View clinical trials related to Myocardial Infarction.
Filter by:The size of the acute myocardial infarction (AMI) is related to ischemia and injury induced by tissue reperfusion. These reperfusion's injuries can be reduced by injection of cyclosporin A (CsA) at the time of reperfusion. This post-conditioning reduces the final infarct size 20 to 40%. This has been demonstrated in STEMI patients non-complicated by cardiogenic shock. Early revascularization in the AMI complicated by cardiogenic shock improves short-term and long term survival by reducing the size of the myocardial infarction. The hypothesis of this study is that the administration of Cyclosporin A to these patients, in addition to mechanical reperfusion, is likely to reduce the severity of the multi-organ failure associated with the cardiogenic shock and improve clinical outcome.
A novel Cardiac MRI sequence, developed by Dr. Maria Altbach (Double Inversion radial fast Spin Echo T2 mapping), has been tested clinically. It demonstrated a high sensitivity to the heart muscle swelling ("edema") in different types of heart injury, including heart attacks. The investigators propose to use T2-Map methodology in patients with acute heart attacks and to compare value of this method with other clinical and imaging parameters in predicting short-term (30 day) clinical outcomes of these patients. If successful, the project will provide an effective risk-stratification tool to identify patients with heart attack as a result of atherosclerotic disease, who require more aggressive therapeutic approach and closer follow-up after initial hospitalization.
The purpose of this study is to assess the safety and tolerability of human allogeneic mesenchymal bone marrow cells (aMBMC) administered intravenously to subjects with ST Segment Elevation Myocardial Infarction (STEMI).
Thi is an observational, non interventional, cohort analysis by using administrative databases (drugs treatment, laboratory and diagnostic tests, specialist visits and hospitalizations) of Sicilia region to evaluate treatment patterns of patients after Acute Coronary Syndrome (ACS) event.
REL-0609 trial's hypothesis is that repeated loading doses of clopidogrel (600 mg) administration in addition to high dose of clopidogrel continuous therapy (150 mg/day) results in higher inhibition of the platelets' aggregation in patients with myocardial infarction undergoing interventional treatment comparing to the standard therapy. Such treatment strategy will not cause increased risk of bleeding complications. In many trials treatment with to repeated loading doses of clopidogrel together with high dose of clopidogrel continuous therapy resulted in: MACE reduction, improvement of the long term therapy results, lower risk of ischemic complications. Currently, data regarding to the results of the above treatment are still limited.
INTRODUCTION: Sudden cardiac death is one of the most important reasons of death at industrialized countries. Despite its importance, nowadays Clinical Guidelines are not as extended as expected, with respect to indications for primary prevention defibrillator implantation, following MADIT II and MUSTT criteria, especially at Latin American countries. OBJECTIVES: This Project is designed with the purpose of providing tools to help spreading primary prevention by the means of clinical evidence on real risk of death in this group of patients. REGISTRY DESIGN: - retrospective (at stage 1); prospective (at stage 2) - multi-center (minimum 25-30 centres) - international (Argentina, Brazil, Colombia, Chile, Mexico and Venezuela) - non randomized. - Sample size: at screening about 12.500 patients and 962 patients at treatment stage REGISTRY DEVICES: CE marked (Conformité Européenne) single-chamber, dual-chamber or CRT (Cardiac Resynchronization Therapy) implantable cardiac defibrillator (ICD).
The objective of this study is to evaluate the safety and tolerability of two active doses of RGN-352 (thymosin beta 4, Tβ4, Injectable Solution) in patients with acute myocardial infarction receiving percutaneous coronary intervention angioplasty with or without stent placement. Approximately 75 subjects will be randomized to receive one of two RGN-352 doses of 1200 mg, or 450 mg, or placebo, administered iv by iv push daily for the first 3 consecutive days and weekly for 4 more weeks.
The purpose of this study is to determine whether the efficacy of tirofiban (a 25mcg/kg i.v. bolus followed by a 0.15mcg/kg/min i.v. infusion during a percutaneous coronary intervention (PCI) plus two hours after the procedure) is more effective than placebo in the setting of standard therapies (e.g. aspirin, a thienopyridine, and unfractionated heparin or bivalirudin) among patients undergoing PCI, as assessed by the incidence of adverse cardiac ischemic events defined as death, myocardial infarction (MI), and urgent target vessel revascularization (uTVR) within 48 hours following study drug initiation. A secondary objective of this study is to assess whether tirofiban (a 25mcg/kg i.v. bolus followed by a 0.15mcg/kg/min i.v. infusion during a PCI plus two hours after the procedure) is safe compared to placebo in the setting of standard therapies (e.g. aspirin, a thienopyridine, and unfractionated heparin or bivalirudin) among patients undergoing PCI, as assessed by the incidence of non-CABG-related TIMI major bleeding within 48 hours following study drug initiation. Patient enrollment is pending.
The pilot prospective randomized trial is designed to determine the safety and feasibility of enrolling patients to surgically correct residual Mitral Regurgitation (MR) following Percutaneous Coronary Intervention (PCI) for Myocardial Infarction (MI) verses ongoing medical management of MR. The investigators hypothesize that if moderate MR is corrected in this patient subset, the patients will have improved outcomes as measured by decreased number of major adverse cardiac events, including death, congestive heart failure requiring hospitalization, atrial fibrillation, deterioration of New York Heart Association (NYHA) functional status and improved quality of life.
Myocardial infarction (heart attack) is usually the consequence of rupture of a fatty 'plaque' in a heart artery. The presence of this fat and debris causes the propagation of a blood clot and blockage of the artery. The heart muscle normally supplied by the artery becomes deprived of oxygen and, if starved for long enough, this area of muscle dies. Much of the heart muscle damage is caused by overactivation of inflammatory cells. Whilst inflammation can be beneficial in healing processes, there is accumulating evidence that overactivation of inflammatory processes contributes to further muscle damage and cell death during myocardial infarction. We have recently developed a means of labelling human blood cells with 'nanoparticles' of iron oxide which can then safely be reinjected into the blood to allow the cells to be tracked and seen in the body using a conventional magnetic resonance scanner. In the proposed study we aim to recruit patients with recent heart attacks to perform similar cell labelling and reinjection of labelled cells into the same volunteer's blood stream via the arm to track the fate of the blood cells over the course of days to months. We think that the labelled inflammatory cells will 'home' to the site of the heart attack and will be visible using magnetic resonance imaging (MRI) of the heart. We aim not only to highlight the role of inflammatory cells in myocardial infarction, but also propose that, if successful, this technique could be used in the future to assess the effects of antiinflammatory treatments currently being developed for the treatment of patients with heart attacks. The technique could also be extended to allow labelling of other cell types, including stem cells, to let us further understand how these cells may contribute to repair of damaged organs including the heart.