Seminars in thrombosis, thrombolysis and vascular biology. 3. Platelet activity in cardiovascular disease.
Platelets contribute to normal hemostasis by adhering to subendothelial tissues after vascular damage has taken place and then recruiting additional platelets through the process of aggregation. Activation of the coagulation cascade ultimately results in fibrin deposition. In pathological conditions, thrombogenic surfaces act as a nidus for platelet adherence and thrombus formation. The ability of platelet-inhibiting agents to prevent or impair platelet-mediated thrombotic and thromboembolic events is of vital importance in the prevention and treatment of cardiovascular diseases, including myocardial infarction, unstable angina and stroke. They also serve as important adjuvants following percutaneous transluminal coronary angioplasty and saphenous vein bypass grafting. Future investigations will likely uncover additional indications.
Becker
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Thrombosis Research Center, University of Massachusetts Medical School, Worcester.
D001792:Blood Platelets / Q000502:physiology*; D003324:Coronary Artery Disease / Q000097:blood / Q000517:prevention & control; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000517:prevention & control; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D013927:Thrombosis / Q000097:blood
D010975:Platelet Aggregation Inhibitors