View clinical trials related to Platelet Aggregation.
Filter by:The aim of the study is to assess blood platelet function and activation in patients undergoing both cement and non cement hip joint total alloplasty. Bone cement is used as a special biomaterial to help fix a hip prosthesis in place but is associated with bone cement implantation syndrome causing such complications as hypotension, cardiac arrhythmias. The pathophysiology of bone cement implantation syndrome is not fully known but one theory supports formation of clots in the bloodstream. This directly would activate platelets but no such study has been performed in humans. As bone reaming could potentially cause platelet activation even without bone cement, the study involves a control group of patients undergoing non cemented joint alloplasty.
About 35% of patients hospitalized with Acute Coronary Syndromes (ACS) have some degree of renal dysfunction. Chronic kidney disease (CKD) is not only associated to worse prognosis in ACS patients, but leads also to an increased risk of bleeding, which may importantly influence the risk-benefit ratio of antiplatelet therapy in this population. The responsible mechanisms for increased rate of ischemic events in this population are not completely elucidated. Antiplatelet therapy is of paramount importance in the treatment of ACS, but its benefit in CKD patients is not well established. This population is often excluded or underrepresented in large clinical trials, and the indication of antiplatelet therapy is often extrapolated from studies in patients with preserved renal function. In recent meta-analysis, Palmer et al. sought to evaluate the benefits and risks of antiplatelet agents in patients with CKD and concluded that in patients with ACS or scheduled for angioplasty already taking aspirin, the addition of clopidogrel or glycoprotein IIb / IIIa inhibitors have little or no impact in reducing the incidence of myocardial infarction, death or need for revascularization. In the PLATO trial, ticagrelor (a new reversible inhibitor of P2Y12 receptor with faster onset of action and greater platelet inhibition) was compared to clopidogrel in patients with high risk ACS and was associated to a 16% risk reduction on the occurrence of death from vascular causes, myocardial infarction, or stroke. In a pre-specified sub-analysis, data from patients with CKD were compared to those obtained from the population with normal renal function and suggests that the benefit of ticagrelor may be even greater in patients with CKD. Two hypotheses were considered to explain these results: 1. Greater and more consistent platelet inhibition achieved with ticagrelor would be more effective in reducing ischemic events in this population at increased thrombotic risk; 2. Pleiotropic effects of ticagrelor besides inhibition of the P2Y12 receptor. Ticagrelor might be associated with an elevation in serum levels of adenosine. This could improve myocardial perfusion through coronary vasodilation, and this effect would be more pronounced in patients with renal dysfunction. This project aims to validate (or not) these hypotheses, analyzing platelet aggregation and circulating adenosine levels in patients taking dual antiplatelet therapy with aspirin and clopidogrel or ticagrelor.
This project aims to evaluate, in recent post-acute myocardial infarction (AMI) patients on dual antiplatelet therapy, the impact of regular exercise training on platelet aggregability and the correlation between the level of platelet aggregability and muscle sympathetic nerve activity (MSNA).
The study is to characterize the AggreGuide ADP Assay's performance.
This clinical trial is examining the role of genetic polymorphism on the effect of clopidogrel (with or without aspirin) on platelet response in persons at high-risk for myocardial infarction or stroke due to family history of early-onset coronary artery disease.
This study is to determine whether the AggreGuide platelet aggregometer can discern the effect of low dose aspirin on subjects platelet aggregation using arachidonic acid as the agonist.
This study is designed to provide data on platelet aggregation of PA32540 plus clopidogrel dosed separately compared to EC aspirin 81 mg plus EC omeprazole 40 mg plus clopidogrel dosed concomitantly.
The objective is to describe and quantify levels of platelet reactivity in three different cohorts of patients taking thienopyridine: patients who report nuisance bleeding, patients who report alarming bleeding, and patients who report no nuisance or alarming bleeding. The investigators hypothesize that patients with nuisance or alarming bleeding events on maintenance thienopyridine therapy will have lower levels of platelet reactivity than patients without nuisance or alarming bleeding on thienopyridine therapy.
Aspirin has been shown to reduce cardiovascular events in at risk individuals. Elucidation of mechanisms of aspirin resistance and a possible loss of effect of aspirin over time with chronic aspirin treatment necessitate a more precise method of measuring the "release phase" of platelet activation, including the release of dense granules from platelets.
Passive smoking is associated with an increased risk for cardiovascular events. However, the exact mechanisms by which passive smoking affects cardiovascular health are not entirely understood. In the present study, the researchers investigate the effects of short-term exposure to secondhand smoke on platelet function and peripheral microvascular endothelial function in healthy individuals. For this purpose, platelet function and endothelial function are measured before and after a 1-hour exposure to secondhand smoke in a concentration that is encountered in bars and restaurants without smoke-free policies. The researchers' hypothesis is that short-term exposure leads to platelet activation and impairment of endothelial function.