resonance imaging (NMRI) confirmed altered fatty acid populations with higher mono-unsaturated fatty acid levels in hearts from Per2−/− mice. Unexpectedly, studies on gene regulation during reperfusion revealed solely pro inflammatory genes as differentially regulated ‘Per2-genes’. Subsequent studies on inflammatory markers showed increasing IL-6 or TNFα levels during reperfusion in Per2−/− mice. In summary, these studies reveal an important role of cardiac Per2 for fatty acid metabolism and inflammation during myocardial ischemia and reperfusion, respectively. PMID:23977055

  15. Saturated fatty acids are not off the hook.

    PubMed

    Dawczynski, C; Kleber, M E; März, W; Jahreis, G; Lorkowski, S

    2015-12-01

    A recent meta-analysis by Chowdhury et al. (2014) has disclaimed the association between coronary artery diseases and either circulating blood levels or the intake of total saturated fatty acids (SFA). Scrutiny revealed that two of the eight studies included in the meta-analysis focused on the proportion of pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0) and their impact on cardiovascular disease (CVD) risk. These odd-chain fatty acids are markers for milk or ruminant fat intake. Both studies indicated inverse associations between milk-fat intake and first-ever myocardial infarction. Neither of the two studies described the association between total circulating blood SFA on coronary outcomes. In contrast to the cardioprotective effects of dairy consumption, we expected that an elevated intake of palmitic acid (C16:0) and stearic acid (C18:0) de novo may raise CVD risk. Thus, it is of particular importance to differentiate the effects of individual circulating SFA on cardiovascular outcomes. Excluding the studies that evaluated the association of fatty acids from milk fat and cardiovascular outcomes revealed a positive association of total SFA blood levels and coronary outcome (RR 1.21, CI 1.04-1.40). Therefore, results obtained from studies of C15:0 and C17:0 cannot be mixed with results from studies of other SFA because of the opposite physiological effects of regular consumption of foods rich in C16:0 and C18:0 compared to high intake of milk or ruminant fat. In our opinion, it is vital to analyze the impact of individual SFA on CVD incidence in order to draw prudent conclusions. PMID:26626084

  16. Heart-type fatty acid-binding protein and its relation with morphological changes in rat myocardial damage model induced by isoproterenol.

    PubMed

    Hasić, Sabaheta; Jadrić, Radivoj; Cosović, Esad; Kiseljaković, Emina; Mornjaković, Zakira; Winterhalter-Jadrić, Mira

    2011-11-01

    We have investigated heart type fatty acid binding protein (H-FABP) rat serum values at different time point following subcutaneous (s.c) isoproterenol (ISO) administration and their correlation with severity of myocardial lesion. Thirty adult, male, Wistar rats were used for this study. Six rats per group were treated with a single dose of either ISO (ISO groups, dose 100 mg/kg, s.c.) at different time point (30', 60', 120', 240') or with saline (control group). Serum H-FABP was determined by enzyme-linked immunosorbent assay (ELISA) and histological analysis was performed by hematoxylin-eosin (HE) method of staining. The first serum H-FABP increase was obtained 30' following ISO administration, but maximal value was reached after 240'. Myocardial histological changes were time-dependent and correlated with serum H-FABP values (p<0.001). The results of the study suggest that H-FABP is sensitive marker for acute rat myocardial injury and its possible inclusion in myocardial injury screening studies in rats. PMID:22117831

  17. Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction

    PubMed Central

    Bank, Sarbashri; Jana, Pradipta; Maiti, Smarajit; Guha, Santanu; Sinha, A. K.

    2014-01-01

    The aggregation of platelets on the plaque rupture site on the coronary artery is reported to cause both acute coronary syndromes (ACS) and acute myocardial infarction (AMI). While the inhibition of platelet aggregation by acetyl salicylic acid was reported to produce beneficial effects in ACS, it failed to do in AMI. The concentration of a stress induced protein (dermcidin isoform-2) was much higher in AMI than that in ACS. Incubation of normal platelet rich plasma (PRP) with dermcidin showed one high affinity (Kd = 40 nM) and one low affinity binding sites (Kd = 333 nM). When normal PRP was incubated with 0.4 μM dermcidin, the platelets became resistant to the inhibitory effect of aspirin similar to that in the case of AMI. Incubation of PRP from AMI with dermcidin antibody restored the sensitivity of the platelets to the aspirin effect. Incubation of AMI PRP pretreated with 15 μM aspirin, a stimulator of the NO synthesis, resulted in the increased production of NO in the platelets that removed the bound dermcidin by 40% from the high affinity binding sites of AMI platelets. When the same AMI PRP was retreated with 10 μM aspirin, the aggregation of platelets was completely inhibited by NO synthesis. PMID:25055737

  18. Genetic variation in fatty acid elongases is not associated with intermediate cardiovascular phenotypes or myocardial infarction

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Elongases 2, 4 and 5, encoded by genes ELOVL2, ELOVL4 and ELOVL5, have a key role in the biosynthesis of very long chain polyunsaturated fatty acids (PUFAs). To date, few studies have investigated the associations between elongase polymorphisms and cardiovascular health. We investigated whether ELOV...

  19. Lipid oxidation by hypochlorous acid: chlorinated lipids in atherosclerosis and myocardial ischemia.

    PubMed

    Ford, David A

    2010-12-01

    Leukocytes, containing myeloperoxidase (MPO), produce the reactive chlorinating species, HOCl, and they have important roles in the pathophysiology of cardiovascular disease. Leukocyte-derived HOCl can target primary amines, alkenes and vinyl ethers of lipids, resulting in chlorinated products. Plasmalogens are vinyl ether-containing phospholipids that are abundant in tissues of the cardiovascular system. The HOCl oxidation products derived from plasmalogens are α-chlorofatty aldehyde and unsaturated molecular species of lysophosphatidylcholine. α-chlorofatty aldehyde is the precursor of both α-chlorofatty alcohol and α-chlorofatty acid. Both α-chlorofatty aldehyde and α-chlorofatty acid accumulate in activated neutrophils and have disparate chemotactic properties. In addition, α-chlorofatty aldehyde increases in activated monocytes, human atherosclerotic lesions and rat infarcted myocardium. This article addresses the pathways for the synthesis of these lipids and their biological targets. PMID:21339854

  20. Impact of 1 wk of diabetes on the regulation of myocardial carbohydrate and fatty acid oxidation.

    PubMed

    Chatham, J C; Gao, Z P; Forder, J R

    1999-08-01

    The aim of this study was to investigate the effect of increasing exogenous palmitate concentration on carbohydrate and palmitate oxidation in hearts from control and 1-wk diabetic rats. Hearts were perfused with glucose, [3-(13)C]lactate, and [U-(13)C]palmitate. Substrate oxidation rates were determined by combining (13)C-NMR glutamate isotopomer analysis of tissue extracts with measurements of oxygen consumption. Carbohydrate oxidation was markedly depressed after diabetes in the presence of low (0.1 mM) but not high (1.0 mM) palmitate concentration. Increasing exogenous palmitate concentration 10-fold resulted in a 7-fold increase in the contribution of palmitate to energy production in controls but only a 30% increase in the diabetic group. Consequently, at 0.1 mM palmitate, the rate of fatty acid oxidation was higher in the diabetic group than in controls; however, at 1.0 mM fatty acid oxidation, it was significantly depressed. Therefore, after 1 wk of diabetes, the major differences in carbohydrate and fatty acid metabolism occur primarily at low rather than high exogenous palmitate concentration. PMID:10444431

  1. Usefulness of serum unbound free fatty acid levels to predict death early in patients with ST-segment elevation myocardial infarction (from the Thrombolysis In Myocardial Infarction [TIMI] II trial).

    PubMed

    Huber, Andrew H; Kampf, J Patrick; Kwan, Thomas; Zhu, Baolong; Adams, Jesse; Kleinfeld, Alan M

    2014-01-15

    Circulating total free fatty acid (FFA) levels are elevated early in myocardial infarction (MI) and have been associated with an increase in mortality. We investigated the association of serum unbound FFA (FFAu) levels with mortality in patients presenting with ST-segment elevation MI in the Thrombolysis In Myocardial Infarction II trial. The Thrombolysis In Myocardial Infarction II trial enrolled patients within 4 hours of chest pain onset. The patients were treated with a recombinant tissue plasminogen activator within 1 hour of enrollment. The FFAu concentration was evaluated in serum samples from 1,834 patients obtained at baseline, before therapy. The FFAu level was an independent risk factor for death as early as at 1 day of hospitalization and continued to be an independent risk factor for the >3.8 years of follow-up. When adjusted for other cardiovascular risk factors, the FFAu levels in the fourth versus the first quartile remained an independent risk factor for death from MI (hazard ratio 5.0, 95% confidence interval 1.9 to 13.0), all cardiac death (hazard ratio 2.4, 95% confidence interval 1.3 to 4.4), and all-cause death (hazard ratio 1.9, 95% confidence interval 1.2 to 3.1). Women were twice as likely to be in the upper 2 FFAu quartiles and had approximately twice the rate of death as men. In conclusion, FFAu elevation is 1 of the earliest molecular biomarkers of mortality in patients with ST-segment elevation MI and was independent of other risk factors known to affect the outcomes after ST-segment elevation MI. PMID:24176067

  2. Cardioprotective effect of resveratrol analogue isorhapontigenin versus omega-3 fatty acids in isoproterenol-induced myocardial infarction in rats.

    PubMed

    Abbas, Amr M

    2016-09-01

    Myocardial infarction (MI) is a common cause of mortality worldwide. Isorhapontigenin is a derivative of stilbene with chemical structure similar to resveratrol. The omega-3 fatty acids (FA) have beneficial effects on neurodegenerative, inflammatory, and cardiovascular diseases. The aim of this study was to investigate the effects of pretreatment with isorhapontigenin and omega-3 FA on rat model of isoproterenol-induced MI. Fifty-six rats were divided into seven groups: normal, normal + isorhapontigenin, normal + omega-3 FA, MI, MI + isorhapontigenin, MI + omega-3 FA, and MI + isorhapontigenin + omega-3 FA. Serum levels of cardiac marker enzymes [lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB)], cardiac troponin I (cTnI), inflammatory markers [tumor necrosis factor-alpha (TNF-α) and interleukin-6], and lipid profile [triglycerides, total cholesterol (T.Ch), high and low density lipoproteins (HDL, LDL), and phospholipids] as well as cardiac levels of malondialdehyde and anti-oxidants [reduced glutathione (GSH), superoxide dismutase (SOD), and catalase)] were measured in all rats. ECG and histopathological examination were performed. Isoproterenol caused a significant elevation of ST segment, decreased R wave amplitude, HDL, and anti-oxidants, and increased LDH, CK-MB, cTnI, TNF-α, interleukin-6, malondialdehyde, triglycerides, T.Ch, LDL, and phospholipids. Omega-3 FA or isorhapontigenin significantly decreased the ST segment elevation, LDH, CK-MB, cTnI, TNF-α, interleukin-6, malondialdehyde, and phospholipids and increased R wave amplitude and anti-oxidants. The effects of combined omega-3 FA and isorhapontigenin were more significant than either of them alone. Therefore, we conclude that omega-3 FA and isorhapontigenin have a cardioprotective effect on rats with isoproterenol-induced MI through their anti-oxidant and anti-inflammatory actions. PMID:27193109

  3. Serum Uric Acid Levels and Renal Impairment among ST-Segment Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Intervention

    PubMed Central

    Shacham, Yacov; Gal-Oz, Amir; Flint, Nir; Keren, Gad; Arbel, Yaron

    2016-01-01

    Background Elevated serum uric acid (UA) levels are associated with adverse outcomes in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). However, the relation between UA and acute kidney injury (AKI) in this population is unclear. We evaluated the effect of elevated UA levels on the risk to develop AKI among consecutive STEMI patients treated with primary PCI. Methods We performed a retrospective analysis of 1,372 consecutive patients admitted with the diagnosis of STEMI between January 2008 and February 2015. Patients were stratified into quartiles according to UA levels as follows: quartile 1, <4.7 mg/dl; quartile 2, 4.8 to <5.6 mg/dl; quartile 3, 5.7 to <6.6 mg/dl, and quartile 4, >6.7 mg/dl. Results STEMI patients with elevated UA levels had a higher frequency of AKI (4 vs. 6% vs. 10 vs. 24%; p < 0.001). In a subgroup analysis of patients with reduced baseline estimated glomerular filtration rate (≤60 ml/min/1.73 m2), an elevated UA level was associated with a significant risk to develop AKI, with 46% of patients developing AKI in the highest UA quartile. In a multivariate logistic regression model, for every 1-mg/dl increase in the UA concentration, the adjusted risk for AKI increased by 46% (OR = 1.46, 95% CI 1.18-1.66; p < 0.001). Conclusions Among STEMI patients undergoing primary PCI, elevated UA levels are an independent predictor of AKI.

  4. Asiatic acid inhibits left ventricular remodeling and improves cardiac function in a rat model of myocardial infarction

    PubMed Central

    HUO, LIANYING; SHI, WENBING; CHONG, LING; WANG, JINLONG; ZHANG, KAI; LI, YUFENG

    2016-01-01

    Left ventricular remodeling results in cardiac dysfunction and accounts for the majority of the morbidity and mortality following myocardial infarction (MI). The aim of the present study was to investigate the effect of asiatic acid (AA) on cardiac function and left ventricular remodeling in a rat model of MI and explore the underlying mechanisms. Rats were subjected to coronary artery ligation to model MI and orally treated with AA. After 4 weeks, cardiac function was assessed by echocardiography. Cardiomyocyte cross-sectional area was recorded, and the expression levels of a number of inflammatory cytokines were detected using ELISA. The degree of interstitial fibrosis was determined by evaluating the mRNA expression levels of collagen II and III. Western blot analysis was performed to detect the expression levels of total and phosphorylated p38 MAPK and ERK1/2, to investigate whether they are involved in the mechanism underlying the effect of AA on the heart. Rats subjected to MI displayed significantly impaired cardiac function compared with those subjected to a sham procedure, while this change was reversed by treatment with AA. Furthermore, AA markedly inhibited cardiac hypertrophy, reduced the mRNA expression levels of inflammatory cytokines and decreased interstitial fibrosis in the infarct border zone of MI model rats compared with those in vehicle-treated MI model rats. Furthermore, the phosphorylation of p38 MAPK and ERK1/2 was blocked by AA in the MI rats but not in the sham rats. In summary, AA treatment preserved cardiac function and inhibited left ventricular remodeling, potentially by blocking the phosphorylation of p38 MAPK and ERK1/2 in the infarct border zone of the ischemic myocardium, indicating that AA may be a novel candidate for development as a therapy for MI. PMID:26889217

  5. JNK/PI3K/Akt signaling pathway is involved in myocardial ischemia/reperfusion injury in diabetic rats: effects of salvianolic acid A intervention.

    PubMed

    Chen, Qiuping; Xu, Tongda; Li, Dongye; Pan, Defeng; Wu, Pei; Luo, Yuanyuan; Ma, Yanfeng; Liu, Yang

    2016-01-01

    Recent studies have demonstrated that diabetes impairs the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway, while insulin resistance syndrome has been associated with alterations of this pathway in diabetic rats after ischemia/reperfusion (I/R), and activation of C-jun N-terminal kinase (JNK) is involved. The present study was designed to investigate whether inhibiting JNK activity would partially restore the PI3K/Akt signaling pathway and protect against myocardial I/R injury in diabetic rats, and to explore the effect of intervention with salvianolic acid A (Sal A). The inhibitor of JNK (SP600125) and Sal A were used in type 2 diabetic (T2D) rats, outcome measures included heart hemodynamic data, myocardial infarct size, the release of lactate dehydrogenase (LDH), SERCA2a activity, cardiomyocyte apotosis, expression levels of Bcl-2, Bax and cleaved caspase-3, and the phosphorylation status of Akt and JNK. The p-Akt levels were increased after myocardial I/R in non-diabetic rats, while there was no change in diabetic rats. Pretreatment with the SP600125 and Sal A decreased the p-JNK levels and increased the p-Akt levels in diabetic rats with I/R, and heart hemodynamic data improved, infarct size and LDH release decreased, SERCA2a activity increased, Bax and cleaved caspase-3 expression levels decreased, and the expression of Bcl-2 and the Bcl-2/Bax ratio increased. Our results suggest that the JNK/PI3K/Akt signaling pathway is involved in myocardial I/R injury in diabetic rats and Sal A exerts an anti-apoptotic effect and improves cardiac function following I/R injury through the JNK/PI3K/Akt signaling pathway in this model. PMID:27398138

  6. JNK/PI3K/Akt signaling pathway is involved in myocardial ischemia/reperfusion injury in diabetic rats: effects of salvianolic acid A intervention

    PubMed Central

    Chen, Qiuping; Xu, Tongda; Li, Dongye; Pan, Defeng; Wu, Pei; Luo, Yuanyuan; Ma, Yanfeng; Liu, Yang

    2016-01-01

    Recent studies have demonstrated that diabetes impairs the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway, while insulin resistance syndrome has been associated with alterations of this pathway in diabetic rats after ischemia/reperfusion (I/R), and activation of C-jun N-terminal kinase (JNK) is involved. The present study was designed to investigate whether inhibiting JNK activity would partially restore the PI3K/Akt signaling pathway and protect against myocardial I/R injury in diabetic rats, and to explore the effect of intervention with salvianolic acid A (Sal A). The inhibitor of JNK (SP600125) and Sal A were used in type 2 diabetic (T2D) rats, outcome measures included heart hemodynamic data, myocardial infarct size, the release of lactate dehydrogenase (LDH), SERCA2a activity, cardiomyocyte apotosis, expression levels of Bcl-2, Bax and cleaved caspase-3, and the phosphorylation status of Akt and JNK. The p-Akt levels were increased after myocardial I/R in non-diabetic rats, while there was no change in diabetic rats. Pretreatment with the SP600125 and Sal A decreased the p-JNK levels and increased the p-Akt levels in diabetic rats with I/R, and heart hemodynamic data improved, infarct size and LDH release decreased, SERCA2a activity increased, Bax and cleaved caspase-3 expression levels decreased, and the expression of Bcl-2 and the Bcl-2/Bax ratio increased. Our results suggest that the JNK/PI3K/Akt signaling pathway is involved in myocardial I/R injury in diabetic rats and Sal A exerts an anti-apoptotic effect and improves cardiac function following I/R injury through the JNK/PI3K/Akt signaling pathway in this model. PMID:27398138

  7. A Study on the Role of Heart Type Fatty Acid Binding Protein in the Diagnosis of Acute Myocardial Infarction

    PubMed Central

    Kabekkodu, Shama Prakash; Mananje, Sudhindra Rao

    2016-01-01

    Introduction Heart type Fatty Acid Binding Protein (H-FABP) has been proposed as an early cardiac biomarker for the diagnosis of acute myocardial Infarction (AMI) using animal models and clinical samples. Aim The study aimed to evaluate the role of H-FABP in early detection of AMI by comparing its sensitivity, specificity and predictive value with Creatinine Kinase-MB (CK-MB) and Cardiac Troponin I (cTnI). Materials and Methods This is a cross-sectional descriptive study of 50 patients admitted with the diagnosis of AMI at a tertiary care hospital in South India. The study group was categorised in to those coming to the hospital within four hours of symptom onset and those coming in between 4 to 12 hours. H-FABP was compared with those of troponin T and myoglobin tests. Results Among patients presenting within four hours of symptom onset, the sensitivity of H-FABP was 60% and was significantly higher than that of cardiac Troponin I (cTnI, 18.8%) and Creatinine Kinase (CK)-MB (12.5%). But specificity was only 23.53% and was less than that of cTnI (66.67%) and CK-MB (100%). In patients presenting during 4 to 12 hours of symptom onset, the sensitivity of H-FABP was 86.96% which was comparable to that of cTnI (90.9%) and CK-MB (77.3%). The specificity was 60% in the 4-12 hours group which was comparable to that of cTnI (50%) and CK-MB (50%). Conclusion The H-FABP is a sensitive biomarker for the diagnosis of AMI in the initial hours after symptom onset when the standard biomarkers may not be elevated, but it is less specific. During 4-12 hours of symptom onset it is as sensitive and specific as standard cardiac biomarkers troponin and CK-MB. Due to these factors H-FABP can be considered as a promising cardiac biomarker which can be used along with troponins and CK-MB at present. PMID:26894106

  8. Influence of stimulation by electroejaculation on myocardial function, acid-base and electrolyte status, and hematobiochemical profiles in male dromedary camels.

    PubMed

    Tharwat, M; Ali, A; Al-Sobayil, F; Derar, R; Al-Hawas, A

    2014-10-01

    This study was carried out to evaluate the effect of electroejaculation (EEJ) on myocardial function, acid-base balance, and hematobiochemical profiles in male dromedary camels. Twenty sexually mature, apparently healthy male camels were assigned to EEJ. Parallel, eight naturally mated male camels were enrolled as a control group. Three blood samples were collected from each camel: just before (T0), directly after (T1), and 24 hours after (T2) EEJ or natural mating. The serum concentrations of the cardiac biomarker troponin I (cTnI), blood gas parameters, and hematobiochemical profiles were determined. Nineteen camels were ejaculated by the end of the second circuit and one by the end of the first circuit. In both groups, the mean heart and respiratory rates had increased significantly immediately after the procedure, but returned to normal values 24 hours after the procedure. The mean serum concentration of cTnI had increased significantly in all camels after EEJ, but not in controls. However, at 24 hours post-EEJ, the serum concentration of cTnI did not differ significantly compared with baseline values. The blood pH and base excess had decreased, and the PCO2 and lactic acid had increased after EEJ. The EEJ provoked decreases in hematocrit and mean corpuscular volume. In the control group, the base excess, HCO3(-), TCO2, anion gap, and lactic acid increased slightly after mating but did not reach a significant level compared with premating values. It is concluded that EEJ in camels results in a reversible myocardial injury, changes in the acid-base status, and increase the lactic acid concentration. PMID:25139755

  9. 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.

  10. Predictors of preinterventional patency of infarct-related artery in patients with ST-segment elevation myocardial infarction: Importance of neutrophil to lymphocyte ratio and uric acid level

    PubMed Central

    Şahin, Durmuş Yıldıray; Gür, Mustafa; Elbasan, Zafer; Yıldız, Ali; Kaya, Zekeriya; İçen, Yahya Kemal; Kıvrak, Ali; Türkoğlu, Caner; Yılmaz, Remzi; Çaylı, Murat

    2013-01-01

    BACKGROUND: Patients with ST-segment elevation myocardial infarction (STEMI) and a patent infarct-related artery (IRA) experience lower mortality and better clinical outcome, but little is known about the predictors of IRA patency before primary percutaneous coronary intervention (PCI) in the setting of STEMI. OBJECTIVE: To assess possible predictors of patency of IRA before primary PCI in patients with STEMI. METHODS: A total of 880 patients with STEMI undergoing primary PCI were prospectively included (646 male, 234 female; mean [± SD] age 58.5±12.4 years). Blood samples were obtained on admission to investigate biochemical markers. Preinterventional thrombolysis in myocardial infarction (TIMI) flow was assessed in all patients. The patients were divided into two groups according to the pre-PCI TIMI flow as impaired flow group (TIMI flow 0, 1 and 2) and normal flow group (TIMI flow 3). Transthoracic echocardiography was performed in all patients. RESULTS: Eighty-three (9.43%) patients had pre-PCI TIMI 3 flow in IRA. Uric acid levels and neutrophil to lymphocyte (N to L) ratio in the normal flow group were lower than in the impaired flow group (P<0.001 for both). However, ejection fraction (EF) was higher in the normal flow group than in the impaired flow group. Multivariate logistic regression analysis showed that IRA patency was independently associated with serum uric acid level (β 0.673 [95% CI 0.548 to 0.826]; P<0.001), N to L ratio (β 0.783 [95% CI 0.683 to 0.897]; P<0.001) and EF (β 1.033 [95% CI 1.006 to 1.061]; P=0.016). CONCLUSION: Serum uric acid level, N to L ratio and EF are independent predictors of the pre-PCI patency of IRA in patients with STEMI undergoing primary PCI. PMID:23940451

  11. A preliminary feasibility study of simultaneous dual-isotope imaging with a solid-state dedicated cardiac camera for evaluating myocardial perfusion and fatty acid metabolism.

    PubMed

    Ko, Toshiyuki; Utanohara, Yuko; Suzuki, Yasuhiro; Kurihara, Makiko; Iguchi, Nobuo; Umemura, Jun; Sumiyoshi, Tetsuya; Tomoike, Hitonobu

    2016-01-01

    Simultaneous dual-isotope SPECT imaging with 201Tl and (123)I-β-methyl-p-iodophenylpentadecanoic acid (BMIPP) is used to study the perfusion-metabolism mismatch. It predicts post-ischemic functional recovery by detecting stunned myocardium. On the other hand, (99m)Tc-MIBI is another radioisotope widely used in myocardial perfusion imaging because of its better image quality and lower radiation exposure than 201Tl. However, since the photopeak energies of (99m)Tc and (123)I are very similar, crosstalk hampers the simultaneous use of these two radioisotopes. To overcome this problem, we conducted simultaneous dual-isotope imaging study using the D-SPECT scanner (Spectrum-Dynamics, Israel) which has a novel detector design and excellent energy resolution. We first conducted a basic experiment using cardiac phantom to simulate the condition of normal perfusion and impaired fatty acid metabolism. Subsequently, we prospectively recruited 30 consecutive patients who underwent successful percutaneous coronary intervention for acute myocardial infarction, and performed (99m)Tc-MIBI/(123)I-BMIPP dual-isotope imaging within 5 days after reperfusion. Images were interpreted by two experienced cardiovascular radiologists to identify the infarcted and stunned areas based on the coronary artery territories. As a result, cardiac phantom experiment revealed no significant crosstalk between (99m)Tc and (123)I. In the subsequent clinical study, (99m)Tc-MIBI/(123)I-BMIPP dual-isotope imaging in all participant yielded excellent image quality and detected infarcted and stunned areas correctly when compared with coronary angiographic findings. Furthermore, we were able to reduce radiation exposure to significantly approximately one-eighth. In conclusion, we successfully demonstrated the practical application of simultaneous assessment of myocardial perfusion and fatty acid metabolism by (99m)Tc-MIBI and (123)I-BMIPP using a D-SPECT cardiac scanner. Compared with conventional (201)Tl

  12. Effects of aluminum oxide (Al2O3) nanoparticles on ECG, myocardial inflammatory cytokines, redox state, and connexin 43 and lipid profile in rats: possible cardioprotective effect of gallic acid.

    PubMed

    El-Hussainy, El-Hussainy M A; Hussein, Abdelaziz M; Abdel-Aziz, Azza; El-Mehasseb, Ibrahim

    2016-08-01

    The objectives of present study were to examine the effects of aluminum oxide (Al2O3) nanoparticles on myocardial functions, electrical activities, morphology, inflammation, redox state, and myocardial expression of connexin 43 (Cx43) and the effect of gallic acid (GA) on these effects in a rat animal model. Forty male albino rats were divided into 4 equal groups: the control (normal) group; the Al2O3 group, rats received Al2O3 (30 mg·kg(-1), i.p.) daily for 14 days; the nano-alumina group, rats received nano-alumina (30 mg·kg(-1), i.p.) daily for 14 days; and the nano-alumina + GA group, rats received GA (100 mg·kg(-1) orally once daily) for 14 days before nano-alumina administration. The results showed disturbed ECG variables and significant increases in serum levels of LDH, creatine phosphokinase (CPK), CK-MB, triglycerides (TGs), cholesterol and LDL, nitric oxide (NO), and TNF-α and myocardial concentrations of NO, TNF-α, and malondialdehyde (MDA), with significant decreases in serum HDL and myocardial GSH, SOD, catalase (CAT), and Cx43 expression in the nano-alumina group. Pretreatment with GA improved significantly all parameters except serum and myocardial NO. We concluded that chronic administration of Al2O3 NPs caused myocardial dysfunctions, and pretreatment with GA ameliorates myocardial injury induced by nano-alumina, probably through its hypolipidaemic, anti-inflammatory, and antioxidant effects and upregulation of Cx43 in heart. PMID:27191243

  13. Plant Natural Products Calycosin and Gallic Acid Synergistically Attenuate Neutrophil Infiltration and Subsequent Injury in Isoproterenol-Induced Myocardial Infarction: A Possible Role for Leukotriene B4 12-Hydroxydehydrogenase?

    PubMed Central

    Cheng, Yuanyuan; Zhao, Jia; Tse, Hung Fat; Le, X. Chris; Rong, Jianhui

    2015-01-01

    Leukotriene B4 12-hydroxydehydrogenase (LTB4DH) catalyzes the oxidation of proinflammatory LTB4 into less bioactive 12-oxo-LTB4. We recently discovered that LTB4DH was induced by two different natural products in combination. We previously isolated gallic acid from Radix Paeoniae through a bioactivity-guided fractionation procedure. The purpose of this study is to test the hypothesis that LTB4DH inducers may suppress neutrophil-mediated inflammation in myocardial infarction. We first isolated the active compound(s) from another plant, Radix Astragali, by the similar strategy. By evaluating LTB4DH induction, we identified calycosin and formononetin from Radix Astragali by HPLC-ESI-MS technique. We confirmed that gallic acid and commercial calycosin or formononetin could synergistically induce LTB4DH expression in HepG2 cells and human neutrophils. Moreover, calycosin and gallic acid attenuated the effects of LTB4 on the survival and chemotaxis of neutrophil cell culture. We further demonstrated that calycosin and gallic acid synergistically suppressed neutrophil infiltration and protected cardiac integrity in the isoproterenol-induced mice model of myocardial infarction. Calycosin and gallic acid dramatically suppressed isoproterenol-induced increase in myeloperoxidase (MPO) activity and malondialdehyde (MDA) level. Collectively, our results suggest that LTB4DH inducers (i.e., calycosin and gallic acid) may be a novel combined therapy for the treatment of neutrophil-mediated myocardial injury. PMID:26265982

  14. 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

  15. Myocardial ischaemia in infancy and childhood

    PubMed Central

    Berry, C. L.

    1967-01-01

    Examination of 135 consecutive necropsy specimens has shown that ischaemic myocardial injury is not uncommon in infancy and childhood. The extent of the myocardial change has been assessed by a technique of staining with acid fuchsin, first described by Selye (1958). The significance of the findings is discussed. Images PMID:4163355

  16. 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. PMID:7680178

  17. Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on isoproterenol-induced myocardial injury in rats

    PubMed Central

    CHEN, MINCHUN; WANG, MINGMING; YANG, QIONG; WANG, MIN; WANG, ZHIPENG; ZHU, YANRONG; ZHANG, YIKAI; WANG, CHAO; JIA, YANYAN; LI, YUWEN; WEN, AIDONG

    2016-01-01

    Oxidative stress plays an important role in the initiation and development of myocardial injury (MI). The peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is considered to be a potential target for cardioprotection in MI. Acetyl-11-keto-β-boswellic acid (AKBA) is the major organic acid component extracted from Boswellia serrata Roxb. ex Colebr. Hydroxysafflor yellow A (HSYA) is the principal active constituent of Carthamus tinctorius L. In the present study, we aimed to investigate the cardioprotective effects of HSYA and AKBA in combination in vivo and in vitro, as well as the underlying mechanisms responsible for these effects. For this purpose, MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol. To model ischemic-like conditions in vitro, H9C2 cells were subjected to oxygen-glucose deprivation (OGD). The levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were examined as well as apoptotic cell death. Mitochondrial reactive oxygen species (ROS) production and mitochondrial membrane potential (ΔΨm or MMP) were measured using MitoSOX Red and 5,5′,6,6′-tetraethylbenzimidazolylcarbocya-nine iodide (JC-1) dye. The expression of PGC-1α and Nrf2 was quantified by western blot analysis and immunohistochemistry. HSYA and AKBA prevented myocardial pathological changes, significantly reduced the blood levels of CK-MB and LDH, and decreased apoptotic cell death. They significantly increased the expression of PGC-1α and Nrf2, and the activity of the antioxidant enzyme SOD and also decreased the levels of MDA and ROS. Moreover, the reduction in MMP was partly prevented by HSYA and AKBA. Taken together, these findings elucidate the underlying mechanisms through which HSYA and AKBA protect against MI. Additionally, HSYA and AKBA appear to act synergistically in order to

  18. Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on isoproterenol-induced myocardial injury in rats.

    PubMed

    Chen, Minchun; Wang, Mingming; Yang, Qiong; Wang, Min; Wang, Zhipeng; Zhu, Yanrong; Zhang, Yikai; Wang, Chao; Jia, Yanyan; Li, Yuwen; Wen, Aidong

    2016-06-01

    Oxidative stress plays an important role in the initiation and development of myocardial injury (MI). The peroxisome proliferator-activated receptor gamma coactivator-1α (PGC‑1α)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is considered to be a potential target for cardioprotection in MI. Acetyl-11-keto-β-boswellic acid (AKBA) is the major organic acid component extracted from Boswellia serrata Roxb. ex Colebr. Hydroxysafflor yellow A (HSYA) is the principal active constituent of Carthamus tinctorius L. In the present study, we aimed to investigate the cardioprotective effects of HSYA and AKBA in combination in vivo and in vitro, as well as the underlying mechanisms responsible for these effects. For this purpose, MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol. To model ischemic-like conditions in vitro, H9C2 cells were subjected to oxygen-glucose deprivation (OGD). The levels of creatine kinase-MB (CK‑MB), lactate dehydrogenase (LDH), malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were examined as well as apoptotic cell death. Mitochondrial reactive oxygen species (ROS) production and mitochondrial membrane potential (ΔΨm or MMP) were measured using MitoSOX Red and 5,5',6,6'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) dye. The expression of PGC-1α and Nrf2 was quantified by western blot analysis and immunohistochemistry. HSYA and AKBA prevented myocardial pathological changes, significantly reduced the blood levels of CK-MB and LDH, and decreased apoptotic cell death. They significantly increased the expression of PGC-1α and Nrf2, and the activity of the antioxidant enzyme SOD and also decreased the levels of MDA and ROS. Moreover, the reduction in MMP was partly prevented by HSYA and AKBA. Taken together, these findings elucidate the underlying mechanisms through which HSYA and AKBA protect against MI. Additionally, HSYA and AKBA appear to act

  19. Epicardial application of cardiac progenitor cells in a 3D-printed gelatin/hyaluronic acid patch preserves cardiac function after myocardial infarction.

    PubMed

    Gaetani, Roberto; Feyen, Dries A M; Verhage, Vera; Slaats, Rolf; Messina, Elisa; Christman, Karen L; Giacomello, Alessandro; Doevendans, Pieter A F M; Sluijter, Joost P G

    2015-08-01

    Cardiac cell therapy suffers from limitations related to poor engraftment and significant cell death after transplantation. In this regard, ex vivo tissue engineering is a tool that has been demonstrated to increase cell retention and survival. The aim of our study was to evaluate the therapeutic potential of a 3D-printed patch composed of human cardiac-derived progenitor cells (hCMPCs) in a hyaluronic acid/gelatin (HA/gel) based matrix. hCMPCs were printed in the HA/gel matrix (30 × 10(6) cells/ml) to form a biocomplex made of six perpendicularly printed layers with a surface of 2 × 2 cm and thickness of 400 μm, in which they retained their viability, proliferation and differentiation capability. The printed biocomplex was transplanted in a mouse model of myocardial infarction (MI). The application of the patch led to a significant reduction in adverse remodeling and preservation of cardiac performance as was shown by both MRI and histology. Furthermore, the matrix supported the long-term in vivo survival and engraftment of hCMPCs, which exhibited a temporal increase in cardiac and vascular differentiation markers over the course of the 4 week follow-up period. Overall, we developed an effective and translational approach to enhance hCMPC delivery and action in the heart. PMID:26043062

  20. Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction

    SciTech Connect

    Kuepper, A.J.V.; Verheugt, F.W.; Peels, C.H.; Galema, T.W.; den Hollander, W.; Roos, J.P.

    1989-04-15

    In this prospective, randomized, placebo-controlled trial the effect of 100 mg acetylsalicylic acid (ASA) once daily on the incidence, hematologic activity and embolic potential of left ventricular (LV) thrombosis was studied in 100 consecutive patients with a first anterior wall acute myocardial infarction (AMI). Patients were randomized to ASA or placebo less than 12 hours after onset of symptoms. Heparin, 5,000 IU subcutaneously twice daily, was given to all patients during immobilization. Echocardiography was performed less than 24 hours, 48 to 72 hours and 1, 2, and 12 weeks after AMI. LV thrombosis was detected by echocardiography in 30 (33%) of the 92 evaluable patients (15 patients given ASA and 15 given placebo). Indium-111 platelet scintigraphy was done in 17 of the 22 patients with an LV thrombus at the second week echocardiogram. Among 7 ASA-treated patients, 4 had positive images; among 10 placebo patients, 5 had positive images. LV thrombus resolution was noted in 3 of 9 patients with a positive scan and in 5 of 8 patients with a negative platelet scan. In 7 of 10 ASA-treated patients and 5 of 12 placebo-treated patients thrombus resolution was observed (difference not significant). Systemic embolism occurred in 2 patients, both given ASA, during the first week after AMI. Thus, low dose ASA has no effect on the incidence, hematologic activity and embolic potential of LV thrombosis in anterior wall AMI.

  1. Circadian rhythms in fatty acid-induced depression of myocardial contractile function: Potential mediation by the circadian clock within the cardiomyocyte

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Circadian rhythms in susceptibility to cardiovascular (CV) pathologic events (e.g., arrhythmias, myocardial infarction) are well established. These phenomena have been explained largely by diurnal variations in neurohumoral influences, such as sympathetic activity. Circadian clocks are intracellular...

  2. Heart-Type Fatty Acid-Binding Protein, in Early Detection of Acute Myocardial Infarction: Comparison with CK-MB, Troponin I and Myoglobin.

    PubMed

    Pyati, Anand K; Devaranavadagi, Basavaraj B; Sajjannar, Sanjeev L; Nikam, Shashikant V; Shannawaz, Mohd; Patil, Satish

    2016-10-01

    The study aimed to investigate whether heart-type fatty acid binding protein (H-FABP) measurement provides additional diagnostic value to that of conventional cardiac markers in acute myocardial infarction (AMI) within first 6 h after the onset of symptoms. The study included 120 subjects: 60 AMI cases and 60 age and sex matched controls. The cases and controls were further divided into 2 subgroups depending on the time since onset of chest pain as (1) subjects within 3 h and (2) between 3 and 6 h of onset of chest pain. In all the cases and controls, serum H-FABP concentration was measured by Immunoturbidimetric method, serum Troponin I and myoglobin concentrations by Chemiluminescence immunoassay and serum CK-MB concentration by Immuno-inhibition method. The sensitivity, specificity, positive and negative predictive values of H-FABP were significantly greater than CK-MB and myoglobin but were lesser than Troponin I in patients with suspected AMI in both within 3 h and 3-6 h groups. Receiver operating characteristic curves demonstrated greatest diagnostic ability for Troponin I (AUC = 0.99, p < 0.001) followed by H-FABP (AUC = 0.906, p < 0.001) within 3 h and 3-6 h after the onset of chest pain. In conclusion, the diagnostic value of H-FABP is greater than CK-MB and myoglobin but slightly lesser than troponin I for the early diagnosis of AMI within first 6 h of chest pain. H-FABP can be used as an additional diagnostic tool for the early diagnosis of AMI along with troponin I. PMID:27605741

  3. N-3 Polyunsaturated fatty acid therapy improves endothelial function and affects adiponectin and resistin balance in the first month after myocardial infarction

    PubMed Central

    Mizia-Stec, Katarzyna; Haberka, Maciej; Mizia, Magdalena; Chmiel, Artur; Gieszczyk, Klaudia; Lasota, Bartosz; Janowska, Joanna; Zahorska-Markiewicz, Barbara; Gąsior, Zbigniew

    2011-01-01

    Introduction N-3 Polyunsaturated fatty acids (n-3 PUFA) exert clinical beneficial effects in patients after acute myocardial infarction (AMI). However, their exact mechanisms of action are not well recognized yet. Our aim was to evaluate effects of early introduced n-3 PUFA supplementation on endothelial function and serum adipokine concentrations in patients with AMI. Material and methods Thirty-eight patients with AMI and successful coronary stent implantation were randomized to the study group (PUFA group: n = 19; standard therapy + PUFA 1 g daily) and the control group (control group: n = 19; standard therapy). The study group patients were given n-3 PUFA (Omacor 1 g daily) starting from the 3rd day of AMI. Ultrasound vascular indexes (flow-mediated dilatation [FMD], nitroglycerine-mediated dilation [NMD]) and serum concentrations of adiponectin and resistin (ELISA) were evaluated before and after 30 days of pharmacotherapy. Results Comparison of the mean delta values (baseline/after 30 days of therapy) between groups revealed significant differences for delta FMD (PUFA 7.6 ±12.4% vs. control –1.7 ±10.5%, p = 0.019) and delta resistin concentrations (PUFA 1.0 ±3.8pg/ml vs. control –1.6 ±2.9pg/ml, p = 0.028). Multiple linear regression analysis for all subjects revealed the n-3 PUFA supplementation (r = 10.933, p = 0.004) and waist circumference (r = –0.467, p = 0.01) as independent factors associated with delta FMD values (R-adjusted 0.29; p = 0.002). Conclusions Early and short-term n-3 PUFA supplementation in AMI with successful primary PCI and optimal pharmacotherapy improves endothelial function. However, increased resistin serum levels observed after 1-month n-3 PUFA supplementation merits further investigations. PMID:22291823

  4. Heart-Type Fatty Acid Binding Protein: A Better Cardiac Biomarker than CK-MB and Myoglobin in the Early Diagnosis of Acute Myocardial Infarction

    PubMed Central

    Devaranavadagi, Basavaraj B; Sajjannar, Sanjeev L; Nikam, Shashikant V; Shannawaz, Mohd; Sudharani

    2015-01-01

    Background Early diagnosis and therapeutic intervention can improve the outcome of acute myocardial infarction (AMI). However, there are no satisfactory cardiac biomarkers for the diagnosis of AMI within 6 hours of onset of symptoms. Among novel biochemical markers of AMI, heart-type fatty acid binding protein (H-FABP) is of particular interest. Aim To compare the diagnostic value of H-FABP with that of CK-MB and myoglobin in suspected AMI patients within first 6 hours after the onset of symptoms. Settings and Design The study includes 40 AMI cases and 40 non-cardiac chest pain otherwise healthy controls. The cases and controls were further divided into 2 groups depending on the time since chest pain as those subjects within 3 hours and those between 3-6 hours of onset of chest pain. Materials and Methods In all the cases and controls, serum H-FABP, CK-MB and myoglobin concentrations were measured by Immunoturbidimetric method, immuno-inhibition method and Chemiluminescence immunoassay respectively. Statistical Analysis Data is presented as mean ± SD values. Differences between means of two groups were assessed by Student t-test. Sensitivity, Specificity, Positive predictive value, Negative predictive values were calculated and ROC curve analysis was done to assess the diagnostic validity of each study parameter. Results The sensitivity, specificity, PPV, NPV of H-FABP were greater than CK-MB and myoglobin and ROC curve analysis demonstrated highest area under curve for H-FABP followed by myoglobin and CK-MB in patients with suspected AMI both within 3 hours and 3-6 hours after the onset of chest pain. Conclusion The diagnostic efficiency of H-FABP is greater than CK-MB and myoglobin for the early diagnosis of AMI within first 6 hours of chest pain. H-FABP can be used as an additional diagnostic tool for the early diagnosis of AMI. PMID:26557510

  5. Association of serum uric acid with all-cause and cardiovascular disease mortality and incident myocardial infarction in the MONICA Augsburg cohort. World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases.

    PubMed

    Liese, A D; Hense, H W; Löwel, H; Döring, A; Tietze, M; Keil, U

    1999-07-01

    Because previous findings have been inconsistent, we explored the association of serum concentrations of uric acid with all-cause and cardiovascular disease mortality and myocardial infarction prospectively. We used data from 1,044 men who are members of the World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) Augsburg cohort. The men, 45-64 years of age in 1984-1985, were followed through 1992. There were 90 deaths, 44 of which were related to cardiovascular disease; 60 men developed incident nonfatal or fatal myocardial infarction. We estimated hazard rate ratios from Cox proportional hazard models. Uric acid levels > or =373 micromol/liter (fourth quartile) vs < or =319 micromol/liter (first and second quartile) independently predicted all-cause mortality [hazard rate ratio = 2.8; 95% confidence interval (CI) = 1.6-5.0] after adjustment for alcohol, total cholesterol/high-density lipoprotein cholesterol ratio, hypertension, use of diuretic drugs, smoking, body mass index, and education. The adjusted risk of cardiovascular disease mortality was 2.2 (95% CI = 1.0-4.8), and that of myocardial infarction was 1.7 (95% CI = 0.8-3.3). Although residual confounding cannot be excluded, our results are among the few, in men, demonstrating a strong positive association of elevated serum uric acid with all-cause mortality. Future investigations may be able to evaluate whether uric acid contributes independently to the development of cardiovascular disease or is simply a component of the atherogenic metabolic condition known as the insulin resistance syndrome. PMID:10401873

  6. Omega-3-fatty acid adds to the protective effect of flax lignan concentrate in pressure overload-induced myocardial hypertrophy in rats via modulation of oxidative stress and apoptosis.

    PubMed

    Ghule, Arvindkumar E; Kandhare, Amit D; Jadhav, Suresh S; Zanwar, Anand A; Bodhankar, Subhash L

    2015-09-01

    Objective of the present investigation was to study the effect of the flax lignan concentrate (FLC) and Omega-3-fatty acid (O-3-FA) on myocardial apoptosis, left ventricular (LV) contractile dysfunction and electrocardiographic abnormalities in pressure overload-induced cardiac hypertrophy. The rats were divided into five groups such as sham, aortic stenosis (AS), AS+FLC, AS+O-3-FA and AS+FLC+O-3-FA. Cardiac hypertrophy was produced in rats by abdominal aortic constriction. The rats were treated with FLC (400mg/kg, p.o.), O-3-FA (400mg/kg, p.o.) and FLC+O-3-FA orally per day for four weeks. The LV function, myocardial apoptosis, and oxidative stress were quantified. FLC+O-3-FA treatment significantly reduced hemodynamic changes, improved LV contractile dysfunction, reduced cardiomyocyte apoptosis and cellular oxidative stress. Moreover, it significantly up-regulated the VEGF expression and decreased TNF-alpha level in serum. The histological analysis also revealed that FLC+O-3-FA treatment markedly preserved the cardiac structure and inhibited interstitial fibrosis. In conclusion, FLC+O-3-FA treatment improved LV dysfunction, inhibited cardiomyocyte apoptosis, improved myocardial angiogenesis, conserved activities of membrane-bound phosphatase enzymes and suppressed inflammation through reduced oxidative stress in an additive manner than FLC alone and O-3-FA alone treatment in pressure overload-induced cardiac hypertrophy. PMID:26277701

  7. Uncommon and dynamic changes detected by 123I-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography in a stunned myocardium induced by coronary microvascular spasm.

    PubMed

    Zen, K; Ito, K; Hikosaka, T; Adachi, Y; Yoneyama, S; Katoh, S; Azuma, A; Sugihara, H; Nakagawa, M

    2000-08-01

    A 55-yr-old man underwent surgery. Soon after the procedure was finished, the patient complained of chest pain, and the electrocardiogram showed increase in the ST-segment in some leads. Emergency angiography showed normal coronary arteries, but there was asynergy in the left ventricle, and delayed filling of contrast medium was observed in the LCA. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment increase in the electrocardiogram. Soon after nicorandil was injected into the LCA, the patient's symptoms, electrocardiogram, and delayed filling of contrast medium dramatically improved. On the second day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate increase in tracer uptake in the apico-anteroseptal region and a moderate decrease in tracer uptake in the lateral region, in which the first left ventriculography showed akinesis, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. On the sixth day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate decrease in tracer uptake in the apical and lateral regions and a mild decrease in tracer uptake in the anteroseptal region, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. By the 30th day, 123I-BMIPP myocardial SPECT had normalized. We consider that these dynamic changes in 123I-BMIPP myocardial SPECT imaging may reflect metabolic changes in fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool. PMID:11023032

  8. A comparative study of the concentrations of hypoxanthine, xanthine, uric acid and allantoin in the peripheral blood of normals and patients with acute myocardial infarction and other ischaemic diseases.

    PubMed

    Kock, R; Delvoux, B; Sigmund, M; Greiling, H

    1994-11-01

    The aim of this study was the elucidation of the role of the xanthine oxidoreductase in the purine metabolism in ischaemic diseases of man. The serum concentrations of hypoxanthine, xanthine, uric acid and allantoin were determined in peripheral blood samples from patients with angina pectoris, cerebral insult and myocardial infarction with thrombolytic therapy and were compared with the concentrations obtained for healthy males and females. No significant differences were observed for the serum hypoxanthine concentrations, xanthine concentrations, the sum (hypoxanthine+xanthine) and the ratio (xanthine/hypoxanthine) between the healthy males, healthy females, the patients suffering from angina pectoris and the patients suffering from cerebral insult. An increase of the serum xanthine concentration in patients with myocardial infarction indicates a significant metabolic involvement of xanthine oxidoreductase in this disease and therefore a possible role in the development of tissue damage in the postischaemic phase due to oxygen radicals generated by the oxidase activity of this enzyme. The serum concentrations of uric acid and allantoin showed no differences between any of the studied groups. Study of the non-enzymatic oxidation of uric acid to allantoin by oxygen radicals, a relevant radical-scavenging mechanism in other diseases, provided no indication of an increased concentration of oxygen radicals due to the xanthine oxidoreductase reaction or other radical-producing mechanisms. PMID:7888480

  9. 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.

  10. α-Lipoic Acid Reduces Infarct Size and Preserves Cardiac Function in Rat Myocardial Ischemia/Reperfusion Injury through Activation of PI3K/Akt/Nrf2 Pathway

    PubMed Central

    Yi, Wei; Ma, Li; Zhao, Bijun; Cheng, Liang; Zhang, Jinzhou; Cao, Feng; Yi, Dinghua

    2013-01-01

    Background The present study investigates the effects and mechanisms of α-Lipoic acid (LA) on myocardial infarct size, cardiac function and cardiomyocyte apoptosis in rat hearts subjected to in vivo myocardial ischemia/reperfusion (MI/R) injury. Methodology/Principal Findings Male adult rats underwent 30 minutes of ischemia followed by 3, 24, or 72 h of reperfusion. Animals were pretreated with LA or vehicle before coronary artery ligation. The level of MI/R- induced LDH and CK release, infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined and compared. Western blot analysis was performed to elucidate the mechanism of LA pretreatment. The level of inflammatory cytokine TNF-α released to serum and accumulated in injured myocardium as well as neutrophil accumulation in injured myocardium were also examined after MI/R injury. Our results reveal that LA administration significantly reduced LDH and CK release, attenuated myocardial infarct size, decreased cardiomyocytes apoptosis, and partially preserved heart function. Western blot analysis showed that LA pretreatment up-regulated Akt phosphorylation and Nrf2 nuclear translocation while producing no impact on p38MAPK activation or nitric oxide (NO) production. LA pretreatment also increased expression of HO-1, a major target of Nrf2. LA treatment inhibited neutrophil accumulation and release of TNF-α. Moreover, PI3K inhibition abolished the beneficial effects of LA. Conclusions/Significance This study indicates that LA attenuates cardiac dysfunction by reducing cardiomyoctyes necrosis, apoptosis and inflammation after MI/R. LA exerts its action by activating the PI3K/Akt pathway as well as subsequent Nrf2 nuclear translocation and induction of cytoprotective genes such as HO-1. PMID:23505496

  11. Idiopathic calcified myocardial mass

    PubMed Central

    Patterson, David; Gibson, Derek; Gomes, Ricardo; McDonald, Lawson; Olsen, Eckhardt; Parker, John; Ross, Donald

    1974-01-01

    Patterson, D., Gibson, D., Gomes, R., McDonald, L., Olsen, E., Parker, J., and Ross, D. (1974).Thorax,29, 589-594. Idiopathic calcified myocardial mass. Myocardial calcification can be subdivided into three groups—metastatic, dystrophic or an extension inwards from the pericardium. This case in which the calcified myocardial mass was initially delineated by radiography and by echocardiography and subsequently removed does not fit into any subdivision and has been termed idiopathic. Images PMID:4279467

  12. [Myocardial responses to ischemia].

    PubMed

    Borisenko, V G; Gubareva, E A; Kade, A Kh

    2010-01-01

    The paper details the types of a myocardial response to impaired blood flow, such as myocardial stunning, hibernation, ischemic preconditioning, warm-up phenomenon, ischemic postconditioning, remodeling, and infarction. According to the pathogenesis, the authors identify several types of myocardial dysfunction in transient ischemic attack--uptake, delivery; and a mixed one. It is concluded the myocardial response to damage depends on a combination of influencing factors, a number of pathophysiological processes starting in the acute phase of ischemia achieve its peak in the late period. PMID:20564927

  13. Transient myocardial ischaemia after acute myocardial infarction.

    PubMed Central

    Currie, P; Saltissi, S

    1990-01-01

    The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications. PMID:2245108

  14. Heart-type fatty acid binding protein and high-sensitivity troponin T are myocardial damage markers that could predict adverse clinical outcomes in patients with peripheral artery disease

    PubMed Central

    Otaki, Yoichiro; Takahashi, Hiroki; Watanabe, Tetsu; Yamaura, Gensai; Funayama, Akira; Arimoto, Takanori; Shishido, Tetsuro; Miyamoto, Takuya; Kubota, Isao

    2015-01-01

    Background Despite many recent advances in endovascular therapy (EVT), peripheral artery disease (PAD) is an increasing health problem with high mortality. Heart-type fatty acid-binding protein (H-FABP) and high-sensitivity troponin T (hsTnT) are markers of ongoing myocardial damage and have been reported to be useful indicators of future cardiovascular events. However, it remains to be determined whether H-FABP and hsTnT can predict adverse clinical outcomes in patients with PAD. Methods and results We enrolled 208 de novo PAD patients who underwent EVT. Serum H-FABP and hsTnT were measured in all patients before EVT. During the median follow-up period of 694 days, there were 40 major adverse cardiovascular and cerebrovascular events (MACCEs) including all-cause deaths, and re-hospitalizations due to cardiovascular and cerebrovascular diseases and amputations. H-FABP and hsTnT were found to be higher in patients with critical limb ischemia (CLI) compared to those without this condition. Multivariate Cox proportional hazard regression analysis revealed that both H-FABP and hsTnT were independent predictors of MACCEs after adjustment for confounding factors. Kaplan–Meier analysis demonstrated that patients in the highest tertile according to H-FABP levels, as well as those in the highest hsTnT tertile, were at greatest risk for MACCEs. The net reclassification index was significantly improved by the addition of H-FABP as well as the addition of hsTnT to traditional risk factors. Conclusion The myocardial damage markers H-FABP and hsTnT were increased in PAD patients with CLI and could predict MACCEs in PAD patients. PMID:26673681

  15. [Energy metabolism and myocardial function in myocardiodystrophy].

    PubMed

    Temirova, K V; Kurlygina, L A; Zavodskaia, I S; Novikova, N A

    1976-09-01

    A total of 92 patients with chronic tonsilitis and cardiovascular changes were subjected to clinical observations, ECG analysis, potassium and nitroglycerine tests, and studies of the lactic acid level and creatinekinase activity as indces of myocardial metabolism. The examinations were conducted prior to and following tonsillectomy. In a majority of patients a correlation was revealed between the degree of ECG changes and the serum lactic acid level, as well as between the ECG improvement and a reduction of the lactic acid level following tonsillectomy. Three stages of tonsillogenic myocardiodystrophy were distinguished. The obtained data indicate the rationale of the used tests for the evaluation of the myocardial meabolism alterations and of the efficacy of treatment of chronic tonsillitis patients. PMID:1011536

  16. Myocardial infarction and marijuana.

    PubMed

    Charles, R; Holt, S; Kirkham, N

    1979-04-01

    Myocardial infarction in the virtual absence of risk factors occurred in a 25-year old man shortly after smoking a cigarette containing marijuana. Subsequent coronary arteriography was normal. PMID:466984

  17. Experimental myocardial infarction

    PubMed Central

    Kumar, Raj; Joison, Julio; Gilmour, David P.; Molokhia, Farouk A.; Pegg, C. A. S.; Hood, William B.

    1971-01-01

    The hemodynamic effects of tachycardia induced by atrial pacing were investigated in left ventricular failure of acute and healing experimental myocardial infarction in 20 intact, conscious dogs. Myocardial infarction was produced by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 10-15 days prior to the study. 1 hr after acute myocardial infarction, atrial pacing at a rate of 180 beats/min decreased left ventricular end-diastolic pressure from 19 to 8 mm Hg and left atrial pressure from 17 to 12 mm Hg, without change in cardiac output. In the healing phase of myocardial infarction 1 wk later, atrial pacing decreased left ventricular end-diastolic pressure from 17 to 9 mm Hg and increased the cardiac output by 37%. This was accompanied by evidence of peripheral vasodilation. In two dogs with healing anterior wall myocardial infarction, left ventricular failure was enhanced by partial occlusion of the circumflex coronary artery. Both the dogs developed pulmonary edema. Pacing improved left ventricular performance and relieved pulmonary edema in both animals. In six animals propranolol was given after acute infarction, and left ventricular function deteriorated further. However the pacing-induced augmentation of cardiac function was unaltered and, hence, is not mediated by sympathetics. The results show that the spontaneous heart rate in left ventricular failure of experimental canine myocardial infarction may be less than optimal and that maximal cardiac function may be achieved at higher heart rates. Images PMID:4395910

  18. Preparation of 3R- and 3S-methyl isomers of the myocardial imaging agent 15-(p-IODOPHENYL)-3-methylpentadecanoic acid ({open_quotes}BMIPP{close_quotes})

    SciTech Connect

    Lin, Q. |; Luo, J.; Mokler, F.

    1996-10-01

    Iodine-123-labeled racemic BMIPP is used for clinical evaluation of heart disease. To evaluate the expected importance of configuration of the asymmetric C-3 center, we have synthesized the 3R-isomer. 6-Phenylhexanoyl chloride was condensed with thiophene (Friedel-Crafts), followed by Wolff-Kishner reduction and subsequent acylation with the ethyl-3-R-methylglutaroyl chloride, Wolff-Kishner reduction and Raney-Ni ring opening. Para Thallation (TTFA)/KI provided 3R-BMIPP, m.p. 51-52{degrees}C, [{alpha}{sub D}] = +0.74{degrees}. The diastereomeric amide mixture was prepared by reaction of racemic 3-R,S-BMIPP with (S)-(-)-{alpha}-methylbenzylamine. Chromatographic separation and HCl hydrolysis (at 175{degrees}C) provided the 3R- and 3S- (m.p. 45-46{degrees}C, [{alpha}{sub D}] = -1.67{degrees}) BMIPP isomers. The more polar amide (m.p. 93-94{degrees}C) was identical with the amide from the synthetic 3R-BMIPP (m.p., HPLC, NMR). Availability of the 3R- and 3S-BMIPP isomers will permit preparation of the radioiodinated isomers and animal evaluation to determine the effects of the methyl group configuration on myocardial uptake and metabolism.

  19. Myocardial Noncompaction Presenting With Myocardial Bridge

    PubMed Central

    Shen, Yuechun; Li, Xinchun; Lu, Dongfeng; Xiao, Aiyi; Li, Jun

    2015-01-01

    Abstract Myocardial noncompaction, namly isolated noncompaction of the left ventricular myocardium (NVM), is a rare congenital disease. It can be either seen in the absence of other cardiac anomalies, or associated with other congenital cardiac defects, mostly stenotic lesions of the left ventricular outflow tract. A myocardial bridge (MB) is thought being associated with coronary heart disease, such as coronary spasm, arrhythmia, and so on. The significance of MB in association with other congenital cardiac conditions is unknown. We report a novel case who was presented NVM and MB. A 34-year-old man complained of chest prickling-like pain and dizzy for 1 year. His blood pressure was 110/70 mm Hg. Echocardiograph revealed increased trabeculations below the level of papillary muscle of left ventricle (LV); deep intertrabecular recesses in the endocardial wall of LV particularly in apex free wall; and LV ejection fraction of 57%. A coronary computerized tomography scan showed that part, 38.9 cm, of left descending artery tunnel was surrounding by cardiac muscles rather than resting on top of the myocardium. The therapeutics interventions included lifestyle cares, agents of anti-ischemia and improvement myocardial cell metabolism. The patient was followed up for 2.6 years, and his general condition was stable. This case indicates that NVM can be developed with MB, and the complete diagnosis of NVM and MB should be made by different image studies. PMID:26356695

  20. Attenuation of post-myocardial infarction depression in rats by n-3 fatty acids or probiotics starting after the onset of reperfusion.

    PubMed

    Gilbert, Kim; Arseneault-Bréard, Jessica; Flores Monaco, Fabio; Beaudoin, Alexanne; Bah, Thierno Madjou; Tompkins, Thomas A; Godbout, Roger; Rousseau, Guy

    2013-01-14

    Proinflammatory cytokines play a central role in depression-like behaviour and apoptosis in the limbic system after myocardial infarction (MI). A PUFA n-3 diet or the combination of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 probiotics, when given before the ischaemic period, reduce circulating proinflammatory cytokines as well as apoptosis in the limbic system. The present study was designed to determine if the same nutritional interventions maintain their beneficial effects when started after the onset of the reperfusion period and attenuate depression-like behaviour observed after MI. MI was induced by the occlusion of the left anterior descending coronary artery for 40 min in rats. After the onset of reperfusion, animals were fed with a high- or low-PUFA n-3 diet, combined or not with one billion live bacteria of L. helveticus and B. longum. At 3 d post-MI, caspase-3 enzymatic activities and terminal 2'-deoxyuridine, 5'-triphosphate (dUTP) nick-end labelling (TUNEL)-positive cells were decreased in the CA1, dentate gyrus (DG) and amygdala with the high-PUFA n-3 diet, as compared to the three other diets. Probiotics attenuated caspase-3 activity and TUNEL-positive cells in the DG and the medial amygdala. At 2 weeks post-MI, depression-like behaviour was observed in the low-PUFA n-3 diet without probiotics-group, and this behaviour was attenuated with the high-PUFA n-3 diet or/and probiotics. These results indicate that a high-PUFA n-3 diet or the administration of probiotics, starting after the onset of reperfusion, are beneficial to attenuate apoptosis in the limbic system and post-MI depression in the rat. PMID:23068715

  1. Comparison of Serum Uric Acid, Bilirubin, and C-Reactive Protein as Prognostic Biomarkers of In-Hospital MACE Between Women and Men With ST-Segment Elevation Myocardial Infarction.

    PubMed

    Baumann, Stefan; Huseynov, Aydin; Koepp, Johanna; Jabbour, Claude; Behnes, Michael; Becher, Tobias; Renker, Matthias; Lang, Siegfried; Borggrefe, Martin; Lehmann, Ralf; Akin, Ibrahim

    2016-03-01

    Levels of C-reactive protein (CRP), uric acid (UA), and total bilirubin (TB) are associated with coronary artery disease and major adverse cardiac events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI). We retrospectively included 1167 patients with STEMI who underwent percutaneous coronary intervention and routine blood sampling. The study cohort consisted of 803 patients (73.1% male, mean age 62.5 ± 13.4 years). In men, the levels of CRP, TB, and UA were significantly higher in the MACE than in the non-MACE group (P < .05). The receiver-operating characteristic (ROC) analysis shows that CRP (area under the curve [AUC]: 0.59; 95% confidence interval [CI]: 0.53-0.66; P = .014) and TB (AUC: 0.58; 95% CI: 0.51-0.65; P = .019) are significantly associated with MACE but not UA (AUC: 0.61; 95% CI: 0.42-0.76; P = .083). Logistic regression revealed CRP (odds ratio [OR] 1.01; 95% CI: 1.00-1.01; P = .006) and TB (OR 2.03; 95% CI: 1.12-3.40; P = .007) as an independent predictor for MACE. In women, none of the biomarkers was associated with MACE by ROC analysis or logistic regression analysis. This study demonstrated that high CRP and TB serum levels have a prognostic association with in-hospital MACE in male patients with STEMI. PMID:26032849

  2. Differences in the relative myocardial/organ ratios of iodine-123-BMIPP and the dimethyl-substituted iodine 123-DMIPP fatty acid analogue in humans

    SciTech Connect

    Sloof, G.W.; Comans, E.F.I.; Visser, F.C.

    1997-05-01

    Radioiodinated fatty acid analogues, modified by methyl-substitution are used for SPECT imaging of the heart. The effect of mono- and dimethyl-substitution on biodistribution was investigated in humans to evaluate their relative merits for SPECT image quality. Planar total body scans were performed in fasting patients with coronary artery disease, but without heart failure, one hour after administration of 111 MBq 15-(p-[I-123]-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP, n=7) or III MBq 15-(p-[I-123]-iodophenyl)-3,3-dimethylpentaderanoic acid (DMIPP, n=4). Because these branched fatty acids are used for cardiac imaging, we focussed on heart/organ ratios, by comparing small roi-counts in heart, liver, lung, muscle (thigh) and bladder. Statistical analysis: t-test for unpaired data. Both tracers showed good visualization of the heart. While DMIPP showed a relatively high liver uptake, increased background, ie lung, activity was found for BMIPP. In contrast to DMIPP, BMIPP also showed elevated activity in the bladder.

  3. Evaluation of ischemia and myocardial viability in patients with coronary artery disease (CAD) with iodine-123-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP)

    SciTech Connect

    Kropp, J.; Joergens, M.; Glaenzer, K.P.; Luederitz, B.; Biersack, H.J.; Knapp, F.F. Jr.

    1993-10-01

    Twenty patients with coronary artery disease (CAD) controlled by coronary arteriography (CA) and biplane left ventricular cineventriculography (LVCV) were investigated with the 15- (p[I-123]iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) fatty acid analogue. During maximal symptom limited exercise 5 mCi (200 MBq) of BMIPP were injected followed by two SPECT studies within three hours. After another 30 min, with the patient at rest a third SPECT was performed after reinjection of 3 mCi (100 MBq) BMIPP. Visual inspection of the short and long axis slices and quantitative comparison of the short axis slices of the tomograms were performed to grade BMIPP uptake and refill and detect turnover abnormalities. These were addressed either as scar or as ischemia and compared to CA and a graded score of regional wall motion by LVCV which provided values for sensitivity (SE) and specificity (SP) to detect CAD. Fifteen infarctions had corresponded clinical, angiographic and scintigraphic findings in 93%.

  4. 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

  5. Comparison of a qualitative measurement of heart-type fatty acid-binding protein with other cardiac markers as an early diagnostic marker in the diagnosis of non-ST - segment elevation myocardial infarction

    PubMed Central

    Gerede, Demet Menekşe; Güleç, Sadi; Kılıçkap, Mustafa; Kaya, Cansın Tulunay; Vurgun, Veysel Kutay; Özcan, Özgür Ulaş; Göksülük, Hüseyin; Erol, Çetin

    2015-01-01

    Summary Objective: Heart-type fatty acid-binding protein (H-FABP) is a novel cardiac marker used in the early diagnosis of acute myocardial infarction (AMI), which shows myocyte injury. Our study aimed to compare bedside H-FABP measurements with routine creatine kinase-MB (CK-MB) and troponin I (TnI) tests for the early diagnosis of non-ST-elevation MI (NSTEMI), as well as for determining its exclusion capacity. Methods A total of 48 patients admitted to the emergency room within the first 12 hours of onset of ischaemic-type chest pain lasting more than 30 minutes and who did not have ST-segment elevation on electrocardiography (ECG) were included in the study. Definite diagnoses of NSTEMI were made in 24 patients as a result of 24-hour follow up, and the remaining 24 patients did not develop MI. Results When various subgroups were analysed according to admission times, H-FABP was found to be a better diagnostic marker compared to CK-MB and TnI (accuracy index 85%), with a high sensitivity (79%) and specificity (93%) for early diagnosis (≤ six hours). The respective sensitivities of bedside H-FABP and TnI tests were 89 vs 33% (p < 0.05) for patients presenting within three hours of onset of symptoms. Conclusion Bedside H-FABP measurements may contribute to correct early diagnoses, as its levels are elevated soon following MI, and measurement is easy, with a rapid result. PMID:26212703

  6. TRIIODOTHYRONINE INCREASES MYOCARDIAL FUNCTION AND PYRUVATE ENTRY INTO THE CITRIC ACID CYCLE AFTER REPERFUSION IN A MODEL OF INFANT CARDIOPULMONARY BYPASS

    SciTech Connect

    Olson, Aaron; Bouchard, Bertrand; Ning, Xue-Han; Isern, Nancy G.; Des Rosiers, Christine; Portman, Michael A.

    2012-03-01

    We utilized a translational model of infant CPB to test the hypothesis that T3 modulates pyruvate entry into the citric acid cycle (CAC) thereby providing the energy support for improved cardiac function after ischemia-reperfusion. Methods and Results: Neonatal piglets received intracoronary [2-13Carbon(13C)]-pyruvate for 40 minutes (8 mM) during control aerobic conditions (Cont) or immediately after reperfusion (IR) from global hypothermic ischemia. A third group (IR-Tr) received T3 (1.2 ug/kg) during reperfusion. We assessed absolute CAC intermediate levels (aCAC) and flux parameters into the CAC through oxidative pyruvate decarboxylation (PDC ) and anaplerotic carboxylation (PC; ) using 13C-labeled pyruvate and isotopomer analysis by gas and liquid chromatography-mass spectrometry and 13C NMR. Neither IR nor IR-Tr modified aCAC. However, compared to IR, T3 (group IR-Tr) increased cardiac power and oxygen consumption after CPB while elevating both PDC and PC (~ four-fold). T3 inhibited IR induced reductions in CAC intermediate molar percent enrichment (MPE) and oxaloacetate(citrate)/malate MPE ratio; an index of aspartate entry into the CAC. Conclusions: T3 markedly enhances PC and PDC thereby providing substrate for elevated cardiac function and work after reperfusion. The increases in pyruvate flux occur with preservation of the CAC intermediate pool. Additionally, T3 inhibition of reductions in CAC intermediate MPEs indicates that T3 reduces the reliance on amino acids (AA) for anaplerosis after reperfusion. Thus, AA should be more available for other functions such as protein synthesis.

  7. Inhibition of L-carnitine biosynthesis and transport by methyl-γ-butyrobetaine decreases fatty acid oxidation and protects against myocardial infarction

    PubMed Central

    Liepinsh, E; Makrecka-Kuka, M; Kuka, J; Vilskersts, R; Makarova, E; Cirule, H; Loza, E; Lola, D; Grinberga, S; Pugovics, O; Kalvins, I; Dambrova, M

    2015-01-01

    Background and Purpose The important pathological consequences of ischaemic heart disease arise from the detrimental effects of the accumulation of long-chain acylcarnitines in the case of acute ischaemia-reperfusion. The aim of this study is to test whether decreasing the L-carnitine content represents an effective strategy to decrease accumulation of long-chain acylcarnitines and to reduce fatty acid oxidation in order to protect the heart against acute ischaemia–reperfusion injury. Key Results In this study, we used a novel compound, 4-[ethyl(dimethyl)ammonio]butanoate (Methyl-GBB), which inhibits γ-butyrobetaine dioxygenase (IC50 3 μM) and organic cation transporter 2 (OCTN2, IC50 3 μM), and, in turn, decreases levels of L-carnitine and acylcarnitines in heart tissue. Methyl-GBB reduced both mitochondrial and peroxisomal palmitate oxidation rates by 44 and 53% respectively. In isolated hearts treated with Methyl-GBB, uptake and oxidation rates of labelled palmitate were decreased by 40%, while glucose oxidation was increased twofold. Methyl-GBB (5 or 20 mg·kg−1) decreased the infarct size by 45–48%. In vivo pretreatment with Methyl-GBB (20 mg·kg−1) attenuated the infarct size by 45% and improved 24 h survival of rats by 20–30%. Conclusions and Implications Reduction of L-carnitine and long-chain acylcarnitine content by the inhibition of OCTN2 represents an effective strategy to protect the heart against ischaemia–reperfusion-induced damage. Methyl-GBB treatment exerted cardioprotective effects and increased survival by limiting long-chain fatty acid oxidation and facilitating glucose metabolism. PMID:25363063

  8. Acute myocardial infarction.

    PubMed

    Rischpler, Christoph

    2016-09-01

    Inflammatory processes after myocardial infarction have gained major interest in recent cardiovascular research. It is believed that not only the degree of cell recruitment to the heart plays a pivotal role in the quality of wound healing after myocardial infarction, but also the balance between different types or even subtypes of cells. It is also this balance which is thought to control key processes in tissue repair, such as apoptosis and neoangiogenesis. In this paper, we aim to review imaging strategies (with a special focus on nuclear molecular imaging strategies) that target cells and processes involved in postischemic inflammation and that have a high potential to be translated into clinic or that are already being used and evaluated in humans. PMID:27225319

  9. Heart-type Fatty acid-binding protein in Acute Myocardial infarction Evaluation (FAME): Background and design of a diagnostic study in primary care

    PubMed Central

    Bruins Slot, Madeleine HE; van der Heijden, Geert JMG; Rutten, Frans H; van der Spoel, Onno P; Mast, E Gijs; Bredero, Ad C; Doevendans, Pieter A; Glatz, Jan FC; Hoes, Arno W

    2008-01-01

    Background Currently used biomarkers for cardiac ischemia are elevated in blood plasma after a delay of several hours and therefore unable to detect acute coronary syndrome (ACS) in a very early stage. General practitioners (GPs), however, are often confronted with patients suspected of ACS within hours after onset of complaints. This ongoing study aims to evaluate the added diagnostic value beyond clinical assessment for a rapid bedside test for heart-type fatty-acid binding protein (H-FABP), a biomarker that is detectable as soon as one hour after onset of ischemia. Methods Participating GPs perform a blinded H-FABP rapid bedside test (Cardiodetect®) in patients with symptoms suggestive of ACS such as chest pain or discomfort at rest. All patients, whether referred to hospital or not, undergo electrocardiography (ECG) and venapunction for a plasma troponin test within 12–36 hours after onset of complaints. A final diagnosis will be established by an expert panel consisting of two cardiologists and one general practitioner (blinded to the H-FABP test result), using all available patient information, also including signs and symptoms. The added diagnostic value of the H-FABP test beyond history taking and physical examination will be determined with receiver operating characteristic curves derived from multivariate regression analysis. Conclusion Reasons for presenting the design of our study include the prevention of publication bias and unacknowledged alterations in the study aim, design or data-analysis. To our knowledge this study is the first to assess the diagnostic value of H-FABP outside a hospital-setting. Several previous hospital-based studies showed the potential value of H-FABP in diagnosing ACS. Up to now however it is unclear whether these results are equally promising when the test is used in primary care. The first results are expected in the end of 2008. PMID:18412949

  10. [Mortality of myocardial infarction].

    PubMed

    Bonnefoy, E; Kirkorian, G

    2011-12-01

    Coronary disease is a major cause of death and disability. From 1975 to 2000, coronary mortality was reduced by half. Better treatments and reduction of risk factors are the main causes. This phenomenon is observed in most developed countries, but mortality from coronary heart disease continues to increase in developing countries. In-hospital mortality of ST elevation myocardial infarction (STEMI) is in the range of 7 to 10% in registries. In infarction without ST segment elevation (NSTEMI), in-hospital mortality is around 5%. More recent studies found a similar in-hospital mortality for STEMI and NSTEMI. Because of patient selection and monitoring, mortality in clinical trials is much lower. After adjustment for the extent of coronary disease, age, risk factors, history of myocardial infarction, the excess mortality observed in women is fading. Many clinical, biological and laboratory parameters are associated with mortality in myocardial infarction. They refer to the immediate risk of death (ventricular rhythm disturbances, shock…), the extent of infarction (number of leads with ST elevation on the ECG, release of biomarkers, ejection fraction…), the presence of heart failure, the failure of reperfusion and the patient's baseline risk (age, renal function…). Risk scores, and more specifically the GRACE risk score, synthesize these different markers to predict the risk of death in a given patient. However, their use for the treatment of myocardial only concerns NSTEMI. Only a limited number of mechanical or pharmacological interventions reduces mortality of heart attack. The main benefits are observed with reperfusion by thrombolysis or primary angioplasty in STEMI, aspirin, heparin, beta-blockers, angiotensin converting enzyme inhibitors. Some medications such as bivalirudin and fondaparinux reduce mortality by decreasing the incidence of hemorrhagic complications. The guidelines classify interventions according to their benefit and especially their ability

  11. Tomoscintigraphic assessment of myocardial metabolic heterogenity

    SciTech Connect

    Roesler, H.; Hess, T.; Weiss, M.; Noelpp, U.; Mueller, G.; Hoeflin, F.; Kinser, J.

    1983-04-01

    I-123-omega-heptadecanoic acid (HDA) was evaluated for myocardial scanning in 59 healthy volunteers and 133 patients, using a 7-pinhole collimator. Early (uptake) and late (retention) images were compared visually. Regional HDA elimination was also followed semiquantitatively based on the calculation of a retention-over-uptake ratio, R(phi), derived from the maximal counts/pixel in 60 midventricular slice sectors. The healthy heart concentrated HDA homogeneously in all segments with no difference between early and late images. The minimal R(phi), taken as representative of that myocardium with the best function, was unchanged after maximal ergometer stress and with dipyramidole-induced hyperperfusion. A circumscribed decreased HDA uptake is the clear-cut criterion for an abnormal finding. HDA tomography of the myocardium had an 86% sensitivity for myocardial infarcts (MIs) up to 4 wk old, and 83% for myocardial scars (MSs). Comparing early and late tomograms, we find a cool-warm sequence more often with acute and subacute MIs. A cool-cool or a cold-cold sequence dominated with MSs. HDA tomoscintigraphy cannot replace TI-201 for the evaluation of regional coronary reserve in coronary heart disease.

  12. Diurnal variations in myocardial metabolism

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The heart is challenged by a plethora of extracellular stimuli over the course of a normal day, each of which distinctly influences myocardial contractile function. It is therefore not surprising that myocardial metabolism also oscillates in a time-of-day dependent manner. What is becoming increasin...

  13. Dipyridamole thallium-201 myocardial scintigraphy

    SciTech Connect

    Not Available

    1988-09-01

    Thallium-201 (/sup 201/Tl) myocardial scintigraphy is a sensitive technique for detecting coronary artery disease. Standardized exercise testing is the most common method for inducing myocardial stress for /sup 201/Tl imaging. Unfortunately, a significant number of patients are unable to undergo adequate treadmill or bicycle exercise. In these patients, pharmacologic stress with dipyridamole provides a safe, efficacious, and reliable alternative.

  14. Spiral MR myocardial tagging.

    PubMed

    Ryf, Salome; Kissinger, Kraig V; Spiegel, Marcus A; Börnert, Peter; Manning, Warren J; Boesiger, Peter; Stuber, Matthias

    2004-02-01

    In the present study, complementary spatial modulation of magnetization (CSPAMM) myocardial tagging was extended with an interleaved spiral imaging sequence. The use of a spiral sequence enables the acquisition of grid-tagged images with a tagline distance as low as 4 mm in a single breath-hold. Alternatively, a high temporal resolution of 77 frames per second was obtained with 8-mm grid spacing. Ten healthy adult subjects were studied. With this new approach, high-quality images can be obtained and the tags persist throughout the entire cardiac cycle. PMID:14755646

  15. Assessment of myocardial viability.

    PubMed

    Travin, Mark I; Bergmann, Steven R

    2005-01-01

    The prevalence of left ventricular (LV) dysfunction and resultant congestive heart failure is increasing. Patients with this condition are at high risk for cardiac death and usually have significant limitations in their lifestyles. Although there have been advances in medical therapy resulting in improved survival and well being, the best and most definitive therapy, when appropriate, is revascularization. In the setting of coronary artery disease, accounting for approximately two thirds of cases of congestive heart failure, LV dysfunction often is not the result of irreversible scar but rather caused by impairment in function and energy use of still viable-myocytes, with the opportunity for improved function if coronary blood flow is restored. Patients with LV dysfunction who have viable myocardium are the patients at highest risk because of the potential for ischemia but at the same time benefit most from revascularization. It is important to identify viable myocardium in these patients, and radionuclide myocardial scintigraphy is an excellent tool for this. Single-photon emission computed tomography perfusion scintigraphy, whether using thallium-201, Tc-99m sestamibi, or Tc-99m tetrofosmin, in stress and/or rest protocols, has consistently been shown to be an effective modality for identifying myocardial viability and guiding appropriate management. Metabolic imaging with positron emission tomography radiotracers frequently adds additional information and is a powerful tool for predicting which patients will have an improved outcome from revascularization, including some patients referred instead for cardiac transplantation. Other noninvasive modalities, such as stress echocardiography, also facilitate the assessment of myocardial viability, but there are advantages and disadvantages compared with the nuclear techniques. Nuclear imaging appears to require fewer viable cells for detection, resulting in a higher sensitivity but a lower specificity than stress

  16. 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

  17. Trauma Induced Myocardial Infarction

    PubMed Central

    Lolay, Georges A.; Abdel-Latef, Ahmed K.

    2016-01-01

    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. PMID:26490501

  18. Simultaneous technetium-99m MIBI angiography and myocardial perfusion imaging

    SciTech Connect

    Baillet, G.Y.; Mena, I.G.; Kuperus, J.H.; Robertson, J.M.; French, W.J.

    1989-01-01

    Resting first-pass radionuclide angiography (FPRNA) was performed with the myocardial perfusion agent technetium-99m MIBI. In 27 patients, it was compared with technetium-99m diethylenetriamine pentaacetic acid FPRNA. A significant correlation was present in left (r = 0.93, p less than 0.001) as well as right (r = 0.92, p less than 0.001) ventricular ejection fraction measured with both radiopharmaceuticals. In 13 patients, MIBI derived segmental wall motion was compared with contrast ventriculography. A high correlation was present (p less than 0.001), and qualitative agreement was found in 38/52 segments. In 19 patients with myocardial infarction a significant correlation was present between MIBI segmental wall motion and perfusion scores (p less than 0.001). In ten patients with a history of myocardial infarction, 18 myocardial segments demonstrated diseased coronary vessels and impaired wall motion at contrast angiography. These segments were all identified by the MIBI wall motion and perfusion study. We conclude that MIBI is a promising agent for simultaneous evaluation of cardiac function and myocardial perfusion at rest.

  19. An unusual myocardial infarction

    PubMed Central

    Di Michele, Sara; Mirabelli, Francesca; Mankad, Sunil

    2014-01-01

    Summary We present a 74-year-old male with a chondrosarcoma, who presented with chest pain. The history, electrocardiogram (ECG), and biomarkers established the diagnosis of myocardial infarction (MI); angiography did not show coronary atherosclerosis and, both initial transthoracic echocardiogram and chest computed tomography (CT), did not demonstrate any cardiac abnormalities. A second echocardiogram following a routine ECG showed presence of a mass involving the right ventricle and the cardiac apex that was confirmed by chest CT scan. We underline the importance of considering cardiac tumors in the clinical arena of MI management. Learning points Cardiac tumors cause ECG changes similar to ischemic heart diseases.Keep in mind cardiac tumors when performing transthoracic echocardiogram (TTE) in the setting of suspected MI.TTE is the technique of choice in detecting cardiac tumors. PMID:26693309

  20. Masquerades of myocardial infarction.

    PubMed Central

    Bean, W. B.

    1976-01-01

    I summarize these observations in Figure 1. It represents every person in a hypothetical population who has myocardial infarction. A large but unknown number, some believe almost half, never get help. Mobile coronary care units are reducing this group, but so far only a little. When the diagnosis is not understood the disease is not recognized. Then come discovery and popularization. Hereafter masquerades hide some cases and the diagnosis is missed. Somewhere fairly early the diagnostic fad leads to false positive diagnosis. As new techniques are discovered, perfected and mastered, false positive errors and masquerades leading to oversights diminish but still exist. All the skill and technical virtuosity in the world will not be applied if we do not think of the disease. When we think of it, even obscure cases may be resolved easily. PMID:960416

  1. Wave Propagation of Myocardial Stretch: Correlation with Myocardial Stiffness

    PubMed Central

    Pislaru, Cristina; Pellikka, Patricia A.; Pislaru, Sorin V.

    2015-01-01

    The mechanism of flow propagation during diastole in the left ventricle (LV) has been well described. Little is known about the associated waves propagating along the heart wall s. These waves may have a mechanism similar to pulse wave propagation in arteries. The major goal of the study was to evaluate the effect of myocardial stiffness and preload on this wave transmission. Methods Longitudinal late diastolic deformation and wave speed (Vp) of myocardial stretch in the anterior LV wall were measured using sonomicrometry in sixteen pigs. Animals with normal and altered myocardial stiffness (acute myocardial infarction) were studied with and without preload alterations. Elastic modulus estimated from Vp (EVP; Moens-Korteweg equation) was compared to incremental elastic modulus obtained from exponential end -diastolic stress-strain relation (ESS). Myocardial distensibility and α-and β-coefficients of stress-strain relations were calculated. Results Vp was higher at reperfusion compared to baseline (2.6±1.3 m/s vs. 1.3±0.4 m/s; p=0.005) and best correlated with ESS (r 2=0.80, p<0.0001), β-coefficient (r2=0.78, p<0.0001), distensibility (r2=0.47, p=0.005), and wall thickness/diameter ratio (r2=0.42, p=0.009). Elastic moduli (EVP and ESS) were strongly correlated (r2=0.83, p<0.0001). Increasing preload increased Vp and EVP and decreased distensibility. At multivariate analysis, ESS, wall thickness, and end-diastolic and systolic LV pressures were independent predictors of Vp (r2model=0.83, p<0.0001). Conclusions The main determinants of wave propagation of longitudinal myocardial stretch were myocardial stiffness and LV geometry and pressure. This local wave speed could potentially be measured noninvasively by echocardiography. PMID:25193091

  2. Characterization and chemical composition of fatty acids content of watermelon and muskmelon cultivars in Saudi Arabia using gas chromatography/mass spectroscopy

    PubMed Central

    Albishri, Hassan M.; Almaghrabi, Omar A.; Moussa, Tarek A. A.

    2013-01-01

    Background: The growth in the production of biodiesel, which is principally fatty acid methyl esters (FAME), has been phenomenal in the last ten years because of the general desire to cut down on the release of greenhouse gases into the atmosphere, and also as a result of the increasing cost of fossil fuels. Objective: Establish whether there is any relationship between two different species (watermelon and muskmelon) within the same family (Cucurbitaceae) on fatty acid compositions and enumerate the different fatty acids in the two species. Materials and Methods: Extraction of fatty acids from the two species and preparation the extract to gas chromatography/mass spectroscopy analysis to determine the fatty acids compositions qualitatively and quantitatively. Results: The analyzed plants (watermelon and muskmelon) contain five saturated fatty acids; tetrdecanoic acid, pentadecanoic acid, hexadecanoic acid, heptadecanoic acid and octadecanoic acid with different concentrations, while muskmelon contains an extra saturated fatty acid named eicosanoic acid. The watermelon plant contains five unsaturated fatty acids while muskmelon contains three only, the two plants share in two unsaturated fatty acids named 9-hexadecenoic acid and 9-octadecenoic acid, the muskmelon plant contains higher amounts of these two acids (2.04% and 10.12%, respectively) over watermelon plant (0.88% and 0.25%, respectively). Conclusion: The chemical analysis of watermelon and muskmelon revealed that they are similar in saturated fatty acids but differ in unsaturated fatty acids which may be a criterion of differentiation between the two plants. PMID:23661995

  3. Modulation of cardiac metabolism during myocardial ischemia.

    PubMed

    Chagas, Antonio C P; Dourado, Paulo M M; Galvão, Tatiana de Fátima Gonçalves

    2008-01-01

    Metabolic modulation during myocardial ischemia is possible by the use of specific drugs, which may induce a shift from free fatty acid towards predominantly glucose utilization by the myocardium to increase ATP generation per unit oxygen consumption. Three agents (trimetazidine, ranolazine, and perhexiline) have well-documented anti-ischaemic effects. However, perhexiline, the most potent agent currently available, requires plasma-level monitoring to avoid hepato-neuro-toxicity. Besides, the long-term safety of trimetazidine and ranolazine has yet to be established. In addition to their effect in ischemia, the potential use of these drugs in chronic heart failure is gaining recognition as clinical and experimental data are showing the improvement of myocardial function following treatment with several of them, even in the absence of ischemia. Future applications for this line of treatment is promising and deserves additional research. In particular, large, randomised, controlled trials investigating the effects of these agents on mortality and hospitalization rates due to coronary artery disease are needed. PMID:18991673

  4. CAD of myocardial perfusion

    NASA Astrophysics Data System (ADS)

    Storm, Corstiaan J.; Slump, Cornelis H.

    2007-03-01

    Our purpose is in the automated evaluation of the physiological relevance of lesions in coronary angiograms. We aim to extract as much as possible quantitative information about the physiological condition of the heart from standard angiographic image sequences. Coronary angiography is still the gold standard for evaluating and diagnosing coronary abnormalities as it is able to locate precisely the coronary artery lesions. The dimensions of the stenosis can be assessed nowadays successfully with image processing based Quantitative Coronary Angiography (QCA) techniques. Our purpose is to assess the clinical relevance of the pertinent stenosis. We therefore analyze the myocardial perfusion as revealed in standard angiographic image sequences. In a Region-of-Interest (ROI) on the angiogram (without an overlaying major blood vessel) the contrast is measured as a function of time (the so-called time-density curve). The required hyperemic state of exercise is induced artificially by the injection of a vasodilator drug e.g. papaverine. In order to minimize motion artifacts we select based on the recorded ECG signal end-diastolic images in both a basal and a hyperemic run in the same projection to position the ROI. We present the development of the algorithms together with results of a small study of 20 patients which have been catheterized following the standard protocol.

  5. Experimental myocardial infarction

    PubMed Central

    Hood, William B.; Bianco, Jesus A.; Kumar, Raj; Whiting, Richard B.

    1970-01-01

    Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction. Images PMID:4914678

  6. 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

  7. Fatty acids in serum and diet--a canonical correlation analysis among toddlers.

    PubMed

    Uusitalo, Liisa; Nevalainen, Jaakko; Salminen, Irma; Ovaskainen, Marja-Leena; Kronberg-Kippilä, Carina; Ahonen, Suvi; Niinistö, Sari; Alfthan, Georg; Simell, Olli; Ilonen, Jorma; Veijola, Riitta; Knip, Mikael; Virtanen, Suvi M

    2013-07-01

    Fatty acid concentrations in blood are potential biomarkers of dietary fat intake, but methodological studies among children are scarce. The large number of fatty acids and their complex interrelationships pose a special challenge in research on fatty acids. Our target was to assess the interrelationships between the total fatty acid profiles in diet and serum of young children. The study subjects were healthy control children from the birth cohort of the Type 1 Diabetes Prediction and Prevention Study. A 3-day food record and a frozen serum sample were available from 135 children at the age of 1 year, from 133 at 2 years, and from 92 at 3 years. The relationship between dietary and serum fatty acid profiles was analysed using canonical correlation analysis. The consumption of fatty milk correlated positively with serum fatty acids, pentadecanoic acid, palmitic acid and conjugated linoleic acid (CLA) at all ages. Correlations between dietary and serum eicosapentaenoic and/or docosahexaenoic acid were observed at 2 and 3 years of age. Serum linoleic acid was positively associated with the consumption of infant formula at the age of 1 year, and with the consumption of vegetable margarine at 2 and 3 years. The results indicate a high quality of the 3-day food records kept by parents and other caretakers of the children, and suitability of non-fasting, un-fractioned serum samples for total fatty acid analyses. The correlation between intake of milk fat and serum proportion of CLA is a novel finding. PMID:22066932

  8. 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.

  9. Dichloroacetate attenuates myocardial acidosis and metabolic changes induced by partial occlusion of the coronary artery in dogs.

    PubMed

    Sakai, K; Ichihara, K; Nasa, Y; Kamigaki, M; Abiko, Y

    1990-01-01

    The present study was undertaken to examine whether dichloroacetate, which inhibits pyruvate dehydrogenase kinase and, therefore, increases the activity of pyruvate dehydrogenase, attenuates myocardial acidosis and metabolic changes induced by coronary occlusion. In dogs anesthetized with pentobarbital, the left anterior descending coronary artery was incompletely occluded to reduce the left anterior descending flow to a half to one third of the original flow (partial occlusion) to produce myocardial (regional) ischemia. Partial occlusion was continued for 90 min, and a bolus injection of saline or dichloroacetate was made intravenously 30 min after the onset of occlusion. Partial occlusion decreased myocardial pH significantly. An injection of dichloroacetate (150 mg/kg) increased myocardial pH that had been lowered by partial occlusion. Myocardial metabolites were measured in other dogs. Partial occlusion decreased the myocardial levels of adenosine triphosphate, creatine phosphate and energy charge potential, and increased that of lactate significantly, without affecting the myocardial levels of pyruvate and nonesterified fatty acids. Dichloroacetate attenuated the ischemia-induced changes in the myocardial levels of adenosine triphosphate, creatine phosphate, energy charge potential and lactate. These results indicate that dichloroacetate attenuates the myocardial acidosis and metabolic changes during coronary partial occlusion. PMID:2095718

  10. 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

  11. 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.

  12. Aqueous extract of Saussurea lappa root ameliorate oxidative myocardial injury induced by isoproterenol in rats

    PubMed Central

    Saleem, T. S. Mohamed; Lokanath, N.; Prasanthi, A.; Madhavi, M.; Mallika, G.; Vishnu, M. N.

    2013-01-01

    Saussurea lappa Clarke (Compositae), is commonly known as Kushta. In Ayurvedha, it is mentioned that the aqueous extract of the root S. lappa was used for treatment of angina pectoris. The present study was designed to investigate the cardioprotective effect of aqueous extract of root of S. lappa against isoproterenol induced myocardial injury. Myocardial injury in rat was induced by the administration of isoproterenol at a dose of 85 mg/kg, i.p., The rats were pretreated with the aqueous extract of S. lappa (AESL) in three different doses (100, 200 and 300 mg/kg, p.o.) through the oral route. Isoproterenol alone-treated rats showed increased serum concentration of lactate dehydrogenase (LDH), creatinine kinase (CK), and aspartate transaminase (AST), increased myocardial thiobarbituric acid reactive substances (TBARS) level, and decreased myocardial glutathione (GSH) level due to myocardial damage produced by isoproterenol. This is further conformed by histopathological changes. Chronic oral administration of AESL in three different doses significantly restored the level of myocardial LDH, CK, AST, TBARS, and GSH. The extract effect was compared with the reference standard α-tocopherol which also offered similar protection in biochemical and histopathological changes. The overall beneficial effect which was observed with the dose of 200 mg/kg indicated that AESL produced significant dose-dependent activity against isoproterenol induced myocardial injury. PMID:23833749

  13. PPARs: Protectors or Opponents of Myocardial Function?

    PubMed Central

    Pol, Christine J.; Lieu, Melissa; Drosatos, Konstantinos

    2015-01-01

    Over 5 million people in the United States suffer from the complications of heart failure (HF), which is a rapidly expanding health complication. Disorders that contribute to HF include ischemic cardiac disease, cardiomyopathies, and hypertension. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor family. There are three PPAR isoforms: PPARα, PPARγ, and PPARδ. They can be activated by endogenous ligands, such as fatty acids, as well as by pharmacologic agents. Activators of PPARs are used for treating several metabolic complications, such as diabetes and hyperlipidemia that are directly or indirectly associated with HF. However, some of these drugs have adverse effects that compromise cardiac function. This review article aims to summarize the current basic and clinical research findings of the beneficial or detrimental effects of PPAR biology on myocardial function. PMID:26713088

  14. Myocardial infarction following bee sting.

    PubMed

    Puvanalingam, A; Karpagam, P; Sundar, C; Venkatesan, S; Ragunanthanan

    2014-08-01

    Bee stings are commonly encountered worldwide. Various manifestations after bee sting have been described. Local reactions are common. Unusually, manifestations like vomiting, diarrhoea, dyspnoea, generalised oedema, acute renal failure, hypotension and collapse may occur. Rarely vasculitis, serum sickness, neuritis and encephalitis have been described which generally develop days to weeks after a sting. Acute coronary syndromes after hymenoptera stings and other environmental exposures are referred to as the Kounis syndrome or allergic myocardial ischaemia and infarction. We report a 60 year old male who developed myocardial infarction after multiple bee stings over his body. PMID:25856951

  15. Myocardial uptake of cocaine and effects of cocaine on myocardial substrate utilization and perfusion in hypertensive rats

    SciTech Connect

    Som, P.; Wang, G.J.; Oster, Z.H.; Knapp, F.F. Jr.; Yonekura, Y.; Fujibayashi, Y.; Yamamoto, K.; Kubota, K.

    1992-12-31

    Cocaine abuse is a problem causing world-wide concern and the number of deaths following cocaine use is increasing. Cardiovascular complications following cocaine include severe tachyarrythmias, pulmonary edema, myocardial infarction, and acute renal failure, which are major problems confronting emergency facilities. While the studies of cocaine effects on the brain have been given the most attention, it is clear that the effects of cocaine on the cardiovascular system are of great importance, given the increasing number of reports on sudden death and myocardial infarctions in young adults related to cocaine use. The precise mechanisms of cardiotoxic actions of cocaine are unclear. We investigated the whole-body distribution of C-14-labeled cocaine to determine the cocaine-binding sites, including blocking experiments to determine the nature of regional binding sites, and differential response of the normal vs. diseased heart (hypertensive cardiomyopathy) in an animal model to mimic a potentially high risk population. We investigated the acute effects of cocaine on myocardial metabolism using two myocardial energy substrate analogs, fatty acid and glucose with comparison with regional perfusion.

  16. Myocardial uptake of cocaine and effects of cocaine on myocardial substrate utilization and perfusion in hypertensive rats

    SciTech Connect

    Som, P.; Wang, G.J. ); Oster, Z.H. ); Knapp, F.F. Jr. ); Yonekura, Y. . Faculty of Medicine); Fujibayashi, Y. . Hospital); Yamamoto, K. . Medical School); Kubota, K. (Tohoku Univ., Sendai

    1992-01-01

    Cocaine abuse is a problem causing world-wide concern and the number of deaths following cocaine use is increasing. Cardiovascular complications following cocaine include severe tachyarrythmias, pulmonary edema, myocardial infarction, and acute renal failure, which are major problems confronting emergency facilities. While the studies of cocaine effects on the brain have been given the most attention, it is clear that the effects of cocaine on the cardiovascular system are of great importance, given the increasing number of reports on sudden death and myocardial infarctions in young adults related to cocaine use. The precise mechanisms of cardiotoxic actions of cocaine are unclear. We investigated the whole-body distribution of C-14-labeled cocaine to determine the cocaine-binding sites, including blocking experiments to determine the nature of regional binding sites, and differential response of the normal vs. diseased heart (hypertensive cardiomyopathy) in an animal model to mimic a potentially high risk population. We investigated the acute effects of cocaine on myocardial metabolism using two myocardial energy substrate analogs, fatty acid and glucose with comparison with regional perfusion.

  17. 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.

  18. Acute myocardial infarction

    PubMed Central

    Domes, Trustin; Szafran, Olga; Bilous, Cheryl; Olson, Odell; Spooner, G. Richard

    2006-01-01

    OBJECTIVE To assess the quality of care of acute myocardial infarction (AMI) in a rural health region. DESIGN Clinical audit employing multiple explicit criteria of care elements for emergency department and in-hospital AMI management. The audit was conducted using retrospective chart review. SETTING Twelve acute care health centres and hospitals in the East Central Health Region, a rural health region in Alberta, where medical and surgical services are provided almost entirely by family physicians. PARTICIPANTS Hospital inpatients with a confirmed discharge diagnosis of AMI (ICD-9-CM codes 410.xx) during the period April 1, 2001, to March 31, 2002, were included (177 confirmed cases). MAIN OUTCOME MEASURES Quality of AMI care was assessed using guidelines from the American College of Cardiology and the American Heart Association and the Canadian Cardiovascular Outcomes Research Team and Canadian Cardiovascular Society. Quality of care indicators at three stages of patient care were assessed: at initial recognition and AMI management in the emergency department, during in-hospital AMI management, and at preparation for discharge from hospital. RESULTS In the emergency department, the quality of care was high for most procedural and therapeutic audit elements, with the exception of rapid electrocardiography, urinalysis, and provision of nitroglycerin and morphine. Average door-to-needle time for thrombolysis was 102.5 minutes. The quality of in-hospital care was high for most elements, but low for nitroglycerin and angiotensin-converting enzyme (ACE) inhibitors, daily electrocardiography, and counseling regarding smoking cessation and diet. Few patients received counseling for lifestyle changes at hospital discharge. Male and younger patients were treated more aggressively than female and older patients. Sites that used care protocols achieved better results in initial AMI management than sites that did not. Stress testing was not readily available in the rural

  19. 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.

  20. 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…

  1. [Sewer gas induced myocardial toxicity].

    PubMed

    Antonelli, Dante; Sabanchiev, Avi; Rosner, Ehud; Turgeman, Yoav

    2014-07-01

    We report the case of a 19 year-old worker who collapsed after acute exposure to sewer gas. He rapidly developed cardiorespiratory failure with electrocardiographic, echocardiographic and laboratory findings of myocardial involvement. The mainstay of the therapy was mainly supportive treatment with a successful outcome. PMID:25189024

  2. Thrombolysis for Acute Myocardial Infarction

    PubMed Central

    Webb, John; Thompson, Christopher

    1992-01-01

    Thrombolysis has an important role in the management of acute myocardial infarction. Early treatment can markedly reduce mortality and morbidity. This new standard of care requires knowledge of accepted indications and contraindications for thrombolysis as well as familiarity with available agents and regimens. ImagesFigure 3 PMID:21221398

  3. Myocardial Oxidative Stress in Infants Undergoing Cardiac Surgery.

    PubMed

    Sznycer-Taub, Nathaniel; Mackie, Stewart; Peng, Yun-Wen; Donohue, Janet; Yu, Sunkyung; Aiyagari, Ranjit; Charpie, John

    2016-04-01

    Cardiac surgery for congenital heart disease often necessitates a period of myocardial ischemia during cardiopulmonary bypass and cardioplegic arrest, followed by reperfusion after aortic cross-clamp removal. In experimental models, myocardial ischemia-reperfusion is associated with significant oxidative stress and ventricular dysfunction. A prospective observational study was conducted in infants (<1 year) who underwent elective surgical repair of a ventricular septal defect (VSD) or tetralogy of Fallot (TOF). Blood samples were drawn following anesthetic induction (baseline) and directly from the coronary sinus at 1, 3, 5, and 10 min following aortic cross-clamp removal. Samples were analyzed for oxidant stress using assays for thiobarbituric acid-reactive substances, protein carbonyl, 8-isoprostane, and total antioxidant capacity. For each subject, raw assay data were normalized to individual baseline samples and expressed as fold-change from baseline. Results were compared using a one-sample t test with Bonferroni correction for multiple comparisons. Sixteen patients (ten with TOF and six with VSD) were enrolled in the study, and there were no major postoperative complications observed. For the entire cohort, there was an immediate, rapid increase in myocardial oxidative stress that was sustained for 10 min following aortic cross-clamp removal in all biomarker assays (all P < 0.01), except total antioxidant capacity. Infant cardiac surgery is associated with a rapid, robust, and time-dependent increase in myocardial oxidant stress as measured from the coronary sinus in vivo. Future studies with larger enrollment are necessary to assess any association between myocardial oxidative stress and early postoperative outcomes. PMID:26843460

  4. The PPAR-α activator fenofibrate fails to provide myocardial protection in ischemia and reperfusion in pigs

    PubMed Central

    Xu, Ya; Lu, Li; Greyson, Clifford; Rizeq, Mona; Nunley, Karin; Wyatt, Beata; Bristow, Michael R.; Long, Carlin S.; Schwartz, Gregory G.

    2010-01-01

    Rodent studies suggest that peroxisome proliferator-activated receptor-α (PPAR-α) activation reduces myocardial ischemia-reperfusion (I/R) injury and infarct size; however, effects of PPAR-α activation in large animal models of myocardial I/R are unknown. We determined whether chronic treatment with the PPAR-α activator fenofibrate affects myocardial I/R injury in pigs. Domestic farm pigs were assigned to treatment with fenofibrate 50 mg·kg−1 ·day−1 orally or no drug treatment, and either a low-fat (4% by weight) or a high-fat (20% by weight) diet. After 4 wk, 66 pigs underwent 90 min low-flow regional myocardial ischemia and 120 min reperfusion under anesthetized open-chest conditions, resulting in myocardial stunning. The high-fat group received an infusion of triglyceride emulsion and heparin during this terminal experiment to maintain elevated arterial free fatty acid (FFA) levels. An additional 21 pigs underwent 60 min no-flow ischemia and 180 min reperfusion, resulting in myocardial infarction. Plasma concentration of fenofibric acid was similar to the EC50 for activation of PPAR-α in vitro and to maximal concentrations achieved in clinical use. Myocardial expression of PPAR-α mRNA was prominent but unaffected by fenofibrate treatment. Fenofibrate increased expression of carnitine palmitoyltransferase (CPT)-I mRNA in liver and decreased arterial FFA and lactate concentrations (each P < 0.01). However, fenofibrate did not affect myocardial CPT-I expression, substrate uptake, lipid accumulation, or contractile function during low-flow I/R in either the low- or high-fat group, nor did it affect myocardial infarct size. Despite expression of PPAR-α in porcine myocardium and effects of fenofibrate on systemic metabolism, treatment with this PPAR-α activator does not alter myocardial metabolic or contractile responses to I/R in pigs. PMID:16339839

  5. Fatty acid constituents of Peganum harmala plant using Gas Chromatography–Mass Spectroscopy

    PubMed Central

    Moussa, Tarek A.A.; Almaghrabi, Omar A.

    2015-01-01

    Fatty acid contents of the Peganum harmala plant as a result of hexane extraction were analyzed using GC–MS. The saturated fatty acid composition of the harmal plant was tetradecanoic, pentadecanoic, tridecanoic, hexadecanoic, heptadecanoic and octadecanoic acids, while the saturated fatty acid derivatives were 12-methyl tetradecanoic, 5,9,13-trimethyl tetradecanoic and 2-methyl octadecanoic acids. The most abundant fatty acid was hexadecanoic with concentration 48.13% followed by octadecanoic with concentration 13.80%. There are four unsaturated fatty acids called (E)-9-dodecenoic, (Z)-9-hexadecenoic, (Z,Z)-9,12-octadecadienoic and (Z,Z,Z)-9,12,15-octadecatrienoic. The most abundant unsaturated fatty acid was (Z,Z,Z)-9,12,15-octadecatrienoic with concentration 14.79% followed by (Z,Z)-9,12-octadecadienoic with concentration 10.61%. Also, there are eight non-fatty acid compounds 1-octadecene, 6,10,14-trimethyl-2-pentadecanone, (E)-15-heptadecenal, oxacyclohexadecan-2 one, 1,2,2,6,8-pentamethyl-7-oxabicyclo[4.3.1]dec-8-en-10-one, hexadecane-1,2-diol, n-heneicosane and eicosan-3-ol. PMID:27081366

  6. Fatty acid constituents of Peganum harmala plant using Gas Chromatography-Mass Spectroscopy.

    PubMed

    Moussa, Tarek A A; Almaghrabi, Omar A

    2016-05-01

    Fatty acid contents of the Peganum harmala plant as a result of hexane extraction were analyzed using GC-MS. The saturated fatty acid composition of the harmal plant was tetradecanoic, pentadecanoic, tridecanoic, hexadecanoic, heptadecanoic and octadecanoic acids, while the saturated fatty acid derivatives were 12-methyl tetradecanoic, 5,9,13-trimethyl tetradecanoic and 2-methyl octadecanoic acids. The most abundant fatty acid was hexadecanoic with concentration 48.13% followed by octadecanoic with concentration 13.80%. There are four unsaturated fatty acids called (E)-9-dodecenoic, (Z)-9-hexadecenoic, (Z,Z)-9,12-octadecadienoic and (Z,Z,Z)-9,12,15-octadecatrienoic. The most abundant unsaturated fatty acid was (Z,Z,Z)-9,12,15-octadecatrienoic with concentration 14.79% followed by (Z,Z)-9,12-octadecadienoic with concentration 10.61%. Also, there are eight non-fatty acid compounds 1-octadecene, 6,10,14-trimethyl-2-pentadecanone, (E)-15-heptadecenal, oxacyclohexadecan-2 one, 1,2,2,6,8-pentamethyl-7-oxabicyclo[4.3.1]dec-8-en-10-one, hexadecane-1,2-diol, n-heneicosane and eicosan-3-ol. PMID:27081366

  7. Influence of Carotino oil on in vitro rumen fermentation, metabolism and apparent biohydrogenation of fatty acids.

    PubMed

    Adeyemi, Kazeem Dauda; Ebrahimi, Mahdi; Samsudin, Anjas Asmara; Alimon, Abd Razak; Karim, Roselina; Karsani, Saiful Anuar; Sazili, Awis Qurni

    2015-03-01

    The study appraised the effects of Carotino oil on in vitro rumen fermentation, gas production, metabolism and apparent biohydrogenation of oleic, linoleic and linolenic acids. Carotino oil was added to a basal diet (50% concentrate and 50% oil palm frond) at the rate of 0, 2, 4, 6 and 8% dry matter of the diet. Rumen inoculum was obtained from three fistulated Boer bucks and incubated with 200 mg of each treatment for 24 h at 39°C. Gas production, fermentation kinetics, in vitro organic matter digestibility (IVOMD), volatile fatty acids (VFA), in vitro dry matter digestibility (IVDMD), metabolizable energy and free fatty acids were determined. Carotino oil did not affect (P > 0.05) gas production, metabolizable energy, pH, IVOMD, IVDMD, methane, total and individual VFAs. However, Carotino oil decreased (P < 0.05) the biohydrogenation of linoleic and linolenic acids but enhanced (P < 0.05) the biohydrogenation of oleic acid. After 24 h incubation, the concentrations of stearic, palmitic, pentadecanoic, myristic, myristoleic and lauric acids decreased (P < 0.05) while the concentration of linolenic, linoleic, oleic and transvaccenic acids and conjugated linoleic acid (CLAc9t11) increased (P < 0.05) with increasing levels of Carotino oil. Carotino oil seems to enhance the accumulation of beneficial unsaturated fatty acids without disrupting rumen fermentation. PMID:25377536

  8. Inflammatory response, neutrophil activation, and free radical production after acute myocardial infarction: effect of thrombolytic treatment.

    PubMed Central

    Bell, D; Jackson, M; Nicoll, J J; Millar, A; Dawes, J; Muir, A L

    1990-01-01

    Activated neutrophils releasing proteolytic enzymes and oxygen free radicals have been implicated in extending myocardial injury after myocardial infarction. Neutrophil elastase was used as a marker of neutrophil activation and the non-peroxide diene conjugate of linoleic acid was used as an indicator of free radical activity in 32 patients after acute myocardial infarction; 17 were treated by intravenous thrombolysis. Patients with acute myocardial infarction had higher plasma concentrations of neutrophil elastase and the non-peroxide diene conjugated isomer of linoleic acid than normal volunteers or patients with stable ischaemic heart disease. Patients treated by thrombolysis had an early peak of neutrophil elastase at eight hours while those who had not been treated by thrombolysis showed a later peak 40 hours after infarction. The plasma concentration of non-peroxide conjugated diene of linoleic acid was highest 16 hours after the infarction irrespective of treatment by thrombolysis. Quantitative imaging with single photon emission tomography showed decreased uptake of indium-111 labelled neutrophils in the infarcted myocardium (as judged from technetium-99m pyrophosphate) in those who had received thrombolysis, suggesting a decreased inflammatory response. The results indicate increased neutrophil activation and free radical production after myocardial infarction; they also suggest that thrombolysis does not amplify the inflammatory response and may indeed suppress it. Images PMID:2317413

  9. Effects of glutamine treatment on myocardial damage and cardiac function in rats after severe burn injury

    PubMed Central

    Yan, Hong; Zhang, Yong; Lv, Shang-jun; Wang, Lin; Liang, Guang-ping; Wan, Qian-xue; Peng, Xi

    2012-01-01

    Treatment with glutamine has been shown to reduce myocardial damage associated with ischemia/reperfusion injury. However, the cardioprotective effect of glutamine specifically after burn injury remains unclear. The present study explores the ability of glutamine to protect against myocardial damage in rats that have been severely burned. Seventy-two Wistar rats were randomly divided into three groups: normal controls (C), burned controls (B) and a glutamine-treated group (G). Groups B and G were subjected to full thickness burns comprising 30% of total body surface area. Group G was administered 1.5 g/ (kg•d) glutamine and group B was given the same dose of alanine via intragastric administration for 3 days. Levels of serum creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST) and blood lactic acid were measured, as well as myocardial ATP and glutathione (GSH) contents. Cardiac function indices and histopathological changes were analyzed at 12, 24, 48 and 72 post-burn hours. In both burned groups, levels of serum CK, LDH, AST and blood lactic acid increased significantly, while myocardial ATP and GSH contents decreased. Compared with group B, CK, LDH, and AST levels were lower and blood lactic acid, myocardial ATP and GSH levels were higher in group G. Moreover, cardiac contractile function inhibition and myocardial histopathological damage were significantly reduced in group G compared to B. Taken together, these results show that glutamine supplementation protects myocardial structure and function after burn injury by improving energy metabolism and by promotedthe synthesis of ATP and GSH in cardiac myocytes. PMID:22977661

  10. Calpain inhibition preserves myocardial structure and function following myocardial infarction.

    PubMed

    Mani, Santhosh K; Balasubramanian, Sundaravadivel; Zavadzkas, Juozas A; Jeffords, Laura B; Rivers, William T; Zile, Michael R; Mukherjee, Rupak; Spinale, Francis G; Kuppuswamy, Dhandapani

    2009-11-01

    Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(2+)-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated (n = 6) and untreated (n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 + or - 2% pre-MI to 30 + or - 4% with MI only vs. 41 + or - 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 + or - 2 microl pre-MI to 73 + or - 4 microl with MI only vs. 55 + or - 4 microl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients. PMID:19734364

  11. Myocardial steatosis and necrosis in atria and ventricles of rats given pyruvate dehydrogenase kinase inhibitors.

    PubMed

    Jones, Huw Bowen; Reens, Jaimini; Johnson, Elizabeth; Brocklehurst, Simon; Slater, Ian

    2014-12-01

    Pharmaceutical therapies for non-insulin-dependent diabetes mellitus (NIDDM) include plasma glucose lowering by enhancing glucose utilization. The mitochondrial pyruvate dehydrogenase (PDH) complex is important in controlling the balance between glucose and fatty acid substrate oxidation. Administration of pyruvate dehydrogenase kinase inhibitors (PDHKIs) to rats effectively lowers plasma glucose but results in myocardial steatosis that in some instances is associated primarily with atrial and to a lesser degree with ventricular pathology. Induction of myocardial steatosis is not dose-dependent, varies from minimal to moderate severity, and is either of multifocal or diffuse distribution. Ventricular histopathology was restricted to few myocardial degenerative fibers, while that in the atrium/atria was of either acute or chronic appearance with the former showing myocardial degeneration/necrosis, acute myocarditis, edema, endothelial activation (rounding up), endocarditis, and thrombosis associated with moderate myocardial steatosis and the latter with myocardial loss, replacement fibrosis, and no apparent or minimal association with steatosis. The evidence from these evaluations indicate that excessive intramyocardial accumulation of lipid may be either primarily adverse or represents an indicator of other adversely affected cellular processes. PMID:24742628

  12. Imaging and Modeling of Myocardial Metabolism

    PubMed Central

    Jamshidi, Neema; Karimi, Afshin; Birgersdotter-Green, Ulrika; Hoh, Carl

    2010-01-01

    Current imaging methods have focused on evaluation of myocardial anatomy and function. However, since myocardial metabolism and function are interrelated, metabolic myocardial imaging techniques, such as positron emission tomography, single photon emission tomography, and magnetic resonance spectroscopy present novel opportunities for probing myocardial pathology and developing new therapeutic approaches. Potential clinical applications of metabolic imaging include hypertensive and ischemic heart disease, heart failure, cardiac transplantation, as well as cardiomyopathies. Furthermore, response to therapeutic intervention can be monitored using metabolic imaging. Analysis of metabolic data in the past has been limited, focusing primarily on isolated metabolites. Models of myocardial metabolism, however, such as the oxygen transport and cellular energetics model and constraint-based metabolic network modeling, offer opportunities for evaluation interactions between greater numbers of metabolites in the heart. In this review, the roles of metabolic myocardial imaging and analysis of metabolic data using modeling methods for expanding our understanding of cardiac pathology are discussed. PMID:20559785

  13. Perioperative myocardial ischemia reperfusion injury.

    PubMed

    Shernan, Stanton K

    2003-09-01

    Myocardial I-R injury contributes to adverse cardiovascular outcomes after cardiac surgery. The pathogenesis of I-R injury is complex and involves the activation, coordination, and amplification of several systemic and local proinflammatory pathways (Fig. 4). Treatment and prevention of perioperative morbidity associated with myocardial I-R will ultimately require a multifocal approach. Combining preoperative risk stratification (co-morbidity and surgical complexity), minimizing initiating factors predisposing to SIRS, limiting ischemia duration, and administering appropriate immunotherapy directed toward systemic and local proinflammatory mediators of I-R injury, should all be considered. In addition, the role of the genetic-environmental interactions in the pathogenesis of cardiovascular disease is also being examined. Thus, in the near future, preoperative screening for polymorphisms of certain inflammatory and coagulation genes should inevitably help reduce morbidity by permitting the identification of high-risk cardiac surgical patients and introducing the opportunity for gene therapy or pharmacogenetic intervention [42,64]. PMID:14562561

  14. 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

  15. Protective Effects of Ultramicronized Palmitoylethanolamide (PEA-um) in Myocardial Ischaemia and Reperfusion Injury in VIVO.

    PubMed

    Di Paola, Rosanna; Cordaro, Marika; Crupi, Rosalia; Siracusa, Rosalba; Campolo, Michela; Bruschetta, Giuseppe; Fusco, Roberta; Pugliatti, Pietro; Esposito, Emanuela; Cuzzocrea, Salvatore

    2016-08-01

    Myocardial infarction is the leading cause of death, occurs after prolonged ischemia of the coronary arteries. Restore blood flow is the first intervention help against heart attack. However, reperfusion of the arteries leads to ischemia/reperfusion injury (I/R). The fatty acid amide palmitoylethanolamide (PEA) is an endogenous compound widely present in living organisms, with analgesic and anti-inflammatory properties. The present study evaluated the effect of ultramicronized palmitoylethanolamide (PEA-um) treatment on the inflammatory process associated with myocardial I/R. Myocardial ischemia reperfusion injury was induced by occlusion of the left anterior descending coronary artery for 30 min followed by 2 h of reperfusion. PEA-um, was administered (10 mg/kg) 15 min after ischemia and 1 h after reperfusion. In this study, we demonstrated that PEA-um treatment reduces myocardial tissue injury, neutrophil infiltration, adhesion molecules (ICAM-1, P-selectin) expression, proinflammatory cytokines (TNF-α, IL-1β) production, nitrotyrosine and PAR formation, nuclear factor kB expression, and apoptosis (Fas-L, Bcl-2) activation. In addition to study whether the protective effect of PEA-um on myocardial ischemia reperfusion injury is also related to the activation of PPAR-α, in a separate set of experiments it has been performed myocardial I/R in PPARα mice. Genetic ablation of peroxisome proliferator activated receptor (PPAR)-α in PPAR-αKO mice exacerbated Myocardial ischemia reperfusion injury when compared with PPAR-αWT mice. PEA-um induced cardioprotection in PPAR-α wild-type mice, but the same effect cannot be observed in PPAR-αKO mice. Our results have clearly shown a modulation of the inflammatory process, associated with myocardial ischemia reperfusion injury, following administration of PEA-um. PMID:26844976

  16. Acute care of myocardial infarction.

    PubMed Central

    Gutman, M. B.; Lee, T. F.; Gin, K.; Ho, K.

    1996-01-01

    Patients with acute myocardial infarct (AMI) need rapid diagnosis and prompt initiation of thrombolytic therapy. Patients with suspected cardiac ischemia must receive a coordinated team response by the emergency room staff including rapid electrocardiographic analysis and a quick but thorough history and physical examination to diagnose AMI. Thrombolysis and adjunct therapies should be administered promptly when indicated. The choice of thrombolytics is predicated by the location of the infarct. PMID:8754702

  17. New radiohalogenated alkenyl tellurium fatty acids

    SciTech Connect

    Srivastava, P.C.; Knapp, F.F. Jr.; Kabalka, G.W.

    1987-01-01

    Radiolabeled long-chain fatty acids have diagnostic value as radiopharmaceutical tools in myocardial imaging. Some applications of these fatty acids are limited due to their natural metabolic degradation in vivo with subsequent washout of the radioactivity from the myocardium. The identification of structural features that will increase the myocardial residence time without decreasing the heart uptake of long-chain fatty acids is of interest. Fatty acids containing the tellurium heteroatom were the first modified fatty acids developed that show unique prolonged myocardial retention and low blood levels. Our detailed studies with radioiodinated vinyliodide substituted tellurium fatty acids demonstrate that heart uptake is a function of the tellurium position. New techniques of tellurium and organoborane chemistry have been developed for the synthesis of a variety of radioiodinated iodoalkenyl tellurium fatty acids. 9 refs., 3 figs., 2 tabs.

  18. 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

  19. 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

  20. [Vectorcardiographic diagnosis of the myocardial inactivatable zone].

    PubMed

    de Micheli, A; Medrano, G A

    1989-01-01

    Clinical importance of the vectorcardiographic exploration (distant and spatial) of the myocardial electrical phenomenon is emphasized. This technique constitutes a useful integration of electrocardiographic exploration (near and analytical). The more characteristic morphological and chronological changes due to an inactivatable area are discussed in the light of ventricular myocardial depolarization. Some typical vectorcardiographic features corresponding to the presence of a myocardial inactivatable zone are presented. The utility of the complementary elements which vectorcardiography can bring to electrocardiography is emphasized. Both of these procedures integrate a rational exploration of electrical activity of the myocardium, the solid base of prognostic and therapeutic decisions in cases of myocardial infarction. PMID:2669657

  1. Myocardial perfusion imaging using contrast echocardiography.

    PubMed

    Pathan, Faraz; Marwick, Thomas H

    2015-01-01

    Microbubbles are an excellent intravascular tracer, and both the rate of myocardial opacification (analogous to coronary microvascular perfusion) and contrast intensity (analogous to myocardial blood volume) provide unique insights into myocardial perfusion. A strong evidence base has been accumulated to show comparability with nuclear perfusion imaging and incremental diagnostic and prognostic value relative to wall motion analysis. This technique also provides the possibility to measure myocardial perfusion at the bedside. Despite all of these advantages, the technique is complicated, technically challenging, and has failed to scale legislative and financial hurdles. The development of targeted imaging and therapeutic interventions will hopefully rekindle interest in this interesting modality. PMID:25817740

  2. Myocardial ischaemia during tracheal intubation and extubation.

    PubMed

    Edwards, N D; Alford, A M; Dobson, P M; Peacock, J E; Reilly, C S

    1994-10-01

    The incidence of myocardial ischaemia during tracheal intubation and extubation was compared using ambulatory ECG monitoring in 60 patients undergoing a variety of different surgical operations. Seven patients had myocardial ischaemia after tracheal intubation and seven patients during tracheal extubation. The patients who developed myocardial ischaemia during tracheal extubation had significantly greater rate-pressure products immediately before tracheal extubation (P < 0.05) and 1 min after tracheal extubation (P < 0.01) compared with those patients who did not develop myocardial ischaemia during extubation. PMID:7999498

  3. Myocardial perfusion scintigraphy: the evidence.

    PubMed

    Underwood, S R; Anagnostopoulos, C; Cerqueira, M; Ell, P J; Flint, E J; Harbinson, M; Kelion, A D; Al-Mohammad, A; Prvulovich, E M; Shaw, L J; Tweddel, A C

    2004-02-01

    This review summarises the evidence for the role of myocardial perfusion scintigraphy (MPS) in patients with known or suspected coronary artery disease. It is the product of a consensus conference organised by the British Cardiac Society, the British Nuclear Cardiology Society and the British Nuclear Medicine Society and is endorsed by the Royal College of Physicians of London and the Royal College of Radiologists. It was used to inform the UK National Institute of Clinical Excellence in their appraisal of MPS in patients with chest pain and myocardial infarction. MPS is a well-established, non-invasive imaging technique with a large body of evidence to support its effectiveness in the diagnosis and management of angina and myocardial infarction. It is more accurate than the exercise ECG in detecting myocardial ischaemia and it is the single most powerful technique for predicting future coronary events. The high diagnostic accuracy of MPS allows reliable risk stratification and guides the selection of patients for further interventions, such as revascularisation. This in turn allows more appropriate utilisation of resources, with the potential for both improved clinical outcomes and greater cost-effectiveness. Evidence from modelling and observational studies supports the enhanced cost-effectiveness associated with MPS use. In patients presenting with stable or acute chest pain, strategies of investigation involving MPS are more cost-effective than those not using the technique. MPS also has particular advantages over alternative techniques in the management of a number of patient subgroups, including women, the elderly and those with diabetes, and its use will have a favourable impact on cost-effectiveness in these groups. MPS is already an integral part of many clinical guidelines for the investigation and management of angina and myocardial infarction. However, the technique is underutilised in the UK, as judged by the inappropriately long waiting times and by

  4. Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα

    PubMed Central

    Yang, Jing

    2016-01-01

    Despite the importance of testosterone as a metabolic hormone, its effects on myocardial metabolism in the ischemic heart remain unclear. Myocardial ischemia leads to metabolic remodeling, ultimately resulting in ATP deficiency and cardiac dysfunction. In the present study, the effects of testosterone replacement on the ischemic heart were assessed in a castrated rat myocardial infarction model established by ligating the left anterior descending coronary artery 2 weeks after castration. The results of real-time PCR and Western blot analyses showed that peroxisome proliferator-activated receptor α (PPARα) decreased in the ischemic myocardium of castrated rats, compared with the sham-castration group, and the mRNA expression of genes involved in fatty acid metabolism (the fatty acid translocase CD36, carnitine palmitoyltransferase I, and medium-chain acyl-CoA dehydrogenase) and glucose transporter-4 also decreased. A decline in ATP levels in the castrated rats was accompanied by increased cardiomyocyte apoptosis and fibrosis and impaired cardiac function, compared with the sham-castration group, and these detrimental effects were reversed by testosterone replacement. Taken together, our findings suggest that testosterone can modulate myocardial metabolic remodeling by upregulating PPARα after myocardial infarction, exerting a protective effect on cardiac function. PMID:27413362

  5. Circadian rhythms in myocardial metabolism and contractile function; influence of workload and oleate

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Multiple extra-cardiac stimuli, such as workload and circulating nutrients (e.g., fatty acids), known to influence myocardial metabolism and contractile function exhibit marked circadian rhythms. The aim of the present study was to investigate whether the rat heart exhibits circadian rhythms in its ...

  6. 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.

  7. Extracellular Ubiquitin: Role in Myocyte Apoptosis and Myocardial Remodeling.

    PubMed

    Scofield, Stephanie L C; Amin, Parthiv; Singh, Mahipal; Singh, Krishna

    2015-01-01

    Ubiquitin (UB) is a highly conserved low molecular weight (8.5 kDa) protein. It consists of 76 amino acid residues and is found in all eukaryotic cells. The covalent linkage of UB to a variety of cellular proteins (ubiquitination) is one of the most common posttranslational modifications in eukaryotic cells. This modification generally regulates protein turnover and protects the cells from damaged or misfolded proteins. The polyubiquitination of proteins serves as a signal for degradation via the 26S proteasome pathway. UB is present in trace amounts in body fluids. Elevated levels of UB are described in the serum or plasma of patients under a variety of conditions. Extracellular UB is proposed to have pleiotropic roles including regulation of immune response, anti-inflammatory, and neuroprotective activities. CXCR4 is identified as receptor for extracellular UB in hematopoietic cells. Heart failure represents a major cause of morbidity and mortality in western society. Cardiac remodeling is a determinant of the clinical course of heart failure. The components involved in myocardial remodeling include-myocytes, fibroblasts, interstitium, and coronary vasculature. Increased sympathetic nerve activity in the form of norepinephrine is a common feature during heart failure. Acting via β-adrenergic receptor (β-AR), norepinephrine is shown to induce myocyte apoptosis and myocardial fibrosis. β-AR stimulation increases extracellular levels of UB in myocytes, and UB inhibits β-AR-stimulated increases in myocyte apoptosis and myocardial fibrosis. This review summarizes intracellular and extracellular functions of UB with particular emphasis on the role of extracellular UB in cardiac myocyte apoptosis and myocardial remodeling. PMID:26756642

  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. Adaptation of Myocardial Substrate Metabolism to a Ketogenic Nutrient Environment*

    PubMed Central

    Wentz, Anna E.; d'Avignon, D. André; Weber, Mary L.; Cotter, David G.; Doherty, Jason M.; Kerns, Robnet; Nagarajan, Rakesh; Reddy, Naveen; Sambandam, Nandakumar; Crawford, Peter A.

    2010-01-01

    Heart muscle is metabolically versatile, converting energy stored in fatty acids, glucose, lactate, amino acids, and ketone bodies. Here, we use mouse models in ketotic nutritional states (24 h of fasting and a very low carbohydrate ketogenic diet) to demonstrate that heart muscle engages a metabolic response that limits ketone body utilization. Pathway reconstruction from microarray data sets, gene expression analysis, protein immunoblotting, and immunohistochemical analysis of myocardial tissue from nutritionally modified mouse models reveal that ketotic states promote transcriptional suppression of the key ketolytic enzyme, succinyl-CoA:3-oxoacid CoA transferase (SCOT; encoded by Oxct1), as well as peroxisome proliferator-activated receptor α-dependent induction of the key ketogenic enzyme HMGCS2. Consistent with reduction of SCOT, NMR profiling demonstrates that maintenance on a ketogenic diet causes a 25% reduction of myocardial 13C enrichment of glutamate when 13C-labeled ketone bodies are delivered in vivo or ex vivo, indicating reduced procession of ketones through oxidative metabolism. Accordingly, unmetabolized substrate concentrations are higher within the hearts of ketogenic diet-fed mice challenged with ketones compared with those of chow-fed controls. Furthermore, reduced ketone body oxidation correlates with failure of ketone bodies to inhibit fatty acid oxidation. These results indicate that ketotic nutrient environments engage mechanisms that curtail ketolytic capacity, controlling the utilization of ketone bodies in ketotic states. PMID:20529848

  10. 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.

  11. [Ischemic myocardial metabolism and antianginal drugs].

    PubMed

    Ichihara, K

    1986-12-01

    The effect of several kinds of antianginal drugs: nitrates, coronary vasodilators, beta-adrenergic blocking agents and calcium entry blocking agents on the myocardial metabolism and myocardial acidosis during ischemia was studied in the dog heart in vivo. Ischemia was induced by ligating the left anterior descending coronary artery. Ischemia accelerated anaerobic metabolism in the myocardium, in which glycogen breakdown, accumulation of glycolytic intermediates, loss of high energy phosphate and tissue acidosis occurred. Nitroglycerin, beta-adrenergic blocking agents such as propranolol, and some calcium entry blocking agents such as diltiazem and flunarizine prevented the myocardial metabolism from shifting to an anaerobic metabolism in spite of ischemia. However, coronary vasodilators and the dihydropyridine type of calcium entry blocking agents were not capable of reducing changes in the myocardial metabolism and myocardial acidosis during ischemia. The author makes a point in the present review that all the drugs which dilate coronary artery are not always effective on the ischemic myocardium. PMID:3549484

  12. [Fibrinolysis in acute myocardial infarct].

    PubMed

    Bleifeld, W

    1987-10-24

    Fibrinolysis has opened up a new avenue in the treatment of acute myocardial infarction (AMI). In principle, the rate of reperfusion depends on the type of compound used, the mode of administration and the time between onset of symptoms and the beginning of treatment. With intracoronary streptokinase the reperfusion rate is of the order of 85%. Intravenous urokinase administered as a bolus results in a reopening rate of 50-60%; a similar rate of reperfusion is achieved with rt-PA as infusion, while i.v. streptokinase produces about 50% reopened coronary vessels. The final infarct size is decreased in 70% of patients if fibrinolysis is initiated within 2.5 hours after the onset of symptoms and followed by reopening of the occluded vessel. This results in a lowering of in-hospital mortality, which in various studies is of the order of 45-60%.- Bearing in mind the contraindications, fibrinolysis should be initiated within 3 hours. Hemodynamic improvement by a decrease of infarct size may also be achieved beyond 3 hours in large anterior myocardial infarctions and in posterior infarctions with cardiogenic shock. Early initiation of thrombolysis is of major importance in improving left ventricular function and lowering mortality following acute myocardial infarction. Therefore, prehospital thrombolytic therapy should be considered. - In the postinfarction phase coronary angiography is indicated in patients with angina at rest, stable angina of ECG signs of ischemia. In this situation transfer to a specialized cardiology division for possible percutaneous transluminal angioplasty is indicated. - Reocclusion after successful thrombolysis occurs in 20-30%, and it is therefore important to avoid reinfarction to improve the long term prognosis after AMI.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:3321420

  13. 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

  14. 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

  15. [Cardiac rehabilitation after myocardial infarction].

    PubMed

    Ghannem, M; Ghannem, L; Ghannem, L

    2015-12-01

    Although the proofs of the benefits of cardiac rehabilitation accumulate, many patients are not sent to rehabilitation units, especially younger and very elderly patients. As the length of stay in acute care units decreases, rehabilitation offers more time to fully assess the patients' conditions and needs. Meta-analyses of randomised trials suggest that mortality can be improved by as much as 20-30%. In addition, rehabilitation helps managing risk factors, including hyperlipidemia, diabetes, smoking and sedentary behaviours. Physical training also helps improving exercise capacity. Because of all of these effects, cardiac rehabilitation for post-myocardial infarction patients has been given a class IA recommendation in current guidelines. PMID:26548984

  16. 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

  17. Inhibition of carnitine synthesis protects against left ventricular dysfunction in rats with myocardial ischemia.

    PubMed

    Aoyagi, T; Sugiura, S; Eto, Y; Yonekura, K; Matsumoto, A; Yokoyama, I; Kobayakawa, N; Omata, M; Kirimoto, T; Hayashi, Y; Momomura, S

    1997-10-01

    During myocardial ischemia, inhibition of the carnitine-mediated transportation of fatty acid may be beneficial because it facilitates glucose utilization and prevents an accumulation of fatty acid metabolites. We orally administered 3-(2,2,2-trimethyl hydrazinium) propionate (MET), an inhibitor of carnitine synthesis, for 20 days to rats. Then we evaluated left ventricular (LV) function during brief ischemia by using a buffer-perfused isovolumic heart model. After 15 min of reoxygenation after the transient ischemia, LV peak systolic pressure (PSP) almost completely returned to the baseline level in rats given MET (96 +/- 4%), whereas it was only partially (77 +/- 16%) recovered in the placebo-treated rats. We induced myocardial infarction in other rats by ligating the left anterior descending coronary artery. Then the animals were given MET for 20 days, and LV function was compared. In the placebo-treated rats (with myocardial infarction, but without drug treatment), LVPSP was lower than that in the sham group [108 +/- 19 (n = 10) vs. 136 +/- 15 mm Hg (n = 13); p < 0.05], and the time constant (T) of LV pressure decay was elongated (36 +/- 4 vs. 30 +/- 7 ms; p < 0.05). In MET-treated groups, however, neither PSP nor T differed from those in the sham group. In conclusion, inhibition of the carnitine-mediated transportation of fatty acid by MET protected against left ventricular dysfunction in acute and chronic myocardial ischemia. PMID:9335406

  18. Cell therapy for myocardial infarction.

    PubMed

    Kwon, Yoo-Wook; Yang, Han-Mo; Cho, Hyun-Jai

    2010-05-01

    Ischemic heart disease, particularly acute myocardial infarction (MI), is the worldwide health care problem and the leading cause of morbidity and mortality. The fundamental treatment of MI remains a major unmet medical need. Although recent tremendous advances have been made in the treatment for acute MI such as percutaneous coronary intervention (PCI) and medical and surgical therapies, myocardial cell loss after ischemia and subsequent, adverse cardiac remodeling and heart failure are demanding for new therapeutic strategy. Since the first experimental studies of adult stem cell therapy into the ischemic heart were performed in the early 1990s, the identification and potential application of stem and/or progenitor cells has triggered attempts to regenerate damaged heart tissue and cell-based therapy is a promising option for treatment of MI. In this review, we would like to discuss the pathogenesis of acute MI, current standard treatments and their limitation, clinical results of recent stem or progenitor cell therapy which have shown a favorable safety profile with modest improvement in cardiac function, and putative mechanisms of benefits. PMID:24855535

  19. Circadian influences on myocardial infarction.

    PubMed

    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

  20. 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

  1. [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. PMID:7500263

  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. Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation and oxidative stress in rat

    PubMed Central

    Chen, Huaguo; Xu, Yongfu; Wang, Jianzhong; Zhao, Wei; Ruan, Huihui

    2015-01-01

    Baicalin belongs to glucuronic acid glycosides and after hydrolysisbaicalein and glucuronic acid come into being. It has such effects as clearing heat and removing toxicity, anti-inflammation, choleresis, bringing high blood pressure down, diuresis, anti-allergic reaction and so on. In this study, we investigated whether baicalin ameliorates isoproterenol-induced acute myocardial infarction and its mechanism. Rat model of acute myocardial infarction was induced by isoproterenol. Casein kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH), cardiac troponin T (cTnT) and infarct size measurement were used to measure the protective effect of baicalin on isoproterenol-induced acute myocardial infarction. iNOS protein expression in rat was analyzed using western blot analysis. Tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), malondialdehyde (MDA) and superoxide dismutase (SOD) and caspase-3 activation levels were explored using commercial ELISA kits. In the acute myocardial infarction experiment, baicalin effectively ameliorates the level of CK, CK-MB, LDH and cTnT, reduced infarct size in acute myocardial infarction rat model. Meanwhile, treatment with baicalin effectively decreased the iNOS protein expression, inflammatory factors and oxidative stresses in a rat model of acute myocardial infarction. However, baicalin emerged that anti-apoptosis activity and suppressed the activation of caspase-3 in a rat model of acute myocardial infarction. The data suggest that the protective effect of baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation and oxidative stress in rat. PMID:26617721

  4. 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. PMID:14740689

  5. Investigation of ischemia modified albumin, oxidant and antioxidant markers in acute myocardial infarction

    PubMed Central

    Hazini, Ahmet; Işıldak, İbrahim; Alpdağtaş, Saadet; Önül, Abdullah; Şenel, Ünal; Kocaman, Tuba; Dur, Ali; Iraz, Mustafa; Uyarel, Hüseyin

    2015-01-01

    Introduction Acute myocardial infarction (AMI) is still one of the most common causes of death worldwide. In recent years, for diagnosis of myocardial ischemia, a new parameter, called ischemia modified albumin (IMA), which is thought to be more advantageous than common methods, has been researched. Aim In this study, systematic analysis of parameters considered to be related to myocardial ischemia has been performed, comparing between control and myocardial ischemia groups. Material and methods We selected 40 patients with AMI and 25 healthy controls for this study. Ischemia modified albumin levels, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) antioxidant enzyme activities and non-enzymatic antioxidants such as retinol, α-tocopherol, β-carotene and ascorbic acid levels were investigated in both groups. Glutathione (GSH) and malondialdehyde (MDA) levels, which are indicators of oxidative stress, were compared between patient and control groups. Results Ischemia modified albumin levels were found significantly higher in the AMI diagnosed group when compared with controls. The MDA level was elevated in the patient group, whereas the GSH level was decreased. SOD, GPx and CAT enzyme levels were decreased in the patient group, where it could be presumed that oxidative stress causes the cardiovascular diseases. Conclusions Due to the increased oxidative stress, non-enzymatic and enzymatic antioxidant capacity was affected. Systematic investigation of parameters related to myocardial infarction has been performed, and it is believed that such parameters can contribute to protection and early diagnosis of AMI and understanding the mechanism of development of the disease. PMID:26677379

  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. 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

  8. Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

    PubMed Central

    de Campos, Dijon Henrique Salomé; Leopoldo, André Soares; Lima-Leopoldo, Ana Paula; do Nascimento, André Ferreira; de Oliveira-Junior, Silvio Assis; da Silva, Danielle Cristina Tomaz; Sugizaki, Mario Mateus; Padovani, Carlos Roberto; Cicogna, Antonio Carlos

    2014-01-01

    Background Obesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished. Objective Study the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity. Methods 30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway. Results Compared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C. Conclusion The energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle. PMID:25352507

  9. SPECT Myocardial Blood Flow Quantitation Concludes Equivocal Myocardial Perfusion SPECT Studies to Increase Diagnostic Benefits.

    PubMed

    Chen, Lung-Ching; Lin, Chih-Yuan; Chen, Ing-Jou; Ku, Chi-Tai; Chen, Yen-Kung; Hsu, Bailing

    2016-01-01

    Recently, myocardial blood flow quantitation with dynamic SPECT/CT has been reported to enhance the detection of coronary artery disease in human. This advance has created important clinical applications to coronary artery disease diagnosis and management for areas where myocardial perfusion PET tracers are not available. We present 2 clinical cases that undergone a combined test of 1-day rest/dipyridamole-stress dynamic SPECT and ECG-gated myocardial perfusion SPECT scans using an integrated imaging protocol and demonstrate that flow parameters are capable to conclude equivocal myocardial perfusion SPECT studies, therefore increasing diagnostic benefits to add value in making clinical decisions. PMID:26053731

  10. Ventricular Aneurysm Following Myocardial Infarction

    PubMed Central

    Walters, M. B.

    1966-01-01

    Cineradiographic examination appears to be the best method for the study of cardiac pulsations. Fifty consecutive patients, who had sustained transmural myocardial infarction at least six months previously, were studied by this technique. Thirty-six had some abnormality of pulsation and eight had dynamic ventricular aneurysm. Six of the eight had suffered severe infarct. Functional recovery in those with aneurysm was not as complete as in the rest of the group. Two made a poor functional recovery, two a fair recovery, and four a moderately good recovery. Clinically, there were no systemic emboli in the patients with dynamic aneurysms. Five of the 50 had persistent ST-segment elevation and “coving” of the T waves; three of these patients had aneurysms. There was no good correlation between the electrocardiographic site of the infarct and the site of the abnormal pulsation. ImagesFig. 1 PMID:5928534

  11. 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

  12. [Thrombolytic treatment of acute myocardial infarct. 1].

    PubMed

    Soares-Costa, J T; Soares-Costa, T J; Gabriel, H M

    1998-05-01

    I-Rationale of thrombolytic therapy in acute myocardial infarction (AMI). II-Thrombolytic drugs. III-Effects of thrombolytic therapy on mortality. IV-Studies comparing the effects of various thrombolytic agents on mortality. PMID:9951051

  13. Repetitive Myocardial Infarctions Secondary to Delirium Tremens

    PubMed Central

    Schwartzberg, David; Shiroff, Adam

    2014-01-01

    Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal. PMID:25197580

  14. Repetitive myocardial infarctions secondary to delirium tremens.

    PubMed

    Schwartzberg, David; Shiroff, Adam

    2014-01-01

    Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal. PMID:25197580

  15. Myocardial hypoperfusion on conventional contrast computed tomography.

    PubMed

    Ching, Shing; Chung, Tak Shun

    2015-10-01

    Non–electrocardiogram (ECG)–gated contrast computed tomography (CT) is commonly performed to exclude aortic dissection in chest pain patients. Besides evaluating the aorta for dissection flap, attention should be paid to the myocardium for areas of hypoenhancement that may suggest ischemia. Current models of multidetector CT enable assessment of myocardial perfusion with minimal motion artifact even without ECG gating. Transmural hypoenhancement with preserved wall thickness in a coronary distribution is highly specific for acute myocardial infarction. We report 2 cases of acute chest pain with initial nondiagnostic studies that underwent CT aortogram to exclude dissection. Instead, the CT showed myocardial hypoenhancement in left anterior descending artery territory. Myocardial hypoenhancement occurred before ST-segment elevation on ECG, suggesting that recognition of this important finding may lead to earlier revascularization decisions. PMID:26321167

  16. 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

  17. Prompt recognition and percutaneous coronary intervention leads to favorable myocardial recovery after ST-segment elevation myocardial infarction secondary to acute promyelocytic leukemia: pediatric case report.

    PubMed

    Thomas, Tamara O; Ramachandran, Preeti; Jefferies, John L; Beekman, Robert H; Hor, Kan; Lorts, Angela

    2013-01-01

    Acute myocardial infarction (AMI) is extremely rare in children, and unlike the adult disease, the etiology of the infarction is rarely due to atherosclerotic coronary disease. This unique reported case involved a 15-year-old boy with severe chest pain who presented with an ST-segment-elevation myocardial infarction secondary to in situ thrombus formation in the left anterior descending (LAD) coronary artery. The initial electrocardiogram (ECG) had a Q-wave pattern in V6 and ST depression in the inferior leads with ST-segment elevation in reciprocal leads. The cardiac enzymes and routine labs showed evidence of myocardial damage. The boy was urgently taken to the cardiac catheterization laboratory for percutaneous coronary intervention, where complete occlusion of the LAD was found and successfully stented. Eventually, a peripheral blood smear showed pancytopenia with 38 % hypergranular blast-like cells consistent with acute myeloid leukemia (AML), and chemotherapy with all-transretinoic acid was implemented. This first pediatric case report of an AML-associated AMI emphasizes the benefit resulting from expedient reperfusion of the ischemic myocardium by quick reestablishment of coronary perfusion. It also emphasizes the limitations of existing noninvasive technologies in detecting myocardial viability. PMID:23263162

  18. [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

  19. Myocardial perfusion imaging with 201Tl.

    PubMed

    Pagnanelli, Robert A; Basso, Danny A

    2010-03-01

    The object of this review is to provide information about (201)Tl-thallous chloride in radionuclide myocardial perfusion imaging. This technique has experienced a recent resurgence because of the shortage of (99m)Tc. After reading this article, the technologist will be able to describe the properties and uptake mechanism of (201)Tl, the procedure for myocardial perfusion imaging with this agent, and the advantages and disadvantages of thallium, compared with the technetium agents. PMID:20159930

  20. 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.

  1. 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

  2. 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

  3. Myocardial Sleeve Tissues in Surgical Lung Specimens.

    PubMed

    Yoshida, Akihiko; Kamata, Tsugumasa; Iwasa, Takeshi; Watanabe, Shun-ichi; Tsuta, Koji

    2015-10-01

    Left atrial myocardial extensions over the pulmonary veins (PVs), known as myocardial sleeves, are present in the physiological anatomy of most individuals. Although this structure has recently received clinical attention as a major origin of paroxysmal atrial fibrillation (AF), it has not been documented in surgical specimens. Here, we examine incidentally identified myocardial sleeve tissue in routinely processed lung resection specimens to determine its incidence and diagnostic implications. Among 694 lung resection specimens with evaluable PV margins, myocardial sleeve tissue was identified in 26 cases (3.7%). The tissue was located within the adventitia of the PVs, mostly in margin preparations, and existed outside the pericardium in the majority of cases. Carcinoma infiltration of the sleeves was evident in 6 cases. No heart injuries were observed, and no tumors invaded the heart. Preoperative electrocardiography showed sinus rhythm in all cases, whereas postoperative monitoring revealed sinus rhythm in all patients except one who showed AF and flutter. Myocardial sleeve tissue is an underrecognized incidental finding in lung resection specimens, and it is not indicative of heart injury. Cancer infiltration into this tissue indicates neither heart invasion nor, by itself, invasion into the pericardium. Although surgical transection of the myocardial sleeve did not evoke immediate arrhythmia in most cases, the overall influence of this procedure on the postsurgical risk of AF remains to be determined in further studies involving extensive rhythm assessment. PMID:26099012

  4. Myocardial Dysfunction and Shock after Cardiac Arrest

    PubMed Central

    Jentzer, Jacob C.; Chonde, Meshe D.; Dezfulian, Cameron

    2015-01-01

    Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies. PMID:26421284

  5. Myocardial Fat Accumulation Is Independent of Measures of Insulin Sensitivity

    PubMed Central

    Noureldin, Radwa; Ouwerkerk, Ronald; Liu, Elizabeth Y.; Madan, Ritu; Abel, Brent S.; Mullins, Katherine; Walter, Mary F.; Skarulis, Monica C.; Gharib, Ahmed M.

    2015-01-01

    Background: Myocardial steatosis, an independent predictor of diastolic dysfunction, is frequently present in type 2 diabetes mellitus. High free fatty acid flux, hyperglycemia, and hyperinsulinemia may play a role in myocardial steatosis. There are no prior studies examining the relationship between insulin sensitivity (antilipolytic and glucose disposal actions of insulin) and cardiac steatosis. Objective: Using a cross-sectional study design of individuals with and without metabolic syndrome (MetSyn), we examined the relationships between cardiac steatosis and the sensitivity of the antilipolytic and glucose disposal actions of insulin. Methods: Pericardial fat (PF) volume, intramyocardial and hepatic fat (MF and HF) content, visceral fat (VF) and sc fat content were assessed by magnetic resonance imaging in 77 subjects (49 without MetSyn and 28 with MetSyn). In a subset of the larger cohort (n = 52), peripheral insulin sensitivity index (SI) and adipocyte insulin sensitivity (Adipo-SI) were determined from an insulin-modified frequently sampled iv glucose tolerance test. The Quantitative Insulin Sensitivity Check Index was used as a surrogate for hepatic insulin sensitivity. Results: Individuals with the MetSyn had significantly higher body mass index, total body fat, and MF, PF, HF, and VF content. HF and VF, but not MF, were negatively correlated with the Quantitative Insulin Sensitivity Check Index, Adipo-SI, and SI. Stepwise regression revealed that waist circumference and serum triglyceride levels independently predicted MF and PF, respectively. Adipo-SI and serum triglyceride levels independently predict HF. Conclusion: Myocardial steatosis is unrelated to hepatic, adipocyte, or peripheral insulin sensitivity. Although it is frequently observed in insulin-resistant subjects, further studies are necessary to identify and delineate pathogenic mechanisms that differentially affect cardiac and hepatic steatosis. PMID:26020762

  6. Apelin-13 protects against myocardial infarction-induced myocardial fibrosis.

    PubMed

    Zhang, Xuemin; Hu, Wenyu; Feng, Feng; Xu, Jian; Wu, Fang

    2016-06-01

    Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensin II receptor-like 1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarction‑induced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin‑13 during myocardial infarction‑induced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin‑13. Apelin‑13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Masson's trichrome staining and western blotting showed that apelin‑13 attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzyme‑linked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin‑13 inhibited the activation of nuclear factor (NF)‑κB signaling in vitro and in vivo. To the best of our knowledge, the present study was the first to demonstrate that apelin‑13 may attenuate myocardial infarction‑induced myocardial fibrosis, and that this protective function may be mediated by inhibition of NF‑κB signaling. The present study suggests a theoretical basis for the effects of apelin‑13 and provides insight into the potential clinical application of apelin-13. PMID:27109054

  7. Clinical experience with technetium-99m teboroxime, a neutral, lipophilic myocardial perfusion imaging agent

    SciTech Connect

    Johnson, L.L.; Seldin, D.W. )

    1990-10-16

    Technetium-99m (Tc-99m) teboroxime is a new technetium-based myocardial perfusion imaging agent (investigational code = SQ30217 (Cardiotec, Squibb Diagnostics)). A member of a class of neutral, lipophilic, technetium-containing complexes known as boronic acid adducts of technetium dioxime (BATO) complexes, this agent is chemically very different from the cationic tracer thallium-201 (Tl-201) and from the cationic technetium complex Tc-99m sestamibi (Cardiolite, Du Pont Imaging Agents). Tc-99m teboroxime has high myocardial extraction, rapid blood clearance, little lung uptake and rapid myocardial washout. A biexponential pattern of myocardial washout is demonstrated in animals and in man. Effective half-lives of the 2 washout components in man are 5.2 minutes and 3.8 hours and represent approximately 66 and 33% of the myocardial activity, respectively. The first half-life for the myocardium is approximately 11 minutes. As the agent washes out of the heart, hepatic uptake occurs, peaking at about 5 minutes after injection. The liver is the major organ of excretion and receives, along with the large bowel, the largest radiation dose. Rapid imaging protocols using standard cameras have achieved good myocardial counts from 3 planar views acquired over a 4- to 5-minute period or for single photon emission computed tomography (SPECT) images acquired over a 10-minute period. An entire stress/rest procedure can be completed in 1 hour. Analysis of data from 155 patients from 4 centers using planar or SPECT imaging showed a sensitivity and specificity for blinded readings of 82 and 91%, respectively, when compared against overall clinical impression. 13 references.

  8. A vesicular sequestration to oxidative deamination shift in myocardial sympathetic nerves in Parkinson's disease.

    PubMed

    Goldstein, David S; Sullivan, Patricia; Holmes, Courtney; Miller, Gary W; Sharabi, Yehonatan; Kopin, Irwin J

    2014-10-01

    In Parkinson's disease (PD), profound putamen dopamine (DA) depletion reflects denervation and a shift from vesicular sequestration to oxidative deamination of cytoplasmic DA in residual terminals. PD also involves cardiac sympathetic denervation. Whether PD entails myocardial norepinephrine (NE) depletion and a sequestration-deamination shift have been unknown. We measured apical myocardial tissue concentrations of NE, DA, and their neuronal metabolites 3,4-dihydroxyphenylglycol (DHPG), and 3,4-dihydroxyphenylacetic acid (DOPAC) from 23 PD patients and 23 controls and ascertained the extent of myocardial NE depletion in PD. We devised, validated in VMAT2-Lo mice, and applied 5 neurochemical indices of the sequestration-deamination shift-concentration ratios of DOPAC:DA, DA:NE, DHPG:NE, DOPAC:NE, and DHPG:DOPAC-and used a kinetic model to estimate the extent of the vesicular storage defect. The PD group had decreased myocardial NE content (p < 0.0001). The majority of patients (70%) had severe NE depletion (mean 2% of control), and in this subgroup all five indices of a sequestration-deamination shift were increased compared to controls (p < 0.001 for each). Vesicular storage in residual nerves was estimated to be decreased by 84-91% in this subgroup. We conclude that most PD patients have severe myocardial NE depletion, because of both sympathetic denervation and decreased vesicular storage in residual nerves. We found that the majority (70%) of Parkinson's disease (PD) patients have profound (98%) myocardial norepinephrine depletion, because of both cardiac sympathetic denervation and a shift from vesicular sequestration to oxidative deamination of cytoplasmic catecholamines in the residual nerves. This shift may be part of a final common pathogenetic pathway in the loss of catecholaminergic neurons that characterizes PD. PMID:24848581

  9. Myocardial infarction in young men. Study of risk factors in nine countries.

    PubMed Central

    Dolder, M A; Oliver, M F

    1975-01-01

    In order to determine whether the development of myocardial infarction in different countries is associated with different risk factors, 240 male survivors, aged 40 or less, were studied in nine countries. In the seven centres in developed countries (Auckland, Melbourne, Los Angles/Atlanta, Cape Town, Tel Avic, Heidelberg, and Edinburgh) there was a high procedure of risk factors, particularly of hyperlipidaemia and cigarette smoking. The prevalence of hypertension, obesity, hyperglycaemia, and hyperuricaemia varied from centre to centre. Risk factors were less prevalent in Bombay and Singapore: the most common risks operating in Bombay seemed to be cigarette smoking and hyperglycaemia, while in Singpore cigarette smoking was the commonest. The mean age of the whole group was 35.4 years. Serum cholesterol levels of 7.25 mmol/l (280 mg/dl) or more were present in 25 per cent of all patients, serum triglyceride levels of 2.26 mmol/l )l200 mg/dl) or more in 35 per cent. 80 per cent of the patients were smokers, and 15 per cent were either for hypertension before myocardial infarction or had a raised blood pressure after myocardial infarction. Obesity was found in 19 per cent of all patients and serum uric acid levels over 0.5 mmol/l (8.5 mg/dl) in 17 per cent. 10 per cent of all patients were either treated for diabetes mellitus before myocardial infarction or showed an abnormal glucose tolerance after myocardial infarction. This collaborative study may help, by showing differences in the prevalence of risk factors, to indicate to each centre and to national and to international organizations, the direction for their future studies into the causation and prevention of myocardial infarction in young men. PMID:1137658

  10. 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.

  11. 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.

  12. 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.

  13. Growth, fatty acid profile in major lipid classes and lipid fluidity of Aurantiochytrium mangroveiSK-02 As a function of growth temperature

    PubMed Central

    Chodchoey, Kanokwan; Verduyn, Cornelis

    2012-01-01

    Aurantiochytrium mangrovei Sk-02 was grown in a medium containing glucose (40 g/l), yeast extract (10 g/L) and sea salts (15 g/L) at temperatures ranging from 12 to 35°C. The fastest growth (µmax= 0.15 h-1) and highest fatty acid content of 415 mg/g-dry cell weight were found in the cells grown at 30°C. However, the cells grown at 12°C showed the highest percentage of polyunsaturated fatty acid (PUFA) (48.6% of total fatty acid). The percentage of docosahexaenoic acid (DHA) and pentadecanoic acid (C15:0) decreased with an increase in the growth temperature, whereas, palmitic acid (C16:0), stearic acid (C18:0) and DPA (C22:5n6) increased with an increase in the growth temperature. The composition of the major lipid class (%w/w) was slightly affected by the growth temperature. The fluidity of the organelle membrane or intracellular lipid (by DPH measurement) decreased with an increase in the growth temperatures, while the plasma membrane fluidity (by TMA-DPH measurement) could still maintain its fluidity in a wide range of temperatures (15 - 37°C). Furthermore, the distribution of DHA was found to be higher (36 – 54%) in phospholipid (PL) as compared to neutral lipid (NL) (20 - 41%). PMID:24031817

  14. Myocardial imaging with a radioiodinated norepinephrine storage analog

    SciTech Connect

    Wieland, D.M.; Brown, L.E.; Rogers, W.L.; Worthington, K.C.; Wu, J.L.; Clinthorne, N.H.; Otto, C.A.; Swanson, D.P.; Beierwaltes, W.H.

    1981-01-01

    Meta-iodobenzylguanidine (M-IBG), an iodinated aromatic analog of the hypotensive drug guanethidine, localizes in the heart of the rat, dog, and rhesus monkey. A comparative study of tissue distribution in the dog has been performed with five myocardiophilic agents: thallium-201, I-125 16-iodohexadecanoic acid, H-3 norepinephrine, C-14 guanethidine and I-125 M-IBG. The last two compounds give heart concentrations and heart-to-blood concentration ratios similar to those of thallium-201. Planar and tomographic images of the hearts of the dog and rhesus monkey were obtained using I-131 or I-123 labeled M-IBG. Blocking studies with reserpine suggest that a major component of myocardial retention of M-IBG is sequestration within the norepinephrine storage vesicles of the adrenergic nerves. The localization of M-IBG in other organs with rich sympathetic innervation and the relative insensitivity of myocardial uptake to a wide range of loading doses lend additional support for a neuronal mode of retention.

  15. Immunological results in myocardial diseases.

    PubMed Central

    Bolte, H. D.; Schultheiss, P.

    1978-01-01

    Immunological studies have shown new diagnostically important changes in alcoholic and viral myocarditis, as well as in congestive cardiomyopathy. Increased heart size correlated with the degree of congestive heart failure, as well as with negative immunofluorescence and an increased IgA concentration in the serum. These findings may serve as a diagnostic aid in patients with myocardial disease due to alcohol abuse. Viral heart disease is characterized by a variety of symptoms and nuclear antibodies (IgM) can be of help in the differential diagnosis. Heart muscle tissue of patients with congestive cardiomyopathy preferentially binds IgG and IgA. In addition to the other changes these findings are of diagnostic importance. It seems likely that results similar to those obtained for humoral antibodies in congestive cardiomyopathy will apply in the correlation of the haemodynamic status of the patients. The pathophysiological implication of these findings is not clear at present, but the evolution of congestive cardiomyopathy appears to be associated with binding of immunoglobulin to the myocardium, as well as with humoral antiheart antibodies. PMID:704517

  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. PMID:26150284

  17. 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

  18. 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

  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. The effect of fatty acid surfactants on the uptake of ozone to aqueous halogenide particles

    NASA Astrophysics Data System (ADS)

    Rouvière, A.; Ammann, M.

    2010-06-01

    The reactive uptake of ozone to deliquesced potassium iodide aerosol particles coated with linear saturated fatty acids (C9, C12, C15, C18 and C20) as surfactants was studied. The experiments were performed in an aerosol flow tube at 293 K and atmospheric pressure. The uptake coefficient on pure deliquesced KI aerosol was γ=(1.10±0.20)×10-2 at 72-75% relative humidity. In presence of organic coatings, the uptake coefficient decreased significantly for long straight chain surfactants (>C15), while it was only slightly reduced for the short ones (C9, C12). We linked the kinetic results to the monolayer properties of the surfactants, and specifically to the phase state of the monolayer formed (liquid expanded or liquid condensed state). We also investigated the effect of organic films to mixed deliquesced aerosol composed of a variable mixture of KI and NaCl, which allowed determining the resistance exerted to O3 at the aqueous surface by the two longer chained surfactants pentadecanoic acid (C15) and stearic acid (C18). Finally, the effect of two-component coatings, consisting of a mixture of long and short chained surfactants, was also studied.

  1. Kinetics of /sup 13/N-ammonia uptake in myocardial single cells indicating potential limitations in its applicability as a marker of myocardial blood flow

    SciTech Connect

    Rauch, B.; Helus, F.; Grunze, M.; Braunwell, E.; Mall, G.; Hasselbach, W.; Kuebler, W.

    1985-02-01

    To study kinetics and principles of cellular uptake of /sup 13/N-ammonia, a marker of coronary perfusion in myocardial scintigraphy, heart muscle cells of adult rats were isolated by perfusion with collagenase and hyaluronidase. Net uptake of /sup 13/N, measured by flow dialysis, reached equilibrium within 20 sec in the presence of sodium bicarbonate and carbon dioxide (pH 7.4, 37 degrees C). Total extraction, 80 sec after the reaction start, was 786 +/- 159 mumol/ml cell volume. Cells destroyed by calcium overload were unable to extract /sup 13/N-ammonia. Omission of bicarbonate and carbon dioxide reduced total extraction to 36% of control. /sup 13/N-Ammonia uptake could also be reduced by 50 muM 4,4' diisothiocyanostilbene 2,2' disulfonic acid, by 100 micrograms/ml 1-methionine sulfoximine, and by preincubation with 5 muM free oleic acid. These results indicate that in addition to metabolic trapping by glutamine synthetase, the extraction of /sup 13/N-ammonia by myocardial cells is influenced by cell membrane integrity, intracellular-extracellular pH gradient, and possibly an anion exchange system for bicarbonate. For this reason, the uptake of /sup 13/N-ammonia may not always provide a valid measurement of myocardial perfusion.

  2. Myocardial infarction size: measurement and modification

    PubMed Central

    Cairns, John A.

    1977-01-01

    The majority of in-hospital deaths from acute myocardial infarction occur as a result of the “power failure” syndrome (severe congestive heart failure and cardiogenic shock), which results from extensive loss of myocardium. The death of myocardial cells is sequential over many hours. Surrounding the central zone of necrosis in an acute myocardial infarction is a zone of ischemic myocardium whose fate might be altered by interventions during the early phase of the infarction. ST-segment mapping, serial measurement of the serum concentration of creatine phosphokinase and myocardial imaging by means of radionuclides are being developed for the noninvasive assessment of infarct size in animals and humans. A number of interventions appear to limit infarct size in animals. There have been relatively few studies in humans to date, but preliminary results suggest that infarct size might be limited by certain interventions. The research has provided important practical benefits in terms of understanding the course of acute myocardial infarction and the potential effects of conventional therapies. For the present, interventions designed to limit infarct size remain in the realm of clinical research; routine clinical use would be inappropriate. PMID:69481

  3. Contemporary perspective on endogenous myocardial regeneration

    PubMed Central

    Milasinovic, Dejan; Mohl, Werner

    2015-01-01

    Considering the complex nature of the adult heart, it is no wonder that innate regenerative processes, while maintaining adequate cardiac function, fall short in myocardial jeopardy. In spite of these enchaining limitations, cardiac rejuvenation occurs as well as restricted regeneration. In this review, the background as well as potential mechanisms of endogenous myocardial regeneration are summarized. We present and analyze the available evidence in three subsequent steps. First, we examine the experimental research data that provide insights into the mechanisms and origins of the replicating cardiac myocytes, including cell populations referred to as cardiac progenitor cells (i.e., c-kit+ cells). Second, we describe the role of clinical settings such as acute or chronic myocardial ischemia, as initiators of pathways of endogenous myocardial regeneration. Third, the hitherto conducted clinical studies that examined different approaches of initiating endogenous myocardial regeneration in failing human hearts are analyzed. In conclusion, we present the evidence in support of the notion that regaining cardiac function beyond cellular replacement of dysfunctional myocardium via initiation of innate regenerative pathways could create a new perspective and a paradigm change in heart failure therapeutics. Reinitiating cardiac morphogenesis by reintroducing developmental pathways in the adult failing heart might provide a feasible way of tissue regeneration. Based on our hypothesis “embryonic recall”, we present first supporting evidence on regenerative impulses in the myocardium, as induced by developmental processes. PMID:26131310

  4. 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

  5. Depression Increases Sympathetic Activity and Exacerbates Myocardial Remodeling after Myocardial Infarction: Evidence from an Animal Experiment

    PubMed Central

    Liu, Tao; Yuan, Xiaoran; Ruan, Bing; Sun, Lifang; Tang, Yanhong; Yang, Bo; Hu, Dan; Huang, Congxin

    2014-01-01

    Depression is an independent risk factor for cardiovascular events and mortality in patients with myocardial infarction (MI). Excessive sympathetic activation and serious myocardial remodeling may contribute to this association. The aim of this study was to discuss the effect of depression on sympathetic activity and myocardial remodeling after MI. Wild-type (WT) rats were divided into a sham group (Sham), a myocardial infarction group (MI), a depression group (D), and a myocardial infarction plus depression group (MI+D). Compared with controls, the MI+D animals displayed depression-like behaviors and attenuated body weight gain. The evaluation of sympathetic activity showed an increased level in plasma concentrations of epinephrine and norepinephrine and higher expression of myocardial tyrosine hydroxylase in the MI+D group than the control groups (p<0.05 for all). Cardiac function and morphologic analyses revealed a decreased fractional shortening accompanied by increased left ventricular dimensions, thinning myocardium wall, and reduced collagen repair in the MI+D group compared with the MI group (p<0.05 for all). Frequent premature ventricular contractions, prolonged QT duration and ventricular repolarization duration, shorted effective refractory period, and increased susceptibility to ventricular arrhythmia were displayed in MI+D rats. These results indicate that sympathetic hyperactivation and exacerbated myocardial remodeling may be a plausible mechanism linking depression to an adverse prognosis after MI. PMID:25036781

  6. 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.

  7. 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.

  8. 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

  9. Fabrication of electrospun poly (lactide-co-glycolide)-fibrin multiscale scaffold for myocardial regeneration in vitro.

    PubMed

    Sreerekha, Perumcherry Raman; Menon, Deepthy; Nair, Shantikumar V; Chennazhi, Krishna Prasad

    2013-04-01

    Myocardial tissue engineering is one of the most promising treatment strategies to restore heart function after a massive heart attack. The biomaterials, cells, and scaffold design play important roles in engineering of heart tissue. In this study, we have developed a fibrin-based multiscale electrospun composite scaffold for myocardial regeneration. Fibrin is the natural wound-healing matrix having angiogenic potential and comprehensively used for tissue engineering applications. It provides a natural environment for cell attachment, migration, and proliferation. Morphological, chemical, and mechanical characterization of the scaffolds was done by scanning electron microscopy, fibrin-specific phosphotungstic acid hematoxylin staining, and mechanical testing. The fiber diameters of fibrin nanofibers range from 50 to 300 nm and that of poly (lactide-co-glycolide) microfibers range from 2 to 4 μm, which mimics the structural hierarchy of native myocardial tissue. Our results indicate that this scaffold enhances the differentiation of mesenchymal stem cells into cardiomyocytes. The cardiac phenotype of the cells was confirmed by the presence of cardiac-specific proteins like α-sarcomeric actinin, troponin, tropomyosin, desmin, and atrial natriuretic peptide Estimation of D-Dimer in the culture supernatant for 2 weeks and analysis of scaffold for 3 weeks of in vitro culture of cardiomyocytes indicated the degradation of fibrin and presence of newly synthesized collagen respectively. Our results demonstrate the promising potential of this scaffold for myocardial tissue engineering applications. PMID:23083104

  10. [Ventricular Septal Perforation after Inferior Myocardial Infarction].

    PubMed

    Sato, Hisashi; Nakayama, Yoshihiro; Tanaka, Hideya; Takahashi, Baku

    2016-07-01

    We report a rare case of ventricular septal perforation (VSP) after inferior myocardial infarction. Surgical repair of VSP after inferior infarction is technically difficult because of its anatomical location. An 81-year-old female presented with dyspnea on the 8th day after percutaneous coronary intervention for acute inferior myocardial infarction. Echocardiography revealed a ventricular septal perforation. Urgent operation was performed. There was a VSP around the base of the ventricular septum. The myocardial infarction extended to the adjacent muscle of the mitral valve annulus. Two bovine pericardial patches were used in the left ventricular cavity. The patches were sewn on the mitral valve annulus which was the only normal tissue in the region. The 1st patch was used to close the VSP directly, and the 2nd patch was sutured to the normal myocardium to exclude the infracted area. No residual shunt flow was observed. The postoperative course was uneventful. PMID:27365060

  11. Myocardial infarction--fusion or confusion?

    PubMed

    Ardhanari, Sivakumar; Shah, Ashok J; Thakur, Ranjan K

    2009-09-01

    A patient with a dualchamber pacemaker with dynamic atrioventricular delay (AVD) experienced acute substernal chest pain. The rhythm strip in the ambulance showed intermittent ST elevation in the inferior leads. An emergent cardiac catheterization revealed nonobstructive coronary artery disease. Rate-responsive dual-chamber pacing with dynamic AVD was responsible for varying devvgrees of ventricular fusion due to competition with the patient's normal conduction. Intermittent ST elevation, evident only during ventricular fusion should have suggested secondary ventricular repolarization and not myocardial injury, but concomitant chest pain and inconspicuous bipolar pacing artifacts added to the confusion. Ventricular pacing may not only mask acute ST-T changes due to myocardial injury, but can also mimic acute myocardial infarction. PMID:19726827

  12. 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.

  13. [Recurrent myocardial infarctions: specific changes in biomarkers and in myocardial remodeling (case-control study)].

    PubMed

    Volkova, E G; Malykhina, O P; Levashov, S Iu

    2007-01-01

    Basing on a case-control study (n=81) with the use of standard methods of myocardial infarction verification, examination of hemogram, troponin T, C-reactive protein, echocardiography data it was established that markers of myocardial infarction (troponin T level) and inflammation (C reactive protein level, lymphopenia) during recurrent infarctions are less pronounced than during first infarctions. Remodeling in recurrent infarctions had the following specific characteristics: increase of left ventricular end diastolic dimension, myocardial mass index, diastolic dysfunction and stroke volume with unchanged ejection fraction. PMID:18260891

  14. Fatty acid uptake in normal human myocardium

    SciTech Connect

    Vyska, K.; Meyer, W.; Stremmel, W.; Notohamiprodjo, G.; Minami, K.; Machulla, H.J.; Gleichmann, U.; Meyer, H.; Koerfer, R. )

    1991-09-01

    Fatty acid binding protein has been found in rat aortic endothelial cell membrane. It has been identified to be a 40-kDa protein that corresponds to a 40-kDa fatty acid binding protein with high affinity for a variety of long chain fatty acids isolated from rat heart myocytes. It is proposed that this endothelial membrane fatty acid binding protein might mediate the myocardial uptake of fatty acids. For evaluation of this hypothesis in vivo, influx kinetics of tracer-labeled fatty acids was examined in 15 normal subjects by scintigraphic techniques. Variation of the plasma fatty acid concentration and plasma perfusion rate has been achieved by modulation of nutrition state and exercise conditions. The clinical results suggest that the myocardial fatty acid influx rate is saturable by increasing fatty acid plasma concentration as well as by increasing plasma flow. For analysis of these data, functional relations describing fatty acid transport from plasma into myocardial tissue in the presence and absence of an unstirred layer were developed. The fitting of these relations to experimental data indicate that the free fatty acid influx into myocardial tissue reveals the criteria of a reaction on a capillary surface in the vicinity of flowing plasma but not of a reaction in extravascular space or in an unstirred layer and that the fatty acid influx into normal myocardium is a saturable process that is characterized by the quantity corresponding to the Michaelis-Menten constant, Km, and the maximal velocity, Vmax, 0.24 {plus minus} 0.024 mumol/g and 0.37 {plus minus} 0.013 mumol/g(g.min), respectively. These data are compatible with a nondiffusional uptake process mediated by the initial interaction of fatty acids with the 40-kDa membrane fatty acid binding protein of cardiac endothelial cells.

  15. 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

  16. 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

  17. 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.

  18. 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

  19. Molecular and cellular mechanisms of myocardial stunning.

    PubMed

    Bolli, R; Marbán, E

    1999-04-01

    The past two decades have witnessed an explosive growth of knowledge regarding postischemic myocardial dysfunction or myocardial "stunning." The purpose of this review is to summarize current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single entity but rather as a "syndrome" that has been observed in a wide variety of experimental settings, which include the following: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after multiple, completely reversible episodes of regional ischemia in vivo; 3) stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; and 6) stunning after exercise-induced ischemia (high-flow ischemia). Whether these settings share a common mechanism is unknown. Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals (oxyradical hypothesis) and by a transient calcium overload (calcium hypothesis) on reperfusion. The final lesion responsible for the contractile depression appears to be a decreased responsiveness of contractile filaments to calcium. Recent evidence suggests that calcium overload may activate calpains, resulting in selective proteolysis of myofibrils; the time required for resynthesis of damaged proteins would explain in part the delayed recovery of function in stunned myocardium. The oxyradical and calcium hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, increased free radical formation could cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a

  20. Hemodialysis-Induced Myocardial Stunning: A Review.

    PubMed

    Brown, Maxine; Burrows, LaVonne; Pruett, Timothy; Burrows, Thaddeus

    2015-01-01

    Patients on hemodialysis have a high incidence of cardiac morbidity and mortality, and echocardiographic evidence of hemodialysis-related myocardial stunning supports a potential link between the hemodialysis treatment itself and cardiac sequelae. Fluid removal rates exceeding 13 mL/kg/hour during hemodialysis have been implicated in the development of myocardial stunning. Providers caring for patients on chronic hemodialysis might improve patient outcomes by the use of modified treatment monitoring methods, alternative dialysis delivery methods, and enhanced patient education regarding risks of excessive interdialytic weight gains. PMID:26290919

  1. Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

    PubMed Central

    Regan, Timothy J.; Khan, Mohammad I.; Ettinger, Philip O.; Haider, Bunyad; Lyons, Michael M.; Oldewurtel, Henry A.; Weber, Marilyn

    1974-01-01

    In view of the variables that obscure the pathogenesis of cardiomyopathy, a study was undertaken in mongrel dogs fed ethanol as 36% of calories for up to 22 mo. Both the experimental and control groups maintained body weight, hematocrit, plasma vitamin, and protein levels. Left ventricular function was evaluated in the intact anesthetized dog using indicator dilution for end-diastolic and stroke volume determinations. During increased afterload with angiotensin, the ethanol group exhibited a larger rise of end-diastolic pressure (P<0.01), whereas end-diastolic and stroke volume responses were significantly less than in controls. Preload increments with saline elicited a significantly higher end-diastolic pressure rise in the ethanol group (P<0.01). No hypertrophy, inflammation, or fibrosis was present and it was postulated that the enhanced diastolic stiffness was related to accumulation of Alcian Blue-positive material in the ventricular interstitium. To evaluate myocardial lipid metabolism, [1-14C]oleic acid was infused systemically. Plasma specific activity and myocardial lipid uptake were similar in both groups. There was a significantly increased incorporation of label into triglyceride, associated with a reduced 14CO2 production, considered the basis for a twofold increment of triglyceride content. In addition, diminished incorporation of [14C]oleic acid into phospholipid was observed accompanied by morphologic abnormalities of cardiac cell membranes. Potassium loss and sodium gain, like the lipid alteration, was more prominent in the subendocardium. Thus, chronic ethanol ingestion in this animal model is associated with abnormalities of ventricular function without evident malnutrition, analogous to the preclinical malfunction described in the human alcoholic. Images PMID:4368946

  2. Abnormal Myocardial Blood Flow Reserve Observed in Cardiac Amyloidosis

    PubMed Central

    Nel, Karen; Senior, Roxy; Greaves, Kim

    2016-01-01

    We performed real-time myocardial contrast echocardiography on a patient with cardiac amyloidosis and previous normal coronary angiography presenting with atypical chest pain to assess myocardial blood flow reserve (MBFR). Myocardial contrast echocardiography was performed and flash microbubble destruction and replenishment analysis was used to calculate myocardial blood flow. Dipyridamole was used to achieve hyperemia. MBFR was derived from the ratio of peak myocardial blood flow at hyperemia and rest. The results show a marked reduction in MBFR in our patient. Previous reports of luminal obstruction of intramyocardial rather than epicardial vessels by amyloid deposition may be causing microvascular dysfunction. PMID:27081447

  3. 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

  4. The effects of changing dairy intake on trans and saturated fatty acid levels- results from a randomized controlled study

    PubMed Central

    2014-01-01

    Background Dairy food is an important natural source of saturated and trans fatty acids in the human diet. This study evaluates the effect of dietary advice to change dairy food intake on plasma fatty acid levels known to be present in milk in healthy volunteers. Methods Twenty one samples of whole fat dairy milk were analyzed for fatty acids levels. Changes in levels of plasma phospholipid levels were evaluated in 180 healthy volunteers randomized to increase, not change or reduce dairy intake for one month. Fatty acids were measured by gas chromatography–mass spectrometry and levels are normalized to d-4 alanine. Results The long chain fatty acids palmitic (13.4%), stearic (16.7%) and myristic (18.9%) acid were most common saturated fats in milk. Four trans fatty acids constituted 3.7% of the total milk fat content. Increased dairy food intake by 3.0 (± 1.2) serves/ day for 1 month was associated with small increases in plasma levels of myristic (+0.05, 95% confidence level-0.08 to 0.13, p = 0.07), pentadecanoic (+0.014, 95% confidence level -0.016 to 0.048, p = 0.02) and margaric acid (+0.02, -0.03 to 0.05, p = 0.03). There was no significant change in plasma levels of 4 saturated, 4 trans and 10 unsaturated fatty acids. Decreasing dairy food intake by 2.5 (± 1.2) serves per day was not associated with change in levels of any plasma fatty acid levels. Conclusion Dietary advice to change dairy food has a minor effect on plasma fatty acid levels. Trial registration ACTRN12612000574842. PMID:24708591

  5. 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

  6. 131Cs myocardial scintigraphy. Application to assessment of anterior myocardial infarction.

    PubMed Central

    Burguet, W; Merchie, G; Kulbertus, H

    1975-01-01

    Earlier studies have indicated that caesium-131 is a good myocardial scanning agent for the demonstration of anterior infarcts. One hundred and ten patients with documented anterior myocardial infarction were studied by 131Cs myocardial scintigraphy. An anterior area of decreased uptake of caesium was noted in all but 3 subjects whose necrotic zone was likely to be of small dimensions. In 20 cases, the scintigram showed a definite, sometimes very large, cold area whereas the electrocardiogram failed to display any diagnostic feature of myocardial necrosis. In most of the latter instances, the electrocardiographic diagnosis was obscured by the presence of intraventricular conduction disturbances. In order to visualize the intracardiac cavities, the 131Cs investigation was usually completed by a 113mIn scintigram, which allowed recognition of a parietal aneurysm in 12 of the 18 patients with extensive anterior lesions. In each case, an index of necrosis was computed from planimetric measurements of the infarcted area as compared to the total left ventricular surfact in both the anteroposterior and left anterior oblique projections. This index was shown to correlate with the incidence of major complications developing after the acute episode of coronary occlusion. The sensitivity, specificity, and accuracy of the method are briefly discussed. It is felt that myocardial scintigraphy represents a sound approach to the semiquantitative assessment of anterior myocardial infarction; the clinical usefulness of the technique seems sufficiently demonstrated to prompt further research in this field. Images PMID:1191417

  7. 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

  8. Myocardial ischemic protection in natural mammalian hibernation

    PubMed Central

    Yan, Lin; Kudej, Raymond K.; Vatner, Dorothy E.

    2015-01-01

    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. Thrombolytic therapy in acute myocardial infarction.

    PubMed

    Woo, K S; White, H D

    1994-07-01

    Thrombolytic therapy has revolutionized the treatment of acute myocardial infarction by reducing mortality and preserving left ventricular function. It is relatively safe and cost-effective. However, it is currently underused in most countries. Patients in whom thrombolysis is indicated include those with ST elevation on the electrocardiogram or bundle branch block pattern who present within 12 hours of myocardial infarction; the indications should be widened to include the elderly, patients who have undergone nontraumatic cardiopulmonary resuscitation, and women during menstruation. The risk-benefit ratio should be assessed for the individual patient. Prehospital thrombolytic treatment has been shown to be feasible with the support of well-trained staff and resuscitation equipment, and may be cost-effective in communities with time delays before hospitalization greater than 1 hour. The most important strategy is to shorten the "door to needle" time in hospital. The importance of full infarct-related artery flow (Thrombolysis in Myocardial Infarction [TIMI] grade 3 flow) for preservation of ventricular function and survival has been documented in the second Thrombolysis Trial of Eminase in Acute Myocardial Infarction (TEAM 2) and the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) studies. Aspirin and heparin are beneficial adjunctive regimens to thrombolytic therapy but optimal epicardial reperfusion is achieved in only about half of patients. Improved thrombolytic, adjunctive antiplatelet, and antithrombotic regimens are required to achieve early full reperfusion, which is crucial to improve survival and quality of life. PMID:7919592

  10. Myocardial protection: what the anesthesiologist does.

    PubMed

    Merin, R G

    1990-09-01

    The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important. PMID:2133851

  11. Myocardial infarction complicated by ventricular septal rupture.

    PubMed

    Sahjian, Michael; Ventriglia, Rich; Bolton, Lauri

    2012-01-01

    Transporting patients with an ST segment elevation myocardial infarction (STEMI) is a fairly common practice for most critical care transport teams. When a STEMI is complicated by ventricular septal rupture, the care can become more challenging, especially if the rupture is not yet diagnosed. This article describes such a transport and reviews the pathophysiology of the process along with treatment options. PMID:22225564

  12. 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.

  13. 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…

  14. 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

  15. Thrombus aspiration in acute myocardial infarction.

    PubMed

    Mahmoud, Karim D; Zijlstra, Felix

    2016-07-01

    The success of primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) is often hampered by incomplete microvascular myocardial reperfusion owing to distal embolization of thrombus resulting in microvascular obstruction. To address this problem, thrombus aspiration devices have been developed that can be used to evacuate coronary thrombus either manually or mechanically. Thrombus aspiration has the potential to reduce the local thrombus load, minimize the need for balloon predilatation, facilitate direct stenting, prevent distal embolization, and ultimately improve myocardial reperfusion. Furthermore, thrombus aspiration has enabled us to study coronary thrombus in vivo, and has facilitated recognition of distinct mechanisms of coronary thrombosis. Clinical trials focusing on manual thrombus aspiration in primary PCI have generally shown improved myocardial reperfusion. However, in two large trials powered for clinical end points, no reduction in 1-year mortality or other adverse clinical events was observed with the use of this strategy. Moreover, one of these trials showed a marginally increased risk of stroke. Consequently, current guidelines do not recommend routine use of thrombus aspiration. Future studies should focus on the identification of subgroups of patients with STEMI who might derive benefit from manual thrombus aspiration, and establish the effect of operator performance on the efficacy and safety of the procedure. PMID:26961064

  16. Perceived Neighborhood Social Cohesion and Myocardial Infarction

    PubMed Central

    Kim, Eric S.; Hawes, Armani M.; Smith, Jacqui

    2015-01-01

    Background The main strategy for alleviating heart disease has been to target individuals and encourage them to change their health behaviors. Though important, emphasis on individuals has diverted focus and responsibility away from neighborhood characteristics, which also strongly influence people’s behaviors. Although a growing body of research has repeatedly demonstrated strong associations between neighborhood characteristics and cardiovascular health, it has typically focused on negative neighborhood characteristics. Only a few studies have examined the potential health enhancing effects of positive neighborhood characteristics, such as perceived neighborhood social cohesion. Methods Using multiple logistic regression models, we tested whether higher perceived neighborhood social cohesion was associated with lower incidence of myocardial infarction. Prospective data from the Health and Retirement Study—a nationally representative panel study of American adults over the age of 50—were used to analyze 5,276 participants with no history of heart disease. Respondents were tracked for four years and analyses adjusted for relevant sociodemographic, behavioral, biological, and psychosocial factors. Results In a model that adjusted for age, gender, race, marital status, education, and total wealth, each standard deviation increase in perceived neighborhood social cohesion was associated with a 22% reduced odds of myocardial infarction (OR = 0.78, 95% CI, 0.63–0.94. The association between perceived neighborhood social cohesion and myocardial infarction remained even after adjusting for behavioral, biological, and psychosocial covariates. Conclusions Higher perceived neighborhood social cohesion may have a protective effect against myocardial infarction. PMID:25135074

  17. 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...

  18. Abnormal Glucose Tolerance Is Associated with a Reduced Myocardial Metabolic Flexibility in Patients with Dilated Cardiomyopathy.

    PubMed

    Tricò, Domenico; Baldi, Simona; Frascerra, Silvia; Venturi, Elena; Marraccini, Paolo; Neglia, Danilo; Natali, Andrea

    2016-01-01

    Dilated cardiomyopathy (DCM) is characterized by a metabolic shift from fat to carbohydrates and failure to increase myocardial glucose uptake in response to workload increments. We verified whether this pattern is influenced by an abnormal glucose tolerance (AGT). In 10 patients with DCM, 5 with normal glucose tolerance (DCM-NGT) and 5 with AGT (DCM-AGT), and 5 non-DCM subjects with AGT (N-AGT), we measured coronary blood flow and arteriovenous differences of oxygen and metabolites during Rest, Pacing (at 130 b/min), and Recovery. Myocardial lactate exchange and oleate oxidation were also measured. At Rest, DCM patients showed a reduced nonesterified fatty acids (NEFA) myocardial uptake, while glucose utilization increased only in DCM-AGT. In response to Pacing, glucose uptake promptly rose in N-AGT (from 72 ± 21 to 234 ± 73 nmol/min/g, p < 0.05), did not change in DCM-AGT, and slowly increased in DCM-NGT. DCM-AGT sustained the extra workload by increasing NEFA oxidation (from 1.3 ± 0.2 to 2.9 ± 0.1 μmol/min/gO2 equivalents, p < 0.05), while DCM-NGT showed a delayed increase in glucose uptake. Substrate oxidation rates paralleled the metabolites data. The presence of AGT in patients with DCM exacerbates both the shift from fat to carbohydrates in resting myocardial metabolism and the reduced myocardial metabolic flexibility in response to an increased workload. This trial is registered with ClinicalTrial.gov NCT02440217. PMID:26798650

  19. Abnormal Glucose Tolerance Is Associated with a Reduced Myocardial Metabolic Flexibility in Patients with Dilated Cardiomyopathy

    PubMed Central

    Tricò, Domenico; Baldi, Simona; Frascerra, Silvia; Venturi, Elena; Marraccini, Paolo; Neglia, Danilo; Natali, Andrea

    2016-01-01

    Dilated cardiomyopathy (DCM) is characterized by a metabolic shift from fat to carbohydrates and failure to increase myocardial glucose uptake in response to workload increments. We verified whether this pattern is influenced by an abnormal glucose tolerance (AGT). In 10 patients with DCM, 5 with normal glucose tolerance (DCM-NGT) and 5 with AGT (DCM-AGT), and 5 non-DCM subjects with AGT (N-AGT), we measured coronary blood flow and arteriovenous differences of oxygen and metabolites during Rest, Pacing (at 130 b/min), and Recovery. Myocardial lactate exchange and oleate oxidation were also measured. At Rest, DCM patients showed a reduced nonesterified fatty acids (NEFA) myocardial uptake, while glucose utilization increased only in DCM-AGT. In response to Pacing, glucose uptake promptly rose in N-AGT (from 72 ± 21 to 234 ± 73 nmol/min/g, p < 0.05), did not change in DCM-AGT, and slowly increased in DCM-NGT. DCM-AGT sustained the extra workload by increasing NEFA oxidation (from 1.3 ± 0.2 to 2.9 ± 0.1 μmol/min/gO2 equivalents, p < 0.05), while DCM-NGT showed a delayed increase in glucose uptake. Substrate oxidation rates paralleled the metabolites data. The presence of AGT in patients with DCM exacerbates both the shift from fat to carbohydrates in resting myocardial metabolism and the reduced myocardial metabolic flexibility in response to an increased workload. This trial is registered with ClinicalTrial.gov NCT02440217. PMID:26798650

  20. [Prehospital thrombolytic therapy in acute myocardial infarction].

    PubMed

    Carlsson, J; Schuster, H P; Tebbe, U

    1997-10-01

    The extent of myocardial damage occurring during acute myocardial infarction is time dependent, and there is abundant evidence from most clinical trials that mortality reduction is greatest in patients treated early with thrombolytic agents, although beneficial effects have been shown with treatment initiated up to 12 h after onset of symptoms. All studies on prehospital thrombolysis have conclusively shown the practicability and safety of patient selection and administration of the thrombolytic agent. The accuracy of diagnosis in the prehospital setting was comparable to trials of in-hospital thrombolysis, e.g., in the Myocardial Infarction Triage and Intervention Project (MITI) 98% of the patients enrolled had subsequent evidence of acute myocardial infarction. With regard to time savings, all randomized studies showed positive results. The smallest time gain was observed in the MITI trial: prehospital-treated patients received thrombolytic therapy an average of 33 min earlier than those treated in hospital. In the European Myocardial Infarction Project (EMIP) the difference in time between prehospital and hospital treatment was a median of 55 min. However, none of these trials was able to show a significant short-term mortality difference between the two groups. Only a meta analysis of five randomized studies with a combined median time gain of about 60 min showed a significant 17% reduction in short-term mortality for patients who received thrombolytic therapy in the prehospital phase. In the Grampian Region Early Anistreplase Trial (GREAT), a study performed in a more rural area than other studies, the time gain by prehospital initiation of thrombolysis was a median of 130 min. GREAT was the only study to date reporting a significant mortality benefit for prehospital-treated patients after 3 months and 1 year. In conclusion, prehospital thrombolysis is feasible and safe. Patients with acute myocardial infarction can be correctly identified and treated with

  1. Effect of angiotensin-converting enzyme inhibitors on myocardial ischemia/reperfusion injury: an overview.

    PubMed

    Zughaib, M E; Sun, J Z; Bolli, R

    1993-01-01

    There are multiple mechanisms whereby ACE inhibitors could be beneficial during myocardial ischemia and reperfusion, including: i) reduced formation of angiotensin II, ii) decreased metabolism of bradykinin, iii) antioxidant activity, and iv) possibly other unknown mechanisms. Reduced formation of angiotensin II should be beneficial because this peptide exerts several actions that are potentially detrimental to the ischemic/reperfused myocardium, including vasoconstriction, increased release of norepinephrine, stimulation of phospholipase C and/or A2, and increased afterload with an attendant increase in oxygen demands. Reduced metabolism of bradykinin could be beneficial by increasing myocardial glucose uptake, by causing vasodilation, and by stimulating production of endothelium-derived relaxing factor and prostacyclin. Although earlier studies suggested that sulfhydryl-containing ACE inhibitors scavenge superoxide anions, recent data have shown that these drugs scavenge hydroxyl radical and hypochlorous acid with no effect on superoxide anion. Studies in isolated hearts have demonstrated that ACE inhibitors attenuate the metabolic, arrhythmic, and contractile dearrangements associated with ischemia and reperfusion, and have suggested that such beneficial effects are mediated by potentiation of bradykinin and/or increased synthesis of prostacyclin. Studies in models of myocardial stunning after brief (15-min) ischemia in vivo (anesthetized dogs) suggest that ACE inhibitors enhance the recovery of contractile function after a single brief ischemic episode. No data are available regarding the effect of these drugs on myocardial stunning after a prolonged, partly reversible episode, after multiple consecutive brief ischemic episodes, and after global ischemia. The mechanism for the salutary effects of ACE inhibitors on stunning remains a mystery. It may involve an antioxidant action (in the case of thiol-containing molecules) or potentiation of prostaglandins (in

  2. Myocardial Tissue Doppler Velocity in Child Growth

    PubMed Central

    Choi, Sun-Ha; Kim, Nam Kyun; Jung, Jo Won; Choi, Jae Young

    2016-01-01

    Background In adults, tissue Doppler imaging (TDI) is a recommended component of routine echocardiography. However, TDI velocities are less accepted in pediatrics, due to their strong variability and age dependence in children. This study examines the distribution of myocardial tissue Doppler velocities in healthy children to assess the effect of age with cardiac growth on the various echocardiographic measurements. Methods Total 144 healthy children were enrolled in this study. They were recruited from the pediatric outpatient clinic for routine well-child visits. The statistical relationships between age and TDI values were analyzed. Also, the statistical relationships between body surface area (BSA) and TDI values, left ventricle end-diastolic dimension (LVEDD) and TDI values were analyzed. Also, we conducted multivariate analysis of cardiac growth parameters such as, age, BSA, LVEDD and TDI velocity data. Results All of the age, BSA, and LVEDD had positive correlations with deceleration time (DT), pressure half-time (PHT), peak early diastolic myocardial velocity, peak systolic myocardial velocity, and had negative correlations with peak late diastolic velocity (A) and the ratio of trans-mitral inflow velocity to early diastolic velocity of mitral annulus (E/E'). In the multivariate analysis, all of the age, BSA, and LVEDD had positive correlations with DT, PHT, and negative correlations with A and E/E'. Conclusion The cardiac growth parameters related alterations of E/E' may suggest that diastolic myocardial velocities are cardiac growth dependent, and diastolic function has positive correlation with cardiac growth in pediatric group. This cardiac growth related myocardial functional variation would be important for assessment of cardiac involvement either in healthy and sick child. PMID:27081443

  3. Influence of myocardial substrate utilization on the oxygen consumption of the heart.

    PubMed

    Kahles, H; Hellige, G; Hunneman, D H; Mezger, V A; Bretschneider, H J

    1982-04-01

    The effect of changing myocardial metabolism from predominantly lipid to predominantly carbohydrate utilization on myocardial oxygen consumption (MVO2) was studied in 10 closed-chest dogs. Oxygen saving potency of different metabolic interventions was quantified over a wide hemodynamic range by comparing the directly determined MVO2 with the hemodynamic parameter total left ventricular energy demand (Et), which correlates closely under control conditions with MVO2 (r = 0.98). Stimulation of carbohydrate metabolism by addition of glucose and beta-pyridyl carbinol or by activation of pyruvate dehydrogenase with dichloroacetate (DCA) shifted the cardiac respiratory quotient during beta-stimulation from 0.73 to 1.00 and 0.89, respectively, the nonesterified fatty acid/albumin ratio decreased from 4.0 to 0.5, or remained unchanged with DCA, and MVO2 was reduced by 25 and 16%, respectively. Therapeutic approaches aimed at decreasing MVO2 by changing substrate utilization are discussed. PMID:7083652

  4. Type 2 myocardial infarction: the chimaera of cardiology?

    PubMed

    Collinson, Paul; Lindahl, Bertil

    2015-11-01

    The term type 2 myocardial infarction first appeared as part of the universal definition of myocardial infarction. It was introduced to cover a group of patients who had elevation of cardiac troponin but did not meet the traditional criteria for acute myocardial infarction although they were considered to have an underlying ischaemic aetiology for the myocardial damage observed. Since first inception, the term type 2 myocardial infarction has always been vague. Although attempts have been made to produce a systematic definition of what constitutes a type 2 myocardial infarction, it has been more often characterised by what it is not rather than what it is. Clinical studies that have used type 2 myocardial infarction as a diagnostic criterion have produced disparate incidence figures. The range of associated clinical conditions differs from study to study. Additionally, there are no agreed or evidence-based treatment strategies for type 2 myocardial infarction. The authors believe that the term type 2 myocardial infarction is confusing and not evidence-based. They consider that there is good reason to stop using this term and consider instead the concept of secondary myocardial injury that relates to the underlying pathophysiology of the primary clinical condition. PMID:26220812

  5. Oligophrenin1 protects mice against myocardial ischemia and reperfusion injury by modulating inflammation and myocardial apoptosis.

    PubMed

    Niermann, Christina; Gorressen, Simone; Klier, Meike; Gowert, Nina S; Billuart, Pierre; Kelm, Malte; Merx, Marc W; Elvers, Margitta

    2016-08-01

    The Rho family of small GTPases has been analyzed in cardiac physiology and pathophysiology including myocardial infarction (MI) in the last years. Contradictory results show either a protective or a declined effect of RhoA and the RhoA effector Rho-associated protein kinase (ROCK) in myocardial ischemia and reperfusion injury that is associated with cardiomyocyte survival and caspase-3 activation. Cardiac-specific deletion of Rac1 reduced ischemia reperfusion injury in diabetic hearts, whereas cardiomyocyte specific overexpression of active Rac1 predisposes the heart to increased myocardial injury with enhanced contractile dysfunction. GTPase-activating proteins (GAPs) control the activation of Rho proteins through stimulation of GTP hydrolysis. However, the impact of GAPs in myocardial ischemia and reperfusion injury remains elusive. Here we analyzed the role of oligophrenin1 (OPHN1), a RhoGAP with Bin/Amphiphysin/Rvs (BAR) domain known to regulate the activity of RhoA, Rac1 and Cdc42 in MI. The expression of Ophn1, RhoA and Rac1 is strongly upregulated 24h after myocardial ischemia. Loss of OPHN1 induced enhanced activity of Rho effector molecules leading to elevated cardiomyocyte apoptosis and increased migration of inflammatory cells into the infarct border zone of OPHN1 deficient mice. Consequently, echocardiography 24h after myocardial ischemia revealed declined left ventricle function in OPHN1 deficient mice. Our results indicate that OPHN1 mediated regulation of RhoA, Rac1 and Cdc42 is crucial for the preservation of cardiac function after myocardial injury. PMID:27117132

  6. Transient myocardial ischaemia after acute myocardial infarction does not induce ventricular arrhythmias.

    PubMed Central

    Currie, P; Saltissi, S

    1993-01-01

    OBJECTIVE--To see whether transient myocardial ischaemia on ambulatory monitoring after myocardial infarction is associated with ventricular arrhythmias. DESIGN--A prospective study. SETTING--The coronary care unit, general medical wards, and cardiorespiratory department of a major teaching hospital. PATIENTS--203 consecutive patients without specific exclusion criteria admitted with acute myocardial infarction. INTERVENTIONS--24 hour ambulatory electrocardiographic monitoring for ventricular arrhythmias and ST depression both early (mean 6.3 days after infarction, n = 201) and late (mean 38 days, n = 177). MAIN OUTCOME MEASURES--Episodes of myocardial ischaemia were identified during ambulatory monitoring by transient ST depression of > or = 1.0 mm lasting for > or = 30 s. Ventricular arrhythmias were single extrasystoles, couplets, or ventricular tachycardia. RESULTS--All ventricular arrhythmias were significantly more frequent in late than early monitoring. The arrhythmias included couplets (in 83/174 (48%) v 49/200 (25%) of patients, p = 0.0000028) and ventricular tachycardia (29/174 (17%) v 15/199 (8%), p = 0.0064). Patients with ST depression (29 early; 56 late), compared with those without ischaemia, did not experience a significant increase in single extrasystoles, couplets (31% v 23% early; 47% v 48% late), or ventricular tachycardia (3% v 8% early; 18% v 16% late). Even patients with frequent (> or = 3 episodes), and deep (> or = 1.5 mm) or prolonged (> or = 20 min) ST depression had no increase in arrhythmias. CONCLUSIONS--Ventricular arrhythmias after myocardial infarction are not associated with transient myocardial ischaemia during daily activities. This study does not support the belief that to abolish silent ischaemia would reduce the incidence of sudden death due to uncontrollable ventricular arrhythmias after myocardial infarction. PMID:8489860

  7. Cardiac troponins as indicators of acute myocardial damage in dogs.

    PubMed

    Burgener, Iwan A; Kovacevic, Alan; Mauldin, G Neal; Lombard, Christophe W

    2006-01-01

    Cardiac troponin I (cTnI) and T (cTnT) have a high sequence homology across phyla and are sensitive and specific markers of myocardial damage. The purpose of this study was to evaluate the Cardiac Reader, a human point-of-care system for the determination of cTnT and myoglobin, and the Abbott Axsym System for the determination of cTnI and creatine kinase isoenzyme MB (CK-MB) in healthy dogs and in dogs at risk for acute myocardial damage because of gastric dilatation-volvulus (GDV) and blunt chest trauma (BCT). In healthy dogs (n = 56), cTnI was below detection limits (<0.1 microg/L) in 35 of 56 dogs (reference range 0-0.7 microg/L), and cTnT was not measurable (<0.05 ng/mL) in all but 1 dog. At presentation, cTnI, CK-MB, myoglobin, and lactic acid were all significantly higher in dogs with GDV (n = 28) and BCT (n = 8) than in control dogs (P < .001), but cTnT was significantly higher only in dogs with BCT (P = .033). Increased cTnI or cTnT values were found in 26 of 28 (highest values 1.1-369 microg/L) and 16 of 28 dogs (0.1-1.7 ng/mL) with GDV, and in 6 of 8 (2.3-82.4 microg/L) and 3 of 8 dogs (0.1-0.29 ng/mL) with BCT, respectively. In dogs suffering from GDV, cTnI and cTnT increased further within the first 48 hours (P < .001). Increased cardiac troponins suggestive of myocardial damage occurred in 93% of dogs with GDV and 75% with BCT. cTnI appeared more sensitive, but cTnT may be a negative prognostic indicator in GDV. Both systems tested seemed applicable for the measurement of canine cardiac troponins, with the Cardiac Reader particularly suitable for use in emergency settings. PMID:16594583

  8. Effects of glycyl-glutamine dipeptide supplementation on myocardial damage and cardiac function in rats after severe burn injury

    PubMed Central

    Zhang, Yong; Yan, Hong; Lv, Shang-Gun; Wang, Lin; Liang, Guang-Ping; Wan, Qian-Xue; Peng, Xi

    2013-01-01

    Glutamine decreases myocardial damage in ischemia/reperfusion injury. However, the cardioprotective effect of glutamine after burn injury remains unclear. Present study was to explore the protective effect of glycyl-glutamine dipeptide on myocardial damage in severe burn rats. Seventy-two Wistar rats were randomly divided into three groups: normal control (C), burned control (B) and glycyl-glutamine dipeptide-treated (GG) groups. B and GG groups were inflicted with 30% total body surface area of full thickness burn. The GG group was given 1.5 g/kg glycyl-glutamine dipeptide per day and the B group was given the same dose of alanine via intraperitoneal injection for 3 days. The serum CK, LDH, AST, and, blood lactic acid levels, as well as the myocardium ATP and GSH contents, were measured. The indices of cardiac contractile function and histopathological change were analyzed at 12, 24, 48, and 72 post-burn hours (PBH). The serum CK, LDH, AST and blood lactic acid levels increased, and the myocardium ATP and GSH content decreased in both burned groups. Compared with B group, the CK, LDH, AST and blood lactic acid levels reduced, myocardium ATP and GSH content increased in GG group. Moreover, the inhibition of cardiac contractile function and myocardial histopathological damage were reduced significantly in GG group. We conclude that myocardial histological structure and function were damaged significantly after burn injury, glycyl-glutamine dipeptide supplementation is beneficial to myocardial preservation by improving cardiocyte energy metabolism, increasing ATP and glutathione synthesis. PMID:23638213

  9. Regional left ventricular myocardial contractility and stress in a finite element model of posterobasal myocardial infarction.

    PubMed

    Wenk, Jonathan F; Sun, Kay; Zhang, Zhihong; Soleimani, Mehrdad; Ge, Liang; Saloner, David; Wallace, Arthur W; Ratcliffe, Mark B; Guccione, Julius M

    2011-04-01

    Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct (T(max_B)), in the myocardium remote from the infarct (T(max_R)), and in the infarct (T(max_I)) were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized T(max_B) was found to be significantly depressed relative to T(max_R), while T(max_I) was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure. PMID:21428685

  10. Effect of Wenxin Granule on Ventricular Remodeling and Myocardial Apoptosis in Rats with Myocardial Infarction

    PubMed Central

    Wu, Aiming; Zhai, Jianying; Zhang, Dongmei; Lou, Lixia; Zhu, Haiyan; Gao, Yonghong; Chai, Limin; Xing, Yanwei; Lv, Xiying; Zhu, Lingqun; Zhao, Mingjing; Wang, Shuoren

    2013-01-01

    Aim. To determine the effect of a Chinese herbal compound named Wenxin Granule on ventricular remodeling and myocardial apoptosis in rats with myocardial infarction (MI). Methods. Male Sprague-Dawley (SD) rats were randomly divided into four groups: the control group, the model group, the metoprolol group, and the Wenxin Granule group (WXKL group) with sample size (n) of 7 rats in each group. An MI model was established in all rats by occlusion of the left anterior descending coronary artery (the control group was without occlusion). Wenxin Granule (1.35 g/kg/day), metoprolol (12 mg/kg/day), and distilled water (5 mL/kg/day for the control and model groups) were administered orally for 4 weeks. Ultrasonic echocardiography was used to examine cardiac structural and functional parameters. Myocardial histopathological changes were observed using haematoxylin and eosin (H&E) dyeing. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) staining. Serum angiotensin II (Ang II) concentration was measured using the enzyme-linked immunosorbent assay (ELISA). Results. It was found that Wenxin Granule could partially reverse ventricular remodeling, improve heart function, alleviate the histopathological damage, inhibit myocardial apoptosis, and reduce Ang II concentration in rats with MI. Conclusions. The results of the current study suggest that Wenxin Granule may be a potential alternative and complementary medicine for the treatment of MI. PMID:23997803

  11. [Quantitative evaluation of acute myocardial infarction by In-111 antimyosin Fab myocardial imaging].

    PubMed

    Naruse, H; Morita, M; Itano, M; Yamamoto, J; Kawamoto, H; Fukutake, N; Ohyanagi, M; Iwasaki, T; Fukuchi, M

    1991-11-01

    For quantitative evaluation of acute myocardial infarction, In-111 antimyosin Fab myocardial imaging (InAM) was performed in 17 patients with myocardial infarction who underwent Tl-201 (TL) and Tc-99m pyrophosphate (PYP) myocardial imaging in acute phase. For calculating the infarct size, voxel counter method was used for analysis in PYP and InAM, and extent and severity score were used on bull's-eye polar map in TL. The most appropriate cut-off level ranged from 65 to 80% by the fundamental experiment using cardiac phantom. The cut-off level of 0.70 (InAM) and 0.65 (PYP) were used for clinical application of voxel counter analysis. The infarct size calculated by InAM and PYP was compared with wall motion abnormality index by echocardiography (WMAI), TL extent score, TL severity score, peak CK and sigma CK. Infarct size by InAM showed the following correlations with other indices. PYP: r = 0.26 (ns), TL extent score: r = 0.72 (p less than 0.01), TL severity score: r = 0.65 (p less than 0.05), WMAI: r = 0.69 (p less than 0.05). The infarct size by PYP did not show any correlations with these indices. Therefore, the infarct size by InAM showed better correlations with TL and WMAI than that of PYP. So InAM was considered superior to PYP for quantitative evaluation of acute myocardial infarction. PMID:1770642

  12. [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

  13. Design and biological properties of iodine-123 labeled. beta. -methyl-branched fatty acids

    SciTech Connect

    Knapp, F.F. Jr.; Goodman, M.M.

    1984-01-01

    The synthetic strategy, synthesis, preclinical evaluation and potential clinical applications of 3-methyl-branched radioiodinated iodophenyl- and iodovinyl-substituted fatty acids are reviewed for use as myocardial imaging agents. 50 references, 6 figures. (ACR)

  14. Prophylactic lidocaine in suspected acute myocardial infarction.

    PubMed

    Goodman, S L; Geiderman, J M; Bernstein, I J

    1979-06-01

    The incidence of serious ventricular arrhythmias following acute myocardial infarction is highest during the first few hours after injury, and thereafter declines. Several investigations into the prophylactic use of lidocaine to prevent the development of arrhythmias have shown that lidocaine, given in therapeutic doses, is effective in preventing ventricular fibrillation and in reducing early mortality. Lidocaine was found to be effective when given either by the intravenous or by the intramuscular routes. The recommended dosage is 100 mg given as an intravenous bolus followed by 2 to 4 mg/min as an infusion, which should be given by infusion pump. Another recommendation is to use two 100 mg boluses 20 minutes apart, along with the same infusion. We recommend that lidocaine be started as soon as possible in all patients suspected of having suffered acute myocardial infarction. PMID:449144

  15. Amphetamine Abuse Related Acute Myocardial Infarction

    PubMed Central

    Lewis, O'Dene; Kumar, Rajan; Yeruva, Sri Lakshmi Hyndavi; Curry, Bryan H.

    2016-01-01

    Amphetamine abuse is a global problem. The cardiotoxic manifestations like acute myocardial infarction (AMI), heart failure, or arrhythmia related to misuse of amphetamine and its synthetic derivatives have been documented but are rather rare. Amphetamine-related AMI is even rarer. We report two cases of men who came to emergency department (ED) with chest pain, palpitation, or seizure and were subsequently found to have myocardial infarction associated with the use of amphetamines. It is crucial that, with increase in amphetamine abuse, clinicians are aware of this potentially dire complication. Patients with low to intermediate risk for coronary artery disease with atypical presentation may benefit from obtaining detailed substance abuse history and urine drug screen if deemed necessary. PMID:26998366

  16. Painless acute myocardial infarction on Mount Kilimanjaro.

    PubMed

    Jamal, Nasiruddin; Rajhy, Mubina; Bapumia, Mustaafa

    2016-01-01

    An individual experiencing dyspnoea or syncope at high altitude is commonly diagnosed to have high-altitude pulmonary edema or cerebral edema. Acute myocardial infarction (AMI) is generally not considered in the differential diagnosis. There have been very rare cases of AMI reported only from Mount Everest. We report a case of painless ST segment elevation myocardial infarction (STEMI) that occurred while climbing Mount Kilimanjaro. A 51-year-old man suffered dyspnoea and loss of consciousness near the mountain peak, at about 5600 m. At a nearby hospital, he was treated as a case of high-altitude pulmonary edema. ECG was not obtained. Two days after the incident, he presented to our institution with continued symptoms of dyspnoea, light-headedness and weakness, but no pain. He was found to have inferior wall and right ventricular STEMI complicated by complete heart block. He was successfully managed with coronary angioplasty, with good recovery. PMID:26989121

  17. Delayed Myocardial Enhancement in Cardiac Magnetic Resonance Imaging

    PubMed Central

    Franco, Arie; Javidi, Saeed; Ruehm, Stefan G

    2015-01-01

    Delayed myocardial enhancement MRI is a highly valuable but non-specific imaging technique that is ancillary in the diagnosis of a variety of diseases including myocardial viability, cardiomyopathy, myocarditis and other infiltrative myocardial processes. The lack of specificity stems from the wide variety of differential diagnoses that may present with overlapping patterns of delayed enhancement. Many of these differential diagnoses have been presented and discussed in this article. PMID:26622933

  18. Radioiodine therapy of hyperthyroidism precludes thallium-201 myocardial scintigraphy

    SciTech Connect

    Orzel, J.A.; Kruyer, W.B.; Borchert, R.D.

    1987-02-01

    The authors attempted to perform Tl-201 myocardial perfusion scintigraphy in a 42-year-old man 23 and 35 days after he received 9.8 mCi of oral I-131 for documented Graves' disease. Interference from primary and scattered photons from residual thyroid I-131 made Tl-201 myocardial scintigraphy technically impossible. A series of phantom and patient studies using I-131 and Tl-201 were performed, yielding guidelines for planning Tl-201 myocardial scintigraphy following radioiodine therapy.

  19. [Mosaic portrait method in the prognosis of myocardial infarct complications].

    PubMed

    Iakovlev, G M; Ardashev, V N; Kats, M D; Galkina, T A

    1981-06-01

    A mosaic portrait of variants of the course of myocardial infarction differing in the clinical picture of the first days of the disease was created by means of methods of Boolean algebra and electronic computers. A total of 354 patients with transmural myocardial infarction were examined., The created models allow the development of some complications of myocardial infarction to be prognosticated exact within 90%. PMID:7021950

  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. Acute Myocardial Infarction in Nephrotic Syndrome.

    PubMed

    Krishna, Kavita; Hiremath, Shirish; Lakade, Sachin; Davakhar, Sudarshan

    2015-11-01

    A 28 year old male, known case of nephrotic syndrome since 12 years, hypertensive presented with acute myocardial infarction (AMI) and accelerated hypertension. Coronary angiography revealed 100% thrombotic occlusion of mid left anterior descending artery, treated with thrombus aspiration and intracoronary tirofiban and nitroglycerine. He was stabilized within 24 hours. The pathogenesis of AMI in nephrotic syndrome has been discussed with this case report. PMID:27608787

  2. PICSO: from myocardial salvage to tissue regeneration.

    PubMed

    Mohl, Werner; Gangl, Clemens; Jusić, Alem; Aschacher, Thomas; De Jonge, Martin; Rattay, Frank

    2015-01-01

    Despite advances in primary percutaneous interventions (PPCI), management of microvascular obstructions in reperfused myocardial tissue remains challenging and is a high-risk procedure. This has led to renewed interest in the coronary venous system as an alternative route of access to the myocardium. This article reviews historical data describing therapeutic options via cardiac veins as well as discussing the clinical potential and limitations of a catheter intervention: pressure controlled intermittent coronary sinus occlusion (PICSO). Collected experimental and clinical information suggest that PICSO also offers the potential for tissue regeneration beyond myocardial salvage. A meta-analysis of observer controlled pICSO application in animal studies showed a dose dependent reduction in infarct size of 29.3% (p < 0.001). Additionally, a 4-fold increase of hemeoxygenase-1 gene expression (p < 0.001) in the center of infarction and a 2.5 fold increase of vascular endothelial growth factor (VEGF) (p < 0.002) in border zones suggest that molecular pathways are initiating structural maintenance. Early clinical evidence confirmed significant salvage and event free survival in patients with acute myocardial infarction and risk reduction for event free survival 5 years after the acute event (p < 0.0001). This experimental and clinical evidence was recently corroborated using modern PICSO technology in PPCI showing a significant reduction of infarct size, when compared to matched controls (p < 0.04). PICSO enhances redistribution of flow towards deprived zones, clearing microvascular obstruction and leading to myocardial protection. Beyond salvage, augmentation of molecular regenerative networks suggests a second mechanism of PICSO involving the activation of vascular cells in cardiac veins, thus enhancing structural integrity and recovery. PMID:25616738

  3. Myocardial Calcinosis in Chronic Renal Failure

    PubMed Central

    Kempf, Ashley E.; Momeni, Maryam Golshan; Saremi, Farhood

    2009-01-01

    The authors are presenting an 18 year old male with history of end stage renal disease and rejected renal transplant. In his workup echocardiogram and non contract CT of chest revealed diffuse endocardial and myocardial calcifications. Extensive cardiac calcification is a rare but important entity in relation to end stage renal disease as it may cause complications such as valvular dysfunction and fatal arrhythmia. PMID:22470643

  4. Thallium-201 myocardial imaging in children

    SciTech Connect

    Sty, J.R.; Starshak, R.J.

    1985-01-01

    The clinical applications of thallium-201 scintigraphy are less well defined in children than in adults. However, the published data indicate several potential applications including assessment of: 1) deficit in left ventricular myocardial perfusion, 2) early right ventricular volume or pressure overload, or both, and 3) the right ventricle in both cyanotic and acyanotic congenital heart disease. In this report, the applications of thallium imaging to pediatric diseases are described and the advantages and disadvantages of the procedure are enumerated.

  5. [Myocardial depression in the burn patient].

    PubMed

    Carrillo-Esper, Raúl; Sánchez-Zúñiga, Martín de Jesús

    2006-01-01

    Myocardial depression and heart failure are frequent complications in critically ill burn patients. The physiopathology is complex and involves the activation of inflammatory pathways, ischemia-reperfusion, oxidative stress and endothelial lesion. Diagnosis should be made early by means of hemodynamic monitoring. Treatment is accomplished by inotropics that act on different pathways of the contractile function and immune response associated with antioxidants and allopurinol. PMID:16887086

  6. [Transition of myocardial ischemia to heart failure].

    PubMed

    Ertl, G; Fraccarollo, D; Gaudron, P; Hu, K; Laser, A; Neubauer, S; Schorb, W

    1998-09-01

    Myocardial ischemia results in myocardial dysfunction. Recovery may be delayed ("stunning"), or persistent if perfusion remains reduced ("hibernation") and ischemia may go on to necrosis, thus, contributing to chronic heart failure. In addition, myocardium not directly affected by ischemia may undergo adaptive processes like hypertrophy and dilatation, which may result in chronic left heart failure. This process is characterized by hemodynamic, neurohumoral, and progressive morphologic changes of the heart which are closely interrelated. Hemodynamic changes basically consist of an increase in left ventricular filling pressure and a decrease in global ejection fraction, and, in most cases years after myocardial infarction, in an increase in systemic vascular resistance and right atrial pressure. Neurohumoral changes consist of an increase in plasma catecholamines, atrial natriuretic factor and vasopressin, and in an activation of the renin-angiotensin-system. Plasma endothelin-1 was recently reported to be increased in patients with heart failure, and prognosis was related to endothelin levels. Diminished response of vessels to endothelium (EDRF/NO) dependent vasodilatation suggests impairment of vascular endothelium in heart failure. Local changes of cardiac neurohumoral systems could contribute to structural changes of the heart, e.g., systemic activation to hemodynamic changes. Structural changes of the heart are characterized by an increase in volume and thickness of surviving myocardium and an expansion of ischemic and necrotic myocardium. Molecular control of these processes which include various cell types, such as cardiomyocytes and cardiofibroblasts, are currently an issue of intense research and could result in specific therapeutic importance. PMID:9816648

  7. Increased myocardial catalase in rats fed ethanol.

    PubMed Central

    Fahimi, H. D.; Kino, M.; Hicks, L.; Thorp, K. A.; Abelman, W. H.

    1979-01-01

    The effects of chronic intake of dietary ethanol upon catalase, an enzyme capable of metabolizing ethanol, as well as upon myocardial morphology and hemodynamics, were studied in the rat. Ethanol, comprising 36% of dietary calories, administered to rats for 5 weeks, was associated with increased myocardial catalase of 45.9 +/- 3.7 IU/mg protein, compared to 21.0 +/- 1.8 IU/mg protein in pair-fed controls. The enzyme activity remained significantly elevated after 18 weeks of ethanol. Hepatic catalase did not differ in these groups. Parallel cytochemical studies confirmed the increase in myocardial catalase by demonstrating an increase in peroxisomes. Gross and light-microscopic examinations revealed no abnormalities at either 5 or 18 weeks. Remarkably few ultrastructural abnormalities were seen in this material fixed by vascular perfusion. Hemodynamic studies after 5 weeks of ethanol revealed decreased left ventricle systolic pressure and decreased mean arterial pressure but no change in ventricular filling pressure. The possibility of catalase playing a metabolic and potentially protective role in rat myocardium chronically exposed to ethanol is discussed. Images Figure 3 Figure 4-6 Figures 1 and 2 Figures 7 and 8 p[389]-a PMID:474705

  8. Multispectral optoacoustic tomography of myocardial infarction

    PubMed Central

    Taruttis, Adrian; Wildgruber, Moritz; Kosanke, Katja; Beziere, Nicolas; Licha, Kai; Haag, Rainer; Aichler, Michaela; Walch, Axel; Rummeny, Ernst; Ntziachristos, Vasilis

    2012-01-01

    Objectives To investigate the feasibility of a high resolution optical imaging strategy for myocardial infarction. Background Near-infrared approaches to imaging cardiovascular disease enable visualization of disease-associated biological processes in vivo. However, even at the scale of small animals, the strong scattering of light prevents high resolution imaging after the first 1–2 mm of tissue, leading to degraded signal localization. Methods Multispectral optoacoustic tomography (MSOT) was used to non-invasively image myocardial infarction (MI) in a murine model of coronary artery ligation at resolutions not possible with current deep-tissue optical imaging methods. Post-MI imaging was based on resolving the spectral absorption signature of a dendritic polyglycerol sulfate-based (dPGS) near-infrared imaging agent targeted to P- and L-selectin. Results In vivo imaging succeeded in detection of the agent in the injured myocardium after intravenous injection. The high anatomic resolution (<200 μm) achieved by the described method allowed signals originating in the infarcted heart to be distinguished from uptake in adjacent regions. Histological analysis found dPGS signal in infarcted areas, originating from leukocytes and endothelial cells. Conclusions MSOT imaging of myocardial infarction provides non-invasive visualization of optical contrast with a high spatial resolution that is not degraded by the scattering of light. PMID:25327410

  9. PARP inhibition and postinfarction myocardial remodeling.

    PubMed

    Halmosi, Robert; Deres, Laszlo; Gal, Roland; Eros, Krisztian; Sumegi, Balazs; Toth, Kalman

    2016-08-01

    Coronary artery disease accounts for the greatest proportion of cardiovascular diseases therefore it is the major cause of death worldwide. Its therapeutic importance is indicated by still high mortality of myocardial infarction, which is one of the most severe forms of CVDs. Moreover, the risk of developing heart failure is very high among survivors. Heart failure is accompanied by high morbidity and mortality rate, therefore this topic is in the focus of researchers' interest. After a myocardial infarct, at first ventricular hypertrophy develops as a compensatory mechanism to decrease wall stress but finally leads to left ventricular dilation. This phenomenon is termed as myocardial remodeling. The main characteristics of underlying mechanisms involve cardiomyocyte growth, vessel changes and increased collagen production, in all of which several mechanical stress induced neurohumoral agents, oxidative stress and signal transduction pathways are involved. The long term activation of these processes ultimately leads to left ventricular dilation and heart failure with decreased systolic function. Oxidative stress causes DNA breaks producing the activation of nuclear poly(ADP-ribose) polymerase-1 (PARP-1) enzyme that leads to energy depletion and unfavorable modulation of different kinase cascades (Akt-1/GSK-3β, MAPKs, various PKC isoforms) and thus it promotes the development of heart failure. Therefore inhibition of PARP enzyme could offer a promising new therapeutical approach to prevent the onset of heart failure among postinfarction patients. The purpose of this review is to give a comprehensive summary about the most significant experimental results and mechanisms in postinfarction remodeling. PMID:27392900

  10. Myocardial perfusion echocardiography and coronary microvascular dysfunction

    PubMed Central

    Barletta, Giuseppe; Del Bene, Maria Riccarda

    2015-01-01

    Our understanding of coronary syndromes has evolved in the last two decades out of the obstructive atherosclerosis of epicardial coronary arteries paradigm to include anatomo-functional abnormalities of coronary microcirculation. No current diagnostic technique allows direct visualization of coronary microcirculation, but functional assessments of this circulation are possible. This represents a challenge in cardiology. Myocardial contrast echocardiography (MCE) was a breakthrough in echocardiography several years ago that claimed the capability to detect myocardial perfusion abnormalities and quantify coronary blood flow. Research demonstrated that the integration of quantitative MCE and fractional flow reserve improved the definition of ischemic burden and the relative contribution of collaterals in non-critical coronary stenosis. MCE identified no-reflow and low-flow within and around myocardial infarction, respectively, and predicted the potential functional recovery of stunned myocardium using appropriate interventions. MCE exhibited diagnostic performances that were comparable to positron emission tomography in microvascular reserve and microvascular dysfunction in angina patients. Overall, MCE improved echocardiographic evaluations of ischemic heart disease in daily clinical practice, but the approval of regulatory authorities is lacking. PMID:26730291

  11. Myocardial infarction: management of the subacute period.

    PubMed

    Mercado, Michael G; Smith, Dustin K; McConnon, Michael L

    2013-11-01

    Optimal management of myocardial infarction in the subacute period focuses on improving the discharge planning process, implementing therapies early to prevent recurrent myocardial infarction, and avoiding hospital readmission. Evidence-based guidelines for the care of patients with acute coronary syndrome are not followed up to 25% of the time. Antiplatelet therapy, renin-angiotensin-aldosterone system inhibitors, beta blockers, and statins constitute the foundation of medical therapy. Early noninvasive stress testing is an important risk assessment tool, especially in patients who do not undergo revascularization. Discharge preparation should include a review of medications, referral for exercise-based cardiac rehabilitation, activity recommendations, education about lifestyle modification and recognition of cardiac symptoms, and a clear follow-up plan. Because nonadherence to medications is common in patients after a myocardial infarction and is associated with increased mortality risk, modifiable factors associated with medication self-discontinuation should be addressed before discharge. Structured discharge processes should be used to enhance communication and facilitate the transition from the hospital to the family physician's care. PMID:24364634

  12. Myocardial perfusion echocardiography and coronary microvascular dysfunction.

    PubMed

    Barletta, Giuseppe; Del Bene, Maria Riccarda

    2015-12-26

    Our understanding of coronary syndromes has evolved in the last two decades out of the obstructive atherosclerosis of epicardial coronary arteries paradigm to include anatomo-functional abnormalities of coronary microcirculation. No current diagnostic technique allows direct visualization of coronary microcirculation, but functional assessments of this circulation are possible. This represents a challenge in cardiology. Myocardial contrast echocardiography (MCE) was a breakthrough in echocardiography several years ago that claimed the capability to detect myocardial perfusion abnormalities and quantify coronary blood flow. Research demonstrated that the integration of quantitative MCE and fractional flow reserve improved the definition of ischemic burden and the relative contribution of collaterals in non-critical coronary stenosis. MCE identified no-reflow and low-flow within and around myocardial infarction, respectively, and predicted the potential functional recovery of stunned myocardium using appropriate interventions. MCE exhibited diagnostic performances that were comparable to positron emission tomography in microvascular reserve and microvascular dysfunction in angina patients. Overall, MCE improved echocardiographic evaluations of ischemic heart disease in daily clinical practice, but the approval of regulatory authorities is lacking. PMID:26730291

  13. Soluble epoxide hydrolase inhibition and gene deletion are protective against myocardial ischemia-reperfusion injury in vivo.

    PubMed

    Motoki, Atsuko; Merkel, Matthias J; Packwood, William H; Cao, Zhiping; Liu, Lijuan; Iliff, Jeffrey; Alkayed, Nabil J; Van Winkle, Donna M

    2008-11-01

    Soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids. EETs are formed from arachidonic acid during myocardial ischemia and play a protective role against ischemic cell death. Deletion of sEH has been shown to be protective against myocardial ischemia in the isolated heart preparation. We tested the hypothesis that sEH inactivation by targeted gene deletion or pharmacological inhibition reduces infarct size (I) after regional myocardial ischemia-reperfusion injury in vivo. Male C57BL\\6J wild-type or sEH knockout mice were subjected to 40 min of left coronary artery (LCA) occlusion and 2 h of reperfusion. Wild-type mice were injected intraperitoneally with 12-(3-adamantan-1-yl-ureido)-dodecanoic acid butyl ester (AUDA-BE), a sEH inhibitor, 30 min before LCA occlusion or during ischemia 10 min before reperfusion. 14,15-EET, the main substrate for sEH, was administered intravenously 15 min before LCA occlusion or during ischemia 5 min before reperfusion. The EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE) was given intravenously 15 min before reperfusion. Area at risk (AAR) and I were assessed using fluorescent microspheres and triphenyltetrazolium chloride, and I was expressed as I/AAR. I was significantly reduced in animals treated with AUDA-BE or 14,15-EET, independent of the time of administration. The cardioprotective effect of AUDA-BE was abolished by the EET antagonist 14,15-EEZE. Immunohistochemistry revealed abundant sEH protein expression in left ventricular tissue. Strategies to increase 14,15-EET, including sEH inactivation, may represent a novel therapeutic approach for cardioprotection against myocardial ischemia-reperfusion injury. PMID:18835921

  14. Hesperidin blunts streptozotocin-isoproternol induced myocardial toxicity in rats by altering of PPAR-γ receptor.

    PubMed

    Agrawal, Yogeeta O; Sharma, Pankaj Kumar; Shrivastava, Birendra; Arya, Dharamvir Singh; Goyal, Sameer N

    2014-08-01

    Hesperidin has been shown to possess cardioprotective and anti-diabetic potential. Hitherto, its molecular mechanism on isoproterenol (ISO)-induced myocardial dysfunction in diabetes is still not explored. Hence, for the first time we sought to investigate whether hesperidin exerts any beneficial effect on the pathophysiology of myocardial infarction (MI) in diabetes through the PPAR-γ pathway by assessing a variety of indices e.g., apoptosis, hemodynamic, biochemical and histoarchitectural changes. Diabetes was induced by a single dose of STZ (50 mg/kg IP). Diabetic rats received either hesperidin (100 mg/kg/day orally), the PPAR-γ antagonist GW9662 (1 mg/kg/day IP), or both for 14 days with concurrent administration of ISO (85 mg/kg SC) on days 13 and 14. ISO-STZ rats resulted in severe myocardial dysfunction (decreased ±LVdP/dt and increased LVEDP). In addition, augmented myocardial thiobarbituric acid-reactive substances and serum troponin-I with a concomitant decrease in level of glutathione and activities of catalase, superoxide dismutase antioxidants with cardiac injury biomarkers creatine kinase-MB isoenzyme, lactate dehydrogenase were seen. Morphological studies of the ISO-STZ challenged myocardium exhibited severe necrosis, edema and inflammatory changes. In Western blot analysis, Bcl-2 and PPAR-γ expression were decreased where as Bax expression was significantly increased, suggesting role of apoptosis in myocardial dysfunction. Interestingly, hesperidin treatment positively modulated these parameters as validated by improved hemodynamic and left ventricular functions, fortified endogenous anti-oxidant defence system and improved structural integrity of the myocardium. However, significant effects were lowered in animals treated with hesperidin plus GW9662. Moreover, down-regulated PPAR-γ and Bcl-2 expressions in myocardial infarcted diabetic hearts were increased by hesperidin treatment. Hence, for the first time the present study suggests that

  15. Combretastatin A4 disodium phosphate-induced myocardial injury

    PubMed Central

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

    2016-01-01

    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.

  16. Quantitation of Acute Necrosis After Experimental Myocardial Infarction

    PubMed Central

    Yeap, Xin-Yi; Dehn, Shirley; Adelman, Jeremy; Lipsitz, Jeremy; Thorp, Edward B.

    2016-01-01

    Myocardial infarction (MI) is death and necrosis of myocardial tissue secondary to ischemia. MI is associated with adverse cardiac remodeling, progressive heart chamber dilation, ventricular wall thinning, and loss of cardiac function. Myocardial necrosis can be experimentally induced in rodents to simulate human MI by surgical occlusion of coronary arteries. When induced in knockout or transgenic mice, this model is useful for the identification of molecular modulators of cell death, cardiac remodeling, and preclinical therapeutic potential. Herein we outline in tandem, methods for microsurgical ligation of the left anterior descending artery followed by quantitation of myocardial necrosis. Necrosis is quantified after staining the heart with triphenyltetrazolium chloride. PMID:23733573

  17. 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

  18. PET: Is myocardial flow quantification a clinical reality?

    PubMed

    Saraste, Antti; Kajander, Sami; Han, Chunlei; Nesterov, Sergey V; Knuuti, Juhani

    2012-10-01

    Positron emission tomography (PET) enables quantitative measurements of myocardial blood flow (MBF) and myocardial flow reserve (MFR). Recent developments and improved availability of PET technology have resulted in growing interest in translation of quantitative flow analysis from mainly a research tool to routine clinical practice. Quantitative PET measurements of absolute MBF and MFR have potential to improve accuracy of myocardial perfusion imaging in diagnosis of multivessel coronary artery disease as well as definition of the extent and functional importance of stenoses. This article reviews recent advances and experience in the quantitative myocardial perfusion imaging together with issues that need to be resolved for quantitative analysis to become clinical reality. PMID:22733534

  19. Internal countershock produces myocardial damage and lactate production without myocardial ischemia in anesthetized dogs

    SciTech Connect

    Gaba, D.M.; Maxwell, M.S.; Merlone, S.; Smith, C.

    1987-04-01

    The global myocardial extraction of lactate was measured in 13 halothane anesthetized dogs to assess the effect of electric countershock applied directly to the heart. Seven animals received two countershocks of 30 delivered joules each, while six animals were not shocked but were atrially paced to a rate of 190-200, both with and without occlusion of the vena cava to produce a mean arterial pressure of 40-50 mmHg. All animals had substantially positive lactate extraction in the baseline state (36 +/- 10% for countershock group vs. 41 +/- 3% for pacing group). Myocardial lactate extraction reached a markedly negative nadir 2.5 min after countershock (-19 +/- 15%), but returned toward normal by 6 min (10 +/- 6%). Lactate extraction was not significantly changed from baseline in the pacing group. The relationship between changes in regional myocardial blood flow (radiolabeled microspheres) and post-countershock myocardial damage (technetium pyrophosphate uptake) was assessed in six dogs shocked as above. Mean myocardial blood flow was increased minimally immediately after countershock (0.78 +/- 0.08 ml X min-1 X g-1 vs. 1.16 +/- 0.3), but there was no difference in blood flow between damaged and undamaged tissue at either time point. The epicardial-to-endocardial ratio of blood flow was unchanged after countershock (0.97 +/- 0.05 vs. 0.99 +/- 0.08). There was no relationship between myocardial damage and either the absolute amount of blood flow after countershock (r = -0.03) or the change in blood flow compared with the pre-shock period (r = 0.01).

  20. Depressive Symptoms Are Associated with Mental Stress-Induced Myocardial Ischemia after Acute Myocardial Infarction

    PubMed Central

    Wei, Jingkai; Pimple, Pratik; Shah, Amit J.; Rooks, Cherie; Bremner, J. Douglas; Nye, Jonathon A.; Ibeanu, Ijeoma; Murrah, Nancy; Shallenberger, Lucy; Raggi, Paolo; Vaccarino, Viola

    2014-01-01

    Objectives Depression is an adverse prognostic factor after an acute myocardial infarction (MI), and an increased propensity toward emotionally-driven myocardial ischemia may play a role. We aimed to examine the association between depressive symptoms and mental stress-induced myocardial ischemia in young survivors of an MI. Methods We studied 98 patients (49 women and 49 men) age 38–60 years who were hospitalized for acute MI in the previous 6 months. Patients underwent myocardial perfusion imaging at rest, after mental stress (speech task), and after exercise or pharmacological stress. A summed difference score (SDS), obtained with observer-independent software, was used to quantify myocardial ischemia under both stress conditions. The Beck Depression Inventory-II (BDI-II) was used to measure depressive symptoms, which were analyzed as overall score, and as separate somatic and cognitive depressive symptom scores. Results There was a significant positive association between depressive symptoms and SDS with mental stress, denoting more ischemia. After adjustment for demographic and lifestyle factors, disease severity and medications, each incremental depressive symptom was associated with 0.14 points higher SDS. When somatic and cognitive depressive symptoms were examined separately, both somatic [β = 0.17, 95% CI: (0.04, 0.30), p = 0.01] and cognitive symptoms [β = 0.31, 95% CI: (0.07, 0.56), p = 0.01] were significantly associated with mental stress-induced ischemia. Depressive symptoms were not associated with ischemia induced by exercise or pharmacological stress. Conclusion Among young post-MI patients, higher levels of both cognitive and somatic depressive symptoms are associated with a higher propensity to develop myocardial ischemia with mental stress, but not with physical (exercise or pharmacological) stress. PMID:25061993

  1. Platelet microparticle number is associated with the extent of myocardial damage in acute myocardial infarction

    PubMed Central

    Puspitawati, Ira; Gharini, Putrika Prastuti Ratna; Setianto, Budi Yuli

    2016-01-01

    Introduction Activated platelets generate microparticles. Increased platelet microparticles occur in acute myocardial infarction (AMI) and contribute to intracoronary thrombosis and subsequent myocardial injury. This study aimed to investigate the impact of platelet microparticles on intracoronary thrombosis by assessing the relationship between platelet microparticles and the extent of myocardial damage in AMI. Material and methods This was a cross sectional study. The subjects were patients with acute coronary syndrome (ACS). Forty-one consecutive subjects with ACS admitted to intensive cardiovascular care unit were enrolled. The clinical spectrum of ACS comprised AMI (n = 26), both ST-elevation AMI (STEMI) and non-ST-elevation AMI (NSTEMI), and unstable angina (n = 15). Platelet microparticles were isolated from peripheral venous blood and detected with anti-CD42b-PE by the flow cytometry method. The extent of myocardial damage was determined by measuring the peak level of serial cardiac enzymes within 24 h of admission. Results Subjects with AMI had a significantly higher number of platelet microparticles than those with unstable angina (4855 ±4509/µl vs. 2181 ±1923/µl respectively; p = 0.036). Subjects with STEMI had the highest number of platelet microparticles, but no significant difference was detected as compared to those with NSTEMI (5775 ±5680/µl vs. 3601 ±1632/µl). The number of platelet microparticles in AMI was positively associated with the extent of myocardial damage (peak CK-MB: r = 0.408, p = 0.019 and peak GOT: r = 0.384, p = 0.026). Conclusions The number of platelet microparticles was increased in AMI as compared to unstable angina and associated with the extent of myocardial damage. PMID:27279844

  2. Radionuclide imaging in myocardial sarcoidosis. Demonstration of myocardial uptake of /sup 99m/Tc pyrophosphate and gallium

    SciTech Connect

    Forman, M.B.; Sandler, M.P.; Sacks, G.A.; Kronenberg, M.W.; Powers, T.A.

    1983-03-01

    A patient had severe congestive cardiomyopathy secondary to myocardial sarcoidosis. The clinical diagnosis was confirmed by radionuclide ventriculography, /sup 201/Tl, /sup 67/Ga, and /sup 99m/Tc pyrophosphate (TcPYP) scintigraphy. Myocardial TcPYP uptake has not been reported previously in sarcoidosis. In this patient, TcPYP was as useful as gallium scanning and thallium imaging in documenting the myocardial process.

  3. Myocardial Hemorrhage After Acute Reperfused ST-Segment–Elevation Myocardial Infarction

    PubMed Central

    Carrick, David; Haig, Caroline; Ahmed, Nadeem; McEntegart, Margaret; Petrie, Mark C.; Eteiba, Hany; Hood, Stuart; Watkins, Stuart; Lindsay, M. Mitchell; Davie, Andrew; Mahrous, Ahmed; Mordi, Ify; Rauhalammi, Samuli; Sattar, Naveed; Welsh, Paul; Radjenovic, Aleksandra; Ford, Ian; Oldroyd, Keith G.

    2016-01-01

    Background— The success of coronary reperfusion therapy in ST-segment–elevation myocardial infarction (MI) is commonly limited by failure to restore microvascular perfusion. Methods and Results— We performed a prospective cohort study in patients with reperfused ST-segment–elevation MI who underwent cardiac magnetic resonance 2 days (n=286) and 6 months (n=228) post MI. A serial imaging time-course study was also performed (n=30 participants; 4 cardiac magnetic resonance scans): 4 to 12 hours, 2 days, 10 days, and 7 months post reperfusion. Myocardial hemorrhage was taken to represent a hypointense infarct core with a T2* value of <20 ms. Microvascular obstruction was assessed with late gadolinium enhancement. Adverse remodeling was defined as an increase in left ventricular end-diastolic volume ≥20% at 6 months. Cardiovascular death or heart failure events post discharge were assessed during follow-up. Two hundred forty-five patients had evaluable T2* data (mean±age, 58 [11] years; 76% men). Myocardial hemorrhage 2 days post MI was associated with clinical characteristics indicative of MI severity and inflammation. Myocardial hemorrhage was a multivariable associate of adverse remodeling (odds ratio [95% confidence interval]: 2.64 [1.07–6.49]; P=0.035). Ten (4%) patients had a cardiovascular cause of death or experienced a heart failure event post discharge, and myocardial hemorrhage, but not microvascular obstruction, was associated with this composite adverse outcome (hazard ratio, 5.89; 95% confidence interval, 1.25–27.74; P=0.025), including after adjustment for baseline left ventricular end-diastolic volume. In the serial imaging time-course study, myocardial hemorrhage occurred in 7 (23%), 13 (43%), 11 (33%), and 4 (13%) patients 4 to 12 hours, 2 days, 10 days, and 7 months post reperfusion. The amount of hemorrhage (median [interquartile range], 7.0 [4.9–7.5]; % left ventricular mass) peaked on day 2 (P<0.001), whereas microvascular

  4. The effect of fatty acid surfactants on the uptake of ozone to aqueous halogenide particles

    NASA Astrophysics Data System (ADS)

    Rouvière, A.; Ammann, M.

    2010-12-01

    The reactive uptake of ozone to deliquesced potassium iodide aerosol particles coated with linear saturated fatty acids (C9, C12, C15, C18 and C20) was studied. The experiments were performed in an aerosol flow tube at 293 K and atmospheric pressure. The uptake coefficient on pure deliquesced KI aerosol was γ = (1.10±0.20)×10-2 at 72-75% relative humidity. In presence of organic coatings, the uptake coefficient decreased significantly for long straight chain surfactants (≥C15), while it was only slightly reduced for the short ones (C9, C12). We linked the kinetic results to the monolayer properties of the surfactants, and specifically to the expected phase state of the monolayer formed (liquid expanded or liquid condensed state). The results showed a decrease of the uptake coefficient by 30% for C12, 85% for C15 and 50% for C18 in presence of a monolayer of a fatty acid at the equilibrium spreading pressure at the air/water interface. The variation among C12, C15 and C18 follows the density of the monolayer at equilibrium spreading pressure, which is highest for the C15 fatty acid. We also investigated the effect of organic films to mixed deliquesced aerosol composed of a variable mixture of KI and NaCl, which allowed determining the resistance exerted to O3 at the aqueous surface by the two longer chained surfactants pentadecanoic acid (C15) and stearic acid (C18). For these, the probability that a molecule hitting the surface is actually transferred to the aqueous phase underneath was βC15=6.8×10-4 and βC18 = 3.3×10-4, respectively. Finally, the effect of two-component coatings, consisting of a mixture of long and short chained surfactants, was studied qualitatively.

  5. Assessment of diagnostic value of technetium-99m pyrophosphate myocardial scintigraphy in 80 patients with possible acute myocardial infarction.

    PubMed Central

    Walsh, W F; Karunaratne, H B; Resnekov, L; Fill, H R; Harper, P V

    1977-01-01

    The diagnostic value of technetium-99m-pyrophosphate (Tc-pyrophosphate) myocardial scintigraphy was determined in 80 consecutive patients who had been admitted to the coronary care unit in order to rule out an acute myocardial infarction. Scintigraphic findings obtained within 5 days of admission were correlated with the final cardiac diagnosis determined for each patient. Significant myocardial uptake of Tc-pyrophosphate (positive scans) occurred in 13 of 22 patients (59%) who had enzyme and/or electrocardiographic proven acute myocardial infarct: 3 out of 5 with transmural myocardial infarct, 9 of 16 with nontransmural myocardial infarct, and 1 patient with left bundle-branch block. Of 58 patients who showed no evidence of acute myocardial infarction, positive scans occurred in 14 of 33 patients who had unstable angina pectoris (42%), 0 of 6 who had congestive heart failure, 6 of 9 who had other acute cardiac syndromes, and in 0 of 10 who had noncardiac chest pain. In the patients with unstable angina pectoris positive scans could not be predicted on the basis of the history, electrocardiographic findings or the arteriographically determined severity of the coronary artery disease. Blood levels of Tc-99m activity measured in 21 cardiac patients and in 6 volunteers did not correlate with the uptake intensity of Tc-pyrophosphate. These findings suggest caution in the use of this imaging method for the diagnosis of acute myocardial infarct in patients admitted with 'rule out myocardial infarction'. Images PMID:907776

  6. Design of a 3D aligned myocardial tissue construct from biodegradable polyesters.

    PubMed

    Kenar, H; Kose, G T; Hasirci, V

    2010-03-01

    The heart does not regenerate new functional tissue when myocardium dies following coronary artery occlusion, or if it is defective. Ventricular restoration involves excising the infarct and replacing it with a cardiac patch to restore the heart to a more healthy condition. The goal of this study was to design and develop a clinically applicable myocardial patch to replace myocardial infarcts and improve long-term heart function. A basic design composed of 3D microfibrous mats that house mesenchymal stem cells (MSCs) was developed from human umbilical cord matrix (Wharton's Jelly) cells aligned in parallel to each other mimicking the native myocardium. Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV), poly(L-D,L-lactic acid) (P(L-D,L)LA) and poly(glycerol sebacate) (PGS) were blended and electrospun into aligned fiber mats with fiber diameter ranging between 1.10 and 1.25 microm. The micron-sized parallel fibers of the polymer blend were effective in cell alignment and cells have penetrated deep within the mat through the fiber interstices, occupying the whole structure; 8-9 cell layers were obtained. Biodegradable macroporous tubings were introduced to serve as nutrient delivery route. It was possible to create a thick myocardial patch with structure similar to the native tissue and with a capability to grow. PMID:19862604

  7. Noninvasive Molecular Imaging of Cell Death in Myocardial Infarction using 111In-GSAO

    PubMed Central

    Tahara, Nobuhiro; Zandbergen, H. Reinier; de Haas, Hans J.; Petrov, Artiom; Pandurangi, Raghu; Yamaki, Takayoshi; Zhou, Jun; Imaizumi, Tsutomu; Slart, Riemer H. J. A.; Dyszlewski, Mary; Scarabelli, Tiziano; Kini, Annapoorna; Reutelingsperger, Chris; Narula, Navneet; Fuster, Valentin; Narula, Jagat

    2014-01-01

    Acute insult to the myocardium is associated with substantial loss of cardiomyocytes during the process of myocardial infarction. In this setting, apoptosis (programmed cell death) and necrosis may operate on a continuum. Because the latter is characterized by the loss of sarcolemmal integrity, we propose that an appropriately labeled tracer directed at a ubiquitously present intracellular moiety would allow non-invasive definition of cardiomyocyte necrosis. A trivalent arsenic peptide, GSAO (4-(N-(S-glutathionylacetyl)amino)phenylarsonous acid), is capable of binding to intracellular dithiol molecules such as HSP90 and filamin-A. Since GSAO is membrane impermeable and dithiol molecules abundantly present intracellularly, we propose that myocardial localization would represent sarcolemmal disruption or necrotic cell death. In rabbit and mouse models of myocardial infarction and post-infarct heart failure, we employed In-111-labelled GSAO for noninvasive radionuclide molecular imaging. 111In-GSAO uptake was observed within the regions of apoptosis seeking agent- 99mTc-Annexin A5 uptake, suggesting the colocalization of apoptotic and necrotic cell death processes. PMID:25351258

  8. Respiratory chain defect of myocardial mitochondria in idiopathic dilated cardiomyopathy of Doberman pinscher dogs.

    PubMed

    McCutcheon, L J; Cory, C R; Nowack, L; Shen, H; Mirsalami, M; Lahucky, R; Kovac, L; O'Grady, M; Horne, R; O'Brien, P J

    1992-11-01

    Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause. We tested the hypothesis that IDCM was associated with a myocardial metabolic defect by determining a comprehensive biochemical profile of metabolite concentrations and enzyme activities for the major metabolic pathways of the myocardium. We used the Doberman pinscher breed as a naturally occurring canine model of IDCM and compared its myocardial profile with that of healthy adult mongrels. Compared with controls, myocardium in IDCM had markedly reduced mitochondrial electron transport activity and myoglobin concentration, in association with acidosis and energy depletion following anoxic challenge: 60% decreased NADH dehydrogenase and 50% decreased ATP synthetase activities; 90% decreased myoglobin concentration; and 30% reduced ATP and 50% increased lactate and proton concentrations. Sarcoplasmic reticulum Ca(2+)-transport ATPase was decreased by 42%. There was a 15% compensatory increase in fatty acid oxidation and Krebs cycle activity. Other biochemical changes were mild by comparison with the mitochondrial defects. We conclude that IDCM is associated with a marked impairment of mitochondrial production of ATP, arising from decreased activity of the mitochondrial electron transport system, including myoglobin. These changes may be secondary to an underlying genetic defect or may indicate a deficiency of the mitochondrial respiratory chain that predisposes this breed to heart failure. PMID:1338376

  9. N-13 ammonia as an indicator of myocardial blood flow. [Dogs

    SciTech Connect

    Schelbert, H.R.; Phelps, M.E.; Huang, S.C.; MacDonald, N.S.; Hansen, H.; Selin, C.; Kuhl, D.E.

    1981-06-01

    We have characterized N-13 ammonia as a myocardial blood flow imaging agent suitable for positron-emission computed tomography. However, the mechanisms of uptake and retention of this agent in myocardium are not known, and effects of altered metabolism were not considered. Therefore, we studied the uptake and retention of N-13 ammonia in myocardium under various hemodynamic and metabolic conditions in open-chest dogs. N-13 ammonia was extracted nearly 100% during its initial capillary transit, followed by metabolic trapping that competed with flow-dependent back diffusion. At control flows, the first capillary transit extraction fraction (E) of N-13 ammonia averaged 0.82 +- 0.06. Inhibition of glutamine synthetase with L-methionine sulfoximine impaired metabolic trapping of N-13 ammonia and implicates te glutamic acid-glutamine reaction as the primary mechanism for ammonia fixation. Blood flow and metabolic trapping are the primary determinants of myocardial uptake and retention of N-13 ammonia. The relative constancy of metabolic trapping over a wide range of hemodynamic and metabolic conditions demonstrates the value of N-13 ammonia as a myocardial blood flow imaging agent.

  10. Conditioning the heart to prevent myocardial reperfusion injury during PPCI

    PubMed Central

    2012-01-01

    For patients presenting with a ST-segment elevation myocardial infarction (STEMI), early myocardial reperfusion by primary percutaneous coronary intervention (PPCI) remains the most effective treatment strategy for limiting myocardial infarct size, preserving left ventricular systolic function, and preventing the onset of heart failure. Recent advances in PCI technology to improve myocardial reperfusion and the introduction of novel anti-platelet and anti-thrombotic agents to maintain the patency of the infarct-related coronary artery continue to optimize PPCI procedure. However, despite these improvements, STEMI patients still experience significant major adverse cardiovascular events. One major contributing factor has been the inability to protect the heart against the lethal myocardial reperfusion injury, which accompanies PPCI. Past attempts to translate cardioprotective strategies, discovered in experimental studies to prevent lethal myocardial reperfusion injury, into the clinical setting of PPCI have been disappointing. However, a number of recent proof-of-concept clinical studies suggest that the heart can be ‘conditioned’ to protect itself against lethal myocardial reperfusion injury, as evidenced by a reduction in myocardial infarct size. This can be achieved using either mechanical (such as ischaemic postconditioning, remote ischaemic preconditioning, therapeutic hypothermia, or hyperoxaemia) or pharmacological (such as cyclosporin-A, natriuretic peptide, exenatide) ‘conditioning’ strategies as adjuncts to PPCI. Furthermore, recent developments in cardiac magnetic resonance (CMR) imaging can provide a non-invasive imaging strategy for assessing the efficacy of these novel adjunctive therapies to PPCI in terms of key surrogate clinical endpoints such as myocardial infarct size, myocardial salvage, left ventricular ejection fraction, and the presence of microvascular obstruction or intramyocardial haemorrhage. In this article, we review the

  11. Cardiac troponin T in the diagnosis of myocardial injury.

    PubMed

    Mair, J; Dienstl, F; Puschendorf, B

    1992-01-01

    In the last several decades serum levels of cardiac enzymes and isoenzymes have become the final arbiters by which myocardial damage is diagnosed or excluded. Because conventionally used enzymes are neither perfectly sensitive nor specific, there is need for a new sensitive and cardiospecific marker of myocardial damage. Cardiac troponin T (TnT) is a contractile protein unique to cardiac muscle and can be differentiated by immunologic methods from its skeletal-muscle isoform. An enzyme immunoassay specific for cardiac TnT is now available in a commercial kit for routine use. The biggest advantage of this assay is its cardiospecificity. TnT measurements, however, are also highly sensitive in diagnosis of myocardial injury and accurately discern even small amounts of myocardial necrosis. TnT measurements are, therefore, particularly useful in patients with borderline CK-MB and in clinical settings in which traditional enzymes fail to diagnose myocardial damage efficiently because of lack of specificity--for example, perioperative myocardial infarction or blunt heart trauma. TnT release kinetics reveal characteristics of both soluble, cytoplasmic, and structurally bound molecules. It starts to increase a few hours after the onset of myocardial damage and remains increased for several days. TnT allows late diagnosis of myocardial infarction. The diagnostic efficiency remains at 98% until 6 d after the onset of infarct-related symptoms. TnT is also useful in monitoring the effectiveness of thrombolytic therapy in myocardial infarction patients. The ratio of peak TnT concentration on day 1 to TnT concentration at day 4 discriminates between patients with successful (greater than 1) and failed (less than or equal to 1) reperfusion. TnT measurements are very sensitive and specific for the early and late diagnosis of myocardial damage and could, therefore, provide a new criterion in laboratory diagnosis of the occurrence of myocardial damage. PMID:1388708

  12. Myocardial blood flow and its transit time, oxygen utilization, and efficiency of highly endurance-trained human heart.

    PubMed

    Heinonen, Ilkka; Kudomi, Nobuyuki; Kemppainen, Jukka; Kiviniemi, Antti; Noponen, Tommi; Luotolahti, Matti; Luoto, Pauliina; Oikonen, Vesa; Sipilä, Hannu T; Kopra, Jaakko; Mononen, Ilkka; Duncker, Dirk J; Knuuti, Juhani; Kalliokoski, Kari K

    2014-07-01

    Highly endurance-trained athlete's heart represents the most extreme form of cardiac adaptation to physical stress, but its circulatory alterations remain obscure. In the present study, myocardial blood flow (MBF), blood mean transit time (MTT), oxygen extraction fraction (OEF) and consumption (MVO2), and efficiency of cardiac work were quantified in highly trained male endurance athletes and control subjects at rest and during supine cycling exercise using [(15)O]-labeled radiotracers and positron emission tomography. Heart rate and MBF were lower in athletes both at rest and during exercise. OEF increased in response to exercise in both groups, but was higher in athletes (70 ± 21 vs. 63 ± 11 % at rest and 86 ± 13 vs. 73 ± 10 % during exercise). MTT was longer and vascular resistance higher in athletes both at rest and during exercise, but arterial content of 2,3-diphosphoglycerate (oxygen affinity) was unchanged. MVO2 per gram of myocardium trended (p = 0.08) lower in athletes both at rest and during exercise, while myocardial efficiency of work and MVO2 per beat were not different between groups. Arterial levels of free fatty acids were ~twofold higher in athletes likely leading to higher myocardial fatty acid oxidation and hence oxygen cost, which may have blunted the bradycardia-induced decrease in MVO2. Finally, the observed group differences in MBF, OEF, MTT and vascular resistance remained significant also after they were controlled for differences in MVO2. In conclusion, in highly endurance-trained human heart, increased myocardial blood transition time enables higher oxygen extraction levels with a lower myocardial blood flow and higher vascular resistance. These physiological adaptations to exercise training occur independently of the level of oxygen consumption and together with training-induced bradycardia may serve as mechanisms to increase functional reserve of the human heart. PMID:24866583

  13. Comparison of myocardial contrast echocardiography with NC100100 and 99mTc sestamibi SPECT for detection of resting myocardial perfusion abnormalities in patients with previous myocardial infarction

    PubMed Central

    Jucquois, I; Nihoyannopoulos, P; D'Hondt, A; Roelants, V; Robert, A; Melin, J; Glass, D; Vanoverschelde, J

    2000-01-01

    OBJECTIVE—To determine whether myocardial contrast echocardiography (MCE) following intravenous injection of perfluorocarbon microbubbles permits identification of resting myocardial perfusion abnormalities in patients who have had a previous myocardial infarction.
PATIENTS AND INTERVENTIONS—22 patients (mean (SD) age 66 (11) years) underwent MCE after intravenous injection of NC100100, a novel perfluorocarbon containing contrast agent, and resting 99mTc sestamibi single photon emission computed tomography (SPECT). With both methods, myocardial perfusion was graded semiquantitatively as 1 = normal, 0.5 = mild defect, and 0 = severe defect.
RESULTS—Among the 203 normally contracting segments, 151 (74%) were normally perfused by SPECT and 145 (71%) by MCE. With SPECT, abnormal tracer uptake was mainly found among normally contracting segments from the inferior wall. By contrast, with MCE poor myocardial opacification was noted essentially among the normally contracting segments from the anterior and lateral walls. Of the 142 dysfunctional segments, 87 (61%) showed perfusion defects by SPECT, and 94 (66%) by MCE. With both methods, perfusion abnormalities were seen more frequently among akinetic than hypokinetic segments. MCE correctly identified 81/139 segments that exhibited a perfusion defect by SPECT (58%), and 135/206 segments that were normally perfused by SPECT (66%). Exclusion of segments with attenuation artefacts (defined as abnormal myocardial opacification or sestamibi uptake but normal contraction) by either MCE or SPECT improved both the sensitivity (76%) and the specificity (83%) of the detection of SPECT perfusion defects by MCE.
CONCLUSIONS—The data suggest that MCE allows identification of myocardial perfusion abnormalities in patients who have had a previous myocardial infarction, provided that regional wall motion is simultaneously taken into account.


Keywords: myocardial contrast echocardiography; NC100100

  14. Cardioprotective actions of Notch1 against myocardial infarction via LKB1-dependent AMPK signaling pathway.

    PubMed

    Yang, Hui; Sun, Wanqing; Quan, Nanhu; Wang, Lin; Chu, Dongyang; Cates, Courtney; Liu, Quan; Zheng, Yang; Li, Ji

    2016-05-15

    AMP-activated protein kinase (AMPK) signaling pathway plays a pivotal role in intracellular adaptation to energy stress during myocardial ischemia. Notch1 signaling in the adult myocardium is also activated in response to ischemic stress. However, the relationship between Notch1 and AMPK signaling pathways during ischemia remains unclear. We hypothesize that Notch1 as an adaptive signaling pathway protects the heart from ischemic injury via modulating the cardioprotective AMPK signaling pathway. C57BL/6J mice were subjected to an in vivo ligation of left anterior descending coronary artery and the hearts from C57BL/6J mice were subjected to an ex vivo globe ischemia and reperfusion in the Langendorff perfusion system. The Notch1 signaling was activated during myocardial ischemia. A Notch1 γ-secretase inhibitor, dibenzazepine (DBZ), was intraperitoneally injected into mice to inhibit Notch1 signaling pathway by ischemia. The inhibition of Notch1 signaling by DBZ significantly augmented cardiac dysfunctions caused by myocardial infarction. Intriguingly, DBZ treatment also significantly blunted the activation of AMPK signaling pathway. The immunoprecipitation experiments demonstrated that an interaction between Notch1 and liver kinase beta1 (LKB1) modulated AMPK activation during myocardial ischemia. Furthermore, a ligand of Notch1 Jagged1 can significantly reduce cardiac damage caused by ischemia via activation of AMPK signaling pathway and modulation of glucose oxidation and fatty acid oxidation during ischemia and reperfusion. But Jagged1 did not have any cardioprotections on AMPK kinase dead transgenic hearts. Taken together, the results indicate that the cardioprotective effect of Notch1 against ischemic damage is mediated by AMPK signaling via an interaction with upstream LKB1. PMID:27015742

  15. Cell-free DNA for diagnosing myocardial infarction: not ready for prime time.

    PubMed

    Lippi, Giuseppe; Sanchis-Gomar, Fabian; Cervellin, Gianfranco

    2015-11-01

    A modest amount of cell-free DNA is constantly present in human blood, originating from programmed cell death, apoptosis and rupture of blood cells or pathogens. Acute or chronic cell injury contributes to enhance the pool of circulating nucleic acids, so that their assessment may be regarded as an appealing perspective for diagnosing myocardial ischemia. We performed a search in Medline, Web of Science and Scopus to identify clinical studies that investigated the concentration of cell-free DNA in patients with myocardial ischemia. Overall, eight case-control studies could be detected and reviewed. Although the concentration of cell-free DNA was found to be higher in the diseased than in the healthy population, the scenario was inconclusive due to the fact that the overall number of subjects studied was modest, the populations were unclearly defined, cases and controls were not adequately matched, the methodology for measuring the reference cardiac biomarkers was inadequately described, and the diagnostic performance of cell-free DNA was not benchmarked against highly sensitive troponin immunoassays. Several biological and technical hurdles were also identified in cell-free DNA testing, including the lack of specificity and unsuitable kinetics for early diagnosis of myocardial ischemia, the long turnaround time and low throughput, the need for specialized instrumentation and dedicated personnel, the lack of standardization or harmonization of analytical techniques, the incremental costs and the high vulnerability to preanalytical variables. Hence it seems reasonable to conclude that the analysis of cell-free DNA is not ready for prime time in diagnostics of myocardial ischemia. PMID:25883207

  16. Selective Cyclooxygenase-2 Inhibition Protects Against Myocardial Damage in Experimental Acute Ischemia

    PubMed Central

    Carnieto, Alberto; Dourado, Paulo Magno Martins; da Luz, Protásio Lemos; Chagas, Antonio Carlos Palandri

    2009-01-01

    BACKGROUND Acute myocardial infarction is associated with tissue inflammation. Early coronary reperfusion clearly improves the outcome but may help propagate the inflammatory response and enhance tissue damage. Cyclooxygenase-2 is an enzyme that catalyzes the initial step in the formation of inflammatory prostaglandins from arachidonic acid. Cyclooxygenase-2 levels are increased when ischemic cardiac events occur. The overall function of COX-2 in the inflammatory process generated by myocardial ischemic damage has not yet been elucidated. GOAL The objective of this study was to determine whether a selective cyclooxygenase-2 inhibitor (rofecoxib) could alter the evolution of acute myocardial infarction after reperfusion. METHODS AND RESULTS This study was performed with 48 mongrel dogs divided into two groups: controls and those treated with the drug. All animals were prepared for left anterior descending coronary artery occlusion. The dogs then underwent 180 minutes of coronary occlusion, followed by 30 minutes of reperfusion. Blood samples were collected from the venous sinus immediately before coronary occlusion and after 30 minutes of reperfusion for measurements of CPK-MB, CPK-MBm and troponin I. During the experiment we observed the mean blood pressure, heart rate and coronary flow. The coronary flow and heart rate did not change, but in the control group, there was blood pressure instability, in addition to maximal levels of CPK-MB post-infarction. The same results were observed for CPK-MBm and troponin I. CONCLUSION In a canine model of myocardial ischemia-reperfusion, selective inhibition of Cyclooxygenase-2 with rofecoxib was not associated with early detrimental effects on the hemodynamic profile or the gross extent of infarction; in fact, it may be beneficial by limiting cell necrosis. PMID:19330252

  17. Assessment of myocardial blood perfusion improved by CD151 in a pig myocardial infarction model

    PubMed Central

    Zuo, Hou-juan; Liu, Zheng-xiang; Liu, Xiao-chun; Yang, Jun; Liu, Tao; Wen, Sha; Wang, Dao-wen; Zhang, Xin

    2009-01-01

    Aim: To appraise the efficacy of CD151-induced myocardial therapeutic angiogenesis in a pig myocardial infarction model. Methods: CD151 and anti-CD151 were constructed into the recombinant adeno-associated virus (rAAV) vector. All 26 pigs were subjected to coronary artery ligation or no surgery. Eight weeks after coronary artery ligation, the expression of CD151 was measured by Western blot and immunostaining. Capillary density was evaluated using immunostaining for von Willebrand factor (vWF). 13N-labeled NH3 positron emission computed tomography ([13N]NH3 PET) was measured to assess regional myocardial perfusion and the defect area. Results: CD151 gene delivery could increase the expression of CD151 at protein level. Over-expression of CD151 increased the density of total capillaries in the ischemic myocardium, significantly improved the blood perfusion and reduced the defect area percentage. Conclusion: This study demonstrated that the rAAV-mediated CD151 gene delivery promoted efficient neovascularization and increased the blood perfusion after myocardial infarction in pigs. PMID:19079294

  18. Improving the early diagnosis of acute myocardial infarction.

    PubMed Central

    Banerjee, A.

    1996-01-01

    The diagnosis of early myocardial infarction, especially in association with atypical clinical presentations, can be difficult to establish. Continued observation of high-risk patients, with multiple serial electrocardiographs and the use of other diagnostic modalities as available, is essential to prevent the inadvertent premature discharge of patients with evolving myocardial infarcts from the accident and emergency department. PMID:9015461

  19. Prognostic value of radionuclide exercise testing after myocardial infarction

    SciTech Connect

    Schocken, D.D.

    1984-08-01

    Abnormal systolic ventricular function and persistent ischemia are sensitive indicators of poor prognosis following myocardial infarction. The use of exercise improves the utility of both radionuclide ventriculography and myocardial perfusion scintigraphy in the identification of postinfarction patients at high risk of subsequent cardiac events. 51 references.

  20. Predictors of Appraisal and Coping Dimensions in Myocardial Infarction Victims.

    ERIC Educational Resources Information Center

    Lee, Hyong Sil; Martin, Peter

    This study attempted to identify predictors of perception and coping after the occurrence of a myocardial infarction. Sixty males and 17 females who had suffered from a myocardial infarction within 3 months prior to the research were recruited from a hospital rehabilitation program. Subjects completed the Peri-Life Events Scale, the 16-PF…

  1. Low High-Density Lipoprotein and Risk of Myocardial Infarction.

    PubMed

    Ramirez, A; Hu, P P

    2015-01-01

    Low HDL is an independent risk factor for myocardial infarction. This paper reviews our current understanding of HDL, HDL structure and function, HDL subclasses, the relationship of low HDL with myocardial infarction, HDL targeted therapy, and clinical trials and studies. Furthermore potential new agents, such as alirocumab (praluent) and evolocumab (repatha) are discussed. PMID:26692765

  2. Low High-Density Lipoprotein and Risk of Myocardial Infarction

    PubMed Central

    Ramirez, A.; Hu, P. P.

    2015-01-01

    Low HDL is an independent risk factor for myocardial infarction. This paper reviews our current understanding of HDL, HDL structure and function, HDL subclasses, the relationship of low HDL with myocardial infarction, HDL targeted therapy, and clinical trials and studies. Furthermore potential new agents, such as alirocumab (praluent) and evolocumab (repatha) are discussed. PMID:26692765

  3. Value of positive myocardial infarction imaging in coronary care units.

    PubMed Central

    Joseph, S P; Pereira-Prestes, A V; Ell, P J; Donaldson, R; Somerville, W; Emanuel, R W

    1979-01-01

    Positive myocardial imaging was undertaken on 120 unselected patients admitted to a coronary care unit with clinical suspicion of acute myocardial infarction. Multipurpose mobile gamma-cameras were used for serial imaging after administration of 99mtechnetium-labelled imidodiphosphonate, a low-cost radiopharmaceutical that is 97% specific for myocardial necrosis, with myocardial uptake and blood clearance most suitable for myocardial imaging. The sensitivty of detection was 94% for patients whose infarction was unequivocal on the ECG; when the presence of raised enzyme concentrations was also used as a criterion for myocardial necrosis, the overall sensitivity for all 120 patients remained 94%. In 73 patients (61%), whose ECGs were unhelpful or difficult to interpret, scintigraphy allowed infarction to be diagnosed in 11 (15%) and to be excluded in five (7%). In 32 (44%) of this group whose ECGs were totally uninterpretable due to previous myocardial damage or disorders of electrical activation, scintigraphy provided confirmation of a diagnosis that otherwise rested only on whether enzyme concentrations were raised. Myocardial imaging is thus a useful technique that permits more definite diagnosis in patients for whom ECG and enzyme data are uncertain. PMID:761017

  4. Myocardial structures over the coronary arteries and their branches.

    PubMed

    Aleksandrowicz, R; Balwierz, P; Barczak, R; Stryjewska-Makuch, G

    1993-01-01

    Myocardial bridges over coronary arteries have been investigated in 30 pig's hearts. Such bridges were found in 26 hearts. Such structures were in form of myocardial loops, bridges or tunnels. The bridges were found most often over the posterior interventricular branch. PMID:8175071

  5. Seasonal changes of buffalo colostrum: physicochemical parameters, fatty acids and cholesterol variation

    PubMed Central

    2013-01-01

    Background Colostrum has many beneficial effects on newborns due to its main compounds (proteins, fats, lactose, essential fatty acids, amino acids) as well as protective antibodies that confer to the body. The buffaloes are the second important species for milk production in the world after cows. The importance of the species is also conferred by a longer longevity, high dry content of milk and a strong organic resistance when compared with cows. The purpose of this study was to investigate the changes of buffalo colostrum compounds such as fatty acids, cholesterol and physicochemical parameters during the first seven days postpartum and under the impact of the season, summer on pasture and winter on dry diet (hay based). Results Fat from colostrum differs depending on the postpartum day showing mean values of 11.31-7.56% (summer season) and 11.22-7.51% (winter season). These values gradually decreased starting with first day postpartum until day seven. Dry substance and protein presented a similar evolution to fat reaching the lowest values at the end of the colostral period. Lactose, ash and pH showed a gradually increase reaching the maximum on day seven postpartum. The highest titres of fatty acids from colostrum are: butyric acid (C4:0), myristic acid (C14:0), palmitic acid (C16:0), oleic acid (C18:1) and the lowest values showed up in myristoleic acid (C14:1), cis-10-pentadecanoic acid (C15:1), pentadecylic acid (C15:0) and margaric acid (C17:0) for both seasons. Higher concentrations have been recorded for the summer season in general. Cholesterol concentration decreased from 12.93 and 12.68 mg/100 mL (summer and winter season) to 9.02 and 7.88 mg/100 mL in the end of the colostral period. Conclusions Physicochemical compounds of buffalo colostrum were influenced by season and postpartum day of milking. Excepting lactose all other parameters gradually decreased during colostral period. Fatty acids and cholesterol showed the same evolution, presenting higher

  6. Protective Role of Ramipril and Candesartan against Myocardial Ischemic Reperfusion Injury: A Biochemical and Transmission Electron Microscopical Study

    PubMed Central

    Reddy, Rajitha Bodd; Punuru, Priyanka; Chakka, Gopinath; Karunakaran, Gauthaman

    2016-01-01

    The present study was designed to investigate the role of combined administration of Ramipril and Candesartan against in vitro myocardial ischemic reperfusion injury in rat. Male Wistar albino rats were divided into five groups (n = 6) and treated with saline (10 mL/kg), Ramipril (2 mg/kg), Candesartan (1 mg/kg), and the combination of both drugs, respectively 24 h before induction of global ischemia (5 min of stabilization, 9 min of global ischemia, and 12 min of reflow). Combination of Ramipril and Candesartan when compared to the monotherapy significantly increased the levels of superoxide dismutase, reduced glutathione, catalase, and nitric oxide and decreased the levels of thiobarbituric acid reactive substances. In addition, the superior protective role of combination of Ramipril and Candesartan on ischemia induced myocardial damage was further confirmed by well preserved myocardial tissue architecture in light microscopy and transmission electron microscopy analysis studies. The combination was proved to be effective in salvaging the myocardial tissue against ischemic reperfusion injury when compared to the monotherapy of individual drugs and further investigations on protective mechanism of drugs by increasing the nitric oxide level at molecular levels are needed. PMID:27042175

  7. [The reduction of stroke risk, risk of myocardial infarction and death by healthy diet and physical activity].

    PubMed

    Droste, D W; Keipes, M

    2013-01-01

    There is no doubt that a healthy diet and regular physical activity improve risk factors for cerebro-cardio-vascular disease and death. However, there is less evidence from prospective randomised controlled trials that they also reduce the actual risk of stroke, myocardial infarction and death. The only evidence from randomised controlled trials is, that a mediterranean diet with nuts and/or native olive oil considerably reduces stroke risk by 47% respectively 31%, however not the risk of myocardial infarction and death. A low-fat diet, a low-salt diet, and the addition of omega-3 fatty acids have no influence. In case of severe obesity with a BMI of > 34-38 kg/m2, weight reduction is the priority, if necessary by means of bariatric surgery. In longitudinal studies mortality (-29%), stroke (-34%), and myocardial infarction (-29%) could thus be reduced. Regular physical activity, whether endurance or more intense activity, leads to weight loss and improved vascular risk factors. An independent impact on stroke, myocardial infarction and mortality has not yet been demonstrated in prospective studies (double-blinding being impossible). Nevertheless, several epidemiological meta-analyses with observation durations of 4 to 28 years using data of up to 880 000 persons, indicate that there is a 2-3 fold risk reduction of cerebro-cardio-vascular death and global mortality in people with regular physical activity versus sedentary behaviour. PMID:24437075

  8. Decreased sulfhydryl groups in the reperfused myocardial tissue of a rat model of myocardial infarction.

    PubMed

    Maezawa, H; Manaka, K; Yamakawa, K; Ogawa, K; Iizuka, M

    1997-02-01

    The aim of this study was to determine whether myocardial injury resulting from temporary ischemia followed by reperfusion can be measured by assaying sulfhydryl groups in the affected tissue of a rat model of myocardial infarction. We studied 3 groups: a control group (n = 6), which underwent surgery without left coronary artery (LCA) ligation; group NoR (n = 9), in which the LCA was ligated for 3 h; and group I + R (n = 7), in which 30 min LCA ligation was followed by 3 h reperfusion. The sulfhydryl group content of myocardial tissue was assayed by measuring the fluorescence produced by incubating heart sections with N-(7-dimethylamino-4-methyl-3-coumarinyl) maleimide (DACM), which binds sulfhydryl groups. The fluorescence intensity (FI) of normal and infarcted myocardium was quantified by our computerized system of microscopic fluorophotometry. Indices such as sulfhydryl group content, the size of the low-FI area [% AREA(lower FI)] and the relative decrease in FI [%FI(decrease)]) in the infarct zone were calculated. Both %AREA(lower FI) and %FI(decrease) were significantly higher in the infarcted zone of animals in NoR and I + R groups than in control animals. Both indices were higher in infarct tissue from animals in the I + R group than in the NoR group. These changes suggest that sulfhydryl group content is significantly reduced in tissue that has been subjected to ischemia-reperfusion. Microscopic fluorophotometry, as defined by DACM staining of myocardial tissue, may help to delineate areas of myocardial reperfusion injury. PMID:9070971

  9. Effect of hydroxy safflower yellow A on myocardial apoptosis after acute myocardial infarction in rats.

    PubMed

    Zhou, M X; Fu, J H; Zhang, Q; Wang, J Q

    2015-01-01

    This study aimed to investigate the effect of hydroxy safflower yellow A (HSYA) on myocardial apoptosis after acute myocardial infarction (AMI) in rats. We randomly divided 170 male Wistar rats into 6 groups (N = 23): normal control, sham, control, SY (90 mg/kg), HSYA high-dose (HSYA-H, 40 mg/kg), and HSYA low-dose groups (HSYA-L, 20 mg/kg). Myocardial ischemic injury was induced by ligating the anterior descending coronary artery, and the degree of myocardial ischemia was evaluated using electrocardiography and nitroblue tetrazolium staining. Bax and Bcl-2 expressions in the ischemic myocardium were determined using immunohistochemical analysis. Peroxisome proliferator-activated receptor-γ (PPAR-γ) expression in the myocardium of rats with AMI was determined using reverse transcription-polymerase chain reaction. Compared to rats in the control group, those in the HYSA-H, HSYA-L, and SY groups showed a decrease in the elevated ST segments and an increase in the infarct size. The rats in the drug-treated groups showed a significantly lower percentage of Bax-positive cells and a significantly higher percentage of Bcl-2-positive cells than those in the control group (P < 0.05). Moreover, mRNA expression of PPAR-γ in the ischemic myocardium of rats in the SY, HSYA-L, and HSYA-H groups was significantly lower than that in the control group (P < 0.05). Thus, HSYA and SY can attenuate myocardial ischemia in rats, possibly by increasing the level of Bcl-2/Bax, and PPAR-γ may be not a necessary link in this process. PMID:25966078

  10. Subacute cardiac rupture complicating myocardial infarction. A case report.

    PubMed

    Rosato, G; Santomauro, M; Stanco, G; Petillo, F; Sauro, R; Chiariello, M; Spampinato, N; Rotiroti, D

    1996-02-01

    The authors have focused this study on the emergence of subacute ventricular free wall rupture in a seventy-six-year-old patient admitted to hospital for inferior acute myocardial infarction. After six days he showed clinical signs of bradycardia and hypotension evolving to electromechanical dissociation. Given an adequate pharmacologic therapy, the patient was submitted to echocardiography, which was believed to be consistent with myocardial rupture, showing a moderate to large pericardial effusion. Pericardiocentesis of 150 mL of bloody fluid resulted in a further improvement in his hemodynamics. The patient underwent cardiac surgery with repair of the myocardial rupture through a large diaphragmatic infarction by a Dacron polyester fiber graft and pacemaker placement. In conclusion the authors confirm the relevant role of clinical data such as persistent chest pain and hemodynamic instability and the value of echocardiography in identifying subacute myocardial free wall rupture after an episode of acute myocardial infarction. PMID:8595015

  11. Reducing myocardial infarct size: challenges and future opportunities

    PubMed Central

    Bulluck, Heerajnarain; Yellon, Derek M; Hausenloy, Derek J

    2016-01-01

    Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is ‘myocardial reperfusion injury’, a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies—however, being able to demonstrate improved clinical outcomes has been elusive. In this article, we review the challenges facing clinical cardioprotection research, and highlight future therapies for reducing MI size and preventing heart failure in patients presenting with STEMI at risk of myocardial reperfusion injury. PMID:26674987

  12. 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

  13. Controversies in cardiovascular care: silent myocardial ischemia

    NASA Technical Reports Server (NTRS)

    Hollenberg, N. K.

    1987-01-01

    The objective evidence of silent myocardial ischemia--ischemia in the absence of classical chest pain--includes ST-segment shifts (usually depression), momentary left ventricular failure, and perfusion defects on scintigraphic studies. Assessment of angina patients with 24-hour ambulatory monitoring may uncover episodes of silent ischemia, the existence of which may give important information regarding prognosis and may help structure a more effective therapeutic regimen. The emerging recognition of silent ischemia as a significant clinical entity may eventually result in an expansion of current therapy--not only to ameliorate chest pain, but to minimize or eliminate ischemia in the absence of chest pain.

  14. ST Elevation Myocardial Infarction in the elderly

    PubMed Central

    Franken, Marcelo; Nussbacher, Amit; Liberman, Alberto; Wajngarten, Mauricio

    2012-01-01

    Acute coronary syndromes (ACS) are the leading causes of death in the elderly. The suspicion and diagnosis of ACS in this age group is more difficult, since typical angina is less frequent. The morbidity and mortality is greater in older age patients presenting ACS. Despite the higher prevalence and greater risk, elderly patients are underrepresented in major clinical trials from which evidence based recommendations are formulated. The authors describe, in this article, the challenges in the diagnosis and management of ST elevation myocardial infarction in the elderly, and discuss the available evidence. PMID:22916055

  15. Succinate metabolism: a new therapeutic target for myocardial reperfusion injury.

    PubMed

    Pell, Victoria R; Chouchani, Edward T; Frezza, Christian; Murphy, Michael P; Krieg, Thomas

    2016-07-15

    Myocardial ischaemia/reperfusion (IR) injury is a major cause of death worldwide and remains a disease for which current clinical therapies are strikingly deficient. While the production of mitochondrial reactive oxygen species (ROS) is a critical driver of tissue damage upon reperfusion, the precise mechanisms underlying ROS production have remained elusive. More recently, it has been demonstrated that a specific metabolic mechanism occurs during ischaemia that underlies elevated ROS at reperfusion, suggesting a unifying model as to why so many different compounds have been found to be cardioprotective against IR injury. This review will discuss the role of the citric acid cycle intermediate succinate in IR pathology focusing on the mechanism by which this metabolite accumulates during ischaemia and how it can drive ROS production at Complex I via reverse electron transport. We will then examine the potential for manipulating succinate accumulation and metabolism during IR injury in order to protect the heart against IR damage and discuss targets for novel therapeutics designed to reduce reperfusion injury in patients. PMID:27194563

  16. Factors affecting myocardial 2-[F-18]fluoro-2-deoxy-D-glucose uptake in positron emission tomography studies of normal humans.

    PubMed

    Choi, Y; Brunken, R C; Hawkins, R A; Huang, S C; Buxton, D B; Hoh, C K; Phelps, M E; Schelbert, H R

    1993-04-01

    The goal of this study was to identify the anatomic and physiologic factors affecting left ventricular myocardial 2-[F-18]fluoro-2-deoxy-D-glucose (FDG) uptake and myocardial glucose utilization rates (MRGlc) in normal humans. Eighteen healthy male volunteers were studied in the fasting state (4-19 h) and 16 after oral glucose loading (100 g dextrose) with positron emission tomography (PET) and FDG. Substrate and hormone concentrations were measured in each study. The kinetics of myocardial FDG uptake were evaluated using both a three-compartment model and Patlak graphical analysis. Systolic blood pressures and rate pressure products were similar in the fasting and postglucose states. MRGlc averaged 0.24 +/- 0.17 mumol/min/g in fasting subjects and rose to 0.69 +/- 0.11 mumol/min/g after glucose loading. Phosphorylation rate constant, k3, and MRGlc were linearly related (P < 0.001). Increases in MRGlc following glucose loading were correlated with plasma glucose, insulin and free fatty acid concentrations, ratios of insulin to glucagon levels, and influx rate constants of FDG. Glucose loading improved the diagnostic image quality due to more rapid clearance of tracer from blood and higher myocardial FDG uptake. When MRGlc, glucose and insulin concentrations, and insulin to glucagon ratios exceeded 0.2 mumol/min/g, 100 mg/dl, 19 microU/ml, and 0.2 microU/pg, respectively, myocardial uptake of FDG was always adequate for diagnostic use. FDG image quality and MRGlc were similar after relatively short (6 +/- 2 h) and overnight (16 +/- 2 h) fasting. Significant (P < 0.05) regional heterogeneity of myocardial FDG uptake and MRGlc was observed in both the fasting and the postglucose studies. MRGlc and FDG uptake values in the posterolateral wall were higher than those in the anterior wall and septum. Thus, both 6-h and overnight fasts resulted in similarly low myocardial glucose utilization rates. While MRGlc and myocardial FDG uptake depended on plasma glucose, free

  17. Human myocardial Na,K-ATPase concentration in heart failure.

    PubMed

    Bundgaard, H; Kjeldsen, K

    1996-01-01

    The Na,K-ATPase is of major importance for active ion transport across the sarcolemma and thus for electrical as well as contractile function of the myocardium. Furthermore, it is receptor for digitalis glycosides. In human studies of the regulatory aspects of myocardial Na,K-ATPase concentration a major problem has been to obtain tissue samples. Methodological accomplishments in quantification of myocardial Na,K-ATPase using vanadate facilitated 3H-ouabain binding to intact samples have, however, made it possible to obtain reliable measurements on human myocardial necropsies obtained at autopsy as well as on biopsies of a wet weight of only 1-2 mg obtained during heart catheterisation. However, access to the ultimately, normal, vital myocardial tissue has come from the heart transplantation programs, through which myocardial samples from cardiovascular healthy organ donors have become available. In the present paper we evaluate the various values reported for normal human myocardial Na,K-ATPase concentration, its regulation in heart disease and the association with digitalization. Normal myocardial Na,K-ATPase concentration level is found to be 700 pmol/g wet weight. No major variations were found between or within the walls of the heart ventricles. During the first few years of life a marked decrease in myocardial Na,K-ATPase concentration is followed by a stable level obtained in early adulthood and normally maintained throughout life. In patients with enlarged cardiac x-ray silhouette a significant positive, linear correlation between left ventricular ejection fraction (EF) and Na,K-ATPase concentration was established. A maximum reduction in Na,K-ATPase concentration of 89% was obtained when EF was reduced to 20%. Generally, heart failure associated with heart dilatation, myocardial hypertrophy as well as ischaemic heart disease is associated with reductions in myocardial Na,K-ATPase concentration of around 25%. During digoxin treatment of heart failure

  18. New perspectives on the role of cardiac magnetic resonance imaging to evaluate myocardial salvage and myocardial hemorrhage after acute reperfused ST-elevation myocardial infarction.

    PubMed

    Mangion, Kenneth; Corcoran, David; Carrick, David; Berry, Colin

    2016-07-01

    Cardiac magnetic resonance (CMR) imaging enables the assessment of left ventricular function and pathology. In addition to established contrast-enhanced methods for the assessment of infarct size and microvascular obstruction, other infarct pathologies, such as myocardial edema and myocardial hemorrhage, can be identified using innovative CMR techniques. The initial extent of myocardial edema revealed by T2-weighted CMR has to be stable for edema to be taken as a retrospective marker of the area-at-risk, which is used to calculate myocardial salvage. The timing of edema assessment is important and should be focused within 2 - 7 days post-reperfusion. Some recent investigations have called into question the diagnostic validity of edema imaging after acute STEMI. Considering the results of these studies, as well as results from our own laboratory, we conclude that the time-course of edema post-STEMI is unimodal, not bimodal. Myocardial hemorrhage is the final consequence of severe vascular injury and a progressive and prognostically important complication early post-MI. Myocardial hemorrhage is a therapeutic target to limit reperfusion injury and infarct size post-STEMI. PMID:27043975

  19. Association of urinary cadmium and myocardial infarction

    SciTech Connect

    Everett, Charles J. Frithsen, Ivar L.

    2008-02-15

    We conducted a cross-sectional analysis of individuals 45-79 years old in the National Health and Nutrition Examination Survey III (1988-1994) (NHANES III). Myocardial infarction was determined by electrocardiogram (ECG). Our sample included 4912 participants, which when weighted represented 52,234,055 Americans. We performed adjusted logistic regressions with the Framingham risk score, pack-years of smoking, race-ethnicity, and family history of heart attack, and diabetes as covariates. Urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.86 (95% CI 1.26-2.75) compared to urinary cadmium <0.43 {mu}g/g creatinine. This result supports the hypothesis that cadmium is associated with coronary heart disease. When logistic regressions were done by gender, women, but not men, showed a significant association of urinary cadmium with myocardial infarction. Women with urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.80 (95% CI 1.06-3.04) compared to urinary cadmium <0.43 {mu}g/g creatinine. When the analysis was restricted to never smokers (N=2187) urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.85 (95% CI 1.10-3.14) compared to urinary cadmium <0.43 {mu}g/g creatinine.

  20. Physiological Implications of Myocardial Scar Structure.

    PubMed

    Richardson, William J; Clarke, Samantha A; Quinn, T Alexander; Holmes, Jeffrey W

    2015-10-01

    Once myocardium dies during a heart attack, it is replaced by scar tissue over the course of several weeks. The size, location, composition, structure, and mechanical properties of the healing scar are all critical determinants of the fate of patients who survive the initial infarction. While the central importance of scar structure in determining pump function and remodeling has long been recognized, it has proven remarkably difficult to design therapies that improve heart function or limit remodeling by modifying scar structure. Many exciting new therapies are under development, but predicting their long-term effects requires a detailed understanding of how infarct scar forms, how its properties impact left ventricular function and remodeling, and how changes in scar structure and properties feed back to affect not only heart mechanics but also electrical conduction, reflex hemodynamic compensations, and the ongoing process of scar formation itself. In this article, we outline the scar formation process following a myocardial infarction, discuss interpretation of standard measures of heart function in the setting of a healing infarct, then present implications of infarct scar geometry and structure for both mechanical and electrical function of the heart and summarize experiences to date with therapeutic interventions that aim to modify scar geometry and structure. One important conclusion that emerges from the studies reviewed here is that computational modeling is an essential tool for integrating the wealth of information required to understand this complex system and predict the impact of novel therapies on scar healing, heart function, and remodeling following myocardial infarction. PMID:26426470

  1. Ventricular myocardial architecture in marine fishes.

    PubMed

    Sanchez-Quintana, D; Hurle, J M

    1987-03-01

    The fiber architecture of the ventricular myocardium has been studied in elasmobranch (Isurus oxyrhinchus, Galeorhinus galeus, Prionace glauca) and teleost (Xiphias gladius, Thunnus thynnus, Thunnus alalunga) fish species with hearts displaying mixed types of ventricular musculature (compact and trabecular). In all cases, the compact myocardium is organized in layers of fiber bundles with an orderly arrangement within the ventricular walls. The number of these layers appears to be dependent on the relative thickness of the compact myocardium. Differences in the pattern of myocardial fiber arrangement were observed among the different fish species. In elasmobranchs the compact myocardium at the level of the atrioventricular orifice is continuous with the trabeculated myocardium. Furthermore, in elasmobranchs the trabeculated myocardium displays a precise arrangement in arcuate trabeculae running from the auriculoventricular to the conoventricular orifices. In teleosts, the compact myocardium is independent of the trabeculated myocardium and a large number of fibers insert into the bulboventricular fibrous ring. The trabeculated myocardium in these species displays an anarchic arrangement except at the level of the bulboventricular orifice, where the fibers tend to be aligned longitudinally, also being inserted into the fibrous ring. Minor differences, consisting mainly of the presence of extra bundles of fibers, were also observed among different individuals of the same species. The possible relationship between myocardial fiber architecture and ventricular shape is discussed. PMID:3578842

  2. Incidence of myocardial infarction and weather

    NASA Astrophysics Data System (ADS)

    Staiger, Henning

    1982-08-01

    Extreme values of temperature and/or humidity in the temperate climate of Hamburg are not able to explain the influence of weather on day-to-day fluctuations of morbidity. Short term changes in weather are described by two objective classifications as deviation from the meteorological past: 1. the temperature-humidity-environment, derived from values of temperature and water vapour pressure at 07.00 h, 2. changes in the cyclonality, derived from the difference of 500 and 850 mbar vorticity values. Their suitability for human biometeorology is illustrated with a material of 1262 subjects who suffered from acute myocardial infarction. For these investigated cases it was known whether angina pectoris was already manifest before the infarction or not. The daily weather conditions have a significant effect on the incidence of acute myocardial infarction according to angina pectoris. Compared to subjects with angina pectoris those without angina pectoris show an increased susceptibility to infarction during changes in weather conditions to warmer/more humid and also during all strong changes in the cyclonality whereby the temperature-humidity-environment seems to leave only the role of an indicator too. Persons with a preceeding angina pectoris are more sensitive agains rapid changes in weather conditions.

  3. [The early ergometric test after myocardial revascularization].

    PubMed

    Mazzucco, G; Conti, M; Biagioli, F; Delpero, P; Del Ponte, S; Gelato, D

    1991-09-01

    Ergometric tests (ET) were used to study 900 patients undergoing surgical myocardial revascularisation during the period between January 1983 and December 1989. ET was carried out without medical therapy between the 30th and 35th day post surgery. The test was positive in 193 subjects (21%); in 42 of the latter (5% of the total and 229 of positive subjects) symptoms of effort angina were found to persist. ET was negative in 557 patients (62%); 150 subjects (17%), although not positive, did not attain a sufficient heart rate to enable a 100% negative diagnosis to be made. No major complication was observed. Maximal short-term ET is a reliable and safe test for checking the efficacy of myocardial revascularisation and to assess functional recovery. In view of the relatively high percentage of positive tests due to ischemia but with the complete absence of symptoms, the authors affirm that the mere onset of anginous symptoms alone cannot be considered indicative of the success of cardiosurgery. PMID:1787892

  4. Current perspectives on direct myocardial revascularization.

    PubMed

    Kornowski, R; Hong, M K; Leon, M B

    1998-04-01

    Direct myocardial revascularization (DMR), either surgical or catheter-based, uses lasers to create channels between ischemic myocardium and the left ventricular cavity to improve perfusion and decrease angina. This technique can also be used to deliver drugs to the damaged tissue. Candidates include patients with chronic, severe, refractory angina and those unable to undergo conventional surgical revascularization or angioplasty because remaining conduits or acceptable target vessels are lacking. Although the mechanism of action of DMR is still not known, several theories have been proposed, including stimulated angiogenesis. Late sequelae also remain to be determined. Channel characteristics differ depending on whether they were created by carbon dioxide or holmium/yttrium-aluminum-garnet (Ho: YAG) lasers. Catheter-based DMR obviates thoracotomy and anesthesia and, in systems that can create electromechanical maps, fluoroscopy. Phase I clinical trials are now under way to evaluate catheter-based DMR, with endpoints that include improvement in symptoms of angina, exercise capacity, and radionuclide myocardial perfusion. PMID:9551594

  5. 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

  6. [Myocardial ischemia-reperfusion injury and melatonin].

    PubMed

    Sahna, Engin; Deniz, Esra; Aksulu, Hakki Engin

    2006-06-01

    It is believed that myocardial ischemia-reperfusion injury is related to increased free radical generated and intracellular calcium overload especially during the period of reperfusion. The pineal secretory product, melatonin, is known to be a potent free radical scavenger, antioxidant and can inhibit the intracellular calcium overload. In this review, we have summarized the fundamental of cardiac ischemia-reperfusion injury and the effects of melatonin on myocardial damage that related to cardiac ischemia-reperfusion injury. The total antioxidant capacity of human serum is related to melatonin levels. Incidence of sudden cardiac death is high in the morning hours. It has been shown that melatonin levels are significantly low at these times and patients with coronary heart disease have lower than normal individuals. These findings thought that melatonin would be valuable to test in clinical trials for prevention of possible ischemia-reperfusion-induced injury, especially life threatening arrhythmias and infarct size, effecting life quality, associated with thrombolysis, angioplasty, coronary artery spasm or coronary bypass surgery. PMID:16766282

  7. Nicardipine in models of myocardial infarction

    PubMed Central

    Alps, B. J.; Calder, C.; Wilson, A.

    1985-01-01

    1 In a dog model of partial myocardial ischaemia, superimposed ST segment elevations in epicardial ECGs were inhibited by nicardipine over a cumulative i.v. dose range of 1-20 μg kg-1. 2 Over the cumulative i.v. dose range of 0.5-166.5 μg kg-1, nicardipine had little overall effect on gross cardiac conduction, at spontaneous heart rate. 3 Dogs that received oral 1-2 mg kg-1 nicardipine daily for 16 weeks and then survived 1 week occlusion of the left anterior descending coronary artery (LAD) developed a superior coronary collateral circulation compared with untreated animals. 4 Nicardipine given by three different dosing schedules to baboons markedly limited myocardial infarction over a 6 h period of LAD occlusion. 5 Compared with a group of completely untreated dogs, there was protection of the myocardium in the animals given nicardipine that survived 3 months occlusion of the LAD. ImagesFigure 7 PMID:4027150

  8. Prognostic significance of transient myocardial ischaemia after first acute myocardial infarction: five year follow up study.

    PubMed Central

    Mickley, H.; Nielsen, J. R.; Berning, J.; Junker, A.; Møller, M.

    1995-01-01

    OBJECTIVE--To assess the five year prognostic significance of transient myocardial ischaemia on ambulatory monitoring after a first acute myocardial infarction, and to compare the diagnostic and long term prognostic value of ambulatory ST segment monitoring, maximal exercise testing, and echocardiography in patients with documented ischaemic heart disease. DESIGN--Prospective study. SETTING--Cardiology department of a teaching hospital. PATIENTS--123 consecutive men aged under 70 who were able to perform predischarge maximal exercise testing. INTERVENTIONS--Echocardiography two days before discharge (left ventricular ejection fraction), maximal bicycle ergometric testing one day before discharge (ST segment depression, angina, blood pressure, heart rate), and ambulatory ST segment monitoring (transient myocardial ischaemia) started at hospital discharge a mean of 11 (SD 5) days after infarction. MAIN OUTCOME MEASURES--Relation of ambulatory ST segment depression, exercise test variables, and left ventricular ejection fraction to subsequent objective (cardiac death or myocardial infarction) or subjective (need for coronary revascularisation) events. RESULTS--23 of the 123 patients had episodes of transient ST segment depression, of which 98% were silent. Over a mean of 5 (range 4 to 6) years of follow up, patients with ambulatory ischaemia were no more likely to have objective end points than patients without ischaemic episodes. If, however, subjective events were included an association between transient ST segment depression and an adverse long term outcome was found (Kaplan-Meier analysis; P = 0.004). The presence of exercise induced angina identified a similar proportion of patients with a poor prognosis (Kaplan-Meier analysis; P < 0.004). Both exertional angina and ambulatory ST segment depression had high specificity but poor sensitivity. The presence of exercise induced ST segment depression was of no value in predicting combined cardiac events. Indeed

  9. Myocardial Oxidative Metabolism and Protein Synthesis during Mechanical Circulatory Support by Extracorporeal Membrane Oxygenation

    SciTech Connect

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

    2013-02-01

    Extracorporeal membrane oxygenation (ECMO) provides mechanical circulatory support essential for survival in infants and children with acute cardiac decompensation. However, ECMO also causes metabolic disturbances, which contribute to total body wasting and protein loss. Cardiac stunning can also occur which prevents ECMO weaning, and contributes to high mortality. The heart may specifically undergo metabolic impairments, which influence functional recovery. We tested the hypothesis that ECMO alters oxidative. We focused on the amino acid leucine, and integration with myocardial protein synthesis. We used a translational immature swine model in which we assessed in heart (i) the fractional contribution of leucine (FcLeucine) and pyruvate (FCpyruvate) to mitochondrial acetyl-CoA formation by nuclear magnetic resonance and (ii) global protein fractional synthesis (FSR) by gas chromatography-mass spectrometry. Immature mixed breed Yorkshire male piglets (n = 22) were divided into four groups based on loading status (8 hours of normal circulation or ECMO) and intracoronary infusion [13C6,15N]-L-leucine (3.7 mM) alone or with [2-13C]-pyruvate (7.4 mM). ECMO decreased pulse pressure and correspondingly lowered myocardial oxygen consumption (~ 40%, n = 5), indicating decreased overall mitochondrial oxidative metabolism. However, FcLeucine was maintained and myocardial protein FSR was marginally increased. Pyruvate addition decreased tissue leucine enrichment, FcLeucine, and Fc for endogenous substrates as well as protein FSR. Conclusion: The heart under ECMO shows reduced oxidative metabolism of substrates, including amino acids, while maintaining (i) metabolic flexibility indicated by ability to respond to pyruvate, and (ii) a normal or increased capacity for global protein synthesis, suggesting an improved protein balance.

  10. Regulation of myocardial ketone body metabolism by the gut microbiota during nutrient deprivation

    PubMed Central

    Crawford, Peter A.; Crowley, Jan R.; Sambandam, Nandakumar; Muegge, Brian D.; Costello, Elizabeth K.; Hamady, Micah; Knight, Rob; Gordon, Jeffrey I.

    2009-01-01

    Studies in mice indicate that the gut microbiota promotes energy harvest and storage from components of the diet when these components are plentiful. Here we examine how the microbiota shapes host metabolic and physiologic adaptations to periods of nutrient deprivation. Germ-free (GF) mice and mice who had received a gut microbiota transplant from conventionally raised donors were compared in the fed and fasted states by using functional genomic, biochemical, and physiologic assays. A 24-h fast produces a marked change in gut microbial ecology. Short-chain fatty acids generated from microbial fermentation of available glycans are maintained at higher levels compared with GF controls. During fasting, a microbiota-dependent, Pparα-regulated increase in hepatic ketogenesis occurs, and myocardial metabolism is directed to ketone body utilization. Analyses of heart rate, hydraulic work, and output, mitochondrial morphology, number, and respiration, plus ketone body, fatty acid, and glucose oxidation in isolated perfused working hearts from GF and colonized animals (combined with in vivo assessments of myocardial physiology) revealed that the fasted GF heart is able to sustain its performance by increasing glucose utilization, but heart weight, measured echocardiographically or as wet mass and normalized to tibial length or lean body weight, is significantly reduced in both fasted and fed mice. This myocardial-mass phenotype is completely reversed in GF mice by consumption of a ketogenic diet. Together, these results illustrate benefits provided by the gut microbiota during periods of nutrient deprivation, and emphasize the importance of further exploring the relationship between gut microbes and cardiovascular health. PMID:19549860

  11. Myocardial oxidative metabolism and protein synthesis during mechanical circulatory support by extracorporeal membrane oxygenation

    PubMed Central

    Priddy, Colleen M. O′Kelly; Kajimoto, Masaki; Ledee, Dolena R.; Bouchard, Bertrand; Isern, Nancy; Olson, Aaron K.; Rosiers, Christine Des

    2013-01-01

    Extracorporeal membrane oxygenation (ECMO) provides essential mechanical circulatory support necessary for survival in infants and children with acute cardiac decompensation. However, ECMO also causes metabolic disturbances, which contribute to total body wasting and protein loss. Cardiac stunning can also occur, which prevents ECMO weaning, and contributes to high mortality. The heart may specifically undergo metabolic impairments, which influence functional recovery. We tested the hypothesis that ECMO alters oxidative metabolism and protein synthesis. We focused on the amino acid leucine and integration with myocardial protein synthesis. We used a translational immature swine model in which we assessed in heart 1) the fractional contribution of leucine (FcLeucine) and pyruvate to mitochondrial acetyl-CoA formation by nuclear magnetic resonance and 2) global protein fractional synthesis (FSR) by gas chromatography-mass spectrometry. Immature mixed breed Yorkshire male piglets (n = 22) were divided into four groups based on loading status (8 h of normal circulation or ECMO) and intracoronary infusion [13C6,15N]-L-leucine (3.7 mM) alone or with [2-13C]-pyruvate (7.4 mM). ECMO decreased pulse pressure and correspondingly lowered myocardial oxygen consumption (∼40%, n = 5), indicating decreased overall mitochondrial oxidative metabolism. However, FcLeucine was maintained and myocardial protein FSR was marginally increased. Pyruvate addition decreased tissue leucine enrichment, FcLeucine, and Fc for endogenous substrates as well as protein FSR. The heart under ECMO shows reduced oxidative metabolism of substrates, including amino acids, while maintaining 1) metabolic flexibility indicated by ability to respond to pyruvate and 2) a normal or increased capacity for global protein synthesis. PMID:23203964

  12. Myocardial ischemia--association with perioperative cardiac morbidity.

    PubMed Central

    Cunningham, A. J.

    1993-01-01

    The development of ambulatory electrocardiographic recorders and analysers and the application of transesophageal echocardiography in the mid-1980's enabled investigators to quantify and describe the occurrence of silent as well as symptomatic ischemia in the perioperative period. Several technical advances which have recently occurred in ECG monitoring include the use of miniaturized digital computing equipment to store and analyze data. In addition, real time ST-segment analysis has become widely available on multicomponent monitors in both the operating room and intensive care units. The incidence of perioperative myocardial ischemia depends on the patient population, the surgical procedure, and the monitoring technique used. Several studies in the early 1990's have shown that cardiac morbidity in patients undergoing major, noncardiac surgery is best predicted by postoperative myocardial ischemia, rather than tradition preoperative clinical predictors. Long duration postoperative ischemia may be the factor most significantly associated with adverse cardiac outcome. Postoperative pain, physiological and emotional stress may all combine to cause tachycardia, hypertension, increase in cardiac output, and fluid shifts which, in high risk patients, might result in subendocardial ischemia and eventual myocardial infarction. If postoperative myocardial ischemia is the cause of late postoperative myocardial infarction in patients undergoing non-cardiac surgery, then treatment of postoperative myocardial ischemia should reduce morbidity. In addition, reducing pain and stress and avoiding postoperative hypoxemia might prevent postoperative myocardial ischemia and minimize the need for extensive preoperative cardiac evaluation. PMID:7825338

  13. Unstable angina pectoris. Clinical, angiographic, and myocardial scintigraphic observations.

    PubMed Central

    Donsky, M S; Curry, G C; Parkey, R W; Meyer, S L; Bonte, F J; Platt, M R; Willerson, J T

    1976-01-01

    The clinical, left ventricular and coronary angiographic data, and the technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigraphic results are presented in 31 patients with unstable angina pectoris. One-third of these patients had positive 99mTc-PYP myocardial scintigrams in a pattern suggesting limited and diffuse subendocardial necrosis. The positive 99mTc-PYP myocardial scintigrams occurred without diagnostic electrocardiographic and cardiac enzyme changes suggestive of myocardial infarction; positive scintigrams seemed to occur more commonly in patients with continuing pain after admission and in those without previous history of myocardial infarction. The positive 99mTc-PYP myocardial scintigrams did not correctly predict coronary anatomical patterns except that positive scintigrams occurred only in patients with coronary artery disease. Neither did the positive scintigrams necessarily occur in that group of patients with the poorest ventricular function though the 2 patients with the lowest ejection fractions both had positive 99mTc-PYP myocardial scintigrams. Finally, when positive 99mTc-PYP scintigrams are the only evidence suggestive of limited subendocardial infarction in patients with unstable angina pectoris, they do not appear to have any prognostic significance in terms of longevity or response to pharmacological or surgical therapy, though the follow-up period so far is short. Images PMID:1259840

  14. Decellularized myocardial matrix hydrogels: In basic research and preclinical studies.

    PubMed

    Wang, Raymond M; Christman, Karen L

    2016-01-15

    A variety of decellularized materials have been developed that have demonstrated potential for treating cardiovascular diseases and improving our understanding of cardiac development. Of these biomaterials, decellularized myocardial matrix hydrogels have shown great promise for creating cellular microenvironments representative of the native cardiac tissue and treating the heart after a myocardial infarction. Decellularized myocardial matrix hydrogels derived from porcine cardiac tissue form a nanofibrous hydrogel once thermally induced at physiological temperatures. Use of isolated cardiac extracellular matrix in 2D and 3D in vitro platforms has demonstrated the capability to provide tissue specific cues for cardiac cell growth and differentiation. Testing of the myocardial matrix hydrogel as a therapy after myocardial infarction in both small and large animal models has demonstrated improved left ventricular function, increased cardiac muscle, and cellular recruitment into the treated infarct. Based on these results, steps are currently being taken to translate these hydrogels into a clinically used injectable biomaterial therapy. In this review, we will focus on the basic science and preclinical studies that have accelerated the development of decellularized myocardial matrix hydrogels into an emerging novel therapy for treating the heart after a myocardial infarction. PMID:26056717

  15. Cardioprotective Properties of Aerobic and Resistance Training Against Myocardial Infarction.

    PubMed

    Barboza, C A; Souza, G I H; Oliveira, J C M F; Silva, L M; Mostarda, C T; Dourado, P M M; Oyama, L M; Lira, F S; Irigoyen, M C; Rodrigues, B

    2016-06-01

    We evaluated the effects of aerobic and resistance exercise training on ventricular morphometry and function, physical capacity, autonomic function, as well as on ventricular inflammatory status in trained rats prior to myocardial infarction. Male Wistar rats were divided into the following groups: sedentary+Sham, sedentary+myocardial infarction, aerobic trained+myocardial infarction, and resistance trained+myocardial infarction. Sham and myocardial infarction were performed after training periods. In the days following the surgeries, evaluations were performed. Aerobic training prevents aerobic (to a greater extent) and resistance capacity impairments, ventricular dysfunction, baroreflex sensitivity and autonomic disorders (vagal tonus decrease and sympathetic tonus increase) triggered by myocardial infarction. Resistance training was able to prevent negative changes to aerobic and resistance capacity (to a greater extent) but not to ventricular dysfunction, and it prevented cardiovascular sympathetic increments. Additionally, both types of training reduced left ventricle inflammatory cytokine concentration. Our results suggest that aerobic and, for the first time, dynamic resistance training were able to reduce sympathetic tonus to the heart and vessels, as well as preventing the increase in pro-inflammatory cytokine concentrations in the left ventricle of trained groups. These data emphasizes the positive effects of aerobic and dynamic resistance training on the prevention of the negative changes triggered by myocardial infarction. PMID:26928914

  16. LAD-Ligation: A Murine Model of Myocardial Infarction

    PubMed Central

    Kolk, Mandy V.V.; Meyberg, Danja; Deuse, Tobias; Tang-Quan, Karis R.; Robbins, Robert C.; Reichenspurner, Hermann; Schrepfer, Sonja

    2009-01-01

    Research models of infarction and myocardial ischemia are essential to investigate the acute and chronic pathobiological and pathophysiological processes in myocardial ischemia and to develop and optimize future treatment. Two different methods of creating myocardial ischemia are performed in laboratory rodents. The first method is to create cryo infarction, a fast but inaccurate technique, where a cryo-pen is applied on the surface of the heart (1-3). Using this method the scientist can not guarantee that the cryo-scar leads to ischemia, also a vast myocardial injury is created that shows pathophysiological side effects that are not related to myocardial infarction. The second method is the permanent ligation of the left anterior descending artery (LAD). Here the LAD is ligated with one single stitch, forming an ischemia that can be seen almost immediately. By closing the LAD, no further blood flow is permitted in that area, while the surrounding myocardial tissue is nearly not affected. This surgical procedure imitates the pathobiological and pathophysiological aspects occurring in infarction-related myocardial ischemia. The method introduced in this video demonstrates the surgical procedure of a mouse infarction model by ligating the LAD. This model is convenient for pathobiological and pathophysiological as well as immunobiological studies on cardiac infarction. The shown technique provides high accuracy and correlates well with histological sections. PMID:19829290

  17. Preservation of canine myocardial high-energy phosphates during low-flow ischemia with modification of hemoglobin–oxygen affinity

    PubMed Central

    Weiss, Robert G.; Mejia, Marco A.; Kass, David A.; DiPaula, Anthony F.; Becker, Lewis C.; Gerstenblith, Gary; Chacko, V.P.

    1999-01-01

    Conventional approaches for the treatment of myocardial ischemia increase coronary blood flow or reduce myocardial demand. To determine whether a rightward shift in the hemoglobin–oxygen saturation curve would reduce the metabolic and contractile effects of a myocardial oxygen-supply imbalance, we studied the impact of a potent synthetic allosteric modifier of hemoglobin–oxygen affinity, a 2-[4-[[(3,5-disubstituted anilino)carbonyl]methyl] phenoxy] -2-methylproprionic acid derivative (RSR13), during low-flow ischemia. Changes in myocardial high-energy phosphate levels and pH were studied by 31P nuclear magnetic resonance (NMR) spectroscopy in 12 open-chest dogs randomized to receive RSR13 or vehicle control during a reversible reduction of left anterior descending (LAD) coronary artery blood flow. Changes in cardiac metabolites and regional ventricular function studied by pressure segment–length relations were also investigated in additional animals before and after RSR13 administration during low-flow LAD ischemia. The intravenous administration of RSR13 before ischemia resulted in a substantial increase in the mean hemoglobin p50 and attenuated the decline in cardiac creatine phosphate/adenosine triphosphate (PCr/ATP), percent PCr, and pH during ischemia without a change in regional myocardial blood flow, heart rate, or systolic blood pressure. RSR13 given after the onset of low-flow ischemia also improved cardiac PCr/ATP ratios and regional function as measured by fractional shortening and regional work. Thus, synthetic allosteric reduction in hemoglobin–oxygen affinity may be a new and important therapeutic strategy to ameliorate the metabolic and functional consequences of cardiac ischemia. J. Clin. Invest. 103:739–746 (1999) PMID:10074492

  18. Preservation of canine myocardial high-energy phosphates during low-flow ischemia with modification of hemoglobin-oxygen affinity.

    PubMed

    Weiss, R G; Mejia, M A; Kass, D A; DiPaula, A F; Becker, L C; Gerstenblith, G; Chacko, V P

    1999-03-01

    Conventional approaches for the treatment of myocardial ischemia increase coronary blood flow or reduce myocardial demand. To determine whether a rightward shift in the hemoglobin-oxygen saturation curve would reduce the metabolic and contractile effects of a myocardial oxygen-supply imbalance, we studied the impact of a potent synthetic allosteric modifier of hemoglobin-oxygen affinity, a 2-[4-[[(3,5-disubstituted anilino)carbonyl]methyl] phenoxy] -2-methylproprionic acid derivative (RSR13), during low-flow ischemia. Changes in myocardial high-energy phosphate levels and pH were studied by 31P nuclear magnetic resonance (NMR) spectroscopy in 12 open-chest dogs randomized to receive RSR13 or vehicle control during a reversible reduction of left anterior descending (LAD) coronary artery blood flow. Changes in cardiac metabolites and regional ventricular function studied by pressure segment-length relations were also investigated in additional animals before and after RSR13 administration during low-flow LAD ischemia. The intravenous administration of RSR13 before ischemia resulted in a substantial increase in the mean hemoglobin p50 and attenuated the decline in cardiac creatine phosphate/adenosine triphosphate (PCr/ATP), percent PCr, and pH during ischemia without a change in regional myocardial blood flow, heart rate, or systolic blood pressure. RSR13 given after the onset of low-flow ischemia also improved cardiac PCr/ATP ratios and regional function as measured by fractional shortening and regional work. Thus, synthetic allosteric reduction in hemoglobin-oxygen affinity may be a new and important therapeutic strategy to ameliorate the metabolic and functional consequences of cardiac ischemia. PMID:10074492

  19. In vitro comparative study of two decellularization protocols in search of an optimal myocardial scaffold for recellularization

    PubMed Central

    Perea-Gil, Isaac; Uriarte, Juan J; Prat-Vidal, Cristina; Gálvez-Montón, Carolina; Roura, Santiago; Llucià-Valldeperas, Aida; Soler-Botija, Carolina; Farré, Ramon; Navajas, Daniel; Bayes-Genis, Antoni

    2015-01-01

    Introduction. Selection of a biomaterial-based scaffold that mimics native myocardial extracellular matrix (ECM) architecture can facilitate functional cell attachment and differentiation. Although decellularized myocardial ECM accomplishes these premises, decellularization processes may variably distort or degrade ECM structure. Materials and methods. Two decellularization protocols (DP) were tested on porcine heart samples (epicardium, mid myocardium and endocardium). One protocol, DP1, was detergent-based (SDS and Triton X-100), followed by DNase I treatment. The other protocol, DP2, was focused in trypsin and acid with Triton X-100 treatments. Decellularized myocardial scaffolds were reseeded by embedding them in RAD16-I peptidic hydrogel with adipose tissue-derived progenitor cells (ATDPCs). Results. Both protocols yielded acellular myocardial scaffolds (~82% and ~94% DNA reduction for DP1 and DP2, respectively). Ultramicroscopic assessment of scaffolds was similar for both protocols and showed filamentous ECM with preserved fiber disposition and structure. DP1 resulted in more biodegradable scaffolds (P = 0.04). Atomic force microscopy revealed no substantial ECM stiffness changes post-decellularization compared to native tissue. The Young’s modulus did not differ between heart layers (P = 0.69) or decellularization protocols (P = 0.15). After one week, recellularized DP1 scaffolds contained higher cell density (236 ± 106 and 98 ± 56 cells/mm2 for recellularized DP1 and DP2 scaffolds, respectively; P = 0.04). ATDPCs in both DP1 and DP2 scaffolds expressed the endothelial marker isolectin B4, but only in the DP1 scaffold ATDPCs expressed the cardiac markers GATA4, connexin43 and cardiac troponin T. Conclusions. In our hands, DP1 produced myocardial scaffolds with higher cell repopulation and promotes ATDPCs expression of endothelial and cardiomyogenic markers. PMID:26045895

  20. Risk of bleeding associated with combined use of selective serotonin reuptake inhibitors and antiplatelet therapy following acute myocardial infarction

    PubMed Central

    Labos, Christopher; Dasgupta, Kaberi; Nedjar, Hacene; Turecki, Gustavo; Rahme, Elham

    2011-01-01

    Background: Patients prescribed antiplatelet treatment to prevent recurrent acute myocardial infarction are often also given a selective serotonin reuptake inhibitor (SSRI) to treat coexisting depression. Use of either treatment may increase the risk of bleeding. We assessed the risk of bleeding among patients taking both medications following acute myocardial infarction. Methods: We conducted a retrospective cohort study using hospital discharge abstracts, physician billing information, medication reimbursement claims and demographic data from provincial health services administrative databases. We included patients 50 years of age or older who were discharged from hospital with antiplatelet therapy following acute myocardial infarction between January 1998 and March 2007. Patients were followed until admission to hospital due to a bleeding episode, admission to hospital due to recurrent acute myocardial infarction, death or the end of the study period. Results: The 27 058 patients in the cohort received the following medications at discharge: acetylsalicylic acid (ASA) (n = 14 426); clopidogrel (n = 2467), ASA and clopidogrel (n = 9475); ASA and an SSRI (n = 406); ASA, clopidogrel and an SSRI (n = 239); or clopidogrel and an SSRI (n = 45). Compared with ASA use alone, the combined use of an SSRI with antiplatelet therapy was associated with an increased risk of bleeding (ASA and SSRI: hazard ratio [HR] 1.42, 95% confidence interval [CI] 1.08–1.87; ASA, clopidogrel and SSRI: HR 2.35, 95% CI 1.61–3.42). Compared with dual antiplatelet therapy alone (ASA and clopidogrel), combined use of an SSRI and dual antiplatelet therapy was associated with an increased risk of bleeding (HR 1.57, 95% CI 1.07–2.32). Interpretation: Patients taking an SSRI together with ASA or dual antiplatelet therapy following acute myocardial infarction were at increased risk of bleeding. PMID:21948719

  1. 4-PBA prevents pressure overload-induced myocardial hypertrophy and interstitial fibrosis by attenuating endoplasmic reticulum stress.

    PubMed

    Luo, Tao; Chen, Baihe; Wang, Xianbao

    2015-12-01

    Our previous study indicated that attenuation of endoplasmic reticulum (ER) stress by administration of 4-phenylbutyric acid (4-PBA) could prevent cardiac rupture and remodeling in a mouse model of myocardial infarction (MI). However, whether 4-PBA is protective in hypertrophic heart disease is unclear. Thus, we tested the therapeutic effect of 4-PBA on pressure-overload induced myocardial hypertrophy. Transverse aortic constriction (TAC) was used to create myocardial hypertrophy in C57BL/6 male mice for 4 weeks. Immediately after surgery, the mice were administrated either 4-PBA (20 mg/kg/day) or 0.9% NaCl by intraperitoneal injection. At the end of 4 weeks, the mice underwent high-resolution echocardiographic imaging. Our results showed that both the left ventricular posterior wall thickness at end systole (LVPWs) and diastole (LVPWd) were increased in the TAC group, compared to control. 4-PBA administration attenuated hypertrophy and decreased the heart weight over body weight ratio. Masson's trichrome staining showed that myocardial interstitial fibrosis and collagen deposition were also decreased by 4-PBA. We next detected the ER stress response in the heart tissues of TAC mice in different time points. Western blotting showed that the expression of ER stress marker, GRP78, CHOP and phosphor-PERK, were persistently increased 4 weeks after TAC. The treatment of 4-PBA inhibited the expression of ER stress markers. We also demonstrated that the 4-PBA at 20 mg/kg/day had no effect on histone 3 deacetylation inhibition, while attenuating ER stress and TAC-induced hypertrophy. These findings suggest that 4-PBA may be a therapeutic strategy to consider in preventing pressure-overload induced myocardial hypertrophy and interstitial fibrosis by selectively attenuating ER stress. PMID:26428355

  2. Assessment of Myocardial Triglyceride Oxidation with PET and 11C-Palmitate

    PubMed Central

    Kisrieva-Ware, Zulfia; Coggan, Andrew R.; Sharp, Terry L.; Dence, Carmen S.; Gropler, Robert J.; Herrero, Pilar

    2010-01-01

    Background The goal of this study was to test whether myocardial triglyceride (TG) turnover including oxidation of TG-derived fatty acids could be assessed with PET and 11C-palmitate. Methods and Results 26 dogs were studied fasted (FAST), during Intralipid infusion (IL), during a hyperinsulinemic-euglycemic clamp without (HIEG) or with Intralipid infusion (HIEG+IL). 11C-palmitate was injected, and 45 min were allowed for labeling of myocardial TG pool. 3-D PET data were then acquired for 60 min, with first 15 min at baseline followed by 45 min during cardiac work stimulated with constant infusion of either phenylephrine (FAST, n=6; IL, n=6; HIEG+IL, n=6) or dobutamine (FAST, n=4; HIEG, n=4). Myocardial 11C washout during adrenergic stimulation (AS) was fitted to a mono-exponential function (Km(PET)). To determine the source of this 11C clearance, Km(PET) was compared to direct coronary sinus-arterial measurements of total 11C activity, 11C-palmitate, and 11CO2. Before AS, PET curves in all groups were flat indicating absence of net clearance of 11C activity from heart. In both FAST groups, AS resulted in negligible net 11C activity and 11CO2 production higher than net 11C-palmitate uptake. AS with phenylephrine resulted in net myocardial uptake of total 11C activity and 11C-palmitate in IL and HIEG+IL, and 11CO2 production lower than 11C-palmitate uptake. In contrast, AS with dobutamine in HIEG resulted in net clearance of all 11C metabolites (total 11C activity, 11C-palmitate and 11CO2) with 11CO2 contributing 66% to endogenous FA oxidation. AS resulted in significant Km(PET) in all groups, except HIEG+IL. However, positive correlation between Km(PET) and 11CO2 was observed only in HIEG (R2=0.83, P=0.09). Conclusions This is the first study to demonstrate that using PET and pre-labeling of intracardiac TG pool with 11C-palmitate, noninvasive assessment of myocardial TG use is feasible under metabolic conditions that favor endogenous TG use such as increased

  3. Static and dynamic assessment of myocardial perfusion by computed tomography.

    PubMed

    Danad, Ibrahim; Szymonifka, Jackie; Schulman-Marcus, Joshua; Min, James K

    2016-08-01

    Recent developments in computed tomography (CT) technology have fulfilled the prerequisites for the clinical application of myocardial CT perfusion (CTP) imaging. The evaluation of myocardial perfusion by CT can be achieved by static or dynamic scan acquisitions. Although both approaches have proved clinically feasible, substantial barriers need to be overcome before its routine clinical application. The current review provides an outline of the current status of CTP imaging and also focuses on disparities between static and dynamic CTPs for the evaluation of myocardial blood flow. PMID:27013250

  4. Regorafenib-Related Myocardial Injury during Atrial Fibrillation

    PubMed Central

    Hsiao, Fu-Chih; Yeh, Chun-Nan; Chu, Pao-Hsien

    2016-01-01

    Multikinase inhibitors with an anti-vascular endothelial growth factor effect have been reported to increase the risk of myocardial infarction or ischemia. We have presented the case of a 72-year-old male who had a metastatic gastrointestinal stromal tumor for which he received targeted therapy and who was admitted to our hospital for recurrent episodes of myocardial injury during atrial fibrillation. Coronary angiography showed insignificant coronary artery stenosis. We also reviewed the incidence of cardiovascular events in patients receiving regorafenib, and the current understanding of the mechanism of targeted therapy-induced myocardial ischemia/infarction. PMID:27122956

  5. New imaging technology: measurement of myocardial perfusion by contrast echocardiography

    NASA Technical Reports Server (NTRS)

    Rubin, D. N.; Thomas, J. D.

    2000-01-01

    Myocardial perfusion imaging has long been a goal for the non-invasive echocardiographic assessment of the heart. However, many factors at play in perfusion imaging have made this goal elusive. Harmonic imaging and triggered imaging with newer contrast agents have made myocardial perfusion imaging potentially practical in the very near future. The application of indicator dilution theory to the coronary circulation and bubble contrast agents is fraught with complexities and sources of error. Therefore, quantification of myocardial perfusion by non-invasive echocardiographic imaging requires further investigation in order to make this technique clinically viable.

  6. Disseminated mucormycosis with myocardial involvement in a renal transplant recipient.

    PubMed

    Nam, Y; Jung, J; Park, S S; Kim, S J; Shin, S J; Choi, J H; Kim, M; Yoon, H E

    2015-12-01

    We report the case of a renal transplant recipient with pulmonary and splenic mucormycosis whose demise was accelerated by a myocardial abscess. Once pulmonary and splenic mucormycosis was diagnosed, liposomal amphotericin B was started and immunosuppressant treatments were discontinued. The pulmonary cavities regressed during treatment, but new myocardial and peri-allograft abscesses developed. The myocardial abscess diffusely infiltrated the left ventricular wall and was associated with akinesia, which led to sudden cardiac arrest. This case demonstrates a rare manifestation of mucormycosis and highlights the fatality and invasiveness of this infection. PMID:26538076

  7. A “PET” area of interest: myocardial metabolism in human systolic heart failure

    PubMed Central

    Kadkhodayan, Ana; Coggan, Andrew R.; Peterson, Linda R.

    2013-01-01

    Myocardial substrate metabolism provides the energy needed for cardiac contraction and relaxation. The normal adult heart uses predominantly fatty acids (FAs) as its primary fuel source. However, the heart can switch and use glucose (and to a lesser extent, ketones, lactate, as well as endogenous triglycerides and glycogen), depending on the metabolic milieu and superimposed conditions. FAs are not a wholly better fuel than glucose, but they do provide more energy per mole than glucose. Conversely, glucose is the more oxygen-efficient fuel. Studies in animal models of heart failure (HF) fairly consistently demonstrate a shift away from myocardial fatty acid metabolism and towards glucose metabolism. Studies in humans are less consistent. Some show the same metabolic switch away from FA metabolism but not all. This may be due to differences in the etiology of HF, sex-related differences, or other mitigating factors. For example, obesity, insulin resistance, and diabetes are all related to an increased risk of HF and may complicate or contribute to its development. However, these conditions are associated with increased FA metabolism. This review will discuss aspects of human heart metabolism in systolic dysfunction as measured by the noninvasive, quantitative method – positron emission tomography. Continued research in this area is vital if we are to ameliorate HF by manipulating heart metabolism with the aim of increasing energy production and/or efficiency. PMID:23180281

  8. Elastomeric electrospun scaffolds of poly(L-lactide-co-trimethylene carbonate) for myocardial tissue engineering.

    PubMed

    Mukherjee, Shayanti; Gualandi, Chiara; Focarete, Maria Letizia; Ravichandran, Rajeswari; Venugopal, Jayarama Reddy; Raghunath, Michael; Ramakrishna, Seeram

    2011-07-01

    In myocardial tissue engineering the use of synthetically bioengineered flexible patches implanted in the infarcted area is considered one of the promising strategy for cardiac repair. In this work the potentialities of a biomimetic electrospun scaffold made of a commercial copolymer of (L)-lactic acid with trimethylene carbonate (P(L)LA-co-TMC) are investigated in comparison to electrospun poly(L)lactic acid. The P(L)LA-co-TMC scaffold used in this work is a glassy rigid material at room temperature while it is a rubbery soft material at 37 °C. Mechanical characterization results (tensile stress-strain and creep-recovery measurements) show that at 37 °C electrospun P(L)LA-co-TMC displays an elastic modulus of around 20 MPa and the ability to completely recover up to 10% of deformation. Cell culture experiments show that P(L)LA-co-TMC scaffold promotes cardiomyocyte proliferation and efficiently preserve cell morphology, without hampering expression of sarcomeric alpha actinin marker, thus demonstrating its potentialities as synthetic biomaterial for myocardial tissue engineering. PMID:21617996

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

    PubMed Central

    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. PMID:26464621

  10. 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

  11. Bone marrow mesenchymal stem cells improve myocardial function in a swine model of acute myocardial infarction.

    PubMed

    Zhao, Jing-Jie; Liu, Xiao-Cheng; Kong, Feng; Qi, Tong-Gang; Cheng, Guang-Hui; Wang, Jue; Sun, Chao; Luan, Yun

    2014-09-01

    The aim of the current study was to confirm the effect and elucidate the mechanism of bone marrow mesenchymal stem cells (BMSCs) in acute myocardial infarction (AMI). AMI was induced in mini‑swine by ligating the left anterior descending coronary artery, and BMSCs (1x107) were injected via a sterile microinjection into the ischemic area. Six months postoperatively, electrocardiograph‑gated single photon emission computed tomography revealed that the myocardial filling defect was reduced and the left ventricular ejection fraction was improved in the BMSC group compared with the control group (P<0.05). Histopathological examination indicated that, in the BMSC treatment group, the percentage of survived myocardial tissue and the vessel density were increased, and the percentage of apoptosis was decreased compared with controls (P<0.05). Reverse transcription‑polymerase chain reaction results indicated that the expression levels of multiple inflammatory factors were significantly upregulated in the BMSC group compared with levels in the control group (P<0.05). In conclusion, the present study demonstrated that BMSC injection significantly improved cardiac function and reduced infarct size in six months, indicating that this method may be valuable for future study in clinical trials. PMID:25060678

  12. Effect of alpha 1-adrenergic blockade on myocardial blood flow during exercise after myocardial infarction.

    PubMed

    Herzog, C A; Dai, X Z; Bache, R J

    1991-08-01

    The effect of alpha 1-adrenergic blockade with prazosin on myocardial blood flow at rest and during two levels of treadmill exercise was assessed in 16 chronically instrumented dogs 9-14 days after myocardial infarction had been produced by occlusion of the left circumflex coronary artery. During resting conditions prazosin did not alter mean myocardial blood flow or the subendocardial-to-subepicardial flow ratio in either normally perfused or collateral-dependent myocardium. However, during exercise at comparable external work loads and comparable rate-pressure products, prazosin significantly increased blood flow to normally perfused (27% increase at the second level of exercise, P less than 0.001) and collateral-dependent myocardium (35% increase at the second level of exercise, P less than 0.001) compared with control. In addition, prazosin caused a small but significant decrease in the subendocardial-to-subepicardial flow ratio in both normal (1.27 +/- 0.04 to 1.19 +/- 0.04; P less than 0.01) and collateral-dependent myocardium (0.57 +/- 0.11 to 0.52 +/- 0.11; P less than 0.01) compared with control, reflecting a disproportionally greater increase in subepicardial flow in response to alpha 1-adrenergic blockade. These data demonstrate that alpha 1-adrenergic vasoconstriction inhibits coronary vasodilation during exercise, even in areas of collateral-dependent myocardium relatively early after coronary artery occlusion. PMID:1678929

  13. Effects of Chromium Methionine Supplementation on Blood Metabolites and Fatty Acid Profile of Beef during Late Fattening Period in Holstein Steers

    PubMed Central

    Nejad, Jalil Ghassemi; Lee, Bae-Hun; Kim, Byong-Wan; Ohh, Sang-Jip; Sung, Kyung Il

    2016-01-01

    The objective of this study was to determine the effects of chromium methionine (Cr-Met) chelate supplementation on blood metabolites and fatty acid profile of beef from Holstein steers during late fattening period. Fifteen Holstein steers were allotted randomly into two groups including the control (non Cr-Met feeding, NCM, ave. body weight [BW] = 483±25.7 kg) and the treatment (Cr-Met feeding for 4 months, 4CM, ave. BW = 486±27.5 kg) group. The feeding amount of Cr-Met to animals was limited to 400 ppb/cow/d and was supplemented to total mixed ration. No difference in blood albumin, alkaline phosphatase, urea-nitrogen, calcium, creatine, glucose, total protein, triglyceride, and cholesterol were observed between the treatment groups (p>0.05). The level of high density lipoprotein was higher in the 4CM group than the NCM group, whereas low density lipoprotein was lower in the 4CM group (p<0.05). The fatty acid composition (caprate, laurate, myristate, pentadecanoate, palmitate, palmitoleate, margarate, cis-11 heptadodecanoate, stearate, oleate, trans-vaccenate, linoleate, cis-11 eicosenoate, docosa hexaenoic acid, and docosa pentaenoic acid) of the beef showed no difference between the two groups (p>0.05). The arachidonic acid level tended to be higher in the 4CM than the NCM group (p = 0.07). Cr-Met had no influence (p>0.05) on the ratio of saturated, unsaturated, unsaturated/saturated, monounsaturated/saturated and polyunsaturated/saturated fatty acids whereas the ratio of polyunsaturated fatty acids (PUFA) in the 4CM group was comparatively higher than the NCM group (p<0.05). This study concluded that feeding Cr-Met supplementation in 400 ppb/d to Holstein steers for 4 months during late fattening period can improve some blood metabolites and beef quality by increasing PUFA and gamma-linoleate compositions of beef. PMID:26950869

  14. Effects of Chromium Methionine Supplementation on Blood Metabolites and Fatty Acid Profile of Beef during Late Fattening Period in Holstein Steers.

    PubMed

    Nejad, Jalil Ghassemi; Lee, Bae-Hun; Kim, Byong-Wan; Ohh, Sang-Jip; Sung, Kyung Il

    2016-03-01

    The objective of this study was to determine the effects of chromium methionine (Cr-Met) chelate supplementation on blood metabolites and fatty acid profile of beef from Holstein steers during late fattening period. Fifteen Holstein steers were allotted randomly into two groups including the control (non Cr-Met feeding, NCM, ave. body weight [BW] = 483±25.7 kg) and the treatment (Cr-Met feeding for 4 months, 4CM, ave. BW = 486±27.5 kg) group. The feeding amount of Cr-Met to animals was limited to 400 ppb/cow/d and was supplemented to total mixed ration. No difference in blood albumin, alkaline phosphatase, urea-nitrogen, calcium, creatine, glucose, total protein, triglyceride, and cholesterol were observed between the treatment groups (p>0.05). The level of high density lipoprotein was higher in the 4CM group than the NCM group, whereas low density lipoprotein was lower in the 4CM group (p<0.05). The fatty acid composition (caprate, laurate, myristate, pentadecanoate, palmitate, palmitoleate, margarate, cis-11 heptadodecanoate, stearate, oleate, trans-vaccenate, linoleate, cis-11 eicosenoate, docosa hexaenoic acid, and docosa pentaenoic acid) of the beef showed no difference between the two groups (p>0.05). The arachidonic acid level tended to be higher in the 4CM than the NCM group (p = 0.07). Cr-Met had no influence (p>0.05) on the ratio of saturated, unsaturated, unsaturated/saturated, monounsaturated/saturated and polyunsaturated/saturated fatty acids whereas the ratio of polyunsaturated fatty acids (PUFA) in the 4CM group was comparatively higher than the NCM group (p<0.05). This study concluded that feeding Cr-Met supplementation in 400 ppb/d to Holstein steers for 4 months during late fattening period can improve some blood metabolites and beef quality by increasing PUFA and gamma-linoleate compositions of beef. PMID:26950869

  15. [Family experiences post-acute myocardial infarction].

    PubMed

    Garcia, Raquel Pötter; Budó, Maria de Lourdes Denardin; Simon, Bruna Sodré; Wünsch, Simone; Oliveira, Stefanie Griebeler; Barbosa, Mariane da Silva

    2013-09-01

    This study aimed to describe the family experiences post-infarction. Qualitative, descriptive and exploratory research, carried out with six families of post-infarction patients. Data collection was conducted in families' homes, in the period of February to May of 2012, through observation and interviews with the family. The software Atlas Ti 6.2 was used to code the interviews and the data were explored with thematic analysis. Two categories emerged "Difficult times": immediate consequence of acute myocardial infarction for the families; and "We reeducate ourselves--we can adapt ourselves": current experience of families. The immediate post-infarction experience is permeated by several feelings, with the need for families to adapt to fit into the needs. The current experience shows changes in families due to the disease. The family is the main responsible for the care giving, although Nursing should exchange and share knowledge. PMID:24344600

  16. Molecular Imaging of Healing After Myocardial Infarction

    PubMed Central

    Naresh, Nivedita K; Ben-Mordechai, Tamar; Leor, Jonathan

    2011-01-01

    The progression from acute myocardial infarction (MI) to heart failure continues to be a major cause of morbidity and mortality. Potential new therapies for improved infarct healing such as stem cells, gene therapy, and tissue engineering are being investigated. Noninvasive imaging plays a central role in the evaluation of MI and infarct healing, both clinically and in preclinical research. Traditionally, imaging has been used to assess cardiac structure, function, perfusion, and viability. However, new imaging methods can be used to assess biological processes at the cellular and molecular level. We review molecular imaging techniques for evaluating the biology of infarct healing and repair. Specifically, we cover recent advances in imaging the various phases of MI and infarct healing such as apoptosis, inflammation, angiogenesis, extracellular matrix deposition, and scar formation. Significant progress has been made in preclinical molecular imaging, and future challenges include translation of these methods to clinical practice. PMID:21869911

  17. Cortical laminar necrosis following myocardial infarction.

    PubMed

    Lattanzi, Simona; Silvestrini, Mauro; Provinciali, Leandro

    2016-01-01

    The cortical laminar necrosis (CLN) is a permanent injury characterized by the selective delayed necrosis of the cerebral cortex, mainly of the third layer, and usually greater in the depths and sides of the sulci than over the crest of the gyri. The damage involves all cellular components - either neurons, glia cells and blood vessels - and results in a focal cortical band of pan-necrosis detectable in late sub-acute or chronic stages of reduced energy supply to the brain. The CLN has been described in different conditions as hypoxia, hypoglycemia and status epilepticus. At brain CT or MR scans it appears with pathognomonic highly hyperdense or T1-hyperintense lesions following the gyral anatomy of the cerebral cortex. We reported a case of CLN associated to myocardial infarct and discussed the underlying mechanisms. PMID:27375142

  18. Caffeine reduces dipyridamole-induced myocardial ischemia

    SciTech Connect

    Smits, P.; Aengevaeren, W.R.; Corstens, F.H.; Thien, T. )

    1989-10-01

    The mechanism of action of coronary vasodilation after dipyridamole may be based on inhibition of cellular uptake of circulating endogenous adenosine. Since caffeine has been reported to be a competitive antagonist of adenosine we studied the effect of caffeine on the outcome of dipiridamole-{sup 201}Tl cardiac imaging in one patient. During caffeine abstinence dipyridamole induced myocardial ischemia with down-slope ST depressions on the ECG, and reversible perfusion defects on the scintigrams. When the test was repeated 1 wk later on similar conditions, but now shortly after infusion of caffeine (4 mg/kg), the ECG showed nodepressions, and the scintigrams only slight signs of ischemia. We conclude that when caffeine abstinence is not sufficient, the widespread use of coffee and related products may be responsible for false-negative findings in dipyridamole-201Tl cardiac imaging.

  19. Clinical disease registries in acute myocardial infarction

    PubMed Central

    Ashrafi, Reza; Hussain, Hussain; Brisk, Robert; Boardman, Leanne; Weston, Clive

    2014-01-01

    Disease registries, containing systematic records of cases, have for nearly 100 years been valuable in exploring and understanding various aspects of cardiology. This is particularly true for myocardial infarction, where such registries have provided both epidemiological and clinical information that was not readily available from randomised controlled trials in highly-selected populations. Registries, whether mandated or voluntary, prospective or retrospective in their analysis, have at their core a common study population and common data definitions. In this review we highlight how registries have diversified to offer information on epidemiology, risk modelling, quality assurance/improvement and original research-through data mining, transnational comparisons and the facilitation of enrolment in, and follow-up during registry-based randomised clinical trials. PMID:24976913

  20. Myocardial tissue engineering for cardiac repair.

    PubMed

    Pecha, Simon; Eschenhagen, Thomas; Reichenspurner, Hermann

    2016-03-01

    The number of patients with heart failure is increasing in the aging population. Heart transplantation remains the only curative treatment option for patients with end-stage heart failure. Because of an organ donor shortage, new organ-independent treatment options are necessary. Different approaches to cardiac repair therapies have been developed and optimized in recent years. One of these promising approaches is myocardial tissue engineering, which refers to the creation of 3-dimensional engineered heart tissue in vitro. This perspective provides an overview of different approaches to tissue engineering, including essentials to improve tissue quality and choice of ideal cell source, as well as an overview of in vitro and in vivo studies. Several hurdles that have to be overcome before clinical application of engineered heart tissue might become a realistic scenario are also addressed. PMID:26856673

  1. Coronary microvascular obstruction in acute myocardial infarction.

    PubMed

    Niccoli, Giampaolo; Scalone, Giancarla; Lerman, Amir; Crea, Filippo

    2016-04-01

    The success of a primary percutaneous intervention (PCI) in the setting of ST elevation myocardial infarction depends on the functional and structural integrity of coronary microcirculation. Coronary microvascular dysfunction and obstruction (CMVO) occurs in up to half of patients submitted to apparently successful primary PCI and is associated to a much worse outcome. The current review summarizes the complex mechanisms responsible for CMVO, including pre-existing coronary microvascular dysfunction, and highlights the current limitations in the assessment of microvascular function. More importantly, at the light of the substantial failure of trials hitherto published on the treatment of CMVO, this review proposes a novel integrated therapeutic approach, which should overcome the limitations of previous studies. PMID:26364289

  2. Computing Myocardial Motion in 4D Echocardiography

    PubMed Central

    Mukherjee, Ryan; Sprouse, Chad; Pinheiro, Aurélio; Abraham, Theodore; Burlina, Philippe

    2012-01-01

    4D (3D spatial+time) echocardiography is gaining widespread acceptance at clinical institutions for its high temporal resolution and relatively low cost. We describe a novel method for computing dense 3D myocardial motion with high accuracy. The method is based on a classical variational optical flow technique, but exploits modern developments in optical flow research to utilize the full capabilities of 4D echocardiography. Using a variety of metrics, we present an in-depth performance evaluation of the method on synthetic, phantom, and intraoperative 4D Transesophageal Echocardiographic (TEE) data. When compared with state-of-the-art optical flow and speckle tracking techniques currently found in 4D echocardiography, the method we present shows notable improvements in error. We believe the performance improvements shown can have a positive impact when the method is used as input for various applications, such as strain computation, biomechanical modeling, or automated diagnostics. PMID:22677256

  3. Adenosine thallium 201 myocardial perfusion scintigraphy

    SciTech Connect

    Verani, M.S. )

    1991-07-01

    Pharmacologic coronary vasodilation as an adjunct to myocardial perfusion imaging has become increasingly important in the evaluation of patients with coronary artery disease, in view of the large number of patients who cannot perform an adequate exercise test or in whom contraindications render exercise inappropriate. Adenosine is a very potent coronary vasodilator and when combined with thallium 201 scintigraphy produces images of high quality, with the added advantages of a very short half-life (less than 10 seconds) and the ability to adjust the dose during the infusion, which may enhance safety and curtail the duration of side effects. The reported sensitivity and specificity of adenosine thallium 201 scintigraphy for the detection of coronary artery disease are high and at least comparable with imaging after exercise or dipyridamole administration. 23 refs.

  4. Acute myocardial infarction in the obstetric patient

    PubMed Central

    Firoz, Tabassum; Magee, Laura A

    2012-01-01

    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.

  5. 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

  6. 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

  7. 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

  8. (1) Coronary Events Caused by Myocardial Bridge

    PubMed Central

    Yoko, Kawawa; Ehiichi, Kohda; Toshiharu, Ishii

    2009-01-01

    Myocardial bridge (MB), which covers a part of the left anterior descending coronary artery (LAD), is a normal anatomical variant structure (45% in frequency by autopsy) in LAD. MB contraction plays the role of a “double-edged sword” on the coronary events, suppressing coronary atherosclerosis under the MB, yet generating abnormal blood flow associated with coronary heart diseases (CHDs). High shear stress driven by MB compression causes the suppression of vascular permeability and vasoactive protein expression such as e-NOS and endothelin-1, which leads to the suppression of atherosclerosis in the LAD segment under the MB. However, despite the prevalent view of MB as benignancy by conventional coronary angiography (5-6% in frequency), with advance of imaging technique such as multislice spiral computed tomography [(MSCT); 16% in frequency], cardiologists are now frequently aware of symptomatic MB occurring not only in hospitalized patients, but also in young athletes free from atherosclerosis. Moreover, the large mass volume of MB muscle induces atherosclerosis evolution at the settled site in LAD proximal to MB and contributes to the occurrence of myocardial infarction. These events upon the coronary events result from the different pathophysiological mechanisms induced by contractile force of MB, which is solely determined just by the integration of anatomical properties of MB, such as the location, length and thickness of MB in an individual LAD. A recent MSCT provides the objective quantification of the anatomical variables that correlate with the histopathological results in relation to the occurrence of CHD. In this review, we therefore discuss the necessity to explore MB as a inherent chance anatomical risk factor for CHD. PMID:23555365

  9. Myocardial bioenergetic abnormalities in experimental uremia

    PubMed Central

    Chesser, Alistair MS; Harwood, Steven M; Raftery, Martin J; Yaqoob, Muhammad M

    2016-01-01

    Purpose Cardiac bioenergetics are known to be abnormal in experimental uremia as exemplified by a reduced phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio. However, the progression of these bioenergetic changes during the development of uremia still requires further study and was therefore investigated at baseline, 4 weeks and 8 weeks after partial nephrectomy (PNx). Methods A two-stage PNx uremia model in male Wistar rats was used to explore in vivo cardiac and skeletal muscles’ bioenergetic changes over time. High-energy phosphate nucleotides were determined by phosphorus-31 nuclear magnetic resonance (31P-NMR) and capillary zone electrophoresis. Results 31P-NMR spectroscopy revealed lower PCr/ATP ratios in PNx hearts compared to sham (SH)-operated animals 4 weeks after PNx (median values given ± SD, 0.64±0.16 PNx, 1.13±0.31 SH, P<0.02). However, 8 weeks after PNx, the same ratio was more comparable between the two groups (0.84±0.15 PNx, 1.04±0.44 SH, P= not significant), suggestive of an adaptive mechanism. When 8-week hearts were prestressed with dobutamine, the PCr/ATP ratio was again lower in the PNx group (1.08±0.36 PNx, 1.55±0.38 SH, P<0.02), indicating a reduced energy reserve during the progression of uremic heart disease. 31P-NMR data were confirmed by capillary zone electrophoresis, and the changes in myocardial bioenergetics were replicated in the skeletal muscle. Conclusion This study provides evidence of the changes that occur in myocardial energetics in experimental uremia and highlights how skeletal muscle bioenergetics mirror those found in the cardiac tissue and so might potentially serve as a practical surrogate tissue during clinical cardiac NMR investigations. PMID:27307758

  10. Copeptin Testing in Acute Myocardial Infarction: Ready for Routine Use?

    PubMed Central

    Reinstadler, Sebastian Johannes; Klug, Gert; Metzler, Bernhard; Mair, Johannes

    2015-01-01

    Suspected acute myocardial infarction is one of the leading causes of admission to emergency departments. In the last decade, biomarkers revolutionized the management of patients with suspected acute coronary syndromes. Besides their pivotal assistance in timely diagnosis, biomarkers provide additional information for risk stratification. Cardiac troponins I and T are the most sensitive and specific markers of acute myocardial injury. Nonetheless, in order to overcome the remaining limitations of these markers, novel candidate biomarkers sensitive to early stage of disease are being extensively investigated. Among them, copeptin, a stable peptide derived from the precursor of vasopressin, emerged as a promising biomarker for the evaluation of suspected acute myocardial infarction. In this review, we summarize the currently available evidence for the usefulness of copeptin in the diagnosis and risk stratification of patients with suspected acute myocardial infarction in comparison with routine biomarkers. PMID:25960596

  11. Acute myocardial infarction due to blunt chest trauma.

    PubMed

    Sinha, Ajay Kumar; Agrawal, R K; Singh, Arun; Kumar, Rajiv; Kumar, Sanjeev; Sinha, Ajay; Saurabh; Kumar, Amit

    2002-01-01

    We report a case of blunt chest injury following a road accident leading to damage of the left main and left anterior descending coronary arteries causing acute myocardial infarction in a young person. PMID:12674188

  12. Inflammatory markers in ST-elevation acute myocardial infarction.

    PubMed

    Seropian, Ignacio M; Sonnino, Chiara; Van Tassell, Benjamin W; Biasucci, Luigi M; Abbate, Antonio

    2016-08-01

    After acute myocardial infarction, ventricular remodeling is characterized by changes at the molecular, structural, geometrical and functional level that determine progression to heart failure. Inflammation plays a key role in wound healing and scar formation, affecting ventricular remodeling. Several, rather different, components of the inflammatory response were studied as biomarkers in ST-elevation acute myocardial infarction. Widely available and inexpensive tests, such as leukocyte count at admission, as well as more sophisticated immunoassays provide powerful predictors of adverse outcome in patients with ST-elevation acute myocardial infarction. We review the value of inflammatory markers in ST-elevation acute myocardial infarction and their association with ventricular remodeling, heart failure and sudden death. In conclusion, the use of these biomarkers may identify subjects at greater risk of adverse events and perhaps provide an insight into the mechanisms of disease progression. PMID:25681486

  13. An Unusual Complication Following Transarterial Chemoembolization: Acute Myocardial Infarction

    SciTech Connect

    Lai Yiliang; Chang Weichou; Kuo Wuhsien; Huang Tienyu; Chu Hengcheng; Hsieh Tsaiyuan; Chang Weikuo

    2010-02-15

    Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.

  14. Asymptomatic myocardial infarction in Kawasaki disease: Long-term prognosis

    SciTech Connect

    Shiraishi, I.; Onouchi, Z.; Hayano, T.; Hamaoka, K.; Kiyosawa, N. )

    1991-04-01

    Eight patients with Kawasaki disease who had sustained asymptomatic myocardial infarction 8-15 years ago (mean, 13.1 years) were reexamined by various noninvasive cardiac function tests to assess long-term prognosis. At present, electrocardiograms (ECGs) are normal in six patients. However, all eight patients had a prolonged preejection period (PEP) to left ventricular ejection time (LVET) ratio 30 s after amylnitrate (AN) inhalation. Six patients had perfusion defects by exercise thallium-201 myocardial scintigraphy, and two patients developed ST segment depression in treadmill exercise testing. These patients are symptom-free even though their physical activity has not been restricted. Yet they proved to have serious abnormalities suggesting sequelae of myocardial infarction or existing myocardial ischemia. Judging from the results of noninvasive cardiac function tests and recently performed coronary angiography, five of the eight patients require coronary bypass surgery.

  15. Role of cardiomyocyte circadian clock in myocardial metabolic adaptation

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Marked circadian rhythmicities in cardiovascular physiology and pathophysiology exist. The cardiomyocyte circadian clock has recently been linked to circadian rhythms in myocardial gene expression, metabolism, and contractile function. For instance, the cardiomyocyte circadian clock is essential f...

  16. Tomographic myocardial perfusion scintigraphy in children with Kawasaki disease

    SciTech Connect

    Spielmann, R.P.; Nienaber, C.A.; Hausdorf, G.; Montz, R.

    1987-12-01

    Myocardial infarction and stenotic coronary lesions are serious late complications in children with Kawasaki disease. For the noninvasive assessment of myocardial perfusion, dipyridamole-redistribution /sup 201/Tl emission computed tomography (ECT) was performed in seven children (age 2 8/12-8 7/12 yr) 3-20 mo after the acute stage of the disease. In all patients, coronary aneurysms had been demonstrated by cross-sectional echocardiography. The scintigrams of six children showed no significant regional reduction of myocardial thallium uptake. These children had remained asymptomatic since the acute stage of Kawasaki disease. Persistent and transient thallium defects were present in one child with documented myocardial infarction. For this patient, obstruction of corresponding coronary vessels was confirmed by contrast angiography. It is suggested, that /sup 201/Tl ECT after dipyridamole-induced vasodilation may be used as a safe alternative to invasive coronary angiography for follow-up investigations in patients with Kawasaki disease.

  17. 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

  18. Imaging considerations for a technetium-99m myocardial perfusion agent

    SciTech Connect

    English, R.J.; Jones, A.G.; Davison, A.; Lister-James, J.; Campbell, S.; Holman, B.L.

    1986-03-01

    Myocardial perfusion imaging with /sup 201/Tl chloride suffers from a number of physical, geometric, and dosimetric constraints that could be diminished if an agent labeled with /sup 99m/Tc were available. The cationic complex /sup 99m/Tc hexakis-(t-butylisonitrile)technetium(I) ((/sup 99m/Tc)TBI) has been shown to concentrate in the myocardial tissue of both animals and humans, with preliminary clinical studies demonstrating a number of technical attributes not possible with /sup 201/Tl. Technetium-99m-TBI is a promising myocardial imaging agent that may permit high quality planar, gated, and tomographic imaging of both myocardial ischemia and infarction with reduced imaging times and improved resolution.

  19. The role of technetium-99m stannous pyrophosphate in myocardial imaging to recognize, localize and identify extension of acute myocardial infarction in patients

    NASA Technical Reports Server (NTRS)

    Willerson, J. T.; Parkey, R. W.; Bonte, F. J.; Stokely, E. M.; Buja, E. M.

    1975-01-01

    The ability of technetium-99m stannous pyrophosphate myocardial scintigrams to aid diagnostically in recognizing, localizing, and identifying extension of acute myocardial infarction in patients was evaluated. The present study is an extension of previous animal and patient evaluations that were recently performed utilizing this myocardial imaging agent.

  20. Systemic Effects of Electromagnetic Fields in Patients with Myocardial Infarction

    NASA Astrophysics Data System (ADS)

    Cañedo-Dorantes, L.; Valle, L.; Uruchurtu, E.; Medel, A.; García-Mayen, F.; Serrano-Luna, G.

    2003-09-01

    Healing of acute myocardial infarction (AMI) is associated with inflammatory response, which promotes healing and scar formation. Activation of a local inflammatory response in patients with sequel of AMI could have an important role to enhance angiogenesis and regeneration of hibernating myocardial tissue. Chronic arterial leg ulcers have a similar etiology, and healing has been promoted by exposure to extremely low frequency electromagnetic fields (ELF). We report the evolution of three AMI patients with sequel of AMI that were exposed to ELF.

  1. Myocardial imaging artifacts caused by mitral valve annulus calcification

    SciTech Connect

    Wagoner, L.E.; Movahed, A.; Reeves, W.C. )

    1991-02-01

    Knowledge of imaging artifact of myocardial perfusion studies with thallium-201 is critical for improving the diagnostic accuracy of coronary artery disease. Three patients are described who underwent exercise or pharmacologic stress thallium-201 imaging studies and had a moderate, fixed myocardial perfusion defect (scar) involving the posterolateral and inferoposterior walls of the left ventricle. This was an imaging artifact caused by a heavily calcified mitral valve annulus.

  2. Circulatory responses to hypoxia in experimental myocardial infarction.

    NASA Technical Reports Server (NTRS)

    Schroll, M.; Robison, S. C.; Harrison, D. C.

    1971-01-01

    Three levels of decreased arterial oxygen saturation elicited a graded circulatory response in dogs, manifested by stepwise increases in cardiac output, left ventricular dp/dt, and stroke volume, and decreases in systemic vascular resistance. Responses to similar hypoxia challenges after experimental myocardial infarction were qualitatively similar but quantitatively less. Although the circulatory compensation for hypoxia was less effective after myocardial infarction, no further deterioration of the haemodynamics was noted.

  3. Radionuclide imaging of myocardial infarction using Tc-99m TBI

    SciTech Connect

    Holman, B.L.; Campbell, S.; Kirshenbaum, J.M.; Lister-James, J.; Jones, A.G.; Davison, A.; Antman, E.

    1985-05-01

    The cationic complex Tc-99m t-butylisonitrile (TBI) concentrates in the myocardial tissue of several animal species. Its myocardial distribution is proportional to blood flow both in zones of ischemia and in normal myocardium at rest. Planar, tomographic, and gated myocardial images have been obtained using Tc-99m TBI in the human. The authors investigated the potential application of Tc-99m TBI imaging to detect and localize myocardial infarction. Four subjects without clinical evidence of cardiovascular disease and five patients with ECG evidence of previous myocardial infarction were studied. Tc-99m TBI (10mCi) was injected intravenously with the patient in a resting state with planar imaging in the anterior, 30 and 70 degree LAO projections beginning one hr after injection. The distribution of the tracer was homogeneous throughout the left ventricular wall in the normal subjects. Regional perfusion defects were present in 4/5 of the patients with myocardial infarction. Location of the defects corresponded to the location of the infarct using ECG criteria (2 inferoposterior and 2 anterior). The patient in whom the Tc-99m TBI image appeared normal had sustained a subendocardial myocardial infarct which could not be localized by ECG; the other 4 pts had transmural infarcts. Anterior and 30 degree LAO images were of excellent quality in all cases; there was overlap of the liver on the inferior wall of the left ventricle on the 70 degree LAO views. The authors conclude that accurate perfusion imaging may be possible using Tc-99m TBI in patients with transmural myocardial infarction.

  4. Identification of myocardial injury in the emergency setting

    PubMed Central

    Kavsak, Peter A.; Worster, Andrew; You, John J.; Oremus, Mark; Elsharif, Adell; Hill, Stephen A.; Devereaux, P.J.; MacRae, Andrew R.; Jaffe, Allan S.

    2013-01-01

    Within the past decade, the use of biomarkers to detect myocardial injury in the emergency department (ED) has been given increasing prominence as evident by the numerous studies and guidelines documenting their use. This review details the scope of the clinical problem, the history of changes in the definition of myocardial infarction (MI) and the new approaches, as well as suggestions for using laboratory biomarkers in the early detection of MI in the ED. PMID:20026097

  5. Identification of myocardial injury in the emergency setting.

    PubMed

    Kavsak, Peter A; Worster, Andrew; You, John J; Oremus, Mark; Elsharif, Adell; Hill, Stephen A; Devereaux, P J; MacRae, Andrew R; Jaffe, Allan S

    2010-04-01

    Within the past decade, the use of biomarkers to detect myocardial injury in the emergency department (ED) has been given increasing prominence as evident by the numerous studies and guidelines documenting their use. This review details the scope of the clinical problem, the history of changes in the definition of myocardial infarction (MI) and the new approaches, as well as suggestions for using laboratory biomarkers in the early detection of MI in the ED. PMID:20026097

  6. Effects of human immunodeficiency virus and metabolic complications on myocardial nutrient metabolism, blood flow, and oxygen consumption: a cross-sectional analysis

    PubMed Central

    2011-01-01

    Background In the general population, peripheral metabolic complications (MC) increase the risk for left ventricular dysfunction. Human immunodeficiency virus infection (HIV) and combination anti-retroviral therapy (cART) are associated with MC, left ventricular dysfunction, and a higher incidence of cardiovascular events than the general population. We examined whether myocardial nutrient metabolism and left ventricular dysfunction are related to one another and worse in HIV infected men treated with cART vs. HIV-negative men with or without MC. Methods Prospective, cross-sectional study of myocardial glucose and fatty acid metabolism and left ventricular function in HIV+ and HIV-negative men with and without MC. Myocardial glucose utilization (GLUT), and fatty acid oxidation and utilization rates were quantified using 11C-glucose and 11C-palmitate and myocardial positron emission tomography (PET) imaging in four groups of men: 23 HIV+ men with MC+ (HIV+/MC+, 42 ± 6 yrs), 15 HIV+ men without MC (HIV+/MC-, 41 ± 6 yrs), 9 HIV-negative men with MC (HIV-/MC+, 33 ± 5 yrs), and 22 HIV-negative men without MC (HIV-/MC-, 25 ± 6 yrs). Left ventricular function parameters were quantified using echocardiography. Results Myocardial glucose utilization was similar among groups, however when normalized to fasting plasma insulin concentration (GLUT/INS) was lower (p < 0.01) in men with metabolic complications (HIV+: 9.2 ± 6.2 vs. HIV-: 10.4 ± 8.1 nmol/g/min/μU/mL) than men without metabolic complications (HIV+: 45.0 ± 33.3 vs. HIV-: 60.3 ± 53.0 nmol/g/min/μU/mL). Lower GLUT/INS was associated with lower myocardial relaxation velocity during early diastole (r = 0.39, p < 0.001). Conclusion Men with metabolic complications, irrespective of HIV infection, had lower basal myocardial glucose utilization rates per unit insulin that were related to left ventricular diastolic impairments, indicating that well-controlled HIV infection is not an independent risk factor for

  7. 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. PMID:26871971

  8. Amelioration of adriamycin and daunorubicin myocardial toxicity by adenosine.

    PubMed

    Newman, R A; Hacker, M P; Krakoff, I H

    1981-09-01

    Primary cultures of rat myocardial cells were used to investigate the dose and time-dependent cellular enzyme release induced by either Adriamycin or daunorubicin, Concentrations of either anthracycline (1.8 or 18 microM) produced significant release of creatine phosphokinase and lactic dehydrogenase from myocardial cells within 24 hr of exposure without a detectable decrease in cell viability. Preincubation of the myocardial cells with varying concentrations of adenosine (10 microM to 1 mM) for 24 hr prior to the addition of anthracycline decreased or prevented drug-induced enzyme release. Other putative myocardial protectants, i.e., N-acetyl-L-cysteine, alpha-tocopherol, or carnitine, were ineffective in preventing anthracycline-induced enzyme release. Although adenosine was an effective myocardial protectant, it had no significant effect on cellular uptake of daunorubicin, nor did adenosine adversely affect the oncolytic activity of daunorubicin against L1210 leukemia cells in vitro. Anthramycin, another oncolytic agent having reported cardiotoxic effects, was also tested in the in vitro system. With this drug, however, no enzyme release was detected at less than lethal doses nor did adenosine have any protective potential against the toxicity of anthramycin. Finally, Adriamycin caused no significant lactic dehydrogenase release when incubated at 1.8 or 18 microM with H9c2 cells, a cell line having primarily skeletal muscle characteristics. This result suggests a specific toxicity of anthracyclines for myocardial but not skeletal muscle cells. PMID:7260911

  9. 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

  10. Early-phase myocardial infarction: Evaluation by MR imaging

    SciTech Connect

    Tscholakoff, D.; Higgins, C.B.; McNamara, M.T.; Derugin, N.

    1986-06-01

    In vivo gated magnetic resonance (MR) imaging was performed in 12 dogs immediately after occlusion of the left anterior descending coronary artery and serially up to 5 hours and again between 4 and 14 days. This was done to evaluate the appearance of acute myocardial infarcts and to determine how soon after coronary artery occlusion MR imaging can demonstrate the site of acute myocardial ischemia. In nine dogs with postmortem evidence of myocardial infarction, regional increase of signal intensity of the myocardium was present by 3 hours after coronary occlusion and conformed to the site of myocardial infarct found at autopsy. The signal intensity on T2-weighted images of the infarcted on T2-weighted images of the infarcted myocardium was significantly greater than that of normal myocardium at 3, 4, and 5 hours after occlusion. The T2 (spin-spin) relaxation time was significantly prolonged in the region of myocardial infarct at 3, 4, and 5 hours post-occlusion compared with normal myocardium. Myocardial wall thinning and increased intracavitary flow signal were found in six dogs with comparable pre- and postocclusion images in late systole.

  11. Role of Endothelial Cells in Myocardial Ischemia-Reperfusion Injury

    PubMed Central

    Singhal, Arun K.; Symons, J. David; Boudina, Sihem; Jaishy, Bharat; Shiu, Yan-Ting

    2014-01-01

    Minimizing myocardial ischemia-reperfusion injury has broad clinical implications and is a critical mediator of cardiac surgical outcomes. “Ischemic injury” results from a restriction in blood supply leading to a mismatch between oxygen supply and demand of a sufficient intensity and/or duration that leads to cell necrosis, whereas ischemia-reperfusion injury occurs when blood supply is restored after a period of ischemia and is usually associated with apoptosis (i.e. programmed cell death). Compared to vascular endothelial cells, cardiac myocytes are more sensitive to ischemic injury and have received the most attention in preventing myocardial ischemia-reperfusion injury. Many comprehensive reviews exist on various aspects of myocardial ischemia-reperfusion injury. The purpose of this review is to examine the role of vascular endothelial cells in myocardial ischemia-reperfusion injury, and to stimulate further research in this exciting and clinically relevant area. Two specific areas that are addressed include: 1) data suggesting that coronary endothelial cells are critical mediators of myocardial dysfunction after ischemia-reperfusion injury; and 2) the involvement of the mitochondrial permeability transition pore in endothelial cell death as a result of an ischemia-reperfusion insult. Elucidating the cellular signaling pathway(s) that leads to endothelial cell injury and/or death in response to ischemia-reperfusion is a key component to developing clinically applicable strategies that might minimize myocardial ischemia-reperfusion injury. PMID:25558187

  12. Sphingolipid Therapy in Myocardial Ischemia-Reperfusion Injury

    PubMed Central

    Gundewar, Susheel; Lefer, David J.

    2009-01-01

    Sphingolipids are known to play a significant physiological role in cell growth, cell differentiation, and critical signal transduction pathways. Recent studies have demonstrated a significant role of sphingolipids and their metabolites in the pathogenesis of myocardial ischemia-reperfusion injury. Our laboratory has investigated the cytoprotective effects of N,N,N-Trimethylsphingosine chloride (TMS), a stable N-methylated synthetic sphingolipid analogue on myocardial and hepatic ischemia reperfusion injury in clinically relevant in vivo murine models of ischemia-reperfusion injury. TMS administered intravenously at the onset of ischemia reduced myocardial infarct size in the wild-type and obese (ob/ob) mice. Following myocardial I/R, there was an improvement in cardiac function in the wild-type mice. Additionally, TMS also decreased serum liver enzymes following hepatic I/R in wild-type mice. The cytoprotective effects did not extend to the ob/ob mice following hepatic I/R or to the db/db mice following both myocardial and hepatic I/R. Our data suggests that although TMS is cytoprotective following I/R in normal animals, the cytoprotective actions of TMS are largely attenuated in obese and diabetic animals which may be due to altered signaling mechanisms in these animal models. Here we review the therapeutic role of TMS and other sphingolipids in the pathogenesis of myocardial ischemia reperfusion injury and their possible mechanisms of cardioprotection. PMID:17928150

  13. Administration of intracoronary eptifibatide during ST-elevation myocardial infarction.

    PubMed

    Pinto, Duane S; Kirtane, Ajay J; Ruocco, Nicholas A; Deibele, Albert J; Shui, Amy; Buros, Jacki; Murphy, Sabina A; Gibson, C Michael

    2005-12-01

    Distal embolization of atherothrombotic material during primary percutaneous coronary intervention (PCI) is associated with impaired myocardial perfusion, abnormal left ventricular function, and higher mortality. At high local concentrations, glycoprotein IIb/IIIa receptor antagonists have been demonstrated to promote clot disaggregation in vitro. Intracoronary administration of eptifibatide in vivo may increase local drug concentration by several orders of magnitude and promote clot disaggregation with a minimal increase in systemic drug concentrations. We hypothesized that intracoronary administration of eptifibatide before primary PCI for ST-elevation myocardial infarction would be safe and would be associated with high rates of normal myocardial perfusion. Clinical and angiographic data were pooled from patients who underwent primary PCI and received intracoronary eptifibatide as part of clinical practice. In-hospital adverse events were collected retrospectively. No deaths, urgent revascularizations, or reinfarctions were observed among the 59 patients who were treated with intracoronary eptifibatide. There were no Thrombolysis In Myocardial Infarction (TIMI) major bleeding events. Two TIMI minor bleeding events were noted. Normal TIMI myocardial perfusion grade 3 flow after PCI was noted in 54.4% of patients. No adverse events. including arrhythmias, were noted during intracoronary eptifibatide administration. In conclusion, intracoronary eptifibatide can be administered safely during primary PCI and is associated with few adverse events. Relatively high rates of normal myocardial perfusion were observed after primary PCI with adjunctive intracoronary eptifibatide. Further prospective randomized trials are warranted to evaluate the efficacy and safety of intracoronary eptifibatide. PMID:16310428

  14. Thallium-201 versus technetium-99m pyrophosphate myocardial imaging in detection and evaluation of patients with acute myocardial infarction

    SciTech Connect

    Pitt, B.; Thrall, J.H.

    1980-12-18

    Thallium-201 myocardial imaging is of value in the early detection and evaluation of patients with suspected acute infarction. Thallium imaging may have a special value in characterizing patients with cardiogenic shock and in detecting patients at risk for subsequent infarction or death or death or both, before hospital discharge. Approximately 95 percent of pateints with transmural or nontransmural myocardial infarction can be detected with technetium-99m pyrophosphate myocardial imaging if the imaging is performed 24 to 72 hours after the onset of symptoms. Pyrophosphate imaging may have an important role in the evaluation of patients during the early follow-up period after hospital discharge from an episode of acute infarction. The finding of a persistently positive pyrophosphate image suggests a poor prognosis and is associated with a relatively large incidence of subsequent myocardial infarction and death.

  15. Contribution of diet and major depression to incidence of acute myocardial infarction (AMI)

    PubMed Central

    2010-01-01

    Background Despite significant improvements in the treatment of coronary heart disease (CHD), it is still a major cause of mortality and morbidity among the Iranian population. Epidemiological studies have documented that risk factors including smoking and the biochemical profile are responsible for the development of acute myocardial infarction (AMI). Psychological factors have been discussed as potential risk factors for coronary heart disease. Among emotional factors, depression correlates with coronary heart disease, particularly myocardial infarction. Methods This case-control study was conducted on 120 cases (69 males and 51 females) of acute myocardial infarction (AMI) and 120 controls, with a mean age of 62.48 ± 15.39 years. Cases and controls were matched by age, residence and sex. Results The results revealed that severe depression was independently associated with the risk of AMI (P = 0.025, OR = 2.6, 95% CI 1.1-5.8). The analysis of variables indicated that risk factors for developing depression were unmarried, low levels of polyunsaturated fatty acids (PUFAs), total dietary fiber (TDF) and carbohydrates. The levels of these dietary factors were lowest in severely depressed patients compared to those categorised as moderate or mild cases. Furthermore, severely depressed subjects were associated with higher levels of total cholesterol, high systolic blood pressure (SBP) and WHR. Age, income, a family history of coronary heart disease, education level, sex, employment and smoking were not associated with severe depression. Conclusion The present study demonstrated that severe depression symptoms are independent risk factors for AMI. Furthermore, severe depression was associated with an unhealthy diet and AMI risk factors. PMID:21087475

  16. Size of myocardial infarction induced by ischaemia/reperfusion is unaltered in rats with metabolic syndrome.

    PubMed

    Thim, Troels; Bentzon, Jacob F; Kristiansen, Steen B; Simonsen, Ulf; Andersen, Heidi L; Wassermann, Karsten; Falk, Erling

    2006-06-01

    Obesity is associated with metabolic syndrome and increased incidence of and mortality from myocardial infarction. The aim of the present study was to develop an animal model with metabolic syndrome and examine how that influences size of myocardial infarcts induced by occlusion and reperfusion of the left anterior descending coronary artery. Sprague-Dawley rats (n = 105) were fed either LF (low-fat) or MHF (moderately high-fat) diets for 13 weeks before coronary occlusion for 45 min, followed by reperfusion for 60 min. Compared with LF-fed and lean MHF-fed rats, obese MHF-fed rats developed metabolic disturbances similar to those seen in the metabolic syndrome, including being overweight by 24% (compared with lean MHF-fed rats), having 74% more visceral fat (compared with LF-fed rats), 15% higher blood pressure (compared with LF-fed rats), 116% higher plasma insulin (compared with lean MHF-fed rats), 10% higher fasting plasma glucose (compared with LF-fed rats), 35% higher non-fasting plasma glucose (compared with lean MHF-fed rats), 36% higher plasma leptin (compared with lean MHF-fed rats) and a tendency to lower plasma adiponectin and higher plasma non-esterified fatty acids. Infarct size was similar in the three groups of rats (36+/-14, 42+/-18 and 41+/-14% in obese MHF-fed, lean MHF-fed and LF-fed rats respectively). In conclusion, rats fed a MHF diet developed metabolic syndrome, but this did not influence myocardial infarct size. PMID:16448385

  17. SPARC mediates early extracellular matrix remodeling following myocardial infarction

    PubMed Central

    McCurdy, Sarah M.; Dai, Qiuxia; Zhang, Jianhua; Zamilpa, Rogelio; Ramirez, Trevi A.; Dayah, Tariq; Nguyen, Nguyen; Jin, Yu-Fang; Bradshaw, Amy D.

    2011-01-01

    Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein that functions in the extracellular processing of newly synthesized collagen. Collagen deposition to form a scar is a key event following a myocardial infarction (MI). Because the roles of SPARC in the early post-MI setting have not been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient (null; n=25) mice at day 3 post-MI. Day 0 WT (n=28) and null (n=20) mice served as controls. Infarct size was 52 ± 2% for WT and 47 ± 2% for SPARC null (P=NS), indicating that the MI injury was comparable in the two groups. By echocardiography, WT mice increased end-diastolic volumes from 45 ± 2 to 83 ± 5 μl (P < 0.05). SPARC null mice also increased end-diastolic volumes but to a lesser extent than WT (39 ± 3 to 63 ± 5 μl; P < 0.05 vs. day 0 controls and vs. WT day 3 MI). Ejection fraction fell post-MI in WT mice from 57 ± 2 to 19 ± 1%. The decrease in ejection fraction was attenuated in the absence of SPARC (65 ± 2 to 28 ± 2%). Fibroblasts isolated from SPARC null left ventricle (LV) showed differences in the expression of 22 genes encoding extracellular matrix and adhesion molecule genes, including fibronectin, connective tissue growth factor (CTGF; CCN2), matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of metalloproteinase-2 (TIMP-2). The change in fibroblast gene expression levels was mirrored in tissue protein extracts for fibronectin, CTGF, and MMP-3 but not TIMP-2. Combined, the results of this study indicate that SPARC deletion preserves LV function at day 3 post-MI but may be detrimental for the long-term response due to impaired fibroblast activation. PMID:21602472

  18. Radioiodinated methyl-branched fatty acids: Evaluation of catabolites formed in vivo

    SciTech Connect

    Knapp, F.F. Jr.; Reske, S.N.; Kirsch, G.; Ambrose, K.R.; Blystone, S.L.; Goodman, M.M.

    1987-01-01

    Radioiodinated terminal iodophenyl-substituted long-chain fatty acids containing either racemic mono-methyl or geminal dimethyl-branching in the alkyl chain have been shown to exhibit delayed myocardial clearance properties which make these agents useful for the SPECT evaluation of myocardial fatty acid uptake patterns. Although the myocardial clearance rate of 15-(p-iodophenyl)-3-R,S- methylpentadecanoic acid (BMIPP) is considerably delayed, in comparison with the IPPA straight-chain analogue, analysis of the radioiodinated lipids present in the outflow tract of isolated rat hearts administered BMIPP have clearly demonstrated the presence of a polar metabolite. The synthesis of ..beta..-hydroxy fatty acids has been developed to allow investigation of the possible formation of ..beta..-hydroxy catabolites in vivo. The preparation of ..beta..-hydroxy BMIPP and ..beta..-hydroxy IPPA are described, and the possible significance of their formation in vivo discussed. 4 figs.

  19. [Coronary artery disease, myocardial perfusion and ventricular function in Q-wave and non-Q-wave myocardial infarcts].

    PubMed

    Macieira-Coelho, E; Garcia-Alves, M; da Costa, B; Cantinho, G; Pedro, P; Dionisio, I; Gouveia, A; de Padua, F

    1997-04-01

    Controversy remains in considering non-Q wave myocardial infarction (NQMI) a distinct pathophysiological entity of Q wave myocardial infarction (QMI). In order to analyze the severity of coronary artery disease, extension of myocardial scar or myocardial ischemia and ventricular function, 78 consecutive patients with QMI and 32 with NQMI, mean age 55.4 +/- 8.5, not submitted to thrombolytic therapy, were studied. Coronary angiography, exercise thallium scintigraphy and radionuclide ventriculography were performed in all at least within 3 months of a prior myocardial infarction. In the present study the occurrence of QMI was significantly more frequent in older patients than NQMI. There was no prevalence of occlusion either in the right, left circumflex or left anterior descending coronary arteries in both groups. Ejection fraction, degree of occlusion and presence of collateral circulation showed an equal prevalence in QMI and NQMI patients. A higher incidence of multivessel disease was found in NQMI that had less necrosis than QMI patients. The prevalence of exercise induced thallium-201 redistribution defects within the infarct zone was substantially higher and involved more scar segments in NQMI patients. Physiological and clinical consequences of coronary thrombosis depends on the size and the number of diseased arteries, the approach the pathophysiologic consequences of coronary disease in terms of fractal structure has been suggested. A pronounced heterogeneity in regional myocardial blood flow in a fractal branching arterial network may be responsible for the pathophysiologic differences of coronary thrombosis between Q-wave and non Q-wave infarction. PMID:9341032

  20. Correlation between myocardial dysfunction and perfusion impairment in diabetic rats with velocity vector imaging and myocardial contrast echocardiography.

    PubMed

    Wei, Zhangrui; Zhang, Haibin; Su, Haili; Zhu, Ting; Zhu, Yongsheng; Zhang, Jun

    2012-11-01

    The purpose of this study was to investigate whether myocardial systolic dysfunction and perfusion impairment occur in diabetic rats, and to assess their relationship using velocity vector imaging (VVI) and myocardial contrast echocardiography (MCE). Forty-six rats were randomly divided into either control or the diabetes mellitus (DM) groups. DM was induced by intraperitoneal administration of streptozotocin. Twelve weeks later, 39 survival rats underwent VVI and MCE in short-axis view at the middle level of the left ventricle, both at rest and after dipyridamole stress. VVI-derived contractile parameters included peak systolic velocity (Vs ), circumferential strain (εc ), strain rate (SRc ), and their reserves. MCE-derived perfusion parameters consisted of myocardial blood flow (MBF) and myocardial flow reserve (MFR). At rest, SRc in the DM group was significantly lower than in the control group, Vs , εc , and MBF did not differ significantly between groups. After dipyridamole stress, all VVI parameters and their reserves in the DM group were significantly lower than those in the control group, MBF and MFR were substantially lower than those in the control group, too. Meanwhile, significant correlations between VVI parameter reserves and MFR were observed in the DM group. Both myocardial systolic function and perfusion were impaired in DM rats. Decreased MFR could be an important contributor to the reduction in myocardial contractile reserve. PMID:22931118

  1. [Alpha-linolenic acid and cardiovascular diseases].

    PubMed

    Ristić-Medić, Danijela; Ristić, Gordana; Tepsić, Vesna

    2003-01-01

    IMPORTANCE AND METABOLISM OF ALPHA-LINOLENIC ACID: Alpha-linolenic acid is an essential fatty acid which cannot be produced in the body and must be taken by food. Both in animals and humans, alpha-linolenic acid is desaturated and elongated into eicosapentaenoic and docosahexaenoic acid. It is also incorporated into plasma and tissue lipids and its conversion is affected by levels of linoleic acid. POTENTIAL ROLE IN PATHOGENESIS OF CARDIOVASCULAR DISEASES: Diet enriched in n-3 fatty acids, especially alpha-linolenic acid, reduces the incidence of cardiac death. Studies have shown that alpha linolenic acid prevents ventricular fibrillation which is the main cause of cardiac death. Studies in rats suggest that alpha-linolenic acid may be more effective in preventing ventricular fibrillations than eicosapentaenoic and docosahexaenoic acid. Furthermore, alpha-linolenic acid is the main fatty acid decreasing platalet aggregation which is an important step in thrombosis i.e. non-fatal myocardial infarction and stroke. DIETARY SOURCES AND NUTRITION RECOMMENDATIONS: Dietary sources include flaxseed and flaxseed oil, canola oil, soybean and soybean oil, pumpkin seed and pumpkin oil, walnuts and walnut oil. Strong evidence supports beneficial effects of alpha-linolenic acid and its dietary sources should be incorporated into balanced diet for prevention of cardiovascular diseases. The recommended daily intake is 2 g with a ratio of 5/1 for linoleic/alpha-linolenic acid. PMID:15510909

  2. 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

  3. Evaluation of cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds on isoprenaline-induced myocardial injury in Wistar albino rats

    PubMed Central

    Patel, Kaksha J.; Panchasara, Ashwin K.; Barvaliya, Manish J.; Purohit, Bhargav M.; Baxi, Seema N.; Vadgama, Vishal K.; Tripathi, C. B.

    2015-01-01

    In the present study, cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds in isoprenaline-induced myocardial infarction in Wistar albino rats was evaluated. In vitro total phenolic, total flavonoid content and 2, 2’-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. In vivo effect of aqueous extract of G. indica was evaluated in Wistar albino rats by isoprenaline-induced myocardial injury model. Thirty six rats were randomly divided in 6 groups. Rats were treated with G. indica 250 mg/kg and 500 mg/kg doses for 21 days and myocardial injury was produced by subcutaneous injection of isoprenaline 85 mg/kg on day 20 and 21. Carvedilol 1 mg/kg for 21 days served as active control. Electrocardiogram parameters, cardiac injury markers (serum troponin-I, uric acid, lactate dehydrogenase, creatinine kinase-MB, aspartate aminotransferase and alanine aminotransferase), oxidative stress markers (superoxide dismutase, catalase and malondialdehyde level) and histopathological changes were evaluated in each group and compared using appropriate statistical tests. In vitro evaluation of aqueous extract showed significant antioxidant property. Isoprenaline produced significant myocardial ischemia as compared to normal control group (P<0.05). Administration of G. indica in both the doses did not significantly recover the altered electrocardiogram, cardiac injury markers, oxidative stress markers and histopathological myocardial damage as compared to disease control group (P>0.05). The aqueous extract of G. indica was not found to be cardioprotective against myocardial injury. Further study with more sample size and higher dose range may be required to evaluate its cardioprotective effect. PMID:26752987

  4. Evaluation of cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds on isoprenaline-induced myocardial injury in Wistar albino rats.

    PubMed

    Patel, Kaksha J; Panchasara, Ashwin K; Barvaliya, Manish J; Purohit, Bhargav M; Baxi, Seema N; Vadgama, Vishal K; Tripathi, C B

    2015-01-01

    In the present study, cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds in isoprenaline-induced myocardial infarction in Wistar albino rats was evaluated. In vitro total phenolic, total flavonoid content and 2, 2'-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. In vivo effect of aqueous extract of G. indica was evaluated in Wistar albino rats by isoprenaline-induced myocardial injury model. Thirty six rats were randomly divided in 6 groups. Rats were treated with G. indica 250 mg/kg and 500 mg/kg doses for 21 days and myocardial injury was produced by subcutaneous injection of isoprenaline 85 mg/kg on day 20 and 21. Carvedilol 1 mg/kg for 21 days served as active control. Electrocardiogram parameters, cardiac injury markers (serum troponin-I, uric acid, lactate dehydrogenase, creatinine kinase-MB, aspartate aminotransferase and alanine aminotransferase), oxidative stress markers (superoxide dismutase, catalase and malondialdehyde level) and histopathological changes were evaluated in each group and compared using appropriate statistical tests. In vitro evaluation of aqueous extract showed significant antioxidant property. Isoprenaline produced significant myocardial ischemia as compared to normal control group (P<0.05). Administration of G. indica in both the doses did not significantly recover the altered electrocardiogram, cardiac injury markers, oxidative stress markers and histopathological myocardial damage as compared to disease control group (P>0.05). The aqueous extract of G. indica was not found to be cardioprotective against myocardial injury. Further study with more sample size and higher dose range may be required to evaluate its cardioprotective effect. PMID:26752987

  5. [Myocardial infarction and thromboembolism during pregnancy].

    PubMed

    Härtel, Dirk; Sorges, Eckhard; Carlsson, Jörg; Römer, Volker; Tebbe, Ulrich

    2003-05-01

    Acute myocardial infarction is a very rare event during pregnancy and bears the problem of misdiagnosis. However, about 150 cases have been published worldwide with a preponderance of anterior wall infarcts. With more women delaying childbearing until an older age and increasing prevalence of smoking in young women, it can be expected that all forms of coronary artery disease--including acute myocardial infarction--will be seen more often in the future. Among the causes of coronary artery occlusion in pregnancy are (1) rupture of very small coronary artery plaques triggered by different events, e.g., hypertension; (2) plain coronary artery disease; (3) dissection of coronary arteries; (4) coronary artery spasms with/without arterial thrombosis. Prompt diagnosis and immediate therapy are necessary to lower the high mortality of mother and fetus. The gold standard in the therapy of acute myocardial infarction during pregnancy is immediate coronary angiography and percutaneous transluminal coronary angioplasty (PTCA) with or without stent implantation. Application of thrombolytics (recombinant tissue plasminogen activator [rt-PA], r-PA, streptokinase [SK], urokinase [UK]) has been reported in single patients but should be limited to cases where acute PTCA is not available and where the infarct occurs before the 14th week of pregnancy because of possible embryopathy. If the patient is in the last 10 weeks of pregnancy, anticipation of delivery should be part of the medical planning. Consultation with an obstetrician must be obtained as soon as the patient enters the hospital. Besides bleeding complications, venous thrombosis with pulmonary embolism is among the most common causes of death during pregnancy. Pregnancy-related changes in physiology - increase in the resistance to flow from the lower extremities to the heart - and congenital coagulation abnormalities are most important to be recognized. This leads to the fact that superficial and deep venous thromboses

  6. Translation of Methodology Used In Human Myocardial Imaging to a Sheep Model of Acute Myocardial Infarction

    PubMed Central

    Bailey, Elizabeth A; Bailey, Dale L; Hunyor, Stephen; Ladd, Leigh; Bautovich, George J

    2013-01-01

    Introduction: Pre-clinical investigation of stem cells for repairing damaged myocardium predominantly uses rodents, however large animals have cardiac circulation closely resembling the human heart. The aim of this study was to evaluate whether SPECT/CT myocardial perfusion imaging (MPI) could be used for assessing sheep myocardium following an acute myocardial infarction (MI) and response to intervention. Methods: Eighteen sheep were enrolled in a pilot study to evaluate [99mTc]-sestamibi MPI at baseline, post-MI and after therapy. Modifications to the standard MPI protocols were developed. All data was reconstructed with OSEM using CT-derived attenuation and scatter correction. Standard analyses were performed and inter-observer agreement was measured using Kappa (κ). Power determined the sample sizes needed to show statistically significant changes due to intervention. Results: Ten sheep completed the full protocol. Data processed was performed with pre-existing hardware and software used in human MPI scanning. No improvement in perfusion was seen in the control group, however improvements of 15%-35% were seen after intra-myocardial stem cell administration. Inter-observer agreement was excellent (К=0.89). Using a target power of 0.9, 28 sheep were required to detect a 10-12% change in perfusion. Conclusion: This study demonstrates the suitability of large animal models for imaging with standard MPI protocols and its feasibility with a manageable number of animals. These protocols could be translated into humans to study the efficacy of stem cell therapy in heart regeneration and repair.

  7. Changes in transmural distribution of myocardial perfusion assessed by quantitative intravenous myocardial contrast echocardiography in humans

    PubMed Central

    Fukuda, S; Muro, T; Hozumi, T; Watanabe, H; Shimada, K; Yoshiyama, M; Takeuchi, K; Yoshikawa, J

    2002-01-01

    Objective: To clarify whether changes in transmural distribution of myocardial perfusion under significant coronary artery stenosis can be assessed by quantitative intravenous myocardial contrast echocardiography (MCE) in humans. Methods: 31 patients underwent dipyridamole stress MCE and quantitative coronary angiography. Intravenous MCE was performed by continuous infusion of Levovist. Images were obtained from the apical four chamber view with alternating pulsing intervals both at rest and after dipyridamole infusion. Images were analysed offline by placing regions of interest over both endocardial and epicardial sides of the mid-septum. The background subtracted intensity versus pulsing interval plots were fitted to an exponential function, y = A (1 − e−βt), where A is plateau level and β is rate of rise. Results: Of the 31 patients, 16 had significant stenosis (> 70%) in the left anterior descending artery (group A) and 15 did not (group B). At rest, there were no differences in the A endocardial to epicardial ratio (A-EER) and β-EER between the two groups (mean (SD) 1.2 (0.6) v 1.2 (0.8) and 1.2 (0.7) v 1.1 (0.6), respectively, NS). During hyperaemia, β-EER in group A was significantly lower than that in group B (1.0 (0.5) v 1.4 (0.5), p < 0.05) and A-EER did not differ between the two groups (1.0 (0.5) v 1.2 (0.4), NS). Conclusions: Changes in transmural distribution of myocardial perfusion under significant coronary artery stenosis can be assessed by quantitative intravenous MCE in humans. PMID:12231594

  8. Early myocardial damage assessment in dystrophinopathies using 99Tcm-MIBI gated myocardial perfusion imaging

    PubMed Central

    Zhang, Li; Liu, Zhe; Hu, Ke-You; Tian, Qing-Bao; Wei, Ling-Ge; Zhao, Zhe; Shen, Hong-Rui; Hu, Jing

    2015-01-01

    Background Early detection of muscular dystrophy (MD)-associated cardiomyopathy is important because early medical treatment may slow cardiac remodeling and attenuate symptoms of cardiac dysfunction; however, no sensitive and standard diagnostic method for MD at an earlier stage has been well-recognized. Thus, the aim of this study was to test the early diagnostic value of technetium 99m-methoxyisobutylisonitrile (99Tcm-MIBI) gated myocardial perfusion imaging (G-MPI) for MD. Methods and results Ninety-one patients underwent 99Tcm-MIBI G-MPI examinations when they were diagnosed with Duchenne muscular dystrophy (DMD) (n=77) or Becker muscular dystrophy (BMD; n=14). 99Tcm-MIBI G-MPI examinations were repeated in 43 DMD patients who received steroid treatments for 2 years as a follow-up examination. Myocardial defects were observed in nearly every segment of the left ventricular wall in both DMD and BMD patients compared with controls, especially in the inferior walls and the apices by using 99Tcm-MIBI G-MPI. Cardiac wall movement impairment significantly correlated with age in the DMD and BMD groups (rs=0.534 [P<0.05] and rs=0.784 [P<0.05], respectively). Intermittent intravenous doses of glucocorticoids and continuation with oral steroid treatments significantly improved myocardial function in DMD patients (P<0.05), but not in BMD patients. Conclusion 99Tcm-MIBI G-MPI is a sensitive and safe approach for early evaluation of cardiomyopathy in patients with DMD or BMD, and can serve as a candidate method for the evaluation of progression, prognosis, and assessment of the effect of glucocorticoid treatment in these patients. PMID:26677332

  9. Technetium radiodiagnostic fatty acids derived from bisamide bisthiol ligands

    DOEpatents

    Jones, Alun G.; Lister-James, John; Davison, Alan

    1988-05-24

    A bisamide-bisthiol ligand containing fatty acid substituted thiol useful for producing Tc-labelled radiodiagnostic imaging agents is described. The ligand forms a complex with the radionuclide .sup.99m Tc suitable for administration as a radiopharmaceutical to obtain images of the heart for diagnosis of myocardial disfunction.

  10. Comparative Myocardial Deformation in 3 Myocardial Layers in Mice by Speckle Tracking Echocardiography

    PubMed Central

    Tee, Nicole; Gu, Yacui; Murni; Shim, Winston

    2015-01-01

    Background. Speckle tracking echocardiography (STE) using dedicated high-resolution ultrasound is a relatively new technique that is useful in assessing myocardial deformation in 3 myocardial layers in small animals. However, comparative studies of STE parameters acquired from murine are limited. Methods. A high-resolution rodent ultrasound machine (VSI Vevo 2100) and a clinically validated ultrasound machine (GE Vivid 7) were used to consecutively acquire echocardiography images from standardized parasternal long axis and short axis at midpapillary muscle level from 13 BALB/c mice. Speckle tracking strain (longitudinal, circumferential, and radial) from endocardial, myocardial, and epicardial layers was analyzed using vendor-specific offline analysis software. Results. Intersystem differences were not statistically significant in the global peak longitudinal strain (−16.8 ± 1.7% versus −18.7 ± 3.1%) and radial strain (46.8 ± 14.2% versus 41.0 ± 9.5%), except in the global peak circumferential strain (−16.9 ± 3.1% versus 27.0 ± 5.2%, P < 0.05). This was corroborated by Bland Altman analysis that revealed a weak agreement in circumferential strain (mean bias ± 1.96 SD of −10.12 ± 6.06%) between endocardium and midmyocardium. However, a good agreement was observed in longitudinal strain between midmyocardium/endocardium (mean bias ± 1.96 SD of −1.88 ± 3.93%) and between midmyocardium/epicardium (mean bias ± 1.96 SD of 3.63 ± 3.91%). Radial strain (mean bias ± 1.96 SD of −5.84 ± 17.70%) had wide limits of agreement between the two systems that indicated an increased variability. Conclusions. Our study shows that there is good reproducibility and agreement in longitudinal deformation of the 3 myocardial layers between the two ultrasound systems. Directional deformation gradients at endocardium, myocardium, and epicardium observed in mice were consistent to those reported in human subjects, thus attesting the clinical relevance of STE

  11. The allometric model in chronic myocardial infarction

    PubMed Central

    2012-01-01

    Background An allometric relationship between different electrocardiogram (ECG) parameters and infarcted ventricular mass was assessed in a myocardial infarction (MI) model in New Zealand rabbits. Methods A total of fifteen animals were used, out of which ten underwent left anterior descending coronary artery ligation to induce infarction (7–35% area). Myocardial infarction (MI) evolved and stabilized during a three month-period, after which, rabbits were sacrificed and the injured area was histologically confirmed. Right before sacrifice, ECGs were obtained to correlate several of its parameters to the infarcted mass. The latter was normalized after combining data from planimetry measurements and heart weight. The following ECG parameters were studied: RR and PR intervals, P-wave duration (PD), QRS duration (QRSD) and amplitude (QRSA), Q-wave (QA), R-wave (RA) and S-wave (SA) amplitudes, T-wave peak amplitude (TA), the interval from the peak to the end of the T-wave (TPE), ST-segment deviation (STA), QT interval (QT), corrected QT and JT intervals. Corrected QT was analyzed with different correction formulae, i.e., Bazett (QTB), Framingham (QTFRA), Fridericia (QTFRI), Hodge (QTHO) and Matsunaga (QTMA) and compared thereafter. The former variables and infarcted ventricular mass were then fitted to the allometric equation in terms of deviation from normality, in turn derived after ECGs in 5 healthy rabbits. Results Six variables (JT, QTB, QA, SA, TA and STA) presented statistical differences among leads. QT showed the best allometric fit (r = 0.78), followed by TA (r = 0.77), STA (r = 0.75), QTFRA (r = 0.72), TPE (r = 0.69), QTFRI (r = 0.68) and QTMA (r = 0.68). Corrected QT’s (QTFRA, QTFRI and QTMA) performed worse than the uncorrected counterpart (QT), the former scaling allometrically with similar goodness of fits. Conclusions QT, TA, STA and TPE could possibly be used to assess infarction extent in an old MI event through the

  12. Significance of U wave polarities in previous anterior myocardial infarction

    SciTech Connect

    Kanemoto, N.; Imaoka, C.; Suzuki, Y. )

    1991-04-01

    The significance of the polarity of U waves in left precordial leads was evaluated in relation to myocardial perfusion (T1 201 myocardial scintigraphy) and left ventricular function (99m Tc radionuclide ventriculography) in 63 patients with clinical and electrocardiographic evidence of a previous anterior myocardial infarction. Patients were divided into three groups according to the polarity of the U waves: positive U waves, flat U waves, and negative U waves. Twelve matched patients served as normal controls. The following parameters were analyzed: (1) total number of abnormal Q waves; (2) total myocardial perfusion index and regional myocardial perfusion index; (3) global ejection fraction; (4) regional ejection fraction; and (5) number of diseased coronary arteries. The total myocardial perfusion index values were 43.9 {plus minus} 1.0 in controls, 40.8 {plus minus} 3.4 in the positive U wave group, 33.4 {plus minus} 3.5 in the flat U wave group, and 30.3 {plus minus} 4.4 in the patients with negative U waves. Global ejection fractions in these groups were, respectively, 63.9 {plus minus} 8.6%, 65.0 {plus minus} 11.8%, 53.6 {plus minus} 8.1%, and 36.5 {plus minus} 13.6%. The sensitivity of negative U waves suggesting a global ejection fraction of less than 45% was 91.6%, and the specificity was 82.1%. Therefore the size of myocardial infarction increased and left ventricular function decreased, in order, from patients with positive U waves, to those with flat U waves, to those with negative U waves, with statistically significant differences.

  13. Myocardial regeneration potential of adipose tissue-derived stem cells

    SciTech Connect

    Bai, Xiaowen; Alt, Eckhard

    2010-10-22

    Research highlights: {yields} Various tissue resident stem cells are receiving tremendous attention from basic scientists and clinicians and hold great promise for myocardial regeneration. {yields} For practical reasons, human adipose tissue-derived stem cells are attractive stem cells for future clinical application in repairing damaged myocardium. {yields} This review summarizes the characteristics of cultured and freshly isolated stem cells obtained from adipose tissue, their myocardial regeneration potential and the, underlying mechanisms, and safety issues. -- Abstract: Various tissue resident stem cells are receiving attention from basic scientists and clinicians as they hold promise for myocardial regeneration. For practical reasons, adipose tissue-derived stem cells (ASCs) are attractive cells for clinical application in repairing damaged myocardium based on the following advantages: abundant adipose tissue in most patients and easy accessibility with minimally invasive lipoaspiration procedure. Several recent studies have demonstrated that both cultured and freshly isolated ASCs could improve cardiac function in animal model of myocardial infarction. The mechanisms underlying the beneficial effect of ASCs on myocardial regeneration are not fully understood. Growing evidence indicates that transplantation of ASCs improve cardiac function via the differentiation into cardiomyocytes and vascular cells, and through paracrine pathways. Paracrine factors secreted by injected ASCs enhance angiogenesis, reduce cell apoptosis rates, and promote neuron sprouts in damaged myocardium. In addition, Injection of ASCs increases electrical stability of the injured heart. Furthermore, there are no reported cases of arrhythmia or tumorigenesis in any studies regarding myocardial regeneration with ASCs. This review summarizes the characteristics of both cultured and freshly isolated stem cells obtained from adipose tissue, their myocardial regeneration potential, and the

  14. T1 Mapping in Characterizing Myocardial Disease: A Comprehensive Review.

    PubMed

    Puntmann, Valentina O; Peker, Elif; Chandrashekhar, Y; Nagel, Eike

    2016-07-01

    Cardiovascular magnetic resonance provides insights into myocardial structure and function noninvasively, with high diagnostic accuracy and without ionizing radiation. Myocardial tissue characterization in particular gives cardiovascular magnetic resonance a prime role among all the noninvasive cardiovascular investigations. Late gadolinium enhancement imaging is an established method for visualizing replacement scar, providing diagnostic and prognostic information in a variety of cardiac conditions. Late gadolinium enhancement, however, relies on the regional segregation of tissue characteristics to generate the imaging contrast. Thus, myocardial pathology that is diffuse in nature and affecting the myocardium in a rather uniform and global distribution is not well visualized with late gadolinium enhancement. Examples include diffuse myocardial inflammation, fibrosis, hypertrophy, and infiltration. T1 mapping is a novel technique allowing to diagnose these diffuse conditions by measurement of T1 values, which directly correspond to variation in intrinsic myocardial tissue properties. In addition to providing clinically meaningful indices, T1-mapping measurements also allow for an estimation of extracellular space by calculation of extracellular volume fraction. Multiple lines of evidence suggest a central role for T1 mapping in detection of diffuse myocardial disease in early disease stages and complements late gadolinium enhancement in visualization of the regional changes in common advanced myocardial disease. As a quantifiable measure, it may allow grading of disease activity, monitoring progress, and guiding treatment, potentially as a fast contrast-free clinical application. We present an overview of clinically relevant technical aspects of acquisition and processing, and the current state of art and evidence, supporting its clinical use. PMID:27390332

  15. Measurement of myocardial perfusion and infarction size using computer-aided diagnosis system for myocardial contrast echocardiography.

    PubMed

    Du, Guo-Qing; Xue, Jing-Yi; Guo, Yanhui; Chen, Shuang; Du, Pei; Wu, Yan; Wang, Yu-Hang; Zong, Li-Qiu; Tian, Jia-Wei

    2015-09-01

    Proper evaluation of myocardial microvascular perfusion and assessment of infarct size is critical for clinicians. We have developed a novel computer-aided diagnosis (CAD) approach for myocardial contrast echocardiography (MCE) to measure myocardial perfusion and infarct size. Rabbits underwent 15 min of coronary occlusion followed by reperfusion (group I, n = 15) or 60 min of coronary occlusion followed by reperfusion (group II, n = 15). Myocardial contrast echocardiography was performed before and 7 d after ischemia/reperfusion, and images were analyzed with the CAD system on the basis of eliminating particle swarm optimization clustering analysis. The myocardium was quickly and accurately detected using contrast-enhanced images, myocardial perfusion was quantitatively calibrated and a color-coded map calibrated by contrast intensity and automatically produced by the CAD system was used to outline the infarction region. Calibrated contrast intensity was significantly lower in infarct regions than in non-infarct regions, allowing differentiation of abnormal and normal myocardial perfusion. Receiver operating characteristic curve analysis documented that -54-pixel contrast intensity was an optimal cutoff point for the identification of infarcted myocardium with a sensitivity of 95.45% and specificity of 87.50%. Infarct sizes obtained using myocardial perfusion defect analysis of original contrast images and the contrast intensity-based color-coded map in computerized images were compared with infarct sizes measured using triphenyltetrazolium chloride staining. Use of the proposed CAD approach provided observers with more information. The infarct sizes obtained with myocardial perfusion defect analysis, the contrast intensity-based color-coded map and triphenyltetrazolium chloride staining were 23.72 ± 8.41%, 21.77 ± 7.8% and 18.21 ± 4.40% (% left ventricle) respectively (p > 0.05), indicating that computerized myocardial contrast echocardiography can

  16. Recommended dairy product intake modulates circulating fatty acid profile in healthy adults: a multi-centre cross-over study.

    PubMed

    Abdullah, Mohammad M H; Cyr, Audrey; Lépine, Marie-Claude; Labonté, Marie-Ève; Couture, Patrick; Jones, Peter J H; Lamarche, Benoît

    2015-02-14

    Dairy products are rich sources of an array of fatty acids (FA) that have been shown individually and in certain clusters to exert varying effects on cardiovascular health, for which the circulating lipid profile is a powerful biomarker. Whether the profile of these FA is reflected in blood upon short terms of intake, possibly contributing to the lipid-related health impacts of dairy products, remains to be fully established. The objectives of the present study were to assess a recommended dairy product consumption in relation to circulating FA and lipid profiles, and to evaluate certain FA in dairy fat as potential biomarkers of intake. In a free-living, multi-centre, cross-over design, 124 healthy individuals consumed 3 servings/d of commercial dairy (DAIRY; 1% fat milk, 1·5% fat yogurt and 34% fat cheese) or energy-equivalent control (CONTROL; fruit and vegetable juice, cashews and a cookie) products for 4 weeks each, separated by a 4-week washout period. Plasma FA and serum lipid profiles were assessed by standard methods at the end of each dietary phase. After 4 weeks of intake, plasma levels of FA pentadecanoic acid (15 : 0) and heptadecanoic acid (17 : 0) were higher (0·26 v. 0·22% and 0·42 v. 0·39% of the total identified FA, respectively) after the DAIRY phase than after the CONTROL phase (P< 0·0001). This was accompanied by a small but significant increase in serum LDL-cholesterol levels after the DAIRY phase compared with the CONTROL phase (+0·08 mmol/l; P= 0·04). In conclusion, intake of 3 servings/d of conventional dairy products may modify certain circulating FA and lipid profiles within 4 weeks, where 15 : 0 and 17 : 0 may be potential short-term biomarkers of intake. PMID:25609231

  17. Polymeric electrospun scaffolds: neuregulin encapsulation and biocompatibility studies in a model of myocardial ischemia.

    PubMed

    Simón-Yarza, Teresa; Rossi, Angela; Heffels, Karl-Heinz; Prósper, Felipe; Groll, Jürgen; Blanco-Prieto, Maria J

    2015-05-01

    Cardiovascular disease represents one of the major health challenges in modern times and is the number one cause of death globally. Thus, numerous studies are under way to identify effective cell- and/or growth factor (GF)-based therapies for repairing damaged cardiac tissue. In this regard, improving the engraftment or survival of regenerative cells and prolonging GF exposure have become fundamental goals in advancing these therapeutic approaches. Biomaterials have emerged as innovative scaffolds for the delivery of both cells and proteins in tissue engineering applications. In the present study, electrospinning was used to generate smooth homogenous polymeric fibers, which consisted of a poly(lactic-co-glycolic acid) (PLGA)/NCO-sP(EO-stat-PO) polymer blend encapsulating the cardioactive GF, Neuregulin-1 (Nrg). We evaluated the biocompatibility and degradation of this Nrg-containing biomaterial in a rat model of myocardial ischemia. Histological analysis revealed the presence of an initial acute inflammatory response after implantation, which was followed by a chronic inflammatory phase, characterized by the presence of giant cells. Notably, the scaffold remained in the heart after 3 months. Furthermore, an increase in the M2:M1 macrophage ratio following implantation suggested the induction of constructive tissue remodeling. Taken together, the combination of Nrg-encapsulating scaffolds with cells capable of inducing cardiac regeneration could represent an ambitious and promising therapeutic strategy for repairing diseased or damaged myocardial tissue. PMID:25707939

  18. Synthesis and evaluation of (18)F-trifluoroborate derivatives of triphenylphosphonium for myocardial perfusion imaging.

    PubMed

    Zhang, Zhengxing; Jenni, Silvia; Zhang, Chengcheng; Merkens, Helen; Lau, Joseph; Liu, Zhibo; Perrin, David M; Bénard, François; Lin, Kuo-Shyan

    2016-04-01

    Four trifluoroborate derivatives of phosphonium cations 2a-d were radiolabeled with fluorine-18 ((18)F) and evaluated for imaging myocardial perfusion with positron emission tomography (PET). Tracers were radiolabeled simply via (18)F-(19)F isotope exchange reaction in acidic (pH 2) aqueous solution. On average, [(18)F]2a-d were obtained in 10-17% non-decay-corrected radiochemical yield with 25.9-48.1GBq/μmol specific activity, and >96% radiochemical purity. In vitro stability study showed no decomposition of [(18)F]2a-d after being incubated in mouse plasma for up to 2h. Myocardial uptake in mice was visualized in PET images by using [(18)F]2b-d but not [(18)F]2a. [(18)F]2a-d were stable against in vivo defluorination as no significant bone uptake was observed. Despite sub-optimal heart uptake of [(18)F]2b-d, we successfully demonstrated that (18)F-(19)F isotope exchange reaction on trifluoroborates could be a promising strategy for the design of potential (18)F-labeled tracers even for intracellular targets. PMID:26922139

  19. Fourier transform infrared spectroscopic imaging of cardiac tissue to detect collagen deposition after myocardial infarction

    NASA Astrophysics Data System (ADS)

    Cheheltani, Rabee; Rosano, Jenna M.; Wang, Bin; Sabri, Abdel Karim; Pleshko, Nancy; Kiani, Mohammad F.

    2012-05-01

    Myocardial infarction often leads to an increase in deposition of fibrillar collagen. Detection and characterization of this cardiac fibrosis is of great interest to investigators and clinicians. Motivated by the significant limitations of conventional staining techniques to visualize collagen deposition in cardiac tissue sections, we have developed a Fourier transform infrared imaging spectroscopy (FT-IRIS) methodology for collagen assessment. The infrared absorbance band centered at 1338 cm-1, which arises from collagen amino acid side chain vibrations, was used to map collagen deposition across heart tissue sections of a rat model of myocardial infarction, and was compared to conventional staining techniques. Comparison of the size of the collagen scar in heart tissue sections as measured with this methodology and that of trichrome staining showed a strong correlation (R=0.93). A Pearson correlation model between local intensity values in FT-IRIS and immuno-histochemical staining of collagen type I also showed a strong correlation (R=0.86). We demonstrate that FT-IRIS methodology can be utilized to visualize cardiac collagen deposition. In addition, given that vibrational spectroscopic data on proteins reflect molecular features, it also has the potential to provide additional information about the molecular structure of cardiac extracellular matrix proteins and their alterations.

  20. Effects of Glucose Concentration on Propofol Cardioprotection against Myocardial Ischemia Reperfusion Injury in Isolated Rat Hearts.

    PubMed

    Yao, Xinhua; Li, Yalan; Tao, Mingzhe; Wang, Shuang; Zhang, Liangqing; Lin, Jiefu; Xia, Zhengyuan; Liu, Hui-Min

    2015-01-01

    The anesthetic propofol confers cardioprotection against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS). However, its cardioprotection on patients is inconsistent. Similarly, the beneficial effect of tight glycemic control during cardiac surgery in patients has recently been questioned. We postulated that low glucose (LG) may promote ROS formation through enhancing fatty acid (FA) oxidation and unmask propofol cardioprotection during IRI. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mM (LG) or 8 mM (G) in the absence or presence of propofol (5 μg/mL) or propofol plus trimetazidine (TMZ). Hearts were subjected to 35 minutes of ischemia followed by 60 minutes of reperfusion. Myocardial infarct size (IS) and cardiac CK-MB were significantly higher in LG than in G group (P < 0.05), associated with reduced left ventricular developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher, accompanied with higher cardiac lipid transporter CD36 protein expression in LG. Propofol reduced IS, improved cardiac function, and reduced CD36 in G but not in LG. TMZ facilitated propofol cardioprotection in LG. Therefore, isolated heart with low glucose lost sensitivity to propofol treatment through enhancing FA oxidation and TMZ supplementation restored the sensitivity to propofol. PMID:26491698

  1. Effects of Glucose Concentration on Propofol Cardioprotection against Myocardial Ischemia Reperfusion Injury in Isolated Rat Hearts

    PubMed Central

    Yao, Xinhua; Li, Yalan; Tao, Mingzhe; Wang, Shuang; Zhang, Liangqing; Lin, Jiefu; Xia, Zhengyuan; Liu, Hui-min

    2015-01-01

    The anesthetic propofol confers cardioprotection against myocardial ischemia-reperfusion injury (IRI) by reducing reactive oxygen species (ROS). However, its cardioprotection on patients is inconsistent. Similarly, the beneficial effect of tight glycemic control during cardiac surgery in patients has recently been questioned. We postulated that low glucose (LG) may promote ROS formation through enhancing fatty acid (FA) oxidation and unmask propofol cardioprotection during IRI. Rat hearts were isolated and randomly assigned to be perfused with Krebs-Henseleit solution with glucose at 5.5 mM (LG) or 8 mM (G) in the absence or presence of propofol (5 μg/mL) or propofol plus trimetazidine (TMZ). Hearts were subjected to 35 minutes of ischemia followed by 60 minutes of reperfusion. Myocardial infarct size (IS) and cardiac CK-MB were significantly higher in LG than in G group (P < 0.05), associated with reduced left ventricular developed pressure and increases in postischemic cardiac contracture. Cardiac 15-F2t-isoprostane was higher, accompanied with higher cardiac lipid transporter CD36 protein expression in LG. Propofol reduced IS, improved cardiac function, and reduced CD36 in G but not in LG. TMZ facilitated propofol cardioprotection in LG. Therefore, isolated heart with low glucose lost sensitivity to propofol treatment through enhancing FA oxidation and TMZ supplementation restored the sensitivity to propofol. PMID:26491698

  2. The triterpenoids of Ganoderma tsugae prevent stress-induced myocardial injury in mice.

    PubMed

    Kuok, Qian-Yu; Yeh, Chen-Yu; Su, Bor-Chyuan; Hsu, Pei-Ling; Ni, Hao; Liu, Ming-Yie; Mo, Fan-E

    2013-10-01

    Ganoderma mushrooms (Lingzhi in Chinese) have well-documented health benefits. Ganoderma tsugae (G. tsugae), one of the ganoderma species, has been commercially cultivated as a dietary supplement. Because G. tsugae has high antioxidant activity and because oxidative stress is often associated with cardiac injury, we hypothesized that G. tsugae protects against cardiac injury by alleviating oxidative stress. We tested the hypothesis using a work-overload-induced myocardial injury model created by challenging mice with isoproterenol (ISO). Remarkably, oral G. tsugae protected the mice from ISO-induced myocardial injury. Moreover, the triterpenoid fraction of G. tsugae, composed of a mixture of nine structurally related ganoderic acids (GAs), provided cardioprotection by inhibiting the ISO-induced expression of Fas/Fas ligand, oxidative stress, and apoptosis. The antioxidant activity of GAs was tested in cultured cardio-myoblast H9c2 cells against the insult of H₂O₂. GAs dissipated the cellular reactive oxygen species imposed by H₂O₂ and prevented cell death. Our findings uncovered the cardioprotective activity of G. tsugae and identified GAs as the bioactive components against cardiac insults. PMID:23610080

  3. Role of risk stratification after myocardial infarction.

    PubMed

    Kuriachan, Vikas; Exner, Derek V

    2009-02-01

    Despite advances in medical and surgical therapy for patients with heart disease, sudden cardiac death remains an important public health problem that prematurely ends the lives of more than 300,000 persons each year in North America. Many of these deaths occur in patients with a history of myocardial infarction (MI). Although severe left ventricular (LV) systolic dysfunction is used to identify patients at risk of sudden death after MI, most cardiac arrests occur in those with only mild LV dysfunction. Further, severe LV dysfunction is not a specific indicator for cardiac arrest. Risk stratification, to identify patients most likely to benefit from implantable defibrillator therapy after MI, is an essential area of investigation. Because the development of cardiac arrest is complex and likely requires the confluence of several factors, using a single test to predict the risk of sudden death or to guide implantable defibrillator therapy is unlikely to be successful. Tests that assess cardiac structure, including repolarization, and those that evaluate autonomic modulation and other factors have been developed with the goal of identifying patients at highest risk of cardiac arrest after MI. These tests, particularly in combination, appear to identify patients who may benefit from implantable defibrillator therapy after MI. Ongoing and planned randomized controlled trials will assess whether these tests can be used to guide implantable defibrillator therapy. Until the data from these studies are available, severe LV dysfunction remains the only proven approach to guide implantable defibrillator therapy after MI. PMID:19141257

  4. Mitochondria, myocardial remodeling, and cardiovascular disease.

    PubMed

    Verdejo, Hugo E; del Campo, Andrea; Troncoso, Rodrigo; Gutierrez, Tomás; Toro, Barbra; Quiroga, Clara; Pedrozo, Zully; Munoz, Juan Pablo; Garcia, Lorena; Castro, Pablo F; Lavandero, Sergio

    2012-12-01

    The process of muscle remodeling lies at the core of most cardiovascular diseases. Cardiac adaptation to pressure or volume overload is associated with a complex molecular change in cardiomyocytes which leads to anatomic remodeling of the heart muscle. Although adaptive at its beginnings, the sustained cardiac hypertrophic remodeling almost unavoidably ends in progressive muscle dysfunction, heart failure and ultimately death. One of the features of cardiac remodeling is a progressive impairment in mitochondrial function. The heart has the highest oxygen uptake in the human body and accordingly it has a large number of mitochondria, which form a complex network under constant remodeling in order to sustain the high metabolic rate of cardiac cells and serve as Ca(2+) buffers acting together with the endoplasmic reticulum (ER). However, this high dependence on mitochondrial metabolism has its costs: when oxygen supply is threatened, high leak of electrons from the electron transport chain leads to oxidative stress and mitochondrial failure. These three aspects of mitochondrial function (Reactive oxygen species signaling, Ca(2+) handling and mitochondrial dynamics) are critical for normal muscle homeostasis. In this article, we will review the latest evidence linking mitochondrial morphology and function with the process of myocardial remodeling and cardiovascular disease. PMID:22972531

  5. Hypertension and acute myocardial infarction: an overview.

    PubMed

    Pedrinelli, Roberto; Ballo, Piercarlo; Fiorentini, Cesare; Denti, Silvia; Galderisi, Maurizio; Ganau, Antonello; Germanò, Giuseppe; Innelli, Pasquale; Paini, Anna; Perlini, Stefano; Salvetti, Massimo; Zacà, Valerio

    2012-03-01

    History of hypertension is a frequent finding in patients with acute myocardial infarction (AMI) and its recurring association with female sex, diabetes, older age, less frequent smoking and more frequent vascular comorbidities composes a risk profile quite distinctive from the normotensive ischemic counterpart.Antecedent hypertension associates with higher rates of death and morbid events both during the early and long-term course of AMI, particularly if complicated by left ventricular dysfunction and/or congestive heart failure. Renin-angiotensin-aldosterone system blockade, through either angiotensin-converting enzyme inhibition, angiotensin II receptor blockade or aldosterone antagonism, exerts particular benefits in that high-risk hypertensive subgroup.In contrast to the negative implications carried by antecedent hypertension, higher systolic pressure at the onset of chest pain associates with lower mortality within 1 year from coronary occlusion, whereas increased blood pressure recorded after hemodynamic stabilization from the acute ischemic event bears inconsistent relationships with recurring coronary events in the long-term follow-up.Whether antihypertensive treatment in post-AMI hypertensive patients prevents ischemic relapses is uncertain. As a matter of fact, excessive diastolic pressure drops may jeopardize coronary perfusion and predispose to new acute coronary events, although the precise cause-effect mechanisms underlying this phenomenon need further evaluation. PMID:22317927

  6. [Model based study of myocardial stimulation mechanisms].

    PubMed

    Weiss, I; Urbaszek, A; Schaldach, M

    1997-01-01

    The present study investigated the mechanisms of electrical stimulation of a myocardial fibre with the aim of developing improved minimally invasive stimulation methods. Using a dynamic myocyte model, the ionic currents crossing the voltage-dependent channels of the membrane are computed. To trigger an action potential, the membrane must first be depolarized to the threshold potential, when further depolarization continues spontaneously through the avalanche-like opening of the sodium channels. For the development of an action potential, not merely the amount of charge injected into the cell during the stimulus is of importance, but an above-threshold magnitude of the stimulation current is also required. The smallest energy required is achieved when the stimulus duration is chosen to be equal to the chronaxie. A second aspect of the study concerned the far-field stimulation of a muscle fibre, achieved by generating a potential gradient along the fibre. First, using a continuous fibre model, the fibre activating function is computed. In a more detailed study, the discrete segmental structure of the fibre determined by the gap junctions is taken into account, and the impact of these junctions on the activating function analysed. By optimizing the electrode configuration, an appropriate activating function results which guarantees successful stimulation when its maximum is above than threshold potential. The most important finding is that the myocardium can be stimulated by floating electrodes, thus opening up new possibilities for a less invasive electro-stimulation of the heart. PMID:9172726

  7. Helicobacter pylori infection and acute myocardial infarction.

    PubMed

    Nakić, Dario; Vcev, Aleksandar; Jović, Albino; Patrk, Jogen; Zekanović, Drazen; Klarin, Ivo; Ivanac, Kresimir; Mrden, Anamarija; Balen, Sanja

    2011-09-01

    The aim of this investigation was to determine whether H. pylori infection is an independent risk factor for acute myocardial infarction (AMI), determine is there a link between H. pylori infection and severity of disease. In this prospective, single centre study, were enrolled 100 patients with AMI and control group was consisted 93 healthy individuals. The results of this study showed no difference between H. pylori seropositivity distribution in the investigate and control group (29 vs. 26 %) and there was no significant difference on the severity of the disease. There was significant association in the patients with three and more risk factors, where the patients with lower blood pressure (124.4/77.4 vs. 145.9/87.7 mmHg) and better controlled diabetes (HbA1c 6.1% vs. 6.9%) had greater risk for AMI if they are H. pylori seropositive. The large multicentric trials would be needed to define a precise role of H. pylori infection on the developement of AMI. PMID:22053556

  8. Spirituality in survivors of myocardial infarction

    PubMed Central

    Momennasab, Marzieh; Moattari, Marzieh; Abbaszade, Abbas; Shamshiri, Babak

    2012-01-01

    Background: Life-threatening and stressful events, such as myocardial infarction (MI) can lead to an actual crisis, which affects the patients spiritually as well as physically, psychologically, and socially. However, the focus of health care providers is on physical needs. Furthermore, the spirituality of the patients experiencing heart attack in the light of our cultural context is not well addressed in the literature. This study is aimed at exploring the spiritual experiences of the survivors of the MI. Materials and Methods: In this qualitative research a grounded theory approach was used. Key informants were 9 MI patients hospitalized in the coronary care units of 3 hospitals in Shiraz. In addition, 7 nurses participated in the study. In-depth interviews and a focus group were used to generate data. Data analysis was done based on Strauss and Corbin method. Constant comparison analysis was performed until data saturation. Results: Five main categories emerged from the data, including perceived threat, seeking spiritual support, referring to religious values, increasing faith, and realization. The latter with its 3 subcategories was recognized as core category and represents a deep understanding beyond knowing. At the time of encountering MI, spirituality provided hope, strength, and peace for the participants. Conclusion: Based on the results we can conclude that connecting to God, religious values, and interconnectedness to others are the essential components of the participants’ spiritual experience during the occurrence of MI. Spirituality helps patients to overcome this stressful life-threatening situation. PMID:23853646

  9. Effects of carbon monoxide on myocardial ischemia

    SciTech Connect

    Allred, E.N.; Pagano, M. ); Bleecker, E.R.; Walden, S.M. ); Chaitman, B.R.; Dahms, T.E. ); Hackney, J.D.; Selvester, R.H. ); Warren, J. ); Gottlieb, S.O.

    1991-02-01

    The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre-versus postexposure exercise test at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.

  10. Nuclear cardiology: Myocardial perfusion and function

    SciTech Connect

    Seldin, D.W. )

    1991-08-01

    Myocardial perfusion studies continue to be a major focus of research, with new investigations of the relationship of exercise-redistribution thallium imaging to diagnosis, prognosis, and case management. The redistribution phenomenon, which seemed to be fairly well understood a few years ago, is now recognized to be much more complex than originally thought, and various strategies have been proposed to clarify the meaning of persistent defects. Pharmacologic intervention with dipyridamole and adenosine has become available as an alternative to exercise, and comparisons with exercise imaging and catheterization results have been described. Thallium itself is no longer the sole single-photon perfusion radiopharmaceutical; two new technetium agents are now widely available. In addition to perfusion studies, advances in the study of ventricular function have been made, including reports of studies performed in conjunction with technetium perfusion studies, new insights into cardiac physiology, and the prognostic and case-management information that function studies provide. Finally, work has continued with monoclonal antibodies for the identification of areas of myocyte necrosis. 41 references.

  11. Renalase deficiency aggravates ischemic myocardial damage.

    PubMed

    Wu, Yanling; Xu, Jianchao; Velazquez, Heino; Wang, Peili; Li, Guoyong; Liu, Dinggang; Sampaio-Maia, Benedita; Quelhas-Santos, Janete; Russell, Kerry; Russell, Raymond; Flavell, Richard A; Pestana, Manuel; Giordano, Frank; Desir, Gary V

    2011-04-01

    Chronic kidney disease (CKD) leads to an 18-fold increase in cardiovascular complications not fully explained by traditional risk factors. Levels of renalase, a recently discovered oxidase that metabolizes catecholamines, are decreased in CKD. Here we show that renalase deficiency in a mouse knockout model causes increased plasma catecholamine levels and hypertension. Plasma blood urea nitrogen, creatinine, and aldosterone were unaffected. However, knockout mice had normal systolic function and mild ventricular hypertrophy but tolerated cardiac ischemia poorly and developed myocardial necrosis threefold more severe than that found in wild-type mice. Treatment with recombinant renalase completely rescued the cardiac phenotype. To gain insight into the mechanisms mediating this cardioprotective effect, we tested if gene deletion affected nitrate and glutathione metabolism, but found no differences between hearts of knockout and wild-type mice. The ratio of oxidized (NAD) to reduced (NADH) nicotinamide adenine dinucleotide in cardiac tissue, however, was significantly decreased in the hearts of renalase knockout mice, as was plasma NADH oxidase activity. In vitro studies confirmed that renalase metabolizes NADH and catecholamines. Thus, renalase plays an important role in cardiovascular pathology and its replacement may reduce cardiac complications in renalase-deficient states such as CKD. PMID:21178975

  12. 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

  13. Nanoparticle-Mediated Delivery of Irbesartan Induces Cardioprotection from Myocardial Ischemia-Reperfusion Injury by Antagonizing Monocyte-Mediated Inflammation

    NASA Astrophysics Data System (ADS)

    Nakano, Yasuhiro; Matoba, Tetsuya; Tokutome, Masaki; Funamoto, Daiki; Katsuki, Shunsuke; Ikeda, Gentaro; Nagaoka, Kazuhiro; Ishikita, Ayako; Nakano, Kaku; Koga, Jun-Ichiro; Sunagawa, Kenji; Egashira, Kensuke

    2016-07-01

    Myocardial ischemia-reperfusion (IR) injury limits the therapeutic effect of early reperfusion therapy for acute myocardial infarction (AMI), in which the recruitment of inflammatory monocytes plays a causative role. Here we develop bioabsorbable poly-lactic/glycolic acid (PLGA) nanoparticles incorporating irbesartan, an angiotensin II type 1 receptor blocker with a peroxisome proliferator-activated receptor (PPAR)γ agonistic effect (irbesartan-NP). In a mouse model of IR injury, intravenous PLGA nanoparticles distribute to the IR myocardium and monocytes in the blood and in the IR heart. Single intravenous treatment at the time of reperfusion with irbesartan-NP (3.0 mg kg‑1 irbesartan), but not with control nanoparticles or irbesartan solution (3.0 mg kg‑1), inhibits the recruitment of inflammatory monocytes to the IR heart, and reduces the infarct size via PPARγ-dependent anti-inflammatory mechanisms, and ameliorates left ventricular remodeling 21 days after IR. Irbesartan-NP is a novel approach to treat myocardial IR injury in patients with AMI.

  14. Nanoparticle-Mediated Delivery of Irbesartan Induces Cardioprotection from Myocardial Ischemia-Reperfusion Injury by Antagonizing Monocyte-Mediated Inflammation

    PubMed Central

    Nakano, Yasuhiro; Matoba, Tetsuya; Tokutome, Masaki; Funamoto, Daiki; Katsuki, Shunsuke; Ikeda, Gentaro; Nagaoka, Kazuhiro; Ishikita, Ayako; Nakano, Kaku; Koga, Jun-ichiro; Sunagawa, Kenji; Egashira, Kensuke

    2016-01-01

    Myocardial ischemia-reperfusion (IR) injury limits the therapeutic effect of early reperfusion therapy for acute myocardial infarction (AMI), in which the recruitment of inflammatory monocytes plays a causative role. Here we develop bioabsorbable poly-lactic/glycolic acid (PLGA) nanoparticles incorporating irbesartan, an angiotensin II type 1 receptor blocker with a peroxisome proliferator-activated receptor (PPAR)γ agonistic effect (irbesartan-NP). In a mouse model of IR injury, intravenous PLGA nanoparticles distribute to the IR myocardium and monocytes in the blood and in the IR heart. Single intravenous treatment at the time of reperfusion with irbesartan-NP (3.0 mg kg−1 irbesartan), but not with control nanoparticles or irbesartan solution (3.0 mg kg−1), inhibits the recruitment of inflammatory monocytes to the IR heart, and reduces the infarct size via PPARγ-dependent anti-inflammatory mechanisms, and ameliorates left ventricular remodeling 21 days after IR. Irbesartan-NP is a novel approach to treat myocardial IR injury in patients with AMI. PMID:27403534

  15. Experimental studies of the physiologic properties of technetium-99m agents: Myocardial transport of perfusion imaging agents

    SciTech Connect

    Meerdink, D.J.; Leppo, J.A. )

    1990-10-16

    The physiologic properties of new technetium-99m-labeled myocardial imaging agents (Tc-99m sestamibi, an isonitrile; and Tc-99m teboroxime, a boronic acid adduct of technetium dioxime) are discussed and compared to thallium-201 (Tl-201). Studies with isolated hearts, subcellular fractions and cell cultures indicate that Tc-99m sestamibi, Tc-99m teboroxime and Tl-201 do not share common transport or sequestration mechanisms. Although peak Tc-99m sestamibi myocardial extraction over time is about half that of Tl-201 at equivalent coronary blood flows, the amount of Tc-99m sestamibi that remains in the heart is similar to that of Tl-201 because of its higher retention efficiency. The high retention efficiency for Tc-99m sestamibi also results in minimal redistribution. In contrast, Tc-99m teboroxime myocardial extraction is higher than that of Tl-201, but its retention is less efficient, resulting in relatively rapid washout characteristics which may quickly result in tracer redistribution. During reperfusion after a no-flow period, Tc-99m sestamibi extraction and retention increase, but for Tc-99m teboroxime and Tl-201 these values tend to decrease. All tracers show adequate transport characteristics for perfusion imaging, and differences in transport and retention should lead to the development of new clinical protocols.27 references.

  16. B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction.

    PubMed

    Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

    2013-10-01

    Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6C(hi) monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell-selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction. PMID:24037091

  17. PGC-1α Regulates Expression of Myocardial Mitochondrial Antioxidants and Myocardial Oxidative Stress After Chronic Systolic Overload

    PubMed Central

    Lu, Zhongbing; Xu, Xin; Hu, Xinli; Fassett, John; Zhu, Guangshuo; Tao, Yi; Li, Jingxin; Huang, Yimin; Zhang, Ping; Zhao, Baolu

    2010-01-01

    Abstract Mitochondria are a principal site for generation of reactive oxygen species (ROS) in the heart. Peroxisome proliferator activated receptor γ coactivator 1α (PGC-1α) plays an important role in regulating mitochondrial biogenesis and myocardial metabolism, but whether PGC-1α can simultaneously upregulate myocardial mitochondrial antioxidants has not been studied. In the present study, we examined the effect of PGC-1α deficiency (PGC-1α−/−) on oxidative stress and expression of a group of mitochondrial antioxidants in normal hearts and in hearts exposed to chronic systolic pressure overload produced by transverse aortic constriction (TAC). We found that PGC-1α−/− caused moderate but significant decreases of myocardial mitochondrial antioxidant enzymes such as SOD2, and thioredoxin (Trx2), but had no effect on expression of myocardial oxidative stress markers and left ventricular (LV) function under basal conditions. However, in response to TAC for 6 weeks, PGC-1α−/− mice showed greater increases of myocardial oxidative stress markers 3’-nitrotyrosine and 4-hydroxynonenal, more severe LV hypertrophy and dilatation, pulmonary congestion, and a greater reduction of LV fractional shortening and dP/dtmax than did wild-type hearts. SOD mimetic MnTMPyP treatment (6 mg/kg/day) significantly attenuated TAC-induced LV hypertrophy and dysfunction in PGC-1α−/− mice. These data indicate that PGC-1α plays an important role in regulating expression of myocardial mitochondrial antioxidants SOD2 and Trx2 and in protecting hearts against TAC-induced myocardial oxidative stress, hypertrophy, and dysfunction. Antioxid. Redox Signal. 13, 1011–1022. PMID:20406135

  18. Regional Longitudinal Myocardial Deformation Provides Incremental Prognostic Information in Patients with ST-Segment Elevation Myocardial Infarction

    PubMed Central

    Jensen, Jan Skov; Pedersen, Sune H.; Galatius, Søren; Fritz-Hansen, Thomas; Bech, Jan; Olsen, Flemming Javier; Mogelvang, Rasmus

    2016-01-01

    Background Global longitudinal systolic strain (GLS) has recently been demonstrated to be a superior prognosticator to conventional echocardiographic measures in patients after myocardial infarction (MI). The aim of this study was to evaluate the prognostic value of regional longitudinal myocardial deformation in comparison to GLS, conventional echocardiography and clinical information. Method In total 391 patients were admitted with ST-Segment elevation myocardial infarction (STEMI), treated with primary percutaneous coronary intervention and subsequently examined by echocardiography. All patients were examined by tissue Doppler imaging (TDI) and two-dimensional strain echocardiography (2DSE). Results During a median-follow-up of 5.3 (IQR 2.5–6.1) years the primary endpoint (death, heart failure or a new MI) was reached by 145 (38.9%) patients. After adjustment for significant confounders (including conventional echocardiographic parameters) and culprit lesion, reduced longitudinal performance in the anterior septal and inferior myocardial regions (but not GLS) remained independent predictors of the combined outcome. Furthermore, inferior myocardial longitudinal deformation provided incremental prognostic information to clinical and conventional echocardiographic information (Harrell's c-statistics: 0.63 vs. 0.67, p = 0.032). In addition, impaired longitudinal deformation outside the culprit lesion perfusion region was significantly associated with an adverse outcome (p<0.05 for all deformation parameters). Conclusion Regional longitudinal myocardial deformation measures, regardless if determined by TDI or 2DSE, are superior prognosticators to GLS. In addition, impaired longitudinal deformation in the inferior myocardial segment provides prognostic information over and above clinical and conventional echocardiographic risk factors. Furthermore, impaired longitudinal deformation outside the culprit lesion perfusion region seems to be a paramount marker of adverse

  19. Severe coronary tortuosity or myocardial bridging in patients with chest pain, normal coronary arteries, and reversible myocardial perfusion defects.

    PubMed

    Gaibazzi, Nicola; Rigo, Fausto; Reverberi, Claudio

    2011-10-01

    We reviewed patients with normal or near-normal coronary angiograms enrolled in the SPAM contrast stress echocardiographic diagnostic study in which 400 patients with chest pain syndrome of suspected cardiac origin with a clinical indication to coronary angiography were enrolled. Patients underwent dipyridamole contrast stress echocardiography (cSE) with sequential analysis of wall motion, myocardial perfusion, and Doppler coronary flow reserve before elective coronary angiography. Ninety-six patients with normal or near-normal epicardial coronary arteries were screened for the presence of 2 prespecified findings: severely tortuous coronary arteries and myocardial bridging. Patients were divided in 2 groups based on the presence (false-positive results, n = 37) or absence (true-negative results, n = 59) of reversible myocardial perfusion defects during cSE and compared for history and clinical and angiographic characteristics. Prevalence of severely tortuous coronary arteries (35% vs 5%, p <0.001) or myocardial bridging (13% vs 2%, p <0.05) was 7 times higher in patients who demonstrated reversible perfusion defects at cSE compared to those without reversible perfusion defects. No significant differences were found between the 2 groups for the main demographic variables and risk factors. Patients in the false-positive group more frequently had a history of effort angina (p <0.001) and ST-segment depression at treadmill electrocardiography (p <0.001). In conclusion, we hypothesize that patients with a positive myocardial perfusion finding at cSE but without obstructive epicardial coronary artery disease have a decreased myocardial blood flow reserve, which may be caused by a spectrum of causes other than obstructive coronary artery disease, among which severely tortuous coronary arteries/myocardial bridging may play a significant role. PMID:21784382

  20. [The protective action of ellagic acid in experimental myocarditis].

    PubMed

    Iakovleva, L V; Ivakhnenko, A K; Buniatian, N D

    1998-01-01

    The article presents the material on the study of the cardioprotective effect of ellagic acid on a model of neoepinephrine myocarditis in rats. In doses of 0.5-1 mg/kg ellagic acid causes a marked antioxidant effect. Restores the disturbed myocardial functions. The reference-agent vitamin E (50 mg/kg) yields to ellagic acid as a cardioprotector. The effect of 0.5 mg/kg of ellagic acid was more stable than that of a 1 mg/kg dose. The cardioprotective activity of the drugs under study was determined according to the POL parameters in a myocardial homogenate and blood serum and according to the EEG parameters and the degree of cardiomyocyte cytolysis. PMID:9690073

  1. Regional Myocardial Perfusion Rates in Patients with Coronary Artery Disease

    PubMed Central

    Cannon, Paul J.; Dell, Ralph B.; Dwyer, Edward M.

    1972-01-01

    Regional myocardial perfusion rates were estimated from the myocardial washout of 133Xenon in 24 patients with heart disease whose coronary arteriograms were abnormal and 17 similar subjects whose coronary arteriograms were judged to be normal. Disappearance rates of 133Xe from multiple areas of the heart were monitored externally with a multiple-crystal scintillation camera after the isotope had been injected into a coronary artery and local myocardial perfusion rates were calculated by the Kety formula. The mean myocardial perfusion rates in the left ventricle exceeded those in the right ventricle or atrial regions in subjects without demonstrable coronary artery disease. In this group there was a significant lack of homogeneity of local perfusion rates in left ventricular myocardium; the mean coefficient of variation of left ventricular local perfusion rates was 15.8%. In the patients with radiographically demonstrable coronary artery disease, a variety of myocardial perfusion patterns were observed. Local capillary blood flow rates were depressed throughout the myocardium of patients with diffuse coronary disease but were subnormal only in discrete myocardial regions of others with localized occlusive disease. Local myocardial perfusion rates were similar to those found in the group with normal coronary arteriograms in patients with slight degrees of coronary disease and in those areas of myocardium distal to marked coronary constrictions or occlusions which were well supplied by collateral vessels. In subjects with right coronary disease, the mean right ventricular perfusion rates were significantly subnormal; in seven subjects of this group perfusion of the inferior left ventricle by a dominant right coronary artery was absent or depressed. The average mean left ventricular perfusion rate of 12 subjects with significant disease of two or more branches of the left coronary artery was significantly lower than that of the group with normal left coronary

  2. 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