View clinical trials related to Coronary Disease.
Filter by:Studies have shown that phytosterols will lower LDL cholesterol. Typical diets can contain between 250 to 500 mg of naturally-occurring phytosterols. Long-term studies with phytosterol-containing products(such as margarines) have not taken into account the amounts of naturally occurring phytosterols in the diet. This means that the effects of small amounts of natural dietary phytosterols on LDL cholesterol are not known. In this study, we will examine the effects of phytosterols across a range of levels. The information will likely be used to further support and possibly extend the current dietary recommendations for phytosterol use.
The investigators goals are: 1. to develop software for quantitative volumetric analysis of myocardial perfusion from MDCT images 2. to test its ability to accurately determine the presence, location, extend and severity of perfusion abnormalities in agreement with conventional diagnostic techniques (ICA and MPI) in patients with normal and abnormal coronary arteries and/or perfusion patterns 3. to test this approach in patients undergoing vasodilator stress tests with MDCT imaging in combination with the new vasodilator stress agent Regadenoson.
The purpose of the DEBIUT study is to assess procedural, clinical and angiographic outcomes of: 1. Provisional T-stenting use for dilation the Paclitaxel-eluting PCI-balloon (DiorTM) in comparison to dilation with a standard balloon prior to the implant of the Liberty Bare Metal Stent in bifurcation lesions (with side branch involvement). 2. Comparison of the results above with the results of using a standard balloon prior to provisional T-stenting with the Paclitaxel-eluting stent TaxusTM LibertéTM.
Coronary heart disease (CHD) is a leading cause of death in the spinal cord injured (SCI) population, occurring at younger ages than in the able-bodied population. Conventional risk factors for CHD include high concentrations of low-density lipoprotein (LDL), low concentrations of high-density lipoprotein (HDL), diabetes mellitus (DM), smoking history, and family history. Other factors that may influence progression of CHD include C-reactive protein (an inflammatory marker), and fibrinogen (a pro-coagulant marker). Individuals with SCI with longer duration and greater completeness of injury are more likely to have significantly worse carbohydrate tolerance compared to other neurological deficit subgroups. Muscle atrophy after SCI is associated with increased insulin resistance. Prolonged inactivity has been shown to be associated with hyperinsulinemia and impaired glucose tolerance. Body composition changes after SCI to indicate significantly more total body fat mass and percent fat and less lean mass compared to able-bodied individuals. Carotid intima-media thickness is correlated with atherosclerosis progression and abdominal adiposity. Individuals with abdominal adiposity are at a higher risk for CHD, DM, hypertension, insulin resistance, and dyslipidemia. Abdominal adiposity and insulin resistance are contributors to postprandial lipemia, which may be a more sensitive indicator of CHD risk and progression. The purpose of this study is to determine the prevalence of conventional risk factors by assessing the 10-year risk for CHD, and identify emerging risk factors for CHD in the spinal cord injured population. Subjects will have the option to participate in a high fat meal test to determine postprandial lipemic responses. Knowledge of this information may be able to detect and prevent future cardiovascular events related to CHD.
The purpose of this study is to assess the safety and performance of the BVS Everolimus Eluting Coronary Stent System (EECSS) in the treatment of patients with a maximum of two de novo native coronary artery lesions located in two different major epicardial vessels. Currently in development at Abbott Vascular. Not available for sale in the United States.
The investigators hypothesize that patients with Acute ST Elevation Myocardial Infarction may benefit from primary angioplasty with use of a drug eluting balloon/bare metal stent combination without impairing the process of normal vascular healing and endothelial function. The goals of this study are: 1. To compare 6-month angiographic outcome after primary angioplasty using drug eluting balloon/bare metal stent combination versus drug eluting stent versus bare metal stent. 2. To compare stent apposition and stent endothelialization after primary angioplasty using drug eluting balloon/bare metal stent versus drug eluting stent versus bare metal stent. 3. To compare coronary endothelial function after primary angioplasty using drug eluting balloon/bare metal stent versus drug eluting stent versus bare metal stent.
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.
A feasibility pilot trial of the self-help, "Cognitive behavioural therapy" based "Living Life to the Full" Materials for use by patients with diabetes type 2 and / or coronary heart disease.
The study will assess the change in coronary atherosclerotic disease as determined by intravascular ultrasound (IVUS) for aliskiren compared to placebo when given in addition to standard therapy in patients with coronary artery disease (CAD) and a blood pressure in the pre-hypertensive range.