Active clinical trials for "Myocardial Infarction"

STEMI is a serious type of coronary heart disease, which is a major cause of disability and death. Morphologically the key feature of remodeling is myocyte hypertrophy, myocyte loss from necrosis or apoptosis, as well as interstitial cell growth especially fibroblast proliferation leading to myocardial fibrosis . Elevated serum LDL-cholesterol concentrations play a proatherogenic role by stimulating inflammation and oxidative processes. Statins have been documented to retard fibrosis and ventricular hypertrophy by the cessation of myofibroblast activity. Clinical studies have proven that statins not only regulate lipids but also improve myocardial fibrosis, regulate cell proliferation and apoptosis, regulate ventricular remodeling, and protect the myocardium

the study is to investigate the relationship of several parameters of complete blood count (CBC) including RDW with N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin T (cTnT) in a cohort of acute myocardial infarction (AMI) patients.

the study is to investigate the relationship of several parameters of complete blood count (CBC) including RDW with N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin T (cTnT) in a cohort of acute myocardial infarction (AMI) patients.

A cardiac arrest event has severe impact on the patient´s health-related quality of life. Survival of cardiac arrest does not innately translate to favorable quality of life. In particular, highly invasive resuscitation strategies, including extracorporeal cardio-pulmonary resuscitation (ECPR) due to therapy-refractory cardiac arrest, may have impact on long-term outcomes. Therefore, apart from acute medical treatment and physical rehabilitation, long-term effects on cardio-pulmonary, physical and neuro-psychiatric functions after cardiac arrest survival have to be evaluated and optimized. We plan to investigate a bundle of cardio-pulmonary, physical and neuro-psychiatric functions in patients who survived a therapy-refratory cardiac arrest with ECPR.

This is a Phase 1, randomised, double-blind, placebo-controlled, single ascending dose (SAD) and multiple ascending dose (MAD) study to evaluate the safety, tolerability, and pharmacokinetic of NP-011 in healthy volunteers.

Acute myocardial infarction (AMI), triggered by myocardial ischemia and reperfusion injury, is a disease with high morbidity and mortality, and there is a tendency for its incidence to increase at younger ages. One of the most worrisome complications of primary percutaneous surgery is contrast-induced nephropathy, which is associated with increased mortality and morbidity in myocardial infarction after coronary interventions. In many studies, inflammatory markers, which are thought to give an idea about the development of contrast-related nephropathy, have been examined. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cytoprotective protein expression driven by antioxidant response agents (AREs) and plays a decisive role in the regulation of oxidative defense and redox homeostasis in cells. There are studies showing the role of Nrf2 in the pathogenesis of kidney damage in some studies. Studies on the effect of Nrf2 level on contrast media nephropathy in patients with contrast media nephropathy (CIN) are limited in the literature. This study also aimed to form a basis for the literature, which is a small number of studies, in later studies.

Stress, anger and depressed can operate as a trigger to an Acute Coronary Syndrome. It is often found in the literature that patients refer excessive anger, anxiety, sadness, pain or acute stress before the acute myocardial infarction (AMI). Moreover, a recent meta-analysis reported a strong association between the occurrence of AMI and many of these acute emotions. Anger is a common manifestation of psychological stress and could trigger off an atherogenic process through several mechanisms. Coronary atherosclerosis features narrowing of coronary arteries on account of endothelial thickening caused by the build up of atheromatous plaques. It is a process characterized by inflammatory and fibroproliferative response of the artery wall, caused by continuous aggression to its surface and whose thickening, evoked by the evolution of fat streaks atherosclerotic lesions, until fiber plaques is quite slow. Endothelial dysfunction also results in the loss of natural anti-thrombotic properties involved in the endothelium patency. According to a study performed by our group, anger management was significantly lower among patients with CAD when compared to those without CAD, and the occurrence of major cardiovascular events (MACE) was significantly higher in patients presented with lower anger control. Both associations were independent from traditional risk factors, occurrence of previous events or another anger aspects. Thus, this study was designed in order to evaluate the effect of the "cognitive training to anger management " on endothelium-dependent vasodilation of the arm artery in patients with acute myocardial infarction with ST segment elevation submitted to primary coronary intervention.

The purpose of this study is to evaluate the efficacy and safety of LCZ696 titrated to a target dose of 200 mg twice daily, compared to ramipril titrated to a target dose of 5 mg twice daily.

Inflammatory processes have been identified as key mediators of ischemia/ reperfusion injury in ST-segment elevation myocardial infarction. They add additional damage to the myocardium and are associated with clinical adverse events (heart failure and cardiovascular death) and poor myocardial recovery. All the different anti-inflammatory approaches to reduce reperfusion injury have been disappointing. Colchicine is a well-known substance with potent anti-inflammatory properties. In a recent pilot study performed in 151 acute STEMI patients treated with primary percutaneous coronary intervention(PPCI) Deftereos et al. showed a 50% reduction of infarct size (creatine kinase release) with a short course treatment of colchicine in comparison to placebo. One mechanism to explain this effect could be the reduction of adverse left ventricular (LV) remodelling. LV remodelling is part of the healing process of myocardium after MI. It is defined as the end diastolic volume (EDV) increase in the first months after MI. Adverse LV remodelling is increased by inflammation and ultimately leads to heart failure. Our main hypothesis is that colchicine with its anti-inflammatory properties significantly reduces the initiation of adverse LV remodelling, together with a significant reduction of infarct size and microvascular obstruction in comparison to placebo in acute STEMI patients referred for PPCI. After inclusion and randomisation, patients will receive the first part of their experimental treatment: colchicine or placebo before PCI, then, the second part after PCI and during 5 days. They will be followed up during their hospitalization and until one year. In order to evaluate LV remodelling, two cardiac magnetic resonance studies will be performed during their participation: one during their hospitalization and a second at 3 months. At 1 year, adverse events will be collected by phone.

Investigators aimed to test the beneficial effect of tirofiban, a GPIIb/IIIa antagonist, for Non-ST-Elevation Acute Coronary Syndrome Patients who has high resistance to clopidogrel.