View clinical trials related to Acute Coronary Syndrome.
Filter by:This study is aimed to investigate whether treatment with Telmisartan is more effective than Candesartan in reducing the ischemic cardiovascular events in high-risk patients with cardiovascular disease.
Thrombin is the most potent activator of platelets, and platelet activation is a hallmark of thrombosis. Coronary artery disease (CAD) is the major cause of mortality and morbidity in the United States and other industrialized countries, and thrombotic sequelae are the key cause of death in diabetes. The accumulation of thrombin at sites of vascular injury provides one of the major mechanisms of recruiting platelets into a hemostatic plug. Thrombin works by activation of the G protein-coupled protease activated receptors PAR1 and PAR4 on human platelets to initiate signaling cascades leading to increases in [Ca]i, secretion of autocrine activators, trafficking of adhesion molecules to the plasma membrane, and shape change, which all promote platelet aggregation. The thrombin receptors work in a progressive manner, with PAR1 activated at low thrombin concentrations, and PAR4 recruited at higher thrombin concentrations. As direct thrombin inhibitors become widely used in clinical practice, it is important to assess their effects on vascular function. Our hypothesis is that PAR1 and PAR4 do not signal through the same G protein pathways, and that PAR4 is not a strong platelet agonist. To investigate this hypothesis, the investigators will study the G protein pathways downstream of PAR4, and assess ex-vivo platelet responsiveness to thrombin, PAR1, and PAR4 agonist peptides, both in normal human subjects, and along the stages of pathology, from patients with stable angina as well as unstable angina who are undergoing angioplasty. Similarly, the investigators will examine platelet function in patients with metabolic syndrome as well as diabetes, along the continuum from insulin resistance to full-blown disease. These studies will provide deeper insight into the G protein pathways used by PARs. They will elucidate the contribution of PAR receptors to normal platelet function as well as the abnormal platelet activation in thrombotic states. The long term goal is to understand the implications for PAR receptors as therapeutic targets for anti-platelet therapies that may carry less bleeding risk.
Thrombin is the most potent activator of platelets, and platelet activation is a hallmark of thrombosis. Coronary artery disease (CAD) is the major cause of mortality and morbidity in the United States and other industrialized countries, and thrombotic sequelae are the key cause of death in diabetes. The accumulation of thrombin at sites of vascular injury provides one of the major mechanisms of recruiting platelets into a hemostatic plug. Thrombin works by activation of the G protein-coupled protease activated receptors PAR1 and PAR4 on human platelets to initiate signaling cascades leading to increases in [Ca]i, secretion of autocrine activators, trafficking of adhesion molecules to the plasma membrane, and shape change, which all promote platelet aggregation. The thrombin receptors work in a progressive manner, with PAR1 activated at low thrombin concentrations, and PAR4 recruited at higher thrombin concentrations. As direct thrombin inhibitors become widely used in clinical practice, it is important to assess their effects on vascular function. Our hypothesis is that PAR1 and PAR4 do not signal through the same G protein pathways, and that PAR4 is not a strong platelet agonist. To investigate this hypothesis, the investigators will study the G protein pathways downstream of PAR4, and assess ex-vivo platelet responsiveness to thrombin, PAR1, and PAR4 agonist peptides, both in normal human subjects, and along the stages of pathology, from patients with stable angina as well as unstable angina who are undergoing angioplasty. Similarly, the investigators will examine platelet function in patients with metabolic syndrome as well as diabetes, along the continuum from insulin resistance to full-blown disease. These studies will provide deeper insight into the G protein pathways used by PARs. They will elucidate the contribution of PAR receptors to normal platelet function as well as the abnormal platelet activation in thrombotic states. The long term goal is to understand the implications for PAR receptors as therapeutic targets for anti-platelet therapies that may carry less bleeding risk.
The investigators' work proposes to evaluate the effectiveness of the Acid Nicotinique (Niaspan®), only molecule currently marketed, ready to raise the plasmatic levels of HDL-c. This effectiveness will be tested among patients having presented recently an acute coronary syndrome. The effectiveness of the molecule will be appreciated versus placebo after randomization. The technique of evaluation of this effectiveness will be the analysis of the vasodilatation endothelial-dependent measured on the level huméral (by echography high resolution). The awaited result is an improvement of 2% in value absolute of this vasodilatation between the initial test and the end of study for the patients receiving the acid nicotinic versus those receiving the placebo (3 months of treatment after inclusion). The calculation of the sample necessary to achieve this goal envisages 70 patients led at the end of the study, divided into two groups of treatment (acid nicotinic or Placebo). Such a result if it were obtained would be higher than that found in studies evaluating the effect on the vasomotricity endothelial statins or inhibitors of the enzyme of conversion.
The ACUTE CT trial is designed to test whether the assessment of chest structures by high-resolution multislice computed tomography (CT) provides equivalent diagnostic accuracy for patient with acute chest pain or other potential cardiac symptoms as compared to a standard of care evaluation.
The purpose of this study is to assess the bleeding safety (the composite endpoint of major and clinically relevant non-major bleeding) of 2 doses of apixaban (2.5 mg BID and 5.0 mg BID) or placebo in combination with standard therapy (aspirin and /or additional antiplatelet therapy) over a 24 week treatment period in selected subjects with recent (≤7 days) acute coronary syndrome.
The main aim of the study is a comparison of serum and plasma concentration of VEGF (Vascular Endothelial Growth Factor), HGF (Hepatocyte Growth Factor) and PDGF (Platelet Derived Growth Factor) with markers of myocardial injury as troponin I, hsCRP, CK-MB and NT-proBNP assessed in patients with first episode of acute coronary syndrome (ACS) in their lives and the estimation of assumed value of VEGF, HGF and PDGF in prognosis of cardiovascular complications at 3 months follow up especially with respect to myocardial infarction (MI), exacerbation of angina, reintervention (PTCA,CABG), symptoms of heart failure, stroke, rehospitalization due to cardiovascular reasons and death. The dynamics of changes in serum and plasma concentration of growth factors in comparison with values of myocardial injury markers will be checked. For the realization of the purpose of the study biochemical measurements will be performed twice i.e. just after admission to hospital and 24h later. Area of a myocardial injury will be estimated by echocardiography examination.
This is a registry of patients with non ST segment elevation Myocardial Infarction (heart attack) and/or unstable acute coronary artery syndrome treated with a standardized protocol including Bivalirudin. Data will be collected on diagnosis, treatment and outcomes.
The purpose of this study is to determine if apixaban is superior to placebo for preventing cardiovascular death, non-fatal myocardial infarction, or ischemic stroke in subjects with a recent acute coronary syndrome
The study will compare the safety and efficacy of prasugrel, administered at different doses with clopidogrel in the treatment of Asian participants with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention.