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Myocardial Infarction Stabilization

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3261. 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

3262. 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

3263. 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

3264. 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

3265. 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

3266. 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

3267. 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

3268. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. Full Text available with Trip Pro

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

3269. 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

3270. [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

3271. 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

3272. Perioperative sympatholysis. Beneficial effects of the alpha 2-adrenoceptor agonist mivazerol on hemodynamic stability and myocardial ischemia. McSPI--Europe Research Group. (Abstract)

Perioperative sympatholysis. Beneficial effects of the alpha 2-adrenoceptor agonist mivazerol on hemodynamic stability and myocardial ischemia. McSPI--Europe Research Group. Mivazerol hydrochloride is a new alpha 2-adrenoceptor agonist. In vitro and animal studies have demonstrated both sympatholytic and antiischemic properties. To evaluate the safety and efficacy of mivazerol in patients during perioperative stress, this multicenter phase II clinical trial studied hemodynamic stability (...) , no rebound response occurred in the 12 h after discontinuation of mivazerol. The high-dose, low-dose, and placebo groups did not differ in the incidence of adverse cardiac outcomes (3%, 2%, and 8%, respectively) or the diagnosis of myocardial infarction (2%, 1%, and 6%, respectively).Continuous, 72-h perioperative administration of mivazerol to high-risk patients appears to be relatively safe, producing no significant hypotension or adverse events but some evidence of bradycardia not associated

1997 Anesthesiology Controlled trial quality: predicted high

3273. Cell transplantation preserves cardiac function after infarction by infarct stabilization: augmentation by stem cell factor. Full Text available with Trip Pro

Cell transplantation preserves cardiac function after infarction by infarct stabilization: augmentation by stem cell factor. We hypothesized that implantation of adult mesenchymal stem cells after acute myocardial infarction mobilizes bone marrow precursor cells by activating the stem cell factor pathway, and that overdriving this pathway would enhance the beneficial effects of cell transplantation.After coronary ligation, medium, mesenchymal stem cells, or stem cell factor-overproducing (...) transplantation resulted in 2.0-fold smaller ventricular volumes (P = .001) and 2.0-fold reduced infarct scar area (P = .056), but had no effect on the volume of spared myocardium. Stem cell factor overproduction imparted greater functional benefit without inducing detectable histologic cardiomyocyte regeneration.Mesenchymal stem cell implantation after myocardial infarction facilitates functional cardiac regeneration without myocyte regeneration through augmentation of endogenous infarct repair, which

2005 Journal of Thoracic and Cardiovascular Surgery

3274. Experimental and clinical pharmacology of bretylium tosylate in acute myocardial infarction: a 15-year journey. (Abstract)

. In a randomized hemodynamic study in acute myocardial infarction patients bretylium induced a significant decrease in heart rate, systolic and mean left ventricular pressures, and in systolic and mean aortic pressures. In addition, a parallel and significant decrease in total pulmonary and systemic resistances was seen, accompanied by decreases in tension time and left ventricular (delta P/delta V) indexes. Bretylium tosylate induces stabilization of electrical systole duration (QTc) in acute myocardial (...) Experimental and clinical pharmacology of bretylium tosylate in acute myocardial infarction: a 15-year journey. Experimental and clinical studies demonstrate the antifibrillatory effectiveness of bretylium tosylate: Experimental ventricular fibrillation induced either by electrical stimulation or by ischemia is prevented by bretylium. In 2,000 acute myocardial infarction patients who received bretylium prophylactically primary ventricular fibrillation occurred in less than 1% of cases

1987 Journal de pharmacologie

3275. Justification for intravenous magnesium therapy in acute myocardial infarction. (Abstract)

Justification for intravenous magnesium therapy in acute myocardial infarction. Recent studies have shown that patients with acute myocardial infarction (AMI) are magnesium-deficient and develop an additional transient decrease in serum magnesium concentrations (S-Mg c) during the acute phase of the infarct. Animal experiments, as well as studies on humans, have indicated that the acute decrease in S-Mg c as well as a more chronic magnesium (Mg) deficiency state are harmful to the myocardium (...) multifactorial; a direct depressive effect on the cardiac conducting system; a peripheral dilatory effect on the arteries, reducing the afterload on the myocardium; a reduced infarct size; an ion-stabilizing effect, maintaining stable intra and extracellular concentrations of potassium, sodium and calcium; an improved energy generation in the myocardium; and an inhibitory effect on platelet aggregation. No side-effects were observed in any of the clinical intervention studies. Against this background

1988 Magnesium research : official organ of the International Society for the Development of Research on Magnesium

3276. Glucose-insulin-potassium induced alterations in individual plasma free fatty acids in patients with acute myocardial infarction. (Abstract)

Glucose-insulin-potassium induced alterations in individual plasma free fatty acids in patients with acute myocardial infarction. Total and individual plasma free fatty acids (FFA) were measured on admission and over the next 4 days in 24 patients admitted to the hospital with chest pain and suspected acute myocardial infarction (AMI). In a prospective randomized fashion, the patients were either given an infusion of 300 gm of glucose, 50 units of insulin, and 80 mEq of KCl per liter at a rate (...) ). Arachidonic acid doubled in percentage of the total FFA value during G-I-K infusion (3.1% to 6.5%, P less than 0.002) and returned to the control value when it was stopped. Thus G-I-K infusion during AMI reduces the total level of plasma FFA while increasing the percent of arachidonic and decreasing the percent of linoleic acid, observations proposed to reflect improved membrane stability of the ischemic myocardium.

1981 American heart journal Controlled trial quality: uncertain

3277. Isosorbide dinitrate alone and in association with intra-aortic balloon counterpulsation in acute myocardial infarction. A clinical study by precordial ECG mapping. (Abstract)

treated with ISDN and IABCP. These findings seem to give evidence that the association of ISDN and IABCP may really be effective in reducing and stabilizing the ECG extent of ischemic myocardial injury in pts with transmural AMI without left ventricular failure; however this aggressive therapy cannot have a widespread indication until more reliable criteria for evaluating infarct size are available and larger randomized clinical trials performed. (...) Isosorbide dinitrate alone and in association with intra-aortic balloon counterpulsation in acute myocardial infarction. A clinical study by precordial ECG mapping. The effects of the association of Isosorbide Dinitrate (ISDN) and Intra-Aortic Balloon Counterpulsation (IABCP) on ECGphic signs (in 24-lead precordial maps) of myocardial damage were studied in 7 patients (pts) with anterior acute myocardial infarction (AMI) without cardiogenic shock and/or pulmonary congestion, admitted to the CCU

1982 Giornale italiano di cardiologia Controlled trial quality: uncertain

3278. Clinical intervention studies on magnesium in myocardial infarction. (Abstract)

Clinical intervention studies on magnesium in myocardial infarction. Patients with acute myocardial infarction (AMI) display a significant decrease in serum magnesium concentrations (S-Mg,c) during the initial 48 h after infarction. This decrease is not due to an increased renal magnesium loss, neither is it a dilution phenomenon. Consequently, a migration of Mg from the extracellular to intracellular space might take place, which probably is due to a catecholamine-induced increased lipolysis (...) , forming insoluble intracellular Mg soaps. As the Mg ion is crucial in maintaining the electrical stability of the myocardium, we found it rational to avoid this postinfarctional hypomagnesemia by administration of Mg. In a double-blind, placebo-controlled trial, 130 patients with AMI were randomly allocated to receive a total of 62 mmol magnesium chloride or placebo intravenously during the initial 48 h in hospital. Mg treatment was associated with a reduction in the acute mortality from 19

1989 Magnesium Controlled trial quality: predicted high

3279. Should the exercise test (ET) be performed at discharge or one month later after an episode of unstable angina or non-Q-wave myocardial infarction? (Abstract)

Should the exercise test (ET) be performed at discharge or one month later after an episode of unstable angina or non-Q-wave myocardial infarction? The diagnostic and prognostic value of symptom limited exercise tests (ET) performed before discharge and after one month were compared in men admitted to hospital after an episode of unstable angina or a non-Q-wave myocardial infarction (MI). A 'Positive ET' was defined as either a maximal work load below 100 W or ST-depression greater than (...) stabilized after an episode of unstable angina or non-Q-wave MI.

1991 International journal of cardiac imaging Controlled trial quality: uncertain

3280. N-terminal proatrial natriuretic factor. An independent predictor of long-term prognosis after myocardial infarction. (Abstract)

N-terminal proatrial natriuretic factor. An independent predictor of long-term prognosis after myocardial infarction. Atrial natriuretic factor (ANF) is a peptide hormone secreted from cardiac atria in response to increased atrial pressure. Because of a longer half-life and greater stability, the N-terminal of ANF prohormone (N-terminal proANF) may be a better integrator of atrial peptide secretion than ANF itself. After myocardial infarction, elevation of ANF and other neurohormones has been (...) associated with a poor prognosis. However, when left ventricular ejection fraction (LVEF) and other important clinical variables are included in multivariate analysis, the independent predictive value of these neurohormones has been reduced markedly.To test the prognostic value of N-terminal proANF after myocardial infarction, its plasma concentration was measured a mean of 12 days after infarction in 246 patients in the Survival and Ventricular Enlargement (SAVE) Study. N-terminal proANF was a much

1994 Circulation

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