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Sample records for myocardial infarction trial

  1. 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

  2. Streptokinase in Recent Myocardial Infarction: A Controlled Multicentre Trial

    PubMed Central

    1971-01-01

    In this controlled multicentre trial treatment with either streptokinase or heparin was allocated at random to patients suffering from myocardial infarction of less than 24 hours' duration. Treatment with either drug was standardized and lasted for 24 hours. A total of 764 patients entered the trial; 34 patient charts were rejected (including all 28 charts from one centre) because of data failure. On retrospective analysis of the 730 remaining patients the two groups were found to have been comparable at the start. The total hospital mortality was 18·5% of 373 patients allotted to streptokinase treatment and 26·3% of 357 given herapin. The mortality after infusion (24 hours) was 10·6% of 340 patients treated with streptokinase and 17·8% of 320 given herapin (P=0·011). Reinfarction in hospital after the 24-hour period of infusion occurred significantly less often in patients treated with streptokinase (P=0·036). Bleeding from puncture sites and pyrexia occurred more frequently during streptokinase treatment. After exclusion of those patients whose diagnosis was unconfirmed on retrospective assessment, the total hospital mortality rate was 19·0% of 357 patients treated with streptokinase and 27·4% of 339 treated with heparin (P=0·011). These results indicate that in recent myocardial infarction streptokinase was superior to heparin in reducing mortality and reinfarction rate during an average period of six weeks in hospital. PMID:4934187

  3. 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.

  4. 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…

  5. ST-Elevation Myocardial Infarction, Thrombus Aspiration, and Different Invasive Strategies. A TASTE Trial Substudy

    PubMed Central

    Fröbert, Ole; Calais, Fredrik; James, Stefan K; Lagerqvist, Bo

    2015-01-01

    Background The clinical effect of thrombus aspiration in ST-elevation myocardial infarction may depend on the type of aspiration catheter and stenting technique. Methods and Results The multicenter, prospective, randomized, open-label trial Thrombus Aspiration in ST-Elevation myocardial infarction in Scandinavia (TASTE) did not demonstrate a clinical benefit of thrombus aspiration compared to percutaneous coronary intervention alone. We assessed the effect of type of aspiration device, stent type, direct stenting, and postdilatation on outcomes at 1 year. There was no difference in all-cause mortality, between the 3 most frequently used aspiration catheters (Eliminate [Terumo] 5.4%, Export [Medtronic] 5.0%, Pronto [Vascular Solutions] 4.5%) in patients randomized to thrombus aspiration. There was no difference in mortality between directly stented patients randomized to thrombus aspiration compared to patients randomized to percutaneous coronary intervention only (risk ratio 1.08, 95% CI 0.70 to 1.67, P=0.73). Similarly, there was no difference in mortality between the 2 randomized groups for patients receiving drug-eluting stents (risk ratio 0.89, 95% CI 0.63 to 1.26, P=0.50) or for those treated with postdilation (risk ratio 0.72, 95% CI 0.49 to 1.07, P=0.11). Furthermore, there was no difference in rehospitalization for myocardial infarction or stent thrombosis between the randomized arms in any of the subgroups. Conclusions In patients with ST-elevation myocardial infarction randomized to thrombus aspiration, the type of aspiration catheter did not affect outcome. Stent type, direct stenting, or postdilation did not affect outcome irrespective of treatment with thrombus aspiration and percutaneous coronary intervention or percutaneous coronary intervention alone. Clinical Trial Registration URL: ClinicalTrials.gov. Unique identifier: NCT01093404, https://clinicaltrials.gov/ct2/show/NCT01093404. PMID:26077585

  6. 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

  7. Design and rationale of the Reduction of Infarct Expansion and Ventricular Remodeling with Erythropoietin After Large Myocardial Infarction (REVEAL) trial

    PubMed Central

    Melloni, Chiara; Rao, Sunil V.; Povsic, Thomas J.; Melton, Laura; Kim, Raymond J.; Kilaru, Rakhi; Patel, Manesh; Talan, Mark; Ferrucci, Luigi; Longo, Dan L.; Lakatta, Edward G.; Najjar, Samer S.; Harrington, Robert A.

    2010-01-01

    Background Acute myocardial infarction (MI) remains a leading cause of death despite advances in pharmacologic and percutaneous therapies. Animal models of ischemia/reperfusion have demonstrated that single-dose erythropoietin (EPO) may reduce infarct size, decrease apoptosis, and increase neovascularization, possibly through mobilization of endothelial progenitor cells (EPCs). Study Design REVEAL is a randomized, double-blind, placebo-controlled, multicenter trial evaluating the effects of epoetin alfa on infarct size and left ventricular (LV) remodeling in patients with large MIs. The trial comprises a dose-escalation safety phase and a single-dose efficacy phase using the highest acceptable epoetin alfa dose up to 60,000 units. Up to 250 STEMI patients undergoing primary or rescue percutaneous coronary intervention (PCI) will be randomized to intravenous epoetin alfa or placebo within 4 hours of successful reperfusion. The primary study endpoint is infarct size expressed as a percentage of LV mass, as measured by cardiac magnetic resonance imaging 2–6 days post study medication administration. Secondary endpoints will assess changes in EPC numbers and changes in indices of ventricular remodeling. Conclusion The REVEAL trial will evaluate the safety and efficacy of the highest tolerated single dose of epoetin alfa in patients who have undergone successful rescue or primary PCI for acute STEMI. PMID:21095264

  8. Prevalence, consequences, and implications for clinical trials of unrecognized myocardial infarction.

    PubMed

    Pride, Yuri B; Piccirillo, Bryan J; Gibson, C Michael

    2013-03-15

    Patients with myocardial infarction (MI) generally present with chest pain or pressure at rest or minimal exertion and have associated electrocardiographic changes and/or elevation of the biomarkers of myocardial necrosis. A subset of patients, however, experience little chest discomfort or do not present to medical attention despite experiencing symptoms. Unrecognized MI might be detected using electrocardiographic or imaging techniques, such as echocardiography, nuclear imaging, or cardiovascular magnetic resonance imaging. Unrecognized MI is a common clinical entity, with an incidence as great as 35% in high-risk populations. Moreover, the risk of a subsequent major adverse cardiovascular event might be similar to the risk after a clinically apparent MI. In the present review, we examined the incidence of unrecognized MI across broad groups of subjects and the subsequent risk of adverse cardiovascular events. Finally, we explored the potential role of including unrecognized MI as a major adverse outcome in randomized clinical trials of agents aimed at reducing cardiovascular morbidity.

  9. Long-term prognosis of women after myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial.

    PubMed

    Benderly, M; Behar, S; Reicher-Reiss, H; Boyko, V; Goldbourt, U

    1997-07-15

    Women sustaining myocardial infarction fare worse than men during hospitalization. Reports on long-term survival in women surviving an acute myocardial infarction are controversial. The Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) registry includes 5,839 consecutive myocardial infarction patients who were hospitalized in 13 coronary care units in Israel between 1981 and 1983. The authors examined sex differences in the long-term survival of 4,808 hospital survivors (1,120 women and 3,688 men). Women exhibited a significantly poorer long-term survival than men. After age adjustment, differences between men and women decreased, leaving a survival probability difference of 11% at the end of 12 years of follow-up. In a subgroup analysis, women exhibited poorer survival than men in a comparison of patients with and without periinfarction congestive heart failure or a history of myocardial infarction preceding the index infarction. The multivariate adjusted hazard ratios associated with female sex in diabetic and nondiabetic patients were 1.46 and 1.13, respectively. In conclusion, a cumulative survival disadvantage for women in comparison with men is still evident after 12 years of follow-up. The mortality difference is diminished but not erased after age adjustment or multivariate adjustment for confounders. The authors' results are compatible with a hypothesis that the main factor underlying the increased long-term mortality in women after myocardial infarction, besides older age, is diabetes mellitus.

  10. 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

  11. Thrombus aspiration in acute myocardial infarction: concepts, clinical trials, and current guidelines.

    PubMed

    Vandermolen, Sebastian; Marciniak, Maciej; Byrne, Jonathan; De Silva, Kalpa

    2016-05-01

    The pathogenesis that underlies acute myocardial infarction is complex and multifactorial. One of the most important components, however, is the role of thrombus formation following atherosclerotic plaque rupture, leading to sudden coronary occlusion and subsequent ischemia and infarction. Thrombus aspiration provides the opportunity of intracoronary clot extraction with the aim to improve coronary and myocardial perfusion, by reducing the risk of no-reflow secondary to distal embolization of thrombus. The utility of thrombus aspiration during primary percutaneous coronary intervention has been assessed in an increasing number of observational and randomized studies. This article reviews the contemporary data and provides insights into the validity of thrombus aspiration in the setting of acute myocardial infarction. PMID:26751424

  12. 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

  13. 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.

  14. Excimer laser angioplasty in acute myocardial infarction (the CARMEL multicenter trial).

    PubMed

    Topaz, On; Ebersole, Douglas; Das, Tony; Alderman, Edwin L; Madyoon, Hooman; Vora, Kishor; Baker, John D; Hilton, David; Dahm, Johannes B

    2004-03-15

    Patients with acute myocardial infarction (AMI) with thrombus-laden lesions constitute a revascularization challenge. Thrombus and atherosclerotic plaque absorb laser energy; thus, we studied the safety and efficacy of excimer laser in AMI. In a multicenter trial, 151 patients with AMI underwent excimer laser angioplasty. Baseline left ventricular ejection fraction was 44 +/- 13%, and 13% of patients were in cardiogenic shock. A saphenous vein graft was the target vessel in 21%. Quantitative coronary angiography and statistical analysis were performed by independent core laboratories. A 95% device success, 97% angiographic success, and 91% overall procedural success rate were recorded. Maximal laser gain was achieved in lesions with extensive thrombus burden (p <0.03 vs small burden). Thrombolysis In Myocardial Infarction (TIMI) trial flow increased significantly by laser: 1.2 +/- 1.1 to 2.8 +/- 0.5 (p <0.001), reaching a final 3.0 +/- 0.2 (p <0.001 vs baseline). Minimal luminal diameter increased by laser from 0.5 +/- 0.5 to 1.6 +/- 0.5 mm (mean +/- SD, p <0.001), followed by 2.7 +/- 0.6 mm after stenting (p <0.001 vs baseline and vs after laser). Laser decreased target stenosis from 83 +/- 17% to 52 +/- 15% (mean +/- SD, p <0.001 vs baseline), followed by 20 +/- 16% after stenting (p <0.001 vs baseline and vs after laser). Six patients (4%) died, each presented with cardiogenic shock. Complications included perforation (0.6%), dissection (5% major, 3% minor), acute closure (0.6%), distal embolization (2%), and bleeding (3%). In a multivariant regression model, absence of cardiogenic shock was a significant factor affecting procedural success. Thus, in the setting of AMI, gaining maximal thrombus dissolution in lesions with extensive thrombus burden, combined with a considerable increase in minimal luminal diameter and restoration of anterograde TIMI flow, support successful debulking by excimer laser. The presence of thrombus does not adversely affect procedural

  15. Novel Trial Designs: Lessons Learned from Thrombus Aspiration During ST-Segment Elevation Myocardial Infarction in Scandinavia (TASTE) Trial.

    PubMed

    Wachtell, Kristian; Lagerqvist, Bo; Olivecrona, Göran K; James, Stefan K; Fröbert, Ole

    2016-01-01

    In ST-elevation myocardial infarction (STEMI), thrombus material is often present in partial or total coronary occlusion of the coronary vessel. However, prior to the thrombus aspiration during ST-Segment Elevation Myocardial Infarction in Scandinavia (TASTE) trial, it remained unclear whether routine thrombus aspiration during percutaneous coronary intervention (PCI) treatment of STEMI would result in patients overall survival benefit. The TASTE trial was a multicenter, prospective, open-label, randomized, controlled clinical trial. In order to randomize patients to treatment and collect data, the infrastructure of a clinical population-based registry was used. Online data collection used the national comprehensive Swedish Coronary Angiography and Angioplasty Registry, a part of the SWEDEHEART registry. Monitoring and adjudication was done as part of the regular registry validation. There was no separate, dedicated monitoring or adjudication of endpoints. Included were 7244 patients with STEMI with chest pain and time of symptoms to hospital admission <24 h, in addition to new electrocardiographic ST-segment elevation or left bundle-branch block. Exclusion criteria were the need for emergency coronary artery bypass grafting. All-cause mortality at 30 days occurred in 2.8 % of the patients in the thrombus-aspiration group, as compared with 3.0 % in the PCI-only group (hazard ratio [HR] 0.94, 95 % confidence interval [CI] 0.72-1.22; p = 0.63). All-cause mortality at 1 year occurred in 5.3 % of the patients in the thrombus-aspiration group, as compared with 5.6 % in the PCI-only group (HR 0.94, 95 % CI 0.78-1.15; p = 0.57). No patients were lost to follow-up at 1 year. The incremental cost for trial execution was approximately US$ 300,000 or $50 per patient. Routine thrombus aspiration during PCI in patients with STEMI did not reduce the rate of all-cause mortality at 1 year. It is possible to design and conduct mega-trial at only small cost compared to a

  16. 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

  17. [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.

  18. Noninvasive risk stratification after myocardial infarction: rationale, current evidence and the need for definitive trials.

    PubMed

    Exner, Derek

    2009-06-01

    Despite advances in therapies for myocardial infarction (MI), death attributed to a cardiac arrest from ventricular tachycardia (VT) or ventricular fibrillation (VF) remains an important problem. The implantable cardioverter defibrillator (ICD) is effective in preventing death from VT/VF, but reliably identifying which post-MI patients would benefit from an ICD remains a major challenge. Beyond the initial post-MI period, the presence of significant left ventricular (LV) dysfunction, alone or in combination with the induction of sustained VT/VF during invasive testing, is the only proven means of selecting patients for a prophylactic ICD. However, these approaches identify only a fraction of those at risk. Furthermore, most patients with significant LV dysfunction after MI have a low, near-term risk of VT/VF. Noninvasive risk stratification tools have been developed to better identify patients likely to benefit from an ICD. To date, none of these tools has been proven useful in this regard. The factors leading to a cardiac arrest are complex, and a single test is unlikely to reliably predict risk. Noninvasive assessment of cardiac structure, conduction and repolarization along with autonomic modulation appear to be useful in predicting the risk of a cardiac arrest after MI, particularly when assessed in combination. However, randomized trials assessing the efficacy of ICD therapy in patients identified as being at risk are required. Until such data are available, significant LV dysfunction alone and in combination with the induction of VT/VF during invasive testing in the nonacute post-MI period remain the only proven methods to guide prophylactic ICD therapy. PMID:19521570

  19. Noninvasive risk stratification after myocardial infarction: Rationale, current evidence and the need for definitive trials

    PubMed Central

    Exner, Derek V

    2009-01-01

    Despite advances in therapies for myocardial infarction (MI), death attributed to a cardiac arrest from ventricular tachycardia (VT) or ventricular fibrillation (VF) remains an important problem. The implantable cardioverter defibrillator (ICD) is effective in preventing death from VT/VF, but reliably identifying which post-MI patients would benefit from an ICD remains a major challenge. Beyond the initial post-MI period, the presence of significant left ventricular (LV) dysfunction, alone or in combination with the induction of sustained VT/VF during invasive testing, is the only proven means of selecting patients for a prophylactic ICD. However, these approaches identify only a fraction of those at risk. Furthermore, most patients with significant LV dysfunction after MI have a low, near-term risk of VT/VF. Noninvasive risk stratification tools have been developed to better identify patients likely to benefit from an ICD. To date, none of these tools has been proven useful in this regard. The factors leading to a cardiac arrest are complex, and a single test is unlikely to reliably predict risk. Noninvasive assessment of cardiac structure, conduction and repolarization along with autonomic modulation appear to be useful in predicting the risk of a cardiac arrest after MI, particularly when assessed in combination. However, randomized trials assessing the efficacy of ICD therapy in patients identified as being at risk are required. Until such data are available, significant LV dysfunction alone and in combination with the induction of VT/VF during invasive testing in the nonacute post-MI period remain the only proven methods to guide prophylactic ICD therapy. PMID:19521570

  20. Noninvasive risk stratification after myocardial infarction: rationale, current evidence and the need for definitive trials.

    PubMed

    Exner, Derek

    2009-06-01

    Despite advances in therapies for myocardial infarction (MI), death attributed to a cardiac arrest from ventricular tachycardia (VT) or ventricular fibrillation (VF) remains an important problem. The implantable cardioverter defibrillator (ICD) is effective in preventing death from VT/VF, but reliably identifying which post-MI patients would benefit from an ICD remains a major challenge. Beyond the initial post-MI period, the presence of significant left ventricular (LV) dysfunction, alone or in combination with the induction of sustained VT/VF during invasive testing, is the only proven means of selecting patients for a prophylactic ICD. However, these approaches identify only a fraction of those at risk. Furthermore, most patients with significant LV dysfunction after MI have a low, near-term risk of VT/VF. Noninvasive risk stratification tools have been developed to better identify patients likely to benefit from an ICD. To date, none of these tools has been proven useful in this regard. The factors leading to a cardiac arrest are complex, and a single test is unlikely to reliably predict risk. Noninvasive assessment of cardiac structure, conduction and repolarization along with autonomic modulation appear to be useful in predicting the risk of a cardiac arrest after MI, particularly when assessed in combination. However, randomized trials assessing the efficacy of ICD therapy in patients identified as being at risk are required. Until such data are available, significant LV dysfunction alone and in combination with the induction of VT/VF during invasive testing in the nonacute post-MI period remain the only proven methods to guide prophylactic ICD therapy.

  1. Intracoronary autologous mononucleated bone marrow cell infusion for acute myocardial infarction: results of the randomized multicenter BONAMI trial

    PubMed Central

    Roncalli, Jérôme; Mouquet, Frédéric; Piot, Christophe; Trochu, Jean-Noel; Le Corvoisier, Philippe; Neuder, Yannick; Le Tourneau, Thierry; Agostini, Denis; Gaxotte, Virginia; Sportouch, Catherine; Galinier, Michel; Crochet, Dominique P.; Teiger, Emmanuel; Richard, Marie-Jeanne; Polge, Anne-Sophie; Beregi, Jean-Paul; Manrique, Alain; Carrie, Didier; Susen, Sophie; Klein, Bernard; Parini, Angelo; Lamirault, Guillaume; Croisille, Pierre; Rouard, Hélène; Bourin, Philippe; Nguyen, Jean-Michel; Delasalle, Béatrice; Vanzetto, Gérald; Van Belle, Eric; Lemarchand, Patricia F.

    2011-01-01

    Aims Intracoronary administration of autologous bone marrow cells (BMCs) leads to a modest improvement in cardiac function, but the effect on myocardial viability is unknown. The aim of this randomized multicenter study was to evaluate the effect of BMC therapy on myocardial viability in patients with decreased left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI) and to identify predictive factors for improvement of myocardial viability. Methods and Results One-hundred one patients with AMI and successful reperfusion, LVEF ≤45%, and decreased myocardial viability (resting Tl201-SPECT) were randomized to either a control group (n=49) or a BMC group (n=52). Primary endpoint was improvement of myocardial viability 3 months after AMI. Baseline mean LVEF measured by radionuclide angiography was 36.3 ± 6.9%. BMC infusion was performed 9.3 ± 1.7 days after AMI. Myocardial viability improved in 16/47 (34%) patients in the BMC group compared to 7/43 (16%) in the control group (p = 0.06). The number of non-viable segments becoming viable was 0.8 ± 1.1 in the control group and 1.2 ± 1.5 in the BMC group (p = 0.13). Multivariate analysis including major post-AMI prognostic factors showed a significant improvement of myocardial viability in BMC vs. control group (p=0.03). Moreover, a significant adverse role for active smoking (p=0.04) and a positive trend for microvascular obstruction (p=0.07) were observed. Conclusions Intracoronary autologous BMC administration to patients with decreased LVEF after AMI was associated with improvement of myocardial viability in multivariate –but not in univariate – analysis. A large multicenter international trial is warranted to further document the efficacy of cardiac cell therapy and better define a group of patients that will benefit from this therapy. PMID:21127322

  2. Intracoronary cardiosphere-derived cells for heart regeneration after myocardial infarction (CADUCEUS): a prospective, randomised phase 1 trial

    PubMed Central

    Makkar, Raj R; Smith, Rachel R; Cheng, Ke; Malliaras, Konstantinos; Thomson, Louise E J; Berman, Daniel; Czer, Lawrence S C; Marbán, Linda; Mendizabal, Adam; Johnston, Peter V; Russell, Stuart D; Schuleri, Karl H; Lardo, Albert C; Gerstenblith, Gary; Marbán, Eduardo

    2015-01-01

    Summary Background Cardiosphere-derived cells (CDCs) reduce scarring after myocardial infarction, increase viable myocardium, and boost cardiac function in preclinical models. We aimed to assess safety of such an approach in patients with left ventricular dysfunction after myocardial infarction. Methods In the prospective, randomised CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction (CADUCEUS) trial, we enrolled patients 2–4 weeks after myocardial infarction (with left ventricular ejection fraction of 25–45%) at two medical centres in the USA. An independent data coordinating centre randomly allocated patients in a 2:1 ratio to receive CDCs or standard care. For patients assigned to receive CDCs, autologous cells grown from endomyocardial biopsy specimens were infused into the infarct-related artery 1·5–3 months after myocardial infarction. The primary endpoint was proportion of patients at 6 months who died due to ventricular tachycardia, ventricular fibrillation, or sudden unexpected death, or had myocardial infarction after cell infusion, new cardiac tumour formation on MRI, or a major adverse cardiac event (MACE; composite of death and hospital admission for heart failure or non-fatal recurrent myocardial infarction). We also assessed preliminary efficacy endpoints on MRI by 6 months. Data analysers were masked to group assignment. This study is registered with ClinicalTrials.gov, NCT00893360. Findings Between May 5, 2009, and Dec 16, 2010, we randomly allocated 31 eligible participants of whom 25 were included in a per-protocol analysis (17 to CDC group and eight to standard of care). Mean baseline left ventricular ejection fraction (LVEF) was 39% (SD 12) and scar occupied 24% (10) of left ventricular mass. Biopsy samples yielded prescribed cell doses within 36 days (SD 6). No complications were reported within 24 h of CDC infusion. By 6 months, no patients had died, developed cardiac tumours, or MACE in either group. Four

  3. 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

  4. 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.

  5. N-Acetylcysteine Administration Prevents Nonthyroidal Illness Syndrome in Patients With Acute Myocardial Infarction: A Randomized Clinical Trial

    PubMed Central

    Vidart, Josi; Wajner, Simone Magagnin; Leite, Rogério Sarmento; Manica, André; Schaan, Beatriz D.; Larsen, P. Reed

    2014-01-01

    Context: The acute phase of the nonthyroidal illness syndrome (NTIS) is characterized by low T3 and high rT3 levels, affecting up to 75% of critically ill patients. Oxidative stress has been implicated as a causative factor of the disturbed peripheral thyroid hormone metabolism. Objective: The objective of the study was to investigate whether N-acetylcysteine (NAC), a potent intracellular antioxidant, can prevent NTIS in patients with acute myocardial infarction. Design: This was a randomized, multicenter clinical trial. Settings: Consecutive patients admitted to the emergency and intensive care units of two tertiary hospitals in southern Brazil were recruited. Patients and intervention included 67 patients were randomized to receive NAC or placebo during 48 hours. Baseline characteristics and blood samples for thyroid hormones and oxidative parameters were collected. Main Outcome: Variation of serum T3 and rT3 levels was measured. Results: Baseline characteristics were similar between groups (all P > .05). T3 levels decreased in the placebo group at 12 hours of follow-up (P = .002) but not in NAC-treated patients (P = .10). Baseline rT3 levels were elevated in both groups and decreased over the initial 48 hours in the NAC-treated patients (P = .003) but not in the control group (P = .75). The free T4 and TSH levels were virtually identical between the groups throughout the study period (P > .05). Measurement of total antioxidant status and total carbonyl content demonstrated that oxidative balance was deranged in acute myocardial infarction patients, whereas NAC corrected these alterations (P < .001). Conclusions: NAC administration prevents the derangement in thyroid hormone concentrations commonly occurring in the acute phase of acute myocardial infarction, indicating that oxidative stress is involved in the NTIS pathophysiology. PMID:25148231

  6. 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

  7. Beta blockade during and after myocardial infarction: an overview of the randomized trials.

    PubMed

    Yusuf, S; Peto, R; Lewis, J; Collins, R; Sleight, P

    1985-01-01

    Long-term beta blockade for perhaps a year or so following discharge after an MI is now of proven value, and for many such patients mortality reductions of about 25% can be achieved. No important differences are clearly apparent among the benefits of different beta blockers, although some are more convenient than others (or have slightly fewer side effects), and it appears that those with appreciable intrinsic sympathomimetic activity may confer less benefit. If monitored, the side effects of long-term therapy are not a major problem, as when they occur they are easily reversible by changing the beta blocker or by discontinuation of treatment. By contrast, although very early IV short-term beta blockade can definitely limit infarct size, more reliable information about the effects of such treatment on mortality will not be available until a large trial (ISIS) reports later this year, with data on some thousands of patients entered within less than 4 hours of the onset of pain. Our aim has been not only to review the 65-odd randomized beta blocker trials but also to demonstrate that when many randomized trials have all applied one general approach to treatment, it is often not appropriate to base inference on individual trial results. Although there will usually be important differences from one trial to another (in eligibility, treatment, end-point assessment, and so on), physicians who wish to decide whether to adopt a particular treatment policy should try to make their decision in the light of an overview of all these related randomized trials and not just a few particular trial results. Although most trials are too small to be individually reliable, this defect of size may be rectified by an overview of many trials, as long as appropriate statistical methods are used. Fortunately, robust statistical methods exist--based on direct, unweighted summation of one O-E value from each trial--that are simple for physicians to use and understand yet provide full

  8. Stem cell mobilisation by granulocyte-colony stimulating factor in patients with acute myocardial infarction. Long-term results of the REVIVAL-2 trial.

    PubMed

    Steppich, Birgit; Hadamitzky, Martin; Ibrahim, Tareq; Groha, Philip; Schunkert, Heribert; Laugwitz, Karl-Ludwig; Kastrati, Adnan; Ott, Ilka

    2016-04-01

    Treatment with granulocyte-colony stimulating factor (G-CSF) mobilises cells from the bone marrow to the peripheral blood. Previous preclinical and early clinical trials may suggest that treatment with G-CSF leads to improved myocardial perfusion and function in acute or chronic ischaemic heart disease. In the REVIVAL-2 study we found that stem cell mobilisation by G-CSF does not influence infarct size, left ventricular function and coronary restenosis in patients with acute myocardial infarction (MI) that underwent successful percutaneous coronary intervention. The objective of the present analysis was to assess the impact of G-CSF treatment on seven-year clinical outcomes from the REVIVAL-2 trial. In the randomized, double-blind, placebo-controlled REVIVAL-2 study, 114 patients with the diagnosis of acute myocardial infarction were enrolled five days after successful reperfusion by percutaneous coronary intervention. Patients were assigned to receive 10 µg/kg G-CSF (n=56) or placebo (n=58) for five days. The primary endpoint for this long-term outcome analysis was the composite of death, myocardial infarction or stroke seven years after randomisation. The endpoint occurred in 14.3 % of patients in the G-CSF group versus 17.2 % assigned to placebo (p=0.67). The combined incidence of death or myocardial infarction occurred in 14.3 % of the patients assigned to G-CSF and 15.5 % of the patients assigned to placebo (p=0.85). In conclusion, these long-term follow-up data show that G-CSF does not improve clinical outcomes of patients with acute myocardial infarction.

  9. 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

  10. 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

  11. 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.

  12. 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

  13. 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

  14. Outcomes after thrombus aspiration for ST elevation myocardial infarction: 1-year follow-up of the prospective randomised TOTAL trial

    PubMed Central

    Jolly, Sanjit S; Cairns, John A; Yusuf, Salim; Rokoss, Michael J; Gao, Peggy; Meeks, Brandi; Kedev, Sasko; Stankovic, Goran; Moreno, Raul; Gershlick, Anthony; Chowdhary, Saqib; Lavi, Shahar; Niemela, Kari; Bernat, Ivo; Cantor, Warren J; Cheema, Asim N; Steg, Philippe Gabriel; Welsh, Robert C; Sheth, Tej; Bertrand, Olivier F; Avezum, Alvaro; Bhindi, Ravinay; Natarajan, Madhu K; Horak, David; Leung, Raymond C M; Kassam, Saleem; Rao, Sunil V; El-Omar, Magdi; Mehta, Shamir R; Velianou, James L; Pancholy, Samir; Džavík, Vladimír

    2016-01-01

    Summary Background Two large trials have reported contradictory results at 1 year after thrombus aspiration in ST elevation myocardial infarction (STEMI). In a 1-year follow-up of the largest randomised trial of thrombus aspiration, we aimed to clarify the longer-term benefits, to help guide clinical practice. Methods The trial of routine aspiration ThrOmbecTomy with PCI versus PCI ALone in Patients with STEMI (TOTAL) was a prospective, randomised, investigator-initiated trial of routine manual thrombectomy versus percutaneous coronary intervention (PCI) alone in 10 732 patients with STEMI. Eligible adult patients (aged ≥18 years) from 87 hospitals in 20 countries were enrolled and randomly assigned (1:1) within 12 h of symptom onset to receive routine manual thrombectomy with PCI or PCI alone. Permuted block randomisation (with variable block size) was done by a 24 h computerised central system, and was stratified by centre. Participants and investigators were not masked to treatment assignment. The trial did not show a difference at 180 days in the primary outcome of cardiovascular death, myocardial infarction, cardiogenic shock, or heart failure. However, the results showed improvements in the surrogate outcomes of ST segment resolution and distal embolisation, but whether or not this finding would translate into a longer term benefit remained unclear. In this longer-term follow-up of the TOTAL study, we report the results on the primary outcome (cardiovascular death, myocardial infarction, cardiogenic shock, or heart failure) and secondary outcomes at 1 year. Analyses of the primary outcome were by modified intention to treat and only included patients who underwent index PCI. This trial is registered with ClinicalTrials.gov, number NCT01149044. Findings Between Aug 5, 2010, and July 25, 2014, 10 732 eligible patients were enrolled and randomly assigned to thrombectomy followed by PCI (n=5372) or to PCI alone (n=5360). After exclusions of patients who did not

  15. Multicenter reperfusion trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: controlled comparison with intracoronary streptokinase.

    PubMed

    Anderson, J L; Rothbard, R L; Hackworthy, R A; Sorensen, S G; Fitzpatrick, P G; Dahl, C F; Hagan, A D; Browne, K F; Symkoviak, G P; Menlove, R L

    1988-06-01

    The recent establishment of a firm therapeutic role for reperfusion in acute myocardial infarction has stimulated interest in the development of more ideal thrombolytic agents. Anisoylated plasminogen streptokinase activator complex (APSAC) is a new plasminogen activator possessing properties that are promising for intravenous thrombolytic application in acute myocardial infarction. To assess the reperfusion potential of intravenous APSAC, a multi-center, angiographically controlled reperfusion trial was performed. An approved thrombolytic regimen of intracoronary streptokinase served as a control. Consenting patients with clinical and electrocardiographic signs of acute myocardial infarction were studied angiographically and 240 qualifying patients with documented coronary occlusion (flow grade 0 or 1) were randomized to treatment in less than 6 h of symptom onset (mean 3.4 h, range 0.4 to 6.0) with either intravenous APSAC (30 U in 2 to 4 min) or intracoronary streptokinase (160,000 U over 60 min). Both groups also received heparin for greater than or equal to 24 h. Reperfusion was evaluated angiographically over 90 min and success was defined as advancement of grade 0 or 1 to grade 2 or 3 flow. Rates of reperfusion for the two treatment regimens were 51% (59 of 115) at 90 min after intravenous APSAC and 60% (67 of 111) after 60 min of intracoronary streptokinase (p less than or equal to 0.18). Reperfusion at any time within the 90 min was observed in 55 and 64%, respectively (p less than or equal to 0.16). Time to reperfusion occurred at 43 +/- 23 min after intravenous and 31 +/- 17 min after intracoronary therapy. The success of intravenous therapy was dependent on the time to treatment: 60% of APSAC patients treated within 4 h exhibited reperfusion compared with 33% of those treated after 4 h (p less than or equal to 0.01). Reperfusion rates were also dependent on initial flow grade (p less than or equal to 0.0001): 48% (81 of 168) for grade 0 (APSAC = 43

  16. Qi-Shen-Yi-Qi Dripping Pills for the Secondary Prevention of Myocardial Infarction: A Randomised Clinical Trial

    PubMed Central

    Shang, Hongcai; Zhang, Junhua; Yao, Chen; Liu, Baoyan; Gao, Xiumei; Ren, Ming; Cao, Hongbao; Dai, Guohua; Weng, Weiliang; Zhu, Sainan; Wang, Hui; Xu, Hongjuan; Zhang, Boli

    2013-01-01

    Background. Several types of drugs have been recommended for the secondary prevention of myocardial infarction (MI). However, these conventional strategies have several limitations, such as low adherence, high cost, and side effects during long time use. Novel approaches to this problem are still needed. This trial aimed to test the effectiveness and safety of Qi-Shen-Yi-Qi Dripping Pills (QSYQ), a multi-ingredient Chinese patent medicine, for the secondary prevention of MI. Methods and Findings. A total of 3505 eligible patients were randomly assigned to QSYQ group (1746 patients) or aspirin group (1759). Patients took their treatments for 12 months. The final follow-up visit took place 6 months after the end of the trial drugs. The 12-month and 18-month estimated incidences of the primary outcome were 2.98% and 3.67%, respectively, in the QSYQ group. The figures were 2.96% and 3.81% in the aspirin group. No significant difference was identified between the groups. Conclusions. This trial did not show significant difference of primary and secondary outcomes between aspirin and QSYQ in patients who have had an MI. Though inconclusive, the result suggests that QSYQ has similar effects to aspirin in the secondary prevention of MI. PMID:23935677

  17. 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

  18. 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

  19. Prognostic evaluation by clinical exercise test scores in patients treated with primary percutaneous coronary intervention or fibrinolysis for acute myocardial infarction (a Danish Trial in Acute Myocardial Infarction-2 Sub-Study).

    PubMed

    Valeur, Nana; Clemmensen, Peter; Grande, Peer; Saunamäki, Kari

    2007-10-01

    The prognostic accuracy of exercise testing after myocardial infarction is low, and different models have been proposed to enhance the predictive value for subsequent mortality. This study tested a simple score against 3 established scores. Patients with ST-elevation myocardial infarctions were randomized in the Danish Trial in Acute Myocardial Infarction-2 (DANAMI-2) to either primary percutaneous coronary intervention or fibrinolysis with predischarge exercise testing. Clinical and exercise test data were collected prospectively and were available for 1,115 patients. A simple score was derived, awarding 1 point for history or new signs of heart failure, 1 point for a left ventricular ejection fraction <40%, 1 point for age >65 years in men and age >70 years in women, and 1 point for exercise capacity <5 METs in men and exercise capacity <4 METs in women. This DANAMI score was compared with the Veterans Affairs Medical Center score, the Duke treadmill score, and the Gruppo Italiano per lo Studio Della Sopravvivenza nell'Infarto Miocardico-2 (GISSI-2) score in multivariate Cox models and receiver-operating characteristic plots. All scoring systems were predictive of adverse outcomes. The DANAMI score performed better, with greater chi-square values (142 vs 53 to 88 for the prediction of death). Areas under the receiver-operating characteristic curves were compared and were larger for the DANAMI score (C-statistic 0.79 vs 0.71 to 0.74 for the other tests regarding mortality). The DANAMI score stratified patients into a small high-risk group (8% of the population with 43% mortality in 6 years), an intermediate-risk group (13% with 16% mortality in 6 years), and a low-risk group (79% with 4% mortality in 6 years). In conclusion, a simple exercise test score composed of age, METs, heart failure, and a left ventricular ejection fraction <40% seems to outperform the Duke treadmill score, Veterans Affairs Medical Center score, and GISSI-2 score in risk stratifying

  20. [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.

  1. 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…

  2. 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

  3. [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.

  4. Primary stent implantation is superior to balloon angioplasty in acute myocardial infarction: final results of the primary angioplasty versus stent implantation in acute myocardial infarction (PASTA) trial. PASTA Trial Investigators.

    PubMed

    Saito, S; Hosokawa, G; Tanaka, S; Nakamura, S

    1999-11-01

    Several studies have shown that stent implantations in acute myocardial infarction (AMI) result in better short- and long-term outcomes than primary balloon angioplasty. These results, however, have not been ascertained in randomized trials. We randomized 136 patients out of 208 patients with AMI within 12 hr from onset into two groups: 69 patients with primary balloon angioplasty (POBA group) and 67 patients with primary stent implantation (STENT group). We compared the incidences of major cardiac events (repeat MI, target lesion revascularization, and cardiac death) and angiographic parameters during hospitalization and follow-up periods up to 12 months in these two groups. There was no significant difference in the reperfusion success rates. The incidences of major cardiac events were lower in the STENT group than in the POBA group during hospitalization, the first 6 months and 12 months (6% vs. 19%, P = 0.023; 21% vs. 46%, P < 0.0001; 22% vs. 49%, P = 0.0011). Minimum lumen diameters were significantly bigger in the STENT group than the POBA group at predischarge angiogram and 6-month follow-up (2.85 +/- 0.62 vs. 2.08 +/- 0.82 mm, P < 0.0001; 2.24 +/- 0.64 vs. 1.72 +/- 0.76, P = 0.002). Restenosis rates at 6-month follow-up were significantly lower in the STENT group than in the POBA group (17% vs. 37.5%, P = 0.02). In selected patients with AMI, primary stent implantation results in a lower incidence of major cardiac events during the first 12 months, postprocedure, and less frequent 6-month restenosis than primary balloon angioplasty.

  5. 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.

  6. 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

  7. 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

  8. 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

  9. 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.

  10. [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.

  11. 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.

  12. 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

  13. The effectiveness of antioxidant vitamins C and E in reducing myocardial infarct size in patients subjected to percutaneous coronary angioplasty (PREVEC Trial): study protocol for a pilot randomized double-blind controlled trial

    PubMed Central

    2014-01-01

    Background Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Oxidative stress has been involved in the ischemia-reperfusion injury in AMI. It has been suggested that reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented.Therefore, we propose that antioxidant reinforcement through vitamins C and E supplementation should protect against the ischemia-reperfusion damage, thus decreasing infarct size. The PREVEC Trial (Prevention of reperfusion damage associated with percutaneous coronary angioplasty following acute myocardial infarction) seeks to evaluate whether antioxidant vitamins C and E reduce infarct size in patients subjected to percutaneous coronary angioplasty after AMI. Methods/Design This is a randomized, 1:1, double-blind, placebo-controlled clinical trial. The study takes place at two centers in Chile: University of Chile Clinical Hospital and San Borja Arriarán Clinical Hospital. The subjects will be 134 adults with acute myocardial infarction with indication for percutaneous coronary angioplasty. This intervention is being performed as a pilot study, involving high-dose vitamin C infusion plus oral administration of vitamin E (Vitamin-treatment group) or placebo (Control group) during the angioplasty procedure. Afterward, the Vitamin-treatment group receives oral doses of vitamins C and E, and the Control group receives placebo for 84 days after coronary angioplasty. Primary outcome is infarct size, assessed by cardiac magnetic resonance (CMR), measured 6 and 84 days after coronary angioplasty. Secondary outcomes are ejection fraction, measured 6 and 84 days after coronary angioplasty with CMR, and biomarkers for oxidative stress, antioxidant status, heart damage, and inflammation, which will be measured at baseline, at the onset of reperfusion, 6 to 8 hours after revascularization, and at hospital discharge. Discussion The ischemia-reperfusion event

  14. Impact of pre-procedural cardiopulmonary instability in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention (from the Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction Trial).

    PubMed

    Brener, Sorin J; Brodie, Bruce R; Guerchicoff, Alejandra; Witzenbichler, Bernhard; Guagliumi, Giulio; Xu, Ke; Mehran, Roxana; Stone, Gregg W

    2014-10-01

    Rapid reperfusion with primary percutaneous coronary intervention improves survival in patients with ST-segment elevation myocardial infarction. Preprocedural cardiopulmonary instability and adverse events (IAE) may delay reperfusion time and worsen prognosis. The aim of this study was to evaluate the relation between preprocedural cardiopulmonary IAE, door-to-balloon time (DBT), and outcomes in the Harmonizing Outcomes With Revascularization and Stents in AMI (HORIZONS-AMI) trial. Preprocedural cardiopulmonary IAE included sustained ventricular or supraventricular tachycardia or fibrillation requiring cardioversion or defibrillation, heart block or bradycardia requiring pacemaker implantation, severe hypotension requiring vasopressors or intra-aortic balloon counterpulsation, respiratory failure requiring mechanical ventilation, and cardiopulmonary resuscitation. Three-year outcomes of patients with and without IAE according to DBT were compared. Among 3,602 patients, 159 (4.4%) had ≥1 IAE. DBT did not differ significantly in patients with and without IAE; however, patients with IAE were less likely to have Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow after percutaneous coronary intervention. Mortality at 3 years was significantly higher in patients with versus those without IAE (17.0% vs 6.3%, p<0.0001), and IAE was an independent predictor of mortality, whereas DBT was not. However, a significant interaction was present such that 3-year mortality was reduced in patients with DBT<99 minutes (the median) versus ≥99 minutes to a greater extent in patients with IAE (9.9% vs 20.7%, hazard ratio 0.43, 95% confidence interval 0.16 to 1.16) compared with those without IAE (5.0% vs 7.2%, hazard ratio 0.69, 95% confidence interval 0.50 to 0.95) (p for interaction=0.004). In conclusion, IAE before PCI is an independent predictor of death and identifies a high-risk group in whom faster reperfusion may be particularly important to improve survival.

  15. Informed shared decision-making programme on the prevention of myocardial infarction in type 2 diabetes: a randomised controlled trial

    PubMed Central

    Buhse, Susanne; Mühlhauser, Ingrid; Heller, Tabitha; Kuniss, Nadine; Müller, Ulrich Alfons; Kasper, Jürgen; Lehmann, Thomas; Lenz, Matthias

    2015-01-01

    Objective To evaluate an informed shared decision-making programme (ISDM-P) for people with type 2 diabetes under high fidelity conditions. Design Randomised, single-blinded trial with sham control intervention and follow-up of 6 months. Setting Single-centre diabetes clinic providing care according to the national disease management programme in Germany. Participants 154 people with type 2 diabetes without diagnosis of ischaemic heart disease or stroke. Interventions The ISDM-P is executed by diabetes educators. Core component is a patient decision aid on the prevention of myocardial infarction supplemented by a 90 min group teaching session. The structurally equivalent control intervention addresses stress issues. Main outcome measures Primary outcome was risk comprehension, including realistic expectations about benefits and harms of interventions. It was assessed by a 12-item questionnaire after the teaching session when patients set and prioritise their treatment goals. Key secondary outcome was adherence to treatment goals, operationalised as achievement of individual goals and medication uptake. ISDM-P teaching sessions were video-taped to monitor intervention fidelity. Results 72 of 77 ISDM-P and 71 of 77 control patients completed the questionnaire (score 0–12). ISDM-P patients achieved higher levels of risk comprehension, mean score 8.25 vs 2.62, difference 5.63 (95% CI 4.82 to 6.44), and realistic expectations (score 0–6), 4.51 vs 0.85, 3.67 (3.23 to 4.11). More ISDM-P patients wished to take statins, 59.2% vs 30.4%, 28.7% (12.9% to 44.5%); more prioritised blood pressure control, 51.4% vs 25.7%, and fewer intensive glucose control, 33.3% vs 60%, p=0.002. More ISDM-P patients achieved their glycated haemoglobin goals, 95.8% vs 85.7%, 10.1% (0.6% to 19.5%). Achievement of prioritised goals and medication uptake were comparable between groups. Conclusions The ISDM-P on preventive measures in type 2 diabetes was effective under high fidelity

  16. 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

  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. Rationale and design of a secondary prevention trial of lowering normal plasma cholesterol levels after acute myocardial infarction: the Cholesterol and Recurrent Events trial (CARE)

    PubMed

    Sacks, F M; Pfeffer, M A; Moye', L; Brown, L E; Hamm, P; Cole, T G; Hawkins, C M; Braunwald, E

    1991-12-01

    Recent clinical trials of primary and secondary prevention of cardiovascular disease have demonstrated that lowering plasma cholesterol decreases the incidence of coronary heart disease in patients with elevated plasma cholesterol. However, it is not known whether patients with established coronary artery disease and normal plasma cholesterol can be benefited. Several previous prevention trials reviewed in this report found that patients who had plasma cholesterol levels at baseline in the upper portion of the eligibility range (e.g., greater than 240 mg/dl) received greater benefit from hypolipidemic diet or drug therapy than patients who had lower plasma cholesterol levels at baseline. The recent availability of drugs that are more potent and less prone to cause adverse reactions than previous regimens permits this important question to be addressed. The Cholesterol and Recurrent Events trial is testing whether pravastatin, a hydroxymethylglutaryl coenzyme A reductase inhibitor, will decrease the sum of fatal coronary heart disease and nonfatal myocardial infarction (MI) in patients who have recovered from a MI and who have normal total cholesterol levels. Fatal cardiovascular disease and total mortality are important secondary end points. The trial is enrolling 4,000 men and women from 80 centers throughout North America, age 21 to 75 years, who have survived MI for 3 to 20 months, who have plasma total cholesterol less than 240 mg/dl (6.2 mmol/liter) and low-density cholesterol of 115 to 174 mg/dl (3.0 to 4.5 mmol/liter), and who are representative of the general population of patients with MI. Patients are randomized to either active or inactive drug therapy. Active therapy consists of pravastatin, 40 mg/day, designed to achieve an average decrease in low-density lipoprotein cholesterol of approximately 30%, and an increase in high-density lipoprotein of 5%. The average duration of follow-up will be greater than or equal to 5 years. To protect against a lower

  19. [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

  20. 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

  1. Strategies to attenuate micro-vascular obstruction during P-PCI: the randomized reperfusion facilitated by local adjunctive therapy in ST-elevation myocardial infarction trial

    PubMed Central

    Nazir, Sheraz A.; McCann, Gerry P.; Greenwood, John P.; Kunadian, Vijay; Khan, Jamal N.; Mahmoud, Islam Z.; Blackman, Daniel J.; Been, Martin; Abrams, Keith R.; Shipley, Lorraine; Wilcox, Robert; Adgey, A.A. Jennifer; Gershlick, Anthony H.

    2016-01-01

    Background Microvascular obstruction (MVO) following primary percutaneous coronary intervention (PPCI) treatment of ST-segment elevation myocardial infarction (STEMI) contributes to infarct expansion, left ventricular (LV) remodelling, and worse clinical outcomes. The REFLO-STEMI trial tested whether intra-coronary (IC) high-dose adenosine or sodium nitroprusside (SNP) reduce infarct size and/or MVO determined by cardiac magnetic resonance (CMR). Methods and results REFLO-STEMI, a prospective, open-label, multi-centre trial with blinded endpoints, randomized (1:1:1) 247 STEMI patients with single vessel disease presenting within 6 h of symptom onset to IC adenosine (2–3 mg total) or SNP (500 μg total) immediately following thrombectomy and again following stenting, or to standard PPCI. The primary endpoint was infarct size % LV mass (%LVM) on CMR undertaken 24–96 h after PPCI (n = 197). Clinical follow-up was to 6 months. There was no significant difference in infarct size (%LVM, median, interquartile range, IQR) between adenosine (10.1, 4.7–16.2), SNP (10.0, 4.2–15.8), and control (8.3, 1.9–14.0), P = 0.062 and P = 0.160, respectively, vs. control. MVO (% LVM, median, IQR) was similar across groups (1.0, 0.0–3.7, P = 0.205 and 0.6, 0.0–2.4, P = 0.244 for adenosine and SNP, respectively, vs. control 0.3, 0.0–2.8). On per-protocol analysis, infarct size (%LV mass, 12.0 vs. 8.3, P = 0.031), major adverse cardiac events (hazard ratio, HR, 5.39 [1.18–24.60], P = 0.04) at 30 days and 6 months (HR 6.53 [1.46–29.2], P = 0.01) were increased and ejection fraction reduced (42.5 ± 7.2% vs. 45.7 ± 8.0%, P = 0.027) in adenosine-treated patients compared with control. Conclusions High-dose IC adenosine and SNP during PPCI did not reduce infarct size or MVO measured by CMR. Furthermore, adenosine may adversely affect mid-term clinical outcome. Clinical Trial registration ClinicalTrials.gov Identifier: NCT01747174; https://clinicaltrials.gov/ct2/show

  2. Computational modeling of acute myocardial infarction.

    PubMed

    Sáez, P; Kuhl, E

    2016-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size. PMID:26583449

  3. 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

  4. Clinical benefit of adenosine as an adjunct to reperfusion in ST-elevation myocardial infarction patients: An updated meta-analysis of randomized controlled trials

    PubMed Central

    Bulluck, Heerajnarain; Sirker, Alex; Loke, Yoon K.; Garcia-Dorado, David; Hausenloy, Derek J.

    2016-01-01

    Background Adenosine administered as an adjunct to reperfusion can reduce coronary no-reflow and limit myocardial infarct (MI) size in ST-segment elevation myocardial infarction (STEMI) patients. Whether adjunctive adenosine therapy can improve clinical outcomes in reperfused STEMI patients is not clear and is investigated in this meta-analysis of 13 randomized controlled trials (RCTs). Methods We performed an up-to-date search for all RCTs investigating adenosine as an adjunct to reperfusion in STEMI patients. We calculated pooled relative risks using a fixed-effect meta-analysis assessing the impact of adjunctive adenosine therapy on major clinical endpoint including all-cause mortality, non-fatal myocardial infarction, and heart failure. Surrogate markers of reperfusion were also analyzed. Results 13 RCTs (4273 STEMI patients) were identified and divided into 2 subgroups: intracoronary adenosine versus control (8 RCTs) and intravenous adenosine versus control (5 RCTs). In patients administered intracoronary adenosine, the incidence of heart failure was significantly lower (risk ratio [RR] 0.44 [95% CI 0.25–0.78], P = 0.005) and the incidence of coronary no-reflow was reduced (RR for TIMI flow<3 postreperfusion 0.68 [95% CI 0.47–0.99], P = 0.04). There was no difference in heart failure incidence in the intravenous adenosine group but most RCTs in this subgroup were from the thrombolysis era. There was no difference in non-fatal MI or all-cause mortality in both subgroups. Conclusion We find evidence of improved clinical outcome in terms of less heart failure in STEMI patients administered intracoronary adenosine as an adjunct to reperfusion. This finding will need to be confirmed in a large adequately powered prospective RCT. PMID:26402450

  5. 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

  6. [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.

  7. 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

  8. Usefulness of local delivery of thrombolytics before thrombectomy in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention (the delivery of thrombolytics before thrombectomy in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention [DISSOLUTION] randomized trial).

    PubMed

    Greco, Cesare; Pelliccia, Francesco; Tanzilli, Gaetano; Tinti, Maria Denitza; Salenzi, Paola; Cicerchia, Cristina; Schiariti, Michele; Franzoni, Ferdinando; Speziale, Giuseppe; Gallo, Pietro; Gaudio, Carlo

    2013-09-01

    Thrombus aspiration during percutaneous coronary intervention can result in improved rates of normal epicardial flow and myocardial perfusion, but several unmet needs remain. The purpose of the Delivery of thrombolytIcs before thrombectomy in patientS with ST-segment elevatiOn myocardiaL infarction Undergoing primary percuTaneous coronary interventION (DISSOLUTION) trial was to evaluate the hypothesis that local delivery of thrombolytics can enhance the efficacy of thrombus aspiration in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. A total of 102 patients with ST-segment elevation myocardial infarction and angiographic evidence of massive thrombosis in the culprit artery were randomly assigned to receive a local, intrathrombus bolus of 200,000 U of urokinase (n = 51) or saline solution (n = 51) by way of an infusion microcatheter, followed by manual aspiration thrombectomy. The end points included the final Thrombolysis In Myocardial Infarction flow grade and frame count, myocardial blush grade, 60-minute ST-segment resolution >70%, and major adverse cardiac and cerebrovascular events, defined as the death, reinfarction, stroke, or clinically driven target vessel revascularization at 6 months. The use of intrathrombus urokinase was associated with a significantly higher incidence of Thrombolysis In Myocardial Infarction flow grade 3 (90% vs 66%, p = 0.008) and lower postpercutaneous coronary intervention Thrombolysis In Myocardial Infarction frame count (19 ± 15 vs 25 ± 17, p = 0.033). The postprocedural myocardial perfusion was significantly increased with the use of urokinase (myocardial blush grade 2 or 3, 68% vs 45%, p = 0.028), with more patients showing ST-segment resolution >70% (82% vs 55%, p = 0.006). At 6 months of follow-up, the patients treated with intrathrombus urokinase showed a better major adverse cardiac event-free survival (6% vs 21%; log-rank p = 0.044). In conclusion, local

  9. 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.

  10. 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

  11. 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

  12. 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)

  13. [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.

  14. 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.

  15. 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

  16. 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.

  17. 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.

  18. 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

  19. 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

  20. 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.

  1. Therapeutic hypothermia for the treatment of acute myocardial infarction-combined analysis of the RAPID MI-ICE and the CHILL-MI trials.

    PubMed

    Erlinge, David; Götberg, Matthias; Noc, Marko; Lang, Irene; Holzer, Michael; Clemmensen, Peter; Jensen, Ulf; Metzler, Bernhard; James, Stefan; Bøtker, Hans Erik; Omerovic, Elmir; Koul, Sasha; Engblom, Henrik; Carlsson, Marcus; Arheden, Håkan; Östlund, Ollie; Wallentin, Lars; Klos, Bradley; Harnek, Jan; Olivecrona, Göran K

    2015-06-01

    In the randomized rapid intravascular cooling in myocardial infarction as adjunctive to percutaneous coronary intervention (RAPID MI-ICE) and rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction CHILL-MI studies, hypothermia was rapidly induced in conscious patients with ST-elevation myocardial infarction (STEMI) by a combination of cold saline and endovascular cooling. Twenty patients in RAPID MI-ICE and 120 in CHILL-MI with large STEMIs, scheduled for primary percutaneous coronary intervention (PCI) within <6 hours after symptom onset were randomized to hypothermia induced by rapid infusion of 600-2000 mL cold saline combined with endovascular cooling or standard of care. Hypothermia was initiated before PCI and continued for 1-3 hours after reperfusion aiming at a target temperature of 33°C. The primary endpoint was myocardial infarct size (IS) as a percentage of myocardium at risk (IS/MaR) assessed by cardiac magnetic resonance imaging at 4±2 days. Patients randomized to hypothermia treatment achieved a mean core body temperature of 34.7°C before reperfusion. Although significance was not achieved in CHILL-MI, in the pooled analysis IS/MaR was reduced in the hypothermia group, relative reduction (RR) 15% (40.5, 28.0-57.6 vs. 46.6, 36.8-63.8, p=0.046, median, interquartile range [IQR]). IS/MaR was predominantly reduced in early anterior STEMI (0-4h) in the hypothermia group, RR=31% (40.5, 28.8-51.9 vs. 59.0, 45.0-67.8, p=0.01, median, IQR). There was no mortality in either group. The incidence of heart failure was reduced in the hypothermia group (2 vs. 11, p=0.009). Patients with large MaR (>30% of the left ventricle) exhibited significantly reduced IS/MaR in the hypothermia group (40.5, 27.0-57.6 vs. 55.1, 41.1-64.4, median, IQR; hypothermia n=42 vs. control n=37, p=0.03), while patients with MaR<30% did not show effect of hypothermia (35

  2. Therapeutic hypothermia for the treatment of acute myocardial infarction-combined analysis of the RAPID MI-ICE and the CHILL-MI trials.

    PubMed

    Erlinge, David; Götberg, Matthias; Noc, Marko; Lang, Irene; Holzer, Michael; Clemmensen, Peter; Jensen, Ulf; Metzler, Bernhard; James, Stefan; Bøtker, Hans Erik; Omerovic, Elmir; Koul, Sasha; Engblom, Henrik; Carlsson, Marcus; Arheden, Håkan; Östlund, Ollie; Wallentin, Lars; Klos, Bradley; Harnek, Jan; Olivecrona, Göran K

    2015-06-01

    In the randomized rapid intravascular cooling in myocardial infarction as adjunctive to percutaneous coronary intervention (RAPID MI-ICE) and rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction CHILL-MI studies, hypothermia was rapidly induced in conscious patients with ST-elevation myocardial infarction (STEMI) by a combination of cold saline and endovascular cooling. Twenty patients in RAPID MI-ICE and 120 in CHILL-MI with large STEMIs, scheduled for primary percutaneous coronary intervention (PCI) within <6 hours after symptom onset were randomized to hypothermia induced by rapid infusion of 600-2000 mL cold saline combined with endovascular cooling or standard of care. Hypothermia was initiated before PCI and continued for 1-3 hours after reperfusion aiming at a target temperature of 33°C. The primary endpoint was myocardial infarct size (IS) as a percentage of myocardium at risk (IS/MaR) assessed by cardiac magnetic resonance imaging at 4±2 days. Patients randomized to hypothermia treatment achieved a mean core body temperature of 34.7°C before reperfusion. Although significance was not achieved in CHILL-MI, in the pooled analysis IS/MaR was reduced in the hypothermia group, relative reduction (RR) 15% (40.5, 28.0-57.6 vs. 46.6, 36.8-63.8, p=0.046, median, interquartile range [IQR]). IS/MaR was predominantly reduced in early anterior STEMI (0-4h) in the hypothermia group, RR=31% (40.5, 28.8-51.9 vs. 59.0, 45.0-67.8, p=0.01, median, IQR). There was no mortality in either group. The incidence of heart failure was reduced in the hypothermia group (2 vs. 11, p=0.009). Patients with large MaR (>30% of the left ventricle) exhibited significantly reduced IS/MaR in the hypothermia group (40.5, 27.0-57.6 vs. 55.1, 41.1-64.4, median, IQR; hypothermia n=42 vs. control n=37, p=0.03), while patients with MaR<30% did not show effect of hypothermia (35

  3. [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

  4. [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.

  5. 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

  6. 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.

  7. Intensive lowering of LDL cholesterol with 80 mg versus 20 mg simvastatin daily in 12 064 survivors of myocardial infarction: a double-blind randomised trial

    PubMed Central

    Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) Collaborative Group

    2010-01-01

    Summary Background Lowering of LDL cholesterol reduces major vascular events, but whether more intensive therapy safely produces extra benefits is uncertain. We aimed to establish efficacy and safety of more intensive statin treatment in patients at high cardiovascular risk. Methods We undertook a double-blind randomised trial in 12 064 men and women aged 18–80 years with a history of myocardial infarction. Participants were either currently on or had clear indication for statin therapy, and had a total cholesterol concentration of at least 3·5 mmol/L if already on a statin or 4·5 mmol/L if not. Randomisation to either 80 mg or 20 mg simvastatin daily was done centrally using a minimisation algorithm. Participants were assessed at 2, 4, 8, and 12 months after randomisation and then every 6 months until final follow-up. The primary endpoint was major vascular events, defined as coronary death, myocardial infarction, stroke, or arterial revascularisation. Analysis was by intention to treat. This study is registered, number ISRCTN74348595. Findings 6031 participants were allocated 80 mg simvastatin daily, and 6033 allocated 20 mg simvastatin daily. During a mean follow-up of 6·7 (SD 1·5) years, allocation to 80 mg simvastatin produced an average 0·35 (SE 0·01) mmol/L greater reduction in LDL cholesterol compared with allocation to 20 mg. Major vascular events occurred in 1477 (24·5%) participants allocated 80 mg simvastatin versus 1553 (25·7%) of those allocated 20 mg, corresponding to a 6% proportional reduction (risk ratio 0·94, 95% CI 0·88–1·01; p=0·10). There were no apparent differences in numbers of haemorrhagic strokes (24 [0·4%] vs 25 [0·4%]) or deaths attributed to vascular (565 [9·4%] vs 572 [9·5%]) or non-vascular (399 [6·6%] vs 398 [6·6%]) causes. Compared with two (0·03%) cases of myopathy in patients taking 20 mg simvastatin daily, there were 53 (0·9%) cases in the 80 mg group. Interpretation The 6% (SE 3·5%) reduction in major

  8. Postmortem detection of inapparent myocardial infarction

    PubMed Central

    McVie, J. G.

    1970-01-01

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

  9. 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.

  10. 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.

  11. 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

  12. 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.

  13. 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.

  14. 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.

  15. Clinical predictors of reinfarction among men and women after a first myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial.

    PubMed

    Kornowski, R; Goldbourt, U; Boyko, V; Behar, S

    1995-01-01

    Independent clinical factors predicting reinfarction in the 1st year following an initial myocardial infarction were identified among 900 women and 2,795 men. Women were older (65.8 vs. 59.3 years; p < 0.001) but tended to suffer from reinfarction at a rate similar to that of men (6.9 vs. 5.6%, p = 0.17). Cumulative 1-month, 1- and 5.5-year all-cause mortality following the first infarction was higher among women who sustained reinfarction (43, 52 and 74%, respectively) than among men (29, 30 and 51%, respectively, p < 0.01 for each). Independent clinical predictors for recurrent myocardial infarction among women were (adjusted relative odds): peripheral vascular disease (3.2), postinfarction angina (2.3), diabetes mellitus (2.2), radiographic evidence of cardiomegaly (1.9), anterior location of the first infarction (2.0), congestive heart failure (1.8), prior angina (1.6) and age (10 years) increment (1.2). Predictive variables for men were: anterior infarct location (1.7), peripheral vascular disease (1.6, prior stroke (1.5), prior angina (1.4), systemic hypertension (1.3) and age (10 years) increment (1.1). Our data indicate (a) different cardiac risk factors for reinfarction among men and women after a first myocardial infarction, and (b) a prognostic advantage for men over women following reinfarction.

  16. 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

  17. 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.

  18. 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

  19. 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

  20. Outcome of patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention during on- versus off-hours (a Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction [HORIZONS-AMI] trial substudy).

    PubMed

    Cubeddu, Roberto J; Palacios, Igor F; Blankenship, James C; Horvath, Sofia A; Xu, Ke; Kovacic, Jason C; Dangas, George D; Witzenbichler, Bernhard; Guagliumi, Giulio; Kornowski, Ran; Dudek, Dariusz; Stone, Gregg W; Mehran, Roxana

    2013-04-01

    Patients with ST-segment elevation myocardial infarction (STEMI) admitted during nonregular working hours (off-hours) have been reported to have greater mortality than those admitted during regular working hours (on-hours), perhaps because of the lower availability of catheterization laboratory services and longer door-to-balloon times. This might not be the case, however, for hospital centers in which primary percutaneous coronary intervention (PCI) is invariably performed. We conducted a substudy using the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction study data to determine whether the STEMI arrival time was associated with differing clinical outcomes. We identified all patients with STEMI admitted to a PCI-capable hospital who underwent primary PCI. Patients presenting during on-hours were compared to those presenting during off-hours. The primary outcome of death, major adverse cardiovascular events, and net adverse clinical events was examined. We identified 2,440 patients (1,205 [49%] on-hours and 1,235 [51%] off-hours). Similar baseline characteristics were observed. The off-hour patients had a significantly longer door-to-balloon time (92 vs 75 minutes; p <0.0001) and total ischemic time (209 vs 194 minutes; p <0.0001). Despite these differences, the risk-adjusted all-cause mortality, major adverse cardiovascular events, and net adverse clinical events rates were similar for both groups during the in-hospital, 1-year, and 3-year follow-up. In conclusion, patients with STEMI presenting to primary PCI hospitals during off-hours might have slightly longer delays to revascularization; however, they experienced similar short- and long-term survival and clinical outcomes as those arriving during on-hours. PMID:23340031

  1. 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…

  2. [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.

  3. Cardiac rehabilitation using the Family-Centered Empowerment Model versus home-based cardiac rehabilitation in patients with myocardial infarction: a randomised controlled trial

    PubMed Central

    Vahedian-Azimi, Amir; Hajiesmaieli, Mohammadreza; Kangasniemi, Mari; Alhani, Fatemah; Jelvehmoghaddam, Hosseinali; Fathi, Mohammad; Farzanegan, Behrooz; Ardehali, Seyed H; Hatamian, Sevak; Gahremani, Mehdi; Mosavinasab, Seyed M M; Rostami, Zohreh; Madani, Seyed J; Izadi, Morteza

    2016-01-01

    Objective To determine if a hybrid cardiac rehabilitation (CR) programme using the Family-Centered Empowerment Model (FCEM) as compared with standard CR will improve patient quality of life, perceived stress and state anxiety of patients with myocardial infarction (MI). Methods We conducted a randomised controlled trial in which patients received either standard home CR or CR using the FCEM strategy. Patient empowerment was measured with FCEM questionnaires preintervention and postintervention for a total of 9 assessments. Quality of life, perceived stress, and state and trait anxiety were assessed using the 36-Item Short Form Health Survey (SF-36), the 14-item Perceived Stress, and the 20-item State and 20-item Trait Anxiety questionnaires, respectively. Results 70 patients were randomised. Baseline characteristics were similar. Ejection fraction was significantly higher in the intervention group at measurements 2 (p=0.01) and 3 (p=0.001). Exercise tolerance measured as walking distance was significantly improved in the intervention group throughout the study. The quality of life results in the FCEM group showed significant improvement both within the group over time (p<0.0001) and when compared with control (p<0.0001). Similarly, the perceived stress and state anxiety results showed significant improvement both within the FCEM group over time (p<0.0001) and when compared with control (p<0.0001). No significant difference was found either within or between groups for trait anxiety. Conclusions The family-centred empowerment model may be an effective hybrid cardiac rehabilitation method for improving the physical and mental health of patients post-MI; however, further study is needed to validate these findings. Clinical Trials.gov identifier NCT02402582. Trial registration number NCT02402582. PMID:27110376

  4. 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.

  5. [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

  6. 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

  7. The Nurse-Led Telephone Follow-Up on Medication and Dietary Adherence among Patients after Myocardial Infarction: A Randomized Controlled Clinical Trial

    PubMed Central

    Najafi, Seyed Saeed; Shaabani, Maryam; Momennassab, Marzieh; Aghasadeghi, Kamran

    2016-01-01

    Background: Adherence to dietary and medication regimen plays an important role in successful treatment and reduces the negative complications and severity of the disease. Therefore, the present study aimed to investigate the effect of nurse-led telephone follow-up on the level of adherence to dietary and medication regimen among patients after Myocardial Infarction (MI). Methods: This non-blinded randomized controlled clinical trial was conducted on 100 elderly patients with MI who had referred to the cardiovascular clinics in Shiraz. Participants were selected and randomly assigned to intervention and control groups using balanced block randomization method. The intervention group received a nurse-led telephone follow-up. The data were collected using a demographic questionnaire, Morisky’s 8-item medication adherence questionnaire, and dietary adherence questionnaire before and three months after the intervention. Data analysis was done by the SPSS statistical software (version 21), using paired t-test for intra-group and Chi-square and t-test for between groups comparisons. Significance level was set at<0.05. Results: The results of Chi-square test showed no statistically significant difference between the intervention and control groups with respect to their adherence to dietary and medication regimen before the intervention (P>0.05). However, a statistically significant difference was found between the two groups in this regard after the intervention (P<0.05). The mean differences of dietary and medication adherence scores between pre- and post-tests were significantly different between the two groups. Independent t-test showed these differences (P=0.001). Conclusion: The results of the present study confirmed the positive effects of nurse-led telephone follow-up as a method of tele-nursing on improvement of adherence to dietary and medication regimen in the patients with MI. Trial Registration Number: IRCT201409148505N8 PMID:27382586

  8. 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

    reinfarction during 4 years of follow-up in stable patients with occlusion of the infarct-related artery 3 to 28 days after myocardial infarction. (ClinicalTrials.gov number, NCT00004562.) PMID:17105759

  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. 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.

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

    SciTech Connect

    Willerson, J.T.

    1983-01-01

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

  12. 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

  13. 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

  14. 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

  15. Amphetamine Abuse Related Acute Myocardial Infarction

    PubMed Central

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

    2016-01-01

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

  16. 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

  17. 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

  18. 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.

  19. 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.

  20. 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.

  1. 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.

  2. 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

  3. Clinical, functional, and angiographic distinctions between Q wave and non-Q wave myocardial infarction: evidence of spontaneous reperfusion and implications for intervention trials

    SciTech Connect

    Gibson, R.S.

    1987-06-01

    We prospectively evaluated 241 consecutive patients with creatine kinase (MB fraction)-confirmed acute myocardial infarction with predischarge quantitative thallium-201 scintigraphy, coronary angiography, radionuclide ventriculography, and 24 hr Holter monitoring. Based on serial electrocardiograms, 154 patients had Q wave (QMI) and 87 had non-Q wave (NQMI) infarction. Despite less myocardial necrosis and better left ventricular function, the NQMI group had the same long-term survival as the QMI group. During 27 months of follow-up, patients with NQMI experienced more reinfarctions (p = .009), had a higher rate of unstable angina pectoris requiring rehospitalization (p = .034), and had a greater likelihood of subsequent bypass surgery or angioplasty (p = .018). Based on our thallium scintigraphic data, the greater clinical instability after NQMI appeared to be related to the presence of a larger residual mass of viable but jeopardized myocardium within the perfusion zone of the infarct-related vessel. Our results also indicate that the pathogenesis of NQMI may involve early spontaneous reperfusion and that patients with NQMI can experience sudden death despite well-preserved left ventricular function.

  4. An evidence-based shared decision making programme on the prevention of myocardial infarction in type 2 diabetes: protocol of a randomised-controlled trial

    PubMed Central

    2013-01-01

    Background Lack of patient involvement in decision making has been suggested as one reason for limited treatment success. Concepts such as shared decision making may contribute to high quality healthcare by supporting patients to make informed decisions together with their physicians. A multi-component shared decision making programme on the prevention of heart attack in type 2 diabetes has been developed. It aims at improving the quality of decision-making by providing evidence-based patient information, enhancing patients’ knowledge, and supporting them to actively participate in decision-making. In this study the efficacy of the programme is evaluated in the setting of a diabetes clinic. Methods/Design A single blinded randomised-controlled trial is conducted to compare the shared decision making programme with a control-intervention. The intervention consists of an evidence-based patient decision aid on the prevention of myocardial infarction and a corresponding counselling module provided by diabetes educators. Similar in duration and structure, the control-intervention targets nutrition, sports, and stress coping. A total of 154 patients between 40 and 69 years of age with type 2 diabetes and no previous diagnosis of ischaemic heart disease or stroke are enrolled and allocated either to the intervention or the control-intervention. Primary outcome measure is the patients’ knowledge on benefits and harms of heart attack prevention captured by a standardised knowledge test. Key secondary outcome measure is the achievement of treatment goals prioritised by the individual patient. Treatment goals refer to statin taking, HbA1c-, blood pressure levels and smoking status. Outcomes are assessed directly after the counselling and at 6 months follow-up. Analyses will be carried out on intention-to-treat basis. Concurrent qualitative methods are used to explore intervention fidelity and to gain insight into implementation processes. Discussion Interventions to

  5. 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

  6. 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…

  7. 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.

  8. 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

  9. 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.

  10. 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

  11. 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.

  12. 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

  13. 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

  14. Incidence and prognostic significance of atrial fibrillation in acute myocardial infarction: the GISSI-3 data

    PubMed Central

    Pizzetti, F; Turazza, F; Franzosi, M; Barlera, S; Ledda, A; Maggioni, A; Santoro, L; Tognoni, G

    2001-01-01

    BACKGROUND—Atrial fibrillation is the most common supraventricular arrhythmia in patients with acute myocardial infarction. Recent advances in pharmacological treatment of myocardial infarction may have changed the impact of this arrhythmia.
OBJECTIVE—To assess the incidence and prognosis of atrial fibrillation complicating myocardial infarction in a large population of patients receiving optimal treatment, including angiotensin converting enzyme (ACE) inhibitors.
METHODS—Data were derived from the GISSI-3 trial, which included 17 944 patients within the first 24 hours after acute myocardial infarction. Atrial fibrillation was recorded during the hospital stay, and follow up visits were planned at six weeks and six months. Survival of the patients at four years was assessed through census offices.
RESULTS—The incidence of in-hospital atrial fibrillation or flutter was 7.8%. Atrial fibrillation was associated with indicators of a worse prognosis (age > 70 years, female sex, higher Killip class, previous myocardial infarction, treated hypertension, high systolic blood pressure at entry, insulin dependent diabetes, signs or symptoms of heart failure) and with some adverse clinical events (reinfarction, sustained ventricular tachycardia, ventricular fibrillation). After adjustment for other prognostic factors, atrial fibrillation remained an independent predictor of increased in-hospital mortality: 12.6% v 5%, adjusted relative risk (RR) 1.98, 95% confidence interval (CI) 1.67 to 2.34. Data on long term mortality (four years after acute myocardial infarction) confirmed the persistent negative influence of atrial fibrillation (RR 1.78, 95% CI 1.60 to 1.99).
CONCLUSIONS—Atrial fibrillation is an indicator of worse prognosis after acute myocardial infarction, both in the short term and in the long term, even in an unselected population.


Keywords: atrial fibrillation; acute myocardial infarction; prognosis PMID:11602545

  15. 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

  16. Cigarette smoking and acute myocardial infarction. A case-control study from the GISSI-2 trial. GISSI-EFRIM Investigators. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto--Epidemiologia dei Fattori di Rischio dell'infarto Miocardioco.

    PubMed

    Negri, E; La Vecchia, C; Nobili, A; D'Avanzo, B; Bechi, S

    1994-08-01

    To make a further quantitative assessment of the relationship between cigarette smoking and the risk of myocardial infarction, a multicentric case-control study was conducted in Italy between September 1988 and June 1989 within the framework of the GISSI-2 trial. Ninety hospitals in various Italian Regions participated. 916 cases of acute myocardial infarction with no history of ischaemic heart disease and 1106 controls admitted to hospital for acute conditions not related to known or suspected risk factors for ischaemic heart disease were studied. Relative risks (RR) and 95% confidence intervals (CI) of myocardial infarction according to various measures of tobacco smoking, were adjusted for identified potential confounding factors using multiple logistic regression. Compared to lifelong non-smokers, the RR was 1.3 (95% CI 1.0 to 1.9) for ex-smokers, 2.0 (95% CI 1.4 to 2.9) for current smokers of less than 15 cigarettes per day, 3.1 (95% CI 2.2 to 4.2) for 15-24 cigarettes per day and 4.9 (95% CI 3.4 to 7.1) for 25 or more cigarettes per day. No trend in risk was evident for the duration, the RR being around 3 for subsequent categories. There was a significant interaction between smoking and age. Below the age 45, smokers of 25 or more cigarettes per day had a 33 times higher risk than non-smokers, compared to 7.5 at in the age group 45-54, 4.4 between the ages 55-64 and 2.5 at the age of 65 or over. The risk estimates were higher in women (RR for > or = 25 cigarettes per day = 10.1), in subjects in the lowest cholesterol tertile (RR = 11.9), with no history of diabetes (RR = 6.8), hypertension (RR = 9.5), no family history ischaemic heart disease (RR = 9.1) and low body mass index (RR = 9.3). The importance of smoking is confirmed as a cause of acute myocardial infarction: about 50% of all nonfatal infarctions in this Italian population could be attributable to cigarette smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

  17. 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.

  18. 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.

  19. 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.

  20. 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.

  1. Thrombus aspiration in ST-segment elevation myocardial infarction.

    PubMed

    Meneguz-Moreno, R A; Costa, R A; A, A; Ribamar Costa, J; Abizaid, A

    2015-12-01

    Primary percutaneous coronary intervention (PCI) has become the treatment of choice in patients with ST-segment elevation myocardial infarction (STEMI) throughout the last years. A significant number of studies have demonstrated a morbidity and mortality benefit over thrombolysis, which has been attributed to better coronary perfusion in patients undergoing primary PCI. Even though it usually achieves normal flow in the affected epicardial vessel, myocardial reperfusion is not fully restored in a significant percentage of patients. This is commonly the result of distal thrombus embolization with subsequent impairment of myocardial microcirculation. Recognition of this has led to the development of a number of devices with different mechanisms, including thrombus aspiration catheters, in order to reduce distal embolization and therefore improve myocardial perfusion. Recent studies indeed demonstrate that the use of such devices offer additional clinical advantage in patients undergoing primary PCI in comparison to the standard PCI, whether in other trials it could not be proved. This paper focuses on general mechanisms of thrombus formation and discusses favorable and unfavorable studies towards thrombus aspiration in STEMI and its main aspects and it comes up with specific subjects that could benefit or not from the procedure of thrombus aspiration. PMID:26603617

  2. 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.

  3. 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.

  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. 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.

  6. 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.

  7. 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

  8. Primary angioplasty vs. fibrinolysis in very old patients with acute myocardial infarction: TRIANA (TRatamiento del Infarto Agudo de miocardio eN Ancianos) randomized trial and pooled analysis with previous studies

    PubMed Central

    Bueno, Héctor; Betriu, Amadeo; Heras, Magda; Alonso, Joaquín J.; Cequier, Angel; García, Eulogio J.; López-Sendón, José L.; Macaya, Carlos; Hernández-Antolín, Rosana; Bueno, Héctor; Hernández-Antolín, Rosana; Alonso, Joaquín J.; Betriu, Amadeo; Cequier, Angel; García, Eulogio J.; Heras, Magda; López-Sendón, José L.; Macaya, Carlos; Azpitarte, José; Sanz, Ginés; Chamorro, Angel; López-Palop, Ramón; Sionis, Alex; Arós, Fernando; García-Fernández, Eulogio; Rubio, Rafael; Hernández, Felipe; Tascón, Juan Carlos; Moreu, José; Betriu, Amadeu; Heras, Magda; Hernández-Antolín, Rosana; Fernández-Ortiz, Antonio; Morís, César; de Posada, Ignacio Sánchez; Cequier, Ángel; Esplugas, Enrique; Melgares, Rafael; Bosa, Francisco; García-González, Martín Jesús; Lezáun, Román; Carmona, José Ramón; Vázquez, José Manuel; Castro-Beiras, Alfonso; Picart, Joan García; de Rozas, José Domínguez; Fernández, José Díaz; Vázquez, Felipe Fernández; Alonso, Norberto; Zueco, José Javier; San José, José María; San Román, Alberto; Hernández, Carolina; García, José María Hernández; Alcántara, Ángel García; Bethencourt, Armando; Fiol, Miquel; Mancisidor, Xabier; Mancisidor, Xabier; Ruiz, Rafael; Hidalgo, Rafael; Sobrino, Nicolás; Maqueda, Isidoro González; Torres, Alfonso; Arós, Fernando; Amaro, Antonio; Jaquet, Michel

    2011-01-01

    Aims To compare primary percutaneous coronary intervention (pPCI) and fibrinolysis in very old patients with ST-segment elevation myocardial infarction (STEMI), in whom head-to-head comparisons between both strategies are scarce. Methods and results Patients ≥75 years old with STEMI <6 h were randomized to pPCI or fibrinolysis. The primary endpoint was a composite of all-cause mortality, re-infarction, or disabling stroke at 30 days. The trial was prematurely stopped due to slow recruitment after enroling 266 patients (134 allocated to pPCI and 132 to fibrinolysis). Both groups were well balanced in baseline characteristics. Mean age was 81 years. The primary endpoint was reached in 25 patients in the pPCI group (18.9%) and 34 (25.4%) in the fibrinolysis arm [odds ratio (OR), 0.69; 95% confidence interval (CI) 0.38–1.23; P = 0.21]. Similarly, non-significant reductions were found in death (13.6 vs. 17.2%, P = 0.43), re-infarction (5.3 vs. 8.2%, P = 0.35), or disabling stroke (0.8 vs. 3.0%, P = 0.18). Recurrent ischaemia was less common in pPCI-treated patients (0.8 vs. 9.7%, P< 0.001). No differences were found in major bleeds. A pooled analysis with the two previous reperfusion trials performed in older patients showed an advantage of pPCI over fibrinolysis in reducing death, re-infarction, or stroke at 30 days (OR, 0.64; 95% CI 0.45–0.91). Conclusion Primary PCI seems to be the best reperfusion therapy for STEMI even for the oldest patients. Early contemporary fibrinolytic therapy may be a safe alternative to pPCI in the elderly when this is not available. Clinicaltrials.gov # NCT00257309. PMID:20971744

  9. 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.

  10. [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

  11. 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.

  12. [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.

  13. An Unusual Complication Following Transarterial Chemoembolization: Acute Myocardial Infarction

    SciTech Connect

    Lai Yiliang; Chang Weichou; Kuo Wuhsien; Huang Tienyu; Chu Hengcheng; Hsieh Tsaiyuan; Chang Weikuo

    2010-02-15

    Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.

  14. 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.

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

    PubMed Central

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

    1989-01-01

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

  16. 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.

  17. 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

  18. 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.

  19. "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.

  20. 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.

  1. 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

  2. Acute Myocardial Infarction in a 26-Year-Old Patient With Familial Hypercholesteremia

    PubMed Central

    Miyayama, Takeshi; Miura, Shin-ichiro; Komaki, Tomo; Kuwano, Takashi; Morii, Joji; Nishikawa, Hiroaki; Saku, Keijiro

    2016-01-01

    A 26-year-old male suffered sustained chest pain. Electrocardiogram showed ST-segment elevation in the anteroseptal wall and reciprocal ST-segment change in the inferior wall. The troponin-I level and the white blood cell count were elevated. We gave a diagnosis of acute myocardial infarction. He underwent urgent coronary angiography, which revealed 90% diffuse stenosis in the middle right coronary artery and total occlusion in the proximal left anterior descending coronary artery (LAD). Since the electrocardiogram indicated that the culprit lesion was in the proximal LAD, we performed percutaneous coronary intervention. The coronary flow in the LAD was classified as thrombolysis in myocardial infarction trial 3. His coronary risk factors were obesity, smoking, family history, hypertension and diabetes, in addition to heterozygous familial hypercholesteremia (FH). Herein, we describe the case of a young patient with acute anteroseptal myocardial infarction and discuss the potential importance of controlling cholesterol levels in FH. PMID:27298669

  3. 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.

  4. [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.

  5. Approaches to Improving Cardiac Structure and Function During and After an Acute Myocardial Infarction: Acute and Chronic Phases.

    PubMed

    Kloner, Robert A; Dai, Wangde; Hale, Sharon L; Shi, Jianru

    2016-07-01

    While progress has been made in improving survival following myocardial infarction, this injury remains a major source of mortality and morbidity despite modern reperfusion therapy. While one approach has been to develop therapies to reduce lethal myocardial cell reperfusion injury, this concept has not translated to the clinics, and several recent negative clinical trials raise the question of whether reperfusion injury is important in humans undergoing reperfusion for acute ST segment elevation myocardial infarction. Therapy aimed at reducing myocardial cell death while the myocytes are still ischemic is more likely to further reduce myocardial infarct size. Developing new therapies to further reduce left ventricular remodeling after the acute event is another approach to preserving structure and function of the heart after infarction. Such therapy may include chronic administration of pharmacologic agents and/or therapies developed from the field of regenerative cardiology, including cellular or non-cellular materials such as extracellular matrix. The optimal therapy will be to administer agents that both reduce myocardial infarct size in the acute phase of infarction as well as reduce adverse left ventricular remodeling during the chronic or healing phase of myocardial infarction. Such a dual approach will help optimize the preservation of both cardiac structure and function.

  6. 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.

  7. 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.

  8. 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.

  9. 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.

  10. [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.

  11. 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.

  12. 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.

  13. 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

  14. 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

  15. 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.

  16. Prediction of functional recovery and prognosis in patients with acute myocardial infarction by 123I-BMIPP and 201Tl myocardial single photon emission computed tomography: a multicenter trial.

    PubMed

    Nishimura, T; Nishimura, S; Kajiya, T; Sugihara, H; Kitahara, K; Imai, K; Muramatsu, T; Takahashi, N; Yoshida, H; Osada, T; Terada, K; Ito, T; Naruse, H; Iwabuchi, M

    1998-10-01

    123I-BMIPP [15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid] was developed for metabolic imaging with SPECT. A multicenter collaborative study was conducted on a large patient series to determine whether 123I-BMIPP and 201Tl myocardial SPECT are of use in predicting the prognosis and ventricular function after acute myocardial infarction (AMI). Patients with uncomplicated first AMI underwent resting 123I-BMIPP and 201Tl myocardial SPECT in the subacute phase after the onset of AMI. Of these, 167 patients who had been followed up for an average of 22 months were retrospectively reviewed to predict serious cardiac events and recurrent ischemia. In addition, the association between changes in radionuclide parameters and recurrent ischemia was investigated in Subgroup A (58 patients) who had repeated SPECT in the chronic phase. Furthermore, prediction of the ejection fraction (EF) was investigated in Subgroup B (94 patients) and Subgroup C (76 patients) in whom left ventriculography was performed at the time of discharge and 90 days or more after the onset, respectively. The prognosis was generally favorable, with 4 cases of cardiac death (2%), 3 of heart failure (2%), 4 of nonfatal reMI (2%), and 25 of recurrent ischemia (15%). The results of Cox multivariate regression analysis revealed a high probability of serious cardiac events in patients who were elderly (p = 0.04), who had 90% or more residual stenosis of the infarct-related artery (p = 0.09), and who had a high BMIPP defect score (p = 0.17). There was a high probability of recurrent ischemia in elderly patients (p = 0.10) who had multi-vessel disease (p = 0.03), but no association was found with radionuclide parameters in the subacute phase. In Subgroup A, however, the probability of recurrent ischemia tended to be high in patients with a large mismatch scorebetween 123I-BMIPP and 201Tl in the subacute to chronic phase. An important observation was that the extent of BMIPP defect was more strongly

  17. Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration.

    PubMed Central

    1994-01-01

    OBJECTIVE--To determine the effects of "prolonged" antiplatelet therapy (that is, given for one month or more) on "vascular events" (non-fatal myocardial infarctions, non-fatal strokes, or vascular deaths) in various categories of patients. DESIGN--Overviews of 145 randomised trials of "prolonged" antiplatelet therapy versus control and 29 randomised comparisons between such antiplatelet regimens. SETTING--Randomised trials that could have been available by March 1990. SUBJECTS--Trials of antiplatelet therapy versus control included about 70,000 "high risk" patients (that is, with some vascular disease or other condition implying an increased risk of occlusive vascular disease) and 30,000 "low risk" subjects from the general population. Direct comparisons of different antiplatelet regimens involved about 10,000 high risk patients. RESULTS--In each of four main high risk categories of patients antiplatelet therapy was definitely protective. The percentages of patients suffering a vascular event among those allocated antiplatelet therapy versus appropriately adjusted control percentages (and mean scheduled treatment durations and net absolute benefits) were: (a) among about 20,000 patients with acute myocardial infarction, 10% antiplatelet therapy v 14% control (one month benefit about 40 vascular events avoided per 1000 patients treated (2P < 0.00001)); (b) among about 20,000 patients with a past history of myocardial infarction, 13% antiplatelet therapy v 17% control (two year benefit about 40/1000 (2P < 0.00001)); (c) among about 10,000 patients with a past history of stroke or transient ischaemic attack, 18% antiplatelet therapy v 22% control (three year benefit about 40/1000 (2P < 0.00001)); (d) among about 20,000 patients with some other relevant medical history (unstable angina, stable angina, vascular surgery, angioplasty, atrial fibrillation, valvular disease, peripheral vascular disease, etc), 9% v 14% in 4000 patients with unstable angina (six month

  18. 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

  19. 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

  20. 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.

  1. 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.

  2. 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

  3. Impact of percutaneous coronary intervention on biomarker levels in patients in the subacute phase following myocardial infarction: the Occluded Artery Trial (OAT) biomarker ancillary study

    PubMed Central

    2013-01-01

    Background The purpose of the Occluded Artery Trial (OAT) Biomarker substudy was to evaluate the impact of infarct related artery (IRA) revascularization on serial levels of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and dynamics of other biomarkers related to left ventricular remodeling, fibrosis and angiogenesis. Methods Patients were eligible for OAT-Biomarker based on the main OAT criteria. Of 70 patients (age 60.8 ± 8.8, 25% women) enrolled in the substudy, 37 were randomized to percutaneous coronary intervention (PCI) and 33 to optimal medical therapy alone. Baseline serum samples were obtained prior to OAT randomization with follow up samples taken at one year. The primary outcome was percent change of NT-proBNP from baseline to 1 year. The secondary outcomes were respective changes of matrix metalloproteinases (MMP) 2 and 9, tissue inhibitor of matrix metalloproteinase 2 (TIMP-2), Vascular Endothelial Growth Factor (VEGF), and Galectin-3. Results Paired (baseline and one-year) serum samples were obtained in 62 subjects. Baseline median NT-proBNP level was 944.8 (455.3, 1533) ng/L and decreased by 69% during follow-up (p < 0.0001). Baseline MMP-2 and TIMP-2 levels increased significantly from baseline to follow-up (p = 0.034, and p = 0.027 respectively), while MMP-9 level decreased from baseline (p = 0.038). Levels of VEGF and Galectin-3 remained stable at one year (p = NS for both). No impact of IRA revascularization on any biomarker dynamics were noted. Conclusions There were significant changes in measured biomarkers related to LV remodeling, stress, and fibrosis following MI between 0 and 12 month. Establishing infarct vessel patency utilizing stenting 24 hours-28 days post MI did not however influence the biomarkers’ release. PMID:24156746

  4. Myocardial infarction and intramyocardial injection models in swine

    PubMed Central

    McCall, Frederic C; Telukuntla, Kartik S; Karantalis, Vasileios; Suncion, Viky Y; Heldman, Alan W; Mushtaq, Muzammil; Williams, Adam R; Hare, Joshua M

    2014-01-01

    Sustainable and reproducible large animal models that closely replicate the clinical sequelae of myocardial infarction (MI) are important for the translation of basic science research into bedside medicine. Swine are well accepted by the scientific community for cardiovascular research, and they represent an established animal model for preclinical trials for US Food and Drug Administration (FDA) approval of novel therapies. Here we present a protocol for using porcine models of MI created with a closed-chest coronary artery occlusion-reperfusion technique. This creates a model of MI encompassing the anteroapical, lateral and septal walls of the left ventricle. This model infarction can be easily adapted to suit individual study design and enables the investigation of a variety of possible interventions. This model is therefore a useful tool for translational research into the pathophysiology of ventricular remodeling and is an ideal testing platform for novel biological approaches targeting regenerative medicine. This model can be created in approximately 8–10 h. PMID:22790084

  5. 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.

  6. Rosiglitazone and Myocardial Infarction in Patients Previously Prescribed Metformin

    PubMed Central

    Dormuth, Colin R.; Maclure, Malcolm; Carney, Greg; Schneeweiss, Sebastian; Bassett, Ken; Wright, James M.

    2009-01-01

    Objective Rosiglitazone was found associated with approximately a 43% increase in risk of acute myocardial infarction (AMI) in a two meta-analyses of clinical trials. Our objective is to estimate the magnitude of the association in real-world patients previously treated with metformin. Research Design and Methods We conducted a nested case control study in British Columbia using health care databases on 4.3 million people. Our cohort consisted of 158,578 patients with Type 2 diabetes who used metformin as first-line drug treatment. We matched 2,244 cases of myocardial infarction (AMI) with up to 4 controls. Conditional logistic regression models were used to estimate matched odds ratios for AMI associated with treatment with rosiglitazone, pioglitazone and sulfonylureas. Results In our cohort of prior metformin users, adding rosiglitazone for up to 6 months was not associated with an increased risk of AMI compared to adding a sulfonylurea (odds ratio [OR] 1.38; 95% confidence interval [CI], 0.91–2.10), or compared to adding pioglitazone (OR for rosi versus pio 1.41; 95% CI, 0.74–2.66). There were also no significant differences between rosiglitazone, pioglitazone and sulfonylureas for longer durations of treatment. Though not significantly different from sulfonylureas, there was a transient increase in AMI risk associated with the first 6 months of treatment with a glitazone compared to not using the treatment (OR 1.53; 95% CI, 1.13–2.07) Conclusions In our British Columbia cohort of patients who received metformin as first-line pharmacotherapy for Type 2 diabetes mellitus, further treatment with rosiglitazone did not increase the risk of AMI compared to patients who were treated with pioglitazone or a sulfonylurea. Though not statistically significantly different compared from each other, an increased risk of AMI observed after starting rosiglitazone or sulfonylureas is a matter of concern that requires more research. PMID:19562036

  7. The high-risk myocardial infarction database initiative.

    PubMed

    Dickstein, Kenneth; Bebchuk, Judith; Wittes, Janet

    2012-01-01

    Coronary artery disease and myocardial infarction represent a major cause of morbidity and mortality. Four randomized, controlled, double-blind clinical trials--VALIANT, EPHESUS, OPTIMAAL, and CAPRICORN evaluated pharmacologic intervention in a total of 28,771 high-risk patients following acute MI complicated with signs of heart failure or evidence of left ventricular dysfunction. The demographic profiles of the 4 study cohorts were similar. The High-Risk MI Database Initiative constructed a common database by merging the data captured by these 4 large trials. The merged data set did not contain the randomized study treatment, so no comparisons could be made between the agents investigated. A total of more than 17,600 subjects experienced a cardiovascular end point. Approximately 5100 deaths occurred, and more than 15,700 subjects experienced a hospitalization. The primary objectives of this initiative were to use this large database to define more precisely the prognostic profile of this high-risk population, to perform rigorous, adequately-sized, subset analyses, to provide epidemiologic information and event rate estimation based on baseline demographics. The methodological challenges and limitations of such an analyses are discussed. It is proposed that some thoughtful foresight and planning could enable us to use the large number of clinical events that accrue during randomized clinical trials to address questions of scientific and clinical interest. PMID:22226005

  8. 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.

  9. 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.

  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. 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

  12. 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

  13. 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

  14. 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

  15. 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

  16. 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.

  17. A randomized, double-blind, placebo-controlled trial to evaluate the safety and effectiveness of intracoronary application of a novel bioabsorbable cardiac matrix for the prevention of ventricular remodeling after large ST-segment elevation myocardial infarction: Rationale and design of the PRESERVATION I trial.

    PubMed

    Rao, Sunil V; Zeymer, Uwe; Douglas, Pamela S; Al-Khalidi, Hussein; Liu, Jingyu; Gibson, C Michael; Harrison, Robert W; Joseph, Diane S; Heyrman, Reinilde; Krucoff, Mitchell W

    2015-11-01

    Postinfarction left ventricular (LV) remodeling can result in chronic heart failure and functional impairment. Although pharmacological strategies for established heart failure can be beneficial, preventing remodeling remains a challenge. Injectable bioabsorbable alginate or "bioabsorbable cardiac matrix" (BCM), composed of an aqueous mixture of sodium alginate and calcium gluconate, is a sterile colorless liquid that is a polysaccharide polymer produced from brown seaweed. When exposed to excess ionized calcium present in infarcted myocardium, BCM assembles to form a flexible gel, structurally resembling extracellular matrix, which provides temporary structural support to the infarct zone through and beyond the time needed for mature fibrotic tissue to develop. The PRESERVATION I trial is an early phase randomized, double-blind, placebo-controlled trial comparing intracoronary application of 4 mL of BCM with saline control in patients who develop large infarctions after successful reperfusion of large ST-segment elevation myocardial infarction (MI). Subjects will be randomized 2:1 to either BCM or saline control and will have the study device deployed through an intracoronary microcatheter in the infarct-related artery 2 to 5 days after index ST-segment elevation MI treated with successful primary or rescue percutaneous coronary intervention. The primary effectiveness end point is the absolute change in LV diastolic volume index as measured by 3-dimensional echocardiography from baseline to 6 months after BCM deployment. Secondary effectiveness end points include clinical outcomes, patient-reported quality of life, additional echocardiographic measures, and functional status measures. In summary, the PRESERVATION I trial is a randomized double-blind trial evaluating the effectiveness and safety of the novel device BCM in preventing LV remodeling patients who have large MIs despite undergoing successful primary or rescue percutaneous coronary intervention.

  18. 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

  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. 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.

  1. 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

  2. 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.

  3. 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

  4. [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.

  5. 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

  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. 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

  9. 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

  10. 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.

  11. 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

  12. 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

  13. 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.

  14. 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.

  15. 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

  16. 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.

  17. 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.

  18. Associations of major bleeding and myocardial infarction with the incidence and timing of mortality in patients presenting with non-ST-elevation acute coronary syndromes: a risk model from the ACUITY trial

    PubMed Central

    Mehran, Roxana; Pocock, Stuart J.; Stone, Gregg W.; Clayton, Tim C.; Dangas, George D.; Feit, Frederick; Manoukian, Steven V.; Nikolsky, Eugenia; Lansky, Alexandra J.; Kirtane, Ajay; White, Harvey D.; Colombo, Antonio; Ware, James H.; Moses, Jeffrey W.; Ohman, E. Magnus

    2009-01-01

    Aims To evaluate the associations of myocardial infarction (MI) and major bleeding with 1-year mortality. Both MI and major bleeding predict 1-year mortality in patients presenting with acute coronary syndrome (ACS). However, the risk of each of these events on the magnitude and timing of mortality has not been well studied. Methods and Results A multivariable Cox regression model was developed relating 13 independent baseline predictors to 1-year mortality for 13 819 patients with moderate and high-risk ACS enrolled in the Acute Catheterization and Urgent Intervention Triage strategy trial. After adjustment for baseline predictors, Cox models with major bleeding and recurrent MI as time-updated covariates estimated the effect of these events on mortality hazard over time. Within 30 days of randomization, 705 patients (5.1%) had an MI, 645 (4.7%) had a major bleed; 524 (3.8%) died within a year. The occurrence of an MI was associated with a hazard ratio of 3.1 compared with patients not yet having an MI, after adjustment for baseline predictors. However, MI within 30 days markedly increased the mortality risk for the first 2 days after the event (adjusted hazard ratio of 17.6), but this risk declined rapidly post-infarct (hazard ratio of 1.4 beyond 1 month after the MI event). In contrast, major bleeding had a prolonged association with mortality risk (hazard ratio of 3.5) which remained fairly steady over time throughout 1 year. Conclusion After accounting for baseline predictors of mortality, major bleeds and MI have similar overall strength of association with mortality in the first year after ACS. MI is correlated with a dramatic increase in short-term risk, whereas major bleeding correlates with a more prolonged mortality risk. PMID:19351691

  19. 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

  20. 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

  1. 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

  2. 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

  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. 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.…

  5. 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

  6. 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

  7. Culprit lesion thrombus burden after manual thrombectomy or percutaneous coronary intervention-alone in ST-segment elevation myocardial infarction: the optical coherence tomography sub-study of the TOTAL (ThrOmbecTomy versus PCI ALone) trial

    PubMed Central

    Bhindi, Ravinay; Kajander, Olli A.; Jolly, Sanjit S.; Kassam, Saleem; Lavi, Shahar; Niemelä, Kari; Fung, Anthony; Cheema, Asim N.; Meeks, Brandi; Alexopoulos, Dimitrios; Kočka, Viktor; Cantor, Warren J.; Kaivosoja, Timo P.; Shestakovska, Olga; Gao, Peggy; Stankovic, Goran; Džavík, Vladimír; Sheth, Tej

    2016-01-01

    Aims Manual thrombectomy has been proposed as a strategy to reduce thrombus burden during primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI). However, the effectiveness of manual thrombectomy in reducing thrombus burden is uncertain. In this substudy of the TOTAL (ThrOmbecTomy versus PCI ALone) trial, we compared the thrombus burden at the culprit lesion using optical coherence tomography (OCT) in patients treated with thrombectomy vs. PCI-alone. Methods and results The TOTAL trial (N = 10 732) was an international, multicentre, randomized trial of thrombectomy (using the Export catheter, Medtronic Cardiovascular, Santa Rosa, CA, USA) in STEMI patients treated with primary PCI. The OCT sub-study prospectively enrolled 214 patients from 13 sites in 5 countries. Optical coherence tomography was performed immediately after thrombectomy or PCI-alone and then repeated after stent deployment. Thrombus quantification was performed by an independent core laboratory blinded to treatment assignment. The primary outcome of pre-stent thrombus burden as a percentage of segment analysed was 2.36% (95% CI: 1.73–3.22) in the thrombectomy group and 2.88% (95% CI: 2.12–3.90) in the PCI-alone group (P = 0.373). Absolute pre-stent thrombus volume was not different (2.99 vs. 3.74 mm3, P = 0.329). Other secondary outcomes of pre-stent quadrants of thrombus, post–stent atherothrombotic burden, and post-stent atherothrombotic volume were not different between groups. Conclusion Manual thrombectomy did not reduce pre-stent thrombus burden at the culprit lesion compared with PCI-alone. Both strategies were associated with low thrombus burden at the lesion site after the initial intervention to restore flow. PMID:25994742

  8. 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.

  9. 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

  10. 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.

  11. 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.

  12. 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

  13. 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

  14. 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.

  15. [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

  16. Clinical Application of Heart Rate Variability after Acute Myocardial Infarction

    PubMed Central

    Huikuri, Heikki V.; Stein, Phyllis K.

    2012-01-01

    Heart rate (HR) variability has been extensively studied in patients surviving an acute myocardial infarction (AMI). The majority of studies have shown that patients with reduced or abnormal HR variability/turbulence have an increased risk of mortality within few years after an AMI. Various measures of HR dynamics, such as time-domain, spectral, and non-linear measures of HR variability, as well as HR turbulence, have been used in risk stratification of post-AMI patients. The prognostic power of various measures, except of those reflecting rapid R–R interval oscillations, has been almost identical, albeit some non-linear HR variability measures, such as short-term fractal scaling exponent, and HR turbulence, have provided somewhat better prognostic information than the others. Abnormal HR variability predicts both sudden and non-sudden cardiac death after AMI. Because of remodeling of the arrhythmia substrate after AMI, early measurement of HR variability to identify those at high risk should likely be repeated later in order to assess the risk of fatal arrhythmia events. Future randomized trials using HR variability/turbulence as one of the pre-defined inclusion criteria will show whether routine measurement of HR variability/turbulence will become a routine clinical tool for risk stratification of post-AMI patients. PMID:22375128

  17. 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

  18. Long-term antithrombotic pharmacotherapy following ST-elevation myocardial infarction.

    PubMed

    Buccheri, Sergio; Capodanno, Davide

    2016-06-01

    The selection and optimal duration of pharmacological agents to counteract thrombotic processes activated in patients with ST-elevation myocardial infarction (STEMI) still remain a debated issue in current clinical practice. Recently published trials have highlighted the potential benefits of dual-antiplatelet therapy (DAPT) extended beyond the currently recommended 12-months term. Anticoagulation with non-vitamin K oral anticoagulants in addition to DAPT has also been explored. Importantly, benefits of prolonged antithrombotic management strategies could be offset by harms following bleeding complications, therefore careful assessment of a patient benefit-risk profile must be used to drive individualized medical decisions. Appraising current available evidence is useful to inform clinical practice and to optimize the pharmacological management of patients with STEMI. Accordingly, we provide an overview of the literature focusing on long-term antithrombotic management strategies in patients with a recent or prior myocardial infarction, with a primary focus on STEMI. PMID:26934659

  19. 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.

  20. 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

  1. 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

  2. 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

  3. 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

  4. 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.

  5. 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

  6. [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

  7. 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

  8. Post-myocardial infarct inflammation and the potential role of cell therapy.

    PubMed

    van Zuylen, Vanessa-leigh; den Haan, Melina C; Geutskens, Sacha B; Roelofs, Helene; Fibbe, Willem E; Schalij, Martin J; Atsma, Douwe E

    2015-02-01

    Myocardial infarction triggers reparative inflammatory processes programmed to repair damaged tissue. However, often additional injury to the myocardium occurs through the course of this inflammatory process, which ultimately can lead to heart failure. The potential beneficial effects of cell therapy in treating cardiac ischemic disease, the number one cause of death worldwide, are being studied extensively, both in clinical trials using adult stem cells as well as in fundamental research on cardiac stem cells and regenerative biology. This review summarizes the current knowledge on molecular and cellular processes implicated in post-infarction inflammation and discusses the potential beneficial role cell therapy might play in this process. Due to its immunomodulatory properties, the mesenchymal stromal cell is a candidate to reverse the disease progression of the infarcted heart towards heart failure, and therefore is emphasized in this review.

  9. 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.

  10. [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.

  11. 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

  12. 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.

  13. 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

  14. 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

  15. 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.

  16. 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.

  17. 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.

  18. 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.

  19. 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

  20. 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

  1. 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

  2. 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.

  3. 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.

  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. 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

  6. [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.

  7. 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.

  8. 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

  9. 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.

  10. 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.

  11. 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

  12. 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.

  13. 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.

  14. 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

  15. [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.

  16. [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

  17. Acetaminophen use and risk of myocardial infarction and stroke in a hypertensive cohort.

    PubMed

    Fulton, Rachael L; Walters, Matthew R; Morton, Ross; Touyz, Rhian M; Dominiczak, Anna F; Morrison, David S; Padmanabhan, Sandosh; Meredith, Peter A; McInnes, Gordon T; Dawson, Jesse

    2015-05-01

    Recent data suggest that self-reported acetaminophen use is associated with increased risk of cardiovascular events and that acetaminophen causes a modest blood pressure rise. There are no randomized trials or studies using verified prescription data of this relationship. We aimed to assess the relationship between verified acetaminophen prescription data and risk of myocardial infarction or stroke in patients with hypertension. We performed a retrospective data analysis using information contained within the UK Clinical Research Practice Datalink. Multivariable Cox proportional hazard models were used to estimate hazard ratios for myocardial infarction (primary end point), stroke, and any cardiovascular event (secondary end points) associated with acetaminophen use during a 10-year period. Acetaminophen exposure was a time-dependent variable. A propensity-matched design was also used to reduce potential for confounding. We included 24,496 hypertensive individuals aged ≥ 65 years. Of these, 10,878 were acetaminophen-exposed and 13,618 were not. There was no relationship between risk of myocardial infarction, stroke, or any cardiovascular event and acetaminophen exposure on adjusted analysis (hazard ratio, 0.98; 95% confidence interval, 0.76-1.27; hazard ratio, 1.09; 95% confidence interval, 0.86-1.38; and hazard ratio, 1.17; 95% confidence interval, 0.99-1.37; respectively). Results in the propensity-matched sample (n=4000 per group) and when men and women were analyzed separately were similar. High-frequency users (defined as receiving a prescription for >75% of months) were also not at increased risk. After allowance for potentially confounding variables, the use of acetaminophen was not associated with an increased risk of myocardial infarction or stroke in a large cohort of hypertensive patients.

  18. 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

  19. 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.

  20. 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.

  1. Mean platelet volume and cardiovascular outcomes in acute myocardial infarction

    PubMed Central

    Ranjith, Mangalachulli Pottammal; DivyaRaj, Rajendran; Mathew, Dolly; George, Biju; Krishnan, Mangalath Narayanan

    2016-01-01

    Objective High levels of mean platelet volume (MPV) may be associated with adverse outcomes in patients with myocardial infarction (MI). We examined the association between MPV and the risk of death and adverse cardiovascular outcomes in patients with MI. Methods We studied consecutive patients with MI admitted to a tertiary-care hospital during a period of 1 year. MPV was measured at admission and at third month. Patients were followed up for 1-year primary composite outcome of cardiovascular death, stroke, fatal or non-fatal MI and cardiac failure. Patients were classified according to tertile of baseline MPV. Results A total of 1206 patients with MI, including 934 men (77.4%) and 272 women (22.6%) were studied. The mean age of the study population was 56 years. At 1-year follow-up, 292 (28.57%) primary outcome occurred: cardiovascular mortality 78 (7.6%), fatal or non-fatal MI 153 (15.0%), stroke 30 (2.9%) and cardiac failure 128 (12.52%). Patients with the highest tertile MPV had higher primary outcome as compared with those with MPV in the lowest tertile (adjusted OR=2.31; 95% CI 1.60 to 3.35; p<0.001). Total mortality was also more in high-MPV group (adjusted OR 2.62; 95% CI 1.47 to 4.70; p<0.001). There were no significant changes in mean MPV values at admission from those at third month interval (9.15, (SD 0.99) vs 9.19 (SD 0.94); p=0.2). Conclusions Elevated MPV was associated with worse outcome in patients with acute MI. Elevated MPV in these patients may be due to inherently large platelets. Trial registration number http://ctri.nic.in/Clinicaltrials/rmaindet.php?trialid=5485&EncHid=98036.61144&modid=1&compid=19; CTRI/2012/12/003222. PMID:27326224

  2. 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

  3. Intravenous tissue plasminogen activator and size of infarct, left ventricular function, and survival in acute myocardial infarction.

    PubMed Central

    Van de Werf, F.; Arnold, A. E.

    1988-01-01

    STUDY OBJECTIVE--To assess effect of intravenous recombinant tissue type plasminogen activator on size of infarct, left ventricular function, and survival in acute myocardial infarction. DESIGN--Double blind, randomised, placebo controlled prospective trial of patients with acute myocardial infarction within five hours after onset of symptoms. SETTING--Twenty six referral centres participating in European cooperative study for recombinant tissue type plasminogen activator. PATIENTS--Treatment group of 355 patients with acute myocardial infarction allocated to receive intravenous recombinant plasminogen activator. Controls comprised 366 similar patients allocated to receive placebo. INTERVENTION--All patients were given aspirin 250 mg and bolus injection of 5000 IU heparin immediately before start of trial. Patients in treatment group were given 100 mg recombinant tissue plasminogen activator over three hours (10 mg intravenous bolus, 50 mg during one hour, and 40 mg during next two hours) by infusion. Controls were given placebo by same method. Full anticoagulation treatment and aspirin were given to both groups until angiography (10-22 days after admission). beta Blockers were given at discharge. END POINT--Left ventricular function at 10-22 days, enzymatic infarct size, clinical course, and survival to three month follow up. MEASUREMENTS AND MAIN RESULTS--Mortality was reduced by 51% (95% confidence interval -76 to 1) in treated patients at 14 days after start of treatment and by 36% (-63 to 13) at three months. For treatment within three hours after myocardial infarction mortality was reduced by 82% (-95 to -31) at 14 days and by 59% (-83 to -2) at three months. During 14 days in hospital incidence of cardiac complications was lower in treated patients than controls (cardiogenic shock, 2.5% v 6.0%; ventricular fibrillation, 3.4% v 6.3%; and pericarditis, 6.2% v 11.0% respectively), but that of angioplasty or artery bypass, or both was higher (15.8% v 9

  4. β blockers and mortality after myocardial infarction in patients without heart failure: multicentre prospective cohort study

    PubMed Central

    Riant, Elisabeth; Aissoui, Nadia; Soria, Angèle; Ducrocq, Gregory; Coste, Pierre; Cottin, Yves; Aupetit, Jean François; Bonnefoy, Eric; Blanchard, Didier; Cattan, Simon; Steg, Gabriel; Schiele, François; Ferrières, Jean; Juillière, Yves; Simon, Tabassome; Danchin, Nicolas

    2016-01-01

    Objective To assess the association between early and prolonged β blocker treatment and mortality after acute myocardial infarction. Design Multicentre prospective cohort study. Setting Nationwide French registry of Acute ST- and non-ST-elevation Myocardial Infarction (FAST-MI) (at 223 centres) at the end of 2005. Participants 2679 consecutive patients with acute myocardial infarction and without heart failure or left ventricular dysfunction. Main outcome measures Mortality was assessed at 30 days in relation to early use of β blockers (≤48 hours of admission), at one year in relation to discharge prescription, and at five years in relation to one year use. Results β blockers were used early in 77% (2050/2679) of patients, were prescribed at discharge in 80% (1783/2217), and were still being used in 89% (1230/1383) of those alive at one year. Thirty day mortality was lower in patients taking early β blockers (adjusted hazard ratio 0.46, 95% confidence interval 0.26 to 0.82), whereas the hazard ratio for one year mortality associated with β blockers at discharge was 0.77 (0.46 to 1.30). Persistence of β blockers at one year was not associated with lower five year mortality (hazard ratio 1.19, 0.65 to 2.18). In contrast, five year mortality was lower in patients continuing statins at one year (hazard ratio 0.42, 0.25 to 0.72) compared with those discontinuing statins. Propensity score and sensitivity analyses showed consistent results. Conclusions Early β blocker use was associated with reduced 30 day mortality in patients with acute myocardial infarction, and discontinuation of β blockers at one year was not associated with higher five year mortality. These findings question the utility of prolonged β blocker treatment after acute myocardial infarction in patients without heart failure or left ventricular dysfunction. Trial registration Clinical trials NCT00673036. PMID:27650822

  5. Digoxin: A systematic review in atrial fibrillation, congestive heart failure and post myocardial infarction

    PubMed Central

    Virgadamo, Sebastiano; Charnigo, Richard; Darrat, Yousef; Morales, Gustavo; Elayi, Claude S

    2015-01-01

    AIM: To review digoxin use in systolic congestive heart failure, atrial fibrillation, and after myocardial infarction. METHODS: A comprehensive PubMed search was performed using the key words “digoxin and congestive heart failure”, “digoxin and atrial fibrillation”, “digoxin, atrial fibrillation and systolic congestive heart failure”, and “digoxin and myocardial infarction”. Only articles written in English were included in this study. We retained studies originating from randomized controlled trials, registries and included at least 500 patients. The studies included patients with atrial fibrillation or heart failure or myocardial infarction and had a significant proportion of patients (at least 5%) on digoxin. A table reviewing the different hazard ratios was developed based on the articles selected. Our primary endpoint was the overall mortality in the patients on digoxin vs those without digoxin, among patients with atrial fibrillation and also among patients with atrial fibrillation and systolic heart failure. We reviewed the most recent international guidelines to discuss current recommendations. RESULTS: A total of 18 studies were found that evaluated digoxin and overall mortality in different clinical settings including systolic congestive heart failure and normal sinus rhythm (n = 5), atrial fibrillation with and without systolic congestive heart failure (n = 9), and myocardial infarction (n = 4). Overall, patients with systolic congestive heart failure with normal sinus rhythm, digoxin appears to have a neutral effect on mortality especially if close digoxin level monitoring is employed. However, most of the observational studies evaluating digoxin use in atrial fibrillation without systolic congestive heart failure showed an increase in overall mortality when taking digoxin. In the studies evaluated in this systematic review, the data among patients with atrial fibrillation and systolic congestive heart failure, as well as post myocardial

  6. 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

  7. Infarct Size, Shock, and Heart Failure: Does Reperfusion Strategy Matter in Early Presenting Patients With ST-Segment Elevation Myocardial Infarction?

    PubMed Central

    Shavadia, Jay; Zheng, Yinggan; Dianati Maleki, Neda; Huber, Kurt; Halvorsen, Sigrun; Goldstein, Patrick; Gershlick, Anthony H; Wilcox, Robert; Van de Werf, Frans; Armstrong, Paul W

    2015-01-01

    Background A pharmacoinvasive (PI) strategy for early presenting ST-segment elevation myocardial infarction nominally reduced 30-day cardiogenic shock and congestive heart failure compared with primary percutaneous coronary intervention (PPCI). We evaluated whether infarct size (IS) was related to this finding. Methods and Results Using the peak cardiac biomarker in patients randomized to PI versus PPCI within the Strategic Reperfusion Early After Myocardial Infarction (STREAM) trial, IS was divided into 3 groups: small (≤2 times the upper limit normal [ULN]), medium (>2 to ≤5 times the upper limit normal) and large (>5 times the upper limit normal). The association between IS and 30-day shock and congestive heart failure was subsequently examined. Data on 1701 of 1892 (89.9%) patients randomized to PI (n=853, 50.1%) versus PPCI (n=848, 49.9%) within STREAM were evaluated. A higher proportion of PPCI patients had a large IS (PI versus PPCI: small, 49.8% versus 50.2%; medium, 56.9% versus 43.1%; large, 48.4% versus 51.6%; P=0.035), despite comparable intergroup ischemic times for each reperfusion strategy. As IS increased, a parallel increment in shock and congestive heart failure occurred in both treatment arms, except for the small IS group. The difference in shock and congestive heart failure in the small IS group (4.4% versus 11.6%, P=0.026) in favor of PI likely relates to higher rates of aborted myocardial infarction with the PI strategy (72.7% versus 54.3%, P=0.005). After adjustment, a trend favoring PI persisted in this subgroup (relative risk 0.40, 95% CI 0.15 to 1.06, P=0.064); no difference in treatment-related outcomes was evident in the other 2 groups. Conclusion A PI strategy appears to alter the pattern of IS after ST-segment elevation myocardial infarction, resulting in more medium and fewer large infarcts compared with PPCI. Despite a comparable number of small infarcts, PI patients in this group had more aborted myocardial infarctions and less

  8. 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.

  9. Impact of Aldosterone Antagonists on Sudden Cardiac Death Prevention in Heart Failure and Post-Myocardial Infarction Patients: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

    PubMed Central

    Le, Hai-Ha; El-Khatib, Chadia; Mombled, Margaux; Guitarian, Frédéric; Al-Gobari, Muaamar; Fall, Mor; Janiaud, Perrine; Marchant, Ivanny; Cucherat, Michel; Bejan-Angoulvant, Théodora; Gueyffier, François

    2016-01-01

    Background and Objectives Sudden cardiac death (SCD) is a severe burden of modern medicine. Aldosterone antagonist is publicized as effective in reducing mortality in patients with heart failure (HF) or post myocardial infarction (MI). Our study aimed to assess the efficacy of AAs on mortality including SCD, hospitalization admission and several common adverse effects. Methods We searched Embase, PubMed, Web of Science, Cochrane library and clinicaltrial.gov for randomized controlled trials (RCTs) assigning AAs in patients with HF or post MI through May 2015. The comparator included standard medication or placebo, or both. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. Event rates were compared using a random effects model. Prospective RCTs of AAs with durations of at least 8 weeks were selected if they included at least one of the following outcomes: SCD, all-cause/cardiovascular mortality, all-cause/cardiovascular hospitalization and common side effects (hyperkalemia, renal function degradation and gynecomastia). Results Data from 19,333 patients enrolled in 25 trials were included. In patients with HF, this treatment significantly reduced the risk of SCD by 19% (RR 0.81; 95% CI, 0.67–0.98; p = 0.03); all-cause mortality by 19% (RR 0.81; 95% CI, 0.74–0.88, p<0.00001) and cardiovascular death by 21% (RR 0.79; 95% CI, 0.70–0.89, p<0.00001). In patients with post-MI, the matching reduced risks were 20% (RR 0.80; 95% CI, 0.66–0.98; p = 0.03), 15% (RR 0.85; 95% CI, 0.76–0.95, p = 0.003) and 17% (RR 0.83; 95% CI, 0.74–0.94, p = 0.003), respectively. Concerning both subgroups, the relative risks respectively decreased by 19% (RR 0.81; 95% CI, 0.71–0.92; p = 0.002) for SCD, 18% (RR 0.82; 95% CI, 0.77–0.88, p < 0.0001) for all-cause mortality and 20% (RR 0.80; 95% CI, 0.74–0.87, p < 0.0001) for cardiovascular mortality in patients treated with AAs. As well, hospitalizations were significantly reduced

  10. 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.

  11. 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

  12. 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.

  13. 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.

  14. Cardiac rehabilitation and mortality reduction after myocardial infarction: the emperor's new clothes? Evidence against cardiac rehabilitation.

    PubMed

    West, Robert; Jones, Dee

    2013-07-01

    No trial of cardiac rehabilitation (CR) following myocardial infarction (MI) (not even the WHO European collaborative) demonstrates significant reduction of mortality, as do trials of secondary prevention. There is potential conflict of interest when therapists report self-evaluations. Reviews of published reports exaggerate publication bias. Meta-analyses show no significant effect of CR on mortality in recent years - since 1990, 23 trials, 6527 patients, relative risk 1.01 (0.88-1.15). It does no service to MI patients - or rehabilitation therapists - to repeat claims derived from poolings of historic trials, undertaken before many significant advances in diagnosis, acute treatment and effective secondary prevention. While CR has a role in good medical/nursing practice and continuity of care, rehabilitation therapists could be more effective elsewhere in the NHS. PMID:23644409

  15. Vorapaxar: A novel agent to be considered in the secondary prevention of myocardial infarction

    PubMed Central

    Kehinde, Obamiro; Kunle, Rotimi

    2016-01-01

    Patients receiving therapy for the secondary prevention of myocardial infarction (MI) are still at high risk of a major cardiovascular event or death despite the use of currently available treatment strategy. Vorapaxar, an oral protease-activated receptor antagonist, is a novel antiplatelet drug that has been recently approved to provide further risk reduction. The results of two Phase III trials (thrombin receptor antagonists for clinical event reduction and the TRA 2°P-TIMI 50) have showed that vorapaxar, in addition to standard of care therapy, has the potential to provide further risk reduction in patients with prior MI. A search was made on PubMed on articles related to clinical trials and clinical consideration with the use of vorapaxar. This review article summarizes the results of Phase II trials, Phase III trials, subgroup analysis, precautions, and drug interaction with the use of vorapaxar. PMID:27134460

  16. Vorapaxar: A novel agent to be considered in the secondary prevention of myocardial infarction.

    PubMed

    Kehinde, Obamiro; Kunle, Rotimi

    2016-01-01

    Patients receiving therapy for the secondary prevention of myocardial infarction (MI) are still at high risk of a major cardiovascular event or death despite the use of currently available treatment strategy. Vorapaxar, an oral protease-activated receptor antagonist, is a novel antiplatelet drug that has been recently approved to provide further risk reduction. The results of two Phase III trials (thrombin receptor antagonists for clinical event reduction and the TRA 2°P-TIMI 50) have showed that vorapaxar, in addition to standard of care therapy, has the potential to provide further risk reduction in patients with prior MI. A search was made on PubMed on articles related to clinical trials and clinical consideration with the use of vorapaxar. This review article summarizes the results of Phase II trials, Phase III trials, subgroup analysis, precautions, and drug interaction with the use of vorapaxar. PMID:27134460

  17. 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

  18. 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.

  19. [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.

  20. 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.

  1. 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.

  2. 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

  3. 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.

  4. 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.

  5. No-Reflow Phoenomenon by Intracoronary Thrombus in Acute Myocardial Infarction

    PubMed Central

    2016-01-01

    Recently, percutaneous coronary intervention has been the treatment of choice in most acute myocardial infarction cases. Although the results of percutaneous coronary interventions have ben good, the no-reflow phenomenon and distal embolization of intracoronary thrombus are still major problems even after successful interventions. In this article, we will briefly review the deleterious effects of no-reflow and distal embolization of intracoronary thrombus during percutaneous coronary interventions. The current trials focused on the prevention and treatment of the no-reflow phenomenon and intracoronary thrombus. PMID:26865998

  6. [Cochrane Corner: Intra-aortic balloon pump in patients with cardiogenic shock following myocardial infarction].

    PubMed

    Caldeira, Daniel; Pereira, Hélder; Costa, João; Vaz-Carneiro, António

    2016-04-01

    Improvement of hemodynamic parameters is the rationale for the use of intra-aortic balloon pump counterpulsation (IABP) in patients with cardiogenic shock following acute myocardial infarction (MI). This Cochrane systematic review evaluated the impact of this intervention in reducing mortality. Seven randomized controlled trials with a total of 790 patients were included (four using medical therapy as a comparator, and three comparing IABP with other ventricular assist devices). IABP did not reduce mortality in either the short or long term. Therefore, the systematic use of IABP in patients with cardiogenic shock following MI cannot be recommended.

  7. [Cochrane Corner: Intra-aortic balloon pump in patients with cardiogenic shock following myocardial infarction].

    PubMed

    Caldeira, Daniel; Pereira, Hélder; Costa, João; Vaz-Carneiro, António

    2016-04-01

    Improvement of hemodynamic parameters is the rationale for the use of intra-aortic balloon pump counterpulsation (IABP) in patients with cardiogenic shock following acute myocardial infarction (MI). This Cochrane systematic review evaluated the impact of this intervention in reducing mortality. Seven randomized controlled trials with a total of 790 patients were included (four using medical therapy as a comparator, and three comparing IABP with other ventricular assist devices). IABP did not reduce mortality in either the short or long term. Therefore, the systematic use of IABP in patients with cardiogenic shock following MI cannot be recommended. PMID:26992744

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

    PubMed

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

    2005-04-01

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

  9. Pharmacological prevention of reperfusion injury in acute myocardial infarction. A potential role for adenosine as a therapeutic agent.

    PubMed

    Quintana, Miguel; Kahan, Thomas; Hjemdahl, Paul

    2004-01-01

    last years, three relatively large placebo-controlled clinical trials have been conducted: Acute Myocardial Infarction Study of Adenosine Trial (AMISTAD) I and II and Attenuation by Adenosine of Cardiac Complications (ATTACC). In the AMISTAD trials, the final infarct size was reduced and the LV systolic function was improved by adenosine treatment, mainly in patients with anterior MI localization. However, morbidity and mortality were not affected. In the ATTACC study, the LV systolic function was not affected by adenosine, however, trends towards improved survival were observed in patients with anterior MI localization. The possibility of obtaining a Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the infarct-related artery in up to 95% of patients with acute MI (increasing the occurrence of reperfusion injury) has turned back the interest towards the protection of myocardial cells from the impending ischemic and reperfusion injury in which adenosine alone or together with other cardio-protective agents may exert important clinical effects. PMID:15134468

  10. 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

  11. Intravenous Erythropoietin in Patients with ST-Segment Elevation Myocardial Infarction

    PubMed Central

    Najjar, Samer S.; Rao, Sunil V.; Melloni, Chiara; Raman, Subha V.; Povsic, Thomas J.; Melton, Laura; Barsness, Gregory W.; Prather, Kristi; Heitner, John F.; Kilaru, Rakhi; Gruberg, Luis; Hasselblad, Vic; Greenbaum, Adam B.; Patel, Manesh; Kim, Raymond J.; Talan, Mark; Ferrucci, Luigi; Longo, Dan L.; Lakatta, Edward G.; Harrington, Robert A.

    2012-01-01

    Context Acute ST-segment elevation myocardial infarction (STEMI) is a leading cause of morbidity and mortality. In experimental models of MI, erythropoietin reduces infarct size and improves left ventricular (LV) function. Objective To evaluate the safety and efficacy of a single intravenous bolus of epoetin alfa in patients with STEMI. Design, Setting, and Patients Prospective, randomized, double-blind, placebo-controlled trial with a dose-escalation safety phase and a single-dose (60,000 units of epoetin alfa) efficacy phase involving 222 patients with STEMI who underwent successful percutaneous coronary intervention (PCI) as a primary or rescue reperfusion strategy. Intervention Participants were randomly assigned to treatment with intravenous epoetin alfa or matching saline placebo administered within 4 hours of reperfusion. Main Outcome Measure Infarct size, expressed as a percentage of LV mass, assessed by cardiac magnetic resonance (CMR) imaging 2–6 days after study medication administration. Results In the efficacy cohort (n=138), infarct size did not differ between groups at either 2–6 days (15.8±10.3 vs. 15.0±10.0, P=.666) or 12±2 weeks (10.6±8.6 vs. 10.4±7.6, P=.886). Left ventricular ejection fraction also did not differ between groups at either the early (48.2±9.1 vs. 48.9±8.7, P=.671) or late (52.5±9.3 vs. 52.0±8.8, P=.760) timepoints. In pre-specified analyses of patients aged ≥70 years (n=21), mean infarct size within the first week was larger in the epoetin alfa arm than in the placebo group (19.9±9.9 vs.11.7±7.2, P=.026). Patients who received epoetin alfa had a higher incidence of the composite endpoint of death, myocardial infarction, stroke, or stent thrombosis (4.0% vs. 0.0%, P=.042), and a higher incidence of serious adverse events (20.0% vs. 10.3%, P=.052). Conclusions In STEMI patients successfully reperfused with primary or rescue PCI, a single intravenous bolus of epoetin alfa did not reduce infarct size and was

  12. 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.

  13. 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

  14. [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.

  15. 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

  16. 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

  17. 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.

  18. 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

  19. 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.

  20. 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

  1. 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.

  2. 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

  3. 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.

  4. 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. PMID:25594408

  5. Remote Zone Extracellular Volume and Left Ventricular Remodeling in Survivors of ST-Elevation Myocardial Infarction

    PubMed Central

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

    2016-01-01

    The natural history and pathophysiological significance of tissue remodeling in the myocardial remote zone after acute ST-elevation myocardial infarction (STEMI) is incompletely understood. Extracellular volume (ECV) in myocardial regions of interest can now be measured with cardiac magnetic resonance imaging. Patients who sustained an acute STEMI were enrolled in a cohort study (BHF MR-MI [British Heart Foundation Magnetic Resonance Imaging in Acute ST-Segment Elevation Myocardial Infarction study]). Cardiac magnetic resonance was performed at 1.5 Tesla at 2 days and 6 months post STEMI. T1 modified Look-Locker inversion recovery mapping was performed before and 15 minutes after contrast (0.15 mmol/kg gadoterate meglumine) in 140 patients at 2 days post STEMI (mean age: 59 years, 76% male) and in 131 patients at 6 months post STEMI. Remote zone ECV was lower than infarct zone ECV (25.6±2.8% versus 51.4±8.9%; P<0.001). In multivariable regression, left ventricular ejection fraction was inversely associated with remote zone ECV (P<0.001), and diabetes mellitus was positively associated with remote zone ECV (P=0.010). No ST-segment resolution (P=0.034) and extent of ischemic area at risk (P<0.001) were multivariable associates of the change in remote zone ECV at 6 months (ΔECV). ΔECV was a multivariable associate of the change in left ventricular end-diastolic volume at 6 months (regression coefficient [95% confidence interval]: 1.43 (0.10–2.76); P=0.036). ΔECV is implicated in the pathophysiology of left ventricular remodeling post STEMI, but because the effect size is small, ΔECV has limited use as a clinical biomarker of remodeling. Clinical Trial Registration— URL: https://www.clinicaltrials.gov. Unique identifier: NCT02072850. PMID:27354423

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

    PubMed Central

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

    1977-01-01

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

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

    PubMed Central

    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 of the influence of infarct size on temporal and spatial alteration of myocardium during progressive myocardial remodeling. MI with three infarct sizes (15%, 25% and 35% of left ventricular wall) was created in an ovine infarction model. The progressive LV remodeling over a 12 week period was studied. Echocardiography, sonomicrometry, histological and molecular analyses were carried out to evaluate cardiac function, regional tissue contractile function and structural remodeling, and regional cardiomycyte hypertrophy and calcium handling proteins. The 15%, 25% and 35% MI groups at 12 weeks after MI 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 a 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. Significant correlation was found between myocardiocyte 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, impairment severity of cellular structure and composition, and regional contractile function at regional tissue level and LV cardiac function at organ level. PMID:26540290

  8. 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.

  9. Unusual mechanism of myocardial infarction in prosthetic valve endocarditis

    PubMed Central

    Atik, Fernando A; Campos, Vanessa G; da Cunha, Claudio R; de Oliveira, Felipe Bezerra Martins; Otto, Maria Estefânia Bosco; Monte, Guilherme U

    2015-01-01

    A 46-year-old man with bicuspid aortic valve and severe calcific aortic stenosis was submitted to aortic valve replacement with a stented bioprosthesis. He developed Staphylococcus epidermidis prosthetic valve endocarditis a month later, presenting in the emergency room with acute myocardial infarction. The mechanism of myocardial ischemia was a large aortic root abscess causing left main extrinsic compression. He was urgently taken to the operating room, and an aortic root replacement with cryopreserved homograft was performed, associated with autologous pericardium patch closure of aortic to right atrium fistula and coronary artery bypass grafting of the left anterior descending. After a difficult postoperative period with multiple problems, he was eventually discharged home. At 36-month follow-up, he is asymptomatic with no recurrent infection, and the left main coronary artery is widely patent on control chest computed tomography. PMID:26045678

  10. [Exercise test after acute myocardial infarction: without therapy?].

    PubMed

    Gregorio, G

    2001-12-01

    In this article we analyze the role of ECG exercise test in the clinical evaluation and prognostic stratification of patients after acute myocardial infarction. Moreover, we analyze if test results may be influenced by drugs. In clinical practice, most of the cardiologists working in hospital perform pre-discharge tests while patients are on medical therapy; after the acute event, exercise test is performed after pharmacological wash-out. In the thrombolytic age exercise test has a well-defined role in the evaluation and prognostic stratification of postinfarction patients, but some aspects regarding the way of performance and the opportunity of a pharmacological wash-out need further investigation.

  11. Small Bowel Obstruction Mimicking Acute ST-Elevation Myocardial Infarction

    PubMed Central

    Chang, Nai-Lun; Shulik, Oleg; DePasquale, Joseph; Shamoon, Fayez

    2015-01-01

    We present a case of a 42-year-old female who presented to our institution with a small bowel obstruction and had emergent surgical decompression. Thirteen days postoperatively, the patient became tachycardic and had worsening epigastric pain. Electrocardiogram showed significant ST-segment elevations in leads II, III, aVF, and V3–V6, suggesting the possibility of acute inferolateral myocardial infarction. Subsequent workup revealed the cause of the ST-elevations to be due to recurrent small bowel obstruction. Although intra-abdominal causes of ST-elevation have been reported, our case may be the first to be associated with small bowel obstruction. PMID:25838963

  12. [Outpatient rehabilitation after myocardial infarction or for heart failure].

    PubMed

    Fischer, H M; Charrier, A; Dörr, R; Spitzer, S G

    2012-02-01

    Reducing cardiac mortality and improving quality of life are the main objectives of cardiac rehabilitation. In recent years, outpatient rehabilitation within easy patient reach has achieved the same status as inpatient rehabilitation. Outpatient rehabilitation permits close involvement of the patient's family and social environment, thus easing reintegration into everyday life. However, the health care system is not yet utilizing outpatient rehabilitation to its full potential. This contribution illustrates the principles of rehabilitation following myocardial infarction or for heart failure in an outpatient setting, as well as its potential and future development.

  13. Noncompaction and embolic myocardial infarction: the importance of oral anticoagulation.

    PubMed

    Pulignano, Giovanni; Tinti, Maria Denitza; Tolone, Stefano; Musto, Carmine; De Lio, Lucia; Pino, Paolo Giuseppe; Minardi, Giovanni; Violini, Roberto; Uguccioni, Massimo

    2015-01-01

    Left ventricular noncompaction (LVNC) is characterized by left ventricular (LV) hypertrabeculations and is associated with heart failure, arrhythmias and embolism. We report the case of a 67-year-old LVNC patient, under oral anticoagulation (OAC) therapy for apical thrombosis. After she discontinued OAC, the thrombus involved almost the whole of the left ventricle; in a few months her condition worsened, requiring hospitalization, and despite heparin infusion she experienced myocardial infarction (MI), caused by embolic occlusion of the left anterior descending artery. Although infrequent as a complication of LVNC, and usually attributable to microvascular dysfunction, in this case MI seems due to coronary thromboembolism from dislodged thrombotic material in the left ventricle.

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

    PubMed

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

    2013-01-01

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

  15. Myocardial infarction with an initially normal electrocardiogram--angiographic findings.

    PubMed

    Caceres, L; Cooke, D; Zalenski, R; Rydman, R; Lakier, J B

    1995-10-01

    To analyze the paradox of acute myocardial infarction (AMI) with an initially normal electrocardiogram (ECG), we reviewed the records of 732 patients discharged with a final diagnosis of AMI over a 2-year period. Twenty-one patient were identified whose initial ECG was normal and who underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinct groups were identified: Group 1: those who subsequently developed ST elevation or Q waves (n = 7), Group 2: those who developed ST depression or T-wave inversion (n = 8), and Group 3: those whose ECG remained normal ( n = 6). Peak creatine kinase (CK), timing of the first ECG change, life-threatening complications, and location of the infarct-related coronary lesion were recorded. Infarct-related coronary lesions were also classified into those in a major coronary trunk versus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in the frequency of coronary artery involvement in the groups studied: left anterior descending (33%), right coronary artery (38%), and circumflex (28%). All ECG changes developed within the first 48 h of hospitalization; 17 +/- 15 in Group 1, and 24 +/- 12 h in Group 2. All six patients who had a persistently normal ECG (Group 3) had lesions in branch vessels (p < 0.05 when compared with Group 1 plus Group 2). Patients who developed ST elevation or Q waves (Group 1) always had a major artery trunk involved (p < 0.05 when compared with Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with the other two groups. Myocardial infarction with an initial normal ECG is uncommon and may result from involvement of any of the three coronary arteries. Electrocardiographic evolution usually occurs within the first 48 h of hospitalization. Patients whose ECGs remain normal appear to have culprit lesions in coronary branches, smaller infarctions, and fewer in

  16. Bronchogenic Carcinoma with Cardiac Invasion Simulating Acute Myocardial Infarction

    PubMed Central

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

    2016-01-01

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

  17. Ethnic differences in mortality of male and female patients surviving acute myocardial infarction: long-term follow-up of 5,700 patients. The Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) Study Group.

    PubMed

    Harpaz, D

    1997-10-01

    In migrant countries, ethnic origin may represent a complex of cultural, behavioral and possibly genetic differences. These have been shown to influence acute myocardial infarction (AMI) incidence. How ethnic origin may affect survival after AMI is unknown. Data from 5,692 patients included in the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) registry were analyzed. Patients were divided into eight different ethnic groups, according to birthplaces from five continents, representing major socio-economic and possibly some genetic variation. Mortality was analyzed after adjustment for baseline characteristics known to predict death from coronary artery disease (CAD) using Jews born in Israel as a reference. The odds ratio for in-hospital mortality was higher in women than in men, but unrelated to ethnic origin. The odds ratio for men ranged between 1.08 (95% confidence interval (CI): 0.67-1.73) for Jews born in Eastern Europe and 1.84 (95% CI: 1.07-3.15) for counterparts born in the Middle East. The odds ratio for women ranged between 0.73 in Jews born in Central Europe (95% CI: 0.35-1.50) and 1.45 (95% CI: 0.76-3.15) for Jewish women born in the Balkan countries. Among 4,686 patients surviving the hospital phase, long-term mortality rates (mean follow-up 7.1 +/- 3.5 years) were 43.3% in men and 57.6% in women. Among 3,586 surviving men, the adjusted risk ratios for 10-year mortality varied between 0.92 (95% CI: 0.72-1.18) for men born in Romania and 1.49 (95% CI: 1.07-2.09) for Israeli born Arabs. The variation among men is within the limits of statistical error. However, among 1,100 surviving women, the risk ratio for 10-year mortality differed significantly, from as low as 1.43 (95% CI: 0.84-2.41) in Jewish women born in Central Europe to as high as 2.83 (95% CI: 1.67-4.79) in counterparts born in the Middle East. The latter observations were consistent with the mortality after 3 years. Thus, ethnic origin of Israelis marginally influenced the

  18. 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.

  19. Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction.

    PubMed

    Wysoczynski, Marcin; Solanki, Mitesh; Borkowska, Sylwia; van Hoose, Patrick; Brittian, Kenneth R; Prabhu, Sumanth D; Ratajczak, Mariusz Z; Rokosh, Gregg

    2014-09-01

    Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kit(pos) cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67(pos) CSPCs and decreased formation of new BrdU(pos) /α-sarcomeric actin(pos) myocytes, and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate that CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function.

  20. Beta-blocker therapy after myocardial infarction: secondary prevention in all patients?

    PubMed

    Griggs, T; Adams, K; Narvarte, H; Sheps, D

    1985-01-01

    The ability of beta-adrenergic blocking drugs to prevent death in patients after myocardial infarction has been demonstrated by several large trials. However, the need to treat patients at low risk has been challenged. Retrospective analysis of the data from one of these studies plus results from many additional studies have shown that electrical, mechanical and ischemic complications after myocardial infarction imply a high risk of subsequent death or recurrent infarction. On the other hand, absence of complications with a negative exercise tolerance test, good exercise tolerance, absence of arrhythmias and normal increase of ejection fraction with exercise documents a very low risk. These considerations lead to the following practical implications: The physician should watch for any evidence of left ventricular dysfunction or arrhythmia. Any such complication justifies treatment or more intensive study. Patients without complications can be further characterized with exercise testing, exercise radionuclide blood pool ventriculography, and Holter monitoring. If these tests expose risk indicators, treatment or more study should again be recommended. Because the beta-blockers are probably life-saving in a considerable portion of the patients with moderate and high risk, the decision to treat or not to treat should be made with due, affirmative consideration. In those patients with a carefully documented uncomplicated course and who have a normal exercise test and appropriate increase in ventricular ejection fraction with stress, beta-blockade is probably of no benefit. Under these conditions, a physician and patient might logically decide not to use the drug.

  1. Fractional flow reserve-guided management in stable coronary disease and acute myocardial infarction: recent developments

    PubMed Central

    Berry, Colin; Corcoran, David; Hennigan, Barry; Watkins, Stuart; Layland, Jamie; Oldroyd, Keith G.

    2015-01-01

    Coronary artery disease (CAD) is a leading global cause of morbidity and mortality, and improvements in the diagnosis and treatment of CAD can reduce the health and economic burden of this condition. Fractional flow reserve (FFR) is an evidence-based diagnostic test of the physiological significance of a coronary artery stenosis. Fractional flow reserve is a pressure-derived index of the maximal achievable myocardial blood flow in the presence of an epicardial coronary stenosis as a ratio to maximum achievable flow if that artery were normal. When compared with standard angiography-guided management, FFR disclosure is impactful on the decision for revascularization and clinical outcomes. In this article, we review recent developments with FFR in patients with stable CAD and recent myocardial infarction. Specifically, we review novel developments in our understanding of CAD pathophysiology, diagnostic applications, prognostic studies, clinical trials, and clinical guidelines. PMID:26038588

  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. Local activation of cardiac stem cells for post-myocardial infarction cardiac repair.

    PubMed

    Wen, Zhuzhi; Mai, Zun; Zhang, Haifeng; Chen, Yangxin; Geng, Dengfeng; Zhou, Shuxian; Wang, Jingfeng

    2012-11-01

    The prognosis of patients with myocardial infarction (MI) and resultant chronic heart failure remains extremely poor despite continuous advancements in optimal medical therapy and interventional procedures. Animal experiments and clinical trials using adult stem cell therapy following MI have shown a global improvement of myocardial function. The emergence of stem cell transplantation approaches has recently represented promising alternatives to stimulate myocardial regeneration. Regarding their tissue-specific properties, cardiac stem cells (CSCs) residing within the heart have advantages over other stem cell types to be the best cell source for cell transplantation. However, time-consuming and costly procedures to expanse cells prior to cell transplantation and the reliability of cell culture and expansion may both be major obstacles in the clinical application of CSC-based transplantation therapy after MI. The recognition that the adult heart possesses endogenous CSCs that can regenerate cardiomyocytes and vascular cells has raised the unique therapeutic strategy to reconstitute dead myocardium via activating these cells post-MI. Several strategies, such as growth factors, mircoRNAs and drugs, may be implemented to potentiate endogenous CSCs to repair infarcted heart without cell transplantation. Most molecular and cellular mechanism involved in the process of CSC-based endogenous regeneration after MI is far from understanding. This article reviews current knowledge opening up the possibilities of cardiac repair through CSCs activation in situ in the setting of MI.

  4. Efficacy of technetium Tc 99m pyrophosphate imaging in patients with equivocal myocardial infarction

    SciTech Connect

    Powers, T.A.; Tyler, J.L.; Kulkarni, M.V.

    1983-03-01

    We studied the efficacy of technetium Tc 99m pyrophosphate imaging in patients with equivocal evidence of acute myocardial infarction. Only patients with positive enzyme findings (regardless of ECG findings) had scans with greater than or equal to 2+ focal uptake. None of 26 patients with negative or equivocal enzyme findings (regardless of ECG findings) had greater than 2+ diffuse uptake. These results support the contention that infarct-avid imaging has little clinical utility in patients with equivocal evidence of myocardial infarction.

  5. Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers

    PubMed Central

    Chen, Min; Li, Yongjun; Wang, YaLing; Zhang, Shijun; Wang, Zhen; Wang, Lin; Ju, Shenghong

    2016-01-01

    We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (<4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers. PMID:27777517

  6. Reduction of myocardial infarct size with ischemic "conditioning": physiologic and technical considerations.

    PubMed

    Przyklenk, Karin

    2013-10-01

    A wealth of evidence has revealed that the heart can be "conditioned" and rendered less vulnerable to ischemia-reperfusion injury via the upregulation of endogenous protective signaling pathways. Three distinct conditioning strategies have been identified: (1) preconditioning, the phenomenon where brief episodes of myocardial ischemia (too brief to cause cardiomyocyte death) limit necrosis caused by a subsequent sustained ischemic insult; (2) postconditioning, the concept that relief of myocardial ischemia in a staged or stuttered manner attenuates lethal ischemia-reperfusion injury; and (3) remote conditioning, or upregulation of a cardioprotective phenotype initiated by ischemia in a remote organ or tissue and "transported" to the heart. Progress has been made in defining the technical requirements and limitations of each of the 3 ischemic conditioning models (including the timing and severity of the protective stimulus), as well as elucidating the molecular mechanisms (in particular, the receptor-mediated signaling pathways) responsible for conditioning-induced myocardial protection. Moreover, phase III clinical trials are in progress, seeking to capitalize on the protection that can be achieved by postconditioning and remote conditioning, and applying these strategies in patients undergoing cardiac surgery or angioplasty for the treatment of acute myocardial infarction. There is, however, a potentially important caveat to the clinical translation of myocardial conditioning: emerging data suggest that the efficacy of ischemic conditioning is compromised in aging, diabetic, and hypertensive cohorts, the specific populations in which myocardial protection is most relevant. Successful clinical application of myocardial conditioning will therefore require an understanding of the potential confounding consequences of these comorbidities on the "conditioned" phenotype.

  7. A case of left ventricular aneurysm caused by localized myocardial infarction.

    PubMed

    Watanabe, Tomoyuki; Iwai-Takano, Masumi; Ohto, Yuriko; Abe, Haruna; Saitoh, Hiromi; Ujiie, Michio; Nozaki, Yoko; Noda, Shigeko

    2013-09-01

    A 73-year-old man was hospitalized for unstable angina pectoris with no history of myocardial infarction. After undergoing percutaneous coronary intervention, left ventriculography incidentally revealed a cavity in the anterior wall, and echocardiography found the cavity wall to be dyskinetic. Myocardial contrast echocardiography revealed that the wall of the cavity was surrounded by myocardial tissue with low perfusion. Furthermore, radial strain in the wall of the cavity was low. Myocardial scintigraphy showed a localized defect on the anterior wall. The patient was finally diagnosed as true aneurysm after asymptomatic and localized myocardial infarction, and has since been followed up by echocardiography in the outpatient clinic. PMID:27278616

  8. Relationship between sympathetic nerve sprouting and repolarization dispersion at peri-infarct zone after myocardial infarction.

    PubMed

    Jiang, Hong; Lu, Zhibing; Yu, Ying; Zhao, Dongdong; Yang, Bo; Huang, Congxin

    2007-07-31

    Sympathetic nerve sprouting is thought to contribute to sudden cardiac death (SCD) in chronic myocardial infarction (MI). However, the mechanisms remain unclear. This study investigated the relationship between sympathetic nerve sprouting and repolarization dispersion at peri-infarct zones after MI. Thirty adult New Zealand White rabbits underwent coronary artery ligation (MI group: n=20) or sham operation (SO group: n=10). Eight weeks after surgery, transmural dispersion of repolarization (TDR) was examined at the peri-infarct zones in MI group and corresponding zones in the SO group at baseline and during sympathetic nerve stimulation. Sympathetic nerve sprouting was detected by immunocytochemical staining using anti-growth associated protein 43 (GAP43) and anti-tyrosine hydroxylase (TH) antibodies. The results demonstrated that TDR was significantly larger at peri-infarct zones in MI group than the corresponding zone in SO group at baseline or during sympathetic nerve stimulation. The densities of both GAP43- and TH-positive nerves were significantly higher at peri-infarct zones in infracted hearts than the corresponding zones in control hearts (both p<0.01). In the MI group, the density of GAP43- or TH-positive nerves at peri-infarct zones had a significantly positive correlation with the TDR or DeltaTDR (change in TDR) at baseline as well as with sympathetic nerve stimulation (p<0.05 for all). These results suggested that sympathetic nerve sprouting is more pronounced and heterogeneous at peri-infarct zones at 8 weeks after MI. The excessive sprouting of sympathetic nerves increases local ventricular TDR, which may be a potential mechanism for SCD in chronic MI.

  9. The relationship between acute myocardial infarction and periodontitis

    PubMed Central

    Khosravi Samani, Mahmoud; Jalali, Farzad; Seyyed Ahadi, Seyyed Masud; Hoseini, Seyyed Reza; Dabbagh Sattari, Farhad

    2013-01-01

    Background: Periodontitis is common in adults and cardiovascular diseases (CVD) are the most common cause of adult death in the world. This study aimed to investigate the relationship between CVD and periodontitis. Methods: Sixty patients with myocardial infarction (MI) as case and 63 subjects with periodontitis without MI as control were studied. Periodontitis was assessed according to Ramfjord periodontal diseases index and the number of missing teeth besides classic risk factors of MI were recorded. Results: The patients who lost more than 10 teeth were at more risk of myocardial infarction (OR=2.73). There was a significant relationship between mean attachment loss and MI (p=0.0001). There was also a relation between attachment loss more than 3 mm and MI with OR of 4. Significant difference between mean PDI (periodontal disease index) was seen in case and control groups (p=0.0001). Subjects with PDI>4 were at more risk of periodontal diseases (OR=7.87). Conclusion: The results show the presence of significant relation between periodontitis and MI which could serve as an alarm to treat periodontitis carefully. PMID:24009957

  10. 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.

  11. Arrhythmic death and ICD implantation after myocardial infarction

    PubMed Central

    LOMBARDI, FEDERICO

    2006-01-01

    Arrhythmic death remains one of the most important causes of mortality after an acute myocardial infarction also in the revascularization era. As a consequence, identification of patients at risk should be performed before discharge. Unfortunately, in the clinical practice, this evaluation is mainly based on detection of a depressed left ventricular ejection. This approach, however, cannot adequately distinguish arrhythmic versus non-arrhythmic risk. This issue is of critical relevance when considering that arrhythmic death can be significantly reduced by appropriate interventions of implantable cardioverter defibrillator. Available evidence, however, indicates that in the first month after myocardial infarction, device implantation does not significantly reduce cardiac mortality: it seems that the reduction of arrhythmic death is counterbalanced by an increase in rate of death from non arrhythmic cause. It is therefore to be hoped that, in the future, arrhythmic risk evaluation will be based not only on the extent of left ventricular dysfunction but also on the analysis of other risk markers such as those reflecting autonomic dysfunction, cardiac electrical instability and presence of subclinical inflammation. PMID:21977246

  12. Measurement of myocardial perfusion and infarction size using computer-aided diagnosis system for myocardial contrast echocardiography.

    PubMed

    Du, Guo-Qing; Xue, Jing-Yi; Guo, Yanhui; Chen, Shuang; Du, Pei; Wu, Yan; Wang, Yu-Hang; Zong, Li-Qiu; Tian, Jia-Wei

    2015-09-01

    Proper evaluation of myocardial microvascular perfusion and assessment of infarct size is critical for clinicians. We have developed a novel computer-aided diagnosis (CAD) approach for myocardial contrast echocardiography (MCE) to measure myocardial perfusion and infarct size. Rabbits underwent 15 min of coronary occlusion followed by reperfusion (group I, n = 15) or 60 min of coronary occlusion followed by reperfusion (group II, n = 15). Myocardial contrast echocardiography was performed before and 7 d after ischemia/reperfusion, and images were analyzed with the CAD system on the basis of eliminating particle swarm optimization clustering analysis. The myocardium was quickly and accurately detected using contrast-enhanced images, myocardial perfusion was quantitatively calibrated and a color-coded map calibrated by contrast intensity and automatically produced by the CAD system was used to outline the infarction region. Calibrated contrast intensity was significantly lower in infarct regions than in non-infarct regions, allowing differentiation of abnormal and normal myocardial perfusion. Receiver operating characteristic curve analysis documented that -54-pixel contrast intensity was an optimal cutoff point for the identification of infarcted myocardium with a sensitivity of 95.45% and specificity of 87.50%. Infarct sizes obtained using myocardial perfusion defect analysis of original contrast images and the contrast intensity-based color-coded map in computerized images were compared with infarct sizes measured using triphenyltetrazolium chloride staining. Use of the proposed CAD approach provided observers with more information. The infarct sizes obtained with myocardial perfusion defect analysis, the contrast intensity-based color-coded map and triphenyltetrazolium chloride staining were 23.72 ± 8.41%, 21.77 ± 7.8% and 18.21 ± 4.40% (% left ventricle) respectively (p > 0.05), indicating that computerized myocardial contrast echocardiography can

  13. Measurement of myocardial perfusion and infarction size using computer-aided diagnosis system for myocardial contrast echocardiography.

    PubMed

    Du, Guo-Qing; Xue, Jing-Yi; Guo, Yanhui; Chen, Shuang; Du, Pei; Wu, Yan; Wang, Yu-Hang; Zong, Li-Qiu; Tian, Jia-Wei

    2015-09-01

    Proper evaluation of myocardial microvascular perfusion and assessment of infarct size is critical for clinicians. We have developed a novel computer-aided diagnosis (CAD) approach for myocardial contrast echocardiography (MCE) to measure myocardial perfusion and infarct size. Rabbits underwent 15 min of coronary occlusion followed by reperfusion (group I, n = 15) or 60 min of coronary occlusion followed by reperfusion (group II, n = 15). Myocardial contrast echocardiography was performed before and 7 d after ischemia/reperfusion, and images were analyzed with the CAD system on the basis of eliminating particle swarm optimization clustering analysis. The myocardium was quickly and accurately detected using contrast-enhanced images, myocardial perfusion was quantitatively calibrated and a color-coded map calibrated by contrast intensity and automatically produced by the CAD system was used to outline the infarction region. Calibrated contrast intensity was significantly lower in infarct regions than in non-infarct regions, allowing differentiation of abnormal and normal myocardial perfusion. Receiver operating characteristic curve analysis documented that -54-pixel contrast intensity was an optimal cutoff point for the identification of infarcted myocardium with a sensitivity of 95.45% and specificity of 87.50%. Infarct sizes obtained using myocardial perfusion defect analysis of original contrast images and the contrast intensity-based color-coded map in computerized images were compared with infarct sizes measured using triphenyltetrazolium chloride staining. Use of the proposed CAD approach provided observers with more information. The infarct sizes obtained with myocardial perfusion defect analysis, the contrast intensity-based color-coded map and triphenyltetrazolium chloride staining were 23.72 ± 8.41%, 21.77 ± 7.8% and 18.21 ± 4.40% (% left ventricle) respectively (p > 0.05), indicating that computerized myocardial contrast echocardiography can

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

    PubMed

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

    2016-01-01

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

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

    PubMed Central

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

    2016-01-01

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

  16. Microvascular resistance of the culprit coronary artery in acute ST-elevation myocardial infarction

    PubMed Central

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

    2016-01-01

    BACKGROUND. Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS. IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire–based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days). RESULTS. Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0–33.0] vs. 17 [13.0–39.0] vs. 37 [21.0–63.0], P < 0.001; CFR: 1.7 [1.4–2.5] vs. 1.5 [1.1–1.8] vs. 1.4 [1.0–1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS. IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR. TRIAL REGISTRATION. NCT02072850. FUNDING. A

  17. Microvascular resistance of the culprit coronary artery in acute ST-elevation myocardial infarction

    PubMed Central

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

    2016-01-01

    BACKGROUND. Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS. IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire–based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days). RESULTS. Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0–33.0] vs. 17 [13.0–39.0] vs. 37 [21.0–63.0], P < 0.001; CFR: 1.7 [1.4–2.5] vs. 1.5 [1.1–1.8] vs. 1.4 [1.0–1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS. IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR. TRIAL REGISTRATION. NCT02072850. FUNDING. A

  18. Acute myocardial infarction after heart irradiation in young patients with Hodgkin's disease

    SciTech Connect

    Joensuu, H.

    1989-02-01

    Forty-seven patients younger than 40 years at the time of the diagnosis, and irradiated to the mediastinum for Hodgkin's disease at Turku University Central Hospital from 1977 to 1982, were regularly followed for 56 to 127 months after therapy. Two patients developed an acute myocardial infarction ten and 50 months after cardiac irradiation at the age of only 28 and 24 years, respectively. None of the patients died from lymphoma within five years from the diagnosis, but one of the infarctions was eventually fatal. Since acute myocardial infarction is rare in this age group, the result suggests strongly that prior cardiac irradiation is a risk factor for acute myocardial infarction. The possibility of radiation-induced myocardial infarction should be taken into account both in treatment planning and follow-up of patients with Hodgkin's disease.

  19. Early radionuclide scans for risk assessment in suspected acute myocardial infarction.

    PubMed Central

    Norris, S. L.; Haywood, L. J.; Sobel, E.; Hung, G. L.; deGuzman, M.; Siegel, M.

    1997-01-01

    First-day thallium-201 myocardial perfusion scans and technetium-99m RBC gated scintiangiography were performed during the initial clinical and prognostic evaluation of 69 patients with suspected acute myocardial infarction. Patients were monitored for clinical course, diagnosis confirmation, and use of specialty services (cardiac catheterization, percutaneous balloon angioplasty, and cardiac surgery) during hospitalization. Myocardial infarction, confirmed in 20 patients, was associated with significantly more left ventricular dilatation, lower ejection fractions, lower peak left ventricular filling rates, wall motion abnormalities, and thallium-201 perfusion defects than nonmyocardial infarction patients. Among all patients, left ventricular dilatation carried a relative risk of myocardial infarction of 5.8; low ejection fraction and right ventricular dilatation were strongly associated with myocardial infarction. A logistic model for congestive heart failure included: left ventricular dilation, lower mean left ventricular filling rates and time to peak filling rates, and abnormal thallium-201 lung:heart uptakes. Among nonmyocardial infarction patients, subsequent cardiac catheterization was predicted by the presence of anterior thallium-201 perfusion defects, Killip functional class II-III, and ischemia on ECG. These findings suggest that early detection of myocardial perfusion defects and cardiac dysfunction by radionuclide scans enhances initial evaluation of suspected acute myocardial infarction patients. Additional studies are needed to confirm these findings. PMID:9433058

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

    PubMed

    Richards, David A B; Denniss, A Robert

    2007-06-01

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

  1. Treatment of non-ST-elevation myocardial infarction and ST-elevation myocardial infarction in patients with chronic kidney disease

    PubMed Central

    Gluba, Anna; Banach, Maciej; Rysz, Jacek

    2013-01-01

    Renal dysfunction is frequent in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Chronic kidney disease (CKD) is associated with very poor prognosis and is an independent predictor of early and late mortality and major bleeding in patients with NSTE-ACS. Patients with NSTE-ACS and CKD are still rarely treated according to guidelines. Medical registers reveal that patients with CKD are usually treated with too high doses of antithrombotics, especially anticoagulants and inhibitors of platelet glycoprotein (GP) IIb/IIIa receptors, and therefore they are more prone to bleeding. Drugs which are excreted mainly or exclusively by the kidney should be administered in a reduced dose or discontinued in patients with CKD. These drugs include enoxaparin, fondaparinux, bivalirudin, and small molecule inhibitors of GP IIb/IIIa inhibitors. In long-term treatment of patients after myocardial infarction, anti-platelet therapy, lipid-lowering therapy and β-blockers are used. Chronic kidney disease patients before qualification for coronary interventions should be carefully selected in order to avoid their use in the group of patients who could not benefit from such procedures. This paper presents schemes of non-ST and ST-segment elevation myocardial infarction treatment in CKD patients in accordance with the current recommendations of the European Society of Cardiology (ESC). PMID:24482645

  2. EPC mobilization after erythropoietin treatment in acute ST-elevation myocardial infarction: the REVEAL EPC substudy

    PubMed Central

    Povsic, Thomas J.; Najjar, Samer S.; Prather, Kristi; Zhou, Jiying; Adams, Stacie D.; Zavodni, Katherine L.; Kelly, Francine; Melton, Laura G.; Hasselblad, Vic; Heitner, John F.; Raman, Subha V.; Barsness, Gregory W.; Patel, Manesh R.; Kim, Raymond J.; Lakatta, Edward G.; Harrington, Robert A.; Rao, Sunil V.

    2014-01-01

    Erythropoietin (EPO) was hypothesized to mitigate reperfusion injury, in part via mobilization of endothelial progenitor cells (EPCs). The REVEAL trial found no reduction in infarct size with a single dose of EPO (60,000 U) in patients with ST-segment elevation myocardial infarction. In a substudy, we aimed to determine the feasibility of cryopreserving and centrally analyzing EPC levels to assess the relationship between EPC numbers, EPO administration, and infarct size. As a prespecified substudy, mononuclear cells were locally cryopreserved before as well as 24 and 48–72 h after primary percutaneous coronary intervention. EPC samples were collected in 163 of 222 enrolled patients. At least one sample was obtained from 125 patients, and all three time points were available in 83 patients. There were no significant differences in the absolute EPC numbers over time or between EPO- and placebo-treated patients; however, there was a trend toward a greater increase in EPC levels from 24 to 48–72 h postintervention in patients receiving ≥30,000 U of EPO (P = 0.099 for CD133+ cells, 0.049 for CD34+ cells, 0.099 for ALDHbr cells). EPC numbers at baseline were inversely related to infarct size (P = 0.03 for CD133+ cells, 0.006 for CD34+ cells). Local whole cell cryopreservation and central EPC analysis in the context of a multicenter randomized trial is feasible but challenging. High-dose (≥30,000 U) EPO may mobilize EPCs at 48–72 h, and baseline EPC levels may be inversely associated with infarct size. PMID:23700090

  3. Magnetic resonance imaging in patients with unstable angina: comparison with acute myocardial infarction and normals

    SciTech Connect

    Ahmad, M.; Johnson, R.F. Jr.; Fawcett, H.D.; Schreiber, M.H.

    1988-09-01

    The role of magnetic resonance imaging in characterizing normal, ischemic and infarcted segments of myocardium was examined in 8 patients with unstable angina, 11 patients with acute myocardial infarction, and 7 patients with stable angina. Eleven normal volunteers were imaged for comparison. Myocardial segments in short axis magnetic resonance images were classified as normal or abnormal on the basis of perfusion changes observed in thallium-201 images in 22 patients and according to the electrocariographic localization of infarction in 4 patients. T2 relaxation time was measured in 57 myocardial segments with abnormal perfusion (24 with reversible and 33 with irreversible perfusion changes) and in 25 normally perfused segments. T2 measurements in normally perfused segments of patients with acute myocardial infarction, unstable angina and stable angina were within normal range derived from T2 measurements in 48 myocardial segments of 11 normal volunteers (42 +/- 10 ms). T2 in abnormal myocardial segments of patients with stable angina also was not significantly different from normal. T2 of abnormal segments in patients with unstable angina (64 +/- 14 in reversibly ischemic and 67 +/- 21 in the irreversibly ischemic segments) was prolonged when compared to normal (p less than 0.0001) and was not significantly different from T2 in abnormal segments of patients with acute myocardial infarction (62 +/- 18 for reversibly and 66 +/- 11 for irreversibly ischemic segments). The data indicate that T2 prolongation is not specific for acute myocardial infarction and may be observed in abnormally perfused segments of patients with unstable angina.

  4. 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.

  5. 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

  6. Myocardial uptake of indium-111-labeled antimyosin in acute subendocardial infarction: Clinical, histochemical, and autoradiographic correlation of myocardial necrosis

    SciTech Connect

    Hendel, R.C.; McSherry, B.A.; Leppo, J.A. )

    1990-11-01

    Indium-111-labeled antimyosin has been utilized in the diagnosis and localization of acute transmural myocardial infarction. The present report describes a patient who presented with a massive subendocardial infarction. Two days after the injection of antimyosin, the patient's clinical status markedly deteriorated and he expired. Postmortem examination demonstrated severe three-vessel coronary artery disease with extensive myocyte death in the endocardium. Autoradiography and histochemical staining of the prosected heart demonstrated high correlation for myocardial necrosis and corresponded to clinical evidence for diffuse subendocardial infarction.

  7. Estimation of infarct size by myocardial emission computed tomography with /sup 201/Tl and its relation to creatine kinase-MB release after myocardial infarction in man

    SciTech Connect

    Tamaki, S.; Nakajima, H.; Murakami, T.

    1982-11-01

    We evaluated emission computed tomography (ECT) /sup 201/Tl myocardial imaging in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar /sup 201/Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of /sup 201/Tl perfusion defects, the infarct area in planar images and the infarct volume in reconstructed ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r . 0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r . 0.69; for the largest infarct area, r . 0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

  8. Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man

    SciTech Connect

    Tamaki, S.; Nakajima, H.; Murakami, T.

    1982-11-01

    Emission computed tomography (ECT) for thallium-201 (/sup 201/Tl) myocardial imaging was evaluated in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar /sup 201/Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of /sup 201/Tl perfusion defects, the infarct area in planar images and the infarct volume in reconsturcted ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r=0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r=0.69; for the largest infarct area, r=0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

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

    PubMed

    Hashmi, Satwat; Al-Salam, Suhail

    2015-01-01

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

  10. 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.

  11. Kounis syndrome: inferior ST-segment elevation myocardial infarction following a bumblebee sting.

    PubMed

    Zanini, Gregoriana; Fontanella, Benedetta; Racheli, Marco; Bortolotti, Monica; Pasini, Gian Franco

    2013-08-01

    The Kounis syndrome was first described in 1991 as'the allergic angina syndrome'which could progress to acute myocardial infarction which was named'allergic myocardial infarction. There are several causes underlying this syndrome including drugs, various conditions and a variety of environmental exposure factors such as animal stings. Hymenoptera stings can induce Kounis syndrome because hymenoptera venom contains allergenic proteins and peptides. The following case report describes a patient who experienced an anaphylactic shock associated with coronary artery ischaemia (inferior ST-segment elevation myocardial infarction) after a bumblebee sting.

  12. Edetate Disodium-Based Treatment for Secondary Prevention in Post-Myocardial Infarction Patients.

    PubMed

    Lamas, Gervasio A; Issa, Omar M

    2016-02-01

    An abundance of data, known for decades, is available linking metals, such as lead and cadmium, with cardiovascular disease. However, the idea that these toxic metals could be a modifiable risk factor for atherosclerosis did not become apparent clinically until the completion of the Trial to Assess Chelation Therapy in 2012. This pivotal study was the first double-blind, randomized, controlled trial of its kind to demonstrate a clear improvement in cardiovascular outcomes with edetate disodium therapy in a secondary prevention, post-myocardial infarction population. This effect size was most striking in diabetic patients, where the efficacy of edetate disodium was comparable, if not superior, to that of current guideline-based therapies. Given the economic burden of diabetes and cardiovascular disease, the potential impact of this therapy could be enormous if the results of this study are replicated.

  13. Glycoprotein IIb/IIIa Receptor Inhibitors During Primary Angioplasty for Acute Myocardial Infarction.

    PubMed

    Gruberg; Lansky; Dangas; Stone

    1999-12-01

    Platelet glycoprotein IIb/IIIa receptors are the final common pathway leading to platelet aggregation and coronary thrombosis during acute myocardial infarction (AMI). Therefore, they are ideal candidates for pharmacologic intervention. The recent development of glycoprotein IIb/IIIa receptor antagonists has led to several studies that have shown the benefits and efficacy of these agents in the treatment of acute coronary syndromes and in the setting of percutaneous intervention. To date, six published trials have examined the safety and efficacy of intravenous abciximab, a mouse/human chimeric version of the 7E3 antibody, as an adjunct to primary mechanical reperfusion in patients with AMI. In this article, we review these trials, as well as new studies currently underway that will provide further information on the long-term benefits of combining these pharmacologic agents and stenting in the treatment of AMI.

  14. 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

  15. Unrecognized Myocardial Infarction Assessed by Cardiac Magnetic Resonance Imaging – Prognostic Implications

    PubMed Central

    Ahlström, Håkan; Bjerner, Tomas; Duvernoy, Olov; Eggers, Kai M.; Fröbert, Ole; Hadziosmanovic, Nermin

    2016-01-01

    Background Clinically unrecognized myocardial infarctions (UMI) are not uncommon and may be associated with adverse outcome. The aims of this study were to determine the prognostic implication of UMI in patients with stable suspected coronary artery disease (CAD) and to investigate the associations of UMI with the presence of CAD. Methods and Findings In total 235 patients late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) imaging and coronary angiography were performed. For each patient with UMI, the stenosis grade of the coronary branch supplying the infarcted area was determined. UMIs were present in 25% of the patients and 67% of the UMIs were located in an area supplied by a coronary artery with a stenosis grade ≥70%. In an age- and gender-adjusted model, UMI independently predicted the primary endpoint (composite of death, myocardial infarction, resuscitated cardiac arrest, hospitalization for unstable angina pectoris or heart failure within 2 years of follow-up) with an odds ratio of 2.9; 95% confidence interval 1.1–7.9. However, this association was abrogated after adjustment for age and presence of significant coronary disease. There was no difference in the primary endpoint rates between UMI patients with or without a significant stenosis in the corresponding coronary artery. Conclusions The presence of UMI was associated with a threefold increased risk of adverse events during follow up. However, the difference was no longer statistically significant after adjustments for age and severity of CAD. Thus, the results do not support that patients with suspicion of CAD should be routinely investigated by LGE-CMR for UMI. However, coronary angiography should be considered in patients with UMI detected by LGE-CMR. Trial Registration ClinicalTrials.gov NTC01257282 PMID:26885831

  16. Possible mechanisms of C-reactive protein mediated acute myocardial infarction.

    PubMed

    Fordjour, Patrick Asare; Wang, Yadong; Shi, Yang; Agyemang, Kojo; Akinyi, Mary; Zhang, Qiang; Fan, Guanwei

    2015-08-01

    Myocardial infarction is a relevant cardiovascular event worldwide for morbidity and mortality. It has been theorized that acute myocardial infarctions (AMIs) and other acute coronary events that are precipitated by atherosclerosis are due to arterial blockage from fat deposits. It is now known, however, that atherosclerosis involves more than just lipids. Inflammation has also been studied extensively to play a substantial role in myocardial infarction. There have been debates and conflicting reports over the past few years about the value of assessing levels of C-reactive protein and other biomarkers of inflammation for the prediction of cardiovascular events. Several studies have shown that CRP is not only an inflammatory marker, but also involved in the pathogenesis of myocardial infarction. Studies have linked atherogenesis and rupture of atherosclerotic lesion to endothelial dysfunction. CRP directly inhibits endothelial cell nitric oxide (NO) production via destabilizing endothelial NO synthase (eNOS). Decreased NO release causes CRP mediated inhibition of angiogenesis, stimulating endothelial cell apoptosis. CRP can also activate the complement system through the classical pathway. Complement activation plays an important role in mediating monocyte and neutrophil recruitment in an injured myocardium and may therefore lead to increase in infarct size. This article discusses the possible roles of CRP in complement activation, endothelial dysfunction and its impact on the development of myocardial infarction. We also reviewed the possible therapeutic approaches to myocardial infarction.

  17. Left ventricular pseudoaneurysm caused by coronary spasm, myocardial infarction, and myocardial rupture.

    PubMed

    Mahilmaran, Asha; Nayar, Pradeep G; Sheshadri, Mukundan; Sudarsana, Gurijala; Abraham, K A

    2002-01-01

    We report a very rare case of a 47-year-old man who had coronary spasm that resulted in a silent myocardial infarction, a ruptured myocardial wall, and a nonruptured left ventricular pseudoaneurysm. The patient presented with a 6-month history of dyspnea on exertion, without evidence of fixed coronary artery stenosis. Coronary angiography showed severe coronary spasm of the left anterior descending and left circumflex arteries; the spasm was relieved promptly by nitroglycerin. Echocardiography and left ventricular angiography revealed the large left ventricular pseudoaneurysm posterolateral to the left ventricle. We performed surgical resection of the pseudoaneurysm and patch repair of the ruptured left ventricular wall, with excellent results. We present this case because of the highly unusual sequence of events. Early surgical intervention resulted in the patient's recovery.

  18. Percutaneous coronary intervention for acute myocardial infarction with mitral regurgitation

    PubMed Central

    Tu, Yan; Zeng, Qing-Chun; Huang, Ying; Li, Jian-Yong

    2016-01-01

    Ischemic mitral regurgitation (IMR) is a common complication of acute myocardial infarction (AMI). Current evidences suggest that revascularization of the culprit vessels with percutaneous coronary artery intervention (PCI) or coronary artery bypass grafting can be beneficial for relieving IMR. A 2.5-year follow-up data of a 61-year-old male patient with ST-segment elevation AMI complicated with IMR showed that mitral regurgitation area increased five days after PCI, and decreased to lower steady level three months after PCI. This finding suggest that three months after PCI might be a suitable time point for evaluating the possibility of IMR recovery and the necessity of surgical intervention of the mitral valve for AMI patient. PMID:27582769

  19. Analysis of myocardial infarction signals using optical technique.

    PubMed

    Mahri, Nurhafizah; Gan, Kok Beng; Mohd Ali, Mohd Alauddin; Jaafar, Mohd Hasni; Meswari, Rusna

    2016-01-01

    The risk of heart attack or myocardial infarction (MI) may lead to serious consequences in mortality and morbidity. Current MI management in the triage includes non-invasive heart monitoring using an electrocardiogram (ECG) and the cardic biomarker test. This study is designed to explore the potential of photoplethysmography (PPG) as a simple non-invasive device as an alternative method to screen the MI subjects. This study emphasises the usage of second derivative photoplethysmography (SDPPG) intervals as the extracted features to classify the MI subjects. The statistical analysis shows the potential of "a-c" interval and the corrected "a-cC" interval to classify the subject. The sensitivity of the predicted model using "a-c" and "a-cC" is 90.6% and 81.2% and the specificity is 87.5% and 84.4%, respectively. PMID:27010162

  20. Post myocardial infarction cardiogenic shock: a review of current therapies.

    PubMed

    Ng, Ramford; Yeghiazarians, Yerem

    2013-01-01

    Cardiogenic shock is often a devastating consequence of acute myocardial infarction (MI) and portends to significant mortality and morbidity. Despite improvements in expediting the time to treatment and enhancements in available medical therapy and reperfusion techniques, cardiogenic shock remains the most common cause of mortality following MI. Post-MI cardiogenic shock most commonly occurs as a consequence of severe left ventricular dysfunction. Right ventricular (RV) MI must also be considered. Mechanical complications including acute mitral regurgitation, ventricular septal rupture, and ventricular free-wall rupture can also lead to cardiogenic shock. Rapid diagnosis of cardiogenic shock and its underlying cause is pivotal to delivering definitive therapy. Intravenous vasoactive agents and mechanical support devices may temporize the patient's hemodynamic status until definitive therapy by percutaneous or surgical intervention can be performed. Despite prompt management, post-MI cardiogenic shock mortality remains high.

  1. Raman spectroscopy of human saliva for acute myocardial infarction detection

    NASA Astrophysics Data System (ADS)

    Chen, Maowen; Chen, Yuanxiang; Wu, Shanshan; Huang, Wei; Lin, Jinyong; Weng, Guo-Xing; Chen, Rong

    2014-09-01

    Raman spectroscopy is a rapidly non-invasive technique with great potential for biomedical research. The aim of this study was to evaluate the feasibility of using Raman spectroscopy of human saliva for acute myocardial infarction (AMI) detection. Raman spectroscopy measurements were performed on two groups of saliva samples: one group from patients (n=30) with confirmed AMI and the other group from healthy controls (n=31). The diagnostic performance for differentiating AMI saliva from normal saliva was evaluated by multivariate statistical analysis. The combination of principal component analysis (PCA) and linear discriminate analysis (LDA) of the measured Raman spectra separated the spectral features of the two groups into two distinct clusters with little overlaps, rendering the sensitivity of 80.0% and specificity of 80.6%. The results from this exploratory study demonstrated that Raman spectroscopy of human saliva can serve as a potentially clinical tool for rapid AMI detection and screening.

  2. Perceived threats of individuals recovering from myocardial infarction.

    PubMed

    Bennett, S J

    1992-01-01

    Lazarus' phenomenological theory of stress and coping provided the basis for this descriptive study of perceived threats after myocardial infarction (MI). Sixty-four post-MI subjects enrolled in phase II cardiac rehabilitation programs identified threats they had experienced in the past month. Perceived threats were defined as situations that were difficult or troubling to the individual and were described by respondents in narrative form. Degree of threat was then measured by one item on which subjects indicated the degree of concern the threatening event had caused them. Responses to the one item were analyzed and categorized into the following five areas: physical problems; medical therapy/self-care; work/physical activity; interpersonal/family; and financial. The results provide an overview of the multiple concerns individuals deal with after a major life-threatening cardiac event.

  3. Percutaneous coronary intervention for acute myocardial infarction with mitral regurgitation.

    PubMed

    Tu, Yan; Zeng, Qing-Chun; Huang, Ying; Li, Jian-Yong

    2016-09-01

    Ischemic mitral regurgitation (IMR) is a common complication of acute myocardial infarction (AMI). Current evidences suggest that revascularization of the culprit vessels with percutaneous coronary artery intervention (PCI) or coronary artery bypass grafting can be beneficial for relieving IMR. A 2.5-year follow-up data of a 61-year-old male patient with ST-segment elevation AMI complicated with IMR showed that mitral regurgitation area increased five days after PCI, and decreased to lower steady level three months after PCI. This finding suggest that three months after PCI might be a suitable time point for evaluating the possibility of IMR recovery and the necessity of surgical intervention of the mitral valve for AMI patient. PMID:27582769

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

    PubMed Central

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

    2014-01-01

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

  5. 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

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

    SciTech Connect

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

    1990-03-01

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

  7. iPS Cells for Post-myocardial Infarction Repair: Remarkable Opportunities and Challenges

    PubMed Central

    Lalit, Pratik A.; Hei, Derek J.; Raval, Amish N.; Kamp, Timothy J.

    2014-01-01

    Coronary artery disease with associated myocardial infarction continues to be a major cause of death and morbidity around the world despite significant advances in therapy. Patients who suffer large myocardial infarctions are at highest risk for progressive heart failure and death, and cell-based therapies offer new hope for these patients. A recently discovered cell source for cardiac repair has emerged as a result of a breakthrough reprogramming somatic cells to induced pluripotent stem cells (iPSCs). The iPSCs can proliferate indefinitely in culture and can differentiate into cardiac lineages including cardiomyocytes, smooth muscle cells, endothelial cells, and cardiac progenitors. Thus large quantities of desired cell products can be generated without being limited by cellular senescence. The iPSCs can be obtained from patients to allow autologous therapy or, alternatively, banks of HLA diverse iPSCs are possible for allogeneic therapy. Preclinical animal studies using a variety of cell preparations generated from iPSCs have shown evidence of cardiac repair. Methodology for the production of clinical grade products from human iPSCs is in place. Ongoing studies of the safety of various iPSC preparations with regard to the risk of tumor formation, immune rejection, induction of arrhythmias, and formation of stable cardiac grafts are needed as the field advances toward the first in man trials of iPSCs post-MI. PMID:24723658

  8. In vivo experience with natural scaffolds for myocardial infarction: the times they are a-changin'.

    PubMed

    Perea-Gil, Isaac; Prat-Vidal, Cristina; Bayes-Genis, Antoni

    2015-12-06

    Treating a myocardial infarction (MI), the most frequent cause of death worldwide, remains one of the most exciting medical challenges in the 21st century. Cardiac tissue engineering, a novel emerging treatment, involves the use of therapeutic cells supported by a scaffold for regenerating the infarcted area. It is essential to select the appropriate scaffold material; the ideal one should provide a suitable cellular microenvironment, mimic the native myocardium, and allow mechanical and electrical coupling with host tissues. Among available scaffold materials, natural scaffolds are preferable for achieving these purposes because they possess myocardial extracellular matrix properties and structures. Here, we review several natural scaffolds for applications in MI management, with a focus on pre-clinical studies and clinical trials performed to date. We also evaluate scaffolds combined with different cell types and proteins for their ability to promote improved heart function, contractility and neovascularization, and attenuate adverse ventricular remodeling. Although further refinement is necessary in the coming years, promising results indicate that natural scaffolds may be a valuable translational therapeutic option with clinical impact in MI repair.

  9. Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction

    SciTech Connect

    Dae, M.W.; Herre, J.M.; O'Connell, J.W.; Botvinick, E.H.; Newman, D.; Munoz, L. )

    1991-05-01

    To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that (1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and (2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.

  10. 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.

  11. Acute myocardial infarct imaging with indium-111-labeled monoclonal antimyosin Fab

    SciTech Connect

    Khaw, B.A.; Yasuda, T.; Gold, H.K.; Leinbach, R.C.; Johns, J.A.; Kanke, M.; Barlai-Kovach, M.; Strauss, H.W.; Haber, E.

    1987-11-01

    Indium-111 monoclonal antimyosin Fab scintigraphy was used to detect myocardial necrosis in 52 of 54 patients (96.3%) with acute myocardial infarction. Infarcts were visualized when coronary arteries were persistently occluded (n = 10), became patent after thrombolysis (n = 33), or became patent after spontaneous reperfusion (n = 7). Posteroinferolateral visualizations were obtained in two patients with clinical and enzymatic evidence of infarction but normal electrocardiograms. Of the two patients in whom no infarcts were visualized, one had an anterior myocardial infarct. This patient underwent successful thrombolytic therapy, with attendant minimization of creatine kinase release. The other patient had a small, nonreperfused inferior myocardial infarct. Five patients with a history of remote infarction and acute necrosis showed antimyosin uptake only in regions concordant with the acute episodes of infarction, and radiolabeled antimyosin Fab localized in neither old infarcts nor normal, noninfarcted myocardium. Antimyosin Fab scintigraphy, thus, appears to be a highly specific means of delineating necrotic myocardium, at least in this limited and selected group of patients.

  12. Photoacoustic tomography of ex vivo mouse hearts with myocardial infarction

    NASA Astrophysics Data System (ADS)

    Holotta, Markus; Grossauer, Harald; Kremser, Christian; Torbica, Pavle; Völkl, Jakob; Degenhart, Gerald; Esterhammer, Regina; Nuster, Robert; Paltauf, Günther; Jaschke, Werner

    2011-03-01

    In the present study, we evaluated the applicability of ex vivo photoacoustic imaging (PAI) on small animal organs. We used photoacoustic tomography (PAT) to visualize infarcted areas within murine hearts and compared these data to other imaging techniques [magnetic resonance imaging (MRI), micro-computed tomography] and histological slices. In order to induce ischemia, an in vivo ligation of the left anterior descending artery was performed on nine wild-type mice. After varying survival periods, the hearts were excised and fixed in formaldehyde. Samples were illuminated with nanosecond laser pulses delivered by a Nd:YAG pumped optical parametric oscillator. Ultrasound detection was achieved using a Mach-Zehnder interferometer (MZI) working as an integrating line detector. The voxel data were computed using a Fourier-domain based reconstruction algorithm, followed by inverse Radon transforms. The results clearly showed the capability of PAI to visualize myocardial infarction and to produce three-dimensional images with a spatial resolution of approximately 120 μm. Regions of affected muscle tissue in PAI corresponded well with the results of MRI and histology. Photoacoustic tomography utilizing a MZI for ultrasound detection allows for imaging of small tissue samples. Due to its high spatial resolution, good soft tissue contrast and comparatively low cost, PAT offers great potentials for imaging.

  13. Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction.

    PubMed

    Malick, Mandy; Gilbert, Kim; Barry, Mathieu; Godbout, Roger; Rousseau, Guy

    2014-10-01

    This study was designed to determine if desvenlafaxine (DV), a serotonin-norepinephrine reuptake inhibitor, can attenuate apoptosis observed in the limbic system after myocardial infarction (MI). MI was induced in rats by occlusion of the left descending artery for 40 min followed by reperfusion. Another group of sham (control) rats was similarly manipulated, but without occlusion. Half of the full cohort received DV (3 mg/kg/day intraperitoneal), starting 5 min after the onset of reperfusion; the other half received the vehicle (0.5 ml of 0.9% saline). Rats were sacrificed after 3 days for biochemical analyses and MI size measurements. Infarct size was significantly smaller in DV- compared to vehicle-treated rats. At 3 days post-MI, caspase-3 and -8 activities and terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling-positive cells were decreased in the amygdala of DV-treated rats compared to MI-vehicle controls. No difference was observed between the sham groups. The data indicates that DV given immediately after an acute MI event can reduce MI size and apoptosis in amygdala when measured three days post-MI.

  14. Injectable Hydrogels for Cardiac Tissue Repair after Myocardial Infarction

    PubMed Central

    Khattab, Ahmad; Islam, Mohammad Ariful; Hweij, Khaled Abou; Zeitouny, Joya; Waters, Renae; Sayegh, Malek; Hossain, Md Monowar; Paul, Arghya

    2016-01-01

    Cardiac tissue damage due to myocardial infarction (MI) is one of the leading causes of mortality worldwide. The available treatments of MI include pharmaceutical therapy, medical device implants, and organ transplants, all of which have severe limitations including high invasiveness, scarcity of donor organs, thrombosis or stenosis of devices, immune rejection, and prolonged hospitalization time. Injectable hydrogels have emerged as a promising solution for in situ cardiac tissue repair in infarcted hearts after MI. In this review, an overview of various natural and synthetic hydrogels for potential application as injectable hydrogels in cardiac tissue repair and regeneration is presented. The review starts with brief discussions about the pathology of MI, its current clinical treatments and their limitations, and the emergence of injectable hydrogels as a potential solution for post MI cardiac regeneration. It then summarizes various hydrogels, their compositions, structures and properties for potential application in post MI cardiac repair, and recent advancements in the application of injectable hydrogels in treatment of MI. Finally, the current challenges associated with the clinical application of injectable hydrogels to MI and their potential solutions are discussed to help guide the future research on injectable hydrogels for translational therapeutic applications in regeneration of cardiac tissue after MI. PMID:27668147

  15. Injectable Hydrogels for Cardiac Tissue Repair after Myocardial Infarction

    PubMed Central

    Khattab, Ahmad; Islam, Mohammad Ariful; Hweij, Khaled Abou; Zeitouny, Joya; Waters, Renae; Sayegh, Malek; Hossain, Md Monowar; Paul, Arghya

    2015-01-01

    Cardiac tissue damage due to myocardial infarction (MI) is one of the leading causes of mortality worldwide. The available treatments of MI include pharmaceutical therapy, medical device implants, and organ transplants, all of which have severe limitations including high invasiveness, scarcity of donor organs, thrombosis or stenosis of devices, immune rejection, and prolonged hospitalization time. Injectable hydrogels have emerged as a promising solution for in situ cardiac tissue repair in infarcted hearts after MI. In this review, an overview of various natural and synthetic hydrogels for potential application as injectable hydrogels in cardiac tissue repair and regeneration is presented. The review starts with brief discussions about the pathology of MI, its current clinical treatments and their limitations, and the emergence of injectable hydrogels as a potential solution for post MI cardiac regeneration. It then summarizes various hydrogels, their compositions, structures and properties for potential application in post MI cardiac repair, and recent advancements in the application of injectable hydrogels in treatment of MI. Finally, the current challenges associated with the clinical application of injectable hydrogels to MI and their potential solutions are discussed to help guide the future research on injectable hydrogels for translational therapeutic applications in regeneration of cardiac tissue after MI. PMID:27668147

  16. Imaging of acute myocardial infarction in pigs with Indium-111 monoclonal antimyosin scintigraphy and MRI

    SciTech Connect

    ten Kate, C.I.; van Kroonenburgh, M.J.; Schipperheyn, J.J.; Doornbos, J.; Hoedemaeker, P.J.; Maes, A.; v.d. Nat, K.H.; Camps, J.A.; Huysmans, H.A.; Pauwels, E.K. )

    1990-07-01

    Indium-111 antimyosin F(ab')2 was used in a series of scintigraphic studies on experimentally induced myocardial infarctions in pigs. Antimyosin distribution recorded by planar images of in vivo pigs and by single photon emission computed tomography (SPECT) of excised hearts delineated areas of myocardial necrosis if infarct volume exceeded 3.3 cm3. Scintigraphic images were compared with magnetic resonance images (MRI) obtained from excised hearts and with photographs of slices of the hearts. Infarct size and localization determined with antimyosin were compared. The MR images, with or without gadolinium-DTPA (Gd-DTPA), of the in vivo pigs were all false-negative; some myocardial wall thinning and high bloodpool signals were visible. Results show that both the antimyosin and the MR technique are specific methods for the visualization of induced myocardial necrosis in this animal model. However, the use of antimyosin is limited to a period ranging from 24 to 72 hours after infarction.

  17. 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.

  18. Persistent uptake of indium-111-antimyosin monoclonal antibody in patients with myocardial infarction

    SciTech Connect

    Matsumori, A.; Yamada, T.; Tamaki, N.; Kawai, C.; Watanabe, Y.; Yonekura, Y.; Endo, K.; Konishi, J.; Yoshida, A.; Tamaki, S. )

    1990-11-01

    Indium-111(111In)-antimyosin scintigraphy was investigated in 27 patients with myocardial infarction. {sup 111}In-antimyosin Fab was administered intravenously, and planar and single photon emission computed tomographic images were obtained 48 hours later. Uptake of {sup 111}In-antimyosin was present in 9 of 10 patients (90%) studied within 6 days of infarction. During the second week positive scans were seen in 16 of 16 patients (100%) including 13 (81%) who had normal creatine kinase levels. The mechanism of persistent positive antimyosin images in the subacute stage of myocardial infarction remains to be clarified. {sup 111}In-antimyosin scintigraphy may be useful as a noninvasive method for the detection of myocardial injury late and early after a suspected acute myocardial infarction.

  19. MOEMS-based cardiac enzymes detector for acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Amritsar, Jeetender; Stiharu, Ion G.; Packirisamy, Muthukumaran; Balagopal, Ganesharam; Li, Xing

    2004-10-01

    Biomedical applications of MOEMS are limited only by the mankind imagination. Precision measurements on minute amounts of biological material could be performed by optical means with a remarkable accuracy. Although available in medical laboratories for general purposes, such analyzers are making their way directly to the users in the form of dedicated equipment. Such an example is a test kit to detect the existence of cardiac enzymes in the blood stream. Apart from the direct users, the medical personnel will make use of such tools given the practicality of the kit. In a large proportion of patients admitted to the hospital suspected of Acute Myocardial Infarction (AMI), the symptoms and electrocardiographic changes are inconclusive. This necessitates the use of biochemical markers of myocardial damage for correct exclusion or conformation of AMI. In this study the concept of MOEMS is applied for the detection of enzyme reaction, in which glass spectrums are scanned optically when enzyme molecules adsorb on their surface. This paper presents the optical behavior of glass spectrums under Horseradish Peroxide (HRP) enzyme reaction. The reported experimental results provide valuable information that will be useful in the development of biosensors for enzymatic detection. This paper also reports the dynamic behavior of different glass spectrums.

  20. Plasma lysosomal enzyme activity in acute myocardial infarction.

    PubMed

    Welman, E; Selwyn, A P; Peters, T J; Colbeck, J F; Fox, K M

    1978-02-01

    N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak. PMID:647716

  1. 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.

  2. Relationship between T-wave normalization on exercise ECG and myocardial functional recovery in patients with acute myocardial infarction

    PubMed Central

    Kim, Kyung Jin; Shim, Wan Joo; Jung, Seong Won; Pak, Hui Nam; Lee, Soo Jin; Song, Woo Hyuk; Kim, Young Hoon; Seo, Hong Seog; Oh, Dong Joo; Ro, Young Moo

    2002-01-01

    Background Several studies suggested that T-wave normalization (TWN) in exercise ECG indicates the presence of viable myocardium. But the clinical implication of this phenomenon in patients with acute myocardial infarction who received proper revascularization therapy was not determined. Precisely the aim of this study was to investigate the relationship between TWN in exercise ECG and myocardial functional recovery after acute myocardial infarction. Methods We studied 30 acute myocardial infarction patients with negative T waves in infarct related electrocardiographic leads and who had received successful revascularization therapy. Exercise ECG was performed 10–14days after infarct onset using Naughton protocol. Patients were divided into 2 groups according to presence (group I; n=14) or not (group II; n=16) of TWN in exercise ECG. Exercise parameters and coronary angiographic findings were compared between groups. Baseline and follow-up (mean 11 months) regional and global left ventricular function was analyzed by echocardiography. Results Exercise parameters were similar between groups. There was no difference in baseline ejection fraction and wall motion score between group I and II (EF; 56±12% vs 52±11%, p=ns. WMS; 21±3 vs 23±4, p=ns) and it was improved at the tenth month by similar magnitude (group I/group II, EF % change=12±12% vs 7±6%, p=ns, WMS % change=6±6% vs 7±5%, p=ns). The finding of no relation between TWN and functional recovery was observed also when the patients were analysed according to infarct location and presence or absence of Q-waves. Conclusion As the exercise-induced TWN in patients with acute myocardial infarction was not related with better functional recovery of dysfunctional regional wall motion and ejection fraction, TWN does not appear to be an indicator of myocardial viability. PMID:12164089

  3. 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

  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. 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.

  6. 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.

  7. ST-Elevation Myocardial Infarction After Sumitriptan Ingestion in Patient with Normal Coronary Arteries

    PubMed Central

    Jensen, Christian; Riddle, Mark

    2015-01-01

    Sumitriptan has been used by millions as a migraine abortant; however, there have been studies showing angina pectoris, coronary vasospasm, and even myocardial infarction in patients with predisposing cardiac risk factors. The majority are patients using the injectable form subcutaneously. We present the case of a patient who presents with ST-elevation myocardial infarction, with no cardiovascular risk factors, after ingesting oral sumitriptan for her typical migraine. PMID:26587110

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

    SciTech Connect

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

    2004-09-15

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

  9. [The role of B type natriuretic peptide in the assessment of post myocardial infarction prognosis].

    PubMed

    Ben Halima, A; Ibn el Hadj, Z; Chrigui, R; Kammoun, I; Lefi, A; Chine, S; Gargouri, S; Keskes, H; Kachboura, S

    2006-10-01

    Recently cardiac peptides have received close attention as cardiovascular markers. Brain (B type) natriuretic peptide is a neurohormone synthesized predominantly in ventricular myocardium. Previous studies have shown that this hormone can provide prognostic information in patients with myocardial infarction. The aim of this review is to evaluate the impact of plasma levels of BNP on prediction of left ventricular ejection fraction and remodelling and major cardiac events after myocardial infarction.

  10. Association of Interleukin 8 and Myocardial Recovery in Patients with ST-Elevation Myocardial Infarction Complicated by Acute Heart Failure

    PubMed Central

    Husebye, Trygve; Eritsland, Jan; Arnesen, Harald; Bjørnerheim, Reidar; Mangschau, Arild; Seljeflot, Ingebjørg; Andersen, Geir Øystein

    2014-01-01

    Background No data from controlled trials exists regarding the inflammatory response in patients with de novo heart failure (HF) complicating ST-elevation myocardial infarction (STEMI) and a possible role in the recovery of contractile function. We therefore explored the time course and possible associations between levels of inflammatory markers and recovery of impaired left ventricular function as well as levosimendan treatment in STEMI patients in a substudy of the LEvosimendan in Acute heart Failure following myocardial infarction (LEAF) trial. Methods A total of 61 patients developing HF within 48 hours after a primary PCI-treated STEMI were randomised double-blind to a 25 hours infusion of levosimendan or placebo. Levels of IL-6, CRP, sIL-6R, sgp130, MCP-1, IL-8, MMP-9, sICAM-1, sVCAM-1 and TNF-α were measured at inclusion (median 22 h, interquartile range (IQR) 14, 29 after PCI), on day 1, day 2, day 5 and 6 weeks. Improvement in left ventricular function was evaluated as change in wall motion score index (WMSI) by echocardiography. Results Only circulating levels of IL-8 at inclusion were associated with change in WMSI from baseline to 6 weeks, r = ÷0.41 (p = 0.002). No association, however, was found between IL-8 and WMSI at inclusion or peak troponin T. Furthermore, there was a significant difference in change in WMSI from inclusion to 6 weeks between patients with IL-8 levels below, compared to above median value, ÷0.44 (IQR÷0.57, ÷0.19) vs. ÷0.07 (IQR÷0.27, 0.07), respectively (p<0.0001). Levosimendan did not affect the levels of inflammary markers compared to control. Conclusion High levels of IL-8 in STEMI patients complicated with HF were associated with less improvement in left ventricular function during the first 6 weeks after PCI, suggesting a possible role of IL-8 in the reperfusion-related injury of post-ischemic myocardium. Further studies are needed to confirm this hypothesis. Trial Registration ClinicalTrials.gov NCT00324766

  11. Physical exertion as a trigger of myocardial infarction and sudden cardiac death.

    PubMed

    Mittleman, M A; Siscovick, D S

    1996-05-01

    The data reviewed in this article indicate that physical exertion can trigger the onset of nonfatal myocardial infarction and sudden cardiac death. In addition, it is clear that although the relative risk associated with heavy exertion may be high, the absolute risk is actually quite small. It also is clear that regular exercise reduces the risk of triggering of myocardial infarction and sudden cardiac death by isolated bouts of exertion. Thus, these data provide further support for encouragement of regular exercise, as recommended by the American Heart Association. Such a program is likely to lower the overall risk of myocardial infarction and sudden cardiac death because it may lower the baseline risk and also decrease the relative risk that an episode of exertion will trigger a myocardial infarction or sudden cardiac death. Specific recommendations for patients with a history of myocardial infarction or angina are complex. Patients with coronary artery disease have the same relative risk of myocardial infarction and sudden cardiac death as those with no such history. Because of their elevated and variable baseline risk, however, specific recommendations regarding the risks and benefits of heavy physical exertion must be provided by their individual physicians, acting on recommended guidelines for exercise in such patients.

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

    PubMed Central

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

    2014-01-01

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

  13. A serial study of platelet reactivity throughout the first six months after myocardial infarction: its modification by sulphinpyrazone.

    PubMed Central

    Kubik, M. M.; Richardson, S. G.

    1987-01-01

    Platelet reactivity was studied immediately after and throughout the first 6 months following myocardial infarction. Its modification by sulphinpyrazone was observed. Out of 65 consecutive patients admitted to the coronary care unit, ten did not meet the protocol criteria. Fifty five received either placebo or sulphinpyrazone in a double-blind trial for 6 months, treatment being started within 6 days of infarction. Forty four patients completed the study (19 on placebo and 25 on sulphinpyrazone). An additional ten patients commenced treatment within one day of infarction and were studied daily for one week. Platelet hyper-reactivity was demonstrable in all patients at presentation and persisted throughout the 6 months in the control group. This effect was reversed by sulphinpyrazone, the modification of reactivity being established by the third day of treatment. PMID:3118351

  14. Heart failure progression is accelerated following myocardial infarction in type II diabetic rats

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Clinical studies have shown a greater incidence of myocardial infarction in diabetic patients and following an infarction, diabetes is associated with an increased risk for the development of left ventricular dysfunction and heart failure. The goal of this study was to determine if the progression o...

  15. Regional myocardial metabolism in patients with acute myocardial infarction assessed by positron emission tomography

    SciTech Connect

    Schwaiger, M.; Brunken, R.; Grover-McKay, M.; Krivokapich, J.; Child, J.; Tillisch, J.H.; Phelps, M.E.; Schelbert, H.R.

    1986-10-01

    Positron emission tomography has been shown to distinguish between reversible and irreversible ischemic tissue injury. Using this technique, 13 patients with acute myocardial infarction were studied within 72 hours of onset of symptoms to evaluate regional blood flow and glucose metabolism with nitrogen (N)-13 ammonia and fluorine (F)-18 deoxyglucose, respectively. Serial noninvasive assessment of wall motion was performed to determine the prognostic value of metabolic indexes for functional tissue recovery. Segmental blood flow and glucose utilization were evaluated using a circumferential profile technique and compared with previously established semiquantitative criteria. Relative N-13 ammonia uptake was depressed in 32 left ventricular segments. Sixteen segments demonstrated a concordant decrease in flow and glucose metabolism. Regional function did not change over time in these segments. In contrast, 16 other segments with reduced blood flow revealed maintained F-18 deoxyglucose uptake consistent with remaining viable tissue. The average wall motion score improved significantly in these segments (p less than 0.01), yet the degree of recovery varied considerably among patients. Coronary anatomy was defined in 9 of 13 patients: patent infarct vessels supplied 8 of 10 segments with F-18 deoxyglucose uptake, while 10 of 13 segments in the territory of an occluded vessel showed concordant decreases in flow and metabolism (p less than 0.01). Thus, positron emission tomography reveals a high incidence of residual tissue viability in ventricular segments with reduced flow and impaired function during the subacute phase of myocardial infarction. Absence of residual tissue metabolism is associated with irreversible injury, while preservation of metabolic activity identifies segments with a variable outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

  16. Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial

    PubMed Central

    2014-01-01

    Background The Fas apoptotic pathway has been implicated in type 2 diabetes and cardiovascular disease. Although a polymorphism (rs7138803; G > A) near the Fas apoptotic inhibitory molecule 2 (FAIM2) locus has been related to obesity, its association with other cardiovascular risk factors and disease remains uncertain. Methods We analyzed the association between the FAIM2-rs7138803 polymorphism and obesity, blood pressure and heart rate in 7,161 participants (48.3% with type 2 diabetes) in the PREDIMED study at baseline. We also explored gene-diet interactions with adherence to the Mediterranean diet (MedDiet) and examined the effects of the polymorphism on cardiovascular disease incidence per diabetes status after a median 4.8-year dietary intervention (MedDiet versus control group) follow-up. Results We replicated the association between the FAIM2-rs7138803 polymorphism and greater obesity risk (OR: 1.08; 95% CI: 1.01-1.16; P = 0.011; per-A allele). Moreover, we detected novel associations of this polymorphism with higher diastolic blood pressure (DBP) and heart rate at baseline (B = 1.07; 95% CI: 0.97-1.28 bmp in AA vs G-carriers for the whole population), that remained statistically significant even after adjustment for body mass index (P = 0.012) and correction for multiple comparisons. This association was greater and statistically significant in type-2 diabetic subjects (B = 1.44: 95% CI: 0.23-2.56 bmp; P = 0.010 for AA versus G-carriers). Likewise, these findings were also observed longitudinally over 5-year follow-up. Nevertheless, we found no statistically significant gene-diet interactions with MedDiet for this trait. On analyzing myocardial infarction risk, we detected a nominally significant (P = 0.041) association in type-2 diabetic subjects (HR: 1.86; 95% CI:1.03-3.37 for AA versus G-carriers), although this association did not remain statistically significant following correction for multiple comparisons. Conclusions We

  17. Myocardial ischaemia and the inflammatory response: release of heat shock protein 70 after myocardial infarction

    PubMed Central

    Dybdahl, B; Slørdahl, S A; Waage, A; Kierulf, P; Espevik, T; Sundan, A

    2005-01-01

    Objectives: To test the hypothesis that heat shock protein (Hsp) 70 may be released into the circulation after acute myocardial infarction (AMI) by exploring the kinetics of Hsp70 release and the relations between Hsp70 and markers of inflammation and myocardial damage in AMI. Design: Blood samples from 24 patients were prospectively collected through to the first day after AMI. Hsp70, interleukin (IL) 6, IL-8, and IL-10 in serum were measured by enzyme linked immunosorbent assay (ELISA). Results: Median Hsp70 concentrations in AMI patients measured at arrival, six hours thereafter, and the following morning were 686, 868, and 607 pg/ml, respectively. These concentrations were all significantly different from those of the control patients with angina with a median serum Hsp70 concentration of 306 pg/ml. Peak Hsp70 correlated with creatine kinase (CK) MB (r  =  0.62, p < 0.01) and cardiac troponin T (r  =  0.58, p < 0.01). Furthermore, serum Hsp70 correlated with IL-6 and IL-8 at six hours (r  =  0.60, p < 0.01 and r  =  0.59, p < 0.01, respectively). Conclusions: In this study, Hsp70 was rapidly released into the circulation after AMI. Circulating Hsp70 is suggested as a marker of myocardial damage. In addition, Hsp70 may have a role in the inflammatory response after AMI. PMID:15710705

  18. 3D perfusion mapping in the intact mouse heart after myocardial infarction using myocardial contrast echocardiography

    NASA Astrophysics Data System (ADS)

    Li, Yinbo; Yang, Zequan; French, Brent A.; Hossack, John A.

    2005-04-01

    An intact mouse model of surgically-induced myocardial infarction (MI) caused by permanent occlusion of the Left Anterior Descending (LAD) coronary artery was studied. Normal mice with no occlusion were also studied as controls. For each mouse, contrast enhanced ultrasound images of the heart were acquired in parallel cross-sections perpendicular to the sternum at millimeter increments. For accurate 3D reconstruction, ECG gating and a tri-axial adjustable micromanipulator were used for temporal and spatial registration. Ultrasound images at steady-state of blood refilling were color-coded in each slice to show relative perfusion. Myocardial perfusion defects and necrosis were also examined postmortem by staining with Phthalo blue and TTC red dyes. Good correlation (R>0.93) in perfused area size was observed between in vivo measurements and histological staining. A 3D multi-slice model and a 3D rendering of perfusion distribution were created and showed a promising match with postmortem results, lending further credence to its use as a more comprehensive and more reliable tool for in vivo assessment of myocardial perfusion than 2D tomographic analysis.

  19. Bioresorbable vascular scaffolds in patients with acute myocardial infarction: a new step forward to optimized reperfusion?

    PubMed Central

    Cuesta, Javier; Bastante, Teresa; Rivero, Fernando; García-Guimaraes, Marcos; Alvarado, Teresa; Benedicto, Amparo; Cortese, Bernardo; Byrne, Robert; Kastrati, Adnan

    2016-01-01

    Bioresorbable vascular scaffolds (BVS) represent a disruptive technology that has caused a new revolution in interventional cardiology. BVS appear to be particularly appealing in patients presenting with an acute myocardial infarction (MI). The available evidence on the value of BVS implantation in this challenging scenario is very promising but still limited. Results come from preliminary small observational studies, prospective registries that include a control group, and from scarce randomized clinical trials with surrogate mechanistic or angiographic primary end-points. Further studies, powered for clinical endpoints, are required to establish the relative safety and efficacy of BVS vs. new-generation metallic drug-eluting stents (DES) in patients with ST-segment elevation acute MI. PMID:27293870

  20. [Diagnosis of myocardial infarction by cine MR imaging--a comparative study with thallium-201 myocardial SPECT].

    PubMed

    Shiozaki, H

    1993-01-25

    The usefulness of cine magnetic resonance (MR) imaging was evaluated in 41 patients with acute (4 cases), subacute (21 cases) and chronic (16 cases) myocardial infarctions on the basis of the findings of thallium-201 myocardial SPECT. The overall rate of diagnostic accordance between cine MR imaging and SPECT was 85.0% (408/480). It was highest at the middle of the left ventricle (89.0%, 146/164) and lowest at the base (82.7%, 129/156). Measurement of wall thickness using the images printed on films was possible in 87.1% of segments (418/480). There was a significant difference in end-diastolic wall thickness and %-thickening between the infarcted and non-infarcted sites except for the base of the left ventricle. However, diastolic wall thinning was not remarkable in acute cases of less than one week after onset. In these cases %-thickening may be useful. Partial volume averaging on MR imaging and the inaccuracy of SPECT findings at the base also made meaningful comparison difficult. The most important diagnostic findings of myocardial infarction on cine MR imaging were end-diastolic wall thinning and abnormal motion such as akinesis and dyskinesis. It is concluded that cine MR imaging is a useful noninvasive examination method for evaluating the status of cardiac function in myocardial infarction.

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

    SciTech Connect

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

    1989-11-01

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

  2. Imaging of experimental myocardial infarction with technetium-99m 2,3-dimercaptosuccinic acid

    SciTech Connect

    Karlsberg, R.P.; Milne, N.; Lyons, K.P.; Aronow, W.S.

    1981-03-01

    We have studied the use of Tc-99m-labeled 2,3-dimercaptosuccinic acid(Tc-99m DMSA) to scintigraph acute myocardial infaction after coronary occlusion in dogs. Optimal images were obtained 5 hr after injection of radiotracer, with consistent delineation 48 hr after occlusion. Delivery of tracer was dependent on blood flow. Uptake of tracer correlated to extent of infarction as determined by the myocardial depletion of creatine kinase. Myocardial Tc-99m DMSA was protein-bound.

  3. Microvolt T-wave alternans during exercise and pacing in patients with acute myocardial infarction.

    PubMed

    Raatikainen, M J Pekka; Jokinen, Vesa; Virtanen, Vesa; Hartikainen, Juha; Hedman, Antti; Huikuri, Heikki V

    2005-01-01

    Cardiac Arrhythmias and Risk Stratification after Myocardial infarction (CARISMA) is a prospective multicenter trial designed to document the incidence of cardiac arrhythmias after acute myocardial infarction (AMI), and to assess the predictive accuracy of various arrhythmic risk markers. In this substudy of the CARISMA trial, microvolt T-wave alternans (TWA) was assessed with specific equipment 6 weeks after AMI during bicycle exercise, atrial (A) pacing, and simultaneous ventricular and atrial (V + A) pacing in 80 patients with left ventricular ejection fraction (LVEF) <40%. The agreement between the acute test results was determined by overall proportion of concordance and the kappa statistic. Sustained TWA was observed in 24, 45, and 50% of the patients during the exercise test, A pacing, and V + A pacing, respectively. The number of indeterminate TWA was significantly lower during V + A pacing (n = 7) than exercise test (n = 34). The TWA concordance rate was 71% between exercise and V + A pacing (kappa= 0.53, P = 0.001), 79% between exercise and A pacing (kappa= 0.54, P < 0.001), and 95% between the two pacing modes (kappa= 0.89, P < 0.001). Patients with positive TWA in all tests had lower LVEF (28 +/- 7% vs 35 +/- 9%, P < 0.01) and wider QT dispersion (99 +/- 44 ms vs 67 +/- 38 ms, P < 0.01) than those with inconsistent test result. The low number of indeterminate tests and high concordance between the test results indicate that V + A pacing may provide a valuable means to assess TWA in patients who cannot complete the exercise test.

  4. Serious Infection Following Acute Myocardial Infarction: Incidence, Clinical Features, and Outcomes

    PubMed Central

    Truffa, Adriano A. M.; Granger, Christopher B.; White, Kyle R.; Newby, L. Kristin; Mehta, Rajendra H.; Hochman, Judith S.; Patel, Manesh R.; Pieper, Karen S.; Al-Khalidi, Hussein R.; Armstrong, Paul W.; Lopes, Renato D.

    2013-01-01

    Background Little is known about the incidence, location, etiologic organisms, and outcomes of infection in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Objectives To address this knowledge gap using the database of the Assessment of Pexelizumab in Acute Myocardial Infarction (APEX-AMI) trial. We also assessed the association between serious infections and 90-day death or death/MI. Methods We analyzed data from 5745 STEMI patients enrolled in the APEX-AMI trial. Detailed information on infection was collected on all patients. We describe characteristics of patients according to infection and details of infection. Cox proportional hazards models were used to assess 90-day outcomes among patients with and without infections after adjusting for associated clinical variables and using infection as a time-dependent covariate. Results Overall, 138 patients developed a serious infection (2.4%), most of whom presented with a single-site infection. The median (25th, 75th percentile) time until diagnosis of infection was 3 (1, 6) days. The most commonly identified organism was Staphylococcus aureus, and the main location of infection was the bloodstream. These patients had more comorbidities and lower procedural success at index PCI than those without infections. Serious infection was associated with significantly higher rates of 90-day death (adjusted hazard ratio [HR] 5.6; 95% confidence interval [CI] 3.8-8.4) and death or MI (adjusted HR 4.9; 95% CI 3.4-7.1). Conclusion Infections complicating the course of patients with STEMI are uncommon but associated with markedly worse 90-day clinical outcomes. Mechanisms for early identification of these high-risk patients, as well as design of strategies to reduce their risk of infection, are warranted. PMID:22814783

  5. Changes in Employment Status after Myocardial Infarction among Men

    PubMed Central

    Şahan, Ceyda; Demiral, Yücel; Kılıç, Bülent; Aslan, Özgür

    2016-01-01

    Background: According to the Turkey Burden of Disease Study, 10% of the national burden of disease is attributed to cardiovascular diseases. Although the standardized coronary heart disease (CHD) rate is falling in general, CHD prevalence among young people is rising. On the other hand, as a result of increased life expectancy and higher retirement ages, the CHD rate among workers is also increasing. Therefore, work ability and return to work after diagnosis are important for population health and well-being. Socioeconomic factors and working conditions may play a key role as well as clinical conditions described in the literature that affect returning to work. Aims: The aims of this qualitative study are exploring the changes in employment and working conditions of the patients after acute myocardial infarction (AMI) and affecting factors such as socioeconomic, personal and environmental. Study design: Qualitative research. Methods: The research population are fifty-three patients who are engaged in paid employment when the people have been diagnosed with myocardial infarction for the first time between 2011 and 2012 at a university hospital coronary care unit. We intended to reach the whole population. Twenty-seven patients were contacted whose phone numbers were accessible from the hospital records. Semi-structured in-depth interviews were conducted with twelve patients in a meeting room at the hospital. The interviews were tape-recorded accompanied by note-taking and the content analysis method were evaluated. Results: While many of the participants continued to work at the same job by working less, one third of them said that they were thinking about getting an easier job if they have the opportunity. On the other hand, in most cases, there were neither assessments about their work ability, nor changes to their working conditions after AMI. They had to cope with their conditions, such as economic or psychosocial, without any support. Conclusions: While the

  6. Changes in Employment Status after Myocardial Infarction among Men

    PubMed Central

    Şahan, Ceyda; Demiral, Yücel; Kılıç, Bülent; Aslan, Özgür

    2016-01-01

    Background: According to the Turkey Burden of Disease Study, 10% of the national burden of disease is attributed to cardiovascular diseases. Although the standardized coronary heart disease (CHD) rate is falling in general, CHD prevalence among young people is rising. On the other hand, as a result of increased life expectancy and higher retirement ages, the CHD rate among workers is also increasing. Therefore, work ability and return to work after diagnosis are important for population health and well-being. Socioeconomic factors and working conditions may play a key role as well as clinical conditions described in the literature that affect returning to work. Aims: The aims of this qualitative study are exploring the changes in employment and working conditions of the patients after acute myocardial infarction (AMI) and affecting factors such as socioeconomic, personal and environmental. Study design: Qualitative research. Methods: The research population are fifty-three patients who are engaged in paid employment when the people have been diagnosed with myocardial infarction for the first time between 2011 and 2012 at a university hospital coronary care unit. We intended to reach the whole population. Twenty-seven patients were contacted whose phone numbers were accessible from the hospital records. Semi-structured in-depth interviews were conducted with twelve patients in a meeting room at the hospital. The interviews were tape-recorded accompanied by note-taking and the content analysis method were evaluated. Results: While many of the participants continued to work at the same job by working less, one third of them said that they were thinking about getting an easier job if they have the opportunity. On the other hand, in most cases, there were neither assessments about their work ability, nor changes to their working conditions after AMI. They had to cope with their conditions, such as economic or psychosocial, without any support. Conclusions: While the

  7. [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

  8. Subarachnoid hemorrhage mimicking ST-segment elevation myocardial infarction after return of spontaneous circulation

    PubMed Central

    Park, Injune; Kim, Youn Jung; Ahn, Shin; Sohn, Chang Hwan; Seo, Dong Woo; Kim, Won Young

    2015-01-01

    Electrocardiogram changes in subarachnoid hemorrhage (SAH) have been described as ST-T changes that mimic acute coronary syndrome and even acute ST-segment elevation myocardial infarction. Elevation of cardiac enzymes and abnormality of regional myocardial wall motion have been reported frequently for SAH. We report a case of an out-of-hospital cardiac arrest survivor with high suspicion of ST-segment elevation myocardial infarction based on the electrocardiogram and bedside echocardiography, who had normal coronary arteries on emergent coronary angiography. The patient was ultimately diagnosed with SAH as a cause of out-of-hospital cardiac arrest. PMID:27752607

  9. Akt-dependent Girdin phosphorylation regulates repair processes after acute myocardial infarction.

    PubMed

    Hayano, Shinji; Takefuji, Mikito; Maeda, Kengo; Noda, Tomonori; Ichimiya, Hitoshi; Kobayashi, Koichi; Enomoto, Atsushi; Asai, Naoya; Takahashi, Masahide; Murohara, Toyoaki

    2015-11-01

    Myocardial infarction is a leading cause of death, and cardiac rupture following myocardial infarction leads to extremely poor prognostic feature. A large body of evidence suggests that Akt is involved in several cardiac diseases. We previously reported that Akt-mediated Girdin phosphorylation is essential for angiogenesis and neointima formation. The role of Girdin expression and phosphorylation in myocardial infarction, however, is not understood. Therefore, we employed Girdin-deficient mice and Girdin S1416A knock-in (Girdin(SA/SA)) mice, replacing the Akt phosphorylation site with alanine, to address this question. We found that Girdin was expressed and phosphorylated in cardiac fibroblasts in vitro and that its phosphorylation was crucial for the proliferation and migration of cardiac fibroblasts. In vivo, Girdin was localized in non-cardiomyocyte interstitial cells and phosphorylated in α-smooth muscle actin-positive cells, which are likely to be cardiac myofibroblasts. In an acute myocardial infarction model, Girdin(SA/SA) suppressed the accumulation and proliferation of cardiac myofibroblasts in the infarcted area. Furthermore, lower collagen deposition in Girdin(SA/SA) mice impaired cardiac repair and resulted in increased mortality attributed to cardiac rupture. These findings suggest an important role of Girdin phosphorylation at serine 1416 in cardiac repair after acute myocardial infarction and provide insights into the complex mechanism of cardiac rupture through the Akt/Girdin-mediated regulation of cardiac myofibroblasts.

  10. 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.

  11. 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

  12. Role of infarction artery status in left ventricular remodeling after acute myocardial infarction.

    PubMed

    Sanchis, J; Insa, L; Bodí, V; Egea, S; Monmeneu, J V; Chorro, F J; Llácer, A; López Merino, V

    1997-04-18

    The aim of this study was to evaluate the relation between the infarction artery status and left ventricular volumes, independently of regional ventricular dysfunction, at 4-6 weeks after a first myocardial infarction. The study group consisted of 100 patients, of whom 80 received thrombolytic treatment. Coronary and contrast left ventricular angiograms were performed at 36+/-5 days postinfarction. Left ventricular end-diastolic and end-systolic volumes were measured. The centerline chord motion method was used to calculate the extent of wall motion abnormality (percentage of chords with hypokinetic motion) and its severity (maximum units of S.D. below the normal wall motion reference). Minimum lumen diameter, patency and collateral flow in the infarction artery were also analyzed. Eight patients (group I) showed occlusion with poor collateral flow in the infarction artery, 22 patients (group II) occlusion with good collateral flow, 38 patients (group III) severe residual stenosis (minimum lumen diameter < or = 1 mm), and 32 patients (group IV) non-severe residual stenosis (minimum lumen diameter > 1 mm). Patients from group I presented greater wall motion abnormality in terms of both extent (P=0.005) and severity (P=0.007), and greater end-diastolic (P=0.07) and end-systolic (P=0.0008) volumes; there were no differences among groups II, III and IV. By stepwise multivariate regression analysis, the extent of wall motion abnormality was the main determinant of end-diastolic (P=0.0001) and end-systolic (P=0.0001) volumes; occlusion with poor collateral flow was also a significant independent factor for end-systolic volume (P=0.03). Total occlusion (including both with and without collaterals) and the minimum lumen diameter did not correlate with end-diastolic and end-systolic volumes. We concluded that (A) the extent of regional dysfunction is the primary determinant of left ventricular volumes at 4-6 weeks postinfarction. (B) The status of the infarction artery is a

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

    PubMed Central

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

    2012-01-01

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

  14. Vitamin C deficiency and risk of myocardial infarction: prospective population study of men from eastern Finland.

    PubMed Central

    Nyyssönen, K.; Parviainen, M. T.; Salonen, R.; Tuomilehto, J.; Salonen, J. T.

    1997-01-01

    OBJECTIVE: To examine the association between plasma vitamin C concentrations and the risk of acute myocardial infarction. DESIGN: Prospective population study. SETTING: Eastern Finland. SUBJECTS: 1605 randomly selected men aged 42, 48, 54, or 60 who did not have either symptomatic coronary heart disease or ischaemia on exercise testing at entry to the Kuopio ischaemic heart disease risk factor study in between 1984 and 1989. MAIN OUTCOME MEASURES: Number of acute myocardial infarctions; fasting plasma vitamin C concentrations at baseline. RESULTS: 70 of the men had a fatal or non-fatal myocardial infarction between March 1984 and December 1992.91 men had vitamin C deficiency (plasma ascorbate < 11.4 mumol/l, or 2.0 mg/l), of whom 12 (13.2%) had a myocardial infarction; 1514 men were not deficient in vitamin C, of whom 58 (3.8%) had a myocardial infarction. In a Cox proportional hazards model adjusted for age, year of examination, and season of the year examined (August to October v rest of the year) men who had vitamin C deficiency had a relative risk of acute myocardial infarction of 3.5 (95% confidence interval 1.8 to 6.7, P = 0.0002) compared with those who were not deficient. In another model adjusted additionally for the strongest risk factors for myocardial infarction and for dietary intakes of tea fibre, carotene, and saturated fats men with a plasma ascorbate concentration < 11.4 mumol/l had a relative risk of 2.5 (1.3 to 5.2, P = 0.0095) compared with men with higher plasma vitamin C concentrations. CONCLUSIONS: Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease. PMID:9066474

  15. Patients treated in a coronary care unit without acute myocardial infarction: identification of high risk subgroup for subsequent myocardial infarction and/or cardiovascular death.

    PubMed Central

    Nordlander, R; Nyquist, O

    1979-01-01

    Consecutive patients admitted to a coronary care unit (CCU) during one year were studied. The diagnosis of acute myocardial infarction was not substantiated by our criteria in 206 of the patients discharged from the CCU. Of these, 193 were retrospectively followed up during one year. Seventeen of the patients (9%) died from cardiovascular causes during the 1-year period. Another 14 patients (7%) had a subsequent non-fatal acute myocardial infarction during the same period. The majority of the patients had coronary artery disease. Only 32 (17%) could be classified as non-coronary cases, and these had an excellent prognosis without any subsequent acute myocardial infarctions or deaths. The occurrence of transient ST-T shifts in serial electrocardiograms obtained during the first 3 days in hospital selected a subgroup of patients who had a high risk for subsequent non-fatal acute myocardial infarction and/or cardiovascular death. This high risk subgroup provides a basis for more aggressive diagnostic and therapeutic intervention. Images PMID:465239

  16. Role of Intravascular Ultrasound in Patients with Acute Myocardial Infarction

    PubMed Central

    Hong, Young Joon; Ahn, Youngkeun

    2015-01-01

    Rupture of a vulnerable plaque and subsequent thrombus formation are important mechanisms leading to the development of an acute myocardial infarction (AMI). Typical intravascular ultrasound (IVUS) features of AMI include plaque rupture, thrombus, positive remodeling, attenuated plaque, spotty calcification, and thin-cap fibroatheroma. No-reflow phenomenon was attributable to the embolization of thrombus and plaque debris that results from mechanical fragmentation of the vulnerable plaque by percutaneous coronary intervention (PCI). Several grayscale IVUS features including plaque rupture, thrombus, positive remodeling, greater plaque burden, decreased post-PCI plaque volume, and tissue prolapse, and virtual histology-IVUS features such as large necrotic corecontaining lesion and thin-cap fibroatheroma were the independent predictors of no-reflow phenomenon in AMI patients. Non-culprit lesions associated with recurrent events were more likely than those not associated with recurrent events to be characterized by a plaque burden of ≥70%, a minimal luminal area of ≤4.0 mm2, or to be classified as thin-cap fibroatheromas. PMID:26240578

  17. An unusual cause of ST elevation myocardial infarction (STEMI)

    PubMed Central

    Monem, Mohammed; Rampat, Rajiv

    2014-01-01

    A 67-year-old Caucasian woman presented to clinic with a 2-month history of worsening shortness of breath on exertion and a single episode of chest pain 1 week before. Her ECG in clinic showed ST elevation inferiorly and she was admitted from clinic for further investigations as inpatient. She was initiated on the acute coronary syndrome protocol and underwent emergency left heart catheterisation on the day of admission. The coronary angiogram revealed large aneurysmal dilations in the right coronary artery and left main stem. A ventriculogram showed poor left ventricular (LV) systolic function in line with subsequent transthoracic echocardiogram, which revealed her to have an left ventricular ejection-fraction (LVEF) of approximately 20%. It was agreed with the cardiothoracic surgeons to treat the aneurysms non-operatively and start low-molecular weight heparin. Furthermore the underlying biventricular impairment was treated with ACE-inhibitors, β-blockers and diuretic therapy (loop and potassium-sparing). The strategy was to prevent further thrombus formation with the aneurysmal vessels and to achieve this the patient was initiated on lifelong warfarin. Other medical risk factors were optimised and patient started on statin medication. The aneurysm was monitored with serial CTs with a view to reconsider surgical intervention if any evidence of dilation. This case highlights an unusual cause of ST elevation myocardial infarction. PMID:25246457

  18. 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

  19. The chronergy of recombinant streptokinase thrombolysis in acute myocardial infarction

    PubMed Central

    WANG, ZHONG-MING; LIU, YA-BING; JIN, QI-CHEN; WANG, XUE-QI; DAI, MENG; SHAO, HUI; ZHAO, WEN-PING; DONG, QIU-LI; WANG, SHU-PING; ZHANG, HAI-TAO; KONG, LI-CHA; LIU, SHAO-YUN; WANG, DONG-YING

    2013-01-01

    The aim of this study was to explore the chronergy of intravenous recombinant streptokinase (r-SK) in patients with acute myocardial infarction (AMI). A total of 114 patients were divided into two groups according to the time of AMI onset: the morning onset (6:01–12:00, n=53) and non-morning onset (12:01–06:00, n=61) groups. The recanalization rate was recorded, as well as anticoagulant and fibrinolytic indices. Statistical analysis was performed to evaluate the recanalization rate following thrombolysis, as well as the anticoagulant and fibrinolytic activities. The recanalization rates following thrombolysis in the morning onset and non-morning onset groups were 60.4 and 82.0%, respectively (P<0.05). The level of plasminogen activator inhibitor-1 (PAI-1) antigen was significantly higher in the morning onset group compared with that in the non-morning onset group (P<0.05). This indicated a resistance to r-SK thrombolysis in the morning at the early stage of AMI, which possibly correlates with increased PAI-1 antigen levels and activity. PMID:23737880

  20. An unusual cause of ST elevation myocardial infarction (STEMI).

    PubMed

    Monem, Mohammed; Rampat, Rajiv

    2014-09-22

    A 67-year-old Caucasian woman presented to clinic with a 2-month history of worsening shortness of breath on exertion and a single episode of chest pain 1 week before. Her ECG in clinic showed ST elevation inferiorly and she was admitted from clinic for further investigations as inpatient. She was initiated on the acute coronary syndrome protocol and underwent emergency left heart catheterisation on the day of admission. The coronary angiogram revealed large aneurysmal dilations in the right coronary artery and left main stem. A ventriculogram showed poor left ventricular (LV) systolic function in line with subsequent transthoracic echocardiogram, which revealed her to have an left ventricular ejection-fraction (LVEF) of approximately 20%. It was agreed with the cardiothoracic surgeons to treat the aneurysms non-operatively and start low-molecular weight heparin. Furthermore the underlying biventricular impairment was treated with ACE-inhibitors, β-blockers and diuretic therapy (loop and potassium-sparing). The strategy was to prevent further thrombus formation with the aneurysmal vessels and to achieve this the patient was initiated on lifelong warfarin. Other medical risk factors were optimised and patient started on statin medication. The aneurysm was monitored with serial CTs with a view to reconsider surgical intervention if any evidence of dilation. This case highlights an unusual cause of ST elevation myocardial infarction.

  1. A Case of Metanephric Adenoma and Acute Myocardial Infarction.

    PubMed

    Dusan, Ruzicic; Relja, Kovacevic; Marija, Mirkovic; Jelena, Radovanovic; Vesna, Krstevska; Milijana, Terzic; Vladimir, Pantelic; Irena, Matic; Dragan, Hrncic

    2016-07-01

    Metanephric adenoma (MA) is a rare neoplasm that acounts for 0.2% of adult renal neoplasms. MAs are typically discover incidentally during detailed examinations for nonspecific symptoms such as abdominal or flank pain, hematuria, fever and palpable abdominal mass. Additionally, polycythemia has occasionally been reported as well. Herein we describe a case of metanephric adenoma which was an incidental finding in the course of a clinical autopsy in a patient with complete AV block and polycythemia. Histologically, the tumor was composed of small and uniform tubular structures reminiscent of renal tubuli, without signs of cellular atypia and pleomorphism. Such tumor histomorphology was consistent with the diagnosis of metanephric adenoma. Thrombosis is a common complication of polycythemia that often causes death. Polycythemia with an increasing number of blood cells causes hyperviscosity and, in 20-40% of cases, lethal thrombosis or hemorrhage. Hyperviscosity and coronary artery disease in our patient caused acute myocardial infarction with the subsequent rupture of posterior left ventricle wall and hemopericardium. PMID:27471365

  2. Medication Adherence and Readmission In Medicare Myocardial Infarction

    PubMed Central

    Zhang, Yuting; Kaplan, Cameron M.; Baik, Seo Hyon; Chang, Chung-Chou H.; Lave, Judith R.

    2014-01-01

    Objectives To examine the relationship between 6-month medication adherence and 1-year down-stream heart-disease related readmission among patients who survived a myocardial infarction (MI). Study Design Retrospective, nested case-control analysis of Medicare fee-for-service beneficiaries who were discharged alive post-MI in 2008 (n = 168,882). Methods Patients in the case group had their first heart-disease related readmission post-MI discharge during 6-9 months and/or 9-12 months. We then used propensity score matching mechanism to identify patients in the control group who had similar characteristics, but did not have a readmission in the same time window. Adherence was defined as the average 6-month medication possession ratio (MPR) prior to the first date of the time-window of defining readmission. Results After controlling for demographic, insurance coverage and clinical characteristics, patients who had a heart-disease related readmission had worse adherence, with MPR of 0.70 and 0.74 in the case and control groups. Odds ratio of MPR ≥0.75 was 0.79 (95% CI 0.75-0.83) among those with a readmission relative to those without. Conclusion Our study shows that better 6-month medication adherence may reduce heart-disease related readmissions within a year after an MI. PMID:25651604

  3. 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.

  4. 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.

  5. The Wedensky test predicts malignant ventricular arrhythmias after myocardial infarction

    PubMed Central

    2013-01-01

    Objectives. Better tools are needed for detection of future malignant ventricular arrhythmias post myocardial infarct (MI). Wedensky Modulation (WM) is a new semi-invasive method: A short low-amplitude electrical impulse is applied synchronized to the QRS between a precordial and dorsal thoracic patch, and changes in the following QRS-T are registered. Design. A total of 357 (MI) ICD patients underwent WM testing. QRS-T wavelet analysis provided WM Indexes for the QRS complex (WMI-R) and T wave (WMI-T). Outcome was the time to first occurrence of appropriate device therapy for ventricular arrhythmia. Patients were followed at 6-month intervals for 2 years. Results. No arrhythmia was induced by the testing. Two-year appropriate arrhythmia treatment occurred in 35% (WMI-R positive) versus 25% (WMI-R negative, p = 0.014), and. 45% versus 26% (p = 0.001) for WMI-T positive versus negative. Two-year event rates of WMI-R or WMI-T positive versus WMI-R and WMI-T negative were 36% versus 22% (p = 0.004). In Cox proportional hazard model, the combination of WMI-R and WMI-T was the only statistically significant event predictor (p = 0.003). Conclusion. Potentially life-threatening ventricular arrhythmic events could be predicted by the WM test. In combination with other risk factors WMI may be useful in these patients. PMID:24050376

  6. Risks for first nonfatal myocardial infarction in Belgrade.

    PubMed

    Ratkov, Isidora; Sipetić-Grujicić, Sandra; Vlajinac, Hristina; Marinković, Jelena; Maksimović, Natasa; Matanović, Dragana; Vasiljević, Zorana

    2013-06-01

    The aim of this study was to investigate which one among possible risk factors are independently related to first nonfatal myocardial infarction (MI) in Belgrade population. Case-control study was conducted in Belgrade during the period 2005-2006. Case group comprised 100 subjects 35-80 years old who were hospitalized because of first nonfatal MI at the coronary care unit in Urgent Center, Belgrade. Control group consisted of 100 persons chosen among patients treated during the same period at the Institute of Rheumatology, Institute for Gastroenterology, and Clinic for Orthopedics, Belgrade, Serbia. Cases and controls were individually matched by sex, age (+/- 2 years) and place of residence (urban/rural communities of Belgrade). According to the multivariate analysis risk factors for MI occurrence were "good" socioeconomic conditions (OR = 2.76), total alcohol consumption (OR = 2.62) and consumption of brandy (OR = 6.73), stressful life events taken together (OR = 3.13) and stress because of close relative Ns death (OR = 3.35), great financial problems (OR = 31.64) and small financial problems (OR = 8.47), hypertension (OR = 2.39), MI among all relatives (OR = 3.66), MI in father (OR = 6.24), and low level of high density lipoprotein cholesterol (OR = 152.41). Amateur sport activity in the past was negatively associated with MI development. The results obtained are mainly in accordance with other studies results and can be of help in development of strategy for coronary heart disease prevention in Serbia.

  7. 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

  8. Improved Bat algorithm for the detection of myocardial infarction.

    PubMed

    Kora, Padmavathi; Kalva, Sri Ramakrishna

    2015-01-01

    The medical practitioners study the electrical activity of the human heart in order to detect heart diseases from the electrocardiogram (ECG) of the heart patients. A myocardial infarction (MI) or heart attack is a heart disease, that occurs when there is a block (blood clot) in the pathway of one or more coronary blood vessels (arteries) that supply blood to the heart muscle. The abnormalities in the heart can be identified by the changes in the ECG signal. The first step in the detection of MI is Preprocessing of ECGs which removes noise by using filters. Feature extraction is the next key process in detecting the changes in the ECG signals. This paper presents a method for extracting key features from each cardiac beat using Improved Bat algorithm. Using this algorithm best features are extracted, then these best (reduced) features are applied to the input of the neural network classifier. It has been observed that the performance of the classifier is improved with the help of the optimized features. PMID:26558169

  9. Percutaneous assist devices in acute myocardial infarction with cardiogenic shock: Review, meta-analysis

    PubMed Central

    Romeo, Francesco; Acconcia, Maria Cristina; Sergi, Domenico; Romeo, Alessia; Francioni, Simona; Chiarotti, Flavia; Caretta, Quintilio

    2016-01-01

    AIM: To assess the impact of percutaneous cardiac support in cardiogenic shock (CS) complicating acute myocardial infarction (AMI), treated with percutaneous coronary intervention. METHODS: We selected all of the studies published from January 1st, 1997 to May 15st, 2015 that compared the following percutaneous mechanical support in patients with CS due to AMI undergoing myocardial revascularization: (1) intra-aortic balloon pump (IABP) vs Medical therapy; (2) percutaneous left ventricular assist devices (PLVADs) vs IABP; (3) complete extracorporeal life support with extracorporeal membrane oxygenation (ECMO) plus IABP vs IABP alone; and (4) ECMO plus IABP vs ECMO alone, in patients with AMI and CS undergoing myocardial revascularization. We evaluated the impact of the support devices on primary and secondary endpoints. Primary endpoint was the inhospital mortality due to any cause during the same hospital stay and secondary endpoint late mortality at 6-12 mo of follow-up. RESULTS: One thousand two hundred and seventy-two studies met the initial screening criteria. After detailed review, only 30 were selected. There were 6 eligible randomized controlled trials and 24 eligible observational studies totaling 15799 patients. We found that the inhospital mortality was: (1) significantly higher with IABP support vs medical therapy (RR = +15%, P = 0.0002); (2) was higher, although not significantly, with PLVADs compared to IABP (RR = +14%, P = 0.21); and (3) significantly lower in patients treated with ECMO plus IABP vs IABP (RR = -44%, P = 0.0008) or ECMO (RR = -20%, P = 0.006) alone. In addition, Trial Sequential Analysis showed that in the comparison of IABP vs medical therapy, the sample size was adequate to demonstrate a significant increase in risk due to IABP. CONCLUSION: Inhospital mortality was significantly higher with IABP vs medical therapy. PLVADs did not reduce early mortality. ECMO plus IABP significantly reduced inhospital mortality compared to IABP. PMID

  10. Late prognostic value of scintigraphic parameters of acute myocardial infarction size in complicated myocardial infarction without heart failure

    SciTech Connect

    Botvinick, E.H.; Perez-Gonzalez, J.F.; Dunn, R.; Ports, T.; Chatterjee, K.; Parmley, W.

    1983-04-01

    Perfusion scintigraphy with thallium-201, infarct scintigraphy with technetium-99m pyrophosphate (TcPYP), and equilibrium blood pool scintigraphy were performed during the initial hospitalization for acute myocardial infarction (MI) in 25 patients without evidence of heart failure who presented with advanced electrocardiographic rhythm and conduction disturbances requiring treatment. Scintigraphic findings during short-term hospitalization were related to the late clinical follow-up performed an average of 14 months later, where patients were grouped as asymptomatic, 8 patients; symptomatic, 9 patients; and deceased, 8 patients. Quantitation of perfusion abnormalities, TcPYP image abnormalities, and left ventricular ejection fraction (EF) revealed that the deceased group had significantly larger TcPYP abnormalities (36 +/- 20 cm2), absolute perfusion abnormalities (32 +/- 16 cm2), and perfusion abnormalities expressed as a percentage of the projected left ventricular area (42 +/- 8%) than the asymptomatic group (13 +/- 8 cm2, 14 +/- 6 cm2, and 20 +/- 9%; p less than 0.05, p greater than 0.05, and p less than 0.01, respectively). The percent perfusion abnormality was significantly larger in the deceased group (42 +/- 8%, p less than 0.01) than in either the symptomatic group (35 +/- 13%, p less than 0.01) or the asymptomatic group (20 +/- 9%), and this parameter in the symptomatic group also differed from that in the asymptomatic group (p less than 0.01). The study indicates that patients with rhythm and conduction disturbances and without congestive heart failure during acute MI may follow an uncomplicated or a complicated late clinical course. Early scintigraphic measurements of MI and perfusion correlate well with this outcome; however, EF could not differentiate among prognostic subgroups.

  11. Early detection and diagnosis of acute myocardial infarction: the potential for improved care with next-generation, user-friendly electrocardiographic body surface mapping.

    PubMed

    Lefebvre, Cedric; Hoekstra, James

    2007-11-01

    Prompt and accurate identification of patients with acute coronary syndrome (ACS) presenting to the emergency department (ED) is paramount to the success of interventional and therapeutic strategies. Accurate diagnosis of ST-segment elevation myocardial infarction or non-ST-segment elevation myocardial infarction is hindered by atypical presentations and suboptimal diagnostic tools. The current standard of care, 12-lead electrocardiogram, has limited efficacy. It does not allow complete imaging of various anatomic segments of the heart and therefore fails to accurately identify some patients who would benefit from immediate therapy. Body surface mapping (BSM) allows greater spatial representation of cardiac electrical activity than 12-lead electrocardiogram, with a more complete view of cardiac electrophysiology and greater sensitivity for detecting acute myocardial infarction. Recent technological advances have overcome previous limitations of BSM, including the need for extensive training, difficulty interpreting results, and cost. The future of BSM in the ED is not yet known but will be aided by the ongoing large-scale Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction trial (OCCULT-MI) trial, which uses PRIME BSM technology.

  12. 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

  13. 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.

  14. Strategies for tissue engineering cardiac constructs to affect functional repair following myocardial infarction.

    PubMed

    Ye, Kathy Yuan; Black, Lauren Deems

    2011-10-01

    Tissue-engineered cardiac constructs are a high potential therapy for treating myocardial infarction. These therapies have the ability to regenerate or recreate functional myocardium following the infarction, restoring some of the lost function of the heart and thereby preventing congestive heart failure. Three key factors to consider when developing engineered myocardial tissue include the cell source, the choice of scaffold, and the use of biomimetic culture conditions. This review details the various biomaterials and scaffold types that have been used to generate engineered myocardial tissues as well as a number of different methods used for the fabrication and culture of these constructs. Specific bioreactor design considerations for creating myocardial tissue equivalents in vitro, such as oxygen and nutrient delivery as well as physical stimulation, are also discussed. Lastly, a brief overview of some of the in vivo studies that have been conducted to date and their assessment of the functional benefit in repairing the injured heart with engineered myocardial tissue is provided.

  15. 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

  16. Role of non-high-density lipoprotein cholesterol in predicting cerebrovascular events in patients following myocardial infarction.

    PubMed

    Mahajan, Nitin; Ference, Brian A; Arora, Natasha; Madhavan, Ramesh; Bhattacharya, Pratik; Sudhakar, Rajeev; Sagar, Amit; Wang, Yun; Sacks, Frank; Afonso, Luis

    2012-06-15

    Although there appears to be a role for statins in reducing cerebrovascular events, the exact role of different lipid fractions in the etiopathogenesis of cerebrovascular disease (CVD) is not well understood. A secondary analysis of data collected for the placebo arm (n = 2,078) of the Cholesterol and Recurrent Events (CARE) trial was performed. The CARE trial was a placebo-controlled trial aimed at testing the effect of pravastatin on patients after myocardial infarction. Patients with histories of CVD were excluded from the study. A Cox proportional-hazards model was used to evaluate the association between plausible risk factors (including lipid fractions) and risk for first incident CVD in patients after myocardial infarction. At the end of 5 years, 123 patients (6%) had incident CVD after myocardial infarction (76 with stroke and 47 with transient ischemic attack). Baseline non-high-density lipoprotein (HDL) cholesterol level emerged as the only significant lipid risk factor that predicted CVD; low-density lipoprotein cholesterol and HDL cholesterol were not significant. The adjusted hazard ratios (adjusted for age, gender, hypertension, diabetes mellitus, and smoking) for CVD were 1.28 (95% confidence interval [CI] 1.06 to 1.53) for non-HDL cholesterol, 1.14 (95% CI 0.96 to 1.37) for low-density lipoprotein cholesterol, and 0.90 (95% CI 0.75 to 1.09) for HDL cholesterol (per unit SD change of lipid fractions). This relation held true regardless of the level of triglycerides. After adjustment for age and gender, the hazard ratio for the highest natural quartile of non-HDL was 1.76 (95% CI 1.05 to 2.54), compared to 1.36 (95% CI 0.89 to 1.90) for low-density lipoprotein cholesterol. In conclusion, non-HDL cholesterol is the strongest predictor among the lipid risk factors of incident CVD in patients with established coronary heart disease.

  17. 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

  18. Exploring diagnostic potentials of radioiodinated sennidin A in rat model of reperfused myocardial infarction.

    PubMed

    Jiang, Cuihua; Gao, Meng; Li, Yue; Huang, Dejian; Yao, Nan; Ji, Yun; Liu, Xuejiao; Zhang, Dongjian; Wang, Xiaoning; Yin, Zhiqi; Jing, Su; Ni, Yicheng; Zhang, Jian

    2015-11-10

    Non-invasive "hot spot imaging" and localization of necrotic tissue may be helpful for definitive diagnosis of myocardial viability, which is essential for clinical management of ischemic heart disease. We labeled Sennidin A (SA), a naturally occurring median dianthrone compound, with (131)I and evaluated (131)I SA as a potential necrosis-avid diagnostic tracer agent in rat model of reperfused myocardial infarction. Magnetic resonance imaging (MRI) was performed to determine the location and dimension of infarction. (131)I-SA was evaluated in rat model of 24-hour old reperfused myocardial infarction using single-photon emission computed tomography/computed tomography (SPECT/CT), biodistribution, triphenyltetrazolium chloride (TTC) histochemical staining, serial sectional autoradiography and microscopy. Gamma counting revealed high uptake and prolonged retention of (131)I SA in necrotic myocardium and fast clearance from non-targeted tissues. On SPECT/CT images, myocardial infarction was persistently visualized as well-defined hotspots over 24h, which was confirmed by perfect matches of images from post-mortem TTC staining and autoradiography. Radioactivity concentration in infarcted myocardium was over 9 times higher than that of the normal myocardium at 24h. With favorable hydrophilicity and stability, radioiodinated SA may serve as a necrosis-avid diagnostic agent for assessment of myocardial viability.

  19. Do antioxidant vitamins reduce infarct size following acute myocardial ischemia/reperfusion?

    PubMed

    Bellows, S D; Hale, S L; Simkhovich, B Z; Kay, G L; Kloner, R A

    1995-02-01

    There is controversy concerning the ability of antioxidant vitamins to reduce myocardial infarct size. We sought to determine whether a brief prophylactic treatment of vitamin C or vitamin C plus Trolox (a water-soluble form of vitamin E) could reduce myocardial infarct size in an experimental model. We used an anesthetized open-chest rabbit model in which a branch of the circumflex coronary artery was ligated for 30 minutes followed by 4 hours of reperfusion. Experiments were performed in a randomized and blinded fashion. An IV injection of normal saline pH balanced to 7.4 (control group n = 15), vitamin C (150 mg/kg, n = 14), or vitamin C plus Trolox (150 mg/kg plus 100 mg/kg, respectively, n = 15) was administered prior to coronary occlusion. Collateral blood flow during coronary occlusion was measured by radioactive microspheres, myocardial risk zone (AR) was assessed by blue dye injection, and myocardial infarct size (AN) was assessed by triphenyltetrazolium chloride staining. All rabbits received comparable ischemic insult: Collateral blood flow and AR were similar among all three groups. Infarct size, measured as a percent of AR, did not differ significantly among the controls (21%), vitamin C (29%), or the vitamin C plus Trolox (18%) groups. Therefore, in this ischemia/reperfusion model, antioxidant vitamins did not alter myocardial infarct size. PMID:7540423

  20. 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.

  1. Cardiac restricted overexpression of membrane type-1 matrix metalloproteinase causes adverse myocardial remodeling following myocardial infarction.

    PubMed

    Spinale, Francis G; Mukherjee, Rupak; Zavadzkas, Juozas A; Koval, Christine N; Bouges, Shenikqua; Stroud, Robert E; Dobrucki, Lawrence W; Sinusas, Albert J

    2010-09-24

    The membrane type-1 matrix metalloproteinase (MT1-MMP) is a unique member of the MMP family, but induction patterns and consequences of MT1-MMP overexpression (MT1-MMPexp), in a left ventricular (LV) remodeling process such as myocardial infarction (MI), have not been explored. MT1-MMP promoter activity (murine luciferase reporter) increased 20-fold at 3 days and 50-fold at 14 days post-MI. MI was then induced in mice with cardiac restricted MT1-MMPexp (n = 58) and wild type (WT, n = 60). Post-MI survival was reduced (67% versus 46%, p < 0.05), and LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT (41 ± 2 versus 32 ± 2%,p < 0.05). In the post-MI MT1-MMPexp mice, LV myocardial MMP activity, as assessed by radiotracer uptake, and MT1-MMP-specific proteolytic activity using a specific fluorogenic assay were both increased by 2-fold. LV collagen content was increased by nearly 2-fold in the post-MI MT1-MMPexp compared with WT. Using a validated fluorogenic construct, it was discovered that MT1-MMP proteolytically processed the pro-fibrotic molecule, latency-associated transforming growth factor-1 binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by 4-fold in the post-MI MT1-MMPexp group. Early and persistent MT1-MMP promoter activity occurred post-MI, and increased myocardial MT1-MMP levels resulted in poor survival, worsening of LV function, and significant fibrosis. A molecular mechanism for the adverse LV matrix remodeling with MT1-MMP induction is increased processing of pro-fibrotic signaling molecules. Thus, a proteolytically diverse portfolio exists for MT1-MMP within the myocardium and likely plays a mechanistic role in adverse LV remodeling.

  2. 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

  3. Creatine kinase radioimmunoassay and isoenzyme electrophoresis compared in the diagnosis of acute myocardial infarction

    SciTech Connect

    Homburger, H.A.; Jacob, G.L.

    1980-07-01

    We compared, in 116 patients, the relative usefulness of results of tests for creatine kinase B-isoenzymes, as measured by radioimmunoassay, and the MB isoenzyme, as measured by electrophoresis, in diagnosis of acute myocardial infarction. The radioimmunoassay was specific for isoenzymes of creatine kinase containing the B subunit. All patients with acute transmural infarcts had positive test results by both techniques, but concentrations of B-isoenzymes were more frequently above normal than were MB bands in the case of patients with acute subendocardial infarcts and in the case of all patients with acute myocardial infarcts from whom sera were collected more than 24 h after onset of chest pain. Concentrations of B-isoenzymes also were increased, even when MB bands were not electrophoretically detectable in specimens from several patients without documented acute myocardial infarcts. These abnormal results presumably were caused by increased concentrations of the BB isoenzyme in serum. Accordingly, an increased concentration of B-isoenzymes had less diagnostic specificity and predictive value for acute myocardial infarction than did a detectable MB band. Results of isoenzyme electrophoresis were more reliable for establishing this diagnosis, but the results of radioimmunoassay were more reliable for excluding it in patients with chest pain as the primary symptom.

  4. Beneficial Effects of Coenzyme Q10 Supplementation on Lipid Profile and Intereukin-6 and Intercellular Adhesion Molecule-1 Reduction, Preliminary Results of a Double-blind Trial in Acute Myocardial Infarction

    PubMed Central

    Mohseni, Mona; Vafa, Mohammadreza; Zarrati, Mitra; Shidfar, Farzad; Hajimiresmail, Seyed Javad; Rahimi Forushani, Abbas

    2015-01-01

    Background: The present investigation was aimed to improve the inflammatory factors and lipoproteins concentration in patients with myocardial infarction (MI) by supplementation with coenzyme Q10 (CoQ10). Methods: In a double-blind, placebo-controlled study, we measured serum concentrations of one soluble cell adhesion molecules (intercellular adhesion molecule-1 [ICAM-1]), serum concentration of intereukin-6 (IL-6) and lipid profiles (high-density lipoprotein-cholesterol [HDL-C], low-density lipoprotein-cholesterol [LDL-C], total cholesterol and triglyceride [TG]) in CoQ10 supplementation group (n = 26) compared with placebo group (n = 26) in hyperlipidemic patients with MI. Fifty-two patients were randomized to receive 200 mg/day of CoQ10 or placebo for 12 weeks. Results: There were no significant differences for serum LDL-C, total cholesterol, and TG between two mentioned groups after the intervention. A significant enhancement in serum HDL-C level was observed between groups after the intervention (55.46 ± 6.87 and 44.07 ± 6.99 mg/dl in CoQ10 and placebo groups, respectively P < 0.001). Concentrations of ICAM-1 (415.03 ± 96.89 and 453.38 ± 0.7 ng/dl CoQ10 and placebo groups, respectively, P = 0.001) and IL-6 (11 ± 9.57 and 12.55 ± 8.76 pg/ml CoQ10 and placebo groups, respectively P = 0.001) in serum were significantly decreased in CoQ10 group. Conclusions: Supplementation with CoQ10 in hyperlipidemic patients with MI that have statin therapy has beneficial effects on their aspects of health. PMID:26330989

  5. PCI Strategies in Patients With ST-Segment Elevation Myocardial Infarction and Multivessel Coronary Artery Disease.

    PubMed

    Bates, Eric R; Tamis-Holland, Jacqueline E; Bittl, John A; O'Gara, Patrick T; Levine, Glenn N

    2016-09-01

    Recent randomized controlled trials have suggested that patients with ST-segment elevation myocardial infarction and multivessel coronary artery disease may benefit more from multivessel percutaneous coronary intervention (PCI) compared with culprit vessel-only primary PCI. The American College of Cardiology, American Heart Association, and Society for Cardiovascular Angiography and Interventions recently published an updated recommendation on this topic. The purpose of this State-of-the-Art Review is to accurately document existing published reports, describe their limitations, and establish a base for future studies. PMID:27585512

  6. 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

  7. Roles of High-Density Lipoprotein Cholesterol in Patients With Acute Myocardial Infarction.

    PubMed

    Lee, Cheol Hyun; Woo, Jong Shin; Park, Chang Bum; Cho, Jin Man; Ahn, Young Keun; Kim, Chong Jin; Jeong, Myung Ho; Kim, Weon

    2016-05-01

    Many observational studies showed hogh-density lipoprotein cholesterol (HDL-C) is a strong inverse predictor of cardiovascular (CV) outcome. However, recent large clinical trials evaluating therapies to raise HDL-C level in those already on statin therapy have been discouraging. This complexity is not well-known.A total of 28,357 acute myocardial infarction (AMI) patients were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR), which was a prospective, multicenter, nationwide, web-based database of AMI in Korea. From this registry, we evaluated 3574 patients with AMI who have follow-up HDL-C level to investigate its association with clinical outcomes. The primary endpoint was the relationship between follow-up change in HDL-C and a 12-month composite of major adverse cardiac events (MACEs).Patients with initial HDL-C ≥ 40 mg/dL showed significantly lower rates of 12-month MACEs, especially cardiac and all-cause mortalities (P < 0.001). When patients were stratified into 4 groups according to the change of HDL-C, patients with decreasing HDL-C showed significantly higher rates of 12-month MACEs as comparable with patients with increasing HLD-C. A multivariate analysis indicated that HDL-C level was a significant predictor of CV events (hazard ratio, 1.38; 95% confidence interval, 1.12-1.71) after correcting for confounding variables.The follow-up change in HDL-C level was significantly related with CV outcomes in patients with AMI. PMID:27149442

  8. Amiodarone therapy in chronic heart failure and myocardial infarction: a review of the mortality trials with special attention to STAT-CHF and the GESICA trials. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina.

    PubMed

    Pinto, J V; Ramani, K; Neelagaru, S; Kown, M; Gheorghiade, M

    1997-01-01

    Amiodarone appears to reduce sudden death in patients with left ventricular dysfunction resulting from an acute MI or a primary dilated cardiomyopathy, particularly if complex ventricular arrhythmias are present. Amiodarone's beneficial effect on mortality in these patients could be unrelated to its antiarrhythmic effects. Multiple factors could account for the improvement in mortality such as the drug's antiischemic effects, neuromodulating effects, its effect on left ventricular function and on heart rate. Moreover, patients with LV dysfunction who have survived an episode of sudden death would potentially benefit from amiodarone therapy. Future trials are needed to determine the precise subsets(s) of patients who would benefit from the drug and the most efficacious dosing regimen for the drug. Based on available data, amiodarone is the only antiarrhythmic agent which has not been shown to increase mortality in patients with chronic heart failure.

  9. The role of technetium-99m stannous pyrophosphate in myocardial imaging to recognize, localize and identify extension of acute myocardial infarction in patients

    NASA Technical Reports Server (NTRS)

    Willerson, J. T.; Parkey, R. W.; Bonte, F. J.; Stokely, E. M.; Buja, E. M.

    1975-01-01

    The ability of technetium-99m stannous pyrophosphate myocardial scintigrams to aid diagnostically in recognizing, localizing, and identifying extension of acute myocardial infarction in patients was evaluated. The present study is an extension of previous animal and patient evaluations that were recently performed utilizing this myocardial imaging agent.

  10. 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