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Myocardial Infarction Stabilization

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3281. A functional SNP in PSMA6 confers risk of myocardial infarction in the Japanese population. (Abstract)

cells reduced activation of the transcription factor NF-kappaB by stabilizing phosphorylated IkappaB. Our results implicate this PSMA6 SNP as a previously unknown genetic risk factor for myocardial infarction. (...) A functional SNP in PSMA6 confers risk of myocardial infarction in the Japanese population. Inflammation is now considered critical in the pathogenesis of myocardial infarction. One of the mechanisms regulating the inflammatory process is the ubiquitin-proteasome system. We investigated whether variants of the 20S proteasome are associated with susceptibility to myocardial infarction and found a common SNP (minor allele frequency of 0.35) in the proteasome subunit alpha type 6 gene (PSMA6

2006 Nature Genetics

3282. Surgical therapies for post-myocardial infarction patients. (Abstract)

Surgical therapies for post-myocardial infarction patients. Occasionally, high-risk patients in the post-myocardial infarction (MI) period require surgical intervention for stabilization and/or revascularization. In a meta-analysis involving 3,088 patients with ischemic heart disease, revascularization was associated with nearly an 80% reduction in the risk of death. Coronary artery bypass graft (CABG) surgery is commonly performed in post-MI patients and is associated with more favorable (...) outcomes than medical therapy. However, several factors have to be considered in proper patient selection for CABG, such as the left ventricular ejection fraction (LVEF), severity of heart failure (HF), and myocardial viability. The ongoing Surgical Treatment for Ischemic Heart Failure (STICH) trial will assess the benefits of CABG in patients with both a low LVEF and HF. Unstable post-MI patients who fail revascularization can be managed via mechanical circulatory support devices or pumps

2008 American Journal of Cardiology

3283. Percutaneous left ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock. (Full text)

Percutaneous left ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock. Cardiogenic shock (CS) remains the most common cause of death in patients with acute myocardial infarction (AMI). In addition to percutaneous coronary intervention, inotropes, and fluids, intraaortic balloon pumping (IABP) is most widely used for initial haemodynamic stabilization. However, the main limitation of IABP is the lack of active circulatory support and the requirement

2007 European Heart Journal PubMed abstract

3284. Perioperative myocardial infarction--aetiology and prevention. (Full text)

Perioperative myocardial infarction--aetiology and prevention. Perioperative myocardial infarction (PMI) is one of the most important predictors of short- and long-term morbidity and mortality associated with non-cardiac surgery. Prevention of a PMI is thus a prerequisite for an improvement in overall postoperative outcome. The aetiology of PMI is multifactorial. The perioperative period induces large, unpredictable and unphysiological alterations in coronary plaque morphology, function (...) and coronary revascularization in high-risk patients, the paradigm is shifting from an emphasis on extensive non-invasive preoperative risk stratification to a combination of selective non-invasive testing and aggressive pharmacological perioperative therapy. Perioperative plaque stabilization by pharmacological means may be as important in the prevention of PMI as an increase in myocardial oxygen supply or a reduction in myocardial oxygen demand.

2005 British Journal of Anaesthesia PubMed abstract

3285. 2004 American College of Cardiology/American Heart Association guidelines for the management of patients with ST-elevation myocardial infarction: implications for emergency department practice. (Abstract)

2004 American College of Cardiology/American Heart Association guidelines for the management of patients with ST-elevation myocardial infarction: implications for emergency department practice. The American College of Cardiology and the American Heart Association last published evidence-based guidelines for the management of ST-segment elevation myocardial infarction (STEMI) in 1999. In mid-2004, in recognition of the evolution and improvement of many of the most basic tenets of clinical (...) management of STEMI since that time, an updated edition of the STEMI guidelines has been published. These guidelines offer many evidence-based recommendations that are pertinent to the out-of-hospital and emergency department care of STEMI patients, including initial evaluation, risk stratification, stabilizing management, and the choice between pharmacologic and mechanical revascularization. These are presented and discussed here.

2005 Annals of Emergency Medicine

3286. Autologous myoblast transplantation after myocardial infarction increases the inducibility of ventricular arrhythmias. (Full text)

Autologous myoblast transplantation after myocardial infarction increases the inducibility of ventricular arrhythmias. Small scale clinical trials suggested the feasibility and the efficacy of autologous myoblast transplantation to improve ventricular function after myocardial infarction. However, these trials were hampered by unexpected episodes of life-threatening ventricular tachyarrhythmias (VT). We investigated cardiac electrical stability after myoblast transplantation (...) to the myocardium.Seven days after coronary ligation, Wistar rats were randomized into 3 groups: a control group receiving no further treatment, a vehicle group injected with culture medium into the infarcted myocardium, and a myoblast group injected with autologous myoblasts. Holter monitoring did not discriminate the myoblast from the vehicle groups. Programmed Electrical Stimulation (PES) was performed to evaluate further a cardiac substrate for arrhythmia susceptibility. The occurrence of sustained VT during PES

2006 Cardiovascular Research PubMed abstract

3287. Reciprocal regulation of angiopoietin-1 and angiopoietin-2 following myocardial infarction in the rat. (Full text)

Reciprocal regulation of angiopoietin-1 and angiopoietin-2 following myocardial infarction in the rat. This study sought to characterize changes in the angiopoietin system in a rat model of myocardial infarction (MI).Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) bind to the endothelial-specific receptor tyrosine kinase, TIE-2. Ang-2 has been suggested to be an antagonist of TIE-2, possibly acting to release endothelial cells from the tonic stabilizing influence of Ang-1. However (...) , on prolonged exposure, Ang-2 has been shown to acquire agonistic activity at TIE-2, raising the possibility that this isoform may play a direct role in neovascularization.Sprague-Dawley rats were subjected to left coronary ligation and myocardial tissues were harvested from the infarct and peri-infarct regions, or from non-infarcted myocardium. Changes in gene expression were determined by RT-PCR and confirmed by Northern analysis. Changes in protein expression were confirmed by Western analysis

2004 Cardiovascular Research PubMed abstract

3288. Aging impairs the beneficial effect of granulocyte colony-stimulating factor and stem cell factor on post-myocardial infarction remodeling. (Full text)

Aging impairs the beneficial effect of granulocyte colony-stimulating factor and stem cell factor on post-myocardial infarction remodeling. Granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) are potential new therapies to ameliorate post-myocardial infarction (post-MI) remodeling, as they enhance endogenous cardiac repair mechanisms and decrease cardiomyocyte apoptosis. Because both of these pathways undergo alterations with increasing age, we hypothesized that therapeutic (...) efficacy of G-CSF and SCF is impaired in old versus young adult rats. MI was induced in 6- and 20-month-old rats by permanent ligation of the left coronary artery. In young animals, G-CSF/SCF therapy stabilized and reversed a decline in cardiac function, attenuated left ventricular dilation, decreased infarct size, and reduced cardiomyocyte hypertrophy. Remarkably, these effects on cardiac structure and function were absent in aged rodents. This could not be attributed to ineffective mobilization

2006 Circulation Research PubMed abstract

3289. Evaluation of markers of endothelial damage in cases of young myocardial infarction. (Abstract)

Evaluation of markers of endothelial damage in cases of young myocardial infarction. The pathogenesis of arterial thrombotic disease involves multiple genetic and environmental factors related to atherosclerosis and thrombosis. The endothelium is a monolayer of polygonal cells that extend continuously over the luminal surface of the entire vasculature. Injury to the endothelium leads to dysfunction. The causes of injury include lipids, immune complexes, microorganisms, smoking, hypertension (...) , aging, diabetes mellitus and trauma. Studies have been done to evaluate the role of different adhesion molecules on the endothelial membrane in the pathogenesis of atherosclerosis. These molecules are intercellular adhesion molecule type-1 (ICAM-1), vascular cell adhesion molecule type-1 (VCAM-1), platelet/endothelial cell adhesion molecule-1 (PECAM-1), soluble P-selectin (sP-selectin) and soluble E-selectin (sE-selectin). One-hundred and twenty patients of myocardial infarction (age below 40 years

2005 Atherosclerosis

3290. Multiple plaque rupture and C-reactive protein in acute myocardial infarction. (Full text)

Multiple plaque rupture and C-reactive protein in acute myocardial infarction. This study sought to investigate the relationship between multiple plaque ruptures, C-reactive protein (CRP), and clinical prognosis in acute myocardial infarction (AMI).Several studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some acute coronary syndrome (ACS) patients. Recent studies have reported that a ruptured plaque (...) at the culprit lesion is associated with elevated CRP, which indicates a poor prognosis in patients with ACS.We performed intravascular ultrasound in 45 infarct-related arteries and another 84 major coronary arteries in 45 first AMI patients.Plaque rupture was observed in 21 patients (47%) at the culprit site. Intravascular ultrasound revealed 17 additional plaque ruptures at remote sites in 11 patients (24%). Patients with multiple risk factors were more frequently found in our multiple-plaque rupture

2005 Journal of the American College of Cardiology PubMed abstract

3291. The role of platelet-derived growth factor signaling in healing myocardial infarcts. (Full text)

The role of platelet-derived growth factor signaling in healing myocardial infarcts. This study sought to examine the role of platelet-derived growth factor (PDGF) signaling in healing myocardial infarcts.Platelet-derived growth factor isoforms exert potent fibrogenic effects through interactions with PDGF receptor (PDGFR)-alpha and PDGFR-beta. In addition, PDGFR-beta signaling mediates coating of developing vessels with mural cells, leading to the formation of a mature vasculature. We (...) hypothesized that PDGFR activation may regulate fibrosis and vascular maturation in healing myocardial infarcts.Mice undergoing reperfused infarction protocols were injected daily with a neutralizing anti-PDGFR-beta antibody (APB5), an anti-PDGFR-alpha antibody (APA5), or control immunoglobulin G, and were killed after 7 days of reperfusion.The PDGF-B, PDGFR-alpha, and PDGFR-beta mRNA expression was induced in reperfused mouse infarcts. Perivascular cells expressing phosphorylated PDGFR-beta were

2006 Journal of the American College of Cardiology PubMed abstract

3292. Color of culprit lesion at 6 months after plain old balloon angioplasty versus stenting in patients with acute myocardial infarction. (Abstract)

Color of culprit lesion at 6 months after plain old balloon angioplasty versus stenting in patients with acute myocardial infarction. Although the healing process of disrupted yellow plaques at myocardial infarction (MI) culprit lesions has been reported, the effect of stenting on this process has not been clarified. Stenting has been reported to deteriorate the endothelial function after percutaneous coronary intervention (PCI). Therefore, we compared the angioscopic morphology of culprit (...) at the culprit lesion.Coronary stenting in patients with acute MI leads to the disappearance of yellow color at a significantly higher rate than POBA; however, whether it stabilizes the plaque requires further investigation.

2004 American Heart Journal

3293. Initial therapy for acute myocardial infarction: socioeconomic implications and limitations. (Full text)

Initial therapy for acute myocardial infarction: socioeconomic implications and limitations. The optimal therapeutic approach for acute myocardial infarction (AMI) is still evolving; however, many would consider one of two basic options: "medical"-only thrombolysis or reperfusion, or an early (invasive), percutaneous coronary intervention (PCI). The decision about which is most appropriate depends (perhaps unfortunately) on more than just medical factors. That is, the choice for some patients (...) is also limited by payor source and the technical capabilities at the site of the initial treatment. Practically speaking, a significant portion of the US population simply does not have the option of (at least, initial) PCI.Kino Community Hospital in Tucson, AZ, serves primarily an indigent population in southern Arizona, near the border with Mexico. This facility does not have in-house capability for PCI. Therefore, shortly after the publication of the original Thrombolysis in Myocardial Infarction

2004 Chest PubMed abstract

3294. Measurement of ejection fraction after myocardial infarction in the population. (Abstract)

Measurement of ejection fraction after myocardial infarction in the population. To assess the secular trends in left ventricular ejection fraction (LVEF) assessment after myocardial infarction (MI) and to identify the determinants of testing.A population-based MI incidence cohort.The use of tests measuring LVEF (echocardiography, radionuclide, and left ventricular [LV] angiography) was examined among all consecutive residents of Olmsted County, MN, hospitalized for a validated incident MI (...) between 1979 and 1998. Baseline characteristics and outcome were ascertained from community medical records.Among 2,317 patients with incident MI, LVEF assessment increased from 1979 to 1986 (22 to 85%; p value for trend = 0.0001) to stabilize thereafter until 1998. During the most recent decade, LVEF was measured during the hospital stay in 81% of the patients. Characteristics associated with lesser use of tests included older age and measurement of ejection fraction within 1 year prior to the index

2004 Chest

3295. Do beta-blockers reduce short-term mortality following acute myocardial infarction? A systematic review and meta-analysis. (Full text)

Do beta-blockers reduce short-term mortality following acute myocardial infarction? A systematic review and meta-analysis. Acute myocardial infarction (AMI) remains a major cause of death and beta-blockers are known to reduce long-term mortality in post-AMI patients. We sought to determine whether patients receiving beta-blockers acutely (within 72 h) following AMI had a lower mortality rate at 6 weeks than patients receiving placebo.We conducted a systematic review of randomized controlled (...) the data and rated study quality using the Jadad score and the adequacy of allocation concealment score, which was adopted by the Cochrane group. We calculated pooled odds ratios (ORs) using a random effect model and performed sensitivity analyses to explore the stability of the overall treatment effect.We included 18 studies (13 were rated high-quality) with 74 643 enrolled participants and had 5095 deaths. Compared with placebo, adding beta-blockers to other interventions within 72 hours after AMI

2008 CJEM PubMed abstract

3296. Weight-change as a prognostic marker in 12 550 patients following acute myocardial infarction or with stable coronary artery disease. (Full text)

Weight-change as a prognostic marker in 12 550 patients following acute myocardial infarction or with stable coronary artery disease. To examine the prognostic importance of weight-change in patients with coronary artery disease (CAD), especially following acute myocardial infarction (AMI).In 4360 AMI patients (OPTIMAAL trial) without baseline oedema, we assessed 3-month weight-change, baseline body mass index (BMI), demographics, patient history, medication, physical examination (...) , and biochemical analyses. Weight-change was defined as change >+/-0.1 kg/baseline BMI-unit. Patients were accordingly categorized into three groups; weight-loss, weight-stability, and weight-gain. Our findings were validated in 4012 AMI patients (CONSENSUS II trial) and 4178 stable CAD patients (79% with prior AMI, 4S trial). Median follow-up was 2.7 years, 3 months, and 4.4 years, respectively. In OPTIMAAL, 3-month weight-loss (vs. weight-stability) independently predicted increased all-cause death [n=471

2006 European heart journal PubMed abstract

3297. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. (Full text)

Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. The leading cause of death in patients hospitalized for acute myocardial infarction is cardiogenic shock. We conducted a randomized trial to evaluate early revascularization in patients with cardiogenic shock.Patients with shock due to left ventricular failure complicating myocardial infarction were randomly (...) . Early revascularization should be strongly considered for patients with acute myocardial infarction complicated by cardiogenic shock.

1999 NEJM Controlled trial quality: predicted high PubMed abstract

3298. Elastin stabilizes an infarct and preserves ventricular function. (Abstract)

Elastin stabilizes an infarct and preserves ventricular function. After a myocardial infarction, the injured region becomes fibrotic and the myocardial scar may expand if the ventricular wall lacks elasticity. Cardiac dilatation may precipitate the vicious cycle of progressive heart failure. The present study evaluated the functional benefits of increasing elastin within a myocardial scar using cell based gene therapy.A myocardial infarction was generated by ligation of the left anterior (...) group.Expressing recombinant elastin within the myocardial scar reduced scar expansion and prevented LV enlargement after a myocardial infarction. Altering matrix remodeling after an infarct preserved the LV function for at least 3 months.

2005 Circulation

3299. [Study on the effect and mechanism of puerarin on the size of infarction in patients with acute myocardial infarction]. (Abstract)

[Study on the effect and mechanism of puerarin on the size of infarction in patients with acute myocardial infarction]. To observe the effect of puerarin on infarction size, fatty acids metabolism, inflammatory response and atherosclerotic plaque stability in patients with acute myocardial infarction (AMI).Sixty-one patients with AMI were randomly divided into two groups, the control group (n = 30) and the treated group (n = 31). All were treated with conventional treatment, but to the treated (...) , after treatment, the three parameters lowered by 30%, 41% and 23%, respectively and the size of infarction significantly reduced in the treated group (P<0.01), while in the control group, no significant change was found (P>0.05).Puerarin treatment could significantly reduce the size of infarction in patients with AMI, the mechanism is possibly related with its effects in lowering plasma levels of FFA, inhibiting inflammation and stabilizing atherosclerotic plaque.

2004 Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban Controlled trial quality: uncertain

3300. Effects of carvedilol early after myocardial infarction: analysis of the first 30 days in Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN). (Abstract)

Effects of carvedilol early after myocardial infarction: analysis of the first 30 days in Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN). In the CAPRICORN trial, carvedilol reduced all-cause mortality by 23% over a mean follow-up of 1.3 years in clinically stabilized post-myocardial infarction (MI) patients with left ventricular dysfunction (LVD) with or without signs of heart failure. This analysis sought to assess the impact of carvedilol within the first (...) 30 days of randomization.The effect of carvedilol initiated after acute MI with LVD (n = 975) was compared with the effect of placebo (n = 984) added to other standard-of-care therapies on mortality, fatal or nonfatal infarction, cardiac arrest, and their composite as well as withdrawals for adverse events during the first 30 days of therapy.The carvedilol group experienced a reduction in mortality in the first 30 days (19 vs 33, hazard ratio [HR] 0.58, 95% CI 0.33-1.02); fatal or nonfatal MI (13

2007 American heart journal Controlled trial quality: uncertain

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