The activation of platelets and their participation in a thrombotic response to rupture of an atherosclerotic plaque are critical determinants of the extent of thrombosis, incremental plaque growth, and the development of occlusive thrombi. Increased adherence of platelets to vessel walls manifesting early atherosclerotic changes and the release of growth factors from a-granules can exacerbate the evolution of atherosclerosis. Patients with diabetes, particularly those with macrovascular disease, have an increased circulating platelet mass secondary to increased ploidy of megakaryocytes (28). Activation of platelets is increased with type 2 diabetes. This is reflected by increased concentrations in urine of a metabolite of thromboxane A2, thromboxane B2, and by the spontaneous aggregation of platelets (29-31) in blood. The prevalence of spontaneous aggregation of platelets correlates with the extent of elevation of concentrations of hemoglobin (Hb)A1c (30). Stringent glycemic control decreases concentrations in urine of thromboxane B2 (29,31). Additionally, platelets isolated from the blood of subjects with diabetes exhibit impaired vasodilatory capacity (32), apparently mediated by release of a short-acting platelet-derived substance(s) that interferes with the ADP-induced dilatory response seen in normal vessels with intact endothelium (33).
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