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Sample records for myocardial infarction effects

  1. [Holiday effect in myocardial infarct].

    PubMed

    Otto, W; Hempel, W E; Goebel, H; Erkens, R

    1975-03-15

    Aimed measures of the organisation of the combat against infarction demand also the observation of temporary frequencies. On the basis of the evaluation of certificates of death of the month December of the years 1969 to 1973 of the GDR with differentiation according to so-called prehospital dead (persons who died at home and on the way to the hospital) and patients who died in the hospital with high significance an unwarrantedly high prehospital mortality during the period from Christmas to the end of the year (25th to 31st December) was established compared with the preceding week (18th to 24th December). Since in contrast to this the hospital cases and the cases "on the way" do not show any significant differences main tasks for the beginning of improvements concerning health policy may be deduced, all the more since the so-called holiday effect, expressed by a high home/clinic-relation of patients who died of myocardial infarction, could be restricted to 6 counties of the GDR on account of the analysis of further localities. From the results the tendency of a retrogression of the holiday effect is to be read off in the course of years. In the discussion an explantation of this peculiarity is attempted, and practicable conclusions for the removal and thus for the improvement the infarct situation are formulated.

  2. Effect of temperature on myocardial infarction in swine.

    PubMed

    Duncker, D J; Klassen, C L; Ishibashi, Y; Herrlinger, S H; Pavek, T J; Bache, R J

    1996-04-01

    Body core temperature in the normothermic range alters infarct size in rabbits. Moreover, temperature may modulate the protection by adenosine during a coronary artery occlusion. We investigated the effect of core temperature within the normothermic range (35-39 degrees C) on myocardial infarct size produced by a 45-min coronary occlusion in open-chest swine (n = 10), and we determined whether adenosine blockade with 8-phenyltheophylline and adenosine deaminase increased infarct size in the normothermic range (n = 9). After 4 h of reperfusion the area at risk and infarct size were determined with Evans blue dye and triphenyltetrazolium chloride. Infarct size strongly correlated with temperature (r2 = 0.71, P = 0.0001) so that at 35 degrees C no infarction occurred and with each 1 degree C increase in temperature 20% of the area at risk became infarcted. In contrast, neither the low levels of collateral flow (0.03 +/- 0.01 ml.min-1.g-1) nor the rate-pressure product correlated with infarct size. In the normothermic range, adenosine blockade had no effect on infarct size. The data demonstrate that temperature can exert a profound effect on infarct size but fail to demonstrate a protective effect on endogenous adenosine at normothermic temperatures. Our findings emphasize the need for stringent control of core temperature during investigation of interventions aimed at reducing infarct size.

  3. Effect of zinc sulphate on infarct size in experimental myocardial infarction in dogs.

    PubMed

    Lal, A

    1991-08-01

    The effect of zinc sulphate on myocardial infarct size following left coronary artery branch occlusion in dogs was studied. Zinc sulphate (10 mg/kg) was administered po, 24 h and 2 h before coronary occlusion in one group of animals. The area at risk was visualised by methylene blue injected intraventricularly. The infarcted area was visualised by triphenyl tetrazolium chloride staining. The infarct size expressed as a percentage of risk zone was 76.54 +/- 3.01 per cent (mean +/- SE) in the control group and 37.96 +/- 2.20 per cent in the zinc sulphate group (P less than 0.001). Zinc sulphate appears to be a potent prophylactic agent for limiting the size of myocardial infarct in the dogs.

  4. Cardioprotective effects of adipokine apelin on myocardial infarction.

    PubMed

    Zhang, Bao-Hai; Guo, Cai-Xia; Wang, Hong-Xia; Lu, Ling-Qiao; Wang, Ya-Jie; Zhang, Li-Ke; Du, Feng-He; Zeng, Xiang-Jun

    2014-09-01

    Angiogenesis plays an important role in myocardial infarction. Apelin and its natural receptor (angiotensin II receptor-like 1, AGTRL-1 or APLNR) induce sprouting of endothelial cells in an autocrine or paracrine manner. The aim of this study is to investigate whether apelin can improve the cardiac function after myocardial infarction by increasing angiogenesis in infarcted myocardium. Left ventricular end-diastolic pressure (LVEDP), left ventricular end systolic pressure (LVESP), left ventricular developed pressure (LVDP), maximal left ventricular pressure development (±LVdp/dtmax), infarct size, and angiogenesis were evaluated to analyze the cardioprotective effects of apelin on ischemic myocardium. Assays of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-bromo-2'-deoxyuridine incorporation, wound healing, transwells, and tube formation were used to detect the effects of apelin on proliferation, migration, and chemotaxis of cardiac microvascular endothelial cells. Fluorescein isothiocyanate-labeled bovine serum albumin penetrating through monolayered cardiac microvascular endothelial cells was measured to evaluate the effects of apelin on permeability of microvascular endothelial cells. In vivo results showed that apelin increased ±LV dp/dtmax and LVESP values, decreased LVEDP values (all p < 0.05), and promoted angiogenesis in rat heart after ligation of the left anterior descending coronary artery. In vitro results showed that apelin dose-dependently enhanced proliferation, migration, chemotaxis, and tube formation, but not permeability of cardiac microvascular endothelial cells. Apelin also increased the expression of vascular endothelial growth factor receptors-2 (VEGFR2) and the endothelium-specific receptor tyrosine kinase (Tie-2) in cardiac microvascular endothelial cells. These results indicated that apelin played a protective role in myocardial infarction through promoting angiogenesis and decreasing permeability of microvascular

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

    PubMed

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

    2005-10-01

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

  6. 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.

  7. 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

    2015-04-10

    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.

  8. Protection effect of survivin protein overexpression on acute myocardial infarction in rats

    PubMed Central

    Yang, Meng; Li, Bo; Liu, Jingwei; Sun, Haiyan

    2015-01-01

    To investigate the protective effect of adenovirus mediated Survivin protein overexpression on acute myocardial infarction in rats. 45 acute myocardial infarction rat models were constructed by suture method and were randomly divided into sham group, model group and treatment group. The treatment group was injected with Survivin gene packed virus via ventricle. The model group was injected with equal titer of adenovirus packed empty vector. The sham group was not ligated. These rats were killed in 96 h after treatment. The levels of Survivin, Caspase-3, caspase-7 mRNA and protein in myocardial tissues were detected by real-time fluorescence quantitative PCR and Western blot. Myocardium tissue cell apoptosis were analyzed by TUNEL staining, the immunology of myocardial infarction tissue was analyzed by TTC staining. Compared with model group and sham group, the level of survivin protein in myocardium tissue of rats in treatment group was significantly increased (P<0.05). Compared with sham group, the levels of caspase-3 and caspase-7 mRNA and protein in myocardial tissue of rats in model group and treatment group were significantly increased, but the treatment group were significantly lower than those of model group (P<0.05). The myocardium cell apoptosis index and myocardial infarction areas of rats in model group and treatment group were significantly higher than those of sham group, but the treatment group were significantly lower than those of model group (P<0.05). In conclusion, Survivin protein overexpression in myocardial tissue can significantly inhibit the expression of apoptosis promoting factor in myocardial tissue of acute myocardial infarction rats, reduce the apoptosis index of myocardial cells and the myocardial infarct size, which has great significance for protecting myocardial function. PMID:26550220

  9. Effects of diabetes on myocardial infarct size and cardioprotection by preconditioning and postconditioning

    PubMed Central

    2012-01-01

    In spite of the current optimal therapy, the mortality of patients with ischemic heart disease (IHD) remains high, particularly in cases with diabetes mellitus (DM) as a co-morbidity. Myocardial infarct size is a major determinant of prognosis in IHD patients, and development of a novel strategy to limit infarction is of great clinical importance. Ischemic preconditioning (PC), postconditioning (PostC) and their mimetic agents have been shown to reduce infarct size in experiments using healthy animals. However, a variety of pharmacological agents have failed to demonstrate infarct size limitation in clinical trials. One of the possible reasons for the discrepancy between the results of animal experiments and clinical trials is that co-morbidities, including DM, modified myocardial responses to ischemia/reperfusion and to cardioprotective agents. Here we summarize observations of the effects of DM on myocardial infarct size and ischemic PC and PostC and discuss perspectives for protection of DM hearts. PMID:22694800

  10. Depression after myocardial infarction.

    PubMed

    Ziegelstein, R C

    2001-01-01

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

  11. Effect of coronary artery recanalization on right ventricular function in patients with acute myocardial infarction

    SciTech Connect

    Verani, M.S.; Tortoledo, F.E.; Batty, J.W.; Raizner, A.E.

    1985-05-01

    The effects of coronary artery recanalization by intracoronary administration of streptokinase on left ventricular function during acute myocardial infarction have received increasing attention in recent years. Although myocardial dysfunction is often more pronounced in the right ventricle than in the left ventricle in patients with acute inferior wall myocardial infarction, the effect of coronary artery recanalization on right ventricular dysfunction has not been previously addressed. Accordingly, in this investigation, 54 patients who participated in a prospective, controlled, randomized trial of recanalization during acute myocardial infarction were studied. Among 30 patients with inferior wall infarction, 19 had right ventricular dysfunction on admission; 11 of these 19 had positive uptake of technetium-99m pyrophosphate in the right ventricle, indicative of right ventricular infarction. Patients with successful recanalization exhibited improved right ventricular ejection fraction from admission to day 10. However, control patients and patients who did not undergo recanalization also exhibited improvement. These data indicate that the right ventricular dysfunction commonly associated with inferior wall infarction is often transient, and improvement is the rule, irrespective of early recanalization of the infarct vessel.

  12. Chronic effects of myocardial infarction on right ventricular function: a noninvasive assessment

    SciTech Connect

    Kaul, S.; Hopkins, J.M.; Shah, P.M.

    1983-10-01

    To assess the chronic effects of myocardial infarction on right ventricular function, 48 subjects were studied utilizing radionuclide angiography and two-dimensional echocardiography. Ten were normal subjects (group I), 11 had previous inferior wall myocardial infarction (group II), 10 had previous anteroseptal infarction (group III), 11 had combined anteroseptal and inferior infarction (group IV) and 6 had extensive anterolateral infarction (group V). The mean (+/- standard deviation) left ventricular ejection fraction was 0.66 +/- 0.03 in group I, 0.58 +/- 0.02 in group II, 0.52 +/- 0.02 in group III, 0.33 +/- 0.03 in group IV and 0.33 +/- 0.01 in group V. No systematic correlation between left and right ventricular ejection fraction was observed among the groups. The mean right ventricular ejection fraction was significantly reduced in the presence of inferior myocardial infarction (0.30 +/- 0.03 in group II and 0.29 +/- 0.03 in group IV compared with 0.43 +/- 0.02 in group I (p less than 0.001)). The group II and IV patients also had increased (p less than 0.001) right ventricular end-diastolic area and decreased (p less than 0.001) right ventricular free wall motion by two-dimensional echocardiography. In the presence of anteroseptal infarction (group III), right ventricular free wall motion was increased (p less than 0.05) compared with normal subjects (group I). Thus, the effects of prior myocardial infarction on right ventricular function depend more on the location of infarction than on the extent of left ventricular dysfunction. Inferior infarction was commonly associated with reduced right ventricular ejection fraction and increased right ventricular end-diastolic area. The right ventricular free wall excursion was increased in the presence of anteroseptal infarction, suggested loss of contribution of interventricular septal contraction to right ventricular ejection.

  13. Dose-dependent effects of atorvastatin on myocardial infarction

    PubMed Central

    Barbarash, Olga; Gruzdeva, Olga; Uchasova, Evgenya; Belik, Ekaterina; Dyleva, Yulia; Karetnikova, Victoria

    2015-01-01

    Background Dyslipidemia is a key factor determining the development of both myocardial infarction (MI) and its subsequent complications. Dyslipidemia is associated with endothelial dysfunction, activation of inflammation, thrombogenesis, and formation of insulin resistance. Statin therapy is thought to be effective for primary and secondary prevention of complications associated with atherosclerosis. Methods This study examined 210 patients with Segment elevated MI (ST elevated MI) who were treated with atorvastatin from the first 24 hours after MI. Group 1 (n=110) were given atorvastatin 20 mg/day. Group 2 (n=100) were given atorvastatin 40 mg/day. At days 1 and 12 after MI onset, insulin resistance levels determined by the homeostasis model assessment of insulin resistance index, lipid profiles, and serum glucose, insulin, adipokine, and ghrelin levels were measured. Results Free fatty acid levels showed a sharp increase during the acute phase of MI. Treatment with atorvastatin 20 mg/day, and especially with 40 mg/day, resulted in a decrease in free fatty acid levels. The positive effect of low-dose atorvastatin (20 mg/day) is normalization of the adipokine status. Administration of atorvastatin 20 mg/day was accompanied with a statistically significant reduction in glucose levels (by 14%) and C-peptide levels (by 38%), and a decrease in the homeostasis model assessment of insulin resistance index on day 12. Conclusion Determination of atorvastatin dose and its use during the in-hospital period and subsequent periods should take into account changes in biochemical markers of insulin resistance and adipokine status in patients with MI. PMID:26170622

  14. Myocardial abscess complicating healed myocardial infarction.

    PubMed Central

    Weisz, S.; Young, D. G.

    1977-01-01

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

  15. 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…

  16. 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

  17. Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function

    SciTech Connect

    Flameng, W.; Sergeant, P.; Vanhaecke, J.; Suy, R.

    1987-07-01

    Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.

  18. [Myocardial infarction caused by exertion].

    PubMed

    Bernard, F; Weber, S

    1997-01-01

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

  19. Effects of ghrelin on Cx43 regulation and electrical remodeling after myocardial infarction in rats.

    PubMed

    Yuan, Ming-Jie; Huang, He; Tang, Yan-Hong; Wu, Gang; Gu, Yong-Wei; Chen, Yong-Jun; Huang, Cong-Xin

    2011-11-01

    Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial effects on ventricular remodeling. In this study, we investigated whether ghrelin could decrease vulnerability to ventricular arrhythmias in rats with myocardial infarction and the possible mechanism. Twenty-four hours after ligation of the anterior descending artery, adult male Sprague-Dawley rats were randomized to ghrelin (100 μg/kg) and saline (control group) for 4 weeks. Sham animals underwent thoracotomy and pericardiotomy, but not LAD ligation. Myocardial endothelin-1 (ET-1) levels were significantly elevated in saline-treated rats at the border zone compared with sham-operated rats. Myocardial connexin43 (Cx43) expression at the border zone was significantly decreased in saline-treated infarcted rats compared with sham-operated rats. Ghrelin significantly decreased the inducibility of ventricular tachyarrhythmias compared with control group. Arrhythmias sores during programmed stimulation in saline-treated rats were significantly higher than scores in those treated with ghrelin. The electrophysiological improvement of fatal ventricular tachyarrhythmias was accompanied with increased immunofluorescence-stained Cx43, myocardial Cx43 protein and mRNA levels in ghrelin treated rats. We also shown that ghrelin significantly decreased tissue ET-1 levels at the infarcted border zone. Thus, ghrelin showed the protective effect on ventricular arrhythmias after myocardial infarction. Although the precise mechanism by which ghrelin modulates the dephosphorylation of Cx43 remains unknown, it is most likely that the ghrelin increased expression of Cx43 through the inhibition of ET-1.

  20. Human cord blood cells and myocardial infarction: effect of dose and route of administration on infarct size.

    PubMed

    Henning, Robert J; Burgos, Jose D; Vasko, Mark; Alvarado, Felipe; Sanberg, Cyndy D; Sanberg, Paul R; Morgan, Michael B

    2007-01-01

    There is no consensus regarding the optimal dose of stem cells or the optimal route of administration for the treatment of acute myocardial infarction. Bone marrow cells, containing hematopoietic and mesenchymal stem cells, in doses of 0.5 x 10(6) to >30 x 10(6) have been directly injected into the myocardium or into coronary arteries or infused intravenously in subjects with myocardial infarctions to reduce infarct size and improve heart function. Therefore, we determined the specific effects of different doses of human umbilical cord blood mononuclear cells (HUCBC), which contain hematopoietic and mesenchymal stem cells, on infarct size. In order to determine the optimal technique for stem cell administration, HUCBC were injected directly into the myocardium (IM), or into the LV cavity with the ascending aorta transiently clamped to facilitate coronary artery perfusion (IA), or injected intravenously (IV) in rats 1-2 h after the left anterior coronary artery was permanently ligated. Immune suppressive therapy was not given to any rat. One month later, the infarct size in control rat hearts treated with only Isolyte averaged 23.7 +/- 1.7% of the LV muscle area. Intramyocardial injection of HUCBC reduced the infarct size by 71% with 0.5 x 10(6) HUCBC and by 93% with 4 x 10(6) HUCBC in comparison with the controls (p < 0.001). Intracoronary injection reduced the infarction size by 47% with 0.5 x 10(6) HUCBC and by 80% with 4 x 10(6) HUCBC (p < 0.001), and IV HUCBC reduced infarct size by 51% with 0.5 x 10(6) and by 75-77% with 16-32 million HUCBC (p < 0.001) in comparison with control hearts. With 4 x 10(6) HUCBC, infarction size was 65% smaller with IM HUCBC than with IA HUCBC and 78% smaller than with IV HUCBC (p < 0.05). Nevertheless, IM, IA, and IV HUCBC all produced significant reductions in infarct size in comparison with Isolyte-treated infarcted hearts without requirements for host immune suppression. The present experiments demonstrate that the optimal dose

  1. Salutary effect of adjunctive intracoronary nicorandil administration on restoration of myocardial blood flow and functional improvement in patients with acute myocardial infarction.

    PubMed

    Sakata, Y; Kodama, K; Komamura, K; Lim, Y J; Ishikura, F; Hirayama, A; Kitakaze, M; Masuyama, T; Hori, M

    1997-06-01

    Salutary effect of nicorandil, a K+ adenosine triphosphate channel opener, on restoration of myocardial blood flow and functional improvement after coronary revascularization was investigated in 20 patients with first anterior acute myocardial infarction. Ten patients received intracoronary administration of nicorandil (2 mg) after coronary revascularization; the other 10 patients received coronary revascularization only and served as control subjects. Myocardial contrast echocardiography and two-dimensional echocardiography were performed to assess microvascular integrity and regional function in the infarcted area. Nicorandil improved peak contrast intensity ratio (p < 0.001), calculated as the ratio of peak contrast intensity in the infarcted and noninfarcted areas, indicating the restoration of myocardial blood flow to the infarcted myocardium. Regional wall motion improved more significantly in 1 month in patients who received nicorandil (p < 0.01). Thus our results suggested the usefulness of intracoronary nicorandil administration after coronary revascularization for restoring blood flow and functional improvement in patients with acute myocardial infarction. PMID:9200388

  2. Synergistic effects of nitric oxide and exercise on revascularisation in the infarcted ventricle in a murine model of myocardial infarction.

    PubMed

    Ranjbar, Kamal; Nazem, Farzad; Nazari, Afshin; Gholami, Mohammadreza; Nezami, Ali Reza; Ardakanizade, Malihe; Sohrabi, Maryam; Ahmadvand, Hasan; Mottaghi, Mohammad; Azizi, Yaser

    2015-01-01

    It has been shown that density of microvessels decreases in the left ventricular after myocardial infarction (MI). The change of angiogenic and angiostatic factors as the main factors in revascularisation after exercise training in area at risk is not determined yet in MI. Therefore, the aim of the present study was the effect of exercise training and L-arginine supplementation on area at risk angiogenesis in myocardial infarction rat. Four weeks after surgery (Left Anterior Descending Coronary artery Ligation), myocardial infarction rats were divided into 4 groups: Sedentary rats (Sed-MI); L-arginine supplementation (La-MI); Exercise training (Ex-MI) and Exercise + L-arginine (Ex+La). Exercise training (ET) lasted for 10 weeks at 17 m/min for 10-50 min day(-1). Rats in the L-arginine-treated groups drank water containing 4 % L-arginine. After ET and L-arginine supplementation, ventricular function was evaluated and angiogenic and angiostatic indices were measured at ~1 mm from the edge of scar tissue (area at risk). Statistical analysis revealed that gene expression of VEGF as an angiogenic factor, angiostatin as an angiostatic factor and caspase-3 at area at risk decrease significantly in response to exercise training compared to the sedentary group. The capillary and arteriolar density in the Ex groups were significantly higher than those of the Sed groups. Compared to the Ex-MI group, the Ex+La group showed a markedly increase in capillary to fiber ratio. No significant differences were found in infarct size among the four groups, but cardiac function increased in response to exercise. Exercise training increases revascularization at area at risk by reduction of angiostatin. L-arginine supplementation causes additional effects on exercise-induced angiogenesis by preventing more reduction of VEGF gene expression in response to exercise. These improvements, in turn, increase left ventricular systolic function and decrease mortality in myocardial infarction rats.

  3. Synergistic effects of nitric oxide and exercise on revascularisation in the infarcted ventricle in a murine model of myocardial infarction

    PubMed Central

    Ranjbar, Kamal; Nazem, Farzad; Nazari, Afshin; Gholami, Mohammadreza; Nezami, Ali Reza; Ardakanizade, Malihe; Sohrabi, Maryam; Ahmadvand, Hasan; Mottaghi, Mohammad; Azizi, Yaser

    2015-01-01

    It has been shown that density of microvessels decreases in the left ventricular after myocardial infarction (MI). The change of angiogenic and angiostatic factors as the main factors in revascularisation after exercise training in area at risk is not determined yet in MI. Therefore, the aim of the present study was the effect of exercise training and L-arginine supplementation on area at risk angiogenesis in myocardial infarction rat. Four weeks after surgery (Left Anterior Descending Coronary artery Ligation), myocardial infarction rats were divided into 4 groups: Sedentary rats (Sed-MI); L-arginine supplementation (La-MI); Exercise training (Ex-MI) and Exercise + L-arginine (Ex+La). Exercise training (ET) lasted for 10 weeks at 17 m/min for 10-50 min day−1. Rats in the L-arginine-treated groups drank water containing 4 % L-arginine. After ET and L-arginine supplementation, ventricular function was evaluated and angiogenic and angiostatic indices were measured at ~1 mm from the edge of scar tissue (area at risk). Statistical analysis revealed that gene expression of VEGF as an angiogenic factor, angiostatin as an angiostatic factor and caspase-3 at area at risk decrease significantly in response to exercise training compared to the sedentary group. The capillary and arteriolar density in the Ex groups were significantly higher than those of the Sed groups. Compared to the Ex-MI group, the Ex+La group showed a markedly increase in capillary to fiber ratio. No significant differences were found in infarct size among the four groups, but cardiac function increased in response to exercise. Exercise training increases revascularization at area at risk by reduction of angiostatin. L-arginine supplementation causes additional effects on exercise-induced angiogenesis by preventing more reduction of VEGF gene expression in response to exercise. These improvements, in turn, increase left ventricular systolic function and decrease mortality in myocardial infarction rats

  4. 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

  5. Short-term effects of atmospheric particulate matter on myocardial infarction: a cumulative meta-analysis.

    PubMed

    Cai, Xianlei; Li, Zhenhong; Scott, E Marian; Li, Xiuyang; Tang, Mengyao

    2016-04-01

    Atmospheric particulate matter (PM) is hypothesized to increase the risk of myocardial infarction (MI). However, the epidemiological evidence is inconsistent. We identified 33 studies with more than 4 million MI patients and applied meta-analysis and meta-regression to assess the available evidence. Twenty-five studies presented the effects of the PM level on hospitalization for MI patients, while eight studies showed the effects on mortality. An increase in PM10 was associated with hospitalization and mortality in myocardial infarction patients (RR per 10 μg/m(3) = 1.011, 95% CI 1.006-1.016; RR per 10 μg/m(3) = 1.008, 95 % CI 1.004-1.012, respectively); PM2.5 also increased the risk of hospitalization and mortality in MI patients (RR per 10 μg/m(3) = 1.024, 95% CI 1.007-1.041 for hospitalization and RR per 10 μg/m(3) = 1.012, 95% CI 1.010-1.015 for mortality). The results of the cumulative meta-analysis indicated that PM10 and PM2.5 were associated with myocardial infarction with the addition of new studies each year. In conclusion, short-term exposure to high PM10 and PM2.5 levels revealed to increase risk of hospitalization and mortality for myocardial infarction. Policy support of pollution control and individual protection was strongly recommended. PMID:26846245

  6. Clinical Effects of Hypertension on the Mortality of Patients with Acute Myocardial Infarction

    PubMed Central

    Kang, Dong Goo; Ahn, Yongkeun; Chae, Shung Chull; Hur, Seung Ho; Hong, Taek Jong; Kim, Young Jo; Seong, In Whan; Chae, Jei Keon; Rhew, Jay Young; Chae, In Ho; Cho, Myeong Chan; Bae, Jang Ho; Rha, Seung Woon; Kim, Chong Jin; Jang, Yang Soo; Yoon, Junghan; Seung, Ki Bae; Park, Seung Jung

    2009-01-01

    The incidence of ischemic heart disease has been increased rapidly in Korea. However, the clinical effects of antecedent hypertension on acute myocardial infarction have not been identified. We assessed the relationship between antecedent hypertension and clinical outcomes in 7,784 patients with acute myocardial infarction in the Korea Acute Myocardial Infarction Registry during one-year follow-up. Diabetes mellitus, hyperlipidemia, cerebrovascular disease, heart failure, and peripheral artery disease were more prevalent in hypertensives (n=3,775) than nonhypertensives (n=4,009). During hospitalization, hypertensive patients suffered from acute renal failure, shock, and cerebrovascular event more frequently than in nonhypertensives. During follow-up of one-year, the incidence of major adverse cardiac events was higher in hypertensives. In multi-variate adjustment, old age, Killip class ≥III, left ventricular ejection fraction <45%, systolic blood pressure <90 mmHg on admission, post procedural TIMI flow grade ≤2, female sex, and history of hypertension were independent predictors for in-hospital mortality. However antecedent hypertension was not significantly associated with one-year mortality. Hypertension at the time of acute myocardial infarction is associated with an increased rate of in-hospital mortality. PMID:19794974

  7. Effect of Prolonged Moderate Exercise on the Changes of Nonneuronal Cells in Early Myocardial Infarction.

    PubMed

    Rinaldi, Barbara; Guida, Francesca; Furiano, Anna; Donniacuo, Maria; Luongo, Livio; Gritti, Giulia; Urbanek, Konrad; Messina, Giovanni; Maione, Sabatino; Rossi, Francesco; de Novellis, Vito

    2015-01-01

    Myocardial infarction (MI) is one of the leading causes of death in developed countries and it is characterized by several associated symptomatologies and poor quality of life. Recent data showed a possible interaction between infarction and brain inflammation and activity. Previous studies have demonstrated the beneficial effect of exercise training on deterioration in cardiac function after MI. In this study we analyzed in sedentary and trained rats the microglia and astrocytes 48 hours after MI in PVN, thalamus, prefrontal cortex, and hippocampus through immunofluorescence approach. We found significant changes in specific microglia phenotypes in the brain areas analyzed together with astrocytes activation. Prolonged exercise normalized these morphological changes of microglia and astrocytes in the prefrontal cortex, hippocampus, and thalamus but not in the PVN. Our data suggest that there is an early brain reaction to myocardial infarction induction, involving nonneuronal cells, that is attenuated by the prolonged exercise. PMID:26266053

  8. 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

  9. Trauma induced myocardial infarction.

    PubMed

    Lolay, Georges A; Abdel-Latif, Ahmed K

    2016-01-15

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

  10. The Effects of Inhalation Aromatherapy on Anxiety in Patients With Myocardial Infarction: A Randomized Clinical Trial

    PubMed Central

    Najafi, Zahra; Taghadosi, Mohsen; Sharifi, Khadijeh; Farrokhian, Alireza; Tagharrobi, Zahra

    2014-01-01

    Background: Anxiety is an important mental health problem in patients with cardiac disease. Anxiety reduces patients’ quality of life and increases the risk of different cardiac complications. Objectives: The aim of this study was to investigate the effects of inhalation aromatherapy on anxiety in patients with myocardial infarction. Patients and Methods: This was a randomized clinical trial conduced on 68 patients with myocardial infarction hospitalized in coronary care units of a large-scale teaching hospital affiliated to Kashan University of Medical Sciences, Kashan, Iran in 2013. By using the block randomization technique, patients were randomly assigned to experimental (33 patients receiving inhalation aromatherapy with lavender aroma twice a day for two subsequent days) and control (35 patients receiving routine care of study setting including no aromatherapy) groups. At the beginning of study and twenty minutes after each aromatherapy session, anxiety state of patients was assessed using the Spielberger’s State Anxiety Inventory. Data was analyzed using SPSS v. 16.0. We used Chi-square, Fisher’s exact, independent-samples T-test and repeated measures analysis of variance to analyze the study data. Results: The study groups did not differ significantly regarding baseline anxiety mean and demographic characteristics. However, after the administration of aromatherapy, anxiety mean in the experimental group was significantly lower than the control group. Conclusions: Inhalation aromatherapy with lavender aroma can reduce anxiety in patients with myocardial infarction. Consequently, healthcare providers, particularly nurses, can use this strategy to improve postmyocardial infarction anxiety management. PMID:25389481

  11. 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.

  12. Long term outcome and cost-effectiveness of stenting versus balloon angioplasty for acute myocardial infarction

    PubMed Central

    Suryapranata, H; Ottervanger, J; Nibbering, E; van't, H; Hoorntje, J; de Boer, M J; Al, M; Zijlstra, F

    2001-01-01

    OBJECTIVE—To investigate the long term clinical outcome and cost-effectiveness of stenting compared with balloon angioplasty in patients with acute myocardial infarction.
METHODS—Patients with acute myocardial infarction were randomly allocated to primary stenting (112) or balloon angioplasty (115). The primary end point was the cumulative first event rate of death, non-fatal reinfarction, or target vessel revascularisation. Secondary end points were restenosis at six months and the cost-effectiveness at follow up.
RESULTS—After 24 months, the combined clinical end point of death/reinfarction was 4% after stenting and 11% after balloon angioplasty (p = 0.04). Subsequent target vessel revascularisation was necessary in 15 patients (13%) after stenting and in 39 (34%) after balloon angioplasty (p < 0.001). The cumulative cardiac event-free survival rate was also higher after stenting (84% v 62%, p < 0.001). The angiographic restenosis rate after stenting was less than after balloon angioplasty (12% v 34%, p < 0.001). Despite the higher initial costs of stenting (Dfl 21 484 v Dfl 18 625, p < 0.001), the cumulative costs at 24 months were comparable with those of balloon angioplasty (Dfl 31 423 v Dfl 32 933, p = 0.83).
CONCLUSIONS—Compared with balloon angioplasty, primary stenting for acute myocardial infarction results in a better long term clinical outcome without increased cost.


Keywords: stenting; angioplasty; myocardial infarction; cost-benefit analysis PMID:11359749

  13. Novel adjunctive treatments of myocardial infarction

    PubMed Central

    Schmidt, Michael Rahbek; Pryds, Kasper; Bøtker, Hans Erik

    2014-01-01

    Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic and pharmacological conditioning, but despite decades of research, the translation into clinical effects has been challenging. Recently published clinical studies, however, prompt optimism as novel techniques allow for improved clinical applicability. Cyclosporine A, the GLP-1 analogue exenatide and rapid cooling by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary surgery and percutaneous coronary intervention. The discovery that RIC can be performed noninvasively using a blood pressure cuff on the upper arm to induce brief episodes of limb ischemia and reperfusion has facilitated the translation of RIC into the clinical arena. This review focus on novel advances in adjunctive therapies in relation to acute and elective coronary procedures. PMID:24976915

  14. Effect of drugs used in different type of myocardial infarction (STEMI or (NTEMI) on mortality.

    PubMed

    Vincze, Z; Brugos, B; Lorincz, I; Paragh, G

    2014-06-01

    We examined 416 patients with acute myocardial infarction. 249 patients had STEMI and 167 NSTEMI. 227 were men and 189 women. 142 men had STEMI and 85 men had NSTEMI. 107 women were diagnosed with STEMI and 82 with NSTEMI. 22.5% of patient with STEMI and 20.2% of patients with NSTEMI died (p = 0.58). We compared the effect of anticoagulant treatment, clopidogrel, salicylate, nitrate, beta-blocker, angiotensin-converting enzyme inhibitor, statin and trimetazidine therapy on mortality in function of the type of myocardial infarction. There were no differences between mortality of patients with STEMI and NSTEMI with respect of use of heparine, salicylate, nitrate, beta-blocker, ACE inhibitor, statin and trimetazidine. While examining the effect of clopidogrel, we observed a significantly lower mortality rate in patients with NSTEMI compared to the STEMI group (p = 0.005). These differences are due to the known variability in clopidogrel absorption and metabolism, which could be influenced by the type of myocardial infarction.

  15. The effect of ibuprofen on accumulation of /sup 111/In-labeled platelets and leukocytes in experimental myocardial infarction

    SciTech Connect

    Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schork, M.A.; Swanson, D.P.; Lucchesi, B.R.

    1982-11-01

    To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 (/sup 111/In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occlusion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p . 0.005). Quantification of the platelet-associated /sup 111/In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes accumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.

  16. The effect of ibuprofen on accumulation of indium-111-labeled platelets and leukocytes in experimental myocardial infarction

    SciTech Connect

    Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schark, M.A.; Swanson, D.P.; Lucchesi, B.R.

    1982-11-01

    To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 (/sup 111/In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occulsion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p=0.005). Quantification of the platelet-associated /sup 111/In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes acumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.

  17. Effects of histidine and vitamin C on isoproterenol-induced acute myocardial infarction in rats.

    PubMed

    Moradi-Arzeloo, Masoumeh; Farshid, Amir Abbas; Tamaddonfard, Esmaeal; Asri-Rezaei, Siamak

    2016-01-01

    In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. Rats were given intraperitoneal injections of histidine (40 mg kg(-1)) and vitamin C (40 mg kg(-1)) alone and combined daily for 21 days. Propranolol (10 mg kg(-1)) was orally administered daily for 10 days (from day 11 to day 21). Myocardial infarction was induced by subcutaneous injections of 150 mg kg(-1) of isoproterenol at an interval of 24 hr on days 20 and 21. Blood and tissue samples were taken for histopathological and biochemical evaluations following electrocardiography recording on day 21. Isoproterenol elevated ST segment, increased heart weight, heart rate, serum activities of aspartate transaminase, lactate dehydrogenase, creatine kinase-MB and heart tissue content of malondialdehyde, and decreased R wave amplitude and superoxide dismutase and catalase activities of heart tissue. Necrosis, edema and inflammatory cells infiltration were observed in myocardial tissue sections. Our results indicated that histidine and vitamin C alone, and especially in combination prevent isoproterenol-induced cardiotoxicity and have similar protective effects with propranolol. Cardioprotective effects of histidine and vitamin C may be associated with their ability to reduce free radical-induced toxic effects. PMID:27226887

  18. 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

  19. Effects of intracoronary melatonin on ischemia-reperfusion injury in ST-elevation myocardial infarction.

    PubMed

    Ekeløf, Sarah V; Halladin, Natalie L; Jensen, Svend E; Zaremba, Tomas; Aarøe, Jens; Kjærgaard, Benedict; Simonsen, Carsten W; Rosenberg, Jacob; Gögenur, Ismail

    2016-01-01

    Acute coronary occlusion is effectively treated by primary percutaneous coronary intervention. However, myocardial ischemia-reperfusion injury is at the moment an unavoidable consequence of the procedure. Oxidative stress is central in the development of ischemia-reperfusion injury. Melatonin, an endogenous hormone, acts through antioxidant mechanisms and could potentially minimize the myocardial injury. The aim of the experimental study was to examine the cardioprotective effects of melatonin in a porcine closed-chest reperfused infarction model. A total of 20 landrace pigs were randomized to a dosage of 200 mg (0.4 mg/mL) melatonin or placebo (saline). The intervention was administered intracoronary and intravenous. Infarct size, area at risk and microvascular obstruction were determined ex vivo by cardiovascular magnetic resonance imaging. Myocardial salvage index was calculated. The plasma levels of high-sensitive troponin T were assessed repeatedly. The experimenters were blinded with regard to treatment regimen. Melatonin did not significantly increase myocardial salvage index compared with placebo [melatonin 21.8% (16.1; 24.8) vs. placebo 20.2% (16.9; 27.0), p = 1.00]. The extent of microvascular obstruction was similar between the groups [melatonin 3.8% (2.7; 7.1) vs. placebo 3.7% (1.3; 7.7), p = 0.96]. The area under the curve for high-sensitive troponin T release was insignificantly reduced by 32% in the melatonin group [AUC melatonin 12,343.9 (6,889.2; 20,147.4) ng h/L vs. AUC placebo 18,285.3 (5,180.4; 23,716.8) ng h/L, p = 0.82]. Combined intracoronary and intravenous treatment with melatonin did not reduce myocardial reperfusion injury. The lack of a positive effect could be due to an ineffective dose of melatonin, a type II error or the timing of administration.

  20. Cardioprotective effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats.

    PubMed

    Gao, Yan; Gao, Jianping; Chen, Changxun; Wang, Huilin; Guo, Juan; Wu, Rong

    2015-05-01

    The purpose of this study was to explore the effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats and to elucidate the underlying mechanisms. A rat model of ventricular remodeling after myocardial infarction was established by left coronary artery ligation. Rats with coronary artery ligation were randomly divided into five groups: control, plus 40 mg/kg captopril, plus 25 mg/kg polydatin, plus 50 mg/kg polydatin, and plus 100 mg/kg polydatin. The sham-operated group was used as a negative control. Rats were administered intragastrically with the corresponding drugs or drinking water for seven weeks. At the end of the treatment, the left ventricular weight index and heart weight index were assessed. The cross-sectional size of cardiomyocytes was measured by staining myocardium tissue with hematoxylin and eosin. Collagen content was counted by Sirius red in aqueous saturated picric acid. The concentrations of angiotensin I, angiotensin II, aldosterone, and endothelin 1 in myocardium or serum were determined by radioimmunoassay. Hydroxyproline and nitric oxide concentrations and glutathione peroxidase and catalase activities in serum were measured by ultraviolet spectrophotometry. Our results showed that seven weeks of polydatin treatment resulted in a significantly reduced left ventricular weight index, heart weight index, serum concentrations of hydroxyproline and aldosterone, an increased concentration of nitric oxide as well as enhanced activities of glutathione peroxidase and catalase. Myocardial angiotensin I, angiotensin II, and endothelin 1 levels were also reduced. The cardiomyocyte cross-sectional area and collagen deposition diminished. This study suggests that polydatin may attenuate ventricular remodeling after myocardial infarction in coronary artery ligation rats through restricting the excessive activation of the renin-angiotensin-aldosterone system and inhibiting peroxidation.

  1. 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

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

    NASA Astrophysics Data System (ADS)

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

    2012-11-01

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

  3. Effect of decellularized tissue powders on a rat model of acute myocardial infarction.

    PubMed

    Tabuchi, Masaki; Negishi, Jun; Yamashita, Akitatsu; Higami, Tetsuya; Kishida, Akio; Funamoto, Seiichi

    2015-11-01

    Many research groups are currently investigating new treatment modalities for myocardial infarction. Numerous aspects need to be considered for the clinical application of these therapies, such as low cell integration and engraftment rates of cell injection techniques. Decellularized tissues are considered good materials for promoting regeneration of traumatic tissues. The properties of the decellularized tissues are sustained after processing to powder form. In this study, we examined the use of decellularized tissue powder in a rat model of acute myocardial infarction. The decellularized tissue powders, especially liver powder, promoted cell integration and neovascularization both in vitro and in vivo. Decellularized liver powder induced neovascularization in the infarct area, resulting in the suppression of myocardial necrosis. The results of this study suggest that decellularized liver powder has good potential for application as a blood supply material for the treatment of myocardial infarction.

  4. Effects of Orem-based nursing intervention on nutritional self-care of myocardial infarction patients.

    PubMed

    Aish, A E; Isenberg, M

    1996-06-01

    The purpose of the study was to investigate the effect of nursing care based on Orem's nursing theory on nutritional self-care of myocardial infarction patients. Self-efficacy was explored as a disposition which may motivate behavioral change. One hundred and four subjects were randomly assigned to treatment or control groups. The nursing intervention, which took place during the first 6 weeks following hospital discharge, was effective in supporting healthy low-fat eating behavior. Nursing care influenced patients' self-care agency but lacked impact on self-efficacy for healthy eating. PMID:8736471

  5. Effects of Orem-based nursing intervention on nutritional self-care of myocardial infarction patients.

    PubMed

    Aish, A E; Isenberg, M

    1996-06-01

    The purpose of the study was to investigate the effect of nursing care based on Orem's nursing theory on nutritional self-care of myocardial infarction patients. Self-efficacy was explored as a disposition which may motivate behavioral change. One hundred and four subjects were randomly assigned to treatment or control groups. The nursing intervention, which took place during the first 6 weeks following hospital discharge, was effective in supporting healthy low-fat eating behavior. Nursing care influenced patients' self-care agency but lacked impact on self-efficacy for healthy eating.

  6. Acute myocardial infarction in rats.

    PubMed

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

    2011-01-01

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

  7. Effect of verapamil on heart rate variability after an acute myocardial infarction. Danish Verapamil Infarction Trial II.

    PubMed

    Vaage-Nilsen, M; Rasmussen, V

    1998-07-01

    Because decreased heart rate variability measured after an acute myocardial infarction (AMI) has been demonstrated to predict subsequent mortality and sudden death, and an efficacy analysis of the Danish Verapamil Infarction Trial II (DAVIT II) demonstrated that long-term postinfarction treatment with verapamil significantly reduced sudden death, the aim of the present substudy was to evaluate the effect of verapamil on heart-rate variability in the time and frequency domain, measured in two 5-minute segments during the day and night. Thirty-eight patients were examined by Holter monitoring, at 1 week, that is, before randomization, and at 1 month after infarction; 22 of the patients were examined 12-16 months after infarction as well. In both treatment groups (verapamil and placebo) no significant alteration of heart rate variability during the day-time was demonstrated from before to after 1 and 12-16 months of treatment. In accord with the known reduction of overall heart rate by verapamil, a significant increase of mean NN interval from before to after 1 (P = 0.0004) and 12-16 months (P = 0.004) of treatment was seen in the verapamil, but not in the placebo, group at night. Parameters generally interpreted as an index of parasympathetic modulation, that is, RMSSD, pNN50, and high-frequency power, increased significantly at 1 month (P = 0.04, P = 0.03, NS, respectively) and 12-16 months (P = 0.03, P = 0.04, P < 0.05) after AMI in the verapamil, but not in the placebo, group. In conclusion, the present study indicates that verapamil shifts the autonomic balance to a vagal preponderance or sympathetic attenuation in the postinfarction period. PMID:9784908

  8. Efforts to limit the size of myocardial infarcts.

    PubMed

    Rude, R E; Muller, J E; Braunwald, E

    1981-12-01

    Throughout the last decade, multiple interventions have been shown to decrease myocardial ischemic injury and limit infarct size in animal models of acute myocardial infarction. Results of pilot studies have suggested that some of these interventions may also have beneficial effects in humans with evolving myocardial infarction. This review focuses on the rationale for limiting infarct size, efficacy of methods for estimating size of infarcts, and current clinical data on specific intervention therapy. No intervention has yet been proved sufficiently efficacious to warrant its routine clinical use. However, treatment with beta-adrenergic blockers, intravenous nitroglycerin, and hyaluronidase has been shown to affect one or more indexes of infarct size in patients with acute myocardial infarction. Large, randomized clinical trials of these and other promising interventions are underway and will provide data on whether infarct size can be limited in humans and whether residual cardiac function and patient prognosis can thereby be improved.

  9. PROTECTIVE EFFECT OF HESPERIDIN ON CARDIOVASCULAR COMPLICATION IN EXPERIMENTALLY INDUCED MYOCARDIAL INFARCTION IN DIABETES IN RATS

    PubMed Central

    Kakadiya, Jagdish; Mulani, Haresh; Shah, Nehal

    2010-01-01

    Present study was designed to evaluate effect Hesperidin on Cardiovascular Complication in isoproterenol induced myocardial infarction in normal and Streptozotocin-Nicotinamide induced in diabetic rats. Hesperidin (100 mg/kg, p.o) was administered for 28 days in rats injected with single dose of Streptozotocin (65 mg/kg, i.p, STZ) and Nicotinamide (110 mg/kg, i.p, NIC) and after isoproterenol (200 mg/kg, s.c.) induced myocardial infarction in rats on 29th and 30th day. At the end of experimental period (i.e. on the day 31) serum and heart tissues sample were collected, and glucose, HbA1c and Total Cholesterol (TC), Triglycerides (TG) and High density lipoprotein (HDL) and cholesterol ester synthetase (CES), lecithin Cholesterol acyl transferase (LCAT), lipoprotein lipase (LPL), systolic and diastolic blood pressure were find out. Administration of STZ–NIC in rats showed a significant (p<0.001) increased in the levels of serum glucose, glycosylated heamoglobin (HbA1c), Total Cholesterol (TC), Triglycerides (TG) and Low density lipoprotein (LDL) whereas the levels of High density lipoprotein (HDL) were found to be non significant but significant (p<0.001) increased in the level of heart tissues CES and significant (p<0.001, p<0.01) decreased LCAT and LPL, significantly (p<0.01) increased systolic and diastolic blood pressure as compared to respective control groups. Treatment with Hesperidin significantly (P<0.05) decreased HbA1c, glucose, CES level and significantly (P<0.01) decreased LDL, TC, TG, systolic and diastolic blood pressure and significant (P<0.01) increased LCAT and LPL level but no significantly change HDL in compared to diabetic control group. We concluded that HES (100 mg/kg) is effective in controlling blood glucose levels and reduced cardiac complication in experimentally induced myocardial infarction diabetic rats. PMID:24825971

  10. Protective effect of hesperidin on cardiovascular complication in experimentally induced myocardial infarction in diabetes in rats.

    PubMed

    Kakadiya, Jagdish; Mulani, Haresh; Shah, Nehal

    2010-03-01

    Present study was designed to evaluate effect Hesperidin on Cardiovascular Complication in isoproterenol induced myocardial infarction in normal and Streptozotocin-Nicotinamide induced in diabetic rats. Hesperidin (100 mg/kg, p.o) was administered for 28 days in rats injected with single dose of Streptozotocin (65 mg/kg, i.p, STZ) and Nicotinamide (110 mg/kg, i.p, NIC) and after isoproterenol (200 mg/kg, s.c.) induced myocardial infarction in rats on 29(th) and 30(th) day. At the end of experimental period (i.e. on the day 31) serum and heart tissues sample were collected, and glucose, HbA1c and Total Cholesterol (TC), Triglycerides (TG) and High density lipoprotein (HDL) and cholesterol ester synthetase (CES), lecithin Cholesterol acyl transferase (LCAT), lipoprotein lipase (LPL), systolic and diastolic blood pressure were find out. Administration of STZ-NIC in rats showed a significant (p<0.001) increased in the levels of serum glucose, glycosylated heamoglobin (HbA1c), Total Cholesterol (TC), Triglycerides (TG) and Low density lipoprotein (LDL) whereas the levels of High density lipoprotein (HDL) were found to be non significant but significant (p<0.001) increased in the level of heart tissues CES and significant (p<0.001, p<0.01) decreased LCAT and LPL, significantly (p<0.01) increased systolic and diastolic blood pressure as compared to respective control groups. Treatment with Hesperidin significantly (P<0.05) decreased HbA1c, glucose, CES level and significantly (P<0.01) decreased LDL, TC, TG, systolic and diastolic blood pressure and significant (P<0.01) increased LCAT and LPL level but no significantly change HDL in compared to diabetic control group. We concluded that HES (100 mg/kg) is effective in controlling blood glucose levels and reduced cardiac complication in experimentally induced myocardial infarction diabetic rats.

  11. [Seasonal variations in the myocardial infarction incidence and possible effects of geomagnetic micropulsations on the cardiovascular system in humans].

    PubMed

    Kleĭmenova, N G; Kozyreva, O V; Breus, T K; Rapoport, S I

    2007-01-01

    The analysis of the ambulance calls in Moscow, related to myocardial infarction (85.000 events), sudden death (71.700 events), and hypertension crises (165.500 events) over the period of 1979-1981 demonstrated their clear seasonal variations with a profound summer minimum and a winter maximum. The same results were obtained in the analysis of statistical monthly data on sudden death from infarction in Bulgaria over the period of 15 years (1970-1985). However, there are a great number of clinical and statistical studies confirming the rises in the incidence of myocardial infarction, hypertension crise, and sudden death during geomagnetic disturbances, which have maximum occurrence near equinox, not in winter. In order to explain this contradiction, we suggested that one of critical factors that affect the human cardiovascular system is geomagnetic micropulsations Pc1 having the frequency comparable with the frequency of heart rate beatings and winter maximum in their occurrence. The results of a comparative analysis of data of ambulance calls in Moscow related to myocardial infarction and sudden death and the catalog of Pc1 observations at the geophysical observatory "Borok" (Yaroslavl region) are presented. It is shown that in approximately 70% of days with an anomalously large number of ambulance calls related to myocardial infarction, Pc1 micropulsations have been registered. The probability of simultaneous occurrence of myocardial infarction and Pc1 in the winter season was 1.5 times greater than their accidental coincidence. Moreover, it was found that in winter the effects of magnetic storms and Pc1 IM(A) were much higher than in summer. We suggested that one of possible reasons for the seasonal variations in the occurrence of myocardial infarction is an increase in the production of the pineal hormone melatonin in winter which leads to an unstable state of the human organism and an increase in its sensitivity to the effect of geomagnetic pulsations. PMID

  12. Effect of myocardial infarction on the function and metabolism of the non-infarcted muscle

    SciTech Connect

    Hansen, C.A.

    1985-01-01

    Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery. After one or three weeks, the hearts were isolated and perfused in vitro. Despite the onset of hypertrophy, ventricular function was more depressed in the one- and three-week infarcted hearts than in acutely ligated hearts. These data suggested that the depressed mechanical function was due not only to the loss of viable tissue, but also to alterations occurring in the non-infarcted tissue. The inotropic response to extracellular calcium was depressed in infarcted hearts, such that the mechanical performance of the infarcted heart was likely to be limited by the availability of extracellular calcium under physiological conditions. No limitation in energy production was found as indicated by the maintenance of ATP levels, the creatine phosphate/creatine ratio and normal lactate concentrations in the infarcted hearts. Comparison of the rates of substrate oxidation with MVO/sub 2/ revealed that, in both the sham and infarcted hearts, substrate oxidation, as estimated by /sup 14/CO/sub 2/ production, could not account for the observed MVO/sub 2/. It was found that the rate of /sup 14/CO/sub 2/ production from exogenous labeled palmitate underestimated the actual rate of fatty acid oxidation. This resulted from incomplete equilibration of added (/sup 14/C)-palmitate with the fatty acyl moieties present in acyl carnitine. However, the rate of /sup 14/CO/sub 2/ production from exogenous palmitate was lower in the infarcted than sham hearts.

  13. Effects of Air Pollutant Exposure on Acute Myocardial Infarction, According to Gender

    PubMed Central

    Tuan, Tássia Soldi; Venâncio, Taís Siqueira; Nascimento, Luiz Fernando Costa

    2016-01-01

    Background: There is evidence of the effects of air pollution on hospital admissions due to cardiovascular diseases, including myocardial infarction. Objective: To estimate the association between exposure to air pollutants and hospital admissions due to myocardial infarction according to gender, between January 1st 2012 and December 31st 2013, in São Jose dos Campos-SP. Methods: An ecological time series study was carried out with daily data of admissions due to AMI, pollutants CO, O3, PM10, SO2, and NO2, according to gender. We used the Poisson regression generalized linear model to estimate the relative risks of hospital admissions with lags of 0-5 days, adjusted for temperature, humidity, seasonality and days of the week. Results: There were 1837 admissions for ischemic heart diseases, with 636 women and 1201 men. For females, the risks were significant for CO in lag 0 (RR = 1,09), lag1 (RR = 1,08) and lag 5 (RR = 1,10) and SO2 in lag 0 (RR = 1,10) and 3 (RR = 1,09). For men there was significance of the CO in, lag 3 and lag 5 (RR = 1,05). There was significance, regardless of gender, for CO at lag 1 (RR = 1,05) and lag 5 (RR = 1,07) and lag 0 for SO2 (RR = 1,06). Conclusion: The data presented show the important role of CO and SO2 in the genesis of myocardial infarction admissions, and responses to pollutant exposure are different if analyzed by gender and together - hence the importance of a stratified analyses. PMID:27533257

  14. Cost-effectiveness analysis of short-term clopidogrel therapy for ST elevation myocardial infarction.

    PubMed

    Gibler, Kyle B; Huskamp, Haiden A; Sabatine, Marc S; Murphy, Sabina A; Cohen, David J; Cannon, Christopher P

    2010-03-01

    Clopidogrel improves outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and is recommended in the guidelines. We sought to determine the incremental cost-effectiveness of clopidogrel therapy in this patient population. We used primary patient-level resource use and clinical outcomes data from 3491 STEMI patients treated with fibrinolysis and either clopidogrel or placebo prior to a diagnostic coronary angiogram in the Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial Infarction 28 (CLARITY-TIMI 28) trial. Costs for each patient were calculated based on diagnosis-related groups-specific Medicare reimbursement rates for all hospitalizations and the average wholesale price of clopidogrel. Cost per event prevented and cost per life year gained (LYG) were calculated using standard methods. The estimate of LYG due to clopidogrel therapy was based on recurrent myocardial infarction and death outcomes. The bootstrap method was used to produce bias-corrected confidence intervals for cost and efficacy estimates as well as the cost per LYG ratio. Total costs and resource use were not significantly different for the clopidogrel and placebo groups ($8128 vs. $8134), indicating that short-term clopidogrel therapy is an economically dominant treatment strategy. Even in a sensitivity analysis accounting for higher long-term medical costs due to greater life expectancy, clopidogrel remained under $6000 per LYG. Clopidogrel therapy was dominant in 35% of the bootstrap simulations and cost less than $50,000 per LYG in 67% of simulations. In conclusion, this analysis finds short-term clopidogrel therapy to be a highly economically attractive therapy, improving patient outcomes at no increase in costs. PMID:20215905

  15. Extracardiac-Lodged Mesenchymal Stromal Cells Propel an Inflammatory Response Against Myocardial Infarction via Paracrine Effects.

    PubMed

    Peng, Yi; Pan, Wei; Ou, Yali; Xu, Weifang; Kaelber, Sussannah; Borlongan, Cesario V; Sun, Meiqin; Yu, Guolong

    2016-01-01

    Transplantation of stem cells, including mesenchymal stromal cells (MSCs), improves the recovery of cardiac function after myocardial infarction (MI) in experimental studies using animal models and in patients. However, the improvement of cardiac function following MSC transplantation remains suboptimal in both preclinical and clinical studies. Understanding the mechanism of cell therapy may improve its therapeutic outcomes, but the mode of action mediating stem cell promotion of cardiac repair is complex and not fully understood. Recent studies suggest that the immunomodulatory effects of MSCs on the macrophage M1/M2 subtype transition allow the transplanted stem cells to inhibit inflammation-induced injury and promote cardiac repair in acute MI. However, equally compelling evidence shows that there is poor survival and minimal graft persistence of transplanted MSCs within the infarcted heart tissues, negating the view that graft survival per se is required for the observed high rate and long duration of the transition from proinflammatory M1 to reparative M2 macrophages in the infarcted myocardium. Therefore, we raised a novel hypothesis that the therapeutic effects of MSC transplantation for acute MI depends not primarily on the grafted cells in infarct myocardium, but that MSCs migrating to and being lodged in the extracardiac organs, demonstrating good graft survival and persistence, may render the therapeutic effects in MI. More specifically, MSC transplantation promotes the transition from M1 to M2 in extracardiac organs, such as spleen and bone marrow, and therapeutic effects are conferred to the infarcted myocardium via paracrine effects. In MSC transplantation, the conversion from proinflammatory M1 to anti-inflammatory M2 monocytes may occur remotely from the heart and may serve as one of the major pathways in regulating the dual effects of inflammation. This hypothesis, if proven valid, may represent an important new mechanism of action to be considered

  16. Effects of myocardial infarction on the distribution and transport of nutrients and oxygen in porcine myocardium.

    PubMed

    Davis, Bryce H; Morimoto, Yoshihisa; Sample, Chris; Olbrich, Kevin; Leddy, Holly A; Guilak, Farshid; Taylor, Doris A

    2012-10-01

    One of the primary limitations of cell therapy for myocardial infarction is the low survival of transplanted cells, with a loss of up to 80% of cells within 3 days of delivery. The aims of this study were to investigate the distribution of nutrients and oxygen in infarcted myocardium and to quantify how macromolecular transport properties might affect cell survival. Transmural myocardial infarction was created by controlled cryoablation in pigs. At 30 days post-infarction, oxygen and metabolite levels were measured in the peripheral skeletal muscle, normal myocardium, the infarct border zone, and the infarct interior. The diffusion coefficients of fluorescein or FITC-labeled dextran (0.3-70 kD) were measured in these tissues using fluorescence recovery after photobleaching. The vascular density was measured via endogenous alkaline phosphatase staining. To examine the influence of these infarct conditions on cells therapeutically used in vivo, skeletal myoblast survival and differentiation were studied in vitro under the oxygen and glucose concentrations measured in the infarct tissue. Glucose and oxygen concentrations, along with vascular density were significantly reduced in infarct when compared to the uninjured myocardium and infarct border zone, although the degree of decrease differed. The diffusivity of molecules smaller than 40 kD was significantly higher in infarct center and border zone as compared to uninjured heart. Skeletal myoblast differentiation and survival were decreased stepwise from control to hypoxia, starvation, and ischemia conditions. Although oxygen, glucose, and vascular density were significantly reduced in infarcted myocardium, the rate of macromolecular diffusion was significantly increased, suggesting that diffusive transport may not be inhibited in infarct tissue, and thus the supply of nutrients to transplanted cells may be possible. in vitro studies mimicking infarct conditions suggest that increasing nutrients available to

  17. 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

  18. Protective effect of dimethyl sulfoxide on acute myocardial infarction in rats.

    PubMed

    Parisi, Antonio; Alfieri, Alessio; Mazzella, Marialuisa; Mazzella, Antonio; Scognamiglio, Mattia; Scognamiglio, Gianluigi; Mascolo, Nicola; Cicala, Carla

    2010-01-01

    Dimethyl sulfoxide (DMSO) is an organic compound widely used as solvent in biological studies and as vehicle for drug administration. DMSO has been shown to possess several biological effects, including antioxidant, anti-inflammatory, antinociceptive effects, and it has been proposed to be therapeutic in several disorders, such as gastrointestinal diseases, rheumatologic diseases, and for the treatment of several manifestations of amyloidosis. To better define the biological profile of DMSO, we investigated its effect on an in vivo model of acute myocardial infarction in rats, caused by left anterior descending coronary artery ligation. Our results show that pretreatment of rats with intraperitoneal (ip) DMSO (500 microL/Kg) for 3 consecutive days before left anterior descending coronary artery ligation significantly (P < 0.05) reduced cardiac damage from 18.75 +/- 4.88% (n = 12) to 4.46 +/- 2.01% (n = 8); serum levels of troponin I from 29.35 +/- 12.32 ng/mL (n = 8) to 2.95 +/- 1.32 ng/mL (n = 4); and serum levels of myoglobin from 46.86 +/- 10.35 ng/mL (n = 7) to 13.75 +/- 0.85 ng/mL (n = 4). Our data demonstrate that DMSO has a protective effect in a model of acute myocardial infarction in rats. PMID:19904216

  19. [Myocardial infarction in young population].

    PubMed

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

    2015-03-01

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

  20. Myocardial infarction following sternal surgery.

    PubMed Central

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

    1996-01-01

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

  1. Effects of morphine on left ventricular dimensions and function in patients with previous myocardial infarction.

    PubMed

    Ryan, W F; Henning, H; Karliner, J S

    1979-12-01

    To assess the effects of morphine sulfate on left ventricular function and dimensions we administered 15 mg of this agent to 11 stable patients with previous transmural myocardial infarction. All studies were carried out in the supine position. Before morphine administration an echocardiogram was obtained, and this procedure was repeated at 15, 30, 60, 120, and 240 min after morphine. Heart rate decreased from a control value of 69 +/- 4 to 62 +/- 5 beats/min 2 h after morphine (p less than 0.01, analysis of variance); this slower heart rate persisted for 4 h after morphine. Serial measurements of blood pressure, echocardiographic ejection fraction, percent of fractional shortening, and mean normalized velocity of circumferential fiber shortening also showed no significant alterations after morphine. We conclude that in stable patients with chronic ischemic heart disease studied in the supine position, 1) morphine exerts no effect on left ventricular dimensions, an observation which does not support the concept that this agent acts in humans by producing a 'pharmacologic phlebotomy'; and 2) morphine does not alter left ventricular function at rest. Whether different results will be found in patients with increased sympathetic activity, such as occurs in the setting of an acute myocardial infarction or during an episode of acute pulmonary edema, remains to be investigated.

  2. Effects of valsartan on ventricular arrhythmia induced by programmed electrical stimulation in rats with myocardial infarction

    PubMed Central

    Jiao, Kun-Li; Li, Yi-Gang; Zhang, Peng-Pai; Chen, Ren-Hua; Yu, Yi

    2012-01-01

    Abstract The impact of angiotensin II receptor blockers (ARBs) on electrical remodelling after myocardial infarction (MI) remains unclear. The purpose of the present study was to evaluate the effect of valsartan on incidence of ventricular arrhythmia induced by programmed electrical stimulation (PES) and potential link to changes of myocardial connexins (Cx) 43 expression and distribution in MI rats. Fifty-nine rats were randomly divided into three groups: Sham (n = 20), MI (n = 20) and MI + Val (20 mg/kg/day per gavage, n = 19). After eight weeks, the incidence of PES-induced ventricular tachycardia (VT) and fibrillation (VF) was compared among groups. mRNA and protein expressions of Cx43, angiotensin II type 1 receptor (AT1R) in the LV border zone (BZ) and non-infarct zone (NIZ) were determined by real-time PCR and Western blot, respectively. Connexins 43 protein and collagen distribution were examined by immunohistochemistry in BZ and NIZ sections from MI hearts. Valsartan effectively improved the cardiac function, reduced the prolonged QTc (163.7 ± 3.7 msec. versus 177.8 ± 4.5 msec., P < 0.05) after MI and the incidence of VT or VF evoked by PES (21.1% versus 55%, P < 0.05). Angiotensin II type 1 receptor expression was significantly increased in BZ and NIZ sections after MI, which was down-regulated by valsartan. The mRNA and protein expressions of Cx43 in BZ were significantly reduced after MI and up-regulated by valsartan. Increased collagen deposition and reduced Cx43 expression in BZ after MI could be partly attenuated by Valsartan. Valsartan reduced the incidence of PES-induced ventricular arrhythmia, this effect was possibly through modulating the myocardial AT1R and Cx43 expression. PMID:22128836

  3. Cardiac telocytes were decreased during myocardial infarction and their therapeutic effects for ischaemic heart in rat.

    PubMed

    Zhao, Baoyin; Chen, Shang; Liu, Juanjuan; Yuan, Ziqiang; Qi, Xufeng; Qin, Junwen; Zheng, Xin; Shen, Xiaotao; Yu, Yanhong; Qnin, Thomas J; Chan, John Yeuk-Hon; Cai, Dongqing

    2013-01-01

    Recently, cardiac telocytes were found in the myocardium. However, the functional role of cardiac telocytes and possible changes in the cardiac telocyte population during myocardial infarction in the myocardium are not known. In this study, the role of the recently identified cardiac telocytes in myocardial infarction (MI) was investigated. Cardiac telocytes were distributed longitudinally and within the cross network of the myocardium, which was impaired during MI. Cardiac telocytes in the infarction zone were undetectable from approximately 4 days to 4 weeks after an experimental coronary occlusion was used to induce MI. Although cardiac telocytes in the non-ischaemic area of the ischaemic heart experienced cell death, the cell density increased approximately 2 weeks after experimental coronary occlusion. The cell density was then maintained at a level similar to that observed 1-4 days after left anterior descending coronary artery (LAD)-ligation, but was still lower than normal after 2 weeks. We also found that simultaneous transplantation of cardiac telocytes in the infarcted and border zones of the heart decreased the infarction size and improved myocardial function. These data indicate that cardiac telocytes, their secreted factors and microvesicles, and the microenvironment may be structurally and functionally important for maintenance of the physiological integrity of the myocardium. Rebuilding the cardiac telocyte network in the infarcted zone following MI may be beneficial for functional regeneration of the infarcted myocardium.

  4. Macrophage Roles Following Myocardial Infarction

    PubMed Central

    Lambert, Jessica M.; Lopez, Elizabeth F.; Lindsey, Merry L.

    2010-01-01

    Following myocardial infarction (MI), circulating blood monocytes respond to chemotactic factors, migrate into the infarcted myocardium, and differentiate into macrophages. At the injury site, macrophages remove necrotic cardiac myocytes and apoptotic neutrophils; secrete cytokines, chemokines, and growth factors; and modulate phases of the angiogenic response. As such, the macrophage is a primary responder cell type that is involved in the regulation of post-MI wound healing at multiple levels. This review summarizes what is currently known about macrophage functions post-MI and borrows literature from other injury and inflammatory models to speculate on additional roles. Basic science and clinical avenues that remain to be explored are also discussed. PMID:18656272

  5. 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

  6. Effects of Peroxisome Proliferator-Activated Receptor-δ Agonist on Cardiac Healing after Myocardial Infarction.

    PubMed

    Park, Jeong Rang; Ahn, Jong Hwa; Jung, Myeong Hee; Koh, Jin-Sin; Park, Yongwhi; Hwang, Seok-Jae; Jeong, Young-Hoon; Kwak, Choong Hwan; Lee, Young Soo; Seo, Han Geuk; Kim, Jin Hyun; Hwang, Jin-Yong

    2016-01-01

    Peroxisome proliferator-activated receptor-delta (PPAR-δ)-dependent signaling is associated with rapid wound healing in the skin. Here, we investigated the therapeutic effects of PPAR-δ-agonist treatment on cardiac healing in post-myocardial infarction (MI) rats. Animals were assigned to the following groups: sham-operated control group, left anterior descending coronary artery ligation (MI) group, or MI with administration of the PPAR-δ agonist GW610742 group. GW610742 (1 mg/kg) was administrated intraperitoneally after the operation and repeated every 3 days. Echocardiographic data showed no differences between the two groups in terms of cardiac function and remodeling until 4 weeks. However, the degrees of angiogenesis and fibrosis after MI were significantly higher in the GW610742-treated rats than in the untreated MI rats at 1 week following MI, which changes were not different at 2 weeks after MI. Naturally, PPAR-δ expression in infarcted myocardium was highest increased in 3 day after MI and then disappeared in 14 day after MI. GW610742 increased myofibroblast differentiation and transforming growth factor-beta 2 expression in the infarct zone at 7 days after MI. GW610742 also increased bone marrow-derived mesenchymal stem cell (MSC) recruitment in whole myocardium, and increased serum platelet-derived growth factor B, stromal-derived factor-1 alpha, and matrix metallopeptidase 9 levels at day 3 after MI. PPAR-δ agonists treatment have the temporal effect on early fibrosis of infarcted myocardium, which might not sustain the functional and structural beneficial effect. PMID:26862756

  7. Acute effects of delayed reperfusion following myocardial infarction: a 3D x-ray imaging analysis

    NASA Astrophysics Data System (ADS)

    Simari, Robert D.; Bell, M. R.; Pao, Y. C.; Gersh, B. J.; Ritman, Erik L.

    1996-04-01

    Clinical and experimental data suggest that delayed reperfusion of the infarct related artery may limit infarct expansion without increasing myocardial salvage. In order to assess the potential mechanisms involved, an acute closed chest canine model of myocardial infarction and delayed reperfusion was studied. Nineteen dogs underwent 3D computed tomography in the Dynamic Spatial Reconstructor (a fast, volume imaging, CT scanner) at baseline and three and four hours later to estimate left ventricular chamber volumes, global distensibility and regional myocardial stiffness. A control group was scanned without intervention. An occlusion group underwent four hours of coronary artery occlusion. A reperfusion group underwent three hours of coronary artery occlusion followed by one hour of reperfusion. Similar infarct sizes were seen in the occlusion and reperfusion groups. Globally reperfusion was associated with increased left ventricular end diastolic pressure and prolongation of global relaxation. Regionally reperfusion was associated with increased myocardial stiffness, intramyocardial blood volume and wall thickness within the infarct zone relative to the not reperfused myocardium.

  8. TARGETED DELETION OF INDUCIBLE HEAT SHOCK PROTEIN 70 ABROGATES THE LATE INFARCT-SPARING EFFECT OF MYOCARDIAL ISCHEMIC PRECONDITIONING

    EPA Science Inventory

    Abstract submitted for 82nd annual meeting of the American Association for Thoracic Surgery, May 4-8, 2002 in Washington D.C.

    Targeted Deletion of Inducible Heat Shock Protein 70 Abrogates the Late Infarct-Sparing Effect of Myocardial Ischemic Preconditioning

    Craig...

  9. Reduced apoptosis after acute myocardial infarction by simvastatin.

    PubMed

    Luo, Ke-qin; Long, Hui-bao; Xu, Bing-can

    2015-03-01

    To observe the effect of simvastatin in patients with acute myocardial infarction in rabbits against myocardial apoptosis, and to explore its possible mechanism. Male New Zealand white rabbits were randomized into three groups, including the myocardial infarction group (12 rabbits), the simvastatin treatment group (15 rabbits), and the sham group (12 rabbits). In the simvastatin treatment and myocardial infarction groups, the rabbits received myocardial infarction surgeries. While in the sham group, loose knots were tied in the left anterior descending coronary artery branches. The simvastatin treatment group was given simvastatin by oral gavage 24 h after surgery. Parameters, which included left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction, and left ventricular mass index, were recorded in these three groups. Edge myocardial infarction and myocardial cell apoptosis were analyzed using TUNEL assay, and Bcl-2, Bax, and Caspase-3 protein levels were detected by Western blot. Acute myocardial infarction model was successfully established in rabbits by ligation of the left anterior descending coronary artery. Compared with the myocardial infarction group, left ventricular end-diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) were significantly reduced and left ventricular ejection fraction (LVEF) increased in the simvastatin treatment group. Compared with the sham group, LVEDD and LVESD were significantly increased and LVEF decreased in the simvastatin treatment group. All the differences were statistically significant (P < 0.05). Left ventricular mass index in the simvastatin treatment group was statistically lower than the myocardial infarction group. Compared with the sham group, left ventricular mass index in both the simvastatin treatment and myocardial infarction groups was significantly increased. The differences of the above comparisons were statistically

  10. [Effectiveness of the physical training of post-myocardial infarction patients with differing exertion tolerances].

    PubMed

    Barats, S S; Lipchenko, A A; Vetrov, A V

    1986-01-01

    A total of 159 men after myocardial infarction were examined. Of them 73 were engaged in physical training for 11 mos. Its efficacy was analysed after the results of bicycle ergometry taking account of initial exercise tolerance. A positive effect of physical training was noted both in the patients with high and low exercise tolerance. Raised physical working capacity was observed in parallel with the improved indices of the left ventricular contractility in accordance with the results of two-dimensional echocardiography. The authors also observed a favorable effect of physical training on lipoprotein metabolism, in particular a decrease in the value of the apo B/apo AI ratio was noted that might suggest a decrease in the inflow of cholesterol to the vascular wall and an enhanced outflow from it.

  11. Primary and Secondary Drug Treatment of Myocardial Infarction

    PubMed Central

    Warnica, J.W.

    1989-01-01

    The management of myocardial infarction has been revolutionized during the last few years. Based on a better understanding of the physiopathology of infarction, aggressive intervention with drug therapy has made great reductions in both mortality and morbidity possible. Early reperfusion of the infarct-related artery with such thrombolytic agents as streptokinase or recombinant tissue plasminogen activator may decrease acute mortality by up to 50%. New uses for older drugs, such as acetylsalicylic acid and nitroglycerin, give them a primary role in acute myocardial infarction. β-Blocking drugs, when given in the early and later phases of myocardial infarction, also clearly reduce mortality and morbidity. Combining early reperfusion and adjunctive therapy with ASA, nitrates, and β-blockers will surely become accepted as the most effective method of treating the pain, limiting the damage, and preventing the complications of myocardial infarction. PMID:21249088

  12. [Acute myocardial infarction during sport].

    PubMed

    Fujiwara, M; Asakuma, S; Nakamura, K; Nakamura, T; Yasutomi, N; Iwasaki, T

    1995-10-01

    Thirty patients with acute myocardial infarction which occurred during sport were investigated to identify the type of sport, prodromata, situations at the onset of disease, habit of exercise, preceding medical evaluation, coronary risk factors, and coronary angiographic findings. Infarction occurred during golf in 12 patients, bowling in 4, gateball in 4, jogging or running in 5, baseball in 2, and tennis or table tennis in 3. The majority of the patients were playing ball games. Twenty-seven patients were men (90%) and 3 were women (10%). All patients had played the same kind of sport for several years. Twenty-four patients had one or more coronary risk factors, and especially 18 patients smoked cigarettes. Nine patients had experienced anterior chest pain but only two patients had received medical evaluation. Coronary angiography was performed in 25 patients (83.3%), revealing single-vessel disease in 14, two-vessel disease in 6, three-vessel disease in 4, and disease of all left main coronary trunks in 1. The acute episode of infarction occurred mainly in spring or fall. Many patients with acute myocardial infarction occurring during sport participate in sports of low or moderate dynamic and low static exercises which are generally regarded safe. Many patients had enjoyed their sports regularly for a long time. Though many patients had coronary risk factors, only a few had received a medical check before their heart attack.

  13. Cocaine, a risk factor for myocardial infarction.

    PubMed

    Galasko, G I

    1997-06-01

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

  14. Effect of EHDP on calcium accumulation and technetium-99m pyrophosphate uptake in experimental myocardial infarction

    SciTech Connect

    Buja, L.M.; Tofe, A.J.; Parkey, R.W.; Francis, M.D.; Lewis, S.E.; Kulkarni, P.V.; Bonte, F.J.; Willerson, J.T.

    1981-11-01

    Ethane-l-hydroxy-1,1-diphosphonate (EHDP) inhibits bone mineral growth. This study was performed to test the hypothesis that EHDP would interfere with the process of calcium uptake and deposition in evolving myocardial infarction and thereby influence other parameters, including technetium-99m pyrophosphate (Tc-99m PYP) uptake and scintigraphic visualization of the infarcts. Permanent occlusion of the left anterior descending coronary artery (LAD) was produced in beagles. In seven dogs, serum EHDP was maintained at 10-15 ..mu..g/ml for 24 hours by continuous i.v. infusion, and seven control dogs were infused with saline. The Tc-99m PYP was infected 2 hours before sacrifice. EHDP-treated dogs showed a mild decrease (20%) in mean calcium content of infarcted myocardium (102.4 +/- 6.4 ..mu..g (+/- SEM) per gram wet weight (n = 51) vs 126.7 +/- 9.5 (n = 49) (p < 0.05)). These dogs showed a prominent decrease (37%) in mean Tc-99m PYP content of infarcted myocardium (18.2 +/- 1.4 (% dose/g x 10/sup -3/) (n = 46) vs 28.9 +/- 4.3 (n = 46) (p < 0.005)) and a marked decrease (65%) in infarct-to-normal ratio (6.1 +/- 0.9 (n = 6) vs 15.9 +/- 3.7 (n = 6) (p < 0.05)). Positive relationships were demonstrated between myocardial Tc-99m PYP and calcium levels in the EHDP-treated dogs (r = 0.69) and the control dogs (r = 0.77). Infarct size and regional myocardial blood flow changes were similar in the EHDP-treated and control dogs. The average grade (0-4+) of the Tc-99m PYP myocardial scintigrams for infarcts greater than 3.5 g was 2.4 +/- 0.2 for control dogs and 1.1 +/- 0.4 for EHDP-treated dogs (p < 0.05). Thus, EHDP infusion at the dose tested produced a mild decrease in calcium accumulation in canine infarcts; however, it produced a greater reduction in Tc-99m PYP uptake in the infarcts.

  15. Perioperative myocardial infarction in patients undergoing myocardial revascularization surgery

    PubMed Central

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

    2015-01-01

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

  16. Effect of postconditioning in patients with ST-elevation acute myocardial infarction.

    PubMed

    Ugata, Yusuke; Nakamura, Tomohiro; Taniguchi, Yousuke; Ako, Junya; Momomura, Shinichi

    2012-01-01

    Postconditioning (PosC), which is a brief period of ischemia performed at the time of reperfusion therapy, reduces the infarct size in animal models. We aim to evaluate the impact of PosC in patients with ST-elevation acute myocardial infarction (STEMI). Between January 2008 and August 2009, 37 STEMI patients received PosC. The control group comprised 42 age- and sex-matched patients diagnosed with STEMI in 2007-2008. In the PosC group, we applied four cycles of 30-s balloon inflation and 30-s balloon deflation within 3 min after thrombectomy, and implanted the stent after PosC. In the control group, we directly implanted the stent after thrombectomy. The number of patients with myocardial blush grade 2 or 3 after the procedure was higher in the PosC group than in the control group (65 vs. 43%, p = 0.04). The ST-segment resolution >50% was greater in the PosC group compared to the control group (81 vs. 57%, p = 0.02). Serial changes of creatine kinase and creatine kinase myocardial fraction after reperfusion were significantly lower in the PosC group than in the control group. In conclusion, PosC is a safe and feasible strategy that might preserve myocardial perfusion and reduce the infarct size in patients with STEMI. PMID:24122635

  17. Apoptosis in myocardial ischaemia and infarction.

    PubMed

    Krijnen, P A J; Nijmeijer, R; Meijer, C J L M; Visser, C A; Hack, C E; Niessen, H W M

    2002-11-01

    Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in animals.

  18. Effect of additional treatment with EXenatide in patients with an Acute Myocardial Infarction (EXAMI): study protocol for a randomized controlled trial

    PubMed Central

    2011-01-01

    Background Myocardial infarction causes irreversible loss of cardiomyocytes and may lead to loss of ventricular function, morbidity and mortality. Infarct size is a major prognostic factor and reduction of infarct size has therefore been an important objective of strategies to improve outcomes. In experimental studies, glucagon-like peptide 1 and exenatide, a long acting glucagon-like peptide 1 receptor agonist, a novel drug introduced for the treatment of type 2 diabetes, reduced infarct size after myocardial infarction by activating pro-survival pathways and by increasing metabolic efficiency. Methods The EXAMI trial is a multi-center, prospective, randomized, placebo controlled trial, designed to evaluate clinical outcome of exenatide infusion on top of standard treatment, in patients with an acute myocardial infarction, successfully treated with primary percutaneous coronary intervention. A total of 108 patients will be randomized to exenatide (5 μg bolus in 30 minutes followed by continuous infusion of 20 μg/24 h for 72 h) or placebo treatment. The primary end point of the study is myocardial infarct size (measured using magnetic resonance imaging with delayed enhancement at 4 months) as a percentage of the area at risk (measured using T2 weighted images at 3-7 days). Discussion If the current study demonstrates cardioprotective effects, exenatide may constitute a novel therapeutic option to reduce infarct size and preserve cardiac function in adjunction to reperfusion therapy in patients with acute myocardial infarction. Trial registration ClinicalTrials.gov: NCT01254123 PMID:22067476

  19. 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.

  20. Myocardial infarction due to lightning strike.

    PubMed

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

    2013-09-01

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

  1. Myocardial infarction due to lightning strike.

    PubMed

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

    2013-09-01

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

  2. Changes in rest and exercise myocardial perfusion and left ventricular function 3 to 26 weeks after clinically uncomplicated acute myocardial infarction: effects of exercise training

    SciTech Connect

    Hung, J.; Gordon, E.P.; Houston, N.; Haskell, W.L.; Goris, M.L.; DeBusk, R.F.

    1984-11-01

    The effects of exercise training on exercise myocardial perfusion and left ventricular (LV) function in the first 6 months after clinically uncomplicated acute myocardial infarction (AMI) were assessed in 53 consecutive men aged 55 +/- 9 years. Symptom-limited treadmill exercise with thallium myocardial perfusion scintigraphy and symptom-limited upright bicycle ergometry with equilibrium gated radionuclide ventriculography were performed 3, 11 and 26 weeks after AMI by 23 men randomized to training and 30 randomized to no training. Peak cycle capacity increased in both groups between 3 and 26 weeks (p less than 0.01), but reached higher levels in trained than in untrained patients (803 +/- 149 vs 648 +/- 182 kg-m/min, p less than 0.01). Reversible thallium perfusion defects were significantly more frequent at 3 than at 26 weeks: 59% and 36% of patients, respectively (p less than 0.05), without significant inter-group differences. Values of LV ejection fraction at rest, submaximal and peak exercise did not change significantly in either group. The increase in functional capacity, i.e., peak treadmill or bicycle workload, that occurred 3 to 26 weeks after infarction was significantly correlated with the increase in peak exercise heart rate (p less than 0.001), but not with changes in myocardial perfusion or LV function determined by radionuclide techniques. Changes in myocardial perfusion or LV function do not appear to account for the improvement in peak functional capacity that occurs within the first 6 months after clinically uncomplicated AMI.

  3. Matrix metalloproteinases: drug targets for myocardial infarction

    PubMed Central

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

    2013-01-01

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

  4. [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

  5. Tombstoning ST-Elevation Myocardial Infarction

    PubMed Central

    Balci, Bahattin

    2009-01-01

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

  6. Erythropoietin has an antiapoptotic effect after myocardial infarction and stimulates in vitro aortic ring sprouting

    SciTech Connect

    Mansson Broberg, Agneta; Grinnemo, Karl-Henrik; Genead, Rami; Danielsson, Christian; Andersson, Agneta B.; Waerdell, Eva; Sylven, Christer

    2008-06-20

    Aims were to explore if darbepoietin-{alpha} in mouse can induce angiogenesis and if moderate doses after myocardial infarction stimulates periinfarct capillary and arteriolar densities, cell proliferation, and apoptosis. Myocardial infarction was induced by ligation of LAD. Mouse aortic rings (0.8 mm) were cultured in matrigel and the angiogenic sprouting was studied after addition of darbepoietin-{alpha} with and without VEGF-165. After 12 days the hemoglobin concentration was 25% higher in the darbepoietin-{alpha} treated mice than in the control group. No difference in capillary densities in the periinfarct or noninfarcted areas was seen with darbepoietin-{alpha}. Cell proliferation was about 10 times higher in the periinfarct area than in the noninfarcted wall. Darbepoietin-{alpha} treatment led to a decrease of cell proliferation (BrdU, (p < 0.02)) and apoptosis (TUNEL, p < 0.005) with about 30% in the periinfarct area. Darbepoietin-{alpha} and VEGF-165 both independently induced sprouting from aortic rings. The results suggest that darbepoietin-{alpha} can induce angiogenesis but that moderate doses after myocardial infarction are not angiogenic but antiapoptotic.

  7. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats

    PubMed Central

    Goyal, Sameer N.; Sharma, Charu; Mahajan, Umesh B.; Patil, Chandragouda R.; Agrawal, Yogeeta O.; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-01-01

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities. PMID:26593900

  8. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats.

    PubMed

    Goyal, Sameer N; Sharma, Charu; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-01-01

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities. PMID:26593900

  9. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats.

    PubMed

    Goyal, Sameer N; Sharma, Charu; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-11-17

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities.

  10. [Comparison between 123I-BMIPP and 201TlCl myocardial imaging by circumferential profile analysis in patients with myocardial infarction--evaluation of effects of vascular reconstruction in patients with myocardial infarction].

    PubMed

    Ohsumi, Y; Watanabe, T; Nagano, T

    1994-10-01

    We quantitatively evaluated the effects of vascular reconstruction according to the stage by 123I-BMIPP and 201TlCl using circumferential profile (CP) curve method in patients with myocardial infarction. (1) Comparison of the CP curves for the two nuclides in normal volunteers (n = 9) showed no difference in distribution. (2) In patient with myocardial infarction (n = 32) the severity score was evaluated using the CP curves obtained in the normal volunteers. Type B (marked decrease in 123I-BMIPP accumulation) accounted for 83% in the group in whom vascular reconstruction was performed in the acute stage (Group I) and 91% in the group in whom vascular reconstruction was performed in the chronic stage (Group II). On the other hand, type E (similar accumulation between the two nuclides) accounted for 79% in the group in whom vascular reconstruction was unsuccessful or was not performed (Group III). The severity score for each nuclide did not significantly differ among Group I, II and III. The 123I-BMIPP/201TlCl ratio was the highest in Group II, followed in order by Group I and Group III (p < 0.05). The assessment of the ratio of "severity scores" for both nuclides is considered to be useful for evaluation of the surviving myocardium, rather than the assessment of a single nuclide. PMID:7807719

  11. 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.

  12. Effects of renal sympathetic denervation on cardiac systolic function after myocardial infarction in rats

    PubMed Central

    Guo, Jiqun; Zhou, Zhongxia; Li, Zhenzhen; Liu, Qian; Zhu, Guoqing; Shan, Qijun

    2016-01-01

    Abstract This study investigated the therapeutic effects of renal denervation on cardiac systolic function after myocardial infarction (MI) in rats and the mechanism involved. Fifty male SD rats were randomly assigned to the sham group (n = 15), the MI group (n = 20), and the MI plus renal denervation group (n = 15). MI was established through thoracotomic ligation of the anterior descending artery. Renal denervation was achieved by laparotomic stripping of the renal arterial adventitial sympathetic nerve, approximately 3 mm from the abdominal aorta. Left ventricular function and hemodynamics were measured several weeks following MI. The left ventricular systolic function of the MI group was significantly reduced and the systolic blood pressure (SBP) remarkably declined. In rats with MI treated with renal denervation, the left ventricular ejection fraction (EF), fractional shortening (FS) and SBP markedly improved compared with the MI group. However, heart rate and fibrosis decreased significantly. These findings suggest that renal denervation has therapeutic effects on post-MI cardiac dysfunction. These effects are associated with increased left ventricular ejection fraction (LVEF) and SBP, as well as reduced heart rate and fibrosis. This may represent a new approach to the treatment of post-MI remodeling and subsequent heart failure.

  13. [ST myocardial infarction with spontaneous coronary reperfusion].

    PubMed

    Uriel, Nir; Moravsky, Gil; Blatt, Alex; Vered, Zvi; Krakover, Ricardo; Kaluski, Edo

    2006-05-01

    ST elevation myocardial infarction continues to be a major medical problem even in the beginning of the 21st century. Treatment guidelines for these patients are based on multiple randomized clinical trials. In order to minimize myocardial damage, early patency of the infarct relating artery must be accomplished. This is the major difference in the treatment strategy between ST elevation myocardial infarction and other acute coronary syndromes. Primary percutaneous coronary intervention and fibrinolysis are the two treatment modalities for achieving myocardial reperfusion. The subgroup of ST elevation myocardial infarction with spontaneous coronary artery reperfusion carries a more favorable prognosis. This review addresses the clinical characteristics, natural history, prognosis and treatment strategies for this group, with special emphasis on the optimal timing for revascularization, and the role of glycoprotein IIb/IIIa inhibitors.

  14. Triggering of Myocardial Infarction by Increased Ambient Fine Particle Concentration: Effect Modification by Source Direction

    PubMed Central

    Hopke, Philip K.; Kane, Cathleen; Utell, Mark J.; Chalupa, David C.; Kumar, Pramod; Ling, Frederick; Gardner, Blake; Rich, David Q.

    2015-01-01

    Background Previously, we reported a 18% increased odds of ST-elevation myocardial infarction (STEMI) associated with each 7.1 µg/m3 increase in PM2.5 concentration in the hour prior to MI onset. We found no association with non-ST elevation myocardial infarction (NSTEMI). We examined if this association was modified by PM2.5 source direction. Methods We used the NOAA HYbrid Single-Particle Lagrangian Trajectory (HYSPLIT) model to calculate each hourly air mass location for the 24 hours before each case or control time period in our previous PM2.5/STEMI case-crossover analysis. Using these data on patients with STEMI (n=338), hourly PM2.5 concentrations, and case-crossover methods, we evaluated whether our PM2.5/STEMI association was modified by whether the air mass passed through each of the 8 cardinal wind direction sectors in the previous 24 hours. Results When the air mass passed through the West-Southwest direction (WSW) any time in the past 24 hours, the odds of STEMI associated with each 7.1 µg/m3 increase in PM2.5 concentration in the previous hour (OR=1.27; 95% CI=1.08, 1.22) was statistically significantly (p=0.01) greater than the relative odds of STEMI associated with increased PM2.5 concentration when the wind arrived from any other direction (OR=0.99; 95% CI=0.80, 1.22). We found no other effect modification by any other source direction. Further, relative odds estimates were largest when the time spent in the WSW was 8-16 hours, compared to ≤7 hours or 17-24 hours, suggesting that particles arising from sources in this direction were more potent in triggering STEMIs. Conclusions Since relative odds estimates were higher when the air mass passed through the WSW octant in the past 24 hours, there may be specific components of the ambient aerosol that are more potent in triggering STEMIs. This direction is associated with substantial emissions from coal-fired power plants and other industrial sources of the Ohio River Valley, many of which are

  15. Effects of KR-32570, a new sodium hydrogen exchanger inhibitor, on myocardial infarction and arrhythmias induced by ischemia and reperfusion.

    PubMed

    Lee, Byung Ho; Yi, Kyu Yang; Lee, Sunkyung; Lee, Sunghou; Yoo, Sung-eun

    2005-10-31

    The present study was performed to evaluate the cardioprotective effects of [5-(2-methoxy-5-chloro-5-phenyl)furan-2-ylcarbonyl]guanidine (KR-32570) in rat and dog models of coronary artery occlusion and reperfusion. In addition, we sought to clarify the efficacy of KR-32570 on reperfusion-induced fatal ventricular arrhythmia. In anesthetized rats subjected to 45-min coronary occlusion and 90-min reperfusion, KR-32570 (i.v. bolus) dose-dependently reduced myocardial infarct size from 58.0% to 50.7%, 35.3%, 33.5% and 27.0% for 0.03, 0.1, 0.3 and 1.0 mg/kg, respectively (P<0.05). In anesthetized beagle dogs that underwent 1.2-h occlusion followed by 3.0-h reperfusion, KR-32570 (3 mg/kg, i.v. bolus) markedly decreased infarct size from 28.9% in vehicle-treated group to 8.0% (P<0.05), and reduced the reperfusion-induced release in creatine kinase isoenzyme MB, lactate dehydrogenase, Troponin-I and glutamic-oxaloacetic transaminase. KR-32570 dose-dependently decreased the incidence of premature ventricular contraction, ventricular tachycardia or ventricular fibrillation induced by ischemia and reperfusion in rats. Similar results were obtained in dogs with reperfusion-induced arrhythmia. In separate experiments to assess the effects of timing of treatment, KR-32570 given 10 min before or at reperfusion in rat models also significantly reduced the myocardial infarct size (40.9% and 46.1%, respectively) compared with vehicle-treated group. In all studies, KR-32570 caused no significant changes in any hemodynamic profiles. Taken together, these results indicate that KR-32570 significantly reduced the myocardial infarction and incidence of arrhythmias induced by ischemia and reperfusion in rats and dogs, without affecting hemodynamic profiles. Thus, it could be potentially useful in the prevention and treatment of myocardial injuries and lethal ventricular arrhythmias.

  16. 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

  17. Serum nickle estimation in acute myocardial infarction.

    PubMed

    Narang, N K; Goyal, R K; Gupta, A K; Balwani, S

    1989-11-01

    Serum nickle was estimated by atomic absorption spectrometer in 20 healthy controls and in 25 cases of acute myocardial infarction at 12 hourly intervals upto 48 hours, after the onset of chest pain. The mean serum nickel was 0.27 micrograms/dl in healthy controls and 0.40,050,049 and 0.30 micrograms/dl in patients of acute myocardial infarction. The serum nickel values were significantly (P less than 0.001) raised upto 36 hours in acute myocardial infarction when compared with controls.

  18. 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.

  19. Effect of β-Blockers on the Risk of Atrial Fibrillation in Patients with Acute Myocardial Infarction

    PubMed Central

    Pesaro, Antonio Eduardo; de Matos Soeiro, Alexandre; Serrano, Carlos Vicente; Giraldez, Roberto Rocha; Ladeira, Renata Teixeira; Nicolau, José Carlos

    2010-01-01

    INTRODUCTION: Oral β-blockers improve the prognosis of patients with acute myocardial infarction, while atrial fibrillation worsens the prognosis of this population. The reduction of atrial fibrillation incidence in patients treated with β-blockers could at least in part explain the benefits of this drug. OBJECTIVE: To investigate the effect of β-blockers on the incidence of atrial fibrillation in patients with acute myocardial infarction. METHODS: We analyzed 1401 patients with acute myocardial infarction and evaluated the occurrence or absence of atrial fibrillation, the use of oral β-blockers and mortality during the first 24 hours. RESULTS: a) The use of β-blockers was inversely correlated with the presence of atrial fibrillation (ρ = 0.004; OR = 0.54). b) Correlations with mortality were as follows: 31.5% in patients with atrial fibrillation, 9.2% in those without atrial fibrillation (ρ < 0.001; Odds Ratio = 4.52), and 17.5% in patients not treated with β-blockers and 6.7% in those who received the drug (ρ < 0.001; OR = 0.34). c) Adjusted Models: The presence of atrial fibrillation was independently correlated with mortality (OR = 2.48, ρ = 0.002). The use of β-blockers was inversely and independently correlated with mortality (OR = 0.53; ρ = 0.002). The patients who used β-blockers showed a lower risk of atrial fibrillation (OR = 0.59; ρ = 0.029) in the adjusted model. CONCLUSION: The presence of atrial fibrillation and the absence of oral β-blockers increased in-hospital mortality in patients with acute myocardial infarction. Oral β-blockers reduced the incidence of atrial fibrillation, which might be at least partially responsible for the drug’s benefit. PMID:20360916

  20. Circadian variation in the onset of myocardial infarction: effect of duration of diabetes.

    PubMed

    Rana, Jamal S; Mukamal, Kenneth J; Morgan, James P; Muller, James E; Mittleman, Murray A

    2003-06-01

    There are conflicting reports regarding circadian variation in the onset of acute myocardial infarction (MI) among patients with diabetes. We therefore, studied the circadian pattern of the incidence of acute MI in patients (n = 3,882) who were enrolled in the Onset Study stratified by the presence, type, and duration of diabetes. The Onset Study was conducted at 64 U.S. medical centers between August 1989 and September 1996. We used harmonic regression model to evaluate the circadian variation of MI symptom onset in patients with and without diabetes. Subgroup analysis was performed according to the presence, type, and duration of diabetes by the chi(2) test (dividing the day into four 6-h intervals). Patients without diabetes exhibited a prominent morning peak in the incidence of acute MI symptom onset (P < 0.001). In contrast, patients with type 1 diabetes and type 2 diabetes > or =5 years had a marked attenuation of the morning peak. Patients who had type 2 diabetes diagnosed within the previous 5 years had a pattern of onset of acute MI similar to patients without diabetes. Patients with type 1 diabetes and those with type 2 diabetes > or =5 years have an attenuation of the morning peak in acute MI. Inconsistency in observation of such an effect in patients with diabetes in the past may well have been due to difference in the duration of diabetes and thus the variable extent of underlying autonomic dysfunction.

  1. Interventions during and after acute myocardial infarction.

    PubMed

    Sleight, P

    1983-01-01

    There is now evidence that infarct size in man can be reduced by early treatment and that some cases of threatened infarction can be aborted. Beta blockade, given intravenously within about 6-8 hours after the onset of pain can reduce infarct size and abort some infarctions. So far we have no conclusive data on mortality. Beta blockers may act by a number of mechanisms, namely reduction of cardiac contractility, heart rate and blood pressure thus reducing cardiac work and oxygen requirement, prevention of cardiac rupture by the same mechanism, and by an early effect on R on T ectopic beats and hence serious ventricular arrhythmia. Early myocardial revascularization either by coronary graft, percutaneous angioplasty or intracoronary streptokinase are all promising but so far unproven by adequate clinical trial. Randomized trials suggest that intravenous streptokinase may be effective and hyaluronidase appears promising, possibly by promotion of collateral vessel flow. Calcium channel blockade may also be helpful and there are some early studies which support this. Lowering work by sodium nitroprusside also reduces infarct size. Heparin may have a place in the treatment of threatened infarction. After recovery it now appears established that beta 1-blockade will lower mortality. We do not know how long this effect persists. Other agents are less well established perhaps because the trials have been too small. Anticoagulants may have a place but their use is not widespread. Anti-platelet agents are also controversial. Studies of dipyridamole and sulphinpyrazone have been suggestive but not conclusive; the studies of aspirin are moderately encouraging, when all trials are pooled. Anti-arrhythmic therapy after infarction has been disappointing, with the exception of beta blockade. Perhaps more emphasis should also be put upon changes in lifestyle, notably stopping smoking, reduction of fat intake and encouraging regular exercise.

  2. Mesenchymal Stem Cells and Mononuclear Cells From Cord Blood: Cotransplantation Provides a Better Effect in Treating Myocardial Infarction.

    PubMed

    Chen, Gecai; Yue, Aihuan; Yu, Hong; Ruan, Zhongbao; Yin, Yigang; Wang, Ruzhu; Ren, Yin; Zhu, Li

    2016-03-01

    The aim of this study was to evaluate the effect of cotransplanting mononuclear cells from cord blood (CB-MNCs) and mesenchymal stem cells (MSCs) as treatment for myocardial infarction (MI). Transplanting CD34+ cells or MSCs separately has been shown effective in treating MI, but the effect of cotransplanting CB-MNCs and MSCs is not clear. In this study, MSCs were separated by their adherence to the tissue culture. The morphology, immunophenotype, and multilineage potential of MSCs were analyzed. CB-MNCs were separated in lymphocyte separation medium 1.077. CD34+ cell count and viability were analyzed by flow cytometry. Infarcted male Sprague-Dawley rats in a specific-pathogen-free grade were divided into four treatment groups randomly: group I, saline; group II, CB-MNCs; group III, MSCs; and group IV, CB-MNCs plus MSCs. The saline, and CB-MNCs and/or MSCs were injected intramyocardially in infarcted rats. Their cardiac function was evaluated by echocardiography. The myocardial capillary density was analyzed by immunohistochemistry. Both cell types induced an improvement in the left ventricular cardiac function and increased tissue cell proliferation in myocardial tissue and neoangiogenesis. However, CB-MNCs plus MSCs were more effective in reducing the infarct size and preventing ventricular remodeling. Scar tissue was reduced significantly in the CB-MNCs plus MSCs group. MSCs facilitate engraftment of CD34+ cells and immunomodulation after allogeneic CD34+ cell transplantation. Cotransplanting MSCs and CB-MNCs might be more effective than transplanting MSCs or CB-MNCs separately for treating MI. This study contributes knowledge toward effective treatment strategies for MI.

  3. microRNA-208a in an early stage myocardial infarction rat model and the effect on cAMP-PKA signaling pathway

    PubMed Central

    Feng, Gao; Yan, Zhang; Li, Chuanchuan; Hou, Yuemei

    2016-01-01

    The expression level of microRNA-208a (miR-208a) in a rat model with myocardial infarction and the effect of cAMP-PKA signaling pathway in early stage of myocardial infarction in rats were investigated. The early myocardial infarction model was established in 12 male Sprague-Dawley rats by ligation of the anterior descending coronary artery, and 12 rats were selected as the control group (sham operation group). Reverse-transcription quantitative PCR was conducted to detect the expression levels of miR-208a in the myocardium of and the expression levels of miR-208a in the serum of rats in the two groups. Western blot analysis was used to evaluate the expression levels of cAMP-PKA protein in the rat tissues in the two groups. After stimulating high levels of miR-208a expression in human myocardial cells (HCM), western blot analysis was used to detect the cAMP-PKA protein levels. The expression levels of miR-208a in myocardial tissues in rats with myocardial infarction were significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The expression levels of miR-208a in the early stage of myocardial infarction rats were also significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The level of cAMP-PKA protein in myocardial tissue in rats with chronic myocardial infarction was also significantly higher. Transfection of human myocardial cells with miR-208a analogue significantly increased the cAMP-PKA protein levels in human myocardial cells. In conclusion, the over expression of miR-208a in myocardial infarction tissue and the high levels of this miRNA in the serum, may be involved in the process of myocardial infarction by influencing the cAMP-PKA signaling pathway in myocardial cells. PMID:27314868

  4. microRNA-208a in an early stage myocardial infarction rat model and the effect on cAMP-PKA signaling pathway.

    PubMed

    Feng, Gao; Yan, Zhang; Li, Chuanchuan; Hou, Yuemei

    2016-08-01

    The expression level of microRNA-208a (miR-208a) in a rat model with myocardial infarction and the effect of cAMP-PKA signaling pathway in early stage of myocardial infarction in rats were investigated. The early myocardial infarction model was established in 12 male Sprague-Dawley rats by ligation of the anterior descending coronary artery, and 12 rats were selected as the control group (sham operation group). Reverse-transcription quantitative PCR was conducted to detect the expression levels of miR-208a in the myocardium of and the expression levels of miR‑208a in the serum of rats in the two groups. Western blot analysis was used to evaluate the expression levels of cAMP-PKA protein in the rat tissues in the two groups. After stimulating high levels of miR‑208a expression in human myocardial cells (HCM), western blot analysis was used to detect the cAMP-PKA protein levels. The expression levels of miR‑208a in myocardial tissues in rats with myocardial infarction were significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The expression levels of miR‑208a in the early stage of myocardial infarction rats were also significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The level of cAMP-PKA protein in myocardial tissue in rats with chronic myocardial infarction was also significantly higher. Transfection of human myocardial cells with miR‑208a analogue significantly increased the cAMP-PKA protein levels in human myocardial cells. In conclusion, the over-expression of miR-208a in myocardial infarction tissue and the high levels of this miRNA in the serum, may be involved in the process of myocardial infarction by influencing the cAMP-PKA signaling pathway in myocardial cells.

  5. [Stem cell perspectives in myocardial infarctions].

    PubMed

    Aceves, José Luis; Archundia, Abel; Díaz, Guillermo; Páez, Araceli; Masso, Felipe; Alvarado, Martha; López, Manuel; Aceves, Rocío; Ixcamparij, Carlos; Puente, Adriana; Vilchis, Rafael; Montaño, Luis Felipe

    2005-01-01

    Myocardial infarction is the leading cause of congestive heart failure and death in industrializated countries. The cellular cardiomyoplasty has emerged as an alternative treatment in the regeneration of infarted myocardial tissue. In animals' models, different cellular lines such as cardiomyocites, skeletal myoblasts, embryonic stem cells and adult mesenchymal stem cells have been used, resulting in an improvement in ventricular function and decrease in amount of infarcted tissue. The first three cells lines have disvantages as they are allogenics and are difficult to obtain. The adult mesenchymal stem cells are autologous and can be obtained throught the aspiration of bone marrow or from peripherical circulation, after stimulating with cytokines (G-CSF). The implantation in humans with recent and old myocardial infarction have shown improvements similar to those shown in animal models. These findings encourage the continued investigation in the mechanism of cellular differentiation and implantation methods in infarcted myocardial tissue.

  6. Effect of Coronary Thrombectomy in Cardiogenic Shock Complicating ST-Segment Elevation Myocardial Infarction.

    PubMed

    Suzuki, Makoto; Sumiyoshi, Tetsuya; Miyachi, Hideki; Yamashita, Jun; Yamasaki, Masao; Miyauchi, Katsumi; Yamamoto, Takeshi; Nagao, Ken; Tomoike, Hitonobu; Takayama, Morimasa

    2015-06-15

    Optimal coronary reflow is the critical key issue to ameliorate clinical outcomes in patients with cardiogenic shock complicating ST-segment elevation myocardial infarction (Shock-STEMI). We investigated our hypothesis that pre-percutaneous coronary intervention (PCI) procedural coronary thrombectomy may provide clinical advantages to attempt optimal coronary reflow in patients with Shock-STEMI. Of 7,650 patients with acute myocardial infarction registered in the Tokyo CCU Network Scientific Council from January 2009 to December 2011, a total of 180 consecutive patients (144 men, 68 ± 13 years) with Shock-STEMI who showed pre-PCI procedural Thrombolysis in Myocardial Infarction flow grade 0 (absent initial coronary flow) were recruited. Achievements of post-PCI procedural Thrombolysis in Myocardial Infarction flow grade 3 (optimal coronary reflow) and also in-hospital mortality were evaluated in those in accordance with and without coronary thrombectomy. Coronary thrombectomy was performed in 128 patients with Shock-STEMI (71% of all). Overall in-hospital mortality was 41% and that in anterior Shock-STEMI with a necessity of mechanical circulatory support increased by 59% (i.e., profound shock). Coronary thrombectomy did not affect any improvements in the achievement of optimal coronary reflow (65% vs 58%, p = 0.368) and in-hospital mortality (42% vs 37%, p = 0.484) in these patients. Even when focused on 76 patients with profound shock, neither an achievement of optimal coronary reflow (56% vs 47%, p = 0.518) nor in-hospital mortality (58% vs 65%, p = 0.601) were different between with and without coronary thrombectomy. Multivariate logistic analysis did not demonstrate any association of coronary thrombectomy (p = 0.798), left main Shock-STEMI (p = 0.258), and use of mechanical circulatory support (p = 0.119) except a concentration of hemoglobin (for each 1 g/dl increase, odds ratio 1.247, 95% confidence interval 1.035 to 1.531, p = 0.019) with optimal

  7. Protective effect of oxymatrine on myocardial fibrosis induced by acute myocardial infarction in rats involved in TGF-β₁-Smads signal pathway.

    PubMed

    Shen, Xiang-Chun; Yang, Yu-Ping; Xiao, Ting-Ting; Peng, Jiao; Liu, Xing-De

    2011-03-01

    Oxymatrine (1), a component extracted from a traditional Chinese herb Sophora japonica (Sophora flavescens Ait.), has been demonstrated to have a variety of pharmacological actions. Abundant experimental evidence indicates that 1 may exert a protective effect on the cardiovascular system. This study was designed to explore the possible role of 1 against myocardial fibrosis induced by acute myocardial infarction (AMI) and its modulation on transforming growth factor beta 1 (TGF-β(1))-Smads signaling pathways. Rats with AMI induced by ligation of left anterior descending branch were randomly assigned to receive 1 50 and 25 mg/kg intragastrically, and model group which were further compared with sham-operated group, and positive group treated with captopril. The effects of 4-week therapy with 1 starting 24 h after infarction had been investigated based on (1) hemodynamics, (2) tissue weights, (3) biochemical indicator (hydroxyproline contents in left ventricle), and (4) TGF-β(1), TGF-β(1) receptor (TβR(1)), Smad3, Smad4, Smad7, Col1, and Col3 expression by semi-quantitative reverse transcription PCR. Treatment with 1 significantly ameliorated hemodynamics, inhibited the expression of TβR(1) mRNA and Smad3 mRNA, and reduced the left ventricle weight/body weight. The results of this research indicated that 1 might protect against myocardial fibrosis and the mechanism may be involved in modulating TGF-β(1)-Smads signal pathway. PMID:21409682

  8. A somatic component to myocardial infarction.

    PubMed Central

    Nicholas, A S; DeBias, D A; Ehrenfeuchter, W; England, K M; England, R W; Greene, C H; Heilig, D; Kirschbaum, M

    1985-01-01

    Sixty two patients were randomised to be seen by osteopathic physicians for palpation of the thoracic paravertebral soft tissue, T1-T8. Twenty five patients had clinically confirmed acute myocardial infarction. Of the remainder, 22 without known cardiovascular disease served as controls and 15 were placed in an excluded group because of diagnosed cardiovascular disease other than myocardial infarction. Observations were described in predetermined standard terminology. The control group was found to have a low incidence of palpable changes throughout the thoracic dorsum, and these changes were uniformly distributed from T1 to T8. Examination of the group with myocardial infarction disclosed a significantly higher incidence of soft tissue changes (increased firmness, warmth, ropiness, oedematous changes, heavy musculature), confined almost entirely to the upper four thoracic levels. The 15 patients who were excluded from the experimental group because they had various cardiovascular diseases other than myocardial infarction also showed significantly different changes on palpation compared with the group with myocardial infarction. These findings suggest that myocardial infarction is accompanied by characteristic paravertebral soft tissue changes which are readily detected by palpation. PMID:3926040

  9. Effect of diltiazem on myocardial infarct size estimated by enzyme release, serial thallium-201 single-photon emission computed tomography and radionuclide angiography

    SciTech Connect

    Zannad, F.; Amor, M.; Karcher, G.; Maurin, P.; Ethevenot, G.; Sebag, C.; Bertrand, A.; Pernot, C.; Gilgenkrantz, J.M.

    1988-06-01

    Diltiazem is a calcium antagonist with demonstrated experimental cardioprotective effects. Its effects on myocardial infarct size were studied in 34 patients admitted within 6 hours after the first symptoms of acute myocardial infarction. These patients were randomized, double-blind to placebo or diltiazem (10-mg intravenous bolus followed by 15 mg/hr intravenous infusion during 72 hours, followed by 4 X 60 mg during 21 days). Myocardial infarct size was assessed by plasma creatine kinase and creatine kinase-MB indexes, perfusion defect scores using single-photon emission computed tomography with thallium-201 and left ventricular ejection fraction measured by radionuclide angiography. Tomographic and angiographic scanning was performed serially before randomization, after 48 hours and 21 days later. Groups were comparable in terms of age, sex, inclusion time and baseline infarct location and size. Results showed no difference in creatine kinase and creatine kinase-MB data between controls and treated patients, a significant decrease in the perfusion defect scores in the diltiazem group (+0.1 +/- 3.0 placebo vs -2.2 +/- 1.9 diltiazem, p less than 0.02) and a better ejection fraction recovery in the diltiazem group (-4.2 +/- 7.4 placebo vs +7.7 +/- 11.2 diltiazem, p less than 0.05). Myocardial infarct size estimates from perfusion defect scores and enzyme data were closely correlated. These preliminary results suggest that diltiazem may reduce ischemic injury in acute myocardial infarction.

  10. [Treatment of acute myocardial infarction with betareceptor blocking agents. I. Hemodynamic effects of Propranolol in combination with digitalis (author's transl)].

    PubMed

    Oeff, M; Lehmann, H U; Witt, E; Hochrein, H

    1981-06-01

    In the acute stage of transmural myocardial infarction, 22 patients ranging in age from 34 to 76 (mean 61.6) were given propranolol- because of its alleged myocardium-protecting properties - intravenously at a dosage of 0.03 to 0.1 mg/kg body weight under conditions of continuous hemodynamic control. Subsequently, the influence of digoxin, administered i. v. at a dosage of 0.01 my/kg body weight, on the negative-inotropic propranolol effects was examined. A hemodynamic comparison was made of the effects of propranolol before and after digitalis administration. In patients with compensated cardiac function (group 1, 16 patients), the propranolol-induced drop in the left ventricular stroke-work-index and rise in the left-ventricular filling pressure was completely compensated again by digitalis. The frequency-decreasing propranolol effect was nor influenced by digitalis. In patients with cardiac decompensation (group 2, 6 patients) digitalis only led to a renewed compensation of the left-ventricular stroke-work-index, the rise of the left-ventricular filling pressure remained unaffected. It follows from that, in cases of myocardial infarction without cardial decompensation, propranolol requires concomitant digitalisation. In cases of already existent myocardial insufficiency, propranolol can produce an unfavorable increase of the decompensation signs. PMID:7257499

  11. The effect of atmospheric temperature and pressure on the occurrence of acute myocardial infarction in Kaunas.

    PubMed

    Radišauskas, Ričardas; Vaičiulis, Vidmantas; Ustinavičienė, Rūta; Bernotienė, Gailutė

    2013-01-01

    OBJECTIVE. The aim of the study was to evaluate the impact of meteorological variables (atmospheric temperature and pressure) on the daily occurrence of acute myocardial infarction (AMI). MATERIAL AND METHODS. The study used the daily values of atmospheric temperature and pressure in 2000-2007. The meteorological data were obtained from the Lithuanian Hydrometeorological Service for Kaunas. The relative risks of event occurrence were computed for 5°C atmospheric temperature and for 10-hPa atmospheric pressure variations by means of the Poisson regression model. RESULTS. The occurrence of AMI and atmospheric temperature showed an inverse linear relationship, while the occurrence of AMI and atmospheric pressure, a positive linear relationship. Among the youngest subjects (25-44 years old), no relationships were detected. Contrary, among the subjects aged 45-64 years and those aged 65 years and older, the occurrence of AMI significantly decreased with higher temperature (P=0.001 and P=0.002, respectively). A decrease in atmospheric temperature by 10ºC reduced the risk of AMI by 8.7% in the age groups of 45-64 and 65 years and older and by 19% in the age group of 25 years and older. Among the first AMI cases, the risk increased by 7.5% in the age group of 45-64-year olds and by 6.4% in the age group of 25-64-year olds. The relationship between atmospheric temperature and pressure, and AMI occurrence was found to be linear but inverse. An increase in atmospheric pressure by 10 hPa resulted in an increase in risk by 4% among the subjects aged 65 years and more and by 3% among the subjects aged 25 years and more. CONCLUSIONS. Atmospheric temperature and pressure variations had the greatest effect on middle-aged and aging subjects (starting from 45 years). At younger age, the effect of such factors on the AMI risk was considerably lower.

  12. Temperature, Myocardial Infarction, and Mortality: Effect Modification by Individual and Area-Level Characteristics

    PubMed Central

    Madrigano, Jaime; Mittleman, Murray A.; Baccarelli, Andrea; Goldberg, Robert; Melly, Steven; von Klot, Stephanie; Schwartz, Joel

    2014-01-01

    Background While several studies have examined associations between temperature and cardiovascular-disease-related mortality, fewer have investigated the association between temperature and the development of acute myocardial infarction (MI). Moreover, little is known about who is most susceptible to the effects of temperature. Methods We analyzed data from the Worcester Heart Attack Study, a community-wide investigation of acute MI in residents of the Worcester (MA) metropolitan area. We used a case-crossover approach to examine the association of apparent temperature with acute MI occurrence and with all-cause in-hospital and post-discharge mortality. We examined effect modification by sociodemographic characteristics, medical history, clinical complications, and physical environment. Results A decrease in an interquartile range (IQR) in apparent temperature was associated with an increased risk of acute MI on the same day (hazard ratio=1.15 [95% confidence interval= 1.01–1.31]). Extreme cold during the 2 days prior was associated with an increased risk of acute MI (1.36 [1.07–1.74]). Extreme heat during the two days prior was also associated with an increased risk of mortality (1.44 [1.06–1.96]). Persons living in areas with greater poverty were more susceptible to heat. Conclusions Exposure to cold increased the risk of acute MI, and exposure to heat increased the risk of dying after an acute MI. Local area vulnerability should be accounted for as cities prepare to adapt to weather fluctuations as a result of climate change. PMID:23462524

  13. Effect of Eye Movement Desensitization and Reprocessing (EMDR) on Depression in Patients With Myocardial Infarction (MI)

    PubMed Central

    Behnammoghadam, Mohammad; Alamdari, Ali Karam; Behnammoghadam, Aziz; Darban, Fatemeh

    2015-01-01

    Background: Coronary heart disease is the most important cause of death and inability in all communities. Depressive symptoms are frequent among post-myocardial infarction (MI) patients and may cause negative effects on cardiac prognosis. This study was conducted to identify efficacy of EMDR on depression of patients with MI. Methods: This study is a clinical trial. Sixty patients with MI were selected by simple sampling, and were separated randomly into experimental and control groups. To collect data, demographic questionnaire and Beck Depression Questionnaire were used. In experimental group, EMDR therapy were performed in three sessions alternate days for 45–90 minutes, during four months after their MI. Depression level of patients was measured before, and a week after EMDR therapy. Data were analyzed using paired –t- test, t–test, and Chi-square. Results: The mean depression level in experimental group 27.26± 6.41 before intervention, and it was 11.76 ± 3.71 after intervention. Hence, it showed a statistically significant difference (P<0.001). The mean depression level in control group was 24.53 ± 5.81 before intervention, and it was 31.66± 6.09 after intervention, so it showed statistically significant difference (P<0.001). The comparison of mean depression level at post treatment, in both groups showed statistically significant difference (P<0.001). Conclusion: EMDR is an effective, useful, efficient, and non-invasive method for treatment and reducing depression in patients with MI. PMID:26153191

  14. [Effect of complications in the acute period of myocardial infarction on physical exertion tolerance at the hospital stage of rehabilitation].

    PubMed

    Al'khimovich, V M; Golubev, V G; Rudina, M D; Rusetskaia, V G

    1988-11-01

    Physical stress tolerance and its hemodynamic support were examined in 95 patients with early myocardial infarction, 50 normal subjects and 25 coronary patients. It is suggested that the stress tolerance test is advisable at an early stage of complicated macrofocal myocardial infarction. The safety of the test improves considerably where it is performed under continuous electrocardiographic and chest-rheographic control. An abnormal diastolic impedance wave, emerging during exercise, may serve an additional diagnostic indicator of stress intolerance.

  15. Exosomes and cardiac repair after myocardial infarction.

    PubMed

    Sahoo, Susmita; Losordo, Douglas W

    2014-01-17

    Myocardial infarction is a leading cause of death among all cardiovascular diseases. The analysis of molecular mechanisms by which the ischemic myocardium initiates repair and remodeling indicates that secreted soluble factors are key players in communication to local and distant tissues, such as bone marrow. Recently, actively secreted membrane vesicles, including exosomes, are being recognized as new candidates with important roles in intercellular and tissue-level communication. In this review, we critically examine the emerging role of exosomes in local and distant microcommunication mechanisms after myocardial infarction. A comprehensive understanding of the role of exosomes in cardiac repair after myocardial infarction could bridge a major gap in knowledge of the repair mechanism after myocardial injury.

  16. Omega-3 Fatty Acids Do Not Protect Against Arrhythmias in Acute Nonreperfused Myocardial Infarction Despite Some Antiarrhythmic Effects.

    PubMed

    Mączewski, Michał; Duda, Monika; Marciszek, Mariusz; Kołodziejczyk, Joanna; Dobrzyń, Paweł; Dobrzyń, Agnieszka; Mackiewicz, Urszula

    2016-11-01

    Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). To elucidate the effect of the omega-3 polyunsaturated fatty acids (PUFAs) on ventricular arrhythmias in acute nonreperfused MI, rats were fed with normal or eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA)-enriched diet for 3 weeks. Subsequently the rats were subjected to either MI induction or sham operation. ECG was recorded for 6 h after the operation and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. Six hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca(2+) handling was assessed and expression of proteins involved in Ca(2+) turnover was studied separately in non-infarcted left ventricle wall and infarct borderzone. EPA and DHA had no effect on occurrence of post-MI ventricular arrhythmias or mortality. Nevertheless, DHA but not EPA prevented Ca(2+) overload in LV cardiomiocytes and improved rate of Ca(2+) transient decay, protecting PMCA and SERCA function. Moreover, both EPA and DHA prevented MI-induced hyperphosphorylation of ryanodine receptors (RyRs) as well as dispersion of action potential duration (APD) in the left ventricular wall. In conclusion, EPA and DHA have no antiarrhythmic effect in the non-reperfused myocardial infarction in the rat, although these omega-3 PUFAs and DHA in particular exhibit several potential antiarrhythmic effects at the subcellular and tissue level, that is, prevent MI-induced abnormalities in Ca(2+) handling and APD dispersion. In this context further studies are needed to see if these potential antiarrhythmic effects could be utilized in the clinical setting. J. Cell. Biochem. 117: 2570-2582, 2016. © 2016 Wiley Periodicals, Inc.

  17. 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

  18. [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

  19. [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.

  20. 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

  1. Effect of Streptokinase on Reperfusion After Acute Myocardial Infarction and Its Complications: An Ex-Post Facto Study

    PubMed Central

    Taheri, Leila; Zargham-Boroujeni, Ali; Jahromi, Marzieh Kargar; Charkhandaz, Maryam; Hojat, Mohsen

    2015-01-01

    Introduction: Emergency treatment of patients with acute myocardial infarction is very important. Streptokinase in Iran is often as the only clot-busting medication is used. The purpose of using streptokinase medication is to revive the ischemic heart tissue, although has dangerous complications too. Therefore, the present study aimed to determine the effect of streptokinase on reperfusion after acute myocardial infarction and its complications, has been designed and conducted. Materials and Methods: This is an Ex-post facto study. The study population included patients who suffer from acute myocardial infarction. The sample size was 300 patients, and 2 groups were matched, in variables of age, sex, underlying disease, frequencies and area of MI. Data collection did by researcher making questionnaire, that accept face and content validity by 10 expert researcher, the reliability was conducted with Spearman’s test (r=0.85) by Test-retest method. Data analysis did by SPSS software: V 12. Findings: Mean of EF in SK group was (46.15±8.11) and in control group was (43.11±12.57). Significant relationship was seen between SK, arrhythmia occurring and improve EF reperfusion by chi-square test (p=0.028), (p=0.020). The most arrhythmia in SK group was Ventricular Tachycardia (20.7%). Significant statistical relation between SK and mortality were found by Chi-square test (p=0.001). But a meaningful statistical relation was not found between SK and pulmonary edema incidence (p=0.071). Conclusions: Nurses of CCU should be aware about SK complications such as hypotension, bleeding and arrhythmias. Proposed compare SK and tissue plasminogen drug in reperfusion and complications effect. PMID:25946921

  2. Effect of exercise training and myocardial infarction on force development and contractile kinetics in isolated canine myocardium.

    PubMed

    Canan, Benjamin D; Haizlip, Kaylan M; Xu, Ying; Monasky, Michelle M; Hiranandani, Nitisha; Milani-Nejad, Nima; Varian, Kenneth D; Slabaugh, Jessica L; Schultz, Eric J; Fedorov, Vadim V; Billman, George E; Janssen, Paul M L

    2016-04-15

    It is well known that moderate exercise training elicits a small increase in ventricular mass (i.e., a physiological hypertrophy) that has many beneficial effects on overall cardiac health. It is also well known that, when a myocardial infarction damages part of the heart, the remaining myocardium remodels to compensate for the loss of viable functioning myocardium. The effects of exercise training, myocardial infarction (MI), and their interaction on the contractile performance of the myocardium itself remain largely to be determined. The present study investigated the contractile properties and kinetics of right ventricular myocardium isolated from sedentary and exercise trained (10-12 wk progressively increasing treadmill running, begun 4 wk after MI induction) dogs with and without a left ventricular myocardial infarction. Exercise training increased force development, whereas MI decreased force development that was not improved by exercise training. Contractile kinetics were significantly slower in the trained dogs, whereas this impact of training was less or no longer present after MI. Length-dependent activation, both evaluated on contractile force and kinetics, was similar in all four groups. The control exercise-trained group exhibited a more positive force-frequency relationship compared with the sedentary control group while both sedentary and trained post-MI dogs had a more negative relationship. Last, the impact of the β-adrenergic receptor agonist isoproterenol resulted in a similar increase in force and acceleration of contractile kinetics in all groups. Thus, exercise training increased developed force but slowed contractile kinetics in control (noninfarcted animals), actions that were attenuated or completely absent in post-MI dogs.

  3. 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

  4. B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

    PubMed Central

    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

    2014-01-01

    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 Ly6Chi 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

  5. 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.

  6. Postmortem detection of inapparent myocardial infarction

    PubMed Central

    McVie, J. G.

    1970-01-01

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

  7. The effect of acute hypercholesterolemia on myocardial infarct size and the no-reflow phenomenon during coronary occlusion-reperfusion.

    PubMed

    Golino, P; Maroko, P R; Carew, T E

    1987-01-01

    The goal of this study was to determine the effects of acute hypercholesterolemia on the evolution of myocardial infarction in a preparation of coronary occlusion-reperfusion. New Zealand white rabbits were fed a 2% cholesterol-enriched diet for 3 days (plasma cholesterol 329 +/- 70 mg/dl), or maintained on the control diet (plasma cholesterol 67 +/- 12 mg/dl). Temporary (30 min) coronary artery occlusion was performed in open-chest rabbits with a suture snare. The snare was released to permit reperfusion. When the animals were killed 5.5 hr later, left ventricles were cut into 3 mm slices. Infarct size was determined by planimetry of tetrazolium-stained slices while the area at risk of infarction (hypoperfused zone) was determined by planimetry of the "cold spots" on autoradiograms of the slices that contained 99m Tc-labeled microspheres that had been injected 1 min after occlusion. Infarct size, expressed as percent of the hypoperfused zone, was 42.8 +/- 1.3% (n = 10) in the control group and was increased by approximately 100% in cholesterol-fed animals to 83.7 +/- 2.0% (n = 10, p less than .001). To test the hypothesis that vascular obstruction (no reflow) might account for the larger infarct size, thioflavin S was injected immediately before the animals were killed to demarcate perfused myocardium in three additional groups of animals: standard chow-fed rabbits (n = 5), cholesterol-fed rabbits (n = 5), and standard chow-fed rabbits that, in addition, received an infusion of isoproterenol (0.1 microgram/kg/min, n = 6), an intervention believed to increase infarct size through a mechanism not dependent on the no-reflow phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

  8. 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.

  9. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    PubMed Central

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Vesey, Alex T; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L; Fletcher, Alison M; van Beek, Edwin J R; Rudd, James H F; Fox, Keith A A; Dweck, Marc R; Newby, David E

    2015-01-01

    Background Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans. Methods and Results Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non–ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI. Conclusions The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization

  10. Effects of creatinol O-phosphate on serum enzymes in acute myocardial infarction.

    PubMed

    Knippel, M; Bana, G; Pusterla, G L

    1979-01-01

    Two groups of 23 patients, each with acute myocardial infarction, were treated. The first group (control) received glucose-insuline-K+ (GIK) over a 3-day period, and the second GIK and N-methyl-N-(beta-hydroxyethyl) guanidine O-phosphate (creatinol O-phosphate, COP) (3.06 g i.v./24 h), again for a 3-day period. The six enzymes investigated, i. e. GOT, GPT, LDH, HBDH, CK and MBCK, all decreased between 33 and 49% in the COP group as compared with the control group, reaching a degree of statistical significance of less than 0.01. The decrease in these enzymes was attributed to the protective action of COP on the cell membrane permeability, in agreement with a series of previous papers.

  11. An unusual adverse effect of sildenafil citrate: acute myocardial infarction in a nitrate-free patient.

    PubMed

    Cakmak, Huseyin Altug; Ikitimur, Baris; Karadag, Bilgehan; Ongen, Zeki

    2012-10-19

    Myocardial infarction (MI) associated with sildenafil citrate is seen rarely in patients without any history of coronary artery disease. We report a nitrate-free patient with a history of cardiovascular risk factors who developed acute MI after taking sildenafil. A 44-year-old man diagnosed with acute anterior ST segment elevation MI 120 min after self-administration of 150 mg sildenafil was admitted before attempting any sexual intercourse. The coronary angiography revealed 99% occlusion of the left anterior descending artery (LAD) and a bare-metal stent was implanted. He was discharged after 5 days without any complication. Sildenafil may cause coronary steal or may lead to vasodilation causing hypotension in patient with pre-existing cardiovascular disease, especially in patients on nitrate therapy. Our patient was nitrate free, with normal blood pressure values. Emotional stimulation associated with anticipated sexual activity may have been a triggering factor for vulnerable coronary plaque rupture.

  12. Nanog expression in heart tissues induced by acute myocardial infarction.

    PubMed

    Luo, Huanhuan; Li, Qiong; Pramanik, Jogen; Luo, Jiankai; Guo, Zhikun

    2014-10-01

    Nanog is a potential stem cell marker and is considered a regeneration factor during tissue repair. In the present study, we investigated expression patterns of nanog in the rat heart after acute myocardial infarction by semi-quantitative RT-PCR, immunohistochemistry and Western blot analyses. Our results show that nanog at both mRNA and protein levels is positively expressed in myocardial cells, fibroblasts and small round cells in different myocardial zones at different stages after myocardial infarction, showing a spatio-temporal and dynamic change. After myocardial infarction, the nanog expression in fibroblasts and small round cells in the infarcted zone (IZ) is much stronger than that in the margin zone (MZ) and remote infarcted zone (RIZ). From day 7 after myocardial infarction, the fibroblasts and small cells strongly expressed nanog protein in the IZ, and a few myocardial cells in the MZ and the RIZ and the numbers of nanog-positive fibroblasts and small cells reached the highest peak at 21 days after myocardial infarction, but in this period the number of nanog-positive myocardial cells decreased gradually. At 28 days after myocardial infarction, the numbers of all nanog-positive cells decreased into a low level. Therefore, our data suggest that all myocardial cells, fibroblasts and small round cells are involved in myocardial reconstruction after cardiac infarction. The nanog-positive myocardial cells may respond to early myocardial repair, and the nanog-positive fibroblasts and small round cells are the main source for myocardial reconstruction after cardiac infarction.

  13. 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

  14. 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.

  15. Management of acute perioperative myocardial infarction: a case report of concomitant acute myocardial infarction and tumor bleeding in the transverse colon

    PubMed Central

    Li, Yu-Feng; Gao, Wen-Qian; Li, Yuan-Xin; Feng, Quan-Zhou; Zhu, Ping

    2016-01-01

    Acute myocardial infarction complicated by bleeding colon tumor is problematic with regard to management, and appropriate balance of antiplatelet or anticoagulation therapy and hemostasis or surgery is crucial for effective treatment. Here, we present a case of concomitant acute myocardial infarction and bleeding tumor in the transverse colon, and share our experience of successfully balancing anticoagulation therapy and hemostasis. PMID:26937182

  16. Association of stroke and myocardial infarction in children.

    PubMed

    Nakashima, M; Takashima, S; Hashimoto, K; Shiraishi, M

    1982-02-01

    A 9-year-old boy with cerebrovascular accident (CVA) and old myocardial infarction with mural thrombi is reported. The cause of the myocardial infarction was congenital coronary artery fistula originating from the left coronary artery and emptying into the right atrium. Although a common cause of strokes in adults, myocardial infarction has infrequently been reported as the source of emboli in children.

  17. Winter weather conditions and myocardial infarctions.

    PubMed

    Ohlson, C G; Bodin, L; Bryngelsson, I L; Helsing, M; Malmberg, L

    1991-03-01

    The daily number of cases of myocardial infarctions admitted to a hospital in middle Sweden over three winter seasons 1984-87 was correlated to the weather conditions on a day-to-day basis. The study encompassed 634 days and all cases younger than 70 years, living within the catchment area, in all 382 subjects. Information on temperature, wind force, precipitation and atmospheric pressure was obtained from the Swedish Institute of Meteorology and Hydrology. A low number of myocardial infarctions was seen on Saturdays and Sundays with a mild wind chill factor and on days with moderate snowfall and high atmospheric pressure. A high number was observed for workdays, especially Mondays, as day of diagnosis. Heterogeneity of the study population and a misclassification of the time relationships between dates of diagnosis and weather changes may have caused an underestimation of the impact of weather conditions. However, weather conditions do not seem to be a major triggering factor of myocardial infarctions in Sweden.

  18. Effects of reestablishing blood flow on extent of myocardial infarction in conscious dogs

    SciTech Connect

    Murdock, R.H. Jr.; Chu, A.; Grubb, M.; Cobb, F.R.

    1985-10-01

    The effects of permanent circumflex coronary artery occlusion (PO) compared with reestablishing blood flow (OR) at 2 and 6 h after occlusion on the final extent of histological infarction (HI) was assessed in chronically instrumented awake dogs. The relationships between the extent of left ventricular ischemia measured by microsphere techniques and HI in the PO group were used as models to predict the expected infarction in the 2- and 6-h OR groups. Mean HI (+/-SD) in the PO and 6- and 2-h OR groups were not significantly different. The extent of HI in samples grouped according to epicardial and endocardial layers and ischemic blood flow ranges was reduced in the 2-h but not 6-h OR group. Analysis of individual animals using total ischemic region blood flow to epicardial and endocardial layers demonstrated that OR at 2 h but not 6 h reduced infarction in most animals but not in certain animals with the largest ischemic regions.

  19. 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

  20. 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.

  1. Effects of liraglutide on left ventricular function in patients with non-ST-segment elevation myocardial infarction.

    PubMed

    Chen, Wei-Ren; Shen, Xue-Qin; Zhang, Ying; Chen, Yun-Dai; Hu, Shun-Ying; Qian, Geng; Wang, Jing; Yang, Jun-Jie; Wang, Zhi-Feng; Tian, Feng

    2016-06-01

    The influence of glucagon-like peptide-1 has been studied in several studies in patients with acute myocardial infarction, but not in patients with non-ST-segment elevation myocardial infarction (NSTEMI). We planned to evaluate the effects of liraglutide on left ventricular function in patients with NSTEMI. A total of 90 patients were randomized 1:1 to receive either liraglutide (0.6 mg for 2 days, 1.2 mg for 2 days, followed by 1.8 mg for 3 days) or placebo for 7 days. Eighty-three patients completed the trial. Transthoracic echocardiography was used to assess left ventricular function. At 3 months, the primary endpoint, the difference in the change in left ventricular ejection fraction between the two groups was +4.7 % (liraglutide vs. placebo 95 % CI +0.7 to +9.2 % P = 0.009) under intention-to-treat analysis. The difference in decrease in serum glycosylated hemoglobin levels was -0.2 % (liraglutide vs. placebo 95 % CI -0.1 to -0.3 %; P < 0.001). Inflammation and oxidative stress improved significantly in the liraglutide group compared to the placebo group. Liraglutide could improve left ventricular function in patients with NSTEMI, making it a potential adjuvant therapy for NSTEMI. PMID:26573925

  2. Multimodality noninvasive imaging for assessing therapeutic effects of exogenously transplanted cell aggregates capable of angiogenesis on acute myocardial infarction.

    PubMed

    Huang, Chieh-Cheng; Wei, Hao-Ji; Lin, Kun-Ju; Lin, Wei-Wen; Wang, Ching-Wen; Pan, Wen-Yu; Hwang, Shiaw-Min; Chang, Yen; Sung, Hsing-Wen

    2015-12-01

    Although the induction of neovascularization by cell-based approaches has demonstrated substantial potential in treating myocardial infarction (MI), the process of cell-mediated angiogenesis and its correlation with therapeutic mechanisms of cardiac repair remain elusive. In this work, three-dimensional (3D) aggregates of human umbilical vein endothelial cells (HUVECs) and cord-blood mesenchymal stem cells (cbMSCs) are constructed using a methylcellulose hydrogel system. By maximizing cell-cell and cell-ECM communications and establishing a hypoxic microenvironment in their inner cores, these cell aggregates are capable of forming widespread tubular networks together with the angiogenic marker αvβ3 integrin; they secret multiple pro-angiogenic, pro-survival, and mobilizing factors when grown on Matrigel. The aggregates of HUVECs/cbMSCs are exogenously engrafted into the peri-infarct zones of rats with MI via direct local injection. Multimodality noninvasive imaging techniques, including positron emission tomography, single photon emission computed tomography, and echocardiography, are employed to monitor serially the beneficial effects of cell therapy on angiogenesis, blood perfusion, and global/regional ventricular function, respectively. The myocardial perfusion is correlated with ventricular contractility, demonstrating that the recovery of blood perfusion helps to restore regional cardiac function, leading to the improvement in global ventricular performance. These experimental data reveal the efficacy of the exogenous transplantation of 3D cell aggregates after MI and elucidate the mechanism of cell-mediated therapeutic angiogenesis for cardiac repair.

  3. Multimodality noninvasive imaging for assessing therapeutic effects of exogenously transplanted cell aggregates capable of angiogenesis on acute myocardial infarction.

    PubMed

    Huang, Chieh-Cheng; Wei, Hao-Ji; Lin, Kun-Ju; Lin, Wei-Wen; Wang, Ching-Wen; Pan, Wen-Yu; Hwang, Shiaw-Min; Chang, Yen; Sung, Hsing-Wen

    2015-12-01

    Although the induction of neovascularization by cell-based approaches has demonstrated substantial potential in treating myocardial infarction (MI), the process of cell-mediated angiogenesis and its correlation with therapeutic mechanisms of cardiac repair remain elusive. In this work, three-dimensional (3D) aggregates of human umbilical vein endothelial cells (HUVECs) and cord-blood mesenchymal stem cells (cbMSCs) are constructed using a methylcellulose hydrogel system. By maximizing cell-cell and cell-ECM communications and establishing a hypoxic microenvironment in their inner cores, these cell aggregates are capable of forming widespread tubular networks together with the angiogenic marker αvβ3 integrin; they secret multiple pro-angiogenic, pro-survival, and mobilizing factors when grown on Matrigel. The aggregates of HUVECs/cbMSCs are exogenously engrafted into the peri-infarct zones of rats with MI via direct local injection. Multimodality noninvasive imaging techniques, including positron emission tomography, single photon emission computed tomography, and echocardiography, are employed to monitor serially the beneficial effects of cell therapy on angiogenesis, blood perfusion, and global/regional ventricular function, respectively. The myocardial perfusion is correlated with ventricular contractility, demonstrating that the recovery of blood perfusion helps to restore regional cardiac function, leading to the improvement in global ventricular performance. These experimental data reveal the efficacy of the exogenous transplantation of 3D cell aggregates after MI and elucidate the mechanism of cell-mediated therapeutic angiogenesis for cardiac repair. PMID:26386627

  4. Sensitive Troponin Assay and the Classification of Myocardial Infarction

    PubMed Central

    Shah, Anoop S.V.; McAllister, David A.; Mills, Rosamund; Lee, Kuan Ken; Churchhouse, Antonia M.D.; Fleming, Kathryn M.; Layden, Elizabeth; Anand, Atul; Fersia, Omar; Joshi, Nikhil V.; Walker, Simon; Jaffe, Allan S.; Fox, Keith A.A.; Newby, David E.; Mills, Nicholas L.

    2015-01-01

    Background Lowering the diagnostic threshold for troponin is controversial because it may disproportionately increase the diagnosis of myocardial infarction in patients without acute coronary syndrome. We assessed the impact of lowering the diagnostic threshold of troponin on the incidence, management, and outcome of patients with type 2 myocardial infarction or myocardial injury. Methods Consecutive patients with elevated plasma troponin I concentrations (≥50 ng/L; n = 2929) were classified with type 1 (50%) myocardial infarction, type 2 myocardial infarction or myocardial injury (48%), and type 3 to 5 myocardial infarction (2%) before and after lowering the diagnostic threshold from 200 to 50 ng/L with a sensitive assay. Event-free survival from death and recurrent myocardial infarction was recorded at 1 year. Results Lowering the threshold increased the diagnosis of type 2 myocardial infarction or myocardial injury more than type 1 myocardial infarction (672 vs 257 additional patients, P < .001). Patients with myocardial injury or type 2 myocardial infarction were at higher risk of death compared with those with type 1 myocardial infarction (37% vs 16%; relative risk [RR], 2.31; 95% confidence interval [CI], 1.98-2.69) but had fewer recurrent myocardial infarctions (4% vs 12%; RR, 0.35; 95% CI, 0.26-0.49). In patients with troponin concentrations 50 to 199 ng/L, lowering the diagnostic threshold was associated with increased healthcare resource use (P < .05) that reduced recurrent myocardial infarction and death for patients with type 1 myocardial infarction (31% vs 20%; RR, 0.64; 95% CI, 0.41-0.99), but not type 2 myocardial infarction or myocardial injury (36% vs 33%; RR, 0.93; 95% CI, 0.75-1.15). Conclusions After implementation of a sensitive troponin assay, the incidence of type 2 myocardial infarction or myocardial injury disproportionately increased and is now as frequent as type 1 myocardial infarction. Outcomes of patients with type 2 myocardial

  5. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction

    PubMed Central

    Hritani, Abdulwahab; Antoun, Patrick

    2016-01-01

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

  6. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction.

    PubMed

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

    2016-01-01

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

  7. Cardioprotective effects of timosaponin B II from Anemarrhenae asphodeloides Bge on isoproterenol-induced myocardial infarction in rats.

    PubMed

    Deng, Xue-Yang; Chen, Jun-Jun; Li, Hong-Yan; Ma, Zhan-Qiang; Ma, Shi-Ping; Fu, Qiang

    2015-10-01

    The aim of the present study was to investigate the cardioprotective effects of Timosaponin B II (TB), a main bioactive constituent from Anemarrhenae asphodeloides Bge, on an isoproterenol (ISO)-induced myocardial infarction model in rats and explore its underlying mechanisms. Rats were treated with TB (50 mg/kg, 100 mg/kg) or diltiazem hydrochloride (DH, 5 mg/kg) by gastric gavage for five days. At the 4th and 5th days, myocardial injury was induced by ISO injection (85 mg/kg) at an interval of 24 h for 2 consecutive days. After the induction, rats were anaesthetized with pentobarbital sodium (30 mg/kg) to record the electrocardiogram. Our research showed that ISO administration resulted in significant elevations in the ST-segment, the levels of cardiac injury biomarkers creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), and concentrations of serum proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Pretreatment with TB significantly reversed these alterations induced by ISO challenge. The cardioprotective effects of TB were further proved by the histopathological examination. Exploration of the underlying mechanisms of its actions revealed that TB pretreatment restored the ISO-induced decrease of super oxide dismutase (SOD) and the increase of malondialdehyde (MDA). Meanwhile, we found that the enhancement of antioxidant defense system might be associated with the increased heme oxygenase isoform 1 (HO-1) induction and activated nuclear respiratory factor 2 (Nrf-2) translocation. Furthermore, the present research also demonstrated that nuclear translocation of Nrf-2 and subsequent HO-1 expression might be associated with nuclear factor kappa B (NF-κB) pathway activation. Taken together, our finding demonstrated that TB might have a potential benefit in preventing ischemic heart diseases like myocardial infarction.

  8. Effects of Intracoronary Administration of Autologous Adipose Tissue-Derived Stem Cells on Acute Myocardial Infarction in a Porcine Model

    PubMed Central

    Lee, Hye Won; Park, Jong Ha; Kim, Bo Won; Ahn, Jinhee; Kim, Jin Hee; Park, Jin Sup; Oh, Jun-Hyok; Choi, Jung Hyun; Cha, Kwang Soo; Hong, Taek Jong; Park, Tae Sik; Kim, Sang-Pil; Song, Seunghwan; Kim, Ji Yeon; Park, Mi Hwa; Jung, Jin Sup

    2015-01-01

    Purpose Adipose-derived stem cells (ADSCs) are known to be potentially effective in regeneration of damaged tissue. We aimed to assess the effectiveness of intracoronary administration of ADSCs in reducing the infarction area and improving function after acute transmural myocardial infarction (MI) in a porcine model. Materials and Methods ADSCs were obtained from each pig's abdominal subcutaneous fat tissue by simple liposuction. After 3 passages of 14-days culture, 2 million ADSCs were injected into the coronary artery 30 min after acute transmural MI. At baseline and 4 weeks after the ADSC injection, 99mTc methoxyisobutylisonitrile-single photon emission computed tomography (MIBI-SPECT) was performed to evaluate the left ventricular volume, left ventricular ejection fraction (LVEF; %), and perfusion defects as well as the myocardial salvage (%) and salvage index. At 4 weeks, each pig was sacrificed, and the heart was extracted and dissected. Gross and microscopic analyses with specific immunohistochemistry staining were then performed. Results Analysis showed improvement in the perfusion defect, but not in the LVEF in the ADSC group (n=14), compared with the control group (n=14) (perfusion defect, -13.0±10.0 vs. -2.6±12.0, p=0.019; LVEF, -8.0±15.4 vs. -15.9±14.8, p=0.181). There was a tendency of reducing left ventricular volume in ADSC group. The ADSCs identified by stromal cell-derived factor-1 (SDF-1) staining were well co-localized by von Willebrand factor and Troponin T staining. Conclusion Intracoronary injection of cultured ADSCs improved myocardial perfusion in this porcine acute transmural MI model. PMID:26446632

  9. [Myocardial infarction as a work-related occurrence].

    PubMed

    Szozda, R; Procek, M

    1995-01-01

    An accident is a work-related event caused by an external factor. The aim of this work is to present a cause-effect relationship between myocardial infarction and working conditions. An attitude of the Supreme Court to the question of certification highlighting key issues and facilitating the understanding of the problem is also presented. Myocardial infarction as a work-related accident is an issue of both law and medicine, and particularly, occupational medicine that will have to deal and solve this problem in the near future.

  10. Cannabis: a trigger for acute myocardial infarction? A case report.

    PubMed

    Cappelli, Francesco; Lazzeri, Chiara; Gensini, Gian Franco; Valente, Serafina

    2008-07-01

    Cannabis smoking is consistently increasing in Europe and after alcohol it is the most common recreational drug in the western world. Users and lay people believe that marijuana or hashish is safe. Over the past four decades, however, it has been well established that cannabis has pathophysiological effects on the cardiovascular system. Information concerning the link between cannabis consumption and myocardial infarction is limited and existing data are controversial on this topic. In our case report, we describe a case of a young man who after smoking marijuana experienced ST elevation myocardial infarction caused by acute thrombosis of the descending artery, submitted to efficacious primary coronary angioplasty. PMID:18545075

  11. 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

  12. Anti-inflammatory, Antithrombotic and Cardiac Remodeling Preventive Effects of Eugenol in Isoproterenol-Induced Myocardial Infarction in Wistar Rat.

    PubMed

    Mnafgui, Kais; Hajji, Raouf; Derbali, Fatma; Gammoudi, Anis; Khabbabi, Gaddour; Ellefi, Hedi; Allouche, Noureddine; Kadri, Adel; Gharsallah, Neji

    2016-10-01

    This study aimed to evaluate the antithrombotic, anti-inflammatory and anti-cardiac remodeling properties of eugenol in isoproterenol-induced myocardial infarction in rats. Male Wistar rats were randomly divided into four groups, control, iso [100 mg/kg body weight was injected subcutaneously into rats at an interval of 24 h for 2 days (6th and 7th day) to induce MI] and pretreated animals with clopidogrel (0.2 mg/kg) and eugenol (50 mg/kg) orally for 7 days and intoxicated with isoproterenol (Iso + Clop) and (Iso + EG) groups. Isoproterenol-induced myocardial infarcted rats showed notable changes in the ECG pattern, increase in heart weight index, deterioration in the hemodynamic function and rise in plasma level of troponin-T, CK-MB and LDH and ALT by 316, 74, 172 and 45 %, respectively, with histological myocardium necrosis and cells inflammatory infiltration. In addition, significant increases in plasma levels of inflammatory biomarkers such as fibrinogen, α1, α2, β1, β2 and γ globulins with decrease level of albumin were observed in infarcted rats as compared to normal ones. Else, the angiotensin-converting enzyme (ACE) activity in plasma, kidney and heart of the isoproterenol-induced rats was significantly increased by 34, 47 and 93 %, respectively, as compared to normal group. However, the administration of eugenol induced a clear improvement in cardiac biomarkers injury, reduced inflammatory mediators proteins, increased heart activities of superoxide dismutase and glutathione peroxidase with reduce in thiobarbituric acid-reactive substances content and inhibition of ventricular remodeling process through inhibition of ACE activity. Overall, eugenol evidences high preventive effects from cardiac remodeling process.

  13. Effect of Beta-Blocker Dose on Survival after Acute Myocardial Infarction

    PubMed Central

    Goldberger, Jeffrey J.; Bonow, Robert O.; Cuffe, Michael; Liu, Lei; Rosenberg, Yves; Shah, Prediman K.; Smith, Sidney C.; Subačius, Haris

    2015-01-01

    Background Beta-blocker therapy after acute myocardial infarction (MI) improves survival. Beta-blocker doses used in clinical practice are often substantially lower than those used in the randomized trials establishing their efficacy. Objective This study evaluated the association of beta-blocker dose with survival after acute MI, hypothesizing that higher dose beta-blocker therapy will be associated with increased survival. Methods A multicenter registry enrolled 7,057 consecutive patients with acute MI. Discharge beta-blocker dose was indexed to the target beta-blocker doses used in randomized clinical trials, grouped as >0% to 12.5%, >12.5% to 25%, >25% to 50%, and >50% of target dose. Follow-up vital status was assessed, with the primary endpoint of time-to-death right-censored at 2 years. Multivariable and propensity score analyses were used to account for group differences. Results Of 6,682 with follow-up (median 2.1 years), 91.5% were discharged on beta-blocker (mean dose 38.1%). Lower mortality was observed with all beta-blocker doses (p < 0.0002) versus no beta-blocker therapy. After multivariable adjustment, hazard ratios (HRs) for 2-year mortality compared with the >50% dose were 0.862 (95% confidence interval [CI]: 0.677 to 1.098), 0.799 (95% CI: 0.635 to 1.005), and 0.963 (95% CI: 0.765 to 1.213) for the >0% to 12.5%, >12.5% to 25%, and >25% to 50% of target dose, respectively. Multivariable analysis with an extended set of covariates and propensity score analysis also demonstrated that higher doses were not associated with better outcome. Conclusions These data do not demonstrate increased survival in patients treated with beta-blocker doses approximating those used in prior randomized clinical trials compared with lower doses. These findings provide the rationale to re-engage in research to establish appropriate beta-blocker dosing following MI to derive optimal benefit from this therapy. (The PACE-MI Registry Study - Outcomes of Beta-blocker Therapy

  14. 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…

  15. [Myocardial infarction after conduction electrical weapon shock].

    PubMed

    Ben Ahmed, H; Bouzouita, K; Selmi, K; Chelli, M; Mokaddem, A; Ben Ameur, Y; Boujnah, M R

    2013-04-01

    Controversy persists over the safety of conducted electrical weapons, which are increasingly used by law enforcement agencies around the world. We report a case of 33-year-old man who had an acute inferior myocardial infarction after he was shot in the chest with an electrical weapon.

  16. Preoperative myocardial ischaemia: its relation to perioperative infarction.

    PubMed Central

    Yousif, H; Davies, G; Westaby, S; Prendiville, O F; Sapsford, R N; Oakley, C M

    1987-01-01

    One hundred consecutive patients undergoing coronary artery bypass surgery were randomly allocated to a preoperative (24 h) intravenous infusion of isosorbide dinitrate (1.5-15 mg/hr) (50 patients) or to placebo (50 patients). The characteristics of the two groups were similar. Evidence of acute myocardial ischaemia was sought by continuous electrocardiographic Holter recordings and acute myocardial infarction by the appearance of new Q waves and increased activity of the creatine kinase MB isoenzyme. Episodes of acute myocardial ischaemia were found in 18% of patients in the control group and in none of those who received isosorbide dinitrate. None the less, the frequency of perioperative myocardial infarction was similar (22% and 18% respectively) in the two groups. Perioperative infarction was significantly more common in women, in patients with unstable angina or poor left ventricular function, in those who had coronary endarterectomy, and in those in whom the aortic clamping time was greater than 50 minutes. These factors may have obscured any effect that prevention of preoperative ischaemia had on perioperative infarction. Preoperative infusion of isosorbide dinitrate eliminated preoperative ischaemia but did not influence the occurrence of perioperative infarction. The probable benefits of prevention of preoperative ischaemia on postoperative left ventricular function, which is a determinant of long term survival, remain to be established. PMID:3304371

  17. Effect of Metformin Treatment on Lipoprotein Subfractions in Non-Diabetic Patients with Acute Myocardial Infarction: A Glycometabolic Intervention as Adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III) Trial

    PubMed Central

    Eppinga, Ruben N.; Hartman, Minke H. T.; van Veldhuisen, Dirk J.; Lexis, Chris P. H.; Connelly, Margery A.; Lipsic, Erik; van der Horst, Iwan C. C.; van der Harst, Pim; Dullaart, Robin P. F.

    2016-01-01

    Objective Metformin affects low density lipoprotein (LDL) and high density (HDL) subfractions in the context of impaired glucose tolerance, but its effects in the setting of acute myocardial infarction (MI) are unknown. We determined whether metformin administration affects lipoprotein subfractions 4 months after ST-segment elevation MI (STEMI). Second, we assessed associations of lipoprotein subfractions with left ventricular ejection fraction (LVEF) and infarct size 4 months after STEMI. Methods 371 participants without known diabetes participating in the GIPS-III trial, a placebo controlled, double-blind randomized trial studying the effect of metformin (500 mg bid) during 4 months after primary percutaneous coronary intervention for STEMI were included of whom 317 completed follow-up (clinicaltrial.gov Identifier: NCT01217307). Lipoprotein subfractions were measured using nuclear magnetic resonance spectroscopy at presentation, 24 hours and 4 months after STEMI. (Apo)lipoprotein measures were obtained during acute STEMI and 4 months post-STEMI. LVEF and infarct size were measured by cardiac magnetic resonance imaging. Results Metformin treatment slightly decreased LDL cholesterol levels (adjusted P = 0.01), whereas apoB remained unchanged. Large LDL particles and LDL size were also decreased after metformin treatment (adjusted P<0.001). After adjustment for covariates, increased small HDL particles at 24 hours after STEMI predicted higher LVEF (P = 0.005). In addition, increased medium-sized VLDL particles at the same time point predicted a smaller infarct size (P<0.001). Conclusion LDL cholesterol and large LDL particles were decreased during 4 months treatment with metformin started early after MI. Higher small HDL and medium VLDL particle concentrations are associated with favorable LVEF and infarct size. PMID:26808474

  18. [The perioperative myocardial infarction - an interdisciplinary task].

    PubMed

    Karatolios, Konstantinos; Rolfes, Caroline; Wulf, Hinnerk; Schieffer, Bernhard

    2016-09-01

    Cardiovascular complications, particularly perioperative myocardial infarction (PMI), are major contributors to mortaliyt after noncardiac surgery. PMI often occurs unnoticed without symptoms or ECG changes. Despite ist silent presentation, PMI is associated with increased mortality. The combination of high associated mortality and diagnostic challenges mandates increased awareness of PMI. Perioperative myocardial infarction may result from plaque rupture (PMI type I) or be caused by a myocardial supply-demand imbalance of oxygen without plaque rupture (PMI type II). Most PMIs occur within the first 3 days after surgery, highlighting the need for clinical monitoring in order to allow fast diagnosis and initiation of appropriate therapy. Measurement of cardiac troponin and 12-lead ECG are the diagnostic cornerstone. Therapy of PMI represents a challenge for physicians and requires a collaboration of surgeons, anesthesiologists and cardiologists. PMID:27631445

  19. 5-Lipoxygenase facilitates healing after myocardial infarction.

    PubMed

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

    2013-07-01

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

  20. Holmium:YAG laser coronary angioplasty in acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Topaz, On; Luxenberg, Michael; Schumacher, Audrey

    1994-07-01

    Patients who sustain complicated acute myocardial infarction in whom thrombolytic agents either fail or are contraindicated often need mechanical revascularization other than PTCA. In 24 patients with acute infarction complicated by continuous chest pain and ischemia who either received lytics or with contraindication to lytics, a holmium:YAG laser (Eclipse Surgical Technologies, Palo Alto, CA) was utilized for thrombolysis and plaque ablation. Clinical success was achieved in 23/24 patients, with 23 patients (94%) surviving the acute infarction. Holmium:YAG laser is very effective and safe in thrombolysis and revascularization in this complicated clinical setting.

  1. Effects of Rosuvastatin and MiR-126 on Myocardial Injury Induced by Acute Myocardial Infarction in Rats: Role of Vascular Endothelial Growth Factor A (VEGF-A)

    PubMed Central

    Fei, Ling; Zhang, Jun; Niu, Heping; Yuan, Chen; Ma, Xiaoli

    2016-01-01

    Background The present study investigated the effects of VEGF-A targeted by miR-126 on myocardial injury after acute myocardial infarction (AMI) in rats, along with the contributions of rosuvastatin to the synergic effect. Material/Methods SD rats were obtained to construct AMI models by ligating their left anterior descending coronary arteries (LAD). We conducted echocardiography to check the 6 involved indexes: left ventricular ejection fractions (LVEF), fractional shortening (FS), left ventricular end-systolic volume (LVV), left ventricular end-diastolic volume (LVVd), cardiac output (CO), and heart rate (HR). Moreover, antibody sandwich enzyme-linked immunosorbent assay was carried out to determine MI markers: creatine kinase (CK), CK Isoenzyme (CK-MB), and Troponin I (cTn I). Dual-Luciferase Reporter Assay was performed to confirm the targeting of miR-126 and VEGF-A. MTT assay provided insight into the proliferation of myocardial fibroblasts. Finally, RT-RCR and Western blot were used for the detection of miR-126 and VEGF-A expressions in vivo and in vitro. Results Luciferase activity assay showed that miR-126 transfection significantly decreased the relative luciferase activity in HEK293T cells when it was bound to normal 3′ UTR of VEGF-A (P<0.05). In comparison to the control group, rats in the AMI model group had significantly lower LVEF, FS, and CO, and substantially higher LVVs, LVVd, HR, CK/U, CK-MB/U, and cTn-1/U (all P<0.05). Down-regulated miR-126 and up-regulated VEGF-A were also observed in MI models (P<0.05). Conclusions miR-126 and rosuvastatin have protective effects on AMI risk, and VEGF-A antagonizes effects on AMI is imposed by. PMID:27376405

  2. 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

  3. Adaptation to a Myocardial Infarction from a Developmental Perspective.

    ERIC Educational Resources Information Center

    Meyer, Robert

    1983-01-01

    Explored the interactional effect between victims' (N=30) adult developmental stage and their coping and emotional reactions following a myocardial infarction (MI). The findings point to the usefulness of adult developmental psychology in understanding the divergent emotional and coping reactions of MI patients across the life-cycle. (Author/JAC)

  4. Myocardial Infarction in a Premenopausal Woman on Leuprolide Therapy

    PubMed Central

    Perez, Irving E.; Menegus, Mark A.; Taub, Cynthia C.

    2015-01-01

    Premenopausal women with chest pain syndrome may have nonatherosclerotic coronary arteries with abnormal coronary flow. Estrogens have cardioprotective effect improving coronary vasodilatation. This case report discusses the consequences of leuprolide use by decreasing estrogen levels which led to acute myocardial infarction. PMID:26199626

  5. Biomaterial strategies for alleviation of myocardial infarction

    PubMed Central

    Venugopal, Jayarama Reddy; Prabhakaran, Molamma P.; Mukherjee, Shayanti; Ravichandran, Rajeswari; Dan, Kai; Ramakrishna, Seeram

    2012-01-01

    World Health Organization estimated that heart failure initiated by coronary artery disease and myocardial infarction (MI) leads to 29 per cent of deaths worldwide. Heart failure is one of the leading causes of death in industrialized countries and is expected to become a global epidemic within the twenty-first century. MI, the main cause of heart failure, leads to a loss of cardiac tissue impairment of left ventricular function. The damaged left ventricle undergoes progressive ‘remodelling’ and chamber dilation, with myocyte slippage and fibroblast proliferation. Repair of diseased myocardium with in vitro-engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for heart failure patients. These events reflect an apparent lack of effective intrinsic mechanism for myocardial repair and regeneration. Motivated by the desire to develop minimally invasive procedures, the last 10 years observed growing efforts to develop injectable biomaterials with and without cells to treat cardiac failure. Biomaterials evaluated include alginate, fibrin, collagen, chitosan, self-assembling peptides, biopolymers and a range of synthetic hydrogels. The ultimate goal in therapeutic cardiac tissue engineering is to generate biocompatible, non-immunogenic heart muscle with morphological and functional properties similar to natural myocardium to repair MI. This review summarizes the properties of biomaterial substrates having sufficient mechanical stability, which stimulates the native collagen fibril structure for differentiating pluripotent stem cells and mesenchymal stem cells into cardiomyocytes for cardiac tissue engineering. PMID:21900319

  6. The Effect of PAI-1 4G/5G Polymorphism and Clinical Factors on Coronary Artery Occlusion in Myocardial Infarction

    PubMed Central

    Parpugga, Tajinder Kumar; Tatarunas, Vacis; Skipskis, Vilius; Kupstyte, Nora; Zaliaduonyte-Peksiene, Diana; Lesauskaite, Vaiva

    2015-01-01

    Objective. Data on the impact of PAI-1-675 4G/5G genotype for fibrinolysis during myocardial infarction are inconsistent. The aim of our study was to evaluate the association of clinical and genetic (PAI-1-675 4G/5G polymorphism) factors with coronary artery occlusion in patients with myocardial infarction. Materials and Methods. PAI-1-675 4G/5G detection was achieved by using Sanger sequencing in a sample of patients hospitalized for stent implantation due to myocardial infarction. We categorized the patients into two groups: patients with coronary artery occlusion and patients without coronary artery occlusion according to angiographic evaluation. Results. We identified n = 122 (32.4%) 4G/4G, n = 186 (49.5%) 4G/5G, and n = 68 (18.1%) 5G/5G PAI-1 genotype carriers. Univariate and multivariate analysis showed that only the 4G/5G genotype was associated with coronary artery occlusion (OR: 1.656 and 95% CI: 1.009–2.718, p = 0.046). Conclusions. Our results showed that carriers of PAI-1 4G/5G genotype with myocardial infarction have increased odds of coronary artery occlusion more than 1.6 times in comparison to the carriers of homozygous genotypes. PMID:26273123

  7. Aliskiren and valsartan mediate left ventricular remodeling post-myocardial infarction in mice through MMP-9 effects.

    PubMed

    Ramirez, Trevi A; Iyer, Rugmani Padmanabhan; Ghasemi, Omid; Lopez, Elizabeth F; Levin, Daniel B; Zhang, Jianhua; Zamilpa, Rogelio; Chou, Youn-Min; Jin, Yu-Fang; Lindsey, Merry L

    2014-07-01

    We evaluated whether aliskiren, valsartan, or a combination of both was protective following myocardial infarction (MI) through effects on matrix metalloproteinase (MMP)-9. C57BL/6J wild type (WT, n=94) and MMP-9 null (null, n=85) mice were divided into 4 groups at 3h post-MI: saline (S), aliskiren (A; 50mg/kg/day), valsartan (V; 40mg/kg/day), or A+V and compared to no MI controls at 28days post-MI. All groups had similar infarct areas, and survival rates were higher in the null mice. The treatments influenced systolic function and hypertrophy index, as well as extracellular matrix (ECM) and inflammatory genes in the remote region, indicating that primary effects were on the viable myocardium. Saline treated WT mice showed increased end systolic and diastolic volumes and hypertrophy index, along with reduced ejection fraction. MMP-9 deletion improved LV function post-MI. Aliskiren attenuated the increase in end systolic volume and hypertrophy index, while valsartan improved end diastolic volumes and aliskiren+valsartan improved the hypertrophy index only when MMP-9 was absent. Extracellular matrix and inflammatory gene expression showed distinct patterns among the treatment groups, indicating a divergence in mechanisms of remodeling. This study shows that MMP-9 regulates aliskiren and valsartan effects in mice. These results in mice provide mechanistic insight to help translate these findings to post-MI patients.

  8. Pesticides and myocardial infarction incidence and mortality among male pesticide applicators in the Agricultural Health Study.

    PubMed

    Mills, Katherine T; Blair, Aaron; Freeman, Laura E Beane; Sandler, Dale P; Hoppin, Jane A

    2009-10-01

    Acute organophosphate and carbamate pesticide poisonings result in adverse cardiac outcomes. The cardiac effects of chronic low-level pesticide exposure have not been studied. The authors analyzed self-reported lifetime use of pesticides reported at enrollment (1993-1997) and myocardial infarction mortality through 2006 and self-reported nonfatal myocardial infarction through 2003 among male pesticide applicators in the Agricultural Health Study. Using proportional hazard models, the authors estimated the association between lifetime use of 49 pesticides and fatal and nonfatal myocardial infarction. There were 476 deaths from myocardial infarction among 54,069 men enrolled in the study and 839 nonfatal myocardial infarctions among the 32,024 participants who completed the follow-up interview. Fatal and nonfatal myocardial infarctions were associated with commonly reported risk factors, including age and smoking. There was little evidence of an association between having used pesticides, individually or by class, and myocardial infarction mortality (e.g., insecticide hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.67, 1.24; herbicide HR = 0.74, 95% CI: 0.49, 1.10) or nonfatal myocardial infarction incidence (e.g., insecticide HR = 0.85, 95% CI: 0.66, 1.09; herbicide HR = 0.91, 95% CI: 0.61, 1.36). There was no evidence of a dose response with any pesticide measure. In a population with low risk for myocardial infarction, the authors observed little evidence of increased risk of myocardial infarction mortality or nonfatal myocardial infarction associated with the occupational use of pesticides.

  9. Pesticides and Myocardial Infarction Incidence and Mortality Among Male Pesticide Applicators in the Agricultural Health Study

    PubMed Central

    Mills, Katherine T.; Blair, Aaron; Freeman, Laura E. Beane; Sandler, Dale P.

    2009-01-01

    Acute organophosphate and carbamate pesticide poisonings result in adverse cardiac outcomes. The cardiac effects of chronic low-level pesticide exposure have not been studied. The authors analyzed self-reported lifetime use of pesticides reported at enrollment (1993–1997) and myocardial infarction mortality through 2006 and self-reported nonfatal myocardial infarction through 2003 among male pesticide applicators in the Agricultural Health Study. Using proportional hazard models, the authors estimated the association between lifetime use of 49 pesticides and fatal and nonfatal myocardial infarction. There were 476 deaths from myocardial infarction among 54,069 men enrolled in the study and 839 nonfatal myocardial infarctions among the 32,024 participants who completed the follow-up interview. Fatal and nonfatal myocardial infarctions were associated with commonly reported risk factors, including age and smoking. There was little evidence of an association between having used pesticides, individually or by class, and myocardial infarction mortality (e.g., insecticide hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.67, 1.24; herbicide HR = 0.74, 95% CI: 0.49, 1.10) or nonfatal myocardial infarction incidence (e.g., insecticide HR = 0.85, 95% CI: 0.66, 1.09; herbicide HR = 0.91, 95% CI: 0.61, 1.36). There was no evidence of a dose response with any pesticide measure. In a population with low risk for myocardial infarction, the authors observed little evidence of increased risk of myocardial infarction mortality or nonfatal myocardial infarction associated with the occupational use of pesticides. PMID:19700503

  10. Effects of combination antiretroviral therapies on the risk for myocardial infarction among HIV patients

    PubMed Central

    Brouwer, Emily S.; Napravnik, Sonia; Eron, Joseph J; Stalzer, Brant; Floris-Moore, Michelle; Simpson, Ross J; Stürmer, Til

    2014-01-01

    Background Cohort studies have demonstrated greater risk of myocardial infarction (MI) associated with specific antiretroviral use, while meta-analyses of randomized controlled trials have not. These differences may be due to inherent biases in the observational study design or to the limited duration of randomized trials. We conducted a new-user, active-comparator cohort study emulating a randomized controlled trial comparing initiation of several antiretrovirals as part of combination antiretroviral therapy (cART) and MI. Methods We included North Carolina (NC) Medicaid beneficiaries infected with HIV between 2002 and 2008 who were previously untreated with cART. We compared hazard ratios (HRs) and 95% confidence intervals (CIs) of MI between abacavir and tenofovir recipients, and lopinavir-ritonavir or atazanavir recipients and non-nucleoside-reverse-transcriptase-inhibitor (NNRTI) recipients. We adjusted for confounding through inverse-probability-weighting methods. Results There were 3,481 NC Medicaid new cART recipients who contributed 6,399 person-years and experienced 38 MI events. Receiving abacavir compared with tenofovir as part of cART was associated with an increased rate of MI unadjusted (HR= 2.70 [95% CI= 1.24 - 5.91]; HR= 2.05 [0.72 - 5.86]). Point estimates also suggest a relationship between receipt of atazanavir or lopinavir-ritonavir compared with an NNRTI and MI, although, estimates were imprecise. Conclusions We found an increased rate of MI among patients initiating abacavir compared with tenofovir although the association was decreased after confounding adjustment. Without a very large prospective comparative clinical trial, a much larger observational study of patients initiating cART would be needed to better define this apparent association. PMID:24713880

  11. Cardiac BMIPP imaging in acute myocardial infarction.

    PubMed

    Nakata, T; Hashimoto, A; Eguchi, M

    1999-02-01

    Fatty acid metabolism functions as a major energy-producing system under aerobic conditions, but it is impaired immediately after myocardial ischaemia. This imaging can provide intracellular information which cannot be obtained by angiographical, perfusional or functional analysis. 123I-BMIPP and perfusion imagings in patients with acute myocardial infarction have demonstrated three different correlations between myocardial perfusion and fatty acid metabolism: concordant defects of perfusion and BMIPP which represent scar or non-viable tissue; lower BMIPP uptake relative to perfusion (perfusion-BMIPP mismatch) which implicates metabolically damaged, often dysynergic, but viable myocardium; and equivalently normal uptakes of perfusion and BMIPP in completely salvaged myocardium. Identification of these perfusion-metabolism correlations contributes to the detection of ischaemia-related myocardial injury in viable and non-viable myocardium, to the prediction of post-ischaemic or post-interventional functional recovery and to the identification of patients who have myocardium at ischaemic risk. Further clinical investigations might reveal more clearly the pathophysiological and prognostic implications of cardiac BMIPP imaging in patients with acute myocardial infarction.

  12. 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.

  13. A History of Streptokinase Use in Acute Myocardial Infarction

    PubMed Central

    Sikri, Nikhil; Bardia, Amit

    2007-01-01

    A serendipitous discovery by William Smith Tillett in 1933, followed by many years of work with his student Sol Sherry, laid a sound foundation for the use of streptokinase as a thrombolytic agent in the treatment of acute myocardial infarction. The drug found initial clinical application in combating fibrinous pleural exudates, hemothorax, and tuberculous meningitis. In 1958, Sherry and others started using streptokinase in patients with acute myocardial infarction and changed the focus of treatment from palliation to “cure.” Initial trials that used streptokinase infusion produced conflicting results. An innovative approach of intracoronary streptokinase infusion was initiated by Rentrop and colleagues in 1979. Subsequently, larger trials of intracoronary infusion achieved reperfusion rates ranging from 70% to 90%. The need for a meticulously planned and systematically executed randomized multicenter trial was fulfilled by the Gruppo Italiano per la Sperimentazione della Streptochinasi nell'Infarto Miocardico (GISSI) trial in 1986, which not only validated streptokinase as an effective therapeutic method but also established a fixed protocol for its use in acute myocardial infarction. Currently, despite the wide use of tissue plasminogen activator in developed nations, streptokinase remains essential to the management of acute myocardial infarction in developing nations. PMID:17948083

  14. Coping with myocardial infarction: evaluation of a coping questionnaire.

    PubMed

    Brink, Eva; Persson, Lars-Olof; Karlson, Björn W

    2009-12-01

    The negative effects of emotional distress on the recovery following myocardial infarction make it important to study coping strategies in this situation. The present study aimed to evaluate the psychometric properties and the validity of a 10 dimensions questionnaire labelled The General Coping Questionnaire (GCQ). The structure of the questionnaire was based on a previous interview study with 26 persons with different diseases. The 10 dimensions are called self-trust, problem-reducing actions, change of values, social trust, minimization, fatalism, resignation, protest, isolation and intrusion. The present study comprised 114 first-time myocardial infarction patients (37 women, 77 men). Five months after myocardial infarction, they answered questions about health-related quality of life, health complaints, sense of coherence and the GCQ. A multi-trait/multi-item analysis showed good item-scale convergent and discriminatory validity when the GCQ was reduced from 47 to 40 items. In conclusion, the results showed that the 40-item GCQ is a well-structured and reliable questionnaire for measuring coping strategies in myocardial infarction patients. PMID:19804373

  15. Cardioprotective effect of methanolic extract of Marrubium vulgare L. on isoproterenol-induced acute myocardial infarction in rats.

    PubMed

    Yousefi, Keyvan; Soraya, Hamid; Fathiazad, Fatemeh; Khorrami, Arash; Hamedeyazdan, Sanaz; Maleki-Dizaji, Nasrin; Garjani, Alireza

    2013-08-01

    Isoproterenol injection (100 mg/kg; sc) produced changes in ECG pattern including ST-segment elevation and suppressed R-amplitude. The methanolic extract of M. vulgare at doses of 10, 20, and 40 mg/kg significantly amended the ECG changes. A severe myocardial necrosis and edematous along with a sharp reduction in the arterial blood pressure, left ventricular contractility (LVdP/dt(max or min)), but a marked increase in the left ventricular end-diastolic pressure (LVEDP) were seen in the isoproterenol group. All parameters were significantly improved by the extract treatment. The extract (10 mg/kg) strongly increased LVdP/dt(max). Similarly, treatment with 40 mg/kg of M. vulgare lowered the elevated LVEDP and the heart to body weight ratio. In addition to in vitro antioxidant activity, the extract suppressed markedly the elevation of malondialdehyde levels both in serum and in myocardium. The results demonstrate that M. vulgare protects myocardium against isoproterenol-induced acute myocardial infarction and suggest that the effects could be related to antioxidant activities.

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

    PubMed

    Engelmann, Markus G; Franz, Wolfgang M

    2006-10-01

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

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

    PubMed

    Royo, Marc B; Fleisher, Lee A

    2016-02-01

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

  18. Electromechanical analysis of infarct border zone in chronic myocardial infarction

    PubMed Central

    Ashikaga, Hiroshi; Mickelsen, Steven R.; Ennis, Daniel B.; Rodriguez, Ignacio; Kellman, Peter; Wen, Han; McVeigh, Elliot R.

    2007-01-01

    To test the hypothesis that alterations in electrical activation sequence contribute to depressed systolic function in the infarct border zone, we examined the anatomic correlation of abnormal electromechanics and infarct geometry in the canine post-myocardial infarction (MI) heart, using a high-resolution MR-based cardiac electromechanical mapping technique. Three to eight weeks after an MI was created in six dogs, a 247-electrode epicardial sock was placed over the ventricular epicardium under thoracotomy. MI location and geometry were evaluated with delayed hyperenhancement MRI. Three-dimensional systolic strains in epicardial and endocardial layers were measured in five short-axis slices with motion-tracking MRI (displacement encoding with stimulated echoes). Epicardial electrical activation was determined from sock recordings immediately before and after the MR scans. The electrodes and MR images were spatially registered to create a total of 160 nodes per heart that contained mechanical, transmural infarct extent, and electrical data. The average depth of the infarct was 55% (SD 11), and the infarct covered 28% (SD 6) of the left ventricular mass. Significantly delayed activation (>mean + 2SD) was observed within the infarct zone. The strain map showed abnormal mechanics, including abnormal stretch and loss of the transmural gradient of radial, circumferential, and longitudinal strains, in the region extending far beyond the infarct zone. We conclude that the border zone is characterized by abnormal mechanics directly coupled with normal electrical depolarization. This indicates that impaired function in the border zone is not contributed by electrical factors but results from mechanical interaction between ischemic and normal myocardium. PMID:15908463

  19. 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

  20. 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

  1. 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.

  2. Atorvastatin administered before myocardial infarction in rats improves contractility irrespective of metabolic changes.

    PubMed

    Lehnen, Tatiana Ederich; Lehnen, Alexandre Machado; Tavares, Angela Maria Vicente; Belló-Klein, Adriane; Markoski, Melissa Medeiros; Machado, Ubiratan Fabres; Schaan, Beatriz

    2014-12-01

    Statins have a beneficial effect after myocardial infarction, but the relationship between glucose transporters and their use before the event has not yet been studied. We assessed the effects of atorvastatin treatment pre- and post-myocardial infarction on cardiovascular function and glucose transporter 4 (GLUT4) in the heart. Wistar-Kyoto rats were treated with 20 mg/kg atorvastatin or vehicle for 14 days before coronary artery occlusion surgery (myocardial infarction) or sham surgery. Echocardiographic evaluations were carried out 48 h after myocardial infarction (protocol A) and after 7 days (protocol B), when atorvastatin was also administered. Plasma inflammatory markers and GLUT4 in the heart were also evaluated. Animals were divided into the following groups: sham-operated and vehicle (C), myocardial infarction and vehicle (I), sham-operated and atorvastatin (CAt) and myocardial infarction and atorvastatin (IAt). After 48 h, myocardial infarction induced higher left ventricular fractional shortening in IAt versus I (~ 60%, P = 0.036), and the ejection fraction was lower (protocol A ~ 37%; protocol B ~ 30%). Myocardial infarction was associated with a rise in plasma membrane GLUT4 after 48 h (~ 40%, P < 0.001), and a reduction in GLUT4 after 7 days (I 25%; IAt 49%, P < 0.001). Atorvastatin treatment for 48 h after the infarction did not change GLUT4 expression, and after 7 days it had an additional negative effect on GLUT4 content (~ 39%, P = 0.030). In conclusion, atorvastatin treatment pre- and post-myocardial infarction improved myocardial contractility after 48 h, but not after 7 days, and was not associated with an increase in GLUT4 expression.

  3. Cardiac effects of the extract and active components of radix stephaniae tetrandrae. II. Myocardial infarct, arrhythmias, coronary arterial flow and heart rate in the isolated perfused rat heart.

    PubMed

    Yu, X C; Wu, S; Wang, G Y; Shan, J; Wong, T M; Chen, C F; Pang, K T

    2001-05-11

    The primary purpose of the present study was to compare the cardioprotective effects of the extract from radix stephaniae tetrandrae (RST) and its individual compounds, tetrandrine (Tet) and fanchinoline (Fan). Secondly, we also compared the cardiac effects of the individual compounds and the RST extract with those of verapamil, a classical Ca2+ channel blocker. The Langendorff isolated perfused rat heart preparation was used. Regional ischaemia and reperfusion was employed to induce myocardial infarct and arrhythmia. Infarct, arrhythmia, heart rate and coronary artery flow were determined in hearts treated with vehicle, RST extract, Tet, Fan, or verapamil. It was found that RST extract, of which only 9% was Tet, and Tet alone produced equally potent ameliorating effects on arrhythmia and infarct induced by ischaemia and reperfusion without further inhibiting ischaemia-reduced heart rate and coronary artery flow. Fan had no effects on arrhythmia and infarct induced by ischaemia and reperfusion; but it induced S-T segment elevation and further reduced heart rate and coronary artery flow during ischaemia. Verapamil also ameliorated the effects of ischaemia and reperfusion on arrhythmia and infarct. It should be noted that 1 microM verapamil, that produced comparable effects on infarct and arrhythmia to the RST extract and Tet, further inhibited heart rate during ischaemia. The results indicate that the RST extract produces equally potent cardioprotective and anti-arrhythmic effects as Tet alone. Both RST extract and Tet may be better choices for the treatment of arrhythmia and infarct induced by myocardial ischaemia and reperfusion than the classical Ca2+ channel blocker, verapamil as they do not further reduce heart rate during ischaemia. PMID:11432452

  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.

  5. Coronary Intervention for Persistent Occlusion after Myocardial Infarction

    PubMed Central

    Hochman, Judith S.; Lamas, Gervasio A.; Buller, Christopher E.; Dzavik, Vladimir; Reynolds, Harmony R.; Abramsky, Staci J.; Forman, Sandra; Ruzyllo, Witold; Maggioni, Aldo P.; White, Harvey; Sadowski, Zygmunt; Carvalho, Antonio C.; Rankin, Jamie M.; Renkin, Jean P.; Steg, P. Gabriel; Mascette, Alice M.; Sopko, George; Pfisterer, Matthias E.; Leor, Jonathan; Fridrich, Viliam; Mark, Daniel B.; Knatterud, Genell L.

    2007-01-01

    BACKGROUND It is unclear whether stable, high-risk patients with persistent total occlusion of the infarct-related coronary artery identified after the currently accepted period for myocardial salvage has passed should undergo percutaneous coronary intervention (PCI) in addition to receiving optimal medical therapy to reduce the risk of subsequent events. METHODS We conducted a randomized study involving 2166 stable patients who had total occlusion of the infarct-related artery 3 to 28 days after myocardial infarction and who met a high-risk criterion (an ejection fraction of <50% or proximal occlusion). Of these patients, 1082 were assigned to routine PCI and stenting with optimal medical therapy, and 1084 were assigned to optimal medical therapy alone. The primary end point was a composite of death, myocardial reinfarction, or New York Heart Association (NYHA) class IV heart failure. RESULTS The 4-year cumulative primary event rate was 17.2% in the PCI group and 15.6% in the medical therapy group (hazard ratio for death, reinfarction, or heart failure in the PCI group as compared with the medical therapy group, 1.16; 95% confidence interval [CI], 0.92 to 1.45; P = 0.20). Rates of myocardial reinfarction (fatal and nonfatal) were 7.0% and 5.3% in the two groups, respectively (hazard ratio, 1.36; 95% CI, 0.92 to 2.00; P = 0.13). Rates of nonfatal reinfarction were 6.9% and 5.0%, respectively (hazard ratio, 1.44; 95% CI, 0.96 to 2.16; P = 0.08); only six reinfarctions (0.6%) were related to assigned PCI procedures. Rates of NYHA class IV heart failure (4.4% vs. 4.5%) and death (9.1% vs. 9.4%) were similar. There was no interaction between treatment effect and any subgroup variable (age, sex, race or ethnic group, infarct-related artery, ejection fraction, diabetes, Killip class, and the time from myocardial infarction to randomization). CONCLUSIONS PCI did not reduce the occurrence of death, reinfarction, or heart failure, and there was a trend toward excess

  6. Cells involved in extracellular matrix remodeling after acute myocardial infarction

    PubMed Central

    Garcia, Larissa Ferraz; Mataveli, Fábio D’Aguiar; Mader, Ana Maria Amaral Antônio; Theodoro, Thérèse Rachell; Justo, Giselle Zenker; Pinhal, Maria Aparecida da Silva

    2015-01-01

    Objective Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Methods Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. Results There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation. Conclusion The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct. PMID:25993074

  7. 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

  8. Cardiac stem cells and their roles in myocardial infarction.

    PubMed

    Hou, Jingying; Wang, Lingyun; Jiang, Jieyu; Zhou, Changqing; Guo, Tianzhu; Zheng, Shaoxin; Wang, Tong

    2013-06-01

    Myocardial infarction leads to loss of cardiomyocytes, scar formation, ventricular remodeling and eventually deterioration of heart function. Over the past decade, stem cell therapy has emerged as a novel strategy for patients with ischemic heart disease and its beneficial effects have been demonstrated by substantial preclinical and clinical studies. Efficacy of several types of stem cells in the therapy of cardiovascular diseases has already been evaluated. However, repair of injured myocardium through stem cell transplantation is restricted by critical safety issues and ethic concerns. Recently, the discovery of cardiac stem cells (CSCs) that reside in the heart itself brings new prospects for myocardial regeneration and reconstitution of cardiac tissues. CSCs are positive for various stem cell markers and have the potential of self-renewal and multilineage differentiation. They play a pivotal role in the maintenance of heart homeostasis and cardiac repair. Elucidation of their biological characteristics and functions they exert in myocardial infarction are very crucial to further investigations on them. This review will focus on the field of cardiac stem cells and discuss technical and practical issues that may involve in their clinical applications in myocardial infarction.

  9. Treatment with the gap junction modifier rotigaptide (ZP123) reduces infarct size in rats with chronic myocardial infarction.

    PubMed

    Haugan, Ketil; Marcussen, Niels; Kjølbye, Anne Louise; Nielsen, Morten Schak; Hennan, James K; Petersen, Jørgen Søberg

    2006-02-01

    Treatment with non-selective drugs (eg, long-chain alcohols, halothane) that reduce gap junction intercellular communication (GJIC) is associated with reduced infarct size after myocardial infarction (MI). Therefore, it has been suggested that gap junction intercellular communication stimulating compounds may increase infarct size. The antiarrhythmic peptide analogue rotigaptide (ZP123) increases cardiac gap junction intercellular communication and the purpose of the present study was to examine the effects of rotigaptide treatment on infarct size. Myocardial infarction was induced in male rats by ligation of the left anterior descending artery (LAD). Rats (n = 156) were treated with rotigaptide at three dose levels or vehicle from the onset of ischemia and for 3 weeks following LAD occlusion. Infarct size was determined using histomorphometry after 3 weeks treatment. Rotigaptide treatment producing steady state plasma levels of 0.8 +/- 0.1, 5.5 +/- 0.5, and 86 +/- 8 nmol/L had no effect on mortality, but reduced infarct size to 90 +/- 10% (P = 0.41), 67 +/- 7% (P = 0.005), and 82 +/- 7% (P = 0.13), respectively relative to vehicle-treated myocardial infarction rats (100 +/- 12%). In contrast to what was predicted, our data demonstrates that rotigaptide treatment was associated with a significant infarct size reduction. We conclude that whereas treatment with non-selective inhibitors of gap junction intercellular communication cause a reduction in infarct size, this information cannot be extrapolated to the effects of compounds that selectively increase gap junction intercellular communication.

  10. Enhanced cell survival and paracrine effects of mesenchymal stem cells overexpressing hepatocyte growth factor promote cardioprotection in myocardial infarction.

    PubMed

    Zhao, Liyan; Liu, Xiaolin; Zhang, Yuelin; Liang, Xiaoting; Ding, Yue; Xu, Yan; Fang, Zhen; Zhang, Fengxiang

    2016-05-15

    Poor cell survival post transplantation compromises the therapeutic benefits of mesenchymal stem cells (MSCs) in myocardial infarction (MI). Hepatocyte growth factor (HGF) is an important cytokine for angiogenesis, anti-inflammation and anti-apoptosis. This study aimed to evaluate the cardioprotective effects of MSCs overexpressing HGF in a mouse model of MI. The apoptosis of umbilical cord-derived MSCs (UC-MSCs) and HGF-UC-MSCs under normoxic and hypoxic conditions was detected. The conditioned medium (CdM) of UC-MSCs and HGF-UC-MSCs under a hypoxic condition was harvested and its protective effect on neonatal cardiomyocytes (NCMs) exposed to a hypoxic challenge was examined. UC-MSCs and HGF-UC-MSCs were transplanted into the peri-infarct region in mice following MI and heart function assessed 4 weeks post transplantation. The apoptosis of HGF-UC-MSCs under hypoxic conditions was markedly decreased compared with that of UC-MSCs. NCMs treated with HGF-UC-MSC hypoxic CdM (HGF-UC-MSCs-hy-CdM) exhibited less cell apoptosis in response to hypoxic challenge than those treated with UC-MSC hypoxic CdM (UC-MSCs-hy-CdM). HGF-UC-MSCs-hy-CdM released the inhibited p-Akt and lowered the enhanced ratio of Bax/Bcl-2 induced by hypoxia in the NCMs. HGF-UC-MSCs-hy-CdM expressed higher levels of HGF, EGF, bFGF and VEGF than UC-MSCs-hy-CdM. Transplantation of HGF-UC-MSCs or UC-MSCs greatly improved heart function in the mouse model of MI. Compared with UC-MSCs, transplantation of HGF-UC-MSCs was associated with less cardiomyocyte apoptosis, enhanced angiogenesis and increased proliferation of cardiomyocytes. This study may provide a novel therapeutic strategy for MSC-based therapy in cardiovascular disease. PMID:27025401

  11. Protective effect of morin on cardiac mitochondrial function during isoproterenol-induced myocardial infarction in male Wistar rats.

    PubMed

    Al Numair, Khalid S; Chandramohan, Govindasamy; Alsaif, Mohammed A; Baskar, Arul Albert

    2012-01-01

    Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Myocardial infarction (MI) in rats was induced by ISO (85 mg/kg) at an interval of 24 hours for 2 days. Morin was given to rats as pre-treatment for 30 days orally using an intragastric tube. ISO-treated rats showed a significant elevation of mitochondrial thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (HP) level and pre-treatment with morin significantly prevented the increase of TBARS and HP level to near normality. The level of enzymic and non-enzymic antioxidants was decreased significantly in ISO-treated rats and pre-treatment with morin significantly increased the levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and reduced glutathione to normality. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were decreased significantly in ISO-treated myocardial ischemic rats and upon pre-treatment with morin restored these enzymes activity to normality. In addition, the decreased activities of cytochrome-C oxidase and NADH-dehydrogenases were observed in ISO-treated rats and pre-treatment with morin prevented the activities of cytochrome-C oxidase and NADH-dehydrogenase to normality. Pre-treatment with morin favorably restored the biochemical and functional parameters to near normal indicating morin to be a significant protective effect on cardiac mitochondrial function against ISO-induced MI in rats.

  12. Vulnerabilities to Temperature Effects on Acute Myocardial Infarction Hospital Admissions in South Korea

    PubMed Central

    Kwon, Bo Yeon; Lee, Eunil; Lee, Suji; Heo, Seulkee; Jo, Kyunghee; Kim, Jinsun; Park, Man Sik

    2015-01-01

    Most previous studies have focused on the association between acute myocardial function (AMI) and temperature by gender and age. Recently, however, concern has also arisen about those most susceptible to the effects of temperature according to socioeconomic status (SES). The objective of this study was to determine the effect of heat and cold on hospital admissions for AMI by subpopulations (gender, age, living area, and individual SES) in South Korea. The Korea National Health Insurance (KNHI) database was used to examine the effect of heat and cold on hospital admissions for AMI during 2004–2012. We analyzed the increase in AMI hospital admissions both above and below a threshold temperature using Poisson generalized additive models (GAMs) for hot, cold, and warm weather. The Medicaid group, the lowest SES group, had a significantly higher RR of 1.37 (95% CI: 1.07–1.76) for heat and 1.11 (95% CI: 1.04–1.20) for cold among subgroups, while also showing distinctly higher risk curves than NHI for both hot and cold weather. In additions, females, older age group, and those living in urban areas had higher risks from hot and cold temperatures than males, younger age group, and those living in rural areas. PMID:26580643

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

    PubMed

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

    2014-07-24

    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.

  14. Acute Myocardial Infarction, Use of Percutaneous Coronary Intervention, and Mortality: A Comparative Effectiveness Analysis Covering Seven European Countries.

    PubMed

    Hagen, Terje P; Häkkinen, Unto; Belicza, Eva; Fatore, Giovanni; Goude, Fanny

    2015-12-01

    Percutaneous coronary interventions (PCI) on acute myocardial infarction (AMI) patients have increased substantially in the last 12-15 years because of its clinical effectiveness. The expansion of PCI treatment for AMI patients raises two questions: How did PCI utilization rates vary across European regions, and which healthcare system and regional characteristic variables correlated with the utilization rate? Were the differences in use of PCI associated with differences in outcome, operationalized as 30-day mortality? We obtained our results from a dataset based on the administrative information systems of the populations of seven European countries. PCI rates were highest in the Netherlands, followed by Sweden and Hungary. The probability of receiving PCI was highest in regions with their own PCI facilities and in healthcare systems with activity-based reimbursement systems. Thirty-day mortality rates differed considerably between the countries with the highest rates in Hungary, Scotland, and Finland. Mortality was lowest in Sweden and Norway. The associations between PCI and mortality were remarkable in all age groups and across most countries. Despite extensive risk adjustment, we interpret the associations both as effects of selection and treatments. We observed a lower effect of PCI in the higher age groups in Hungary.

  15. The effects of smoke-free legislation on acute myocardial infarction: a systematic review and meta-analysis

    PubMed Central

    2013-01-01

    Background Comprehensive smoke-free legislation has been implemented in many countries. The current study quantitatively examined the reduction in risk of acute myocardial infarction (MI) occurrence following the legislations and the relationship with the corresponding smoking prevalence decrease. Methods PubMed, EMBASE, and Google Scholar databases and bibliographies of relevant studies and reviews were searched for potential original studies published from January 1, 2004, through October 31, 2011. Meta-analysis was performed using a random effect model to estimate the overall effects of the smoking-free legislations. Meta-regression was used to investigate possible causes of heterogeneity in risk estimates. Results A total of 18 eligible studies with 44 estimates of effect size were used in this study. Meta-analysis produced a pooled estimate of the relative risk of 0.87 (95% confidence interval (CI): 0.84 to 0.91). There was significant heterogeneity in the risk estimates (overall I2 = 96.03%, p<0.001). In meta-regression analysis, studies with greater smoking prevalence decrease produced larger relative risk (adjusted coefficient −0.027, 95% CI: -0.049 to −0.006, p=0.014). Conclusion Smoke-free legislations in public and work places were associated with significant reduction in acute MI risk, which might be partly attributable to reduced smoking prevalence. PMID:23721370

  16. The effect of written material and verbal method education on anxiety and depression in patients with myocardial infarction in selected hospitals in Iran

    PubMed Central

    AGHAKHANI, NADER; KHADEMVATAN, KAMAL; DEHGHANI, MOHAMMAD REZA

    2014-01-01

    Introduction: Myocardial infarction (MI) is the damage to the heart muscle, or myocardium, resulting from the lack of blood flow to the heart. MI patients experience mental and emotional problems such as depression and anxiety. These complications could cause delay in resuming work, decreased quality of life and increased risk of death. The role of education in facilitating adaptation is very important in these patients. The purpose of this study was to determine the effect of written material and verbal method education on anxiety and depression in patients with myocardial infarction in Urmia hospital in 2009. Methods: This study was a quasi-experimental study, comparing the effect of education on anxiety and depression in patients with myocardial infarction in hospitals affiliated to Urmia University of Medical Science. 124 patients were selected randomly and divided into two groups. The experimental group was educated through face to face training and an educational booklet (Written Material and Verbal Method). The control group did not receive any intervention. The level of anxiety and depression was evaluated, using HADS questionnaire at 3 intervals: after 48 hours of admission, the discharge day and 2 months after discharge. Results: The findings suggested that MI patients were worried about their social role, interpersonal relations and personal health. Such problems can aggravate symptoms and complicate the future care. There was no significant difference between the control and experimental groups before the intervention, but after the intervention, anxiety and depression in the experimental group was significantly less than that in the control group (p<0.05). Conclusion: Considering the beneficial results obtained from written materials and verbal method education on reducing anxiety and depression in cases with myocardial infarction, this may be one of the health care goals. More research on more patients is required to achieve more conclusive results

  17. Effects of KR-33028, a novel Na+/H+ exchanger-1 inhibitor, on ischemia and reperfusion-induced myocardial infarction in rats and dogs.

    PubMed

    Oh, Kwang-Seok; Seo, Ho Won; Yi, Kyu Yang; Lee, Sunkyung; Yoo, Sung-eun; Lee, Byung Ho

    2007-06-01

    The present study was performed to evaluate the cardioprotective effects of KR-33028, a novel Na+/H+ exchanger subtype 1 (NHE-1) inhibitor, in rat and dog models of coronary artery occlusion and reperfusion. In anesthetized rats subjected to a 45-min coronary occlusion and a 90-min reperfusion, KR-33028 at 5 min before occlusion (i.v. bolus) dose-dependently reduced myocardial infarct size from 58.0% to 46.6%, 40.3%, 39.7%, 33.1%, and 27.8% for 0.03, 0.1, 0.3, 1.0, and 3.0 mg/kg respectively (P < 0.05). In anesthetized beagle dogs that underwent a 1.0-h occlusion followed by a 3.0-h reperfusion, KR-33028 (3 mg/kg, i.v. bolus) markedly decreased infarct size from 45.6% in vehicle-treated group to 16.4% (P < 0.05), and reduced the reperfusion-induced release in creatine kinase myocardial band isoenzyme (MB), lactate dehydrogenase, troponin-I, glutamic oxaloacetic transaminase, and glutamic pyruvic transaminase. In separate experiments to assess the effects of timing of treatment, KR-33028 (1 mg/kg, i.v. bolus) given 10 min before or at reperfusion in rat models also significantly reduced the myocardial infarct size (46.3% and 44.1% respectively) compared with vehicle-treated group. In all studies, KR-33028 caused no significant changes in any hemodynamic profiles. In an isolated rat heart model of hypothermic cardioplegia, KR-33028 (30 mum), which was added to the heart preservation solution (histidin-tryptophan-ketoglutarate) during hypothermic cardioplegic arrest, significantly improved the recovery of left ventricular developed pressure, heart rate and dP/dt(max) after reperfusion. Taken together, these results indicate that KR-33028 significantly reduced the myocardial infarction induced by ischemia and reperfusion in rats and dogs, without affecting hemodynamic profiles.

  18. 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

  19. 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

  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. Acute myocardial infarction in a young woman on isotretinoin treatment.

    PubMed

    Lorenzo, Natalia; Antuña, Paula; Dominguez, Lourdes; Rivero, Fernando; Bastante, Teresa; Alfonso, Fernando

    2015-02-15

    The use of isotretinoin has been associated with mild changes in the metabolic profile of adolescents. In very rare cases, a possible association with myocardial infarction, stroke and thromboembolic events has been reported. In this report we describe the potential association of isotretinoin with the occurrence of an acute myocardial infarction in a very young girl. OCT provided unique visualization of the culprit lesion.

  2. Effects of paroxetine-mediated inhibition of GRK2 expression on depression and cardiovascular function in patients with myocardial infarction

    PubMed Central

    Tian, Xiuqing; Wang, Qing; Guo, Rui; Xu, Lingling; Chen, Qin M; Hou, Yinglong

    2016-01-01

    Background Paroxetine is a selective serotonin reuptake inhibitor utilized in the treatment of depression and anxiety disorders. Recent studies have identified paroxetine as a G protein-coupled receptor kinase-2 (GRK2) inhibitor capable of reversing cardiac dysfunction and remodeling in experimental models of acute myocardial infarction (AMI). We determine the clinical importance of paroxetine on cardiac functions in patients having AMI with depression (AMID) in comparison with fluoxetine, an unrelated selective serotonin reuptake inhibitor that does not inhibit GRK2. Methods Diagnosis of depression was based on the 17-item Hamilton Depression Scale and Self-rating Depression Scale in AMI patients after hospital admission. AMID patients were randomly assigned to paroxetine or fluoxetine for treatment of depression. Heart rate variability and cardiac function were evaluated. GRK2 protein levels were measured using peripheral lymphocytes and Western blot. Results GRK2 expression in AMID patients was significantly higher than that in AMI patients without depression. In AMID patients, GRK2 levels were positively correlated with the 17-item Hamilton Depression Scale and the Self-rating Depression Scale scores, and negatively correlated with heart rate variability. Treatment of AMID patients with paroxetine significantly reduced the expression of GRK2, normalized the autonomic nervous system function, and improved cardiac performance. In contrast, fluoxetine normalized the autonomic nervous system but did not reduce the expression of GRK2 nor improved cardiac performance. Conclusion This study suggests that paroxetine is effective for improving cardiac function in patients with AMID and such effect correlates with GRK2 reduction.

  3. Effectiveness of a Myocardial Infarction Protocol in Reducing Door-to-Ballon Time

    PubMed Central

    Correia, Luis Cláudio Lemos; Brito, Mariana; Kalil, Felipe; Sabino, Michael; Garcia, Guilherme; Ferreira, Felipe; Matos, Iracy; Jacobs, Peter; Ronzoni, Liliana; Noya-Rabelo, Márcia

    2013-01-01

    Background An adequate door-to-balloon time (<120 minutes) is the necessary condition for the efficacy of primary angioplasty in infarction to translate into effectiveness. Objective To describe the effectiveness of a quality of care protocol in reducing the door-to-balloon time. Methods Between May 2010 and August 2012, all individuals undergoing primary angioplasty in our hospital were analyzed. The door time was electronically recorded at the moment the patient took a number to be evaluated in the emergency room, which occurred prior to filling the check-in forms and to the triage. The balloon time was defined as the beginning of artery opening (introduction of the first device). The first 5 months of monitoring corresponded to the period of pre-implementation of the protocol. The protocol comprised the definition of a flowchart of actions from patient arrival at the hospital, the team's awareness raising in relation to the prioritization of time, and provision of a periodic feedback on the results and possible inadequacies. Results A total of 50 individuals were assessed. They were divided into five groups of 10 sequential patients (one group pre-and four groups post-protocol). The door-to-balloon time regarding the 10 cases recorded before protocol implementation was 200 ± 77 minutes. After protocol implementation, there was a progressive reduction of the door-to-balloon time to 142 ± 78 minutes in the first 10 patients, then to 150 ± 50 minutes, 131 ± 37 minutes and, finally, 116 ± 29 minutes in the three sequential groups of 10 patients, respectively. Linear regression between sequential patients and the door-to-balloon time (r = - 0.41) showed a regression coefficient of - 1.74 minutes. Conclusion The protocol implementation proved effective in the reduction of the door-to-balloon time. PMID:23702814

  4. Importance of magnesium chloride repletion after myocardial infarction.

    PubMed

    Sheehan, J

    1989-04-18

    Data pertinent to the role of magnesium deficits in coronary artery disease and myocardial infarction are reviewed. Results of clinical, laboratory and epidemiologic studies indicate an association between magnesium deficiency and a poor prognostic outcome in patients who have had myocardial infarction. It therefore appears to be a reasonable prophylactic measure to monitor closely magnesium status in patients with coronary heart disease and other patients at risk of acute myocardial infarction, and to supplement with magnesium chloride when clinically necessary. In addition, recent studies provide supportive evidence that supplementation of magnesium chloride may reduce the incidence of fatal and nonfatal arrhythmias after an infarct.

  5. 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

  6. Changes in Hsp60 level of the failing heart following acute myocardial infarction and the effect of long-term treatment with trandolapril.

    PubMed

    Toga, Wakako; Tanonaka, Kouichi; Takeo, Satoshi

    2007-01-01

    Changes in heat shock protein (Hsp) 60 of the viable left ventricular muscle (viable LV) after myocardial infarction in rats and the effect of the angiotensin I-converting enzyme inhibitor (ACEI) trandolapril were examined. Myocardial infarction was induced in rats by ligation of the left coronary artery. The coronary artery-ligated (CAL) and sham-operated (Sham) rats were orally treated with 3 mg/kg/d trandolapril from the 2nd to 8th week after surgery. Hemodynamic parameters and tissue weights of the left and right ventricles of the animals at the 8th week after CAL (8w-CAL rats) showed signs indicating chronic heart failure. An increase in Hsp60 content, a decrease in mitochondrial oxygen consumption rate (OCR), and an increase in the mitochondrial thiobarbiturate-reacting substance (TRS) of the viable LV were detected. Eight weeks after CAL. Long-term treatment of the CAL rats with trandolapril improved the hemodynamic parameters, attenuated the CAL-induced increase in Hsp60 content, the decrease in mitochondrial OCR, and the increase in the mitochondrial TRS content of the viable LV at the 8th week after myocardial infarction. The increase in Hsp60 content was closely related to the decrease in the mitochondrial OCR and to a rise in the LVEDP of the CAL animal at the 8th week after myocardial infarction. These results suggest that a series of pathophysiological alterations, including a reduction in mitochondrial function, appearance of reactive oxygen stress, and production of Hsp60 is involved in the development of cardiac failure and that trandolapril is beneficial for preventing these alterations.

  7. MiRNA-711-SP1-collagen-I pathway is involved in the anti-fibrotic effect of pioglitazone in myocardial infarction.

    PubMed

    Zhao, Na; Yu, Haiyi; Yu, Haitao; Sun, Min; Zhang, Youyi; Xu, Ming; Gao, Wei

    2013-05-01

    Although microRNAs (miRNAs) have been intensively studied in cardiac fibrosis, their roles in drug-mediated anti-fibrotic therapy are still unknown. Previously, Pioglitazone attenuated cardiac fibrosis and increased miR-711 experimentally. We aimed to explore the role and mechanism of miR-711 in pioglitazone-treated myocardial infarction in rats. Our results showed that pioglitazone significantly reduced collagen-I levels and increased miR-711 expression in myocardial infarction heart. Pioglitazone increased the expression of miR-711 in cardiac fibroblasts, and overexpression of miR-711 suppressed collagen-I levels in angiotensin II (Ang II)-treated or untreated cells. Transfection with antagomir-711 correspondingly abolished the pioglitazone-induced reduction in collagen-I levels. Bioinformatics analysis identified SP1, which directly promotes collagen-I synthesis, as the putative target of miR-711. This was confirmed by luciferase assay and western blot analysis. Additionally, increased SP1 expression was attenuated by pioglitazone in myocardial infarction heart. Furthermore, transfection of antagomir-711 attenuated pioglitazone-reduced SP1 expression in cardiac fibroblasts with or without Ang II stimulation. We conclude that pioglitazone up-regulated miR-711 to reduce collagen-I levels in rats with myocardial infarction. The miR-711-SP1-collagen-I pathway may be involved in the anti-fibrotic effects of pioglitazone. Our findings may provide new strategies for miRNA-based anti-fibrotic drug research.

  8. Silent ST segment elevation myocardial infarction with multi-segmental renal infarction: an unusual presentation.

    PubMed

    Chang, Hung-Yu; Yang, Yung-Nien

    2011-01-01

    A 36-year-old diabetic man came to our institution presenting with constant left flank pain. Left renal embolic infarction was found by abdominal computed tomography. Silent ST segment elevation myocardial infarction was noted on 12-lead electrocardiogram. Emergent coronary angiography revealed large thrombus burdens with complete occlusion at the left anterior descending artery ostium, which may be the embolic origin. Silent ST segment elevation myocardial infarction with acute flank pain and multiple segmental renal infarction is an unusual presentation. High vigilance may prevent delay of the "golden hour" to treat acute myocardial infarction.

  9. Scorpion envenomation-induced acute thrombotic inferior myocardial infarction.

    PubMed

    Baykan, Ahmet Oytun; Gür, Mustafa; Acele, Armağan; Şeker, Taner; Çaylı, Murat

    2016-01-01

    The occurrence of a serious cardiac emergency following scorpion envenomation has rarely been reported and, when so, mostly presented as non-ST segment elevation myocardial infarction, cardiogenic shock, or myocarditis. Possible mechanisms include imbalance in blood pressure and coronary vasospasm caused by the combination of sympathetic excitation, scorpion venom-induced release of catecholamines, and the direct effect of the toxin on the myocardium. We report a case of a 55-year-old man who presented with acute inferior wall myocardial infarction (MI) within 2 h of being stung by a scorpion. Coronary angiogram revealed total thrombotic occlusion of the left circumflex artery, which was treated successfully with glycoprotein IIb/IIIa inhibitor, thrombus aspiration, antivenom serum, and supportive therapy. Therefore, life-threatening MI can complicate the clinical course during some types of scorpion envenomation and should be managed as an acute coronary syndrome. PMID:26875137

  10. Myocarditis confirmed by biopsy presenting as acute myocardial infarction.

    PubMed Central

    Costanzo-Nordin, M R; O'Connell, J B; Subramanian, R; Robinson, J A; Scanlon, P J

    1985-01-01

    Two cases of acute myocardial infarction occurred in association with myocarditis, which was confirmed by biopsy. The first patient suffered an anteroseptal and the second patient an inferior wall myocardial infarction shortly after an acute viral illness. In both patients, coronary angiography showed normal coronary arteries, and right ventricular endomyocardial biopsy confirmed myocarditis. Histological abnormalities attributable to ischaemic heart disease were absent. The first patient's condition became stable after immunosuppressive treatment. Myocarditis resolved spontaneously within three months in the second patient. Coronary artery spasm and myocardial involvement with a systemic disease were unlikely. Endomyocardial biopsy in patients with acute myocardial infarction and normal coronary arteries may be useful in identifying myocarditis associated with myocardial necrosis. Myocarditis in acute myocardial infarction in the absence of coronary artery obstruction has not previously been documented during life. Images PMID:3966948

  11. Effect of Hurricane Katrina on chronobiology at onset of acute myocardial infarction during the subsequent three years.

    PubMed

    Peters, Matthew N; Katz, Morgan J; Moscona, John C; Alkadri, Mohi E; Khazi Syed, Rashad H; Turnage, Thomas A; Nijjar, Vikram S; Bisharat, Mohannad B; Delafontaine, Patrice; Irimpen, Anand M

    2013-03-15

    The onset of acute myocardial infarction (AMI) has been shown to occur in a nonrandom pattern, with peaks in midmorning and on weekdays (especially Monday). The incidence of AMI has been shown to increase locally after natural disasters, but the effect of catastrophic events on AMI biorhythms is largely unknown. To assess the differences in the chronobiology of AMI in residents of New Orleans before and after Hurricane Katrina, the onset of AMI in patients at Tulane University Health Sciences Center in the 6 years before and the 3 years after Hurricane Katrina was retrospectively examined. Compared to the pre-Katrina group, the post-Katrina cohort demonstrated significant decreases in the onset of AMI during mornings (p = 0.002), Mondays (p <0.0001), and weekdays (p <0.0001) and significant increases in onset during weekends (p <0.0001) and nights (p <0.0001). These changes persisted during all 3 years after the storm. In conclusion, the normal pattern of AMI onset was altered after Hurricane Katrina, and expected morning, weekday, and Monday peaks were eliminated.

  12. Effect of Hurricane Katrina on chronobiology at onset of acute myocardial infarction during the subsequent three years.

    PubMed

    Peters, Matthew N; Katz, Morgan J; Moscona, John C; Alkadri, Mohi E; Khazi Syed, Rashad H; Turnage, Thomas A; Nijjar, Vikram S; Bisharat, Mohannad B; Delafontaine, Patrice; Irimpen, Anand M

    2013-03-15

    The onset of acute myocardial infarction (AMI) has been shown to occur in a nonrandom pattern, with peaks in midmorning and on weekdays (especially Monday). The incidence of AMI has been shown to increase locally after natural disasters, but the effect of catastrophic events on AMI biorhythms is largely unknown. To assess the differences in the chronobiology of AMI in residents of New Orleans before and after Hurricane Katrina, the onset of AMI in patients at Tulane University Health Sciences Center in the 6 years before and the 3 years after Hurricane Katrina was retrospectively examined. Compared to the pre-Katrina group, the post-Katrina cohort demonstrated significant decreases in the onset of AMI during mornings (p = 0.002), Mondays (p <0.0001), and weekdays (p <0.0001) and significant increases in onset during weekends (p <0.0001) and nights (p <0.0001). These changes persisted during all 3 years after the storm. In conclusion, the normal pattern of AMI onset was altered after Hurricane Katrina, and expected morning, weekday, and Monday peaks were eliminated. PMID:23291089

  13. Quantitative assessment of oscillatory components in blood circulation: classification of the effect of aging, diabetes, and acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Bernjak, Alan; Stefanovska, Aneta; Urbancic-Rovan, Vilma; Azman-Juvan, Katja

    2005-04-01

    The human cardiovascular system is a complex system with the pumping activity of the heart as the main generator of oscillations. Besides the heartbeat there are several other oscillatory components which determine its dynamics. Their nonlinear nature and a weak coupling between them both require special treatment while studying this system. A particular characteristic of the oscillatory components is their frequency fluctuations in time. Consequently, their interactions also fluctuate in time. Therefore the wavelet transform is applied to trace the oscillatory components in time, and specific quantitative measures are introduced to quantify the contribution of each of the oscillatory components involved on the time scale of up to three minutes. Oscillatory components are then analysed from signals obtained by simultaneous measurements of blood flow in the microcirculation, ECG, respiration and blood pressure. Based on quantitative evaluation of the oscillatory components related to (I) the heart beat (0.6-2Hz), (II) respiration (0.145-0.6Hz), (III) intrinsic myogenic activity (0.052-0.145Hz), (IV) sympathetic activity (0.021-0.052Hz), (V, VI) endothelial related activity (0.0095-0.021Hz, 0.005 - 0.0095 Hz), 30-minutes recording taken on 109 healthy subjects, 75 patients with diabetes, and 82 patients after acute myocardial infarction (AMI) were analysed. Classification of the effect of ageing, diabetes and AMI from blood flow signals simultaneously recorded in the skin of four extremities, the heart rate and heart rate variability from R-R intervals will be presented and discussed.

  14. ST-segment depression on the initial electrocardiogram in acute myocardial infarction-prognostic significance and its effect on short-term mortality: A report from the National Registry of Myocardial Infarction (NRMI-2, 3, 4).

    PubMed

    Pitta, Sridevi R; Grzybowski, Mary; Welch, Robert D; Frederick, Paul D; Wahl, Robert; Zalenski, Robert J

    2005-04-01

    This study analyzed 255,256 patients who had acute myocardial infarction and were enrolled in the National Registry of Myocardial Infarction 2, 3, and 4 (1994 to 2002). The objective was to determine in-hospital mortality rate among patients who had ST-segment depression on the initial electrocardiogram. Patients who had ST-segment depression had an in-hospital mortality rate (15.8%) similar to that of patients who had ST-segment elevation or left bundle branch block (15.5%). After adjusting for observed differences, ST-segment depression was associated with only a slightly lower odds ratio (0.91) of mortality compared with ST-segment elevation or left bundle branch block. PMID:15781012

  15. Characterization of nontransmural myocardial infarction by positron-emission tomography

    SciTech Connect

    Geltman, E.M.; Biello, D.; Welch, M.J.; Ter-Pogossian, M.M.; Roberts, R.; Sobel, B.E.

    1982-04-01

    The present study was performed to determine whether positron emission tomography (PET) performed after i.v. 11C-palmitate permits detection and characterization of nontransmural myocardial infarction. PET was performed after the i.v. injection of 11C-palmitate in 10 normal subjects, 24 patients with initial nontransmural myocardial infarction (defined electrocardiographically), and 22 patients with transmural infarction. Depressed accumulation of 11C-palmitate was detected with sagittal, coronal and transverse reconstructions, and quantified based on 14 contiguous transaxial reconstructions. Defects with homogeneously intense depression of accumulation of tracer were detected in all 22 patients with transmural infarction (100%). Abnormalities of the distribution of 11C-palmitate in the myocardium were detected in 23 patients with nontransmural infarction (96%). Thallium scintigrams were abnormal in only 11 of 18 patients with nontransmural infarction (61%). Tomographically estimated infarct size was greater among patients with transmural infarction (50.4 +/- 7.8 PET-g-Eq/m2 (+/- SEM SEM)) compared with those with nontransmural infarction (19 +/- 4 PET-g-Eq, p less than 0.01). Residual accumulation of 11C-palmitate within regions of infarction was more intensely depressed among patients with transmural compared to nontransmural infarction (33 +/- 1 vs 39 +/- 1% maximal myocardial radioactivity, p less than 0.01). Thus, PET and metabolic imaging with 11C-palmitate is a sensitive means of detecting, quantifying and characterizing nontransmural and transmural myocardial infarction.

  16. Design and rationale of a multicentre, randomised, double-blind, placebo-controlled clinical trial to evaluate the effect of vitamin D on ventricular remodelling in patients with anterior myocardial infarction: the VITamin D in Acute Myocardial Infarction (VITDAMI) trial

    PubMed Central

    Tuñón, José; González-Hernández, Ignacio; Llanos-Jiménez, Lucía; Alonso-Martín, Joaquín; Escudier-Villa, Juan M; Tarín, Nieves; Cristóbal, Carmen; Sanz, Petra; Pello, Ana M; Aceña, Álvaro; Carda, Rocío; Orejas, Miguel; Tomás, Marta; Beltrán, Paula; Calero Rueda, Marta; Marcos, Esther; Serrano-Antolín, José María; Gutiérrez-Landaluce, Carlos; Jiménez, Rosa; Cabezudo, Jorge; Curcio, Alejandro; Peces-Barba, Germán; González-Parra, Emilio; Muñoz-Siscart, Raquel; González-Casaus, María Luisa; Lorenzo, Antonio; Huelmos, Ana; Goicolea, Javier; Ibáñez, Borja; Hernández, Gonzalo; Alonso-Pulpón, Luis M; Farré, Jerónimo; Lorenzo, Óscar; Mahíllo-Fernández, Ignacio; Egido, Jesús

    2016-01-01

    Introduction Decreased plasma vitamin D (VD) levels are linked to cardiovascular damage. However, clinical trials have not demonstrated a benefit of VD supplements on left ventricular (LV) remodelling. Anterior ST-elevation acute myocardial infarction (STEMI) is the best human model to study the effect of treatments on LV remodelling. We present a proof-of-concept study that aims to investigate whether VD improves LV remodelling in patients with anterior STEMI. Methods and analysis The VITamin D in Acute Myocardial Infarction (VITDAMI) trial is a multicentre, randomised, double-blind, placebo-controlled trial. 144 patients with anterior STEMI will be assigned to receive calcifediol 0.266 mg capsules (Hidroferol SGC)/15 days or placebo on a 2:1 basis during 12 months. Primary objective: to evaluate the effect of calcifediol on LV remodelling defined as an increase in LV end-diastolic volume ≥10% (MRI). Secondary objectives: change in LV end-diastolic and end-systolic volumes, ejection fraction, LV mass, diastolic function, sphericity index and size of fibrotic area; endothelial function; plasma levels of aminoterminal fragment of B-type natriuretic peptide, galectin-3 and monocyte chemoattractant protein-1; levels of calcidiol (VD metabolite) and other components of mineral metabolism (fibroblast growth factor-23 (FGF-23), the soluble form of its receptor klotho, parathormone and phosphate). Differences in the effect of VD will be investigated according to the plasma levels of FGF-23 and klotho. Treatment safety and tolerability will be assessed. This is the first study to evaluate the effect of VD on cardiac remodelling in patients with STEMI. Ethics and dissemination This trial has been approved by the corresponding Institutional Review Board (IRB) and National Competent Authority (Agencia Española de Medicamentos y Productos Sanitarios (AEMPS)). It will be conducted in accordance with good clinical practice (International Council for Harmonisation of

  17. Personality and mortality after myocardial infarction.

    PubMed

    Denollet, J; Sys, S U; Brutsaert, D L

    1995-01-01

    Previous research showed: a) emotional distress is a risk factor for mortality after myocardial infarction (MI) and b) emotional distress is linked to stable personality traits. In this study, we examined the role of these personality traits in mortality after MI. Subjects were 105 men, 45 to 60 years of age, who survived a recent MI. Baseline assessment included biomedical and psychosocial risk factors, as well as each patient's personality type. After 2 to 5 (mean, 3.8) years of follow-up, 15 patients (14%) had died. Rate of death for patients with a distressed personality type (11/28 = 39%) was significantly greater than that for patients with other personality types (4/77 = 5%) (p < .0001). Patients with this personality type tend simultaneously to experience distress and inhibit expression of emotions. Low exercise tolerance, previous MI (p < .005), anterior MI, smoking, and age (p < .05) were also associated with mortality. A logistic regression model including these biomedical factors had a sensitivity for mortality of only 27%. The addition of distressed personality type in this model more than doubled its sensitivity. Of note, among patients with poor physical health, those with a distressed personality type had a five-fold mortality risk (p < .005). Consistent with the findings of other investigators, depression (p < .005), life stress, use of benzodiazepines (p < .01), and somatization (p < .05) were also related to post-MI mortality. These psychosocial risk factors were more prevalent in the distressed personality type than in the other personality types (p < .001-.05). Multiple logistic regression indicated that these psychosocial factors did not add to the predictive value of the distressed personality type. Hence, an important personality effect was observed despite the low power. This suggests that personality traits may play a role in the detrimental effect of emotional distress in MI patients.

  18. Loss of quality adjusted days as a trial endpoint: effect of early thrombolytic treatment in suspected myocardial infarction. Grampion Region Early Anistreplase Trial (GREAT).

    PubMed Central

    Rawles, J; Light, J

    1993-01-01

    STUDY OBJECTIVES--(1) To measure the quality of life and the loss of quality adjusted days (QADS) after suspected acute myocardial infarction in patients who received thrombolytic treatment either at home or in hospital. (2) To compare the loss of QADS as a trial endpoint with the conventional endpoints of mortality and Q-wave infarction. DESIGN--Randomised double blind parallel group trial of anistreplase (30 U given intravenously) and placebo given either at home or in hospital. SETTING--Rural practices in Grampian admitting patients to teaching hospitals in Aberdeen. PATIENTS--A total of 311 patients with suspected acute myocardial infarction and no contraindications to thrombolytic treatment seen at home within four hours of the onset of symptoms. MEASUREMENTS AND MAIN RESULTS--Loss of quality adjusted days (QADS) in the first 100 days after suspected myocardial infarction (365 QADS = 1 QALY) was the main outcome measure. Compared with later administration in hospital, anistreplase at home resulted in a relative reduction of mortality of 49% (95% confidence interval 3.95%, 2p = 0.04), and a relative reduction of 26% in the proportion of survivors with infarction who had Q-waves (95% CI 7.44%, 2p = 0.007). During the 100 day follow up, the median loss of QADS was 25 for all patients. This loss was significantly greater in those who died than in survivors (65 v 18, 2p < 0.001), and in survivors with infarction than in survivors without infarction (26 v 13, 2p < 0.01). However, there was no significant difference in loss of QADS in those with infarction with or without Q-waves (29 v 21, NS), and the median loss of QADS was not significantly different in those who had thrombolytic treatment at home or in hospital (median difference 0, 95% CI -5, +4 QADS). CONCLUSIONS--Loss of QADS had two serious limitations as an outcome measure: it was less sensitive than mortality and it failed to reflect physiological benefit. Palliative treatment with no physiological effect

  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. Recurrent coronary stent thromboses and myocardial infarctions.

    PubMed

    Chen, Jack; Rajeev, Angampally

    2007-11-01

    Although stent thrombosis is a recognized complication of coronary intervention, recurrent stent thrombosis is rarely reported. We present a patient who suffered 3 ST-segment elevation myocardial infarctions associated with repeated stent thromboses within a month and a half. Although a potentially mechanical cause of thrombosis was identified in the only baremetal stent implanted in this case, no predisposing factors were seen for the 2 drug-eluting stents (DES). While recent worrisome data have suggested a slight increase in the incidence of late angiographic stent thrombosis (defined as occurring beyond 30 days) with drug-eluting stents (DES), their risk of subacute thrombosis (from 1 to 30 days) is reported to be equivalent to that of BMS. Therefore, this rare occurrence serves as a sobering reminder of the risks of subacute thrombosis with both BMS and DES. Marked neointimal inhibition, allergic reactions, as well as thienopyridine resistance, may all contribute to the pathophysiology of DES thrombosis. The Food and Drug Administration advisory panel has concluded that when these devices are used for "on-label" indications, the counterbalance of dramatic target lesion revascularization reduction versus rare incidence of late angiographic stent thrombosis results in no overall increase in DES myocardial infarction or mortality risk. Furthermore, a minimum of 1 year of dual antiplatelet therapy is recommended for all recipients of DES at low risk of bleeding.

  1. Cost-effectiveness of a European ST-segment elevation myocardial infarction network: results from the Catalan Codi Infart network

    PubMed Central

    Bosch, Julia; Martín-Yuste, Victoria; Rosas, Alba; Faixedas, Maria Teresa; Gómez-Hospital, Joan Antoni; Figueras, Jaume; Curós, Antoni; Cequier, Angel; Goicolea, Javier; Fernández-Ortiz, Antonio; Macaya, Carlos; Tresserras, Ricard; Pellisé, Laura; Sabaté, Manel

    2015-01-01

    Objectives To evaluate the cost-effectiveness of the ST-segment elevation myocardial infarction (STEMI) network of Catalonia (Codi Infart). Design Cost-utility analysis. Setting The analysis was from the Catalonian Autonomous Community in Spain, with a population of about 7.5 million people. Participants Patients with STEMI treated within the autonomous community of Catalonia (Spain) included in the IAM CAT II-IV and Codi Infart registries. Outcome measures Costs included hospitalisation, procedures and additional personnel and were obtained according to the reperfusion strategy. Clinical outcomes were defined as 30-day avoided mortality and quality-adjusted life-years (QALYs), before (N=356) and after network implementation (N=2140). Results A substitution effect and a technology effect were observed; aggregate costs increased by 2.6%. The substitution effect resulted from increased use of primary coronary angioplasty, a relatively expensive procedure and a decrease in fibrinolysis. Primary coronary angioplasty increased from 31% to 89% with the network, and fibrinolysis decreased from 37% to 3%. Rescue coronary angioplasty declined from 11% to 4%, and no reperfusion from 21% to 4%. The technological effect was related to improvements in the percutaneous coronary intervention procedure that increased efficiency, reducing the average length of the hospital stay. Mean costs per patient decreased from €8306 to €7874 for patients with primary coronary angioplasty. Clinical outcomes in patients treated with primary coronary angioplasty did not change significantly, although 30-day mortality decreased from 7.5% to 5.6%. The incremental cost-effectiveness ratio resulted in an extra cost of €4355 per life saved (30-day mortality) and €495 per QALY. Below a cost threshold of €30 000, results were sensitive to variations in costs and outcomes. Conclusions The Catalan STEMI network (Codi Infart) is cost-efficient. Further studies are needed in geopolitical

  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. Long-Term Effects of Autologous Bone Marrow Stem Cell Treatment in Acute Myocardial Infarction: Factors That May Influence Outcomes

    PubMed Central

    Clifford, David M.; Fisher, Sheila A.; Brunskill, Susan J.; Doree, Carolyn; Mathur, Anthony; Clarke, Mike J.; Watt, Suzanne M.; Martin-Rendon, Enca

    2012-01-01

    Aims To investigate whether there are important sources of heterogeneity between the findings of different clinical trials which administer autologous stem cell treatment for acute myocardial infarction (AMI) and to evaluate what factors may influence the long-term effects of this treatment. Methods and Results MEDLINE (1950-January 2011), EMBASE (1974-January 2011), CENTRAL (The Cochrane Library 2011, Issue 1), CINAHL (1982-January 2011), and ongoing trials registers were searched for randomised trials of bone marrow stem cells as treatment for AMI. Hand-searching was used to screen recent, relevant conference proceedings (2005–2010/11). Meta-analyses were conducted using random-effects models and heterogeneity between subgroups was assessed using chi-squared tests. Planned analyses included length of follow-up, timing of cell infusion and dose, patient selection, small trial size effect, methodological quality, loss of follow-up and date of publication. Thirty-three trials with a total of 1,765 participants were included. There was no evidence of bias due to publication or time-lag, methodological quality of included studies, participant drop-out, duration of follow-up or date of the first disclosure of results. However, in long-term follow-ups the treatment seemed more effective when administered at doses greater than 108 cells and to patients with more severe heart dysfunction. Conclusions Evaluation of heterogeneity between trials has not identified significant sources of bias in this study. However, clinical differences between trials are likely to exist which should be considered when undertaking future trials. PMID:22655042

  4. 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.

  5. Role of adenosine as adjunctive therapy in acute myocardial infarction.

    PubMed

    Forman, Mervyn B; Stone, Gregg W; Jackson, Edwin K

    2006-01-01

    Although early reperfusion and maintained patency is the mainstay therapy for ST elevation myocardial infarction, experimental studies demonstrate that reperfusion per se induces deleterious effects on viable ischemic cells. Thus "myocardial reperfusion injury" may compromise the full potential of reperfusion therapy and may account for unfavorable outcomes in high-risk patients. Although the mechanisms of reperfusion injury are complex and multifactorial, neutrophil-mediated microvascular injury resulting in a progressive decrease in blood flow ("no-reflow" phenomenon) likely plays an important role. Adenosine is an endogenous nucleoside found in large quantities in myocardial and endothelial cells. It activates four well-characterized receptors producing various physiological effects that attenuate many of the proposed mechanisms of reperfusion injury. The cardio-protective effects of adenosine are supported by its role as a mediator of pre- and post-conditioning. In experimental models, administration of adenosine in the peri-reperfusion period results in a marked reduction in infarct size and improvement in ventricular function. The cardioprotective effects in the canine model have a narrow time window with the drug losing its effect following three hours of ischemia. Several small clinical studies have demonstrated that administration of adenosine with reperfusion therapy reduces infarct size and improves ventricular function. In the larger AMISTAD and AMISTAD II trials a 3-h infusion of adenosine as an adjunct to reperfusion resulted in a striking reduction in infarct size (55-65%). Post hoc analysis of AMISTAD II showed that this was associated with significantly improved early and late mortality in patients treated within 3.17 h of symptoms. An intravenous infusion of adenosine for 3 h should be considered as adjunctive therapy in high risk-patients undergoing reperfusion therapy. PMID:16961725

  6. Cost-effectiveness of amlodipine compared with valsartan in preventing stroke and myocardial infarction among hypertensive patients in Taiwan

    PubMed Central

    Chan, Lung; Chen, Chen-Huan; Hwang, Juey-Jen; Yeh, San-Jou; Shyu, Kou-Gi; Lin, Ruey-Tay; Li, Yi-Heng; Liu, Larry Z; Li, Jim Z; Shau, Wen-Yi; Weng, Te-Chang

    2016-01-01

    Hypertension is a major risk factor for strokes and myocardial infarction (MI). Given its effectiveness and safety profile, the calcium channel blocker amlodipine is among the most frequently prescribed antihypertensive drugs. This analysis was conducted to determine the costs and quality-adjusted life years (QALYs) associated with the use of amlodipine and valsartan, an angiotensin II receptor blocker, in preventing stroke and MI in Taiwanese hypertensive patients. A state transition (Markov) model was developed to compare the 5-year costs and QALYs for amlodipine and valsartan. Effectiveness data were based on the NAGOYA HEART Study, local studies, and a published meta-analysis. Utility data and costs of MI and stroke were retrieved from the published literature. Medical costs were based on the literature and inflated to 2011 prices; drug costs were based on National Health Insurance prices in 2014. A 3% discount rate was used for costs and QALYs and a third-party payer perspective adopted. One-way sensitivity and scenario analyses were conducted. Compared with valsartan, amlodipine was associated with cost savings of New Taiwan Dollars (NTD) 2,251 per patient per year: costs were NTD 4,296 and NTD 6,547 per patient per year for amlodipine and valsartan users, respectively. Fewer cardiovascular events were reported in patients receiving amlodipine versus valsartan (342 vs 413 per 10,000 patients over 5 years, respectively). Amlodipine had a net gain of 58 QALYs versus valsartan per 10,000 patients over 5 years. Sensitivity analyses showed that the discount rate and cohort age had a larger effect on total cost and cost difference than on QALYs. However, amlodipine results were more favorable than valsartan irrespective of discount rate or cohort age. When administered to Taiwanese patients for hypertension control, amlodipine was associated with lower cost and more QALYs compared with valsartan due to a lower risk of stroke and MI events. PMID:27330323

  7. Early Effects of Treatment Low-Dose Atorvastatin on Markers of Insulin Resistance and Inflammation in Patients with Myocardial Infarction

    PubMed Central

    Gruzdeva, Olga; Uchasova, Evgenya; Dyleva, Yulia; Akbasheva, Olga; Karetnikova, Victoria; Barbarash, Olga

    2016-01-01

    Dyslipidemia is one of the primary causes of cardiovascular disease. Therefore, attention has been focused on the development of drugs that normalize lipid levels and exert an effect on markers of atherothrombosis, insulin resistance (IR), and inflammation. Atorvastatin is a drug with not only lipid-lowering potential, but it has multiple non-lipid effects. This study aimed to evaluate atorvastatin effects on lipid, adipokine, IR, and inflammatory statuses in patients with myocardial infarction (MI) in an in-hospital setting. This study included 66 patients with confirmed ST-segment elevation MI, who were treated with atorvastatin 20 mg/day starting on day 1 of MI, without any dose changes. The comparison group consisted of 60 patients receiving standard anti-anginal and anti-thrombotic therapy. During the hospital stay, both groups showed a reduction in total cholesterol level and free fatty acids and increased concentrations of apolipoprotein A, especially those patients receiving atorvastatin. On day 1 of MI, patients in both groups had elevated levels of leptin by 2.9- to 3.3-fold, but the leptin levels decreased by 40.3% and were significantly lower than in patients not taking statins. The treatment with atorvastatin was associated with a decrease in C-reactive protein and interleukin-6 by 23.1 and 49.2%, respectively, compared with baseline values. In the group of patients on standard therapy, there was a decrease of interleukin-6 by 31.7%. Atorvastatin administered early on during hospitalization to patients with MI contributed to the improvement of lipid, adipokine and pro-inflammatory statuses and decreased IR. PMID:27725801

  8. Cost-effectiveness of amlodipine compared with valsartan in preventing stroke and myocardial infarction among hypertensive patients in Taiwan.

    PubMed

    Chan, Lung; Chen, Chen-Huan; Hwang, Juey-Jen; Yeh, San-Jou; Shyu, Kou-Gi; Lin, Ruey-Tay; Li, Yi-Heng; Liu, Larry Z; Li, Jim Z; Shau, Wen-Yi; Weng, Te-Chang

    2016-01-01

    Hypertension is a major risk factor for strokes and myocardial infarction (MI). Given its effectiveness and safety profile, the calcium channel blocker amlodipine is among the most frequently prescribed antihypertensive drugs. This analysis was conducted to determine the costs and quality-adjusted life years (QALYs) associated with the use of amlodipine and valsartan, an angiotensin II receptor blocker, in preventing stroke and MI in Taiwanese hypertensive patients. A state transition (Markov) model was developed to compare the 5-year costs and QALYs for amlodipine and valsartan. Effectiveness data were based on the NAGOYA HEART Study, local studies, and a published meta-analysis. Utility data and costs of MI and stroke were retrieved from the published literature. Medical costs were based on the literature and inflated to 2011 prices; drug costs were based on National Health Insurance prices in 2014. A 3% discount rate was used for costs and QALYs and a third-party payer perspective adopted. One-way sensitivity and scenario analyses were conducted. Compared with valsartan, amlodipine was associated with cost savings of New Taiwan Dollars (NTD) 2,251 per patient per year: costs were NTD 4,296 and NTD 6,547 per patient per year for amlodipine and valsartan users, respectively. Fewer cardiovascular events were reported in patients receiving amlodipine versus valsartan (342 vs 413 per 10,000 patients over 5 years, respectively). Amlodipine had a net gain of 58 QALYs versus valsartan per 10,000 patients over 5 years. Sensitivity analyses showed that the discount rate and cohort age had a larger effect on total cost and cost difference than on QALYs. However, amlodipine results were more favorable than valsartan irrespective of discount rate or cohort age. When administered to Taiwanese patients for hypertension control, amlodipine was associated with lower cost and more QALYs compared with valsartan due to a lower risk of stroke and MI events.

  9. FGF21 attenuates pathological myocardial remodeling following myocardial infarction through the adiponectin-dependent mechanism.

    PubMed

    Joki, Yusuke; Ohashi, Koji; Yuasa, Daisuke; Shibata, Rei; Ito, Masanori; Matsuo, Kazuhiro; Kambara, Takahiro; Uemura, Yusuke; Hayakawa, Satoko; Hiramatsu-Ito, Mizuho; Kanemura, Noriyoshi; Ogawa, Hayato; Daida, Hiroyuki; Murohara, Toyoaki; Ouchi, Noriyuki

    2015-03-27

    Ischemic heart disease is one of the leading causes of death. Fibroblast growth factor 21 (FGF21) is a circulating factor with an anti-diabetic property. Skeletal muscle is an important source of FGF21 production. Here, we investigated whether skeletal muscle-derived FGF21 modulates cardiac remodeling in a murine model of myocardial infarction. Myocardial infarction was produced in C57BL/6J wild-type (WT) mice by the permanent ligation of the left anterior descending coronary artery (LAD). Adenoviral vectors expressing FGF21 (Ad-FGF21) or control β-galactosidase were intramuscularly injected into mice at 3 days before permanent LAD ligation. Intramuscular injection of Ad-FGF21 increased plasma FGF21 levels in WT mice compared with control. Treatment of WT mice with Ad-FGF21 led to improvement of left ventricular systolic dysfunction and dilatation at 2 weeks after LAD ligation. Ad-FGF21 administration to WT mice also led to enhancement of capillary density in the infarct border zone, and reduction of myocyte apoptosis in the remote zone, which were accompanied by decreased expression of pro-inflammatory cytokines. Furthermore, treatment of WT mice with Ad-FGF21 increased plasma levels of adiponectin, which is a cardioprotective adipokine. The beneficial effects of Ad-FGF21 on cardiac dysfunction and inflammatory response after myocardial infarction were diminished in adiponectin-knockout mice. These data suggest that muscle-derived FGF21 ameliorates adverse cardiac remodeling after myocardial infarction, at least in part, through an adiponectin-dependent mechanism.

  10. Cardioprotective Effects of Essential Oil of Lavandula angustifolia on Isoproterenol-induced Acute Myocardial Infarction in Rat.

    PubMed

    Ziaee, Mojtaba; Khorrami, Arash; Ebrahimi, Maryam; Nourafcan, Hassan; Amiraslanzadeh, Masoumeh; Rameshrad, Maryam; Garjani, Mehraveh; Garjani, Alireza

    2015-01-01

    Myocardial infarction (MI) is a common presentation of the ischemic heart disease. Lavandula angustifolia is an herbaceous plant with antioxidative effects. This study was designed to investigate the cardioprotective effects of lavandula angustifolia essential oil against isoproterenol-induced MI in rats. The dried sample was subjected to hydrodistillation by using a Clevenger and the oils were dried over anhydrous Na2SO4. Male Wistar rats were assigned to 6 groups of control, sham, isoproterenol and treatment with 5, 10, 20 mg/Kg of the essential oil. MI was induced by subcutaneous injection of Isoproterenol (100 mg/Kg) for 3 consecutive days at an interval of 24 h. The essential oil was given intraperitoneally every 24 h started at MI induction. Following anesthesia, hemodynamic parameters were measured. After sacrificing the animals, the hearts were removed to measure the heart to body weight ratio and histopathological examination. Myeloperoxidase (MPO) and Malondialdehyde (MDA) were measured in heart tissues for evaluating the activity of neutrophils and lipid peroxidation, respectively. The essential oil amended ECG pattern by suppressing ST-segment elevation and increasing R-amplitude. 10 mg/Kg of the essential oil significantly decreased heart to body weight ratio (P<0.001) and the elevation of MDA and MPO in myocardium, it also increased dp/dtmax from 2793 ± 210 to 4488 ± 253 mmHg/sec (P<0.001), and 20 mg/Kg of it significantly lowered LVEDP from 14 ± 3.43 to 4.3 ± 0.83 mmHg (P<0.001).The results demonstrated that L. angustifolia protects myocardium against isoproterenol-induced MI that it could be related to its antioxidant properties. PMID:25561934

  11. Comparison of the electrophysiological effects of Org 7797, disopyramide, mexiletine and propafenone in anaesthetized dogs with myocardial infarcts.

    PubMed Central

    Campbell, J. K.; Marshall, R. J.; Winslow, E.

    1991-01-01

    1. The electrophysiological effects of intravenously administered Org 7797 were compared with those of disopyramide (class Ia), mexiletine (Ib) and propafenone (Ic) in anaesthetized dogs with 5-6 day-old left ventricular myocardial infarcts. 2. Org 7797 (0.5 mg kg-1) slowed conduction at all levels of the myocardium as shown by increases in St-A, AH, HV and QRS intervals, very modestly prolonged atrial and ventricular refractory periods and slightly shortened ventricular repolarization. Sinus node recovery time was increased whilst the RR interval was unchanged. A higher dose (2 mg kg-1) prolonged RR and rendered 5 out of 8 dogs unable to follow an atrial pacing stimulus of mean cycle length 322 ms. 3. Electrophysiological changes induced by propafenone (2 mg kg-1) were qualitatively similar to those of Org 7797 (0.5 mg kg-1). 4. Electrophysiological changes induced by mexiletine (2 mg kg-1) were small or insignificant. The most noticeable effect was a modest increase in the St-A interval and a slight shortening of ventricular repolarization. A higher dose (8 mg kg-1) additionally slowed conduction in the His-Purkinje system and in the ventricular myocardium. 5. Disopyramide (2 and 5 mg kg-1) prolonged all cardiac intervals including JTc, QTc and QT during pacing and prolonged cardiac refractory periods. 6. It was concluded that the electrophysiological profile of Org 7797 is more like that of the Ic agent propafenone than that of the class Ia and Ib drugs, disopyramide and mexiletine. PMID:1797309

  12. Effects of paroxetine-mediated inhibition of GRK2 expression on depression and cardiovascular function in patients with myocardial infarction

    PubMed Central

    Tian, Xiuqing; Wang, Qing; Guo, Rui; Xu, Lingling; Chen, Qin M; Hou, Yinglong

    2016-01-01

    Background Paroxetine is a selective serotonin reuptake inhibitor utilized in the treatment of depression and anxiety disorders. Recent studies have identified paroxetine as a G protein-coupled receptor kinase-2 (GRK2) inhibitor capable of reversing cardiac dysfunction and remodeling in experimental models of acute myocardial infarction (AMI). We determine the clinical importance of paroxetine on cardiac functions in patients having AMI with depression (AMID) in comparison with fluoxetine, an unrelated selective serotonin reuptake inhibitor that does not inhibit GRK2. Methods Diagnosis of depression was based on the 17-item Hamilton Depression Scale and Self-rating Depression Scale in AMI patients after hospital admission. AMID patients were randomly assigned to paroxetine or fluoxetine for treatment of depression. Heart rate variability and cardiac function were evaluated. GRK2 protein levels were measured using peripheral lymphocytes and Western blot. Results GRK2 expression in AMID patients was significantly higher than that in AMI patients without depression. In AMID patients, GRK2 levels were positively correlated with the 17-item Hamilton Depression Scale and the Self-rating Depression Scale scores, and negatively correlated with heart rate variability. Treatment of AMID patients with paroxetine significantly reduced the expression of GRK2, normalized the autonomic nervous system function, and improved cardiac performance. In contrast, fluoxetine normalized the autonomic nervous system but did not reduce the expression of GRK2 nor improved cardiac performance. Conclusion This study suggests that paroxetine is effective for improving cardiac function in patients with AMID and such effect correlates with GRK2 reduction. PMID:27695334

  13. Stimulating Myocardial Regeneration with Periostin Peptide in Large Mammals Improves Function Post-Myocardial Infarction but Increases Myocardial Fibrosis

    PubMed Central

    Ladage, Dennis; Yaniz-Galende, Elisa; Rapti, Kleopatra; Ishikawa, Kiyotake; Tilemann, Lisa; Shapiro, Scott; Takewa, Yoshiaki; Muller-Ehmsen, Jochen; Schwarz, Martin; Garcia, Mario J.; Sanz, Javier; Hajjar, Roger J.; Kawase, Yoshiaki

    2013-01-01

    Aims Mammalian myocardium has a finite but limited capacity to regenerate. Experimentally stimulating proliferation of cardiomyocytes with extracellular regeneration factors like periostin enhances cardiac repair in rodents. The aim of this study was to develop a safe method for delivering regeneration factors to the heart and to test the functional and structural effects of periostin peptide treatment in a large animal model of myocardial infarction (MI). Methods and Results We developed a controlled release system to deliver recombinant periostin peptide into the pericardial space. A single application of this method was performed two days after experimental MI in swine. Animals were randomly assigned to receive either saline or periostin peptide. Experimental groups were compared at baseline, day 2, 1 month and 3 months. Treatment with periostin peptide increased the EF from 31% to 41% and decreased by 22% the infarct size within 12 weeks. Periostin peptide-treated animals had newly formed myocardium strips within the infarct scar, leading to locally improved myocardial function. In addition the capillary density was increased in animals receiving periostin. However, periostin peptide treatment increased myocardial fibrosis in the remote region at one week and 12 weeks post-treatment. Conclusion Our study shows that myocardial regeneration through targeted peptides is possible. However, in the case of periostin the effects on cardiac fibrosis may limit its clinical application as a viable therapeutic strategy. PMID:23700403

  14. No reflow phenomenon in percutaneous coronary interventions in ST-segment elevation myocardial infarction.

    PubMed

    Gupta, Sanjiv; Gupta, Madan Mohan

    2016-01-01

    Percutaneous coronary intervention (PCI) is effective in opening the infarct related artery and restoring thrombolysis in myocardial infarction flow 3 (TIMI-flow 3) in large majority of ST-elevation myocardial infarction (STEMI). However there remain a small but significant proportion of patients, who continue to manifest diminished myocardial reperfusion despite successful opening of the obstructed epicardial artery. This phenomenon is called no-reflow. Clinically it manifests with recurrence of chest pain and dyspnea and may progress to cardiogenic shock, cardiac arrest, serious arrhythmias and acute heart failure. No reflow is regarded as independent predictor of death or recurrent myocardial infarction. No reflow is a multi-factorial phenomenon. However micro embolization of atherothrombotic debris during PCI remains the principal mechanism responsible for microvascular obstruction. This review summarizes the pathogenesis, diagnostic methods and the results of various recent randomized trials and studies on the prevention and management of no-reflow. PMID:27543480

  15. Effect of Hurricane Katrina on incidence of acute myocardial infarction in New Orleans three years after the storm.

    PubMed

    Jiao, Zhen; Kakoulides, Socrates V; Moscona, John; Whittier, Jabar; Srivastav, Sudesh; Delafontaine, Patrice; Irimpen, Anand

    2012-02-15

    To detect a long-term increase in the incidence of acute myocardial infarction (AMI) after Hurricane Katrina and to investigate the pertinent contributing factors, we conducted a single-center retrospective cohort observational study. The patients admitted with AMI to Tulane University Hospital in the 2 years before Katrina and the 3 years after the hospital reopened were identified from the hospital medical records. The pre- and post-Katrina groups were compared for prespecified demographic and clinical data. In the 3-year post-Katrina group, 418 admissions (2.0%) for AMI occurred of a total census of 21,092 patients compared to 150 (0.7%) of a census of 21,079 in the 2-year pre-Katrina group (p <0.0001). The post-Katrina group had a greater prevalence of unemployment (p <0.0001), lack of medical insurance (p <0.001), smokers (p <0.01), medical noncompliance (p <0.0001), first-time hospitalizations (p <0.001), history of coronary artery disease (p <0.01), multiple vessel disease (p <0.05), and percutaneous coronary interventions (p <0.0001). The mean age of onset of AMI decreased from 62 years before Katrina to 59 years after Katrina (p <0.05), and a significantly greater percentage of patients were men (p <0.05). No significant differences were found between the two groups in terms of race, substance abuse, and a history of hypertension or diabetes mellitus. Our data suggest that chronic stress after natural disasters may significantly affect cardiovascular risk factors such as tobacco abuse and increase medical noncompliance. In conclusion, our data is consistent with a significant change in the overall health of the population and support the need for additional study into the health effects of chronic stress after natural disasters.

  16. Computerized measurement of myocardial infarct size on contrast-enhanced magnetic resonance images

    NASA Astrophysics Data System (ADS)

    Hsu, Li-Yueh; Kellman, Peter; Natanzon, Alex; Hirsch, Glenn A.; Aletras, Anthony H.; Arai, Andrew E.

    2005-04-01

    Purpose: To validate a computer algorithm for measuring myocardial infarct size on gadolinium enhanced MR images. The results of computer infarct sizing are studied on phase-sensitive and magnitude imaging against a histopathology reference. Materials and Methods: Validations were performed in 9 canine myocardial infarctions determined by triphenyltetrazolium chloride (TTC). The algorithm analyzed the pixel intensity distribution within manually traced myocardial regions. Pixels darker than an automatically determined threshold were first excluded from further analysis. Selected image features were used to remove false positive regions. A threshold 50% between bright and dark regions was then used to minimize partial volume errors. Post-processing steps were applied to identify microvascular obstruction. Both phase sensitive and magnitude reconstructed MR images were measured by the computer algorithm in units of % of the left ventricle (LV) infarction and compared to TTC. Results: Correlations of MR and TTC infarct size were 0.96 for both phase sensitive and magnitude imaging. Bland Altman analysis showed no consistent bias as a function of infarct size. The average error of computer infarct sizing was less than 2% of the LV for both reconstructions. Fixed intensity thresholding was less accurate compared to the computer algorithm. Conclusions: MR can accurately depict myocardial infarction. The proposed computer algorithm accurately measures infarct size on contrast-enhanced MR images against the histopathology reference. It is effective for both phase-sensitive and magnitude imaging.

  17. Clenbuterol and anabolic steroids: a previously unreported cause of myocardial infarction with normal coronary arteriograms.

    PubMed

    Goldstein, D R; Dobbs, T; Krull, B; Plumb, V J

    1998-08-01

    During the last 10 years, several cases of myocardial infarction associated with anabolic steroid use have been reported. Postulated mechanisms to explain this association have included changes in lipid levels, the fibrinolytic system, and platelet aggregation. Clenbuterol is a beta 2-agonist with anabolic properties that has not been seen previously with myocardial infarction. We report a case of myocardial infarction in an otherwise healthy 26-year-old body-builder who recently used clenbuterol and anabolic steroids. In this case, synergistic effects of the two agents seem likely to have played a role in the infarct. The normal coronary arteriograms before any anticoagulant or thrombolytic therapy strongly suggest coronary spasm as the mechanism of the infarct. PMID:9715231

  18. Intramyocardial transplantation of cardiac telocytes decreases myocardial infarction and improves post-infarcted cardiac function in rats.

    PubMed

    Zhao, Baoyin; Liao, Zhaofu; Chen, Shang; Yuan, Ziqiang; Yilin, Chen; Lee, Kenneth K H; Qi, Xufeng; Shen, Xiaotao; Zheng, Xin; Quinn, Thomas; Cai, Dongqing

    2014-05-01

    The midterm effects of cardiac telocytes (CTs) transplantation on myocardial infarction (MI) and the cellular mechanisms involved in the beneficial effects of CTs transplantation are not understood. In the present study, we have revealed that transplantation of CTs was able to significantly decrease the infarct size and improved cardiac function 14 weeks after MI. It has established that CT transplantation exerted a protective effect on the myocardium and this was maintained for at least 14 weeks. The cellular mechanism behind this beneficial effect on MI was partially attributed to increased cardiac angiogenesis, improved reconstruction of the CT network and decreased myocardial fibrosis. These combined effects decreased the infarct size, improved the reconstruction of the LV and enhanced myocardial function in MI. Our findings suggest that CTs could be considered as a potential cell source for therapeutic use to improve cardiac repair and function following MI, used either alone or in tandem with stem cells.

  19. Pentoxifylline does not reduce infarct size in a canine model of acute myocardial infarction.

    PubMed Central

    Campbell, C. A.; Clavenna, C. F.; Wynne, J.; Kloner, R. A.

    1988-01-01

    1. The effect of the haemorrheological agent pentoxifylline was investigated in a canine model of acute myocardial infarction, induced by occlusion of the left anterior descending coronary for 6 h. Thirty minutes post-occlusion the dogs were randomized to receive either distilled water or pentoxifylline (0.3 mg kg-1 min-1 for 1 h followed by 0.15 mg kg-1 min-1 for 4.5 h) intravenously. 2. At 6 h post-occlusion the in vivo area at risk was determined with monastral blue dye and the area of necrosis was determined with triphenyltetrazolium chloride. The area at risk was 16.5 +/- 1.3% in the control group (n = 10) and 17.2 +/- 1.8% in the pentoxifylline treated group (n = 10; NS). The area of necrosis was 12.3 +/- 1.9% in the control group and 11.9 +/- 2.2% in the pentoxifylline treated group (NS). The area of necrosis expressed as a percentage of the area at risk was 69.3 +/- 7.7% in the control group and 63.6 +/- 7.4% in the pentoxifylline treated group (NS). 3. Pentoxifylline had no significant effects on heart rate, systolic or diastolic blood pressure. Regional myocardial blood flow, measured by the radioactive microsphere technique, was not significantly different between the groups. 4. Thus, pentoxifylline does not reduce infarct size in this model of acute myocardial infarction and does not enhance coronary collateral blood flow. PMID:3370389

  20. Lives of rural women after myocardial infarction.

    PubMed

    Caldwell, Patricia; Arthur, Heather M; Rideout, Elizabeth

    2005-03-01

    This study examines the influences of rurality on the lives of women post-myocardial infarction (MI). Using a critical ethnographic approach, the researchers analyze in-depth interviews with 12 women from southwestern Ontario, Canada, for the ways in which their experiences were related to social, political, and cultural forces associated with rurality. Data analysis revealed 4 themes: reticence, characterized by a tendency to minimize worry and accept one's life post-MI; referral games, or the challenges associated with accessing tertiary care; resourcefulness in managing one's recovery; and relationships, with rural health professionals and institutions being highly valued. The findings have relevance for nurses in both rural and urban settings who care for women post-MI and form a basis for supporting and building culturally specific post-MI care.

  1. Mad honey poisoning mimicking acute myocardial infarction.

    PubMed

    Chen, Sammy P L; Lam, Y H; Ng, Vember C H; Lau, F L; Sze, Y C; Chan, W T; Mak, Tony W L

    2013-08-01

    We report a case of acute poisoning in a 48-year-old man who presented with chest pain, abdominal pain, dizziness, sweatiness, blurred vision, and severe hypotension after ingestion of honey. His electrocardiogram showed sinus bradycardia and transient ST elevation. He made a good recovery after treatment with atropine and close monitoring. Grayanotoxin was detected in his urine and the honey he ingested, which confirmed a diagnosis of mad honey poisoning. This is a condition prevalent in the Black Sea region around Turkey but rarely seen locally. Although mad honey poisoning is life-threatening, early use of atropine is life-saving. Such poisoning may present with ST elevation in the electrocardiogram and symptoms mimicking acute myocardial infarction. It is therefore essential for clinicians to recognise this unusual form of poisoning and avoid the disastrous use of thrombolytic therapy.

  2. 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.

  3. Myocardial infarction among men below age 40.

    PubMed Central

    Bergstrand, R; Vedin, A; Wilhelmsson, C; Wallin, J; Wedel, H; Wilhelmsen, L

    1978-01-01

    Studies were made in Göteborg over a period of 6 years of all cases of acute myocardial infarction diagnosed among men below the age of 40. Thirty-six cases were registered and 8 of these died outside hospital. Three patients died early during the hospital stay. The remaining 25 patients were compared with a random sample from the general population in Göteborg with respect to conventional risk factors. Smoking, and high plasma cholesterol values were dominating findings among the patients, whereas there was no significant differences in blood pressure levels. Coronary angiography was performed in 18 patients of whom 2 showed normal coronary arteries and left ventricular angiograms. These 2 patients were the only ones free from risk factors. Of the remaining 16 patients, 10 had only one vessel affected. PMID:687475

  4. Effects Of Recombinant Human Erythropoietin On Platelet Activation In Acute Myocardial Infarction: Results Of A Double-Blind, Placebo-Controlled Randomized Trial

    PubMed Central

    Tang, Yi-Da; Hasan, Faisal; Giordano, Frank J.; Pfau, Stephen; Rinder, Henry M.; Katz, Stuart D.

    2009-01-01

    Background Erythropoietin mitigates myocardial damage and improves ventricular performance after experimental ischemic injury. This study assessed safety and efficacy markers relevant to the biological activity of recombinant human erythropoietin (rHuEpo) in patients with acute myocardial infarction. Methods We conducted a prospective, placebo-controlled, randomized, double-blind trial to determine the effects of intravenous rHuEpo (200 U/kg daily for 3 consecutive days) on measures of platelet and endothelial cell activation, soluble Fas ligand, and peripheral blood mononuclear cell (PBMC) expression of angiogenesis signaling proteins in 44 subjects with acute myocardial infarction (MI) treated with aspirin and clopidogrel after successful percutaneous coronary intervention. Results rHuEpo did not alter bleeding time, platelet function assay closure time, von Willebrand factor levels, soluble P-selectin, or soluble Fas ligand levels when compared with placebo. By contrast, rHuEpo significantly increased expression of erythropoietin receptor, vascular endothelial growth factor receptor Flt-1, and phosphorylated phosphatidylinositol 3-kinase in PBMC’s when compared with placebo (all p<0.05). Conclusions In acute MI patients treated with aspirin and clopidogrel, short-term administration of rHuEpo did not alter markers of platelet and endothelial cell activation associated with thrombosis, yet did increase expression of angiogenesis signaling proteins in PBMC’s when compared with placebo. These data provide preliminary evidence of safety and biologic activity of rHuEpo at this dosing and support continued enrollment in ongoing efficacy trials. PMID:19958860

  5. Cardiac oxidative stress and inflammatory cytokines response after myocardial infarction.

    PubMed

    Neri, Margherita; Fineschi, Vittorio; Di Paolo, Marco; Pomara, Cristoforo; Riezzo, Irene; Turillazzi, Emanuela; Cerretani, Daniela

    2015-01-01

    Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protection. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-α (Tumor Necrosis Factor α), IL-1β (Interleukin- 1β) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injury.

  6. [On the actual nomenclature of myocardial infarcts].

    PubMed

    Medrano, Gustavo A; Aranda, Alberto; Meléndez, Gabriela; de Micheli, Alfredo

    2010-01-01

    Certain criteria are examined for infarctions currents defined as inferior or inferolateral. To do this, certain considerations on the anatomical aspects of isolated and in situ heart are laid out. The topographical relationship of the in situ heart with other adjacent thoracic organs is described. The heart is schematically represented as a pyramid with a triangular base and its walls and borders are related to walls of the thorax. The spatial orientation of the main resulting vectors from ventricular depolarization and repolarization are summarized also. Usefulness of registering the unipolar thoracic leads V7, V8, V9 or a complete electrocardiographic thoracic circle, is underlined. This method allows to detect for of the existence of an acute myocardial infarction in the inferior and inferolateral segments in as third basal and mid cardiac regions previously denominated posterolateral. On the base of previous electroanatomical comparisons, it is concluded that the thoracic posterior leads V7 - V9, as well as the magnetic resonance images, explore the same heart regions. Therefore, these two methods: electrocardiography which is an essentially functional method and magnetic resonance that especially focus on structural changes are not contradictory but rather complementary tests." PMID:21147577

  7. Severe Plasmodium falciparum infection mimicking acute myocardial infarction.

    PubMed

    Sulaiman, Helmi; Ismail, Muhammad Dzafir; Jalalonmuhali, Maisarah; Atiya, Nadia; Ponnampalavanar, Sasheela

    2014-08-30

    This case report describes a case of presumed acute myocardial infarction in a returned traveler who was later diagnosed to have severe malaria. Emergency coronary angiography was normal and subsequent peripheral blood film was positive for Plasmodium falciparum.

  8. [Specifically adapted management of diabetics after myocardial infarct].

    PubMed

    Passa, P

    1998-06-13

    Approximately 20% of all patients hospitalized for myocardial infarction have diabetes. The percentage has been increasing constantly and mortality is significantly higher in these patients. The highest rate is observed in women. Despite continuing progress in patient management there has been no reduction in the overmortality after myocardial infarction in diabetic patients. The majority of these deaths are unwarranted and could be avoided if diabetic patients were given specifically adapted treatment after myocardial infarction. Unfortunately, as shown by the EURASPIRE study, there is a gap between intensive care unit discharge prescriptions and follow-up care. With the explosive "epidemic" of noninsulin-diabetes and population aging the number of patients with coronary artery disease and diabetes will rise in the future. Wouldn't it be reasonable to establish special cardiodiabetic units where such patients could benefit from close, and daily, cooperation between diabetologists and cardiologists? Such facilities could be expected to significantly reduce the overmortality in diabetic patients after myocardial infarction.

  9. 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.

  10. 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.

  11. 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

  12. Cardiovascular gene therapy for myocardial infarction

    PubMed Central

    Scimia, Maria C; Gumpert, Anna M; Koch, Walter J

    2014-01-01

    Introduction Cardiovascular gene therapy is the third most popular application for gene therapy, representing 8.4% of all gene therapy trials as reported in 2012 estimates. Gene therapy in cardiovascular disease is aiming to treat heart failure from ischemic and non-ischemic causes, peripheral artery disease, venous ulcer, pulmonary hypertension, atherosclerosis and monogenic diseases, such as Fabry disease. Areas covered In this review, we will focus on elucidating current molecular targets for the treatment of ventricular dysfunction following myocardial infarction (MI). In particular, we will focus on the treatment of i) the clinical consequences of it, such as heart failure and residual myocardial ischemia and ii) etiological causes of MI (coronary vessels atherosclerosis, bypass venous graft disease, in-stent restenosis). Expert opinion We summarise the scheme of the review and the molecular targets either already at the gene therapy clinical trial phase or in the pipeline. These targets will be discussed below. Following this, we will focus on what we believe are the 4 prerequisites of success of any gene target therapy: safety, expression, specificity and efficacy (SESE). PMID:24328708

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

    PubMed

    Sjögren, Bengt; Gunnare, Sara; Sandler, Håkan

    2002-06-01

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

  14. "My parents died of myocardial infarction: is that my destiny?".

    PubMed

    Narula, Nupoor; Rapezzi, Claudio; Tavazzi, Luigi; Arbustini, Eloisa

    2012-01-01

    This article presents an overview of clinical and molecular genetics of myocardial infarction (MI). Discussion includes the partial overlapping of risk factors for myocardial infarction and atherosclerosis, the impact of a positive family history on the risk of MI, the "familial" nongenetic, environmental factors, the inherited risk associated with the low-dose input of many genes, and a simple approach to stratify the individual risk in genetic counseling.

  15. Anaesthetic management of myocardial infarction in a parturient.

    PubMed

    Aglio, L S; Johnson, M D

    1990-08-01

    Myocardial infarction is encountered rarely during pregnancy, but when it occurs the event is life-threatening to both mother and fetus. Data on maternal and fetal outcome are limited, but overall maternal mortality approaches 35%, and 40% of deaths occur during the third trimester. We present a case of myocardial infarction occurring at 38 weeks gestation, and discuss the anaesthetic management of the problems encountered during labour and delivery. PMID:2121201

  16. Myocardial Infarction and Functional Outcome Assessment in Pigs

    PubMed Central

    Koudstaal, Stefan; Jansen of Lorkeers, Sanne J.; Gho, Johannes M.I.H.; van Hout, Gerardus P.J; Jansen, Marlijn S.; Gründeman, Paul F.; Pasterkamp, Gerard; Doevendans, Pieter A.

    2014-01-01

    Introduction of newly discovered cardiovascular therapeutics into first-in-man trials depends on a strictly regulated ethical and legal roadmap. One important prerequisite is a good understanding of all safety and efficacy aspects obtained in a large animal model that validly reflect the human scenario of myocardial infarction (MI). Pigs are widely used in this regard since their cardiac size, hemodynamics, and coronary anatomy are close to that of humans. Here, we present an effective protocol for using the porcine MI model using a closed-chest coronary balloon occlusion of the left anterior descending artery (LAD), followed by reperfusion. This approach is based on 90 min of myocardial ischemia, inducing large left ventricle infarction of the anterior, septal and inferoseptal walls. Furthermore, we present protocols for various measures of outcome that provide a wide range of information on the heart, such as cardiac systolic and diastolic function, hemodynamics, coronary flow velocity, microvascular resistance, and infarct size. This protocol can be easily tailored to meet study specific requirements for the validation of novel cardioregenerative biologics at different stages (i.e. directly after the acute ischemic insult, in the subacute setting or even in the chronic MI once scar formation has been completed). This model therefore provides a useful translational tool to study MI, subsequent adverse remodeling, and the potential of novel cardioregenerative agents. PMID:24796715

  17. IL-17A promotes ventricular remodeling after myocardial infarction.

    PubMed

    Zhou, Su-Feng; Yuan, Jing; Liao, Meng-Yang; Xia, Ni; Tang, Ting-Ting; Li, Jing-Jing; Jiao, Jiao; Dong, Wen-Yong; Nie, Shao-Fang; Zhu, Zheng-Feng; Zhang, Wen-Cai; Lv, Bing-Jie; Xiao, Hong; Wang, Qing; Tu, Xin; Liao, Yu-Hua; Shi, Guo-Ping; Cheng, Xiang

    2014-10-01

    Inflammatory responses play an important role in the pathogenesis of adverse ventricular remodeling after myocardial infarction (MI). We previously demonstrated that interleukin (IL)-17A plays a pathogenic role in myocardial ischemia/reperfusion injury and viral myocarditis. However, the role of IL-17A in post-MI remodeling and the related mechanisms have not been fully elucidated. Acute MI was induced by permanent ligation of the left anterior descending coronary artery in C57BL/6 mice. Repletion of IL-17A significantly aggravated both early- and late-phase ventricular remodeling, as demonstrated by increased infarct size, deteriorated cardiac function, increased myocardial fibrosis, and cardiomyocyte apoptosis. By contrast, genetic IL-17A deficiency had the opposite effect. Additional studies in vitro indicated that IL-17A induces neonatal cardiomyocyte (from C57BL/6 mice) apoptosis through the activation of p38, p53 phosphorylation, and Bax redistribution. These data demonstrate that IL-17A induces cardiomyocyte apoptosis through the p38 mitogen-activated protein kinase (MAPK)-p53-Bax signaling pathway and promotes both early- and late-phase post-MI ventricular remodeling. IL-17A might be an important target in preventing heart failure after MI. Key message: We demonstrated that IL-17A plays a pathogenic role both in the early and late stages of post-MI remodeling. IL-17A induces murine cardiomyocyte apoptosis. IL-17A induces murine cardiomyocyte apoptosis through the p38 MAPK-p53-Bax signaling pathway.

  18. Highly purified omega-3 polyunsaturated fatty acids are effective as adjunct therapy for secondary prevention of myocardial infarction.

    PubMed

    Verboom, Cees N

    2006-12-01

    Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione was the first large randomized trial to produce evidence that a pharmaceutical preparation of highly purified omega-3 polyunsaturated fatty acids (PUFAs), administered as an adjunct to other accepted interventions, had a favorable effect on hard clinical end-points in post-myocardial infarction patients. Much of the 20% all-cause mortality benefit recorded during the study could be attributed to a 45% reduction in sudden death--a fatal outcome that traditionally has proved resistant to medical intervention. These results were obtained with an omega-3 PUFA dose of 1 g/day, which is much lower than was routinely being used at the time the study was initiated (e.g. 4 g/day for hypertriglyceridemia). One consequence of this low-dose regimen was that the tolerability profile of omega-3 PUFAs during GISSI-Prevenzione was considered highly satisfactory, with low adverse event incidence rates and low rates of discontinuation due to adverse events. Time-course analysis established that much of the survival benefit of omega-3 PUFA treatment in GISSI-Prevenzione was realized during the early months of the trial. The beneficial effects of omega-3 PUFA treatment were observed on top of standard, secondary pharmacological prevention therapy like anti-platelet agents, statins, beta-blockers and angiotensin-converting enzyme (ACE) inhibitors. The benefits of omega-3 PUFA therapy were also apparent in patients at all standards of adherence to a healthy diet and may have been augmented in patients with the best dietary profile. Patients with diabetes mellitus (approximately 15% of the study cohort) appeared to benefit from omega-3 PUFAs to at least the same extent as the general study population; the treatment effect on sudden death was progressively more pronounced as left ejection fraction declined. Cost-effectiveness analyses undertaken from a third-party payer perspective for Italy

  19. 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.

  20. Multiscale Characterization of Impact of Infarct Size on Myocardial Remodeling in an Ovine Infarct Model.

    PubMed

    Zhang, Pei; Li, Tielou; Griffith, Bartley P; Wu, Zhongjun J

    2015-01-01

    The surviving myocardium initially compensates the loss of injured myocardium after myocardial infarction (MI) and gradually becomes progressively dysfunctional. There have been limited studies on the effect of infarct size on temporal and spatial alterations in the myocardium during progressive myocardial remodeling. MI with three infarct sizes, i.e. 15, 25 and 35% of the left ventricular (LV) wall, was created in an ovine infarction model. The progressive LV remodeling over a 12-week period was studied. Echocardiography, sonomicrometry, and histological and molecular analyses were carried out to evaluate cardiac function, regional tissue contractile function, structural remodeling and cardiomyocyte hypertrophy, and calcium handling proteins. Twelve weeks after MI, the 15, 25 and 35% MI groups had normalized LV end diastole volumes of 1.4 ± 0.2, 1.7 ± 0.3 and 2.0 ± 0.4 ml/kg, normalized end systole volumes of 1.0 ± 0.1, 1.0 ± 0.2 and 1.3 ± 0.3 ml/kg and LV ejection fractions of 43 ± 3, 42 ± 6 and 34 ± 4%, respectively. They all differed from the sham group (p < 0.05). All the three MI groups exhibited larger wall areal expansion (remodeling strain), larger cardiomyocyte size and altered expression of calcium handing proteins in the adjacent myocardium compared to the remote counterpart from the infarct. A significant correlation was found between cardiomyocyte size and remodeling strain in the adjacent zone. A comparative analysis among the three MI groups showed that a larger infarct size (35 vs. 15% MI) was associated with larger remodeling strain, more serious impairment in the cellular structure and composition, and regional contractile function at regional tissue level and LV function at organ level.

  1. Acute inferior myocardial infarction with right ventricular infarction is more prone to develop cardiogenic shock.

    PubMed

    Bari, M A; Roy, A K; Islam, M Z; Aditya, G; Bhuiyan, A S

    2015-01-01

    Cardiogenic shock is rare in isolated acute inferior myocardial infarction but there is relationship of cardiogenic shock with inferior myocardial infarction if associated with right ventricular infarction. A prospective study was carried out to see the association of cardiogenic shock with inferior myocardial infarction if associated with right ventricular infarction. This study was conducted from January 2011 to November 2011. A total of 100 cases were selected as study population which was taken from the Department of Cardiology, Mymensingh Medical College Hospital, Mymensingh, Bangladesh. Among them 50 were in Group A and 50 were in Group B. Group A was the patients of acute myocardial infarction with right ventricular infarction. Group B was the patients of acute myocardial infarction without right ventricular infarction. It revealed that 9(18%) in Group A and 3(6%) in Group B developed cardiogenic shock which is statistically significant (p<0.05). The study concluded that AMI (Inf) with RVI is significantly associated with cardiogenic shock.

  2. 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.

  3. The Effect of Exercise Training on Diastolic and Systolic Function After Acute Myocardial Infarction: A Randomized Study.

    PubMed

    Fontes-Carvalho, Ricardo; Azevedo, Ana Isabel; Sampaio, Francisco; Teixeira, Madalena; Bettencourt, Nuno; Campos, Lilibeth; Gonçalves, Francisco Rocha; Ribeiro, Vasco Gama; Azevedo, Ana; Leite-Moreira, Adelino

    2015-09-01

    After acute myocardial infarction (AMI), diastolic dysfunction is frequent and an important determinant of adverse outcome. However, few interventions have proven to be effective in improving diastolic function. We aimed to determine the effect of exercise training on diastolic and systolic function after AMI.One month after AMI, 188 patients were prospectively randomized (1:1) to an 8-week supervised program of endurance and resistance exercise training (n = 86; 55.9 ± 10.8 years) versus standard of care (n = 89; 55.4 ± 10.3 years). All patients were submitted to detailed echocardiography and cardiopulmonary exercise test, at baseline and immediately after the study. Diastolic function was evaluated by the determination of tissue-Doppler derived early diastolic velocities (E' velocity at the septal and lateral sides of mitral annulus) and by the E/E' (ratio between the E wave velocity from mitral inflow and the E' velocity) as recommended in the consensus document for diastolic function assessment.At the end of the study, there was no significant change in E' septal velocity or E/E' septal ratio in the exercise group. We observed a small, although nonsignificant, improvement in E' lateral (mean change 0.1 ± 2.0 cm/s; P = 0.40) and E/E' lateral ratio (mean change of -0.3 ± 2.5; P = 0.24), while patients in the control group had a nonsignificant reduction in E' lateral (mean change -0.4 ± 1.9 cm/s; P = 0.09) and an increase in E/E' lateral ratio (mean change + 0.3 ± 3.3; P = 0.34). No relevant changes occurred in other diastolic parameters. The exercise-training program also did not improve systolic function (either tissue Doppler systolic velocities or ejection fraction).Exercise capacity improved only in the exercise-training group, with an increase of 1.6 mL/kg/min in pVO2 (P = 0.001) and of 1.9 mL/kg/min in VO2 at anaerobic threshold (P < 0.001).After AMI, an 8-week endurance plus

  4. Myocardial protection of early extracorporeal membrane oxygenation (ECMO) support for acute myocardial infarction with cardiogenic shock in pigs.

    PubMed

    Zhu, Gang-jie; Sun, Li-na; Li, Xing-hai; Wang, Ning-fu; Wu, Hong-hai; Yuan, Chen-xing; Li, Qiao-qiao; Xu, Peng; Ren, Ya-qi; Mao, Bao-gen

    2015-09-01

    The aim of this study was to explore myocardial protection of early extracorporeal membrane oxygenation (ECMO) support for acute myocardial infarction with cardiogenic shock in pigs. 24 male pigs (34.6 ± 1.3 kg) were randomly divided into three groups-control group, drug therapy group, and ECMO group. Myocardial infarction model was created in drug therapy group and ECMO group by ligating coronary artery. When cardiogenic shock occurred, drugs were given in drug therapy group and ECMO began to work in ECMO group. The pigs were killed 24 h after cardiogenic shock. Compared with in drug therapy group, left ventricular end-diastolic pressure in ECMO group decreased significantly 6 h after ligation (P < 0.05). At the end of the experiments, LV - dp/dt among three groups was significantly different, drug therapy group < ECMO group < control group. There was no difference in LV + dp/dt between drug therapy group and ECMO group. Compared with drug group, myocardial infarct size of ECMO group did not reduce significantly, but myocardial enzyme and troponin-I decreased significantly. Compared with drug therapy, ECMO improves left ventricular diastolic function, and may improve systolic function. ECMO cannot reduce myocardial infarct size without revascularization, but may have positive effects on ischemic areas by avoiding further injuring.

  5. ECG findings after myocardial infarction in children after Kawasaki disease

    SciTech Connect

    Nakanishi, T.; Takao, A.; Kondoh, C.; Nakazawa, M.; Hiroe, M.; Matsumoto, Y.

    1988-10-01

    Standard 12-lead ECGs were evaluated in 17 children with myocardial infarction and 78 children without myocardial infarction after Kawasaki disease; sensitivity and specificity of the ECG infarction criteria were determined. The presence or absence of myocardial infarction was determined from either clinical examination results (coronary angiography, ventriculography, and thallium-201 myocardial imaging) or autopsy findings. Of seven patients with inferior infarction, abnormally deep Q waves in lead II, III, or aVF were observed in six, but the duration was greater than 0.04 second in only one (14%). The sensitivity and specificity of inferior infarction criteria based on Q wave amplitude were 86% and 97%, respectively. Of eight patients with anterior infarction, seven (88%) had abnormally deep and wide (greater than or equal to 0.04 second) Q waves in anterior chest leads. The sensitivity and specificity of the infarction criteria based on the amplitude and duration of the Q wave were 75% and 99%, respectively. Of seven patients with lateral infarction, Q waves were observed in lead I, aVL, or both in four patients, and in all of these patients Q waves were wider than 0.04 second. In two patients with both inferior and anterior infarction, Q waves were observed only in leads II, III, and aVF; in only one patient were the Q waves wider than 0.04 second. Thus deep Q waves in lead II, III, or aVF that are not wider than 0.04 second may indicate inferior infarction in children. Q waves in lead I, aVL, and chest leads associated with anterolateral infarction are in most instances deep and wide.

  6. 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.

  7. Myocardial infarction association with the Riley-Day syndrome.

    PubMed

    Reshef, R; Aderka, D; Suprun, H; Manelis, G; Manelis, J

    1977-10-01

    The "sudden death" of a 23-year-old Ashkenazy Jew, suffering from "familial dysautonomia" was probably caused by an arrhythmia accompanying a myocardial infarction. Such a report is unique. Diffuse coronary atherosclerosis and direct myocardial "catecholamine cardiomyopathy" seem responsible for the myocardial damage. However, diversion of the endocardial blood flow toward dpicardium and a "coronary steal" phenomenon, both the result of a sudden catecholamine discharge, could aggravate the ischemic injury.

  8. A new cooperative approach for ST-elevation myocardial infarction patients to receive timely and effective percutaneous coronary reperfusion in China

    PubMed Central

    Yan, Jin-Chuan; Yan, Yang; Wang, Cui-Ping; Xu, Liang-Jie; Liang, Yi

    2016-01-01

    Background Acute myocardial infarction (AMI) is the most serious type of coronary heart disease. However, less than 30% of these patients have been treated effectively in China. Delayed treatment is a leading cause. This study aimed to evaluate a new regional cooperative model for improving the first medical contact-to-device time and the therapeutic effects on AMI patients. Methods A retrospective analysis of 458 ST-elevation myocardial infarction (STEMI) patients was performed. Patients were divided into two groups in terms of before or after the model were implemented. First medical contact-to-device time (FMC2D), Door to device time (D2D), referral time, cardiac functions, mean cost, days of hospitalization, and major adverse cardiac events (MACE) were analyzed. Results The mean FMC2D time, D2D time and referral time of the model group were significantly lower than the control group. The left ventricular ejection fraction of the model group increased but the left ventricular end-diastolic dimension decreased compared with the control group at 6 months after discharge. These results also showed that mean costs and days of hospitalization were reduced. The MACE rate was reduced in the model group. Conclusions These results suggested that the new model decreased the FMC2D time, which could improve the cardiac function and therapeutic effect of STEMI patients as well as decreased the financial burden. PMID:27605941

  9. Increasing mean arterial pressure in cardiogenic shock secondary to myocardial infarction: effects on hemodynamics and tissue oxygenation.

    PubMed

    Perez, Pierre; Kimmoun, Antoine; Blime, Vincent; Levy, Bruno

    2014-04-01

    There are very few data regarding the effects of norepinephrine uptitration on global and regional hemodynamics in cardiogenic shock. We studied 25 patients with shock secondary to myocardial infarction successfully treated with percutaneous coronary intervention. Before the inclusion, 16 of 25 patients presented a cardiac arrest in the presence of medical staff. Norepinephrine was titrated to increase mean arterial pressure (MAP) from 65 to 85 mmHg during 1 h. Swan-Ganz variables, arterial and mixed venous blood gases, lactate, and thenar near-infrared spectroscopy variables (muscle tissue oxygen saturation [StO2] and its changes during a vascular occlusion test) were measured before, 1 h after norepinephrine uptitration, and 1 h after norepinephrine downtitration. To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.6 (0.28-1.2) to 1.53 µg · kg · min (0.76-2.6 µg · kg · min) (P < 0.00001) (median and interquartile range), with no change in heart rate. Norepinephrine uptitration significantly increased cardiac index (2.3 ± 0.5 to 2.8 ± 0.1 L · min · m), cardiac power index (0.40 ± 0.1 to 0.55 ± 0.1 W/m), mixed venous oxygen saturation (69% ± 9% to 73% ± 9%), and coronary perfusion pressure (32 ± 3 to 43 ± 4 mmHg). Lactate level decreased from 2.6 ± 1.7 to 1.6 ± 0.4 mmol/L (P < 0.05). Pulmonary artery occlusion pressure remained unchanged. Regarding near-infrared spectroscopy variables, all values except StO2 were significantly pathological when compared with healthy volunteers. The StO2 recovery slope and delta StO2, respectively, increased from 3.0% ± 1.3%/s to 3.6% ± 1.3%/s and 10% ± 3% to 14% ± 4%, whereas StO2 did not change (83% ± 6% to 83% ± 7%). After H1, norepinephrine was decreased to basal values, and all variables returned to baseline. In conclusion, a short-term increase in MAP with norepinephrine in resuscitated cardiogenic shock complicated by postreperfusion disease is associated with better cardiac performance and

  10. 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.

  11. 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

  12. Effects of sildenafil and/or muscle derived stem cells on myocardial infarction

    PubMed Central

    2012-01-01

    Background Previous studies have shown that long-term oral daily PDE 5 inhibitors (PDE5i) counteract fibrosis, cell loss, and the resulting dysfunction in tissues of various rat organs and that implantation of skeletal muscle-derived stem cells (MDSC) exerts some of these effects. PDE5i and stem cells in combination were found to be more effective in non-MI cardiac repair than each treatment separately. We have now investigated whether sildenafil at lower doses and MDSC, alone or in combination are effective to attenuate LV remodeling after MI in rats. Methods MI was induced in rats by ligature of the left anterior descending coronary artery. Treatment groups were: “Series A”: 1) untreated; 2) oral sildenafil 3 mg/kg/day from day 1; and “Series B”: intracardiac injection at day 7 of: 3) saline; 4) rat MDSC (106 cells); 5) as #4, with sildenafil as in #2. Before surgery, and at 1 and 4 weeks, the left ventricle ejection fraction (LVEF) was measured. LV sections were stained for collagen, myofibroblasts, apoptosis, cardiomyocytes, and iNOS, followed by quantitative image analysis. Western blots estimated angiogenesis and myofibroblast accumulation, as well as potential sildenafil tachyphylaxis by PDE 5 expression. Zymography estimated MMPs 2 and 9 in serum. Results As compared to untreated MI rats, sildenafil improved LVEF, reduced collagen, myofibroblasts, and circulating MMPs, and increased cardiac troponin T. MDSC replicated most of these effects and stimulated cardiac angiogenesis. Concurrent MDSC/sildenafil counteracted cardiomyocyte and endothelial cells loss, but did not improve LVEF or angiogenesis, and upregulated PDE 5. Conclusions Long-term oral sildenafil, or MDSC given separately, reduce the MI fibrotic scar and improve left ventricular function in this rat model. The failure of the treatment combination may be due to inducing overexpression of PDE5. PMID:22871104

  13. Comparison of radionuclide and enzymatic estimate of infarct size in patients with acute myocardial infarction

    SciTech Connect

    Hirsowitz, G.S.; Lakier, J.B.; Marks, D.S.; Lee, T.G.; Goldberg, A.D.; Goldstein, S.

    1983-06-01

    A comparison was made of the estimated size of the myocardial infarction occurring in 26 patients with a first infarction using creatine kinase (CK) enzyme release between radionuclide gated blood pool measurement of total and regional ventricular function and thallium-201 scintigraphic measurement of myocardial perfusion defects. Creatine kinase estimates of infarct size (enzymatic infarct size) correlated closely with the percent of abnormal contracting regions, left ventricular ejection fraction and thallium-201 estimates of percent of abnormal perfusion area (r . 0.78, 0.69 and 0.74, respectively, p less than 0.01). A close correlation also existed between percent abnormal perfusion area and percent of abnormal contracting regions (r . 0.81, p less than 0.01) and left ventricular ejection fraction (r . 0.69, p less than 0.01). Enzymatic infarct size was larger in anterior (116 +/- 37 CK-g-Eq) than inferior (52 +/- 29 CK-g-Eq) myocardial infarction (p less than 0.01) and was associated with significantly more left ventricular functional impairment as determined by left ventricular ejection fraction (33 +/- 7 versus 60 +/- 10%) (p less than 0.01) and percent abnormal perfusion area (58 +/- 14 versus 13 +/- 12) (p less than 0.01). No significant correlation was observed between enzymatic infarct size and right ventricular ejection fraction. These different methods of estimating infarct size correlated closely with each other in these patients with a first uncomplicated myocardial infarction.

  14. Comparing the effects of MSCs and CD34+ cell therapy in a rat model of myocardial infarction.

    PubMed

    Shalaby, Sally M; El-Shal, Amal S; Zidan, Haidy E; Mazen, Nehad F; Abd El-Haleem, Manal R; Abd El Motteleb, Dalia M

    2016-05-01

    Stem cell therapy is considered as a promising approach in the treatment of myocardial infarction (MI). This study was designed as a comparison of human umbilical cord blood (HUCB)-derived CD34+ and HUCB-derived MSCs for the repair of cardiac tissue by induction of the angiogenesis. Forty-eight male rats were randomized into four groups: sham-operated group, MI group, MSCs-treated group, and CD34+ cells-treated group. After 4 weeks, the rats were sacrificed. All sections from left ventricles of all groups were subjected to hematoxylin & eosin, Masson's trichrome, and immunohistochemical stains (CD133, CD44, and α-smooth muscle actin). RNA was extracted for gene expression of the angiogenic markers. A significant reduction of the infarct size and the amplitude of T-wave in the CD34+ cells-treated group when compared with the MSCs-treated group were determined. Histologically, the MI group showed scar tissue, congested blood capillaries around the infarcted area, some necrotic cells, and inflammatory cells. Administration of either MSCs or CD34+ cells had a therapeutic potential to induce regenerative changes in the myocardium with better results in CD34+cells-treated group. Quantitative RT-PCR analysis revealed a significant increase in the expression of vascular endothelial growth factor (VEGF), VEGFR-2, Ang-1, and Tie-2 and a significant decreased expression of Ang-2 in stem cells transplanted groups when compared with the noncell transplanted hearts. A significant increase of VEGF, VEGFR-2, Ang-1, and Tie-2 expression in the group receiving CD34+ cells than those receiving MSCs was found. Finally, there was an upregulation of both human VEGF and human hypoxia-inducible factor 1α in the infarcted hearts treated by CD34+ cells than that treated by MSCs. We first revealed a superior efficacy of CD34+ cells when compared with MSCs in induction of regenerative changes in the MI model. Both cell therapies may repair the damaged heart tissue primarily by secretion of

  15. Effect of a real-time tele-transmission system of 12-lead electrocardiogram on the first-aid for athletes with ST-elevation myocardial infarction.

    PubMed

    Zhang, Huan; Song, Donghan; An, Lina

    2016-05-01

    To study the effect of a real-time tele-transmission system of 12-lead electrocardiogram on door-to-balloon time in athletes with ST-elevation myocardial infarction. A total of 60 athletes with chest pain diagnosed as ST-elevation myocardial infarction (STEMI) from our hospital were randomly divided into group A (n=35) and group B (n=25), the patients in group A transmitted the real-time tele-transmission system of 12-lead electrocardiogram to the chest pain center before arriving in hospital, however, the patients in group B not. The median door-to-balloon time was significant shorter in-group A than group B (38min vs 94 min, p<0.01) and the ratio of door-to-balloon time below 90 min was remarkable higher in-group A (94.2% vs 60%, p<0.01). The rate of catheter laboratory occupied was 5.7% in-group A and 40% in group B respectively (p=0.001). There was no statistically difference in mortality between the two groups (5.7% vs 4%, p>0.05). The median length of stay was significant reduced in-group A (5 days vs 7 days, p<0.01). Real-time tele-transmission system of 12 lead electrocardiogram is beneficial to the pre-hospital diagnosis of STEMI. PMID:27383498

  16. 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

  17. 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

  18. Natural and unnatural triggers of myocardial infarction.

    PubMed

    Kloner, Robert A

    2006-01-01

    Previous analyses have suggested that factors that stimulate the sympathetic nervous system and catecholamine release can trigger acute myocardial infarction. The wake-up time, Mondays, winter season, physical exertion, emotional upset, overeating, lack of sleep, cocaine, marijuana, anger, and sexual activity are some of the more common triggers. Certain natural disasters such as earthquakes and blizzards have also been associated with an increase in cardiac events. Certain unnatural triggers may play a role including the Holiday season. Holiday season cardiac events peak on Christmas and New Year. A number of hypotheses have been raised to explain the increase in cardiac events during the holidays, including overeating, excessive use of salt and alcohol, exposure to particulates, from fireplaces, a delay in seeking medical help, anxiety or depression related to the holidays, and poorer staffing of health care facilities at this time. War has been associated with an increase in cardiac events. Data regarding an increase in cardiac events during the 9/11 terrorist attack have been mixed. Understanding the cause of cardiovascular triggers will help in developing potential therapies.

  19. Potential role of renin-angiotensin system blockade for preventing myocardial ischemia/reperfusion injury and remodeling after myocardial infarction.

    PubMed

    Dai, Wangde; Kloner, Robert A

    2011-03-01

    Experimental and clinical studies have demonstrated that myocardial ischemia induces activation of various components of the renin-angiotensin system (RAS), including angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensins, and angiotensin receptors, in the acute phase of myocardial infarction and the postinfarction remodeling process. Pharmacological inhibition of the RAS by administration of renin inhibitors, ACE inhibitors, and angiotensin receptor blockers has shown beneficial effects on the pathological processes of myocardial infarction in both experimental animal studies and clinical trials. However, the potential mechanisms responsible for the cardioprotection of RAS inhibition remain unclear. In this review, we discuss roles of RAS blocking in the prevention of myocardial ischemia/reperfusion injury and postinfarction remodeling.

  20. Reducing myocardial infarct size: challenges and future opportunities.

    PubMed

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

    2016-03-01

    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.

  1. 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

  2. Does the addition of losartan improve the beneficial effects of ACE inhibitors in patients with anterior myocardial infarction? A pilot study

    PubMed Central

    Di, P; Bucca, V; Scalzo, S; Cannizzaro, S; Giubilato, A; Paterna, S

    1999-01-01

    OBJECTIVE—To verify the efficacy of the combination of captopril (75 mg day) and losartan (25 mg/day) in early postinfarction phases of reperfused anterior acute myocardial infarction.
DESIGN AND PATIENTS—99 patients, hospitalised for suspected anterior acute myocardial infarction within four hours from the onset of symptoms, were randomised into two groups: group A included 50 patients who received captopril 75 mg/day and placebo; group B included 49 patients who received captopril 75 mg/day within three days of admission plus losartan 12.5 mg, as a first dose, and 25 mg/day successively. An additional 23 patients with anterior acute myocardial infarction received losartan 25 mg alone and acted as controls (group C) to check the effects of losartan on plasma angiotensin II (AII) concentrations. Noradrenaline (norepinephrine) (NA) and AII plasma concentrations were measured on the third and 10th day after admission in 93 patients (35 from group A, 35 from group B, and 23 from group C). 90 days after admission patients underwent echocardiography to determine end systolic volume (ESV) and ejection fraction (EF).
RESULTS—Patients in groups A and B were similar with regard to age, sex, creatine kinase peak, EF, ESV, and risk factors. Group B (captopril plus losartan) patients showed a significant reduction in mean (SD) systolic blood pressure within the group (basal 128 (10) mm Hg; 10 days after admission 105 (9) mm Hg, p < 0.001), and in comparison with group A (captopril) patients (basal 127 (11) mm Hg; 10 days after admission 116 (10) mm Hg, p < 0.001). Diastolic blood pressure was also lower in group B patients versus group A (66 (11) v 77 (11) mm Hg). Group C (losartan) patients also showed a significant reduction in systolic blood pressure (131 (13) mm Hg down to 121 (12) mm Hg, p < 0.001). Neither NA nor AII plasma concentrations in groups A and B differed significantly in basal samples (NA 673 (138) v 675

  3. Environmental temperature and mortality from acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Mannino, Joseph A.; Washburn, Richard A.

    1989-03-01

    Mortality from acute myocardial infarction (MI) over the 5 year period 1982 1987 in Brown County, Wisconsin, was analyzed to assess the relationship with environmental temperature. Deaths occurrring on the day of and the day following a significant snowfall as well as deaths occuring in health care facilities were eliminated from consideration because the focus was upon temperature, not snowfall or events within a hospital. These criteria resulted in the inclusion of 1,802 days and 926 cases of acute MI. The mean temperature on the day of death was obtained from climatological data and were grouped into six categories covering a range of temperatures from<-17.8°C (0°F) to 16.1°C (61°F). The number of deaths in each category was tabulated. The effect of temperature, sex, and age were analyzed by regression analysis. The results indicated a linear increase in mortality as mean daily temperature decreased over the temperature range. The inverse temperature effect was most pronounced in males over the age of 60. These results indicate that cold temperatures appear to be associated with an increased mortality from myocardial infarction.

  4. Pharmacologic Effects of Cannabidiol on Acute Reperfused Myocardial Infarction in Rabbits: Evaluated With 3.0T Cardiac Magnetic Resonance Imaging and Histopathology.

    PubMed

    Feng, Yuanbo; Chen, Feng; Yin, Ting; Xia, Qian; Liu, Yewei; Huang, Gang; Zhang, Jian; Oyen, Raymond; Ni, Yicheng

    2015-10-01

    Cannabidiol (CBD) has anti-inflammatory effects. We explored its therapeutic effects on cardiac ischemia-reperfusion injury with an experimental imaging platform. Reperfused acute myocardial infarction (AMI) was induced in rabbits with a 90-minute coronary artery occlusion followed by 24-hour reperfusion. Before reperfusion, rabbits received 2 intravenous doses of 100 μg/kg CBD (n = 10) or vehicle (control, n = 10). Evans blue was intravenously injected for later detection of the AMI core. Cardiac magnetic resonance imaging was performed to evaluate cardiac morphology and function. After euthanasia, blood troponin I (cTnI) was assessed, and the heart was excised and infused with multifunctional red iodized oil dye. The heart was sliced for digital radiography to quantify the perfusion density rate, area at risk (AAR), and myocardial salvage index, followed by histomorphologic staining. Compared with controls, CBD treatment improved systolic wall thickening (P < 0.05), significantly increased blood flow in the AAR (P < 0.05), significantly decreased microvascular obstruction (P < 0.05), increased the perfusion density rate by 1.7-fold, lowered the AMI core/AAR ratio (P < 0.05), and increased the myocardial salvage index (P < 0.05). These improvements were associated with reductions in serum cTnI, cardiac leukocyte infiltration, and myocellular apoptosis (P < 0.05). Thus, CBD therapy reduced AMI size and facilitated restoration of left ventricular function. We demonstrated that this experimental platform has potential theragnostic utility.

  5. Comparison of the effects of EPA and DHA alone or in combination in a murine model of myocardial infarction.

    PubMed

    Madingou, Ness; Gilbert, Kim; Tomaro, Leandro; Prud'homme Touchette, Charles; Trudeau, François; Fortin, Samuel; Rousseau, Guy

    2016-08-01

    The aim of this project was to investigate the impact of two dietary omega-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), alone or in combination, on infarct size. Adult, male Sprague-Dawley rats were fed for 14 days with different omega-3 diets. The animals were subjected to ischemia for 40min followed by reperfusion. Infarct size, Akt (protein kinase B) activation level, caspase-3 activity and mitochondrial permeability transition pore (mPTP) opening were measured. The results indicate that EPA or DHA alone significantly reduced infarct size compared to the other diets. Akt activity was increased in the group fed EPA or DHA alone, whereas no significant activation was observed in the other groups compared to no omega-3 PUFA. DHA alone reduced caspase-3 activity and conferred resistance to mPTP opening. In conclusion, our results demonstrate that EPA and DHA are individually effective in diminishing infarct size in our experimental model while their combination is not. PMID:27499449

  6. 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.

  7. Effects of an early treatment with lisinopril and isosorbide-5-mononitrate on hemodynamics and late ventricular remodelling in rats with 9-week myocardial infarction.

    PubMed

    Riva, E; Kurosaki, M; Porzio, S; Latini, R; Lagrasta, C; Olivetti, G

    1995-06-01

    This study was undertaken to assess whether the converting enzyme inhibitor lisinopril, and the long-acting nitrate, isosorbide-5-mononitrate, affect left ventricle dysfunction and anatomical remodelling in rats with myocardial infarction. Lisinopril, isosorbide-5-mononitrate or vehicle were given to rats (n = 10-14 per group) immediately after coronary artery occlusion (by an intravenous bolus) and then for nine weeks (in drinking water). At the end of the study, left ventricular pressures were measured, the heart arrested in diastole, and infarct size, left ventricular chamber volume and wall thicknesses measured. Lisinopril significantly lowered systemic blood pressure and left ventricular systolic pressure in rats with small (< 15% scarred tissue of the left ventricle) and large (> 15%) infarcts; the weight of the left ventricle (including the septum) was reduced by 24% and 28% in animals with small and large infarcts, respectively. Lisinopril lowered left ventricular end-diastolic pressure (by 33% and 39%) and chamber volume (by 4% and 34%) in rats with small and large infarcts, respectively, compared with controls (NS). The combined anatomical and hemodynamic changes led to a reduction of the circumferential wall stress by 20% and 44% in lisinopril-treated rats with small and large infarcts, respectively (NS). No significant changes were seen in the nitrate-treated hearts compared with controls. Lisinopril, given early after myocardial infarction and continued for nine weeks, significantly affected cardiac hemodynamics and ventricular weights in rats with infarcts of different sizes.(ABSTRACT TRUNCATED AT 250 WORDS)

  8. 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.

  9. Bone Marrow Mesenchymal Stem Cells (BM-MSCs) Improve Heart Function in Swine Myocardial Infarction Model through Paracrine Effects

    PubMed Central

    Cai, Min; Shen, Rui; Song, Lei; Lu, Minjie; Wang, Jianguang; Zhao, Shihua; Tang, Yue; Meng, Xianmin; Li, Zongjin; He, Zuo-Xiang

    2016-01-01

    Stem cells are promising for the treatment of myocardial infarction (MI) and large animal models should be used to better understand the full spectrum of stem cell actions and preclinical evidences. In this study, bone marrow mesenchymal stem cells (BM-MSCs) were transplanted into swine heart ischemia model. To detect glucose metabolism in global left ventricular myocardium and regional myocardium, combined with assessment of cardiac function, positron emission tomography-computer tomography (PET-CT) and magnetic resonance imaging (MRI) were performed. To study the changes of glucose transporters and glucose metabolism-related enzymes and the signal transduction pathway, RT-PCR, Western-blot, and immunohistochemistry were carried out. Myocardium metabolic evaluation by PET-CT showed that mean signal intensity (MSI) increased in these segments at week 4 compared with that at week 1 after BM-MSCs transplantation. Moreover, MRI demonstrated significant function enhancement in BM-MSCs group. The gene expressions of glucose transporters (GLUT1, GLUT4), glucose metabolism-related enzymes phosphofructokinase (PFK), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH)) and 70-kDa ribosomal protein S6 kinase (p70s6k) in BM-MSCs injected areas were up-regulated at week 4 after BM-MSCs transplantation and this was confirmed by Western-blot and immunohistochemistry. In conclusions, BM-MSCs transplantation could improve cardiac function in swine MI model by activation of mTOR signal transduction pathway. PMID:27321050

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

    PubMed

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

    2015-07-01

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

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

    PubMed

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

    2015-07-01

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

  12. Recurrent myocardial infarction secondary to Prinzmetal’s variant angina

    PubMed Central

    Murdoch, Dale; Dhillon, Priyanka; Niranjan, Selvanayagam

    2015-01-01

    Prinzmetal’s variant angina describes chest pain secondary to reversible coronary artery vasospasm in the context of both diseased and non-diseased coronary arteries. Symptoms typically occur when the patient is at rest and are associated with transient ST-segment elevation. Acute episodes respond to glyceryl trinitrate, but myocardial infarction and other potentially fatal complications can occur, and long-term management can be challenging. Although it is not well understood, the underlying mechanism appears to involve a combination of endothelial damage and vasoactive mediators. In this case, a 35-year-old woman with myocardial infarction secondary to coronary artery vasospasm experienced recurrent chest pain. Coronary angiography revealed severe focal stenosis in the mid left anterior descending artery, which completely resolved after administration of intracoronary glyceryl trinitrate. The patient was discharged on nitrates and calcium channel blockers. The patient re-presented with another myocardial infarction, requiring up-titration of medical therapy. PMID:26034323

  13. Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

    PubMed Central

    Curaj, Adelina; Simsekyilmaz, Sakine; Staudt, Mareike; Liehn, Elisa

    2015-01-01

    Myocardial infarction still remains the main cause of death in western countries, despite considerable progress in the stent development area in the last decades. For clarification of the underlying mechanisms and the development of new therapeutic strategies, the availability of valid animal models are mandatory. Since we need new insights into pathomechanisms of cardiovascular diseases under in vivo conditions to combat myocardial infarction, the validity of the animal model is a crucial aspect. However, protection of animals are highly relevant in this context. Therefore, we establish a minimally invasive and simple model of myocardial infarction in mice, which assures a high reproducibility and survival rate of animals. Thus, this models fulfils the requirements of the 3R principle (Replacement, Refinement and Reduction) for animal experiments and assure the scientific information needed for further developing of therapeutical strategies for cardiovascular diseases. PMID:25992740

  14. Dipyridamole 201Tl scintigraphy in the evaluation of prognosis after myocardial infarction

    SciTech Connect

    Okada, R.D.; Glover, D.K.; Leppo, J.A. )

    1991-09-01

    Dipyridamole 201Tl imaging has been proposed as an alternative to exercise ECG testing for the prehospital discharge evaluation of patients recovering from myocardial infarction. The rationale is that many postinfarction patients with exercise-induced ischemia experience later cardiac events, and the sensitivity of predischarge exercise ECG testing in patients with multivessel disease ranges from only 45% to 62%. In addition, several groups of investigators have shown the sensitivity of submaximum exercise 201Tl imaging to be less than ideal. This report summarizes the current status of dipyridamole 201Tl imaging in the period of 1-13 days after myocardial infarction. Although the number of studies performed to date is limited, the following conclusions can be drawn: dipyridamole 201Tl imaging after myocardial infarction was associated with no serious side effects, and those present could be quickly reversed with aminophylline; redistribution with dipyridamole 201Tl images definitely correlates with prognosis after uncomplicated myocardial infarction; dipyridamole 201Tl imaging is definitely useful in patients unable to exercise for a variety of reasons; and future studies are definitely indicated to further define the role of dipyridamole 201Tl imaging for assessing prognosis, especially in those patients undergoing interventional therapy after acute myocardial infarction.

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

    PubMed

    Fujibayashi, Daisuke; Morino, Yoshihiro; Ikari, Yuji

    2008-07-01

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

  16. Unstable Angina Pectoris and the Progression to Acute Myocardial Infarction

    PubMed Central

    Willerson, James T.; Yao, Sheng-Kun; Ferguson, James J.; Anderson, H. Vernon; Golino, Paolo; Buja, L. Maximilian

    1991-01-01

    The conversion from stable to unstable angina and the further progression to myocardial infarction are usually associated with atherosclerotic plaque fissuring or ulceration at sites of coronary artery stenosis and subsequent development of a thrombus. This thrombus formation is initiated by platelet adhesion and aggregation; these, in turn, are promoted by the local release and accumulation of thromboxane A2 and serotonin. This accumulation and the resulting platelet aggregation at sites of endothelial injury cause dynamic vasoconstriction. With time, the platelet-initiated thrombus expands to include white and red blood cells in a fibrin mesh. Thus, a fully occlusive coronary thrombus may develop and cause the progression from unstable angina to acute myocardial infarction, often Q-wave myocardial infarction. We believe that the connection between unstable angina and acute myocardial infarction is a continuum relative to the processes of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary stenosis lasts only a few minutes and is repetitive, unstable angina or non-Q wave myocardial infarction occurs. However, when complete coronary artery occlusion lasts for longer than 4 hours, a transmural or Q-wave myocardial infarction results. Recently, in experimental animal models with mechanically induced coronary artery stenoses and endothelial injury, we have found that other mediators, including adenosine diphosphate and thrombin, also contribute to coronary artery thrombosis. Moreover, in humans with limiting angina, we have identified spontaneous coronary blood flow variations in a pattern similar to the variations caused by alternating platelet attachment and dislodgement in experimental canine modes. In this review, we add information to our previous observations in order to present the possible mechanisms of conversion from chronic to acute coronary heart

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

    PubMed

    García, Eulogio

    2005-05-01

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

  18. 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

  19. Comparison of enzymic with cineangiocardiographic estimations of myocardial infarct size.

    PubMed Central

    Sammel, N L; Stuckey, J G; Brandt, P W; Norris, R M

    1980-01-01

    Comparisons were made between enzymic indices of myocardial infarct size (total creatine kinase appearance and peak enzyme activity) measured during the acute state of a first myocardial infarct in 32 male patients, and analysis of contraction abnormalities in biplane left ventricular cineangiocardiograms performed one month later. The cineangiocardiograms were analysed independently by two radiologists, each using two different methods for quantification of subjectively classified abnormalities of left ventricular wall motion. A very strong correlation was found between the two enzymic indices of infarct size and somewhat weaker correlations between assessment of contractility abnormalities made by the two radiologists using the same method, or by the same radiologist using the two different methods. Comparisons between enzymic and angiocardiographic indices for all infarcts showed correlation coefficients (r) within the range of 0.53 to 0.72. With all comparisons of enzymic with radiological indices r values were higher for anterior infarcts than for inferior infarcts, and there was a tendency for higher enzyme levels for a given degree of left ventricular damage in inferior than in anterior infarction. This may be the result of variable degrees of right ventricular damage in inferior infarction. PMID:7426141

  20. Management of cardiogenic shock complicating acute myocardial infarction.

    PubMed

    Van Herck, Jozef L; Claeys, Marc J; De Paep, Rudi; Van Herck, Paul L; Vrints, Christiaan J; Jorens, Philippe G

    2015-06-01

    Cardiogenic shock complicates approximately 5-10% of cases with acute myocardial infarction and carries a poor prognosis. Early revascularization remains the cornerstone treatment of cardiogenic shock complicating myocardial infarction. Inotropic and/or vasopressor agents can be used for haemodynamic stabilization, although this comes at the expense of increased myocardial oxygen consumption and extended myocardial ischaemia. In recent years, the use of mechanical circulatory support has significantly increased. However, there is only limited data available from randomized trials evaluating the different percutaneous support systems. This review summarizes the available literature concerning the management of cardiogenic shock and gives an overview of the recommendations of the European and German-Austrian guidelines on cardiogenic shock.

  1. 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.

  2. The effect of carvedilol in patients with impaired left ventricular systolic function following an acute myocardial infarction. How do the treatment effects on total mortality and recurrent myocardial infarction in CAPRICORN compare with previous beta-blocker trials?

    PubMed

    Otterstad, Jan Erik; Ford, Ian

    2002-08-01

    In previous beta-blocker trials, post-myocardial infarction (MI) patients were essentially treated with a beta-blocker or placebo. In the CAPRICORN trial, patients were selected on the basis of a left ventricular (LV) ejection fraction (EF) <40% following the index MI and randomised to carvedilol or placebo, in addition to modern secondary prophylaxis with ACE inhibitors, aspirin and statins. In 1959 patients with a mean LVEF of 33%, treatment with carvedilol over a mean follow-up period of 15 months reduced total mortality from 15.3% with placebo to 11.9% with carvedilol [relative risk reduction (RRR) =23%, absolute risk reduction (ARR) =3.4%]. The incidence of recurrent MI was reduced from 5.8 to 2.3% (RRR 41%, ARR 2.3%). The number needed to treat (NNT) to prevent one death was 28 for the entire study period and 43 for 1 year of treatment. The results of the CAPRICORN trial are compared with three previous beta-blocker post-MI trials: the Gothenburg metoprolol trial (GMT), the Norwegian timolol trial (NTT) and the beta-blocker heart attack trial (BHAT). The RRRs for total mortality were 36% in the GMT and NTT, and 27% in BHAT. The respective NNTs for total mortality were 32, 18 and 38. NNT for 1 year of treatment was 25 in NTT and 80 in BHAT. The RRR for recurrent MIs were 28% in NTT and 16% in BHAT. The reduction of mortality and recurrent MIs in CAPRICORN is within the range of previous post-MI beta-blocker studies. In post-MI patients with LVEF<40%, add-on treatment with a beta-blocker should be given >48 h after initiation with an angiotensin-converting enzyme inhibitor (ACEI) and then with a slow dose escalation as applied in CAPRICORN.

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

    PubMed Central

    Osula, S; Bell, G; Hornung, R

    2002-01-01

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

  4. Acute anteroseptal myocardial infarction in a patient with dextrocardia.

    PubMed

    Alzand, Becker S N; Dennert, Robert; Kalkman, Robert; Gorgels, Anton P M

    2009-01-01

    Dextrocardia with situs inversus is an uncommon congenital condition in which the major visceral organs are reversed. The clinical diagnosis and electrocardiographic localization of myocardial infarctions in these patients remain a great challenge. We report a case of a 64-year-old man known with dextrocardia and situs inversus totalis presenting with acute chest pain irradiating to the right arm. The admission and reversed "normalized" electrocardiogram are presented, allowing for correct diagnosis of an acute anteroseptal myocardial infarction. The present case emphasizes the importance of performing a reversed electrocardiogram in patients with dextrocardia.

  5. Imaging Macrophage Development and Fate in Atherosclerosis and Myocardial Infarction

    PubMed Central

    Swirski, Filip K.; Nahrendorf, Matthias

    2013-01-01

    Macrophages are central regulators of disease progression in both atherosclerosis and myocardial infarction. In atherosclerosis, macrophages are the dominant leukocyte population that influences lesional development. In myocardial infarction, which is caused by atherosclerosis, macrophages accumulate readily and play important roles in inflammation and healing. Molecular imaging has grown considerably as a field and can reveal biological process at the molecular, cellular, and tissue levels. Here we explore how various imaging modalities, from intravital microscopy in mice to organ-level imaging in patients, are contributing to our understanding of macrophages and their progenitors in cardiovascular disease. PMID:23207281

  6. Paradoxical coronary artery embolism - a rare cause of myocardial infarction.

    PubMed

    Hakim, Fayaz A; Kransdorf, Evan P; Abudiab, Muaz M; Sweeney, John P

    2014-01-01

    Paradoxical coronary artery embolism is a rare, but often an underdiagnosed cause of acute myocardial infarction. It should be considered in patient who presents with chest pain and otherwise having a low risk profile for atherosclerosis coronary artery disease. We describe a case of paradoxical coronary artery embolism causing ST segment elevation myocardial infarction in a patient with upper extremity venous thrombosis. Echocardiography demonstrated a patent foramen ovale (PFO) with bidirectional shunt. In addition to treatment of acute coronary event closure of the PFO should be considered to prevent a recurrence. PMID:25774255

  7. Paradoxical Coronary Artery Embolism - A Rare Cause of Myocardial Infarction

    PubMed Central

    Hakim, Fayaz A.; Kransdorf, Evan P.; Abudiab, Muaz M.; Sweeney, John P.

    2014-01-01

    Paradoxical coronary artery embolism is a rare, but often an underdiagnosed cause of acute myocardial infarction. It should be considered in patient who presents with chest pain and otherwise having a low risk profile for atherosclerosis coronary artery disease. We describe a case of paradoxical coronary artery embolism causing ST segment elevation myocardial infarction in a patient with upper extremity venous thrombosis. Echocardiography demonstrated a patent foramen ovale (PFO) with bidirectional shunt. In addition to treatment of acute coronary event closure of the PFO should be considered to prevent a recurrence. PMID:25774255

  8. Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration.

    PubMed

    Blom, Jessica N; Lu, Xiangru; Arnold, Paul; Feng, Qingping

    2016-01-01

    Myocardial infarction induced by coronary artery ligation has been used in many animal models as a tool to study the mechanisms of cardiac repair and regeneration, and to define new targets for therapeutics. For decades, models of complete heart regeneration existed in amphibians and fish, but a mammalian counterpart was not available. The recent discovery of a postnatal window during which mice possess regenerative capabilities has led to the establishment of a mammalian model of cardiac regeneration. A surgical model of mammalian cardiac regeneration in the neonatal mouse is presented herein. Briefly, postnatal day 1 (P1) mice are anesthetized by isoflurane and placed on an ice pad to induce hypothermia. After the chest is opened, and the left anterior descending coronary artery (LAD) is visualized, a suture is placed around the LAD to inflict myocardial ischemia in the left ventricle. The surgical procedure takes 10-15 min. Visualizing the coronary artery is crucial for accurate suture placement and reproducibility. Myocardial infarction and cardiac dysfunction are confirmed by triphenyl-tetrazolium chloride (TTC) staining and echocardiography, respectively. Complete regeneration 21 days post myocardial infarction is verified by histology. This protocol can be used to as a tool to elucidate mechanisms of mammalian cardiac regeneration after myocardial infarction. PMID:27286473

  9. Effects of no-reflow phenomenon on ventricular systolic synchrony in patients with acute anterior myocardial infarction after percutaneous coronary intervention

    PubMed Central

    Wang, Le; Liu, Gang; Liu, Jun; Zheng, Mingqi; Li, Liang

    2016-01-01

    Objectives The aim of this study was to investigate the effect of no-reflow phenomenon on ventricular systolic synchrony via myocardial blush grades (MBGs) in patients with acute anterior myocardial infarction after percutaneous coronary intervention (PCI). Patients and methods All patients were divided into two groups and assessed by MBGs. To observe the parameters of the left ventricular function and left ventricular systolic synchrony, equilibrium radionuclide angiography was performed 1 week after PCI and repeated 6 months after acute myocardial infarction (AMI). Measurement data were compared and analyzed by the Student’s t-test, and the count data were evaluated by the χ2 test. A multivariate regression analysis was performed to assess the contribution of confounding factors. Results A total of 100 patients were enrolled in this study: 26 in the no-reflow and 74 in the reflow group. There was no significant difference in terms of age, sex, hypertension history, diabetes history, hyperlipidemia history, and smoking history between the two groups. However, the incidence rate of heart failure with Killip’s grade ≥2 in the no-reflow group was significantly higher than that in the reflow group (38.46% vs 18.92%, P<0.05). Six months after the AMI-PCI, the left ventricular ejection fraction, peak ejection rate, and peak filling rate in the no-reflow group were significantly lower than those in the reflow group (t=2.21, 2.29, and 2.03, P<0.05 for all comparisons), but the values of the time to peak ejection rate, time to peak filling rate, phase shift, full width at half maximum, and peak phase standard deviation were all higher (t=2.41, 2.46, 2.00, 2.55, and 2.49, P<0.05 for all comparisons), and the incidence rate of major adverse cardiac events in the no-reflow group was also more elevated than that in the reflow group (53.85% vs 8.11%, χ2=34.49, P<0.001). Conclusion The no-reflow phenomenon identified by MBGs reflects the no-reperfusion status in the

  10. Limitation of enzymatic models for predicting myocardial infarct size.

    PubMed Central

    Thygesen, K; Hørder, M; Petersen, P H; Nielsen, B L

    1983-01-01

    The possibility of predicting myocardial infarct size from early enzyme measurements was studied using a physiological two compartment distribution model. Based on this the time dependent appearance function in plasma was calculated for creatine kinase, aspartate aminotransferase, and lactate dehydrogenase in 29 patients suffering from acute myocardial infarction. On average, the appearance function of the three enzymes started four hours after the onset of symptoms, and the maximum was reached after 12 hours for creatine kinase, 13 hours for aspartate aminotransferase, and 22 hours for lactate dehydrogenase. The cumulated appearance function was used as an acceptable estimate of infarct size. The prediction of infarct size from defined points of the appearance function curve for each of the three enzymes was attempted according to a set schedule during the first 25 hours after the onset of myocardial infarction. The prediction using creatine kinase was superior to the other enzymes. Even so, a reliable prediction could only be established at the very earliest from nine hours and this is too late, as irreversible loss of myocardium occurs rapidly after the onset of symptoms. This, together with the fact that other models have unacceptable variability of the prediction, lead to the conclusion that enzymatic predictive models are of no practical value in clinical intervention studies to reduce infarct size. PMID:6860513

  11. Emodin-mediated protection from acute myocardial infarction via inhibition of inflammation and apoptosis in local ischemic myocardium.

    PubMed

    Wu, Yanxia; Tu, Xin; Lin, Guosheng; Xia, Hao; Huang, Hao; Wan, Jing; Cheng, Zhide; Liu, Mengyuan; Chen, Gao; Zhang, Haimou; Fu, Jinrong; Liu, Qian; Liu, Dong-Xu

    2007-10-13

    Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappaB activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis.

  12. Energetic differences between viable and non-viable myocardium in patients with recent myocardial infarction are not an effect of differences in wall thinning- a multivoxel (31)P-MR-spectroscopy and MRI study.

    PubMed

    Beer, Meinrad; Machann, Wolfram; Sandstede, Jörn; Buchner, Stefan; Lipke, Claudia; Köstler, Herbert; Lorenz, Reinhard; Harre, Kerstin; Spindler, Matthias; Hahn, Dietbert

    2007-05-01

    To evaluate multivoxel (31)P-MR spectroscopy (MRS) for assessment of energy metabolism in patients with myocardial infarction (MI) in correlation to left ventricular (LV) wall thickness and the outcome of revascularization. Thirty patients with subacute anterior myocardial infarction and planned revascularization were enrolled. 3D-chemical shift imaging was applied to determine PCr/ATP ratios in two areas: infarcted/anterior and noninfarcted/septal myocardium. MRI was used to evaluate LV function and wall thickness, and was repeated 6 months after revascularization to assess myocardial viability. Fifteen volunteers were controls. Fifteen patients showed normalization of wall motion abnormalities after revascularization (Group 1; viable), 15 not (Group 2; non-viable). Regarding infarcted/anterior myocardium, Group 2 had lower PCr/ATP ratios (0.81 +/- 0.60 vs 1.17 +/- 0.25), and PCr/ATP ratios were reduced in both groups compared to controls (1.45 +/- 0.29). Regarding noninfarcted/septal myocardium, again Group 2 had lower ratios (0.93 +/- 0.53 vs 1.31 +/- 0.38); however, compared to controls (1.51 +/- 0.32) a reduction of PCr/ATP ratios was only found in Group 2. For both myocardial regions, no correlations between PCr/ATP ratios and LV wall thickness were detected. The more severe energetic alteration in irreversibly damaged myocardium is not an effect of differences of wall thinning. Additional alterations of noninfarcted, adjacent myocardium can be detected.

  13. Spatial analysis of myocardial infarction in Iran: National report from the Iranian myocardial infarction registry

    PubMed Central

    Ahmadi, Ali; Soori, Hamid; Mehrabi, Yadollah; Etemad, Koorosh

    2015-01-01

    Background: Myocardial infarction (MI) is a leading cause of mortality and morbidity in Iran. No spatial analysis of MI has been conducted to date. The present study was conducted to determine the pattern of MI incidence and to identify the associated factors in Iran by province. Materials and Methods: This study has two parts. One part is prospective and hospital-based, and the other part is an ecological study. In this study, the data of 20,750 new MI cases registered in Iranian Myocardial Infarction Registry in 2012 were used. For spatial analysis in global and local, spatial autocorrelation, Moran's I, Getis-Ord, and logistic regression models were used. Data were analyzed by Stata software and ArcGIS 9.3. Results: Based on autocorrelation coefficient, a specific pattern was observed in the distribution of MI incidence in different provinces (Moran's I: 0.75, P < 0.001). Spatial pattern of incidence was approximately the same in men and women. MI incidence was clustering in six provinces (North Khorasan, Yazd, Kerman, Semnan, Golestan, and Mazandaran). Out of the associated factors with clustered MI in six provinces, temperature, humidity, hypertension, smoking, and body mass index (BMI) could be mentioned. Hypertension, smoking, and BMI contributed to clustering with, respectively, 2.36, 1.31, and 1.31 odds ratio. Conclusion: Addressing the place-based pattern of incidence and clarifying their epidemiologic dimension, including spatial analysis, has not yet been implemented in Iran. Report on MI incidence rate by place and formal borders is useful and is used in the planning and prioritization in different levels of health system. PMID:26487871

  14. Protective mechanism of quercetin on acute myocardial infarction in rats.

    PubMed

    Li, B; Yang, M; Liu, J W; Yin, G T

    2016-03-11

    To investigate the protective mechanism of quercetin on acute myocardial infarction (AMI) rats, an AMI rat model was established by ligating the left coronary anterior descending branch. The rats were randomly divided into the model group and low- and high-dose quercetin groups. The control group comprised sham-operated rats. The rats in the low- and high-dose quercetin groups were administered 100 and 400 mg/kg quercetin, respectively, by gavage. The rats in the control and model groups were administered isometric normal saline once daily for one week. The mRNA and protein levels of TNF-α and IL-1β in the myocardial tissue of rats were detected in each group by real time polymerase chain reaction and enzyme-linked immunosorbent assay. Malondialdehyde (MDA) content in the myocardial tissue and superoxide dismutase (SOD) and catalase (CAT) activities were detected using a colorimetric method. The level of apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. Compared with those in the control group, the mRNA and protein levels of TNF-α, IL-1β and MDA content in the model, low-, and high-dose groups significantly increased. SOD and CAT activities decreased significantly. The cell apoptosis index increased significantly  (P < 0.05). Compared with those in the model group, the mRNA and protein levels of TNF-α and IL-1β and MDA content in myocardial tissue of rats in the low-dose and high-dose groups decreased significantly. SOD and CAT activities increased significantly. The cell apoptosis index significantly reduced (P < 0.05). In conclusion, quercetin has significant anti-inflammatory, antioxidant, and anti-apoptotic effects on AMI rats and can effectively protect against myocardium damage.

  15. Timely reperfusion for ST-segment elevation myocardial infarction: Effect of direct transfer to primary angioplasty on time delays and clinical outcomes.

    PubMed

    Estévez-Loureiro, Rodrigo; López-Sainz, Angela; Pérez de Prado, Armando; Cuellas, Carlos; Calviño Santos, Ramón; Alonso-Orcajo, Norberto; Salgado Fernández, Jorge; Vázquez-Rodríguez, Jose Manuel; López-Benito, Maria; Fernández-Vázquez, Felipe

    2014-06-26

    Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion therapy for patients presenting with ST-segment elevation myocardial infarction (STEMI) when it can be performed expeditiously and by experienced operators. In spite of excellent clinical results this technique is associated with longer delays than thrombolysis and this fact may nullify the benefit of selecting this therapeutic option. Several strategies have been proposed to decrease the temporal delays to deliver PPCI. Among them, prehospital diagnosis and direct transfer to the cath lab, by-passing the emergency department of hospitals, has emerged as an attractive way of diminishing delays. The purpose of this review is to address the effect of direct transfer on time delays and clinical events of patients with STEMI treated by PPCI.

  16. Effect of early bisoprolol administration on ventricular arrhythmia and cardiac death in patients with non-ST elevation myocardial infarction

    PubMed Central

    Maclean, Edd; Zheng, Sean; Nabeebaccus, Adam; O'Gallagher, Kevin; Stewart, Adrian; Webb, Ian

    2015-01-01

    Objective To investigate the impact of early oral beta blockade in patients presenting with acute non-ST elevation myocardial infarction (NSTEMI). Methods We retrospectively identified 890 consecutive patients presenting with NSTEMI to a single UK centre from 2012 to 2014. Included patients all received standardised antiplatelet therapy plus low-dose oral bisoprolol (1.25–2.5 mg) within 4 h (mean 2.2±1.36; ‘Early Group’) or within 5–24 h (mean 15.4±5.7; ‘Late Group’) of presentation. Patients were followed up for the duration of hospital stay with the incidence of major adverse cardiovascular events (MACE—defined as ventricular arrhythmia, cardiac death or repeat infarction) set as the primary outcome. Multivariate logistic regression models analysed early versus late bisoprolol administration and adjusted for potential confounders. Results 399 patients were included. Of the patient parameters, only the GRACE score was significantly different between the early (n=99, GRACE 164.5±29.6) and late (n=300, GRACE 156.7±31.4) groups (p=0.033). The early group had significantly fewer ventricular arrhythmias (1 vs 20, p=0.034), cardiac deaths (0 vs 13, p=0.044) and consequently MACE (1 vs 27, p=0.005) than the late group. After adjusting for the confounders of pulse, blood pressure, smoking and creatinine, logistic regression analysis identified early bisoprolol administration as protective for ventricular arrhythmia (p=0.038, OR 0.114, CI 0.015 to 0.885) and MACE (p=0.011, OR 0.064, CI 0.008 to 0.527). There was one episode of symptomatic bradycardia in the late group. Conclusions This study suggests that low-dose oral bisoprolol administered to patients with NSTEMI within 4 h of admission may be protective and lead to reduced inpatient MACE. PMID:27326220

  17. Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture.

    PubMed

    Lu, Shuangshuang; Du, Pan; Shan, Congjia; Wang, Yaohe; Ma, Changsheng; Dong, Jianzeng

    2016-09-30

    Previous studies have demonstrated a significantly lower level of Hand1 in ischemic cardiomyopathy than in normal heart tissue. The role of decreased Hand1 in myocardial infarction remains unclear. This study was designed to investigate the effects of haploinsufficiency of Hand1 on mouse heart after myocardial infarction. 8-10 weeks old male heterozygous Hand1-deficient (Hand1(+/-)) mice and wild-type littermates (control) were subjected to sham operation or ligation of the left anterior descending coronary artery to induce acute myocardial infarction (AMI). Hand1(+/-) mice have low incidence of left ventricular free wall rupture in the first week after operation than control mice. Then we found lower MMP9 activity and less cardiomyocytes apoptosis in Hand1(+/-) than in control mice. All of these contribute to the protection role of haploinsufficiency of Hand1 after AMI.

  18. [Myocardial infarction as work-related accident: medical and legal problems].

    PubMed

    Szozda, Ryszard; Procek, Marek

    2002-01-01

    An accident is a work-related event caused by an external factor. Therefore, myocardial infarction is also considered, in specific conditions, as a work-related accident. The aim of this study was to present the cause-effect relationship between myocardial infarction and working conditions in the context of a work-related accident characterized by: urgency of event, external factor and relation with working conditions. The attitude of the Supreme Court to the question of certification, highlighting the key issues and facilitating the understanding of the problem and opinions of legal experts on this matter is also discussed. Myocardial infarction as a work-related accident is an issue involving both law and medicine, particularly occupational medicine, that will have to tackle and solve this problem in its several dimensions, including periodical examinations.

  19. 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.

  20. Cardioprotective effects and pharmacokinetic properties of a controlled release formulation of a novel hydrogen sulfide donor in rats with acute myocardial infarction

    PubMed Central

    Tran, Ba Hieu; Huang, Chengrong; Zhang, Qiuyan; Liu, Xu; Lin, Shizhou; Liu, Hongrui; Wang, Shujun; Zhu, Yi Zhun

    2015-01-01

    We previously reported that S-propargyl-cysteine (SPRC) exerts cardioprotective effects by elevating H2S levels via the CSE/H2S pathway. In the present study, we investigated the cardioprotective effects and pharmacokinetic properties of a controlled release formulation of SPRC (CR-SPRC) in an in vivo rat model of myocardial infarction (MI). Rats were randomly assigned to seven groups that were pre-treated with CR-SPRC daily for 7 days prior to ligation of the left anterior descending coronary artery to induce MI. Cardiac function and infarct size were determined after MI, and we examined the activity of antioxidant enzymes, expression of anti-inflammation proteins and hydrogen sulfide levels. Mixed-mode, reversed-phase and cation-exchange HPLC–MS/MS were used to compare the pharmacokinetic properties of CR-SPRC and SPRC. CR-SPRC significantly reduced infarct size and creatine kinase (CK) and lactate dehydrogenase (LDH) leakage and it preserved cardiac function during MI. CR-SPRC displayed antioxidant properties, preserving glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) levels whereas reducing malondialdehyde (MDA) levels. Moreover, CR-SPRC significantly reduced the protein levels of inflammatory biomarkers (phospho-NF-κB p65/NF-κB p65, TNF-α) and increased cystathionine-γ-lyase (CSE) and Iκ-Bα protein levels. CR-SPRC had better pharmacokinetic properties than SPRC, with a reduced concentration peak (Cmax), prolonged time to reach peak concentration (Tmax), prolonged mean residence time (MRTinf) and increased AUC0–t. CR-SPRC showed protective effects against MI via the CSE/H2S pathway and demonstrated better cardioprotective effects than SPRC by prolonging the release of endogenous H2S. PMID:26182378

  1. The effect of metformin on cardiovascular risk profile in patients without diabetes presenting with acute myocardial infarction: data from the Glycometabolic Intervention as adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III) trial

    PubMed Central

    Lexis, Chris P H; van der Horst-Schrivers, Anouk N A; Lipsic, Erik; Valente, Mattia A E; Muller Kobold, Anneke C; de Boer, Rudolf A; van Veldhuisen, Dirk J; van der Harst, Pim; van der Horst, Iwan C C

    2015-01-01

    Objective In patients with diabetes mellitus, metformin treatment is associated with reduced mortality and attenuation of cardiovascular risk. As a subanalysis of the Glycometabolic Intervention as adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III) study, we evaluated whether metformin treatment in patients with ST-segment elevation myocardial infarction (STEMI) without diabetes improves the cardiovascular risk profile. Methods A total of 379 patients, without known diabetes, presenting with STEMI were randomly allocated to receive metformin 500 mg twice daily or placebo for 4 months. Results After 4 months, the cardiovascular risk profile of patients receiving metformin (n=172) was improved compared with placebo (n=174); glycated hemoglobin (5.83% (95% CI 5.79% to 5.87%) vs 5.89% (95% CI 5.85% to 5.92%); 40.2 mmol/mol (95% CI 39.8 to 40.6) vs 40.9 mmol/mol (40.4 to 41.2), p=0.049); total cholesterol (3.85 mmol/L (95% CI 3.73 to 3.97) vs 4.02 mmol/L (95% CI 3.90 to 4.14), p=0.045); low-density lipoprotein cholesterol (2.10 mmol/L (95% CI 1.99 to 2.20) vs 2.3 mmol/L (95% CI 2.20 to 2.40), p=0.007); body weight (83.8 kg (95% CI 83.0 to 84.7) vs 85.2 kg (95% CI 84.4 to 86.1), p=0.024); body mass index (26.8 kg/m2 (95% CI 26.5 to 27.0) vs 27.2 kg/m2 (95% CI 27.0 to 27.5), p=0.014). Levels of fasting glucose, postchallenge glucose, insulin, high-density lipoprotein cholesterol, and blood pressure were similar in both groups. Conclusions Among patients with STEMI without diabetes, treatment with metformin for 4 months resulted in a modest improvement of the cardiovascular risk profile compared with placebo. Trial register number NCT01217307. PMID:26688733

  2. Interrater reliability of a national acute myocardial infarction register

    PubMed Central

    Govatsmark, Ragna Elise Støre; Sneeggen, Sylvi; Karlsaune, Hanne; Slørdahl, Stig Arild; Bønaa, Kaare Harald

    2016-01-01

    Background Disease-specific registers may be used for measuring and improving healthcare and patient outcomes, and for disease surveillance and research, provided they contain valid and reliable data. The aim of this study was to assess the interrater reliability of all variables in a national myocardial infarction register. Methods We randomly selected 280 patients who had been enrolled from 14 hospitals to the Norwegian Myocardial Infarction Register during the year 2013. Experienced audit nurses, who were blinded to the data about the 280 patients already in the register, completed the Norwegian Myocardial Infarction paper forms for 240 patients by review of medical records. We then extracted all registered data on the same patients from the Norwegian Myocardial Infarction Register. To compare the interrater reliability between the register and the audit nurses, we calculated intraclass correlations coefficient for continuous variables, Cohen’s kappa and Gwet’s first agreement coefficient (AC1) for nominal variables, and quadratic weighted Cohen’s kappa and Gwet’s second AC for ordinal variables. Results We found excellent (AC1 >0.80) or good (AC1 0.61–0.80) agreement for most variables, including date and time variables, medical history, investigations and treatments during hospitalization, medication at discharge, and ST-segment elevation or non-ST-segment elevation acute myocardial infarction. However, only moderate agreement (AC1 0.41–0.60) was found for family history of coronary heart disease, diagnostic electrocardiography, and complications during hospitalization, whereas fair agreement (AC1 0.21–0.40) was found for acute myocardial infarction location. A high percentage of missing data was found for symptom onset, family history, body mass index, infarction location, and new Q-wave. Conclusion Most variables in Norwegian Myocardial Infarction Register had excellent or good reliability. However, some important variables had lower

  3. Temperature, air pollution, and mortality from myocardial infarction in São Paulo, Brazil.

    PubMed

    Sharovsky, R; César, L A M; Ramires, J A F

    2004-11-01

    An increase in daily mortality from myocardial infarction has been observed in association with meteorological factors and air pollution in several cities in the world, mainly in the northern hemisphere. The objective of the present study was to analyze the independent effects of environmental variables on daily counts of death from myocardial infarction in a subtropical region in South America. We used the robust Poisson regression to investigate associations between weather (temperature, humidity and barometric pressure), air pollution (sulfur dioxide, carbon monoxide, and inhalable particulate), and the daily death counts attributed to myocardial infarction in the city of São Paulo in Brazil, where 12,007 fatal events were observed from 1996 to 1998. The model was adjusted in a linear fashion for relative humidity and day-of-week, while nonparametric smoothing factors were used for seasonal trend and temperature. We found a significant association of daily temperature with deaths due to myocardial infarction (P < 0.001), with the lowest mortality being observed at temperatures between 21.6 and 22.6 degrees C. Relative humidity appeared to exert a protective effect. Sulfur dioxide concentrations correlated linearly with myocardial infarction deaths, increasing the number of fatal events by 3.4% (relative risk of 1.03; 95% confidence interval = 1.02-1.05) for each 10 microg/m(3) increase. In conclusion, this study provides evidence of important associations between daily temperature and air pollution and mortality from myocardial infarction in a subtropical region, even after a comprehensive control for confounding factors.

  4. Nitric oxide synthase inhibitors in post-myocardial infarction cardiogenic shock--an update.

    PubMed

    Kaluski, Edo; Hendler, Alberto; Blatt, Alex; Uriel, Nir

    2006-11-01

    Cardiogenic shock (CS) in acute myocardial infarction, after successful coronary angioplasty, still carries a case fatality rate of 50%. These patients succumb to a systemic metabolic storm, superimposed on extensive myocardial necrosis and stunning. Nitric oxide (NO) overproduction contributes to the pathophysiology of this morbid state. Current data regarding the physiologic effects of NO and nitric oxide synthase (NOS) inhibitors on the cardiovascular system are reviewed. Clinical trials assessing the safety and efficacy of NOS inhibitors in CS are summarized.

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

    PubMed

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

    2016-09-01

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

  6. Reducing case fatality from acute myocardial infarction in Cienfuegos, Cuba, 1994-2009.

    PubMed

    Navarro, Víctor René; Falcón, Arelys; Iraola, Marcos D; Valladares, Francisco; Ordúñez, Pedro O

    2012-10-01

    Between 1994 and 2009, the Dr Gustavo Aldereguía University Hospital of Cienfuegos, Cuba implemented a series of interventions that reduced acute myocardial infarction case fatality rate from 47% to 15%. These interventions were part of an institutional plan for myocardial infarction included in the hospital's overall quality assurance strategy. Outcomes resulted primarily from organizational changes (from upgrading of the hospital emergency department and provincial emergency system to creation of a comprehensive coronary care unit and a chest pain center); optimizing use of effective drugs (streptokinase, aspirin, ACE inhibitors and beta blockers); adherence to clinical practice guidelines; and continual and participatory evaluation and adjustment.

  7. In vivo differentiation of human amniotic epithelial cells into cardiomyocyte-like cells and cell transplantation effect on myocardial infarction in rats: comparison with cord blood and adipose tissue-derived mesenchymal stem cells.

    PubMed

    Fang, Cheng-Hu; Jin, Jiyong; Joe, Jun-Ho; Song, Yi-Sun; So, Byung-Im; Lim, Sang Moo; Cheon, Gi Jeong; Woo, Sang-Keun; Ra, Jeong-Chan; Lee, Young-Yiul; Kim, Kyung-Soo

    2012-01-01

    Human amniotic epithelial cells (h-AECs), which have various merits as a cell source for cell therapy, are known to differentiate into cardiomyocytes in vitro. However, the ability of h-AECs to differentiate into cardiomyocytes in vivo and their cell transplantation effects on myocardial infarction are still unknown. In this study, we assessed whether h-AECs could differentiate into cardiomyocytes in vivo and whether h-AECs transplantation can decrease infarct size and improve cardiac function, in comparison to transplantation of cord blood-derived mesenchymal stem cells (MSCs) or adipose tissue-derived MSCs. For our study, we injected h-AECs, cord blood-derived MSCs, adipose tissue-derived MSCs, and saline into areas of myocardial infarction in athymic nude rats. After 4 weeks, 3% of the surviving h-AECs expressed myosin heavy chain, a marker specific to the myocardium. Compared with the saline group, all cell-implanted groups showed a higher ejection fraction, lower infarct area by positron emission tomography and histology, and more abundant myocardial gene and protein expression in the infarct area. We showed that h-AECs can differentiate into cardiomyocyte-like cells, decrease infarct size, and improve cardiac function in vivo. The beneficial effects of h-AECs were comparable to those of cord blood and adipose tissue-derived MSCs. These results support the need for further studies of h-AECs as a cell source for myocardial regeneration due to their plentiful availability, low immunity, and lack of ethical issues related to their use.

  8. In vivo differentiation of human amniotic epithelial cells into cardiomyocyte-like cells and cell transplantation effect on myocardial infarction in rats: comparison with cord blood and adipose tissue-derived mesenchymal stem cells.

    PubMed

    Fang, Cheng-Hu; Jin, Jiyong; Joe, Jun-Ho; Song, Yi-Sun; So, Byung-Im; Lim, Sang Moo; Cheon, Gi Jeong; Woo, Sang-Keun; Ra, Jeong-Chan; Lee, Young-Yiul; Kim, Kyung-Soo

    2012-01-01

    Human amniotic epithelial cells (h-AECs), which have various merits as a cell source for cell therapy, are known to differentiate into cardiomyocytes in vitro. However, the ability of h-AECs to differentiate into cardiomyocytes in vivo and their cell transplantation effects on myocardial infarction are still unknown. In this study, we assessed whether h-AECs could differentiate into cardiomyocytes in vivo and whether h-AECs transplantation can decrease infarct size and improve cardiac function, in comparison to transplantation of cord blood-derived mesenchymal stem cells (MSCs) or adipose tissue-derived MSCs. For our study, we injected h-AECs, cord blood-derived MSCs, adipose tissue-derived MSCs, and saline into areas of myocardial infarction in athymic nude rats. After 4 weeks, 3% of the surviving h-AECs expressed myosin heavy chain, a marker specific to the myocardium. Compared with the saline group, all cell-implanted groups showed a higher ejection fraction, lower infarct area by positron emission tomography and histology, and more abundant myocardial gene and protein expression in the infarct area. We showed that h-AECs can differentiate into cardiomyocyte-like cells, decrease infarct size, and improve cardiac function in vivo. The beneficial effects of h-AECs were comparable to those of cord blood and adipose tissue-derived MSCs. These results support the need for further studies of h-AECs as a cell source for myocardial regeneration due to their plentiful availability, low immunity, and lack of ethical issues related to their use. PMID:22776022

  9. Space weather and myocardial infarction diseases at subauroral latitudes

    NASA Astrophysics Data System (ADS)

    Samsonov, Sergey; Kleimenova, Natalia; Petrova, Palmira

    The relationship of the number of calls for the emergency medical care in Yakutsk (subauroral latitudes) in connection with myocardial infarction diseases during years near the maximum (1992) and minimum (1998) of the 11-year geomagnetic disturbance cycle to space weather parameters has been studied. It is found that at subauroral latitudes, the increase of geomagnetic activity, namely, the occurrence of night magnetospheric substorms, plays the important role in the exacerbation of myocardial infarctions. Substorms are accompanied by Pi1 irregular geomagnetic pulsations with periods of (0.5-3.0) Hz, coinciding with heart rhythms of a human being, thus, these waves can be a biotropic factor negatively influencing on the occurrence of myocardial infarctions. The comparison of seasonal change of the number of calls for emergency medical care to patients at subauroral latitudes with a simultaneous seasonal change of fatal endings because of an infarction at low latitudes (Bulgaria) has shown their essential difference. Thus, in Bulgaria the maximum of infarctions have been marked in winter, and minimum - in summer, and in Yakutsk a few maxima coinciding with the sharp and considerable increases of the level of the planetary geomagnetic disturbances have been observed. In this case, in Bulgaria the infarctions could be connected with availability of the Pc1 geomagnetic pulsations. Thus, the stable quasi-sinusoidal Pc1 pulsations can be a biotropic factor influencing on the development of myocardial infarctions at middle latitudes and the Pi1 irregular geomagnetic pulsations, which do not propagate to the lower latitudes, could be a biotropic factor at subauroral latitudes.

  10. Relation of impaired Thrombolysis In Myocardial Infarction myocardial perfusion grades to residual thrombus following the restoration of epicardial patency in ST-elevation myocardial infarction.

    PubMed

    Kirtane, Ajay J; Weisbord, Aaron; Karmpaliotis, Dimitrios; Murphy, Sabina A; Giugliano, Robert P; Cannon, Christopher P; Antman, Elliott M; Ohman, E Magnus; Roe, Matthew T; Braunwald, Eugene; Gibson, C Michael

    2005-01-15

    Clinical and angiographic data were analyzed from 929 patients who had ST-elevation myocardial infarction and open epicardial arteries after fibrinolytic therapy. Residual angiographically evident thrombus was associated with more frequent Thrombolysis In Myocardial Infarction (TIMI) grade 2 flow (33.6% vs 26.8%, p = 0.03), higher corrected TIMI frame counts (34 vs 31 frames, p = 0.0003), and lower TIMI myocardial perfusion grades (43.0% vs 32.0% TIMI myocardial perfusion grades 0/1, p = 0.001) among all patients and among patients who had TIMI grade 3 flow (33.5% vs 26.0% TIMI myocardial perfusion grades 0/1, p = 0.043). In multivariate analyses, angiographically evident thrombus was associated with higher corrected TIMI frame counts and worsened myocardial perfusion independent of clinical and angiographic covariates, including TIMI grade 3 flow.

  11. Beneficial effects of selective HDL-raising gene transfer on survival, cardiac remodelling and cardiac function after myocardial infarction in mice.

    PubMed

    Gordts, S C; Muthuramu, I; Nefyodova, E; Jacobs, F; Van Craeyveld, E; De Geest, B

    2013-11-01

    Post-myocardial infarction (MI) ejection fraction is decreased in patients with low high-density lipoprotein (HDL) cholesterol levels, independent of the degree of coronary atherosclerosis. The objective of this study is to evaluate whether selective HDL-raising gene transfer exerts cardioprotective effects post MI. Gene transfer in C57BL/6 low-density lipoprotein receptor (LDLr)(-/-) mice was performed with the E1E3E4-deleted adenoviral vector AdA-I, inducing hepatocyte-specific expression of human apo A-I, or with the control vector Adnull. A ligation of the left anterior descending coronary artery was performed 2 weeks after transfer or saline injection. HDL cholesterol levels were persistently 1.5-times (P<0.0001) higher in AdA-I mice compared with controls. Survival was increased (P<0.01) in AdA-I MI mice compared with control MI mice during the 28-day follow-up period (hazard ratio for mortality 0.42; 95% confidence interval 0.24-0.76). Longitudinal morphometric analysis demonstrated attenuated infarct expansion and inhibition of left ventricular (LV) dilatation in AdA-I MI mice compared with controls. AdA-I transfer exerted immunomodulatory effects and increased neovascularisation in the infarct zone. Increased HDL after AdA-I transfer significantly improved systolic and diastolic cardiac function post MI, and led to a preservation of peripheral blood pressure. In conclusion, selective HDL-raising gene transfer may impede the development of heart failure.

  12. When to consider an implantable cardioverter defibrillator following myocardial infarction?

    PubMed

    Szwejkowski, Benjamin R; Wright, Gary A; Connelly, Derek T; Gardner, Roy S

    2015-12-01

    After reading this article the reader should be familiar with: Current guidelines for implantable cardioverter defibrillator (ICD) use post myocardial infarction (MI) and ischaemic cardiomyopathy. Primary prevention ICD guidelines. Secondary prevention ICD guidelines. Non-sustained ventricular tachycardia in patients post MI and the use of ICDs. Programming ICDs. PMID:26526420

  13. Psychological rehabilitation after myocardial infarction: multicentre randomised controlled trial.

    PubMed Central

    Jones, D. A.; West, R. R.

    1996-01-01

    OBJECTIVE: To evaluate rehabilitation after myocardial infarction. DESIGN: Randomised controlled trial of rehabilitation in unselected myocardial infarction patients in six centres, baseline data being collected on admission and by structured interview (of patients and spouses) shortly after discharge and outcome being assessed by structured interview at six months and clinical examination at 12 months. SETTING: Six district general hospitals. SUBJECTS: All 2328 eligible patients admitted over two years with confirmed myocardial infarction and discharged home within 28 days. INTERVENTIONS: Rehabilitation programmes comprising psychological therapy, counselling, relaxation training, and stress management training over seven weekly group outpatient sessions for patients and spouses. MAIN OUTCOME MEASURES: Anxiety, depression, quality of life, morbidity, use of medication, and mortality. RESULTS: At six months there were no significant differences between rehabilitation patients and controls in reported anxiety (prevalence 33%) or depression (19%). Rehabilitation patients reported a lower frequency of angina (median three versus four episodes a week), medication, and physical activity. At 12 months there were no differences in clinical complications, clinical sequelae, or mortality. CONCLUSIONS: Rehabilitation programmes based on psychological therapy, counselling, relaxation training, and stress management seem to offer little objective benefit to patients who have experienced myocardial infarction compared with previous reports of smaller trials. PMID:8978226

  14. Thrombolytic therapy for myocardial infarction. Treatment introduced in northern Ontario.

    PubMed Central

    Hutten-Czapski, P.

    1993-01-01

    In remote regions of Canada, most patients with acute myocardial infarctions (MI) are treated by general practitioners. In hospitals served by cardiologists, intravenous thrombolytic therapy for MI is now routinely available. In a survey of northern Ontario general hospitals, 32 of 45 offered IV thrombolytic therapy. The use of streptokinase in one family physician-run hospital was also reviewed. PMID:8257484

  15. Phaeochromocytoma presenting with ST segment elevation myocardial infarction.

    PubMed

    Ahmed, Mohamed A; Abdullah, Abdullah Sayied; Kiernan, Thomas John

    2016-01-01

    Phaeochromocytoma is a rare endocrine disorder with different cardiovascular presentations. In this brief report, we discuss a case of a 59-year-old woman who presented with acute ST segment elevation myocardial infarction secondary to phaeochromocytoma. Coronary angiogram showed non-obstructive coronary artery disease. PMID:26857585

  16. Does Cardiac Rehabilitation After Myocardial Infarction Favorably Affect Prognosis?

    ERIC Educational Resources Information Center

    Shephard, Roy J.

    1988-01-01

    This article discusses the limitations of 14 randomized controlled trials of exercise rehabilitation for patients who sustained myocardial infarction. The difficulty of sampling patients and controlling the sample size is discussed and the benefits of pooled statistical evidence are considered. (JL)

  17. Controlled Trial of Psychological Intervention in Myocardial Infarction.

    ERIC Educational Resources Information Center

    Oldenburg, Brian; And Others

    1985-01-01

    Compared hospital-based psychological interventions for improving the physical, psychological, and life-style status of patients after myocardial infarction with routine medical and nursing care. Follow-ups showed intervention groups performed significantly better on measures of psychological and life-style functioning; they also reported fewer…

  18. Group Counseling Approaches with Persons Who Have Sustained Myocardial Infarction.

    ERIC Educational Resources Information Center

    Livneh, Hanoch; Sherwood-Hawes, Ardis

    1993-01-01

    Presents group counseling strategies for working with clients who have sustained myocardial infarctions, or heart attacks. MI victims can be assisted with transition from hospital, readjustment to daily life, coping with fears and frustrations of life and the illness. Advantages of counseling, primary goals, and common topics are discussed.…

  19. Modeling Myocardial Infarction in Mice: Methodology, Monitoring, Pathomorphology

    PubMed Central

    Ovsepyan, A.A.; Panchenkov, D.N.; Prokhortchouk, E.B.; Telegin, G.B.; Zhigalova, N.A.; Golubev, E.P.; Sviridova, T.E.; Matskeplishvili, S.T.; Skryabin, K.G.; Buziashvili, U.I.

    2011-01-01

    Myocardial infarction is one of the most serious and widespread diseases in the world. In this work, a minimally invasive method for simulating myocardial infarction in mice is described in the Russian Federation for the very first time; the procedure is carried out by ligation of the coronary heart artery or by controlled electrocoagulation. As a part of the methodology, a series of anesthetic, microsurgical and revival protocols are designed, owing to which a decrease in the postoperational mortality from the initial 94.6 to 13.6% is achieved. ECG confirms the development of large-focal or surface myocardial infarction. Postmortal histological examination confirms the presence of necrosis foci in the heart muscles of 87.5% of animals. Altogether, the medical data allow us to conclude that an adequate mouse model for myocardial infarction was generated. A further study is focused on the standardization of the experimental procedure and the use of genetically modified mouse strains, with the purpose of finding the most efficient therapeutic approaches for this disease. PMID:22649679

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

    PubMed

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

    2012-09-01

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

  1. Low doses of hyperbaric oxygenation effectively decrease the size of necrotic zone in rats with experimental myocardial infarction.

    PubMed

    Dotsenko, E A; Nikulina, N V; Salivonchik, D P; Lappo, O G; Gritsuk, A I; Bastron, A S

    2015-04-01

    We studied the effect of a single session of hyperbaric oxygenation on the size of risk, ischemic, and necrotic zones in rat myocardium after irreversible occlusion of the coronary artery and excessive oxygen pressure of 0.02 and 0.1 MPa. Myocardium infarction was reproduced by ligation of the left coronary artery. The size of the risk, ischemic, and necrotic zones was planimetrically evaluated. Hyperbaric oxygenation (60-min session) was performed 3 h after artery occlusion at excessive oxygen pressure of 0.02 and 0.1 MPa. In rats not exposed to hyperbaric oxygenation, the risk zone median was 31.7% of the left ventricle weight, while after the session it did not exceed 25%. In spontaneous course of myocardium infarction, the ischemia to necrosis zone ratio was 1.7:1, while under conditions of hyperbaric oxygenation at oxygen pressure of 0.1 and 0.02 MPa, the these values were 0.6:1 and 2:1, respectively. Excessive oxygen pressure of 0.02 mPa is better than traditionally used 0.1 MPa, because it promotes redistribution of the ischemic and necrotic areas in the risk zone: the area of necrotic zone decreased at the expense of the ischemic zone. Hyperbaric oxygenation produces a positive effect on the myocardium under conditions of total occlusion of the coronary artery. PMID:25900609

  2. Senescent cardiac fibroblast is critical for cardiac fibrosis after myocardial infarction.

    PubMed

    Zhu, Fuli; Li, Yulin; Zhang, Junmeng; Piao, Chunmei; Liu, Tingting; Li, Hui-Hua; Du, Jie

    2013-01-01

    Senescence is a recognized mechanism of cardiovascular diseases; however, its contribution to myocardial fibrosis and rupture after infarction and the underlying mechanisms remain unclear. Here we showed that senescent cardiac fibroblasts markedly accumulated in heart after myocardial infarction. The expression of key senescence regulators, especially p53, was significantly up-regulated in the infarcted heart or hypoxia-treated fibroblasts. Furthermore, knockdown of endogenous p53 by siRNA in fibroblasts markedly reduced hypoxia-induced cell senescence, cytokine expression but increased collagen expression, whereas increased expression of p53 protein by adenovirus infection had opposite effects. Consistent with in vitro results in cardiac fibroblasts, p53 deficiency in vivo significantly decreased the accumulation of senescent fibroblasts, the infiltration of macrophages and matrix metalloproteinases, but enhanced collagen deposition after myocardial infarction. In conclusion, these results suggest that the p53-mediated fibroblast senescence limits cardiac collagen production, and inhibition of p53 activity could represent a novel therapeutic target to increase reparative fibrosis and to prevent heart rupture after myocardial infarction.

  3. 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.

  4. Inhibition of the nitric oxide/cyclic guanosine monophosphate pathway limited the cardioprotective effect of post-conditioning in hearts with apical myocardial infarction.

    PubMed

    Correa, Francisco; Buelna-Chontal, Mabel; Chagoya, Victoria; García-Rivas, Gerardo; Vigueras, Rosa María; Pedraza-Chaverri, José; García-Niño, Wylly Ramsés; Hernández-Pando, Rogelio; León-Contreras, Juan Carlos; Zazueta, Cecilia

    2015-10-15

    Reperfusion damage involves opening of the mitochondrial permeability transition pore (mPTP) and loss of ATP synthesis. Several cardioprotective pathways are activated by ischemic or pharmacological post-conditioning (PC). The mechanisms that are activated by PC in no co-morbidity murine models include: activation of rescue kinases, oxidative stress reduction, glycolytic flux regulation and preservation of ATP synthesis. However, relatively scarce efforts have been made to define whether the efficacy of PC signaling is blunted by risk factors or systemic diseases associated with ischemic heart pathology. Experimental evidence has shown that the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling is a main mechanism activated by PC in hearts without pathological history. In this work we evaluated the participation of the NO pathway, through downstream kinase activation and inhibition of mPTP in hearts with previous infarct. Myocardial infarction was induced with a single dose of isoproterenol (85 mg/kg i.p.) to male Wistar rats. After 24 h, the hearts were mounted into the Langendorff system and subjected to 30 min of ischemia and 60 min of reperfusion. PC consisted of 5 cycles of 30 s of reperfusion/30 s of ischemia, then the hearts were reperfused with or without inhibitors of the NO/cGMP pathway. PC activates the NO/cGMP pathway, as increased cGMP and NO levels were detected in isoproterenol-treated hearts. The cardioprotective effect of PC was abolished with both L-NAME (inhibitor of constitutive NO synthase) and ODQ (inhibitor of soluble guanylate cyclase), whereas the NO donor (DETA-NO) restored cardioprotection even in the presence of L-NAME or ODQ. We also found that mitochondrial structure and function was preserved in PC hearts. We conclude that PC exerts cardioprotection in hearts with previous infarct by maintaining mitochondrial structure and function through NO-dependent pathway.

  5. Acute myocardial infarction and renal infarction in a bodybuilder using anabolic steroids.

    PubMed

    Ilhan, Erkan; Demirci, Deniz; Güvenç, Tolga Sinan; Calık, Ali Nazmi

    2010-06-01

    A 41-year-old male bodybuilder was admitted with acute inferior myocardial infarction. The patient had been using oxymetholone and methenolone to increase his performance for 15 years and quitted smoking three years before. He underwent successful primary percutaneous coronary intervention (PCI) and bare metal stenting for total occlusion of the proximal right coronary artery. Angiography also showed a critical lesion in the left anterior descending (LAD) coronary artery. Five hours after primary PCI, the patient had severe right flank pain. Abdominal computed tomography showed a large renal infarction in the right kidney. Subcutaneous enoxaparin was added to dual antiplatelet treatment. Doppler renal ultrasound performed on the eighth day showed findings of reperfusion in the right kidney and normal-size kidneys. Transthoracic echocardiography demonstrated disappearance of previously detected thrombus remnant in the left ventricle and only mild hypokinesia around the apical and middle segments of the inferior and inferoseptal walls. The patient was discharged on the 10th day. Renal arteriography during elective LAD intervention 18 days after discharge showed complete revascularization, stent patency, and improved blood flow. This is the first case of renal infarction that developed in the early hours of primary PCI, despite effective anticoagulant and antiplatelet treatment. Intensive coronary artery and left ventricular thrombi may be explained by the use of anabolic steroids.

  6. Photoluminescent Mesoporous Silicon Nanoparticles with siCCR2 Improve the Effects of Mesenchymal Stromal Cell Transplantation after Acute Myocardial Infarction

    PubMed Central

    Lu, Wenbin; Xie, ZhuoYing; Tang, Yong; Bai, Ling; Yao, Yuyu; Fu, Cong; Ma, Genshan

    2015-01-01

    Background: Despite the benefits of mesenchymal stromal cell (MSC) transplantation in cardiac tissue, detailed in vivo observations have shown that MSCs only survive for a brief period after transplantation due to harsh microenvironmental conditions, including ischemia, inflammation and anoikis, in the infarcted myocardium. Thus, new strategies are needed to enhance MSC survival and inhibit cardiac remodeling. Studies have now demonstrated that chemokine [C-C motif] ligand 2 (CCL2) and its cognate receptor C-C chemokine receptor 2 (CCR2) promote excessive Ly6Chigh inflammatory monocyte infiltration at the infarct in response to ischemic myocardial injury. Therefore, decreasing the activities of these monocytes immediately after acute myocardial infarction (AMI) could be beneficial for AMI patients. Objectives: This study tested the hypothesis that therapeutic siRNA-loaded photoluminescent mesoporous silicon nanoparticles (PMSNs) targeting CCR2 expression in Ly6Chigh inflammatory monocytes decrease the accumulation of these cells in the infarct, improve the efficacy of MSC transplantation and attenuate myocardial remodeling. Methods: PMSNs carrying therapeutic siCCR2 were first synthesized without the inclusion of fluorescent materials or dyes. After AMI BALB/c mice were established, 105 5-ethynyl-2'- deoxyuridine (EdU)-labeled MSCs suspended in 100 µl of phosphate buffered saline (PBS) were injected into the border zone of the infarct of each mouse. PMSNs-siCCR2 (25 µg/g) were also intravenously injected via the tail vein immediately following AMI induction. Control mice were injected with an equal amount of PMSNs without siCCR2. PMSNs-siCCR2 were examined in vivo using near-infrared imaging technology. The therapeutic effects of PMSNs-siCCR2 for MSC transplantation were determined at the mRNA, protein and functional levels. Results: PMSNs-siCCR2 circulated freely in vivo and were cleared in a relatively short period of time (t½=37 min) with no evidence of

  7. Acute Anteroseptal Myocardial Infarction after a Negative Exercise Stress Test.

    PubMed

    Al-Alawi, Abdullah M; Janardan, Jyotsna; Peck, Kah Y; Soward, Alan

    2016-05-01

    A myocardial infarction is a rare complication which can occur after an exercise stress test. We report a 48-year-old male who was referred to the Mildura Cardiology Practice, Victoria, Australia, in August 2014 with left-sided chest pain. He underwent an exercise stress test which was negative for myocardial ischaemia. However, the patient presented to the Emergency Department of the Mildura Base Hospital 30 minutes after the test with severe retrosternal chest pain. An acute anteroseptal ST segment elevation myocardial infarction was observed on electrocardiography. After thrombolysis, he was transferred to a tertiary hospital where coronary angiography subsequently revealed significant left anterior descending coronary artery stenosis. Thrombus aspiration and a balloon angioplasty were performed. The patient was discharged three days after the surgical procedure in good health.

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

    PubMed

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

    2014-01-01

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

  9. Risk of Myocardial Infarction Immediately After Alcohol Consumption

    PubMed Central

    Mostofsky, Elizabeth; van der Bom, Johanna G.; Mukamal, Kenneth J.; Maclure, Malcolm; Tofler, Geoffrey H.; Muller, James E.; Mittleman, Murray A.

    2014-01-01

    Background Habitual moderate alcohol consumption is associated with a lower risk of acute myocardial infarction (MI) whereas heavy (binge) drinking is associated with higher cardiovascular risk. However, less is known about the immediate effects of alcohol consumption on the risk of acute MI and whether any association differs by beverage type or usual drinking patterns. Methods We conducted a case-crossover analysis of 3,869 participants from the Determinants of Myocardial Infarction Onset Study who were interviewed during hospitalization for acute MI in one of 64 medical centers across the United States in 1989–1996. We compared the observed number of times that each participant consumed wine, beer or liquor in the hour preceding MI symptom onset with the expected frequency based on each participant’s control information, defined as the number of times the participant consumed alcohol in the past year. Results Among 3869 participants, 2119 (55%) reported alcohol consumption in the past year, including 76 within 1 hour before acute MI onset. The incidence rate of acute MI onset was elevated 1.72-fold (95% confidence interval [CI]=1.37–2.16) within 1 hour after alcohol consumption. The association was stronger for liquor than for beer or wine. The higher rate was not apparent for daily drinkers. For the 24 hours after consumption, there was a 14% lower rate (relative risk=0.86 [95% CI=0.79–0.95]) of MI compared with periods with no alcohol consumption. Conclusions Alcohol consumption is associated with an acutely higher risk of MI in the subsequent hour among people who do not typically drink alcohol daily. PMID:25563434

  10. Prognosis after myocardial infarction: results of 15 year follow up.

    PubMed Central

    Merrilees, M A; Scott, P J; Norris, R M

    1984-01-01

    A total of 271 out of 757 patients who had suffered a myocardial infarction during 1966-7 were still alive after six years; these patients were subsequently followed up 15 years after the infarction. Two hundred and sixty eight (99%) of the patients alive at six years and 519 (95%) of the 549 originally discharged from hospital were traced. A coronary prognostic index, which had predicted survival both to three years and from three to six years after recovery from the infarct also predicted survival from six to 15 years after recovery. The major factor affecting survival to 15 years was age at the time of the original infarct. Among patients aged under 60 at the time of infarction women fared better than men (p = 0.027). Factors in the coronary prognostic index that were associated with impairment of left ventricular function at the time of infarction and that had predicted mortality to three years and from three to six years also predicted mortality from six to 15 years. These factors were cardiac enlargement, pulmonary venous congestion, and the presence of infarction before the index infarct. The dominant cause of death remained coronary heart disease and its complications. PMID:6229313

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

    PubMed

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

    2009-01-24

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

  12. 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.

  13. [Pharmacologic limitation of the size of the myocardial infarction (excluding thrombolysis)].

    PubMed

    Zannad, F; Gilgenkrantz, J M; Royer, R J

    1985-01-01

    Several pharmacological agents possess cardio-protective properties. Some of these agents have been evaluated in the context of the limitation of the size of the myocardial infarction. In this study, controlled randomised trials evaluated the effects of a solution of glucose-insulin-potassium (GIK), hyaluronidase, nitrate derivatives, calcium antagonists and beta-blockers administered during the first few hours following acute myocardial infarction. Despite promising results, we do not yet have any proof of the effectiveness of the GIK solution, hyaluronidase or nitrate derivatives. Nifedipine appears to be devoid of any effect and other calcium antagonists are currently under investigation. The numerous trials have been performed with beta-blockers generally support their beneficial effect on the limitation of the size of the infarction, which is usually accompanied by a reduction in the mid and long term mortality. They are therefore recommended in this indication and their practical use is discussed.

  14. [Trans and postoperative myocardial infarct in heart surgery].

    PubMed

    Rotberg, T; Macías, R; Correa-Suárez, R; Luna, P; Malo, R

    1976-01-01

    1. A study was made of 34 cases (33%) of myocardial infarction trans and immediately postoperative which occurred in 11,210 surgical interventions with and without extracorporeal circulation. 2. This presents a statistical relation of the frequency of myocardial infarction in realtion to the heart disease acquired with or without extracorporeal circulation with the mitral, aortic, and double prosthesis of the mitral and aortic valves. A correlation was also made with the ischemic heart disease subjected to revascularization. The same analysis was carried out in the congenital heart disease with or without extracorporeal circulation. 3. In all cases the antecedents, precipitating factors, and the clinical picture were studied and in 12 cases the necropsy was analized. The principal finding was transmural myocardial infarction with electrocardiographic proof and serial enzymes. 4. The group was divided into two sub-groups; Group "A" with acute myocardial infarction transoperative, and Group "B" with acute myocardial infarction in the first eight postoperative days. The electrical and mechanical complications were analized. 5. A correlation was made of the causes of mortality related to the type of congenital or acquired heart disease with or without extracorporeal circulation. 6. The frequency of this entity was studied with the total time of aortic clamping, and the complications such as the low cardiac output syndrome, rupture of the wall, aneurysms, acute pulmonary edema, and with the disturbances of rhythm and conduction. 7. The presence of 33.3% of normal coronaries in these of necropsy was emphasized. 8. The importance of the coronary profile of this group in relation to the consequences of a stress from anesthesia, surgery, extracorporeal circulation, and aortic clamping is mentioned. 9. The diagnostic parameters such as arterial hypotension with or without the low cardiac output syndrome, enzyme levels, and the action of the potassium ion are mentioned. 10

  15. Carbon monoxide and ST-elevation myocardial infarction: case reports.

    PubMed

    Sward, Douglas G; Sethuraman, Kinjal N; Wong, Jennifer S; Rosenthal, Robert E

    2016-01-01

    We describe two cases of myocardial infarction with ST-segment elevation on electrocardiogram associated with carbon monoxide (CO) poisoning, a condition rarely reported in the literature. The first was a 62-year-old woman who experienced chest pain in the emergency department (ED) while being assessed for exposure to carbon monoxide in her home. The second was an 80-year-old man who fainted at home and was found to have ST elevation during the ED workup. After hospitalization, he returned home and soon thereafter had difficulty walking and speaking. The responding paramedics detected a very high CO level in the home. Both patients received hyperbaric oxygen therapy within the first several hours of presentation. For this combination of conditions, it is difficult to derive evidence-based management recommendations, given the paucity of cases reported to date. We conclude that rapid consultation with interventional cardiology and consideration of angioplasty or stenting are appropriate, especially when electrocardiographic findings and echocardiography point to a specific coronary distribution. Hyperbaric oxygen therapy might have a role in the treatment, based on its effects on myocardial ischemia and injury in other models.

  16. Pathological observation of acute myocardial infarction in Chinese miniswine

    PubMed Central

    Wang, Chuang; Wang, Shao-Xin; Dong, Ping-Shuan; Wang, Li-Ping; Duan, Na-Na; Wang, Yan-Yu; Wang, Ke; Li, Zhuan-Zhen; Wei, Li-Juan; Meng, Ya-Li; Cheng, Jian-Xin

    2015-01-01

    The acute myocardial infarction (AMI) model in Chinese miniswine was built by percutaneous coronary artery occlusion. Pathological observation of AMI was performed, and the expression of tumor necrosis factor alpha (TNF-α) in the infarct sites was detected at different days after modeling in Chinese miniswine. The experimental findings may be used as the basis for blood flow reconstruction and intervention after AMI. Seven experimental Chinese miniswine were subjected to general anesthesia and Seldinger right femoral artery puncture. After coronary angiography, the gelfoam was injected via the microtube to occlude the obtuse marginal branch (OM branch). At 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 17 d after modeling, hetatoxylin-eosin (HE) staining was performed to observe the pathological changes and to detect the expression of TNF-α in the myocardial tissues. Cytoplasmic acidophilia of the necrotic myocardial tissues at 1 d after modeling was enhanced, and cytoplasmic granules were formed; at 3 d, the margins of the necrotic myocardial tissues were infiltrated by a large number of inflammatory cells; at 5 d, the nuclei of the necrotic myocardial cells were fragmented; at 7 d, extensive granulation tissues were formed at the margin of the necrotic myocardial tissues; at 10 d, part of the granulation tissues were replaced by fibrous scar tissues; at 14-17 d, all granulation tissues were replaced by fibrous scar tissues. Immunohistochemical detection indicated that no TNF-α expression in normal myocardial tissues. The TNF-α expression was first detected at 3 d in the necrotic myocardial tissues and then increased at 5 d and 7 d. After reaching the peak at 10 d, the expression began to decrease at 14 d and the decrease continued at 17 d. Coronary angiography showed the disappearance of blood flow at the distal end of OM branch occluded by gelfoam, indicating that AMI model was constructed successfully. The repair of the infarcted myocardium began at 10-17 d after

  17. Ventricular function and infarct size: the Western Washington Intravenous Streptokinase in Myocardial Infarction Trial

    SciTech Connect

    Ritchie, J.L.; Cerqueira, M.; Maynard, C.; Davis, K.; Kennedy, J.W.

    1988-04-01

    The Western Washington Intravenous Streptokinase in Acute Myocardial Infarction Trial randomized 368 patients with symptoms and signs of acute myocardial infarction of less than 6 h duration to either conventional care or 1.5 million units of intravenous streptokinase. The mean time to randomization was 209 min and 52% of patients were randomized within 3 h of symptom onset. Quantitative, tomographic thallium-201 infarct size and radionuclide ejection fraction were measured at 8.2 +/- 7.5 weeks in 207 survivors who lived within a 100 mile radius of a centralized laboratory. Overall, infarct size as a percent of the left ventricle was 19 +/- 13% for control subjects and 15 +/- 13% for treatment patients (p = 0.03). For anterior infarction in patients entered within 3 h of symptom onset, infarct size was 28 +/- 13% in the control group versus 19 +/- 15% for the treatment group (p = 0.09). Left ventricular ejection fraction was 47 +/- 15% in the control versus 51 +/- 15% in the treatment group (p = 0.08). For anterior infarction of less than 3 h duration, the ejection fraction was 38 +/- 16% in the control versus 48 +/- 20% in the treatment group (p = 0.13). By statistical analysis incorporating the nonsurvivors, p values for all of these variables were less than or equal to 0.08. There was no benefit for patients with inferior infarction or for anterior infarction of greater than 3 h duration. It is concluded that intravenous streptokinase, when given within 3 h of symptom onset to patients with anterior infarction, reduces infarct size and improves ventricular function.

  18. Eplerenone attenuates cardiac dysfunction and oxidative stress in β-receptor stimulated myocardial infarcted rats

    PubMed Central

    Reddy, Navya M; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Ojha, Shreesh; Goyal, Sameer N

    2015-01-01

    Eplerenone is a competitive antagonist of the aldosterone receptor with an additional PI3K-Akt activity. The existing cram has been intended to explore, whether eplerenone treatment attenuates the expansion of myocardial infarction in isoproterenol treated rats by restoring hemodynamic, biochemical, and histopathological changes. Isoproterenol induced cardiotoxicity was evidenced by marked ST elevation, decrease in systolic, diastolic, mean arterial pressures. Maximal positive rate of developed left ventricular pressure (+LVdP/dt max, a indicator of myocardial contraction), maximal negative rate of developed left ventricular pressure (-LVdP/dt max, a meter of myocardial relaxation) and an increase in left ventricular end-diastolic pressure (LVEDP, a marker of pre-load) were also shown. In addition, a significant reduction in activities of myocardial creatine kinase-MB isoenzyme, lactate dehydrogenase, superoxide dismutase, catalase, and reduced glutathione level along with increase in malondialdehyde content were observed. Oral pre-treatment with eplerenone (50, 100 and 150 mg/kg) daily for a period of 14 days, constructively modulated the studied parameters in isoproterenol-induced myocardial injury. The protective role of eplerenone on isoproterenolinduced myocardial damage was further confirmed by histopathological examinations. Eplerenone at doses of 100 mg/kg and 150 mg/kg produced more pronounced protective effects than 50 mg/kg body weight. Together, our study provides evidence for protective effects of eplerenone on myocardium in experimentally induced myocardial infarction. PMID:26550459

  19. Eplerenone attenuates cardiac dysfunction and oxidative stress in β-receptor stimulated myocardial infarcted rats.

    PubMed

    Reddy, Navya M; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Ojha, Shreesh; Goyal, Sameer N

    2015-01-01

    Eplerenone is a competitive antagonist of the aldosterone receptor with an additional PI3K-Akt activity. The existing cram has been intended to explore, whether eplerenone treatment attenuates the expansion of myocardial infarction in isoproterenol treated rats by restoring hemodynamic, biochemical, and histopathological changes. Isoproterenol induced cardiotoxicity was evidenced by marked ST elevation, decrease in systolic, diastolic, mean arterial pressures. Maximal positive rate of developed left ventricular pressure (+LVdP/dt max, a indicator of myocardial contraction), maximal negative rate of developed left ventricular pressure (-LVdP/dt max, a meter of myocardial relaxation) and an increase in left ventricular end-diastolic pressure (LVEDP, a marker of pre-load) were also shown. In addition, a significant reduction in activities of myocardial creatine kinase-MB isoenzyme, lactate dehydrogenase, superoxide dismutase, catalase, and reduced glutathione level along with increase in malondialdehyde content were observed. Oral pre-treatment with eplerenone (50, 100 and 150 mg/kg) daily for a period of 14 days, constructively modulated the studied parameters in isoproterenol-induced myocardial injury. The protective role of eplerenone on isoproterenolinduced myocardial damage was further confirmed by histopathological examinations. Eplerenone at doses of 100 mg/kg and 150 mg/kg produced more pronounced protective effects than 50 mg/kg body weight. Together, our study provides evidence for protective effects of eplerenone on myocardium in experimentally induced myocardial infarction.

  20. Microstructural characterization of myocardial infarction with optical coherence tractography and two-photon microscopy.

    PubMed

    Goergen, Craig J; Chen, Howard H; Sakadžić, Sava; Srinivasan, Vivek J; Sosnovik, David E

    2016-09-01

    Myocardial infarction leads to complex changes in the fiber architecture of the heart. Here, we present a novel optical approach to characterize these changes in intact hearts in three dimensions. Optical coherence tomography (OCT) was used to derive a depth-resolved field of orientation on which tractography was performed. Tractography of healthy myocardium revealed a smooth linear transition in fiber inclination or helix angle from the epicardium to endocardium. Conversely, in infarcted hearts, no coherent microstructure could be identified in the infarct with OCT Additional characterization of the infarct was performed by the measurement of light attenuation and with two-photon microscopy. Myofibers were imaged using autofluorescence and collagen fibers using second harmonic generation. This revealed the presence of two distinct microstructural patterns in areas of the infarct with high light attenuation. In the presence of residual myofibers, the surrounding collagen fibers were aligned in a coherent manner parallel to the myofibers. In the absence of residual myofibers, the collagen fibers were randomly oriented and lacked any microstructural coherence. The presence of residual myofibers thus exerts a profound effect on the microstructural properties of the infarct scar and consequently the risk of aneurysm formation and arrhythmias. Catheter-based approaches to segment and image myocardial microstructure in humans are feasible and could play a valuable role in guiding the development of strategies to improve infarct healing. PMID:27650248

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

    SciTech Connect

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

    1990-08-01

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

  2. Declines in Acute Myocardial Infarction following Smokefree Laws and Individual Risk Attributable to Secondhand Smoke

    PubMed Central

    Lightwood, James M; Glantz, Stanton

    2010-01-01

    Background The estimated effects of recent pubic and workplace smoking restriction laws suggest that they produce significant declines in community rates of heart attack. The consistency of these declines with existing estimates of the relative risk of heart attack in individuals attributable to passive smoking exposure is poorly understood. The objective is to determine the consistency of estimates of reductions in community rates heart attacks from smoking restriction laws with estimates of the relative risk of heart disease in individuals exposed to passive smoking. Methods and Results Meta-analysis of existing estimates of declines in community rates were compared to a mathematical model of the relationship between individual risk and community rates. Outcome measure is the ratio of community rates of acute myocardial infarction: after, divided by before, a smoking restriction law. There is a significant drop in the rate of acute myocardial infarction hospital admissions associated with implementation of strong smokefree legislation. The primary reason for heterogeneity in results of different studies is the duration of follow-up period after adoption of the law. The pooled random effects estimate of the rate of acute myocardial infarction hospitalization 12 months following implementation of the law is 0.83 (0.80, 0.87) and this benefit grows with time. This drop in admissions is consistent with a range of plausible individual risk and exposure scenarios. Conclusions Passage of strong smokefree legislation produces rapid and substantial benefits in terms of reduced acute myocardial infarctions and these benefits grow with time. PMID:19770392

  3. MRI evaluation of injectable hyaluronic acid-based hydrogel therapy to limit ventricular remodeling after myocardial infarction.

    PubMed

    Dorsey, Shauna M; McGarvey, Jeremy R; Wang, Hua; Nikou, Amir; Arama, Leron; Koomalsingh, Kevin J; Kondo, Norihiro; Gorman, Joseph H; Pilla, James J; Gorman, Robert C; Wenk, Jonathan F; Burdick, Jason A

    2015-11-01

    Injectable biomaterials are an attractive therapy to attenuate left ventricular (LV) remodeling after myocardial infarction (MI). Although studies have shown that injectable hydrogels improve cardiac structure and function in vivo, temporal changes in infarct material properties after treatment have not been assessed. Emerging imaging and modeling techniques now allow for serial, non-invasive estimation of infarct material properties. Specifically, cine magnetic resonance imaging (MRI) assesses global LV structure and function, late-gadolinium enhancement (LGE) MRI enables visualization of infarcted tissue to quantify infarct expansion, and spatial modulation of magnetization (SPAMM) tagging provides passive wall motion assessment as a measure of tissue strain, which can all be used to evaluate infarct properties when combined with finite element (FE) models. In this work, we investigated the temporal effects of degradable hyaluronic acid (HA) hydrogels on global LV remodeling, infarct thinning and expansion, and infarct stiffness in a porcine infarct model for 12 weeks post-MI using MRI and FE modeling. Hydrogel treatment led to decreased LV volumes, improved ejection fraction, and increased wall thickness when compared to controls. FE model simulations demonstrated that hydrogel therapy increased infarct stiffness for 12 weeks post-MI. Thus, evaluation of myocardial tissue properties through MRI and FE modeling provides insight into the influence of injectable hydrogel therapies on myocardial structure and function post-MI.

  4. [The effect of extracorporeal thermal-modified autologous plasma exchanges on dynamics of hormone-metabolic homeostasis indices in patients with acute myocardial infarction].

    PubMed

    Ust'iantseva, I M; Kreĭnes, V M; Panin, L E; Petukhova, O V; Khokhlova, O I; Agadzhanian, V V

    1998-01-01

    Changes of biochemical indexes in the blood of 56 patients with acute myocardial infarction against the background of conventional and complex treatment using plasma exchange of extracorporeal-termally modified autoplasma have been analysed. The findings show that complex treatment of patients with AMI, using plasma exchange of extracorporal-thermally modified autoplasma, leads to much earlier decrease of KPK, LDH, LDH-1 enzyme activity in blood; it indicates the reduction of the period of myocardiocyte function restoration. The usage of plasma exchange of extracorporeal-thermally modified autoplasma in patients with acute myocardial infarction is accompanied by the absence of increase of glucose concentration in blood (owing to the normalization of insulin production), favourable influence on stress-reaction of biological systems of organism decrease of atherogenity index. Optimisation and efficiency of AMI therapy during treatment in the hospital is possible, with plasma exchange of extracorporeal-thermally modified autoplasma included in complex therapy. PMID:9575618

  5. Role of lymphocytes in myocardial injury, healing, and remodeling after myocardial infarction.

    PubMed

    Hofmann, Ulrich; Frantz, Stefan

    2015-01-16

    A large body of evidence produced during decades of research indicates that myocardial injury activates innate immunity. On the one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial infarction (MI). On the other hand, innate immunity activation contributes to myocardial healing, as exemplified by monocytes' central role in the formation of a stable scar and protection against intraventricular thrombi after acute infarction. Although innate leukocytes can recognize a wide array of self-antigens via pattern recognition receptors, adaptive immunity activation requires highly specific cooperation between antigen-presenting cells and distinct antigen-specific receptors on lymphocytes. We have only recently begun to examine lymphocyte activation's relationship to adaptive immunity and significance in the context of ischemic myocardial injury. There is some experimental evidence that CD4(+) T-cells contribute to ischemia-reperfusion injury. Several studies have shown that CD4(+) T-cells, especially CD4(+) T-regulatory cells, improve wound healing after MI, whereas depleting B-cells is beneficial post MI. That T-cell activation after MI is induced by T-cell receptor signaling implicates autoantigens that have not yet been identified in this context. Also, the significance of lymphocytes in humans post MI remains unclear, primarily as a result of methodology. This review summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk with innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeling after myocardial infarction.

  6. The Effect of Face-to-Face Education and Educational Booklet on Heart Health Indexes of the Hospitalized Patients with Myocardial Infarction

    PubMed Central

    Esmaeili Vardanjani, Safar Ali; Fanisaberi, Laleh; Alirezaee Shahraki, Firozeh; Khalilzadeh, Ahmad; Tavakoli Vardanjani, Abdolazim; Ghani Dehkordi, Fatemeh

    2013-01-01

    Management of risk factors and heart health indexes in the patients who have been diagnosed with myocardial infarction will result in prevention of secondary myocardial infarction, reduction of postimprovement mortality, increase of life span and improvement of life quality. Patient education has been found to be one of the most fundamental and essential care programs on the basis of identification and control of the patients' health criteria. The study is a quasi-experimental research consisting of two groups. In this study, 112 patients with myocardial infarction who were below the age of 70 were selected randomly and divided into two groups (case group and control group) after being matched based on age and sex. The researcher first measured the health indexes including smoking, cholesterol level, body mass, level of anxiety, and amount of systolic and diastolic blood pressure in patients who have been diagnosed with myocardial infarction for the first time. He performed education program in case group and analyzed the said variables after four months. He also compared the behaviors in the two groups after being educated. The data was analyzed by SPSS software, version 15 (This product is licensed to FeFDBi, ABiComputer, 1337), and the two groups were compared by using appropriate statistical tests. According to the results, after education period, systolic blood pressure of the case group improves compared with control group (P < 0.05/P = 0.022), case group tends to quit smoking more than control group does (P = 0.013), cholesterol level of case group improves compared with control group (P < 0.0001), changes of body mass are more positive in case group compared with control group (P = 0.012), and anxiety of case group reduces compared with control group (P < 0.0001). PMID:23781336

  7. Heart Rate Turbulence as Risk-Predictor after Myocardial Infarction

    PubMed Central

    Zuern, Christine S.; Barthel, Petra; Bauer, Axel

    2011-01-01

    Heart rate turbulence (HRT) is the baroreflex-mediated short-term oscillation of cardiac cycle lengths after spontaneous ventricular premature complexes. HRT is composed of a brief heart rate acceleration followed by a gradual heart rate deceleration. In high risk patients after myocardial infarction (MI) HRT is blunted or diminished. Since its first description in 1999 HRT emerged as one of the most potent risk factors after MI. Predictive power of HRT has been studied in more than 10,000 post-infarction patients. This review is intended to provide an overview of HRT as risk-predictor after MI. PMID:22180744

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

    PubMed

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

    2015-11-01

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

  9. Cocaine use and delayed myocardial ischaemia and/or infarction

    PubMed Central

    Phang, Kee Wei; Wood, Alice

    2014-01-01

    A 37-year-old woman was admitted into the coronary care unit following chest pain after using cocaine. She was found to have significant myocardial ischaemia on blood and ECG investigations despite a recent coronary angiogram that had not demonstrated flow-limiting coronary disease. This case report summarises the risks of myocardial ischaemia and/or infarction for patients taking cocaine and the pathophysiology behind it, focusing in particular on the risks of delayed reaction some time after cocaine ingestion. PMID:25201873

  10. Effects of a beta-blocker on ventricular late potentials in patients with acute anterior myocardial infarction receiving successful thrombolytic therapy.

    PubMed

    Evrengul, Harun; Dursunoglu, Dursun; Kayikcioglu, Meral; Can, Levent; Tanriverdi, Halil; Kaftan, Asuman; Kilic, Mustafa

    2004-01-01

    Late potentials (LP) detected on the signal-averaged electrocardiogram (SAECG) predict arrhythmic events after acute myocardial infarction (AMI). It is also well established that successful thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the effects of a beta-blocker on LP in patients receiving thrombolytic therapy. We studied 40 patients presenting with anteroseptal AMI (< 6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Eighteen patients received metoprolol (5 mg IV on admission followed by 50 mg BID). SAECG recordings were obtained serially using an ART system (40-250 Hz filter, noise < 0.5 mV) prior to thrombolytic therapy, after 48 hours and after 10 days. LP was defined as posi-tive if the SAECG met at least 2 of the Gomes criteria. Changes observed in SAECG recordings after thrombolytic therapy were correlated with angiographic and clinical data with regard to the usage of BB. The frequencies of LP before and after thrombolytic therapy were compared with the McNemar test. There were no significant differences between the clinical characteristics, risk factors, and angiographic findings (including infarct related artery patency and LV functions) of the groups. Baseline SAECG findings were also similar between the groups. The incidence of LP significantly decreased after TT in the BB group, however, this change was not observed in patients who did not receive BB (P = 0.012, McNemar test). Beta-blockers reduce the incidence of LPs following thrombolytic therapy in patients with anterior AMI. This might be explained by the possible beneficial effect of BB on the arrhythmogenic substrate.

  11. Left ventricular muscle and fluid mechanics in acute myocardial infarction.

    PubMed

    Nucifora, Gaetano; Delgado, Victoria; Bertini, Matteo; Marsan, Nina Ajmone; Van de Veire, Nico R; Ng, Arnold C T; Siebelink, Hans-Marc J; Schalij, Martin J; Holman, Eduard R; Sengupta, Partho P; Bax, Jeroen J

    2010-11-15

    Left ventricular (LV) diastolic filling is characterized by the formation of intraventricular rotational bodies of fluid (termed "vortex rings") that optimize the efficiency of LV ejection. The aim of the present study was to evaluate the morphology and dynamics of LV diastolic vortex ring formation early after acute myocardial infarction (AMI), in relation to LV diastolic function and infarct size. A total of 94 patients with a first ST-segment elevation AMI (59 ± 11 years; 78% men) were included. All patients underwent primary percutaneous coronary intervention. After 48 hours, the following examinations were performed: 2-dimensional echocardiography with speckle-tracking analysis to assess the LV systolic and diastolic function, the vortex formation time (VFT, a dimensionless index for characterizing vortex formation), and the LV untwisting rate; contrast echocardiography to assess LV vortex morphology; and myocardial contrast echocardiography to identify the infarct size. Patients with a large infarct size (≥ 3 LV segments) had a significantly lower VFT (p <0.001) and vortex sphericity index (p <0.001). On univariate analysis, several variables were significantly related to the VFT, including anterior AMI, LV end-systolic volume, LV ejection fraction, grade of diastolic dysfunction, LV untwisting rate, and infarct size. On multivariate analysis, the LV untwisting rate (β = -0.43, p <0.001) and infarct size (β = -0.33, p = 0.005) were independently associated with VFT. In conclusion, early in AMI, both the LV infarct size and the mechanical sequence of diastolic restoration play key roles in modulating the morphology and dynamics of early diastolic vortex ring formation.

  12. [Exertion tolerance in the early period after myocardial infarction, the results of echocardiographic examination and the clinical course of infarction].

    PubMed

    Straburzyńska-Migaj, E

    1992-01-01

    The relation between exercise test, echocardiography and clinical course of acute myocardial infarction was investigated. 17-34 days after an acute myocardial infarction, before hospital discharge, 58 patients underwent exercise test and 17-28 days- echocardiography. Low exercise capacity was significant related to angina before infarction, maximal CKNAC and complications during clinical course. There was inverted correlation of asynergy index calculated from echocardiography with maximal workload achieved during exercise test.

  13. Effects of mir-21 on Cardiac Microvascular Endothelial Cells After Acute Myocardial Infarction in Rats: Role of Phosphatase and Tensin Homolog (PTEN)/Vascular Endothelial Growth Factor (VEGF) Signal Pathway

    PubMed Central

    Yang, Feng; Liu, Wenwei; Yan, Xiaojuan; Zhou, Hanyun; Zhang, Hongshen; Liu, Jianfei; Yu, Ming; Zhu, Xiaoshan; Ma, Kezhong

    2016-01-01

    Background This study investigated how miR-21 expression is reflected in acute myocardial infarction and explored the role of miR-21 and the PTEN/VEGF signaling pathway in cardiac microvascular endothelial cells. Material/Methods We used an in vivo LAD rat model to simulate acute myocardial infarction. MiR-21 mimics and miR-21 inhibitors were injected and transfected into model rats in order to alter miR-21 expression. Cardiac functions were evaluated using echocardiographic measurement, ELISA, and Masson staining. In addition, lenti-PTEN and VEGF siRNA were transfected into CMEC cells using standard procedures for assessing the effect of PTEN and VEGE on cell proliferation, apoptosis, and angiogenesis. MiR-21, PTEN, and VEGF expressions were examined by RT-PCR and Western blot. The relationship between miR-21 and PTEN was determined by the luciferase activity assay. Results We demonstrated that miR-21 bonded with the 3′-UTR of PTEN and suppressed PTEN expressions. Established models significantly induced cardiac infarct volume and endothelial injury marker expressions as well as miR-21 and PTEN expressions (P<0.05). MiR-21 mimics exhibited significantly protective effects since they down-regulated both infarction size and injury marker expressions by increasing VEGF expression and inhibiting PTEN expression (P<0.05). In addition, results from in vitro research show that lenti-PTEN and VEGF siRNA can notably antagonize the effect of miR-21 on cell proliferation, apoptosis, and angiogenesis (P<0.05). Conclusions MiR-21 exerts protective effects on endothelial injury through the PTEN/VEGF pathway after acute myocardial infarction. PMID:27708252

  14. A Case of Post Myocardial Infarction Papillary Muscle Rupture.

    PubMed

    Anuwatworn, Amornpol; Milnes, Christopher; Kumar, Vishesh; Raizada, Amol; Nykamp, Verlyn; Stys, Adam

    2016-06-01

    Papillary muscle rupture is a rare, life-threatening post myocardial infarction mechanical complication. Without surgical intervention, prognosis is very poor. Clinicians need to recognize this complication early, as prompt therapy is crucial. We present a case of inferior ST elevation myocardial infarction complicated by posteromedial papillary muscle rupture resulting in severe acute mitral regurgitation (flail anterior mitral leaflet), acute pulmonary edema and cardiogenic shock. In our patient, a new mitral regurgitation murmur suggested this mechanical complication. Complete disruption of papillary muscle was visualized by transesophageal echocardiography. This case illustrates the importance of good physical examination for early diagnosis of papillary muscle rupture, so that life-saving treatment can be administered without delay. PMID:27443107

  15. Myocardial infarction: stem cell transplantation for cardiac regeneration.

    PubMed

    Carvalho, Edmund; Verma, Paul; Hourigan, Kerry; Banerjee, Rinti

    2015-11-01

    It is estimated that by 2030, almost 23.6 million people will perish from cardiovascular disease, according to the WHO. The review discusses advances in stem cell therapy for myocardial infarction, including cell sources, methods of differentiation, expansion selection and their route of delivery. Skeletal muscle cells, hematopoietic cells and mesenchymal stem cells (MSCs) and embryonic stem cells (ESCs)-derived cardiomyocytes have advanced to the clinical stage, while induced pluripotent cells (iPSCs) are yet to be considered clinically. Delivery of cells to the sites of injury and their subsequent retention is a major issue. The development of supportive scaffold matrices to facilitate stem cell retention and differentiation are analyzed. The review outlines clinical translation of conjugate stem cell-based cellular therapeutics post-myocardial infarction.

  16. Polycythemia vera presenting as acute myocardial infarction: An unusual presentation

    PubMed Central

    Bahbahani, Hussain; Aljenaee, Khaled; Bella, Abdelhaleem

    2014-01-01

    Acute myocardial infarction (AMI) is usually seen in the setting of atherosclerosis and its associated risk factors. Myocardial infarction in the young poses a particular challenge, as the disease is less likely, due to atherosclerosis. We report the case of a 37-year-old female patient who presented with ST segment elevation anterolateral AMI. The only abnormality on routine blood investigation was raised hemoglobin and hematocrit. After further testing, she was diagnosed according to the World Health Organization (WHO) criteria with polycythemia vera. This case illustrates the importance of recognizing polycythemia vera as an important cause of thrombosis, which can present initially as AMI, and to emphasize the early recognition of the disease in order to initiate appropriate management strategies. PMID:25544823

  17. 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.

  18. Prognostic implications of cardiac scintigraphic parameters obtained in the early phase of acute myocardial infarction

    SciTech Connect

    Suzuki, A.; Matsushima, H.; Satoh, A.; Hayashi, H.; Sotobata, I.

    1988-06-01

    A cohort of 76 patients with acute myocardial infarction was studied with infarct-avid scan, radionuclide ventriculography, and thallium-201 myocardial perfusion scintigraphy. Infarct area, left ventricular ejection fraction, and defect score were calculated as radionuclide indices of the extent of myocardial infarction. The correlation was studied between these indices and cardiac events (death, congestive heart failure, postinfarction angina, and recurrence of myocardial infarction) in the first postinfarction year. High-risk patients (nonsurvivors and patients who developed heart failure) had a larger infarct area, a lower left ventricular ejection fraction, and a larger defect score than the others. Univariate linear discriminant analysis was done to determine the optimal threshold of these parameters for distinguishing high-risk patients from others. Radionuclide parameters obtained in the early phase of acute myocardial infarction were useful for detecting both patients with grave complications and those with poor late prognosis during a mean follow-up period of 2.6 years.

  19. Myocardial infarction caused by myocardial bridging in a male adolescent athlete.

    PubMed

    Zhu, Cheng-Gang; Liu, Jun; Liu, Wei-Dong; Xu, Yan-Lu; Wu, Na-Qiong; Guo, Yuan-Lin; Tang, Yi-Da; Jiang, Li-Xin; Li, Jian-Jun

    2012-02-01

    Myocardial bridging is a common congenital abnormality of a coronary artery, and is usually thought to be a benign anatomical variant. Although rare, previous studies have reported that patients with myocardial bridging may suffer from myocardial ischemia, myocardial infarction (MI), arrhythmias and even sudden death. Here we report the case of an 18-year-old adolescent athlete with myocardial bridging resulting in MI. Coronary angiography revealed 80% luminal narrowing by systolic compression in the proximal and mid segments of the left anterior descending coronary artery, which returned to normal during diastole. We considered that heavy sports might be a potential trigger for his MI attack. Therefore, special attention should be paid to this kind of athlete, especially if adolescent.

  20. 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.

  1. Structural racism and myocardial infarction in the United States

    PubMed Central

    Lukachko, Alicia; Hatzenbuehler, Mark L.; Keyes, Katherine M.

    2014-01-01

    There is a growing research literature suggesting that racism is an important risk factor undermining the health of Blacks in the United States. Racism can take many forms, ranging from interpersonal interactions to institutional/structural conditions and practices. Existing research, however, tends to focus on individual forms of racial discrimination using self-report measures. Far less attention has been paid to whether structural racism may disadvantage the health of Blacks in the United States. The current study addresses gaps in the existing research by using novel measures of structural racism and by explicitly testing the hypothesis that structural racism is a risk factor for myocardial infarction among Blacks in the United States. State-level indicators of structural racism included four domains: (1) political participation; (2) employment and job status; (3) educational attainment; and (4) judicial treatment. State-level racial disparities across these domains were proposed to represent the systematic exclusion of Blacks from resources and mobility in society. Data on past-year myocardial infarction were obtained from the National Epidemiologic Survey on Alcohol and Related Conditions (non-Hispanic Black: N = 8245; non-Hispanic White: N = 24,507), a nationally representative survey of the U.S. civilian, non-institutionalized population aged 18 and older. Models were adjusted for individual-level confounders (age, sex, education, household income, medical insurance) as well as for state-level disparities in poverty. Results indicated that Blacks living in states with high levels of structural racism were generally more likely to report past-year myocardial infarction than Blacks living in low-structural racism states. Conversely, Whites living in high structural racism states experienced null or lower odds of myocardial infarction compared to Whites living in low-structural racism states. These results raise the provocative possibility that structural

  2. Structural racism and myocardial infarction in the United States.

    PubMed

    Lukachko, Alicia; Hatzenbuehler, Mark L; Keyes, Katherine M

    2014-02-01

    There is a growing research literature suggesting that racism is an important risk factor undermining the health of Blacks in the United States. Racism can take many forms, ranging from interpersonal interactions to institutional/structural conditions and practices. Existing research, however, tends to focus on individual forms of racial discrimination using self-report measures. Far less attention has been paid to whether structural racism may disadvantage the health of Blacks in the United States. The current study addresses gaps in the existing research by using novel measures of structural racism and by explicitly testing the hypothesis that structural racism is a risk factor for myocardial infarction among Blacks in the United States. State-level indicators of structural racism included four domains: (1) political participation; (2) employment and job status; (3) educational attainment; and (4) judicial treatment. State-level racial disparities across these domains were proposed to represent the systematic exclusion of Blacks from resources and mobility in society. Data on past-year myocardial infarction were obtained from the National Epidemiologic Survey on Alcohol and Related Conditions (non-Hispanic Black: N = 8245; non-Hispanic White: N = 24,507), a nationally representative survey of the U.S. civilian, non-institutionalized population aged 18 and older. Models were adjusted for individual-level confounders (age, sex, education, household income, medical insurance) as well as for state-level disparities in poverty. Results indicated that Blacks living in states with high levels of structural racism were generally more likely to report past-year myocardial infarction than Blacks living in low-structural racism states. Conversely, Whites living in high structural racism states experienced null or lower odds of myocardial infarction compared to Whites living in low-structural racism states. These results raise the provocative possibility that structural

  3. Chronobiology of Takotsubo Syndrome and Myocardial Infarction: Analogies and Differences.

    PubMed

    Manfredini, Roberto; Manfredini, Fabio; Fabbian, Fabio; Salmi, Raffaella; Gallerani, Massimo; Bossone, Eduardo; Deshmukh, Abhishek J

    2016-10-01

    Several pathophysiologic factors, not harmful if taken alone, are capable of triggering unfavorable events when presenting together within the same temporal window (chronorisk), and the occurrence of many cardiovascular events is not evenly distributed in time. Both acute myocardial infarction and takotsubo syndrome seem to exhibit a temporal preference in their onset, characterized by variations according to time of day, day of the week, and month of the year, although with both analogies and differences. PMID:27638023

  4. Effect of coronary artery revascularization on in-hospital outcomes and long-term prognoses in acute myocardial infarction patients with prior ischemic stroke

    PubMed Central

    Li, Bo-Yu; Li, Xiao-Ming; Zhang, Yan; Wei, Zhan-Yun; Li, Jing; Hua, Qi

    2016-01-01

    Objective To investigate whether coronary artery revascularization therapies (CART), including percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), can improve the in-hospital and long-term outcomes for acute myocardial infarction (AMI) patients with prior ischemic stroke (IS). Methods A total of 387 AMI patients with prior IS were enrolled consecutively from January 15, 2005 to December 24, 2011 in this cohort study. All patients were categorized into the CART group (n = 204) or the conservative medications (CM) group (n = 183). In-hospital cardiocerebral events and long-term mortality of the two groups after an average follow-up of 36 months were recorded by Kaplan-Meier survival curves and compared by Logistic regression and the Cox regression model. Results The CART patients were younger (66.5 ± 9.7 years vs. 71.7 ± 9.7 years, P < 0.01), had less non-ST segment elevation myocardial infarction (11.8% vs. 20.8%, P = 0.016) and more multiple-vascular coronary lesions (50% vs. 69.4%, P = 0.031). The hospitalization incidence of cardiocerebral events in the CART group was 9.3% while 26.2% in the CM group (P < 0.01). CART significantly reduced the risk of in-hospital cardiocerebral events by 65% [adjusted odds ratio (OR) = 0.35, 95% CI: 0.13–0.92]. By the end of follow-up, 57 cases (41.6%) died in CM group (n = 137) and 24 cases (12.2%) died in CART group (n = 197). Cox regression indicated that CART decreased the long-term mortality by 72% [adjusted hazard ratio (HR) = 0.28, 95% CI: 0.06–0.46], while categorical analysis indicated no significant difference between PCI and CABG. Conclusions CART has a significant effect on improving the in-hospital and long-term prognoses for AMI patients with prior IS. PMID:27168740

  5. Capsular contracture simulating myocardial infarction on ECG.

    PubMed

    Peters, W; McEwan, P

    1993-03-01

    A patient is presented with severe bilateral class IV capsular contractures who presented 16 years after prepectoral breast augmentation with a "septal infarct" pattern on ECG. This abnormal ECG proved to be an artifact caused by unavoidable misplacement of the V2 and V3 leads because of the severe capsular contracture. Following open capsulotomy, normal anatomic lead placement was possible, and a normal ECG was produced.

  6. Xylan polysaccharides fabricated into nanofibrous substrate for myocardial infarction.

    PubMed

    Venugopal, J; Rajeswari, R; Shayanti, M; Sridhar, R; Sundarrajan, S; Balamurugan, R; Ramakrishna, S

    2013-04-01

    Myocardial infarction, a main cause of heart failure, leads to loss of cardiac tissue impairment of left ventricular function. Repair of diseased myocardium with in vitro engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for myocardial infarction. We attempted to solve these problems by in vitro study by selecting a plant based polysaccharides beech wood Xylan for the normal functioning of infarcted myocardium. The present study fabricated Xylan based nanofibrous scaffolds cross-linked with glutaraldehyde (Glu) vapors for 24 h, 48 h and 1% Glu blended fibers for the culture of neonatal rat cardiac cells for myocardial infarction. These nanofibers were characterized by SEM, FT-IR, tensile testing and cell culture studies for the normal expression of cardiac proteins. The observed results showed that the Xylan/polyvinyl alcohol (PVA) 24h Glu vapor cross-linked nanofibers (427 nm) having mechanical strength of 2.43 MPa and Young modulus of 3.74 MPa are suitable for the culture of cardiac cells. Cardiac cells proliferation increased only by 11% in Xylan/PVA 24h Glu cross-linked nanofibers compared to control tissue culture plate (TCP). The normal cardiac cell morphology was observed in 24h cross-linked Xylan/PVA nanofibers but 48 h cross-linked fibers cell morphology was changed to flattened and elongated on the fibrous surfaces. Confocal analysis for cardiac expression proteins actinin, connexin 43 was observed normally in 24h Glu cross-linked nanofibers compared to all other nanofibrous scaffolds. The fabricated Xylan/PVA nanofibrous scaffold may have good potential for the normal functioning of infarcted myocardium.

  7. Gemella Endocarditis Presenting as an ST-Segment-Elevation Myocardial Infarction

    PubMed Central

    Chaudhry, Sunit-Preet; Stockwell, Philip H.

    2016-01-01

    Acute myocardial infarction from septic embolization is a rare initial presentation of endocarditis. We report the case of a 67-year-old man who presented with acute chest pain, in whom emergency cardiac catheterization revealed findings that suggested coronary embolism. The patient was found to have Gemella endocarditis, with its initial presentation an embolic acute ST-segment-elevation myocardial infarction. We suggest that endocarditis be considered among the potential causes of acute myocardial infarction. PMID:27303246

  8. [Acute myocardial infarction secondary to anaphylactic reaction following shellfish ingestion. The need for rescue coronary angioplasty].

    PubMed

    López-Mínguez, J R; González Fernández, R; Millán Núñez, V; Merchán Herrera, A; Altozano Gómez, J C; García-Andoaín, J M

    2000-12-01

    During anaphylactic (or anaphylactoid) reactions severe cardiovascular events may occur, acute myocardial infarction among them. This etiology of myocardial infarction, is known, although it is infrequent and only sporadically reported in literature. A case of acute myocardial infarction secondary to anaphylactic reaction following shellfish ingestion, treated with subcutaneous epinephrine and in whom a rescue coronary angioplasty was necessary is reported. The mechanism of coronary occlusion in this kind of reaction and the possible influence on the efficacy of treatment is discussed.

  9. Association of fragmented QRS complex with myocardial reperfusion in acute ST-elevated myocardial infarction.

    PubMed

    Erdem, Fatma Hizal; Tavil, Yusuf; Yazici, Hüseyin; Aygül, Nazif; Abaci, Adnan; Boyaci, Bülent

    2013-01-01

    In this study, we aimed to evaluate the relationship between TIMI myocardial perfusion (TMP) grade, as an indicator of myocardial reperfusion, and fragmented QRS (fQRS) in standard 12-lead electrocardiogram. Also, we evaluate fQRS is an additional indicator of myocardial reperfusion. One hundred patients admitted with first STEMI to Coronary Intensive Care Unit and who were used thrombolytic therapy was included in this retrospective study. Standard 12-lead electrocardiogram records of patients simultaneous with coronary angiography (second day) were assessed and analysed for the presence of fQRS. Also, coronary angiography images were analyzed to identify the infarct related artery, TIMI grade of infarct related artery and TMP grade of infarct related artery. The patients with fQRS demonstrated a significantly lower TMP grade, TIMI grade and ejection fraction compared with the non-fQRS patients (P = 0.004, P = 0.003, P = 0.02 respectively). The patients with inadequate myocardial reperfusion demonstrated a significantly higher fQRS compared with the adequate myocardial reperfusion patients. (56.9% versus 23.5%, P = 0.002 respectively). On correlation analysis, there was a significant negative correlation between fQRS and left ventricular ejection fraction (r = -232, P = 0.02) TMP grade and adequate myocardial reperfusion (TMP 3) showed significant negative correlation with fQRS (r = -0.370, P = 0.000; r = -0.318, P = 0.001 respectively). Presence of fragmented QRS in STEMI patients was associated with inadequate myocardial reperfusion and it can be used as a simple, noninvasive parameter to evaluate myocardial reperfusion.

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

    PubMed

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

    2014-01-01

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

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

    PubMed

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

    2014-01-01

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

  12. Thrombospondins in the transition from myocardial infarction to heart failure.

    PubMed

    Kirk, Jonathan A; Cingolani, Oscar H

    2016-01-01

    The heart's reaction to ischemic injury from a myocardial infarction involves complex cross-talk between the extra-cellular matrix (ECM) and different cell types within the myocardium. The ECM functions not only as a scaffold where myocytes beat synchronously, but an active signaling environment that regulates the important post-MI responses. The thrombospondins are matricellular proteins that modulate cell--ECM interactions, functioning as "sensors" that mediate outside-in and inside-out signaling. Thrombospondins are highly expressed during embryonic stages, and although their levels decrease during adult life, can be re-expressed in high quantities in response to cardiac stress including myocardial infarction and heart failure. Like a Swiss-army knife, the thrombospondins possess many tools: numerous binding domains that allow them to interact with other elements of the ECM, cell surface receptors, and signaling molecules. It is through these that the thrombospondins function. In the present review, we provide basic as well as clinical evidence linking the thrombospondin proteins with the post myocardial infarction response, including inflammation, fibrotic matrix remodeling, angiogenesis, as well as myocyte hypertrophy, apoptosis, and contractile dysfunction in heart failure. We will describe what is known regarding the intracellular signaling pathways that are involved with these responses, paving the road for future studies identifying these proteins as therapeutic targets for cardiac disease.

  13. Patterns of endocrine reactivity in patients with recent myocardial infarction

    PubMed Central

    Ceremużyński, L.; Kuch, J.; Markiewicz, L.; Lawecki, J.; Taton, J.

    1970-01-01

    The following endocrine function parameters were studied serially in a group of 10 patients with recent myocardial infarction: blood and urinary levels of epinephrine and norepinephrine, urinary excretion of vanillyl-mandelic acid; protein-bound iodine, Hamolsky test (Hamolsky, Stein, and Freedberg, 1957); blood insulin; 24-hour urinary excretion of 17-hydroxycorticoids, sodium, and potassium. The acute phase of myocardial infarction, especially in those patients with a severe clinical course (rhythm disturbances, coronary insufficiency, circulatory failure), was associated with disturbed endocrine reactivity. The most frequent and the earliest feature was the increased level of the 24-hour urinary excretion of epinephrine, combined with a pronounced decrease in blood insulin level. Later in the course of the disease, as the adrenergic reactivity returned to normal, there was an increase in blood insulin to normal levels. In 3 patients with severe clinical symptoms of acute myocardial infarction, there were, in addition to the increased 24-hour urinary excretion of catecholamines, a decreased blood insulin, higher than normal levels of protein-bound iodine, and of the Hamolsky test. One of these patients developed hypoadrenia. It is possible that the abnormal endocrine reactions accelerate the catabolic processes within cardiac tissue (catecholamines, thyroid hormones), especially when there is a possible functional deficiency of hormones, occurring as a general adaptation reaction to stress (cortisol, insulin). The disturbances that follow may be dangerous for the patient. PMID:4097104

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

    PubMed

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

    1997-11-01

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

  15. Association Between Smoking and Physician-Diagnosed Stroke and Myocardial Infarction in Male Adults in Korea.

    PubMed

    Chang, Sounghoon; Kim, Hyeongsu; Kim, Vitna; Lee, Kunsei; Jeong, Hyoseon; Lee, Jung-Hyun; Shin, Soon-Ae; Shin, Eunyoung; Park, Minsu; Ko, Eunjung

    2016-01-25

    To evaluate the association between smoking and physician-diagnosed stroke and myocardial infarction, this study used Community Health Survey data from 2009 on 92,082 males over the age of 30 years. Using multiple logistic regression, association index between smoking and physician-diagnosed stroke and myocardial infarction was calculated after adjusting the effects of age, hypertension, and diabetes. The odds ratios (95% confidence interval) of the physician-diagnosed stroke and myocardial infarction in the smoking group were 1.12 (1.02-1.24) and 1.21 (1.06-1.38) compared to the non-smoking group. The values of the physician-diagnosed stroke and myocardial infarction were 0.84 (0.74-0.94) and 0.96 (0.82-1.12) in the current-smoking subgroup, 1.38 (1.24-1.53) and 1.45 (1.26-1.67) in the ex-smoking subgroup, 1.39 (1.18-1.63) and 1.85 (1.53-2.24) in the 10- to 19-year smokers groups, 1.39 (1.22-1.58) and 1.36 (1.15-1.60) in the 30- to 40-year smokers groups, and 0.53 (0.44-0.63) and 0.47 (0.36-0.63) in those who had smoked for over 50 years. These results showed smoking was a risk factor for stroke and myocardial infarction in Korean males. This objective evidence should guide policy-making and public health interventions in the fields of smoking prevention and prohibition.

  16. Association Between Smoking and Physician-Diagnosed Stroke and Myocardial Infarction in Male Adults in Korea

    PubMed Central

    Chang, Sounghoon; Kim, Hyeongsu; Kim, Vitna; Lee, Kunsei; Jeong, Hyoseon; Lee, Jung-Hyun; Shin, Soon-Ae; Shin, Eunyoung; Park, Minsu; Ko, Eunjung

    2016-01-01

    To evaluate the association between smoking and physician-diagnosed stroke and myocardial infarction, this study used Community Health Survey data from 2009 on 92,082 males over the age of 30 years. Using multiple logistic regression, association index between smoking and physician-diagnosed stroke and myocardial infarction was calculated after adjusting the effects of age, hypertension, and diabetes. The odds ratios (95% confidence interval) of the physician-diagnosed stroke and myocardial infarction in the smoking group were 1.12 (1.02–1.24) and 1.21 (1.06–1.38) compared to the non-smoking group. The values of the physician-diagnosed stroke and myocardial infarction were 0.84 (0.74–0.94) and 0.96 (0.82–1.12) in the current-smoking subgroup, 1.38 (1.24–1.53) and 1.45 (1.26–1.67) in the ex-smoking subgroup, 1.39 (1.18–1.63) and 1.85 (1.53–2.24) in the 10- to 19-year smokers groups, 1.39 (1.22–1.58) and 1.36 (1.15–1.60) in the 30- to 40-year smokers groups, and 0.53 (0.44–0.63) and 0.47 (0.36–0.63) in those who had smoked for over 50 years. These results showed smoking was a risk factor for stroke and myocardial infarction in Korean males. This objective evidence should guide policy-making and public health interventions in the fields of smoking prevention and prohibition. PMID:26821036

  17. Comparative Analysis of Methods to Induce Myocardial Infarction in a Closed-Chest Rabbit Model

    PubMed Central

    Isorni, Marc-Antoine; Casanova, Amaury; Piquet, Julie; Bellamy, Valérie; Pignon, Charly; Puymirat, Etienne; Menasche, Philippe

    2015-01-01

    Objective. To develop a rabbit model of closed-chest catheter-induced myocardial infarction. Background. Limitations of rodent and large animal models justify the search for clinically relevant alternatives. Methods. Microcatheterization of the heart was performed in 47 anesthetized 3-4 kg New Zealand rabbits to test five techniques of myocardial ischemia: free coils (n = 4), interlocking coils (n = 4), thrombogenic gelatin sponge (n = 4), balloon occlusion (n = 4), and alcohol injection (n = 8). In order to limit ventricular fibrillation, an antiarrhythmic protocol was implemented, with beta-blockers/amiodarone before and xylocaine infusion during the procedure. Clinical, angiographic, and echographic data were gathered. End points included demonstration of vessel occlusion (TIMI flow grades 0 and 1 on the angiogram), impairment of left ventricular function at 2 weeks after procedure (by echocardiography), and pathologically confirmed myocardial infarction. Results. The best arterial access was determined to be through the right carotid artery. The internal mammary guiding catheter 4-Fr was selected as the optimal device for selective intracoronary injection. Free coils deployed prematurely and tended to prolapse into the aorta. Interlocking coils did not deploy completely and failed to provide reliable results. Gelatin sponge was difficult to handle, adhered to the catheter, and could not be clearly visualized by fluoroscopy. Balloon occlusion yielded inconsistent results. Alcohol injection was the most efficient and reproducible method for inducing myocardial infarction (4 out of 6 animals), the extent of which could be fine-tuned by using a coaxial balloon catheter as a microcatheter (0.52 mm) to achieve a superselective injection of 0.2 mL of alcohol. This approach resulted in a 20% decrease in LVEF and infarcted myocardium was confirmed histologically. Conclusions. By following a stepwise approach, a minimally invasive, effective, and reproducible

  18. Effects of Bulbus allii macrostemi on clinical outcomes and oxidized low-density lipoprotein and plasminogen in unstable angina/non-ST-segment elevation myocardial infarction patients.

    PubMed

    Liu, Yan; Zhang, Lei; Liu, Yun-Fang; Yan, Fang-Fang; Zhao, Yu-Xia

    2008-11-01

    Unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI) is associated with an increased risk of cardiac death and an efficacious drug with few side effects is necessary. The study aimed to evaluate the effects of Bulbus allii macrostemi (B. macrostemi) on UA/NSTEMI patients as well as to elucidate possible mechanisms. 79 patients were randomly divided into two groups: the trial group received B. macrostemi plus baseline therapy, the control group was given placebo plus baseline therapy. The trial lasted 8 weeks. The evaluation involved main clinical symptoms, changes of electrocardiogram and biochemical examination. After treatment, the trial group showed more significant improvement on clinical manifestation. The plasma oxidized low-density lipoprotein (ox-LDL) level decreased significantly in the trial group (p < 0.01); the plasminogen activator inhibitor-1 (PAI-1) level decreased in both groups and it decreased more significantly in the trial group (p < 0.01). In contrast, the activity of plasminogen (PLG) increased in both groups and the change was more marked in the trial group (p < 0.01). The results suggested that B. macrostemi combined with baseline therapy could improve clinical symptoms of UA/NSTEMI patients by decreasing the ox-LDL and PAI-1 levels and enhancing the activity of PLG. PMID:18688814

  19. Class effect of beta-blockers in survivors of ST-elevation myocardial infarction: A nationwide cohort study using an insurance claims database.

    PubMed

    Lin, Ting-Tse; Arnold Chan, K; Chen, Ho-Min; Lai, Chao-Lun; Lai, Mei-Shu

    2015-09-02

    Beta-blockers can help reduce mortality following acute myocardial infarction (MI); however, whether beta-blockers exert a class effect remains controversial. This study identified all patients with first ST-elevation MI for the period of 2003 to 2010 from the National Health Insurance claims database, Taiwan. We compared patients prescribed carvedilol, bisoprolol, and propranolol. Study outcomes included all-cause death, cardiovascular death, and recurrence of MI. The propensity scores were constructed using multinomial logistic regression to model the receipt of different beta-blockers. Treating carvedilol group as a reference, we employed a simultaneous three-group comparison approach using the Cox regression model with adjustment for the propensity scores to compare the relative risks of various outcomes. Among the 16836 patients, 7591 were prescribed carvedilol, 5934 bisoprolol, and 3311 propranolol. Mean follow-up time was one year. After accounting for baseline differences, patients treated with bisoprolol (HR 0.87, 95% CI 0.72-1.05, p = 0.14) or propranolol (HR 1.07, 95% CI 0.84-1.36, p = 0.58) had a similar risk of all-cause death in comparison with carvedilol. No significant differences were observed among three beta-blocker groups with regard to the risks of cardiovascular death and recurrence of MI. Our results suggest that beta-blockers exert a possible class effect in the treatment of acute MI.

  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. Class effect of beta-blockers in survivors of ST-elevation myocardial infarction: A nationwide cohort study using an insurance claims database

    PubMed Central

    Lin, Ting-Tse; Arnold Chan, K.; Chen, Ho-Min; Lai, Chao-Lun; Lai, Mei-Shu

    2015-01-01

    Beta-blockers can help reduce mortality following acute myocardial infarction (MI); however, whether beta-blockers exert a class effect remains controversial. This study identified all patients with first ST-elevation MI for the period of 2003 to 2010 from the National Health Insurance claims database, Taiwan. We compared patients prescribed carvedilol, bisoprolol, and propranolol. Study outcomes included all-cause death, cardiovascular death, and recurrence of MI. The propensity scores were constructed using multinomial logistic regression to model the receipt of different beta-blockers. Treating carvedilol group as a reference, we employed a simultaneous three-group comparison approach using the Cox regression model with adjustment for the propensity scores to compare the relative risks of various outcomes. Among the 16836 patients, 7591 were prescribed carvedilol, 5934 bisoprolol, and 3311 propranolol. Mean follow-up time was one year. After accounting for baseline differences, patients treated with bisoprolol (HR 0.87, 95% CI 0.72–1.05, p = 0.14) or propranolol (HR 1.07, 95% CI 0.84–1.36, p = 0.58) had a similar risk of all-cause death in comparison with carvedilol. No significant differences were observed among three beta-blocker groups with regard to the risks of cardiovascular death and recurrence of MI. Our results suggest that beta-blockers exert a possible class effect in the treatment of acute MI. PMID:26328923

  2. Neural Mechanisms and Delayed Gastric Emptying of Liquid Induced Through Acute Myocardial Infarction in Rats

    PubMed Central

    Nunez, Wilson Ranu Ramirez; Ozaki, Michiko Regina; Vinagre, Adriana Mendes; Collares, Edgard Ferro; de Almeida, Eros Antonio

    2015-01-01

    Background In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE) of liquid in rats. Objective Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABAB receptors and also participation of paraventricular nucleus (PVN) of the hypothalamus in GE and gastric compliance (GC) in infarcted rats. Methods Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH) group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABAB receptors, baclofen was injected via icv (intracerebroventricular). Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1mA/10s electrical current and GE was determined by measuring the percentage of gastric retention (% GR) of a saline meal. Results No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABAB receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Conclusion Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN. PMID:25494017

  3. Smad3 inactivation and MiR-29b upregulation mediate the effect of carvedilol on attenuating the acute myocardium infarction-induced myocardial fibrosis in rat.

    PubMed

    Zhu, Jie-Ning; Chen, Ren; Fu, Yong-Heng; Lin, Qiu-Xiong; Huang, Shuai; Guo, Lin-Lin; Zhang, Meng-Zhen; Deng, Chun-Yu; Zou, Xiao; Zhong, Shi-Long; Yang, Min; Zhuang, Jian; Yu, Xi-Yong; Shan, Zhi-Xin

    2013-01-01

    Carvedilol, a nonselective β-adrenoreceptor antagonist, protects against myocardial injury induced by acute myocardium infarction (AMI). The mechanisms underlying the anti-fibrotic effects of carvedilol are unknown. Recent studies have revealed the critical role of microRNAs (miRNAs) in a variety of cardiovascular diseases. This study investigated whether miR-29b is involved in the cardioprotective effect of carvedilol against AMI-induced myocardial fibrosis. Male SD rats were randomized into several groups: the sham surgery control, left anterior descending (LAD) surgery-AMI model, AMI plus low-dose carvedilol treatment (1 mg/kg per day, CAR-L), AMI plus medium-dose carvedilol treatment (5 mg/kg per day, CAR-M) and AMI plus high-dose carvedilol treatment (10 mg/kg per day, CAR-H). Cardiac remodeling and impaired heart function were observed 4 weeks after LAD surgery treatment; the observed cardiac remodeling, decreased ejection fraction, and fractional shortening were rescued in the CAR-M and CAR-H groups. The upregulated expression of Col1a1, Col3a1, and α-SMA mRNA was significantly reduced in the CAR-M and CAR-H groups. Moreover, the downregulated miR-29b was elevated in the CAR-M and CAR-H groups. The in vitro study showed that Col1a1, Col3a1, and α-SMA were downregulated and miR-29b was upregulated by carvedilol in a dose-dependent manner in rat cardiac fibroblasts. Inhibition of ROS-induced Smad3 activation by carvedilol resulted in downregulation of Col1a1, Col3a1, and α-SMA and upregulation of miR-29b derived from the miR-29b-2 precursor. Enforced expression of miR-29b significantly suppressed Col1a1, Col3a1, and α-SMA expression. Taken together, we found that smad3 inactivation and miR-29b upregulation contributed to the cardioprotective activity of carvedilol against AMI-induced myocardial fibrosis.

  4. Smad3 inactivation and MiR-29b upregulation mediate the effect of carvedilol on attenuating the acute myocardium infarction-induced myocardial fibrosis in rat.

    PubMed

    Zhu, Jie-Ning; Chen, Ren; Fu, Yong-Heng; Lin, Qiu-Xiong; Huang, Shuai; Guo, Lin-Lin; Zhang, Meng-Zhen; Deng, Chun-Yu; Zou, Xiao; Zhong, Shi-Long; Yang, Min; Zhuang, Jian; Yu, Xi-Yong; Shan, Zhi-Xin

    2013-01-01

    Carvedilol, a nonselective β-adrenoreceptor antagonist, protects against myocardial injury induced by acute myocardium infarction (AMI). The mechanisms underlying the anti-fibrotic effects of carvedilol are unknown. Recent studies have revealed the critical role of microRNAs (miRNAs) in a variety of cardiovascular diseases. This study investigated whether miR-29b is involved in the cardioprotective effect of carvedilol against AMI-induced myocardial fibrosis. Male SD rats were randomized into several groups: the sham surgery control, left anterior descending (LAD) surgery-AMI model, AMI plus low-dose carvedilol treatment (1 mg/kg per day, CAR-L), AMI plus medium-dose carvedilol treatment (5 mg/kg per day, CAR-M) and AMI plus high-dose carvedilol treatment (10 mg/kg per day, CAR-H). Cardiac remodeling and impaired heart function were observed 4 weeks after LAD surgery treatment; the observed cardiac remodeling, decreased ejection fraction, and fractional shortening were rescued in the CAR-M and CAR-H groups. The upregulated expression of Col1a1, Col3a1, and α-SMA mRNA was significantly reduced in the CAR-M and CAR-H groups. Moreover, the downregulated miR-29b was elevated in the CAR-M and CAR-H groups. The in vitro study showed that Col1a1, Col3a1, and α-SMA were downregulated and miR-29b was upregulated by carvedilol in a dose-dependent manner in rat cardiac fibroblasts. Inhibition of ROS-induced Smad3 activation by carvedilol resulted in downregulation of Col1a1, Col3a1, and α-SMA and upregulation of miR-29b derived from the miR-29b-2 precursor. Enforced expression of miR-29b significantly suppressed Col1a1, Col3a1, and α-SMA expression. Taken together, we found that smad3 inactivation and miR-29b upregulation contributed to the cardioprotective activity of carvedilol against AMI-induced myocardial fibrosis. PMID:24086569

  5. Psychological Stress in Wives of Patients with Myocardial Infarction

    PubMed Central

    Skelton, M.; Dominian, J.

    1973-01-01

    In a study of the psychological consequences of myocardial infarction on 65 wives of husbands admitted to a coronary care unit feelings of loss, depression, and guilt were common at the time of infarction. Many wives (38%) found the period of convalescence after discharge very stressful, attributing this to fears of a recurrent infarct and marital tension owing to their husbands' increased irritability and dependency. These anxieties and tensions gradually diminished and at one year after the initial illness only eight wives whose husbands had made a good physical recovery still showed considerable psychological disturbance. It is suggested that unnecessary emotional distress, particularly in the initial period after discharge from hospital, can be alleviated by increased help and support from the hospital and family doctor. PMID:4700299

  6. [Myocardial infarction and acute coronary syndrome: definitions, classification, and diagnostic criteria].

    PubMed

    Zaĭrat'iants, O V; Mishnev, O D; Kakturskiĭ, L V

    2014-01-01

    The review gives the definitions and classification of and diagnostic criteria for myocardial infarction and acute coronary syndrome in accordance with the "The third universal definition of myocardial infarction" adopted in 2012 (Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction, 2012). It also discusses the clinical and morphological comparisons of and the problems in the differential diagnosis of myocardial infarction as a nosological entity within coronary heart disease with other coronarogenic and non-coronarogenic necroses of the myocardium.

  7. Improving myocardial injury, infarct size, and myocardial salvage in the era of primary PCI for STEMI.

    PubMed

    Ndrepepa, Gjin

    2015-06-01

    ST-segment elevation myocardial infarction (STEMI) is a major cause of mortality and disability worldwide. Reperfusion therapy by thrombolysis or primary percutaneous coronary intervention (PPCI) improves survival and quality of life in patients with STEMI. Despite the proven efficacy of timely reperfusion, mortality from STEMI remains high, particularly among patients with suboptimal reperfusion. Reperfusion injury following opening of occluded coronary arteries mitigates the efficacy of PPCI by further accentuating ischemic damage and increasing infarct size (IS). On the basis of experimental studies, it is assumed that nearly 50% of the final IS is because of the reperfusion injury. IS is a marker of ischemic damage and adequacy of reperfusion that is strongly related to mortality in reperfused patients with STEMI. Many therapeutic strategies including pharmacological and conditioning agents have been proven effective in reducing reperfusion injury and IS in preclinical research. Mechanistically, these agents act either by inhibiting reperfusion injury cascades or by activating cellular prosurvival pathways. Although most of these agents/strategies are at the experimental stage, some of them have been tested clinically in patients with STEMI. This review provides an update on key pharmacological agents and postconditioning used in the setting of PPCI to reduce reperfusion injury and IS. Despite intensive research, no strategy or intervention has been shown to prevent reperfusion injury or enhance myocardial salvage in a consistent manner in a clinical setting. A number of novel therapeutic strategies to reduce reperfusion injury in the setting of PPCI in patients with STEMI are currently under investigation. They will lead to a better understanding of reperfusion injury and to more efficient strategies for its prevention.

  8. Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era

    PubMed Central

    Dominguez-Rodriguez, Alberto; Abreu-Gonzalez, Pedro; Reiter, Russel J

    2014-01-01

    In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification of several promising pharmacological (cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proof-of-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease. PMID:24669291

  9. Short-Term Effect of Autologous Bone Marrow Stem Cells to Treat Acute Myocardial Infarction: A Meta-Analysis of Randomized Controlled Clinical Trials.

    PubMed

    Cong, Xiao-Qiang; Li, Ying; Zhao, Xin; Dai, Yan-Jian; Liu, Ya

    2015-06-01

    Bone marrow stem cells (BMSCs) have been used to treat patient with ST-segment elevation myocardial infarction (STEMI) via intracoronary route. We performed a meta-analysis to evaluate the short-term efficacy and safety of this modality. Seventeen randomized controlled trials (RCTs) of BMSC-based therapy for STEMI, delivered with 9 days of reperfusion and followed up shorter than 12 months, were identified by systematic review. Intracoronary BMSC therapy resulted in an overall significant improvement in left ventricular ejection fraction (LVEF) by 2.74 % (95 % confidence interval (CI) 2.09-3.39, P < 0.00001, I(2) = 84 %) at 3-6-month follow-up and 5.1 % (95 % CI 4.16-6.03, P < 0.00001 and I(2) = 85 %) at 12 months. The left ventricular end-systolic volume (LVESV) and wall motion score index (WMSI) were also reduced at 3-6 months. At 12 months, left ventricular end-diastolic volume (LVEDV), LVESV, and WMSI were significantly reduced in BMSC group. In conclusion, intracoronary BMSC therapy at post-STEMI is safe and effective in patient with acute STEMI.

  10. Effect on short- and long-term major adverse cardiac events of statin treatment in patients with acute myocardial infarction and renal dysfunction.

    PubMed

    Lim, Sang Yup; Bae, Eun Hui; Choi, Joon Seok; Kim, Chang Seong; Park, Jeong Woo; Ma, Seong Kwon; Jeong, Myung Ho; Kim, Soo Wan

    2012-05-15

    The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) reduce major adverse cardiac events (MACE) and mortality in patients with acute coronary syndrome. We investigated the effectiveness of statin therapy in reducing MACE in patients with acute myocardial infarction (AMI) and renal dysfunction (RD). In the present retrospective study of 12,853 patients with AMI, the patients were categorized into 4 groups: group I, statin therapy and no RD (estimated glomerular filtration rate ≥60 ml/min/1.73 m(2)); group II, neither statin therapy nor RD; group III, statin therapy and RD; group IV, no statin therapy but RD. The primary end points were death and complications during the hospital course. The secondary end points were MACE during 1 year of follow-up after AMI. Significant differences in the composite MACE during 12 months of follow-up were observed among the 4 groups (group I, 11.7%; group II, 19.0%; group III, 26.7%; and group IV, 45.5%; p <0.001). In a Cox proportional hazards model, mortality at 12 months increased stepwise from group II to IV compared to group I. Moreover, MACE-free survival in the severe RD group (estimated glomerular filtration rate <30 mL/min/1.73 m(2)) was also greater in the statin-treated group. In conclusion, statin therapy reduced MACE at 1 year of follow-up in patients with AMI regardless of RD.

  11. Life Expectancy after Myocardial Infarction, According to Hospital Performance.

    PubMed

    Bucholz, Emily M; Butala, Neel M; Ma, Shuangge; Normand, Sharon-Lise T; Krumholz, Harlan M

    2016-10-01

    Background Thirty-day risk-standardized mortality rates after acute myocardial infarction are commonly used to evaluate and compare hospital performance. However, it is not known whether differences among hospitals in the early survival of patients with acute myocardial infarction are associated with differences in long-term survival. Methods We analyzed data from the Cooperative Cardiovascular Project, a study of Medicare beneficiaries who were hospitalized for acute myocardial infarction between 1994 and 1996 and who had 17 years of follow-up. We grouped hospitals into five strata that were based on case-mix severity. Within each case-mix stratum, we compared life expectancy among patients admitted to high-performing hospitals with life expectancy among patients admitted to low-performing hospitals. Hospital performance was defined by quintiles of 30-day risk-standardized mortality rates. Cox proportional-hazards models were used to calculate life expectancy. Results The study sample included 119,735 patients with acute myocardial infarction who were admitted to 1824 hospitals. Within each case-mix stratum, survival curves of the patients admitted to hospitals in each risk-standardized mortality rate quintile separated within the first 30 days and then remained parallel over 17 years of follow-up. Estimated life expectancy declined as hospital risk-standardized mortality rate quintile increased. On average, patients treated at high-performing hospitals lived between 0.74 and 1.14 years longer, depending on hospital case mix, than patients treated at low-performing hospitals. When 30-day survivors were examined separately, there was no significant difference in unadjusted or adjusted life expectancy across hospital risk-standardized mortality rate quintiles. Conclusions In this study, patients admitted to high-performing hospitals after acute myocardial infarction had longer life expectancies than patients treated in low-performing hospitals. This survival benefit

  12. Treatment with bone morphogenetic protein 2 limits infarct size after myocardial infarction in mice.

    PubMed

    Ebelt, Henning; Hillebrand, Ina; Arlt, Stephan; Zhang, Ying; Kostin, Sawa; Neuhaus, Herbert; Müller-Werdan, Ursula; Schwarz, Elisabeth; Werdan, Karl; Braun, Thomas

    2013-04-01

    Various strategies have been devised to reduce the clinical consequences of myocardial infarction, including acute medical care, revascularization, stem cell transplantations, and more recently, prevention of cardiomyocyte cell death. Activation of embryonic signaling pathways is a particularly interesting option to complement these strategies and to improve the functional performance and survival rate of cardiomyocytes. Here, we have concentrated on bone morphogenetic protein 2 (BMP-2), which induces ectopic formation of beating cardiomyocytes during development in the mesoderm and protects neonatal cardiomyocytes from ischemia-reperfusion injury. In a mouse model of acute myocardial infarction, an i.v. injection of BMP-2 reduced infarct size in mice when given after left anterior descending artery ligation. Mice treated with BMP-2 are characterized by a reduced rate of apoptotic cardiomyocytes both in the border zone of the infarcts and in the remote myocardium. In vitro, BMP-2 increases the frequency of spontaneously beating neonatal cardiomyocytes and the contractile performance under electrical pacing at 2 Hz, preserves cellular adenosine triphosphate stores, and decreases the rate of apoptosis despite the increased workload. In addition, BMP-2 specifically induced phosphorylation of Smad1/5/8 proteins and protected adult cardiomyocytes from long-lasting hypoxia-induced cellular damage and oxidative stress without activation of the cardiodepressant transforming growth factor-β pathway. Our data suggest that BMP-2 treatment may have considerable therapeutic potential in individuals with acute and chronic myocardial ischemia by improving the contractility of cardiomyocytes and preventing cardiomyocyte cell death.

  13. Simvastatin ameliorates ventricular remodeling via the TGF-β1 signaling pathway in rats following myocardial infarction

    PubMed Central

    XIAO, XIANGBIN; CHANG, GUANGLEI; LIU, JIAN; SUN, GUANGYUN; LIU, LI; QIN, SHU; ZHANG, DONGYING

    2016-01-01

    Statins are widely used in patients with cardiovascular diseases. A considerable number of previous studies revealed that the intracellular signaling of transforming growth factor (TGF)-β1 mediated the development of cardiomyocyte hypertrophy and interstitial fibrosis. However, whether statins can ameliorate ventricular remodeling in post-myocardial infarction via the TGF-β1 signaling pathway remains to be rigorously tested. The left anterior descending artery was ligated to induce a rat model of myocardial infarction. The rat model of myocardial infarction was treated with simvastatin through gastric gavage (10, 20 or 40 mg kg−1·d−1). All rats were sacrificed on day 28 after the myocardial infarction operation. The results revealed that simvastatin significantly improved the hemodynamic indexes, left ventricular mass index, the myocardial tissue structure, the cardiomyocyte cross-sectional area and the collagen volume fraction, and also showed that the levels of TGF-β1, TGF-activated kinase (TAK)1 and drosophila mothers against decapentaplegic (Smad)3 were significantly reduced following treatment with simvastatin, while the levels of Smad7 in the simvastatin treatment groups were markedly increased. The results of the present study suggested that statins ameliorated ventricular remodeling in post-myocardial infarction rats via the TGF-β1 signaling pathway, which provided a novel explanation for the pleiotropic effects of statins that benefit the cardiovascular system. PMID:27121011

  14. Myocardial Connective Tissue Growth Factor (CCN2/CTGF) Attenuates Left Ventricular Remodeling after Myocardial Infarction

    PubMed Central

    Gravning, Jørgen; Ørn, Stein; Kaasbøll, Ole Jørgen; Martinov, Vladimir N.; Manhenke, Cord; Dickstein, Kenneth; Edvardsen, Thor; Attramadal, Håvard; Ahmed, Mohammed Shakil

    2012-01-01

    Aims Myocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI. Methods and Results Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15. Conclusion Increased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis. PMID:23284892

  15. [Pulmonary complications of acute myocardial infarct. Therapeutic orientation].

    PubMed

    Cano, A E; Meaney, E

    1975-01-01

    The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the

  16. iPSC-derived human mesenchymal stem cells improve myocardial strain of infarcted myocardium.

    PubMed

    Miao, Qingfeng; Shim, Winston; Tee, Nicole; Lim, Sze Yun; Chung, Ying Ying; Ja, K P Myu Mia; Ooi, Ting Huay; Tan, Grace; Kong, Geraldine; Wei, Heming; Lim, Chong Hee; Sin, Yoong Kong; Wong, Philip

    2014-08-01

    We investigated global and regional effects of myocardial transplantation of human induced pluripotent stem cell (iPSC)-derived mesenchymal stem cells (iMSCs) in infarcted myocardium. Acute myocardial infarction (MI) was induced by ligation of left coronary artery of severe combined immunodeficient mice before 2 × 10(5) iMSCs or cell-free saline were injected into peri-infarcted anterior free wall. Sham-operated animals received no injection. Global and regional myocardial function was assessed serially at 1-week and 8-week by segmental strain analysis by using two dimensional (2D) speckle tracking echocardiography. Early myocardial remodelling was observed at 1-week and persisted to 8-week with global contractility of ejection fraction and fractional area change in saline- (32.96 ± 14.23%; 21.50 ± 10.07%) and iMSC-injected (32.95 ± 10.31%; 21.00 ± 7.11%) groups significantly depressed as compared to sham control (51.17 ± 11.69%, P < 0.05; 34.86 ± 9.82%, P < 0.05). However, myocardial dilatation was observed in saline-injected animals (4.40 ± 0.62 mm, P < 0.05), but not iMSCs (4.29 ± 0.57 mm), when compared to sham control (3.74 ± 0.32 mm). Furthermore, strain analysis showed significant improved basal anterior wall strain (28.86 ± 8.16%, P < 0.05) in the iMSC group, but not saline-injected (15.81 ± 13.92%), when compared to sham control (22.18 ± 4.13%). This was corroborated by multi-segments deterioration of radial strain only in saline-injected (21.50 ± 5.31%, P < 0.05), but not iMSC (25.67 ± 12.53%), when compared to sham control (34.88 ± 5.77%). Improvements of the myocardial strain coincided with the presence of interconnecting telocytes in interstitial space of the infarcted anterior segment of the heart. Our results show that localized injection of iMSCs alleviates ventricular remodelling, sustains global and regional myocardial strain by paracrine-driven effect on neoangiogenesis and myocardial deformation/compliance via parenchymal and

  17. Association between polymorphisms in the beta2-adrenergic receptor gene with myocardial infarction and ischaemic stroke in women.

    PubMed

    Schürks, Markus; Kurth, Tobias; Ridker, Paul M; Buring, Julie E; Zee, Robert Y L

    2009-02-01

    Results from studies investigating the association between polymorphisms in the beta2-adrenergic receptor gene (ADRB2) and cardiovascular disease (CVD) are controversial. Using haplotype-based analysis, we have previously shown a protective effect of the Gly16-Gln27-Ile164 haplotype on myocardial infarction in men. We sought to replicate these findings in women and further investigated whether the gene variants exert differential effects on myocardial infarction and ischaemic stroke. We performed a prospective study among 25,224 women, participating in the Women's Health Study and free of CVD at study entry. We had information on polymorphisms Gly16Arg, Gln27Glu, and Thr164Ile in the ADRB2. Incident CVD was self-reported and confirmed after medical record review. We used proportional hazards models to investigate the association between genotypes and haplotypes with any myocardial infarction, any ischaemic stroke, and CVD death. During a mean of 11.8 years of follow-up, 274 myocardial infarctions, 299 ischaemic strokes, and 159 CVD deaths occurred. Among the whole cohort genotype- and haplotype-based analyses did not show an association for any of the gene variants with any of the CVD outcomes. When we focused on Caucasian women, the haplotype-based analysis, however, suggested an inverse association of the haplotype Gly16-Gln27-Thr164 with incident myocardial infarction (multivariable-adjusted hazard ratio 0.75; 95% confidence interval 0.58-0.97; p = 0.03). We did not find associations in the haplotype-based analyses with incident ischaemic stroke or CVD death. Our results suggest that the haplotype Gly16-Gln27-Thr164 is associated with reduced risk of incident myocardial infarction but not ischaemic stroke in Caucasian women and suggest differential pathophysiologies for myocardial infarction and stroke.

  18. Influence of HMGB1 and MSCs transplantation on rat cardiac angiogenesis with acute myocardial infarction.

    PubMed

    Jiang, Youxu; Wang, Xiaoman; Jiang, Xiaodong; Niu, Shaohui; Zhang, Lihua

    2016-07-01

    To observe whether HMGB1could enhance the paracrine effect of MSCs when the Mesenchymal stem cells (Mesenchymal stem cells, MSCs) are pre-proccessed by High Mobility Group Box-1 (High Mobility Group Box-1, HMGB1). And to observe whether it can further increase the quantity of local angiogenesis in myocardial infarcts on the rat model with acute myocardial infarction, HMGB1 was combined with MSCs transplantation. MSCs in rats were cultivated with adherence and centrifugation method. Receptors of TLR4and RAGE in HMGB1 were tested. The MSCs were interfered by HMGB1 with different concentration gradient respectively, then the expression of VEGF was tested with ELISA method. SD male rats were divided into four groups: the model group, the MSCs transplantation group, the HMGB1 injection group, the HMGB1 injection plus MSCs transplantation group (n = 24), preparing rat model with acute myocardial infarction. The serum VEGF concentration levels were detected on the 3rd day, 7th and 28th day with ELISA method. On the 28th day after post operation the density of angiogenesis in infarction area was detected by immunohistochemal. (1) MSCs owned the expression of TLR4 and RAGE. (2) the secretion of VEGF increased significantly after the intervention of HMGB1 with concentration of 12.5 ng/mL, 25 ng/mL, 50 ng/mL, 100 ng/mL and 200ng/ml on MSCs compared with the control group. While the concentration was 400ng/ml or 800ng/ml, the secretion of VEGF decreased compared with the control group (P < 0.05). (3) detection of the serum VEGF on the 3rd or7th day after post operation was arranged: The results showed that: HMGB1 injection plus MSCs transplantation group > MSCs transplantation group >HMGB1 injection group >model group (P < 0.05). (4) the quantity of CD31 stained angiogenesis in HMGB1 injection plus MSCs transplantation group increased obviously. Combining MSCs transplantation, contributed to new angiogenesis of rats with acute myocardial infarction in myocardial infarction

  19. 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

  20. Delayed clopidogrel transit during myocardial infarction evident on angiography.

    PubMed

    Ghobrial, Joanna; Gibson, C Michael; Pinto, Duane S

    2015-05-01

    We describe the case of a patient with non-ST segment elevation myocardial infarction (NSTEMI) where a limitation of oral clopidogrel loading prior to percutaneous coronary intervention (PCI) was directly visualized on angiography. Clopidogrel is a thienopyridine antiplatelet agent used in acute coronary syndromes. It reduces platelet aggregation via inhibition of the P2Y12 receptor. Clopidogrel is an inactive metabolite that is metabolized into the active metabolite by the cytochrome P450 isoenzymes located mostly in the liver and partly in the gastrointestinal system. As such, it requires at least 2 hours to reach maximal effect. A 63-year-old female went to an outside facility where she was diagnosed with NSTEMI and underwent angiography. She was administered 324 mg of aspirin and 600 mg of clopidogrel, and was transferred to our facility. Upon arrival, approximately 1.5 hours after the oral loading dose, the clopidogrel tablets were visualized intact in the stomach during angiography, implying a very low likelihood of adequate absorption or antiplatelet effect. This observation raises the concern that delayed gastrointestinal transit, apart from other metabolic derangements, may be a factor in achieving optimal platelet inhibition using oral agents. PMID:25929306

  1. Solar Activity, Different Geomagnetic Activity Levels and Acute Myocardial Infarction

    NASA Astrophysics Data System (ADS)

    Dimitrova, Svetla; Jordanova, Malina; Stoilova, Irina; Taseva, Tatiana; Maslarov, Dimitar

    Results on revealing a possible relationship between solar activity (SA) and geomagnetic activity (GMA) and acute myocardial infarction (AMI) morbidity are presented. Studies were based on medical data covering the period from 1.12.1995 to 31.12.2004 and concerned daily distribution of patients with AMI diagnose (in total 1192 cases) from Sofia region on the day of admission at the hospital. Analysis of variance (ANOVA) was applied to check the significance of GMA intensity effect and the type of geomagnetic storms, those caused by Magnetic Clouds (MC) and by High Speed Solar Wind Streams (HSSWS), on AMI morbidity. Relevant correlation coefficients were calculated. Results revealed statistically significant positive correlation between considered GMA indices and AMI. ANOVA revealed that AMI number was signifi- cantly increased from the day before (-1st) till the day after (+1st) geomagnetic storms with different intensities. Geomagnetic storms caused by MC were related to significant increase of AMI number in comparison with the storms caused by HSSWS. There was a trend for such different effects even on -1st and +1st day.

  2. Early intervention in acute myocardial infarction: significance for myocardial salvage of immediate intravenous streptokinase therapy followed by coronary angioplasty

    SciTech Connect

    Miller, H.I.; Almagor, Y.; Keren, G.; Chernilas, J.; Roth, A.; Eschar, Y.; Shapira, I.; Shargorodsky, B.; Berenfeld, D.; Laniado, S.

    1987-03-01

    Sixteen patients with acute myocardial infarction underwent treatment with streptokinase up to 3 hours after the onset of chest pain. Nine patients (group I) received streptokinase within 1 hour of the onset of pain, and seven patients (group II) received it within 2 to 3 hours. All underwent multigated radionuclide ventriculography after streptokinase therapy and 1 week later. Percutaneous transluminal coronary angioplasty of the infarct artery was performed within 24 hours in all patients. An effort-limited treadmill stress test was performed before discharge. There was no mortality or serious complication. Mean peak total creatine kinase was 521 +/- 289 mU/ml in group I, and 1,614 +/- 709 mU/ml in group II (p less than 0.05). The mean initial left ventricular ejection fraction was 47 +/- 11% in group I and 37 +/- 10% in group II. After early angioplasty (within 24 hours) and at 1 week recovery, left ventricular ejection fraction increased to 53 +/- 9% in group I (p less than 0.05) and to 40 +/- 7% in group II (p = NS). Seven of the nine patients in group I had normal radionuclide ventriculograms at discharge compared with none of the seven patients in group II. Thrombolytic therapy administered less than 1 hour after the onset of symptoms of acute myocardial infarction followed by angioplasty of the infarct artery results in preservation of left ventricular function, whereas therapy given after 2 hours has only a limited effect.

  3. Improve Myocardial T1 Measurement in Rats with a New Regression Model: Application to Myocardial Infarction and Beyond

    PubMed Central

    Zhang, Haosen; Ye, Qing; Zheng, Jie; Schelbert, Erik B; Hitchens, T. Kevin; Ho, Chien

    2013-01-01

    Purpose To improve myocardial and blood T1 measurements with a multi-variable T1 fitting model specifically modified for a segmented multi-shot FLASH sequence. Methods The proposed method was first evaluated in a series of phantoms simulating realistic tissues, and then in healthy rats (n = 8) and rats with acute myocardial infarction (MI) induced by coronary artery ligation (n = 8). Results By accounting for the saturation effect caused by sampling α-train pulses, and the longitudinal magnetization recovery between readouts, our model provided more accurate T1 estimate than the conventional three-parameter fit in phantoms under realistic gating procedures (error of −0.42 ± 1.73% vs. −3.40 ± 1.46%, respectively, when using the measured inversion efficiency, β). The baseline myocardial T1 values in healthy rats was 1636.3 ± 23.4 ms at 7 T. One day post ligation, the T1 values in the remote and proximal myocardial areas were 1637.5 ± 62.6 ms and 1740.3 ± 70.5 ms, respectively. In rats with acute MI, regional differences in myocardial T1 values were observed both before and after the administration of gadolinium. Conclusion The proposed method has improved T1 estimate in phantoms and could advance applications utilizing quantitative myocardial T1 mapping in rodents. PMID:24142881

  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. Collagen remodeling after myocardial infarction in the rat heart.

    PubMed Central

    Cleutjens, J. P.; Verluyten, M. J.; Smiths, J. F.; Daemen, M. J.

    1995-01-01

    In this study changes in the amount and distribution of types I and III collagen mRNA and protein were investigated in the rat heart after induction of a left ventricular myocardial infarction (MI). Sham operated rats served as controls. The animals were sacrificed at different time intervals after operation. Northern blotting of cardiac RNA and hybridization with cDNA probes for types I and III procollagen revealed a 5- to 15-fold increase in the infarcted left ventricle. Type III procollagen mRNA levels were already increased at day 2 after MI, whereas type I procollagen mRNA followed this response at day 4 after MI. This increase was sustained for at least 21 days in the infarcted left ventricle for type III procollagen mRNA, whereas type 1 procollagen mRNA levels were still elevated at 90 days after MI. In the noninfarcted right ventricle a 5- to 7-fold increase was observed for both type I and type III procollagen mRNA levels, but only at day 4 after MI. In the non-infarcted septum a transient increase was observed for type I procollagen mRNA from day 7-21 (4- to 5-fold increase) and a decline to sham levels thereafter. In the septum type III procollagen mRNA levels were only elevated at 7 days after MI (4- to 5-fold increase) compared with sham operated controls. In situ hybridization with the same types I and III procollagen probes showed procollagen mRNA-producing cells in the infarcted area around necrotic cardiomyocytes, and in the interstitial cells in the non-infarcted part of the myocardium. No labeling was detected above cardiomyocytes. Combined in situ hybridization and immunohistochemistry showed that the collagen mRNA producing cells have a myofibroblast-like phenotype in the infarcted myocardium and are fibroblasts in the noninfarcted septum and right ventricle. The increase in types I and III procollagen mRNA in both infarcted and non-infarcted myocardium was followed by an increased collagen deposition, measured by computerized morphometry on

  6. 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.

  7. Acute myocardial infarction in the obstetric patient.

    PubMed

    Firoz, Tabassum; Magee, Laura A

    2012-06-01

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

  8. Understanding prehospital delay behavior in acute myocardial infarction in women.

    PubMed

    Waller, Cynthia G

    2006-12-01

    Studies demonstrate that acute myocardial infarction (AMI) mortality can be reduced if reperfusion therapy is initiated within 1 hour of AMI symptom onset. However, a considerable number of men and women arrive at the emergency department outside of the time frame for thrombolytic and angioplasty effectiveness. This is especially true for women who have been shown to delay longer than men due to their prehospital decision-making process utilized. With a mean total delay time greater than 4 hours, the time interval from symptom onset to transport activation to the hospital consumes the majority of the prehospital phase of emergency cardiac care. The health belief model, self-regulation model, theory of reasoned action, and theory of planned behavior have all been used to describe the prehospital decision-making process of both men and women with an AMI and the variables that impact that process. These models have identified the importance of symptom attribution to cardiac-related causes as a target variable for research and interventions related to care-seeking behavior.

  9. Understanding prehospital delay behavior in acute myocardial infarction in women.

    PubMed

    Waller, Cynthia G

    2006-12-01

    Studies demonstrate that acute myocardial infarction (AMI) mortality can be reduced if reperfusion therapy is initiated within 1 hour of AMI symptom onset. However, a considerable number of men and women arrive at the emergency department outside of the time frame for thrombolytic and angioplasty effectiveness. This is especially true for women who have been shown to delay longer than men due to their prehospital decision-making process utilized. With a mean total delay time greater than 4 hours, the time interval from symptom onset to transport activation to the hospital consumes the majority of the prehospital phase of emergency cardiac care. The health belief model, self-regulation model, theory of reasoned action, and theory of planned behavior have all been used to describe the prehospital decision-making process of both men and women with an AMI and the variables that impact that process. These models have identified the importance of symptom attribution to cardiac-related causes as a target variable for research and interventions related to care-seeking behavior. PMID:18340239

  10. Assessment of Myocardial Infarction by Cardiac Magnetic Resonance Imaging and Long-Term Mortality

    PubMed Central

    Petriz, João Luiz Fernandes; Gomes, Bruno Ferraz de Oliveira; Rua, Braulio Santos; Azevedo, Clério Francisco; Hadlich, Marcelo Souza; Mussi, Henrique Thadeu Periard; Taets, Gunnar de Cunto; do Nascimento, Emília Matos; Pereira, Basílio de Bragança; e Silva, Nelson Albuquerque de Souza

    2015-01-01

    Background Cardiac magnetic resonance imaging provides detailed anatomical information on infarction. However, few studies have investigated the association of these data with mortality after acute myocardial infarction. Objective To study the association between data regarding infarct size and anatomy, as obtained from cardiac magnetic resonance imaging after acute myocardial infarction, and long-term mortality. Methods A total of 1959 reports of “infarct size” were identified in 7119 cardiac magnetic resonance imaging studies, of which 420 had clinical and laboratory confirmation of previous myocardial infarction. The variables studied were the classic risk factors – left ventricular ejection fraction, categorized ventricular function, and location of acute myocardial infarction. Infarct size and acute myocardial infarction extent and transmurality were analyzed alone and together, using the variable named “MET-AMI”. The statistical analysis was carried out using the elastic net regularization, with the Cox model and survival trees. Results The mean age was 62.3 ± 12 years, and 77.3% were males. During the mean follow-up of 6.4 ± 2.9 years, there were 76 deaths (18.1%). Serum creatinine, diabetes mellitus and previous myocardial infarction were independently associated with mortality. Age was the main explanatory factor. The cardiac magnetic resonance imaging variables independently associated with mortality were transmurality of acute myocardial infarction (p = 0.047), ventricular dysfunction (p = 0.0005) and infarcted size (p = 0.0005); the latter was the main explanatory variable for ischemic heart disease death. The MET-AMI variable was the most strongly associated with risk of ischemic heart disease death (HR: 16.04; 95%CI: 2.64-97.5; p = 0.003). Conclusion The anatomical data of infarction, obtained from cardiac magnetic resonance imaging after acute myocardial infarction, were independently associated with long-term mortality, especially for

  11. [Effect of the depth of myocardial infarction on the tolerance to physical exertion and hemodynamics in patients in the early rehabilitation period].

    PubMed

    Baĭdun, S

    1991-06-01

    Veloergometry (VEM) with determination of the threshold load power and indices of the hemodynamics in 135 patients with a varying depth of myocardial infarction (MI) with an uncomplicated course showed that the presence of asymptomatic coronary insufficiency limiting the tolerance to physical load does not allow to evaluate the physical state depending on the MI depth. Hemodynamic provision in loads and rest is determined by the functional state of the myocardium and does not always depend on the MI depth. VEM and determination of hemodynamic indices is of importance for revealing difference in the physical working capacity of patients with different MI depth, asymptomatic coronary insufficiency in patients with uncomplicated MI.

  12. The scientific achievements of the decades in Korean Acute Myocardial Infarction Registry.

    PubMed

    Kim, Hyun Kuk; Jeong, Myung Ho; Lee, Seung Hun; Sim, Doo Sun; Hong, Young Joon; Ahn, Youngkeun; Kim, Chong Jin; Cho, Myeong Chan; Kim, Young Jo

    2014-11-01

    The Korea Acute Myocardial Infarction Registry (KAMIR) was the first nationwide registry data collection designed to track outcomes of patients with acute myocardial infarction (AMI). These studies reflect the current therapeutic approaches and management for AMI in Korea. The results of KAMIR could help clinicians to predict the prognosis of their patients and identify better diagnostic and treatment tools to improve the quality of care. The KAMIR score was proposed to be a predictor of the prognosis of AMI patients. Triple antiplatelet therapy, consisting of aspirin, clopidogrel and cilostazol, was effective at preventing major adverse clinical outcomes. Drug-eluting stents were effective and safe in AMI patients with no increased risk of stent thrombosis. Statin therapy was effective in Korean AMI patients, including those with very low levels of low density cholesterol. The present review summarizes the 10-year scientific achievements of KAMIR from admission to outpatient care during long-term clinical follow-up.

  13. Symptom-limited maximal treadmill testing after myocardial infarction.

    PubMed

    Roberts, K C; Logan, R L

    1980-11-12

    In this paper we report our experience of routine symptom limited maximal treadmill assessment, and the methodology used with patients at the end of their convalescence after myocardial infarction. Sixty-one of 68 (90 percent) consecutive patients, mean age 55.7 years (21 to 69 years), were studied at the median time after infarction of six weeks (three to 16 weeks). No complications occurred during or after the tests. Fifty-six percent of the patients studied achieved a work capacity which was within the average range reported for healthy people of the smae age. Thirty-two percent experienced chest pain thought to be angina and 31 percent developed ST segment depression of at least 1 mm without chest pain. Although ventricular premature beats occurred in half the tests the only arrhythmia requiring any treatment was a supraventricular tachycardia. The assessment of work capacity and limiting symptoms in this way after myocardial infarction is safe and is of considerable help in patient management.

  14. [Characteristics of therapy of acute myocardial infarction in diabetes].

    PubMed

    Motz, W; Kerner, W

    2012-05-01

    Therapy of acute myocardial infarction (STEMI and NSTEMI) in diabetics does not principally differ from that of non-diabetic patients. Due to the higher mortality in diabetics reperfusion measures, such as direct percutaneous coronary intervention (PCI), should be rapidly performed. An intensive drug treatment with thrombocyte aggregation inhibitors, angiotensin-converting enzyme (ACE) inhibitors and beta-receptor blocking agents must be carried out according to the current guidelines. An important factor is the high risk of renal failure due to the contrast dye administered during PCI in the presence of pre-existing diabetic kidney damage which should be limited to 100 ml if possible. Direct PCI should be limited to the infarcted vessel. After stabilization a comprehensive strategy to cure coronary artery disease, whether with PCI or coronary artery bypass graft (CABG) should be finalized. If severe coronary 3-vessel disease is present, CABG should be favored in diabetic patients. After surviving an acute myocardial infarction differentiated metabolic monitoring is mandatory.

  15. Holmium:YAG laser angioplasty: treatment of acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Topaz, On

    1993-06-01

    We report our clinical experience with a group of 14 patients who presented with acute myocardial infarction. A holmium:YAG laser was applied to the infarct-related artery. This laser emits 250 - 600 mJ per pulse, with a pulse length of 250 microseconds and repetition rate of 5 Hz. Potential benefits of acute thrombolysis by lasers include the absence of systemic lytic state; a shortened thrombus clearing time relative to using thrombolytics; safe removal of the intracoronary thrombus and facilitation of adjunct balloon angioplasty. Potential clinical difficulties include targeting the obstructive clot and plaque, creation of debris and distal emboli and laser-tissue damage. It is conceivable that holmium:YAG laser can be a successful thrombolytic device as its wave length (2.1 microns) coincides with strong water absorption peaks. Since it is common to find an atherosclerotic plaque located under or distal to the thrombotic occlusion, this laser can also be applied for plaque ablation, and the patient presenting with acute myocardial infarction can clearly benefit from the combined function of this laser system.

  16. Risk stratification after acute myocardial infarction in the reperfusion era.

    PubMed

    Michaels, A D; Goldschlager, N

    2000-01-01

    Historically, risk stratification for survivors of acute myocardial infarction (AMI) has centered on 3 principles: assessment of left ventricular function, detection of residual myocardial ischemia, and estimation of the risk for sudden cardiac death. Although these factors still have important prognostic implications for these patients, our ability to predict adverse cardiac events has significantly improved over the last several years. Recent studies have identified powerful predictors of adverse cardiac events available from the patient history, physical examination, initial electrocardiogram, and blood testing early in the evaluation of patients with AMI. Numerous studies performed in patients receiving early reperfusion therapy with either thrombolysis or primary angioplasty have emphasized the importance of a patent infarct related artery for long-term survival. The predictive value of a variety of noninvasive and invasive tests to predict myocardial electrical instability have been under active investigation in patients receiving early reperfusion therapy. The current understanding of the clinically important predictors of clinical outcomes in survivors of AMI is reviewed in this article. PMID:10661780

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

    SciTech Connect

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

    1987-12-01

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

  18. Cyclosporin variably and inconsistently reduces infarct size in experimental models of reperfused myocardial infarction: a systematic review and meta-analysis.

    PubMed

    Lim, W Y; Messow, C M; Berry, C

    2012-04-01

    Cyclosporin is an immunosuppressant that has recently been proposed as a treatment to prevent reperfusion injury in acute myocardial infarction (MI). We aimed to determine the overall efficacy of cyclosporin in experimental studies of acute reperfused MI. We conducted a systematic review and stratified meta-analysis of published studies describing the efficacy of cyclosporin in experimental models of acute reperfused MI. We included all in vivo publications of cyclosporin where infarct size was measured. A literature search identified 29 potential studies of which 20 fulfilled the eligibility criteria. In these studies (involving four species of animals), cyclosporin reduced myocardial infarct size by a standardized mean (95% confidence interval) difference of -1.60 (-2.17, -1.03) compared with controls. Cyclosporin failed to demonstrate a convincing benefit in studies involving pigs. Despite this observation, the overall efficacy of cyclosporin did not differ across species (P= 0.358). The dose of cyclosporin given did not affect final infarct size (P= 0.203). Funnel plots of these data suggested heterogeneity among the studies. Cyclosporin had variable effects on infarct size compared with placebo. Cyclosporin had no effect on myocardial infarct size in swine, raising a question over the potential cardioprotective effects of cyclosporin in man.

  19. [Metformin and left ventricular remodeling after acute myocardial infarction: molecular mechanisms and clinical implications].

    PubMed

    Paneni, Francesco; Costantino, Sarah; Cosentino, Francesco

    2015-04-01

    Despite clear advances in reperfusion therapy and pharmacological treatment, a large proportion of patients with an acute myocardial infarction will die of its consequences. In this regard, it is very important to understand the molecular processes underpinning ischemia-reperfusion injury and occurrence of left ventricular dysfunction, with the aim to develop mechanism-based therapeutic strategies. Experimental evidence indicates that metformin, a biguanide often used in the treatment of diabetes, has favorable effects on left ventricular function. This effect is largely mediated by activation of AMP-activated protein kinase (AMPK), a key molecule orchestrating many biochemical processes such as glucose uptake, glycolysis, oxidation of free fatty acids and mitochondrial biogenesis. These processes significantly contribute to raise ATP levels and restore myocardial contractile efficiency. AMPK also activates endothelial nitric oxide synthase and promotes autophagy, thus preventing inflammation and cellular death. These basic studies prompted many researchers to test the cardioprotective effects of metformin in the clinical setting. In diabetic patients with ST-elevation myocardial infarction (STEMI), retrospective analyses showed that metformin is associated with reduced infarct size as compared to non-metformin-based strategies, implicating beneficial effects beyond glucose control. A recent randomized trial, the GIPS-III study, has postulated that metformin may improve left ventricular function following STEMI even in patients without diabetes. Metformin (500 mg twice/day), administered 3h after percutaneous coronary intervention, did not result in improved left ventricular ejection fraction after 4-month follow-up. Based on these results, it remains unclear whether metformin exerts a cardioprotective effect regardless of glycemic control. Further randomized studies in diabetic and nondiabetic patients are required to address these important questions. The present

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

    PubMed

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

    2015-01-01

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

  1. Epistatic and pleiotropic effects of polymorphisms in the fibrinogen and coagulation factor XIII genes on plasma fibrinogen concentration, fibrin gel structure and risk of myocardial infarction.

    PubMed

    Mannila, Maria Nastase; Eriksson, Per; Ericsson, Carl-Göran; Hamsten, Anders; Silveira, Angela

    2006-03-01

    An intricate interplay between the genes encoding fibrinogen gamma (FGG), alpha (FGA) and beta (FGB), coagulation factor XIII (F13A1) and interleukin 6 (IL6) and environmental factors is likely to influence plasma fibrinogen concentration, fibrin clot structure and risk of myocardial infarction (MI). In the present study, the potential contribution of SNPs harboured in the fibrinogen, IL6 and F13A1 genes to these biochemical and clinical phenotypes was examined. A database and biobank based on 387 survivors of a first MI and population-based controls were used. Sixty controls were selected according to FGG 9340T > C [rs1049636] genotype for studies on fibrin clot structure using the liquid permeation method. The multifactor dimensionality reduction method was used for interaction analyses. We here report that the FGA 2224G > A [rs2070011] SNP (9.2%), plasma fibrinogen concentration (13.1%) and age (8.1%) appeared as independent determinants of fibrin gel porosity. The FGA 2224G > A SNP modulated the relation between plasma fibrinogen concentration and fibrin clot porosity. The FGG-FGA*4 haplotype, composed of the minor FGG 9340C and FGA 2224A alleles, had similar effects, supporting its reported protective role in relation to MI. Significant epistasis on plasma fibrinogen concentration was detected between the FGA 2224G > A and F13A1 Val34Leu [rs5985] SNPs (p < 0.001). The FGG 9340T > C and FGB 1038G > A [rs1800791] SNPs appeared to interact on MI risk, explaining the association of FGG-FGB haplotypes with MI in the absence of effects of individual SNPs. Thus, epistatic and pleiotropic effects of polymorphisms contribute to the variation in plasma fibrinogen concentration, fibrin clot structure and risk of MI.

  2. Meteorological factors and the time of onset of chest pain in acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Thompson, David R.; Pohl, Jurgen E.; Tse, Yiu-Yu S.; Hiorns, Robert W.

    1996-09-01

    Analysis of the time of onset of chest pain in 2254 patients with a myocardial infarction admitted to a coronary care unit in Leicester during a 10-year period shows an association with temperature and humidity. During both the most cold and humid times of the year, the relationship is a strong one. A generalized linear model with a log link was used to fit the data and the backward elimination selection procedure suggested a humid, cold day might help to trigger the occurrence of myocardial infarction. In addition, cold weather was found to have a stronger effect on the male population while those men aged between 50 and 70 years were more sensitive to the effect of high humidity.

  3. Induction of a chronic myocardial infarction in the laboratory animal - experimental model

    PubMed Central

    POP, IONEL CIPRIAN; GRAD, NICOLAE-OVIDIU; PESTEAN, COSMIN; TAULESCU, MARIAN; MIRCEAN, MIRCEA; MIRONIUC, ION-AUREL

    2013-01-01

    Introduction Ischemic heart disease is a major public health problem in western countries. Appropriate animal experimental models of chronic myocardial infarction is an essential first step in order to investigate and develop new therapeutic interventions. Aim The aim of this study was to find an optimal place for a coronary artery ligation to induce an optimal chronic myocardial infarction and also a new heart approach that will not require oro-tracheal intubation. Material and methods To achieve these goals we used a group of rabbits and after induction of anesthesia and cardiac exposure by rib osteotomy (rib III, IV and V) at the costo-sternal junction level on the right side we performed three different left anterior descending artery (LAD) ligation at different distances (5, 10 and 15 mm) in relation to the apex. Thirty days after the acute myocardial infarction, we correlated laboratory investigations (serology, ECG, cardiac ultrasound) with histopathological findings. Results Heart approach achieved by rib osteotomy (rib III, IV and V) at the costo-sternal junction level on the right side, maintains the integrity of the ribcage, allowing it to take part in respiratory movements and the animal model does not need oro-tracheal intubation. Ligation of LAD at 15 mm from the apex was incompatible with life; ligation of LAD at 5 mm from the apex does not achieved transmural myocardial infarction and ligation of LAD at 10 mm from the apex achieved a transmural myocardial infarction of the left ventricle which also involved the distal part of the interventricular septum. Conclusion Ligation of LAD at 10 mm from the apex achieved a transmural myocardial infarction of the left ventricle, is in an easily accessible area from technical point of view, it is sufficiently expanded to induce hemodynamic effects that can be quantified with paraclinical examination and also it is compatible with the experimental animal life. If the heart is approached by rib III, IV and V

  4. Myocardial perfusion of infarcted and normal myocardium in propofol-anesthetized minipigs using (82)Rubidium PET.

    PubMed

    Rasmussen, Thomas; Follin, Bjarke; Kastrup, Jens; Christensen, Thomas Emil; Hammelev, Karsten Pharao; Kjær, Andreas; Hasbak, Philip

    2016-06-01

    Cardiac Rubidium-82 ((82)Rb) positron-emission-tomography (PET) is a good method for quantification of myocardial blood flow in man. Quantification of myocardial blood flow in animals to evaluate new treatment strategies or to understand underlying disease is also of great interest but raises some challenges. Animals, which have been anesthetized during PET acquisition, might react differently to used stress medications, and therefore difficulties might exist while evaluating the resulting PET images using standard software packages from commercial vendors optimized for human hearts. Furthermore propofol, used for anesthesia, can influence myocardial perfusion and coronary flow reserve due to its vasorelaxant effect, and interactions might exist between propofol and used stress agents, potentially affecting the result of the examination. We present cardiac (82)Rb-PET studies performed in propofol-anesthetized minipigs with normal and infarcted myocardium stressed with both adenosine and dipyridamole. Despite the mentioned challenges, we were able to trace the small minipig heart with software designed for human cardiac PET and to achieve blood flow measurements comparable with results in humans with both adenosine and dipyridamole. We found dipyridamole to be a superior stress agent for this experimental setup. Finally, we were able to clearly identify the myocardial perfusion defect after an induced myocardial infarction. PMID:26931633

  5. Incidentally found situs inversus with dextrocardia: inferior myocardial infarction in an 86-year-old woman.

    PubMed

    Hudzik, Bartosz; Polonski, Lech

    2012-10-01

    Situs inversus with dextrocardia is a rare condition. Yet, the incidence of atheroclerosis and myocardial infarction in patients with dextrocardia is similar to that in general population. The diagnosis of acute myocardial infarction is somewhat tricky and difficult if the dextrocardia is not recognized. We present the electrocardiogram, coronary angiograms, and chest radiogram of a patient with incidentally found situs inversus with dextrocardia.

  6. Multiple bee stings resulting in ST elevation myocardial infarction (the Kounis syndrome).

    PubMed

    Pelli, Joseph R; Wieters, J Scott; Firozgary, Bahrom; Montalvo, Timothy

    2016-07-01

    Kounis syndrome consists of angina pectoris or myocardial infarction that is triggered by the release of inflammatory mediators in the setting of an allergic reaction. We present the case of a 61-year-old man who presented to the emergency department with anaphylaxis after being stung by >100 bees. During resuscitation, he subsequently developed ST elevation myocardial infarction. PMID:27365877

  7. [Myocardial infarction related to the association of physical exertion and the ingestion of cold drinks].

    PubMed

    Marcuschamer Miller, J; Pérez de Juan Romero, M A; Castellano Reyes, C; Murrieta Gutiérrez, T; Fernández Domínguez, L

    1987-01-01

    We describe 3 young individuals with acute myocardial infarction that developed after extenous stress followed by the intake of cold fluids. The patients had retrosternal chest pain and EKG changes suggestive of posterior-inferior myocardial infarction. Coronartiography demonstrated 40% and 50% narrowing of the right coronary artery. The remaining case had normal coronary arteries.

  8. Multiple bee stings resulting in ST elevation myocardial infarction (the Kounis syndrome)

    PubMed Central

    Pelli, Joseph R.; Firozgary, Bahrom; Montalvo, Timothy

    2016-01-01

    Kounis syndrome consists of angina pectoris or myocardial infarction that is triggered by the release of inflammatory mediators in the setting of an allergic reaction. We present the case of a 61-year-old man who presented to the emergency department with anaphylaxis after being stung by >100 bees. During resuscitation, he subsequently developed ST elevation myocardial infarction. PMID:27365877

  9. Effects of carnosine on prooxidant-antioxidant status in heart tissue, plasma and erythrocytes of rats with isoproterenol-induced myocardial infarction.

    PubMed

    Evran, Betül; Karpuzoğlu, Hande; Develi, Seval; Kalaz, Esra Betül; Soluk-Tekkeşin, Merva; Olgaç, Vakur; Doğru-Abbasoğlu, Semra; Uysal, Müjdat

    2014-02-01

    Rats were injected with isoproterenol (ISO; 110 mg/kg, ip, 2 doses, 24 h interval) to induce acute myocardial infarction (AMI) and were sacrificed 6 and 24 h after the last ISO injection. The heart tissue, plasma and erythrocytes of these rats were evaluated for cardiac markers and oxidative stress parameters. Levels of cardiac troponin T (cTnT) and the activities of creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) in plasma were increased 6 and 24 h after ISO treatment. The levels of malondialdehyde (MDA), diene conjugate (DC), and protein carbonyl (PC) were increased in heart tissue and plasma, while levels of erythrocyte MDA and glutathione (GSH) and plasma ferric reducing antioxidant power (FRAP) were also increased. However, GSH levels and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased in heart tissue of rats with AMI. We also investigated the effects of carnosine (CAR) treatment on these parameters 24 h after the last ISO injection. CAR (250 mg/kg/day; ip) treatments were carried out either 10 days before ISO injection or 2 days concomitant with ISO. Pretreatment with CAR decreased plasma LDH and AST activities and ameliorated cardiac histopathological changes in ISO-treated rats. Cardiac MDA, DC and PC levels decreased, but GSH levels and SOD and GSH-Px activities increased. However, the increases in plasma MDA and PC levels as well as erythrocyte H(2)O(2)-induced MDA and GSH levels did not change due to CAR pretreatment. In conclusion, our findings indicate that CAR pretreatment may have protective effects on ISO-induced cardiac toxicity by decreasing oxidative stress.

  10. Effectiveness of Practices for Improving the Diagnostic Accuracy of Non-ST Elevation Myocardial Infarction in the Emergency Department: A Laboratory Medicine Best Practices Systematic Review

    PubMed Central

    Layfield, Christopher; Rose, John; Alford, Aaron; Snyder, Susan R.; Apple, Fred S.; Chowdhury, Farah M.; Kontos, Michael C.; Newby, L. Kristin; Storrow, Alan B.; Tanasijevic, Milenko; Leibach, Elizabeth; Liebow, Edward B.; Christenson, Robert H.

    2016-01-01

    Objectives This article presents evidence from a systematic review of the effectiveness of four practices (assay selection, decision point cardiac troponin (cTn) threshold selection, serial testing, and point of care testing) for improving the diagnostic accuracy for Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) in the Emergency Department. Design and Methods The CDC-funded Laboratory Medicine Best Practices (LMBP™) Initiative systematic review A6 Method for Laboratory Best Practices was used. Results The current guidelines (e.g., ACC/AHA) recommend using cardiac troponin assays with a 99th percentile upper reference limit (URL) diagnostic threshold to diagnose NSTEMI. The evidence in this systematic review indicates that contemporary sensitive cTn assays meet the assay profile requirements (sensitivity, specificity, PPV, and NPV) to more accurately diagnose NSTEMI than alternate tests. Additional biomarkers did not increase diagnostic effectiveness of cTn assays. Sensitivity, specificity, and negative predictive value (NPV) were consistently high and low positive predictive value (PPV) improved with serial sampling. Evidence for use of cTn point of care testing (POCT) was insufficient to make recommendations, though some evidence suggests cTn POCT may result in reduction to patient length of stay and costs. Conclusions Two best practice recommendations emerged from the systematic review and meta-analysis of literature conducted using the LMBP™ A6 Method criteria: Testing with cardiac troponin assays, using the 99th percentile URL as the clinical diagnostic threshold for the diagnosis of NSTEMI and without additional biomarkers, is recommended. Also recommended is serial cardiac troponin sampling with one sample at presentation and at least one additional sample taken a minimum of 6 hours later to identify a rise or fall in the troponin level. Testing with high-sensitivity cardiac troponin assays, at presentation and again within 6 hours, is the

  11. Weather fronts and acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Kveton, Vit

    1991-03-01

    Some methodological aspects are discussed of the investigation of acute infarct myocarditis (AIM) in relation to weather fronts. Results of a new method of analysis are given. Data were analysed from about the hour of the onset of symptoms, and led to the diagnosis of AIM either immediately or within a few hours or days (3019 cases observed over 4.5 years during 1982 1986 in Plzen, Czechoslovakia). Weather classification was based on three factors (the type of the foregoing front, the type of the subsequent front, the time section of the time interval demarcated by the passage of the surfaces of the fronts). AIM occurrence increased in particular types of weather fronts: (i) by 30% during 7 12 h after a warm front, if the time span between fronts exceeded 24 h; (ii) by 10% in time at least 36 h distant from the foregoing cold or occlusion front and from the succeeding warm or occlusion front; (iii) by 20% during 0 2 h before the passage of the front, provided the foregoing front was not warm and the interval between fronts exceeded 5 h. AIM occurrence decreased by 15% 20% for time span between fronts > 24 h at times 6 11, 6 23 and 6 35 h before a coming warm or occlusion front (for interfrontal intervals 25 48, 49 72 and possibly > 72 h), and also at 12 23 and possibly 12 35 h before a cold front (for intervals 49 72 and possibly > 72 h), if the foregoing front was cold or an occlusion front.

  12. Telomere Length Variation in Juvenile Acute Myocardial Infarction

    PubMed Central

    Fornengo, Cristina; Di Gaetano, Cornelia; Ricceri, Fulvio; Guarrera, Simonetta; Critelli, Rossana; Anselmino, Matteo; Piazza, Alberto; Gaita, Fiorenzo; Bergerone, Serena; Matullo, Giuseppe

    2012-01-01

    Leukocyte telomere length (LTL) provides a potential marker of biological age, closely related to the endothelial dysfunction and consequently to the atherosclerotic process. To investigate the relationship between the LTL and the risk of premature acute myocardial infarction and to evaluate the predictive value of LTL on the onset of major cardiovascular events, 199 patients from 18 to 48 years old with first diagnosis of acute myocardial infarction were enrolled and were matched with 190 controls for sex and age (±1 year). Clinical data and coronary artery disease were evaluated at enrollment and at follow up. LTL was measured at enrollment using a quantitative PCR-based method. No significant differences were observed in LTL between cases and controls (p = 0.20) and with the presence of coronary artery disease in patients (p = 0.47). Hypercholesterolemic cases presented LTL significantly longer than cases without hypercholesterolemia (t/s: 0.82±0.16 p = 0.79 and t/s norm: 0.79±0.19 p = 0.01), as confirmed in multivariate regression analysis (p = 0.005, β = 0.09). Furthermore, multivariate regression analysis showed LTL significantly shorter in hypertensive cases than in normotensive cases (p = 0.04, β = −0.07). One hundred seventy-one cases (86%) ended the average follow up of 9±5 years, 92 (54%) presented a major cardiovascular event. At multivariate regression analysis the LTL detected at enrollment did not represent a predictive factor of major cardiovascular events nor it significantly impacted with cumulative events. Based on present cohort of young Italian patients, the LTL did not represent a marker of acute myocardial infarction nor had a predictive role at medium term follow up. PMID:23145125

  13. Relation Between Myocardial Infarction Deaths and Solar Activity in Mexico

    NASA Astrophysics Data System (ADS)

    Diaz-Sandoval, R.

    2002-05-01

    We study the daily incidence of myocardial infarction deaths in Mexico for 4 years (1996-99) with a total of 129 917 cases in all the country, collected at the General Directorate of Epidemiology (National Ministry of Health). We divided the cases by sex and age and perform two kinds of analysis. First, we did an spectral analysis using the Maximum Entropy Method, considering the complete period, and minimum and maximum epochs of solar activity. The results show that the most persistent periodicity at higher frequencies in the myocardial infarction death occurrence is that of seven days. Considering the solar cycle phases, we found that during solar minimum times some frequencies are not detectable compared with solar maximum epochs, particularly that of seven days. Biological rhythms close to seven days, the circaseptans, are in general thought to be only the result of the social organization of life. However, this cannot be the only explanation, because the 7-days periodicity has been encountered in lower organisms not related with our rhythms of life. Thus, it has been proposed that biological rhythms could be evolutionary adaptations to environmental conditions, particularly, solar activity. In the second analysis we compared two solar activity-related phenomena: the Forbush decreases of cosmic rays and the geomagnetic index Ap for various levels of geomagnetic perturbations. The results show that during decreases of cosmic ray fluxes, for most cases there is a higher average myocardial infarction deaths occurrence, compared with the average incidence in days of no decreases. For geomagnetic activity we find the same situation in most cases. Furthermore, this behavior is more pronounced as the level of the perturbation increases and in times of maximum solar activity.

  14. Genotype/allelic combinations as potential predictors of myocardial infarction.

    PubMed

    Nasibullin, Timur R; Timasheva, Yanina R; Sadikova, Regina I; Tuktarova, Ilsiyar A; Erdman, Vera V; Nikolaeva, Irina E; Sabo, Jan; Kruzliak, Peter; Mustafina, Olga E

    2016-01-01

    In order to find new informative predictors of myocardial infarction, we performed an analysis of genotype frequencies of polymorphic markers of SELE (rs2076059, 3832T > C), SELP (rs6131, S290 N), SELL (rs1131498, F206L), ICAM1 (rs5498, K469E), VCAM1 (rs3917010, c.928 + 420A > C), PECAM1 (rs668, V125L), VEGFA (rs35569394, -2549(18)I/D), CCL2 (rs1024611, -2518A > G), NOS3 (rs1799983, E298D), and DDAH1 (rs669173, c.303 + 30998A > G) genes in the group of Russian men with myocardial infarction (N = 315) and the control group of corresponding ethnicity, gender, and age (N = 286). Using Markov chain Monte-Carlo method (APSampler), we found genotype combinations associated with increased and decreased risk of myocardial infarction. The most significant associations were detected for PECAM1*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005) SELE*C + VEGFA*I + CCL2*G + VCAM1*A + NOS3*D (OR = 2.74 CI 1.66-4.52 Pperm = 2.09 × 10(-5)), and VEGFA*D/D + CCL2*A + DDAH1*C (OR = 0.44 CI 0.28-0.7 Pperm = 7.89 × 10(-5)) genotype combinations. PMID:26662939

  15. Haemodynamic profile of acebutolol in acute myocardial infarction.

    PubMed

    Wan, S H; Seah, C S; Teh, L B; Letchmana, K

    1980-10-01

    This paper evaluates the haemodynamics of intravenous Acebutolol (SECTRAL) (0.5 mgm/Kgm) in the acute phase of myocardial infarction uncomplicated by hypertension, cardiac failure or conduction abnormalities. Nineteen observations were made on 15 consecutive patients. Haemodynamic parameters were recorded just before, and at 15 and 30 min after injections, using Swan-Ganz Catheter-Thermister and Edslab Cardiac Output Computer (9520) in the Intensive Care Unit. All patients survived; none had extension of infarction. The Heart Rate dropped by 9 +/- 1% (+/- SEM) (from 90.2 +/- 4.0 to 81.6 +/- 3.1 per min, P less than 0.001) but systolic and mean Blood Pressures were not significantly altered. Pulmonary Capillary Pressure was elevated by 2.5 +/- 6% (from 11.6 +/- 0.8 to 14.4 +/- 0.9 mmHg P less than 0.001) but cardiac failure hardly ever developed clinically. The mean Pulmonary Arterial Pressure rose by 10 +/- 2% (P less than 0.005) while the Right Atrial mean increased from 6.0 +/- 1.0 to 8.3 +/- 1.3 mm Hg (P less than 0.005). Although the Cardiac Index was depressed by 11 +/- 2% (from 3.0 +/- 0.1 to 2.7 +/- 0.1 L/min/M2; P less than 0.001), the Stroke Index remained virtually unaffected. Myocardial oxygen consumption per min as reflected by Heart Rate x BP product declined by 12 +/- 2% (P less than 0.001), while the Stroke Work Index was lowered by 9 +/- 3% (P less than 0.005). The haemodynamic profile indicates that intravenous Acebutolol in uncomplicated infarcts is well tolerated, and that it could be employed with advantage to manipulate determinants of myocardial oxygen consumption through reduction of Heart Rate Pressure product and Stroke Work Index.

  16. Monolayered mesenchymal stem cells repair scarred myocardium after myocardial infarction.

    PubMed

    Miyahara, Yoshinori; Nagaya, Noritoshi; Kataoka, Masaharu; Yanagawa, Bobby; Tanaka, Koichi; Hao, Hiroyuki; Ishino, Kozo; Ishida, Hideyuki; Shimizu, Tatsuya; Kangawa, Kenji; Sano, Shunji; Okano, Teruo; Kitamura, Soichiro; Mori, Hidezo

    2006-04-01

    Mesenchymal stem cells are multipotent cells that can differentiate into cardiomyocytes and vascular endothelial cells. Here we show, using cell sheet technology, that monolayered mesenchymal stem cells have multipotent and self-propagating properties after transplantation into infarcted rat hearts. We cultured adipose tissue-derived mesenchymal stem cells characterized by flow cytometry using temperature-responsive culture dishes. Four weeks after coronary ligation, we transplanted the monolayered mesenchymal stem cells onto the scarred myocardium. After transplantation, the engrafted sheet gradually grew to form a thick stratum that included newly formed vessels, undifferentiated cells and few cardiomyocytes. The mesenchymal stem cell sheet also acted through paracrine pathways to trigger angiogenesis. Unlike a fibroblast cell sheet, the monolayered mesenchymal stem cells reversed wall thinning in the scar area and improved cardiac function in rats with myocardial infarction. Thus, transplantation of monolayered mesenchymal stem cells may be a new therapeutic strategy for cardiac tissue regeneration. PMID:16582917

  17. Strategies for recruitment of stem cells to treat myocardial infarction.

    PubMed

    Shafiq, Muhammad; Lee, Sang-Hoon; Jung, Youngmee; Kim, Soo Hyun

    2015-01-01

    Heart failure is one of the most prominent causes of morbidity and mortality worldwide. According to the World Health Organization, coronary artery disease and myocardial infarction (MI) are responsible for 29% of deaths worldwide. MI results in obstruction of the blood supply to the heart and scar formation, and causes substantial death of cardiomyocytes in the infarct zone followed by an inflammatory response. Current treatment methodologies of MI and heart failure include organ transplantation, coronary artery bypass grafting, ventricular remodeling, cardiomyoplasty, and cellular therapy. Each of these methodologies has associated risks and benefits. Cellular cardiomyoplasty is a viable option to decrease the fibrosis of infarct scars, adverse post-ischemic remodeling, and improve heart function. However, the low rate of cell survival, shortage of cell sources and donors, tumorigenesis, and ethical issues hamper full exploitation of cell therapy for MI treatment. Consequently, the mobilization and recruitment of endogenous stem/progenitor cells from bone marrow, peripheral circulation, and cardiac tissues has immense potential through harnessing the host's own reparative capacities that result from interplay among cytokines, chemokines, and adhesion molecules. Therapeutic treatments to enhance the mobilization and homing of stem cells are under development. In this review, we present state-of-the-art approaches that are being pursued for stem cell mobilization and recruitment to regenerate infarcted myocardium. Potential therapeutic interventions and delivery strategies are discussed in detail.

  18. Strategies for recruitment of stem cells to treat myocardial infarction.

    PubMed

    Shafiq, Muhammad; Lee, Sang-Hoon; Jung, Youngmee; Kim, Soo Hyun

    2015-01-01

    Heart failure is one of the most prominent causes of morbidity and mortality worldwide. According to the World Health Organization, coronary artery disease and myocardial infarction (MI) are responsible for 29% of deaths worldwide. MI results in obstruction of the blood supply to the heart and scar formation, an