View clinical trials related to Infarction.
Filter by:The study will perform UC-MSCs transplantation in 2 groups and 1 control group with standard treatment. Each group consists of 5 subjects. In the first group UC-MSCs will be transplanted via intravenous (IV) route and the second group via intracoronary (IC) route. The IV group will receive 2 million cells/kg for each subject and the dosage of IC group is 50 million cells for each subject. All groups will be observed until 1 year.
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 compare the two cardioplegia solutions (blood cardioplegia by means of MPS ® vs. Cardioplexol ®) regarding perioperative outcome and with special attention to cardiac markers in patients with a recent heart attack.
The purpose of this study is to try to find the best dose of the new drug BAY 2433334 to give to participants and to look at how well BAY 2433334 works on top of a dual antiplatelet therapy (acetylsalicylic acid +/- clopidogrel) in patients following a recent heart attack (myocardial infarction) that happens when a blood vessel in the heart suddenly becomes blocked. BAY 2433334, works by blocking a step of the blood clotting process in our body and thins the blood and is a so called oral FXIa inhibitor.
The purpose of this study is to explore the serum levels of pro- and anti-inflammatory biomarkers and angiogenic growth factors and SNP polymorphisms of the promoter regions of their genes as well as to determine their role in the development of adverse cardiac remodeling in patients with acute ST-segment elevation myocardial infarction.
Stroke is the third leading cause of death and the first cause of physical disability and dementia worldwide. Ischemic stroke caused by large vessel occlusion (LVO) is responsible for the vast majority of deaths and disabilities. A very effective and safe treatment, called mechanical thrombectomy (MT) is available for LVO patients. Nevertheless, no blood biomarkers able to identify LVO patients rapidly and to direct them to CT angiography and thrombectomy currently exist. The TIME study is an observational prospective cohort study. All Patients referred to the emergency department or stroke unit with a suspected stroke as identified by paramedics, nurses or clinicians will be enrolled in the study. A panel of blood biomarkers will be analysed retrospectively via standard laboratory assays. The main outcome of the TIME study will be the evaluation of the clinical diagnostic performance of a panel of blood biomarkers, in conjunction with clinical data, for the identification of large vessel occlusion ischemic stroke subtype. This study will allow the identification and evaluation of a final panel of biomarkers and will prompt the development of a test for LVO stroke diagnosis.
The aim of this study is to determine the prevalence of Helicobacter pylori (Hp) infection in patients with myocardial infarction (MI). This is performed to establish the feasibility of a large trial examining whether systematic screening for and subsequent eradication therapy significantly reduces the risk of hospitalization for upper gastrointestinal (GI) bleeding in patients after MI.
RUC-4 is a novel, promising and fast acting (5-15 minutes) αIIbβ3 receptor antagonist with a high-grade inhibition of platelet aggregation (≥80%) shortly after subcutaneous administration. This study is designed to extend the findings in CEL-01 to patients with ST-elevation myocardial Infarction (STEMI) presenting to the cardiac catheterization laboratory with planned coronary angioplasty.
The purpose of this study is to examine the feasibility and effectiveness of a lower extremity telerehabilitation protocol with aims to improve lower extremity recovery among community-living stroke survivors across Canada.
Myocardial infarction is a polygenic disease that may occur due to various environmental risk factors. Mortality risk of the disease; sex, age, smoking, systolic blood pressure, total cholesterol, and high-density lipoprotein levels. The paraoxonase-1 phenotype is expressed as the paraoxonase/arylesterase ratio and is closely related to high-density lipoprotein, acting as an endogenous defense mechanism against vascular oxidative stress, thus contributing to the prevention of atherosclerosis. Serum concentration and activity depend on environmental factors as well as genetic polymorphism. This decrease in enzyme concentration causes changes in gene expression (1). Numerous data on Paraoxonase-1 levels have been found in studies, especially with decreasing serum paraoxonase and arylesterase activities with age, associated with increased risk of systemic oxidative stress and atherosclerosis in humans. Many studies have shown that serum Paraoxonase-1 activity is significantly reduced in people with myocardial infarction, dyslipidemia, atherosclerosis, and chronic kidney disease. The most important risk factor for these and similar diseases is aging. Diversity of conditions such as genetic predisposition, malnutrition, stress, and smoking, which increases vascular dysfunction due to oxidative stress, classify individuals with acute myocardial infarction according to age groups and investigate whether there is a relationship between serum Paraoxonase-1 activity and severity of coronary artery disease in young patients. The paraoxonase-1 enzyme, which is known to decrease blood levels with age, is found to be significantly lower in patients with myocardial infarction at a young age compared to the healthy control group.