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STROKES caused by thromboembolic occlusive events may involve the platelet in several ways: (1) production of platelet-fibrin thrombi, (2) containment of bleeding into the area of ischemia, and (3) participation in atheroma formation. One accepted pathogenesis for small recurrent strokes (transient ischemic attacks or TIAs) is recurrent embolization of platelet-fibrin thrombi or atheromatous material from extracranial atheroma. Therefore, drugs which inhibit platelet participation in thrombus or atheromatous formation might help prevent strokes, provided that bleeding distal to an occlusion is minimal, that hemostasis can be achieved by alternative mechanisms, and that antiplatelet agents (APAs) selectively allow platelets to promote hemostasis while impairing other platelet activities. Full understanding of the use of these drugs in patients with cerebrovascular accidents requires knowledge about the role of platelets in hemostasis, thrombosis, and atherogenesis; the relationships of specific biochemical events in the platelet-to-platelet function; and empiric observations about the use of so-called APAs.

Platelet and antiplatelet agents in strokes.