To assess platelet function profiles in diabetic and nondiabetic patients on aspirin and clopidogrel therapy, two patient populations were included to investigate the 1) acute effects of a 300-mg clopidogrel loading dose (group 1, n ‫؍‬ 52) and 2) long-term effects of clopidogrel (group 2, n ‫؍‬ 120) on platelet function in diabetic compared with nondiabetic patients already on aspirin treatment. Patients were stratified according to the presence of type 2 diabetes. Platelet aggregation was assessed using light transmittance aggregometry (groups 1 and 2). Platelet activation (P-selectin expression and PAC-1 binding) was determined using wholeblood flow cytometry (group 2). Clopidogrel response was also assessed. In group 1, platelet aggregation was significantly increased in diabetic (n ‫؍‬ 16) compared with nondiabetic (n ‫؍‬ 36) patients at baseline and up to 24 h following a 300-mg loading dose (P ‫؍‬ 0.005). In group 2, platelet aggregation and activation were increased in diabetic (n ‫؍‬ 60) compared with nondiabetic (n ‫؍‬ 60) subjects (P < 0.05 for all platelet function assays). Diabetic subjects had a higher number of clopidogrel nonresponders (P ‫؍‬ 0.04). Diabetic patients have increased platelet reactivity compared with nondiabetic subjects on combined aspirin and clopidogrel treatment. Reduced sensitivity to antiplatelet drugs may contribute to the increased atherothombotic risk in diabetic patients. Diabetes 54:2430 -2435, 2005 D iabetes is commonly associated with accelerated atherosclerosis, clinically resulting in premature coronary artery disease (CAD), increased risk of cerebrovascular disease, and severe peripheral vascular disease (1). Patients with type 2 diabetes have a two-to fourfold increase in the risk of CAD, and diabetic patients without prior myocardial infarction have the same risk for a subsequent acute coronary event as nondiabetic patients with a previous myocardial infarction (2,3). Recurrent ischemic events are also more frequent in patients with type 2 diabetes than in nondiabetic patients (4 -6). Platelet dysfunction, among other mechanisms, contribute to the increased risk of atherothrombotic complications in the diabetic population (7-9). Such altered platelet function is revealed by hypersensitivity to aggregants observed in in vitro studies.Platelets from diabetic subjects are also less sensitive to aspirin (10 -11). Importantly, reduced sensitivity, or "poor response," to aspirin has been associated with an increased risk of ischemic events (12-15). Combining clopidogrel to aspirin enhances platelet inhibition and has been associated with a reduction in ischemic events compared with the use of aspirin alone (16 -19). However, the magnitude of antiplatelet effects may be depressed in diabetic patients. The aim of this study was to compare platelet function profiles in diabetic and nondiabetic patients on combined aspirin and clopidogrel therapy. RESEARCH DESIGN AND METHODSTwo patient populations were included to investigate the 1) acute effects of a 300-mg loading dose of...

OCT provides unique insights in patients with SCAD that allow an early diagnosis and adequate management. Most of these findings are undetectable by angiography.

The P2Y12-dependent and -independent pathways of platelet reactivity are altered in T2DM compared with nondiabetic patients, and ITDM have greater ADP-induced platelet aggregation compared with NITDM.

Physiologic assessment of MB should include dobutamine challenge. Because the overshooting of systolic pressure interferes with and is a cause of error in FFR measurements based on mean pressures, diastolic FFR appears to be the technique of choice for MB assessment, whereas mean FFR should be used with caution.