Active clinical trials for "Myocardial Infarction"

Enrollment of a population-based, prospective cohort of 3298 stroke-free adults was completed in 2001 and annual follow-up has continued since then. This collaborative study is the first prospective cohort study among whites, blacks and Caribbean Hispanics living in the same community. This grant supports continued follow-up and outcome detection and expansion of data collection in this cohort. The aims are to evaluate the relationship between vascular outcomes (stroke, myocardial infarction (MI), and vascular death) and insulin resistance, carotid intima-media thickness, carotid distensibility, and quantitative magnetic resonance imaging (MRI) measures of vascular subclinical brain disease and to determine if MRI subclinical disease accounts for race/ethnic differences in cognitive impairment. To accomplish these aims further data collection using the population-based, prospective cohort study is proposed. Stored baseline serum will be used to measure fasting insulin levels to evaluate insulin resistance. High-resolution carotid imaging data will be collected at subsequent visits to expand the measurements of subclinical carotid disease to 1300 subjects. MRIs and a neuropsychological battery emphasizing frontal executive domains will be done on 1300 subjects and quantitative analyses performed to measure white matter hyperintensities, silent infarcts, and silent cerebral microbleeds. Starting in 2005, subjects enrolled in the MRI substudy began to have echocardiograms and 24hour ambulatory blood pressure monitoring. Subjects will be followed by annual telephone interviews to ascertain stroke, MI, death, and changes in cognitive state. In-person assessment will be done for all subjects who screen positive. Community stroke surveillance will be maintained to insure stroke detection among the cohort. Specific diagnostic committees classify stroke, MI and vascular death.

Glucagon-like peptide-1 (GLP-1), produced mainly in enteroendocrine cells, participates in energy homeostasis and glucose metabolism by regulating islet hormone secretion, gastrointestinal motility, and food intake, making GLP-1 agonist a treatment for diabetes and obesity. Pre-clinical and clinical studies have demonstrated that GLP-1 also has cardio-protection effects. GLP-1 agonists is able to improve markers of cardiac function, reduce myocardial infarct size and post-myocardial infarction remodeling in experimental myocardial infarction. And GLP-1 infusion improved left ventricular function and increases myocardial salvage in patients with acute myocardial infarction (AMI). The investigators' previous study found that GLP-1 analogues attenuated ischemia-reperfusion induced apoptosis of stem- and myocardial microvascular endothelial cells, and liraglutide (a GLP-1 analog) usage during hospital stay can prevent no-reflow and improve heart function in AMI. Therefore, the investigators carried out a cohort study to evaluate the association between plasma GLP-1 and in-hospital complications in patients with ST-segment elevation myocardial infarction.

This study is to build a Xinjiang people registry and surveillance system for acute myocardial infarction(AMI) information about patient's basic information, patient characteristics, diagnostic test mode, the program of treatment and hospitalization outcomes including mortality, treatment complications, the cost of hospitalization and follow-up events (death, major adverse cardiac events, stroke, heart failure) of AMI patients; And to propose scientific precaution strategies aimed to prevent effectively from the incidence of AMI; And to optimize the management and outcomes of AMI patients through implementation of guideline recommendations in clinical practice, and to perform analyses and development of effective treatment strategies and predictive models of clinical ourtcomes.

Many studies have shown that acute cerebral dysfunction can impair cardiac function and autonomic control of blood pressure, heart rate and vascular tone, however, the size of the stroke is rarely reported. Involvement of the insular cortex seems to predispose to cardiac damage and autonomic dysfunction. However, it is not clear whether cardiac dysfunction is merely a marker of large strokes or location of the stroke is critical.

Thirty patients with acute ST-elevation myocardial infarction treated with primary PCI and aspiration of thrombus material from the infarct related coronary artery will be included. Both cellular and non cellular content of the thrombus will be examined with morphological and immunohistochemical methods and related to time from onset of symptoms to PCI, as well as to the degree of myocardial necrosis. Furthermore, mRNA expression of selected signal molecules will be performed. In addition, peripheral venous blood samples will be drawn and analyzed for signalling molecules and corresponding mRNA expression in circulating leukocytes.

The purpose of this study is to assess the impact of text message reminders on adherence to medications and exercise in patients recently discharged from the hospital after a myocardial infarction (MI).

Reperfusion therapy for acute ST segment elevation myocardial infarction (STEMI) can significantly reduce mortality, but patients may still have heart failure and adverse cardiovascular events due to massive myocardial loss. About 20% of patients present with acute heart failure (AHF) at admission, It is the most important cause of hospital death in acute myocardial infarction. Because of the large necrotic area of acute anterior myocardial infarction, heart failure still occurs in a considerable number of patients even after revascularization (PCI). Myocardial protection of ischemic myocardium is a hot topic in clinical research. Both ESC and Chinese heart failure guidelines recommend levosimendan for the treatment of acute decompensated heart failure. A large number of studies have proved that levosimendan can significantly reduce myocardial injury and improve cardiac function in patients with acute STEMI complicated with left ventricular dysfunction and cardiogenic shock compared with placebo. Basic research has confirmed that levosimendan can reduce the myocardial infarction area after acute coronary occlusion, improve the left ventricular function, and exert the effects of anti myocardial ischemia, myocardial injury, myocardial fibrosis, ventricular remodeling and anti apoptosis. However, there is still a lack of early preventive application of levosimendan in acute anterior myocardial infarction after PCI to improve ventricular remodeling and reduce the incidence of heart failure. The purpose of this study was to investigate the effect of early prophylactic levosimendan on left ventricular remodeling, ischemic myocardial protection and the development of heart failure in patients with acute anterior myocardial infarction after PCI.

The transradial access (TRA) is currently the preferred approach for percutaneous coronary intervention (PCI). However, in patients with ACUTE ST-segment elevation myocardial infarction (STEMI) after emergency PCI, the high incidence of THE radial artery RAO limits the future choice of the radial artery for percutaneous intervention. The literature reported that distal transradial access (dTRA) significantly reduced RAO after elective PCI, but the application of dTRA in emergency PCI in STEMI has not been reported. We have completed 126 cases of dTRA undergoing emergency PCI after STEMI, which has been preliminarily confirmed to be safe and effective. A single-center, open, prospective, randomized controlled study is planned to compare the use of dTRA and TRA in emergency PCI in STEMI patients. The primary endpoint was the INCIDENCE of RAO within 24 hours after surgery. This clinical study verified that dTRA compared with TRA could reduce the RAO incidence of STEMI patients after emergency PCI. The project will explore a new artery approach to reduce RAO, and provide a basis for the selection of artery approach in STEMI emergency PCI patients.

The relationship between the immune system and the myocardium after myocardial ischemia is an evolving field of research. Crosstalk occurs between macrophages and cardiac myocytes to promote cardio-protection and resolution of inflammation after myocardial ischemia and reperfusion injury (MI/R injury). Myeloid-epithelial-reproductive tyrosine kinase (MerTK), a member of the TAM family of tyrosine kinase receptors (Tyro-Axl-MerTK), is a macrophage receptor that mediates efferocytosis, anti-inflammatory signaling, and resolution of inflammation. After MI/R injury, intact MerTK is necessary for the phagocytosis of dead cardiac myocytes and to promote anti-inflammatory signaling. Proteolytic cleavage of MerTK to its inactive form, soluble MER, restricts the capacity of macrophages to phagocytize dead cardiac myocytes and impairs MerTK-dependent anti-inflammatory signaling resulting in suppressive effects on cardiac remodeling and function. The Thorp lab at Northwestern University has previously measured soluble MER levels in both adult mice and humans and found that soluble MER concentrations increase after MI/R injury. In adult MI patients, soluble MER was measured post coronary artery reperfusion and was found to be increased (average 3200 pg/mL compared to 1700 pg/mL) compared to controls with stable cardiovascular disease. Based on murine data, the lab further postulated that reperfusion injury may directly interfere with MerTK-dependent cardiac repair as reactive oxygen species formed during reperfusion injury induce proteolytic cleavage of MerTK to soluble MER. Myocardial infarctions are rare events in pediatric patients. However, pediatric hearts are exposed to periods of hypoperfusion, ischemia, and inflammation during times of stress such as cardiac bypass and critical illness, and it is unknown how soluble MER levels change in response to these events. Thus, I was interested in investigating how soluble MER levels change after MI/R injury induced by cardiac bypass as well as in the utility of soluble MER as a biomarker of cardiac inflammation and injury in pediatric patients.

The goal of this study is to predict and prevent adverse drug events by investigating the impact of genetic variants, demographics, and environmental factors in subjects status post myocardial infarction and percutaneous coronary insertion who have experienced adverse drug events while on P2Y12 inhibitors.