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Myocardial Infarction Stabilization

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3261. Regulation of the ankyrin-B-based targeting pathway following myocardial infarction. Full Text available with Trip Pro

Regulation of the ankyrin-B-based targeting pathway following myocardial infarction. Ion channel reorganization is a critical step in the pro-arrhythmogenic remodelling process that occurs in heart disease. Ankyrin-B (AnkB) is required for targeting and stabilizing ion channels, exchangers, and pumps. Despite a wealth of knowledge implicating the importance of AnkB in human cardiovascular physiology, nothing is known regarding the role of AnkB in common forms of acquired human disease.We (...) present the first report of AnkB regulation following myocardial infarction (MI). AnkB protein levels were reduced in the infarct border zone 5 days following coronary artery occlusion in the canine. We also observed a dramatic increase in AnkB mRNA levels 5 days post-occlusion. Surprisingly, the expression of the upstream AnkB cytoskeletal component beta2-spectrin was unchanged in post-infarct tissues. However, protein levels and/or membrane expression of downstream AnkB-associated ion channels

2008 Cardiovascular Research

3262. IL-10 Inhibits Inflammation and Attenuates Left Ventricular Remodeling After Myocardial Infarction via Activation of STAT3 and Suppression of HuR. Full Text available with Trip Pro

IL-10 Inhibits Inflammation and Attenuates Left Ventricular Remodeling After Myocardial Infarction via Activation of STAT3 and Suppression of HuR. Persistent inflammatory response has adverse effects on left ventricular (LV) function and remodeling following acute myocardial infarction. We hypothesized that suppression of inflammation with interleukin (IL)-10 treatment attenuates LV dysfunction and remodeling after acute myocardial infarction. After the induction of acute myocardial infarction (...) functions, reduced infarct size, and attenuated infarct wall thinning. Myocardial infarction-induced increase in matrix metalloproteinase (MMP)-9 expression and activity was associated with increased fibrosis, whereas IL-10 treatment reduced both MMP-9 activity and fibrosis. Small interfering RNA knockdown of HuR mimicked IL-10-mediated reduction in MMP-9 expression and activity in NIH3T3 cells. Moreover, IL-10 treatment significantly increased capillary density in the infarcted myocardium which

2008 Circulation Research

3263. Immediate Diagnosis of Acute Inferior Wall Myocardial Infarction with Electrocardiographic Pattern of Only R-wave Loss in Inferior Leads: A Case Report. (Abstract)

that has acute R-wave loss in inferior leads as an initial manifestation of acute inferior wall myocardial infarction. The patient was stabilized by coronary angioplasty.Copyright 2010 Elsevier Inc. All rights reserved. (...) Immediate Diagnosis of Acute Inferior Wall Myocardial Infarction with Electrocardiographic Pattern of Only R-wave Loss in Inferior Leads: A Case Report. The 12-lead electrocardiogram is an easily obtained, non-invasive method to assist in the diagnosis of an acute myocardial infarction. Traditional electrocardiographic criteria for diagnosing inferior myocardial infarction emphasize abnormalities of the initial large Q wave or ST segment elevation in leads II, III, and aVF. We report a case

2007 Journal of Emergency Medicine

3264. An administrative claims model suitable for profiling hospital performance based on 30-day mortality rates among patients with an acute myocardial infarction. Full Text available with Trip Pro

An administrative claims model suitable for profiling hospital performance based on 30-day mortality rates among patients with an acute myocardial infarction. A model using administrative claims data that is suitable for profiling hospital performance for acute myocardial infarction would be useful in quality assessment and improvement efforts. We sought to develop a hierarchical regression model using Medicare claims data that produces hospital risk-standardized 30-day mortality rates (...) and to validate the hospital estimates against those derived from a medical record model.For hospital estimates derived from claims data, we developed a derivation model using 140,120 cases discharged from 4664 hospitals in 1998. For the comparison of models from claims data and medical record data, we used the Cooperative Cardiovascular Project database. To determine the stability of the model over time, we used annual Medicare cohorts discharged in 1995, 1997, and 1999-2001. The final model included 27

2006 Circulation

3265. 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

3266. 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

3267. Percutaneous left ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock. Full Text available with Trip Pro

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

3268. Perioperative myocardial infarction--aetiology and prevention. Full Text available with Trip Pro

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

3269. 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

3270. Autologous myoblast transplantation after myocardial infarction increases the inducibility of ventricular arrhythmias. Full Text available with Trip Pro

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

3271. Reciprocal regulation of angiopoietin-1 and angiopoietin-2 following myocardial infarction in the rat. Full Text available with Trip Pro

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

3272. Aging impairs the beneficial effect of granulocyte colony-stimulating factor and stem cell factor on post-myocardial infarction remodeling. Full Text available with Trip Pro

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

3273. 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

3274. Multiple plaque rupture and C-reactive protein in acute myocardial infarction. Full Text available with Trip Pro

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

3275. The role of platelet-derived growth factor signaling in healing myocardial infarcts. Full Text available with Trip Pro

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

3276. 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

3277. Initial therapy for acute myocardial infarction: socioeconomic implications and limitations. Full Text available with Trip Pro

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

3278. 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

3279. Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats Full Text available with Trip Pro

Biochemical Studies on the Cardioprotective Effect of Glutamine on Tissue Antioxidant Defense System in Isoprenaline-Induced Myocardial Infarction in Rats Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarction of human beings. Levels of diagnostic (...) and antiperoxidative enzymes in heart tissue was also observed. Prior oral administration of glutamine significantly prevented isoprenaline-induced adverse effects and maintained myocardial antioxidant status at near normal status. The cardioprotective effect of glutamine is probably related to a strengthening of the myocardial membrane by its membrane stabilizing action, or to a counteraction of free radicals by its antioxidant property, or to its ability to maintain near to normal status the activities of free

2006 Journal of clinical biochemistry and nutrition

3280. To Assess Safety and Efficacy of Myoblast Implantation Into Myocardium Post Myocardial Infarction

To Assess Safety and Efficacy of Myoblast Implantation Into Myocardium Post Myocardial Infarction To Assess Safety and Efficacy of Myoblast Implantation Into Myocardium Post Myocardial Infarction - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove (...) one or more studies before adding more. To Assess Safety and Efficacy of Myoblast Implantation Into Myocardium Post Myocardial Infarction (MARVEL) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT00526253 Recruitment Status : Active, not recruiting First Posted : September 10, 2007 Last Update

2007 Clinical Trials

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