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Abstract
Platelets have assumed a role in the development of focal cerebral ischemia by virtue of their participation in thromboemboli that may initiate stroke symptoms. Platelets are one component of the blood-vascular axis responsible for preventing hemorrhage. Activated platelets initiate hemostatic plug formation and provide a scaffolding for coagulation activation. Platelets are activated by a number of stimuli, such as exposure of the vascular subendothelium, fibrin deposition, and abnormal surfaces, e.g., atheromata. A number of observations, including the appearance of platelet thrombi on atheromata in situ, indicate that platelet physiology is relevant to stroke. In addition, certain antiplatelet agents (e.g., aspirin) significantly reduce the incidence of ischemic stroke after initial transient ischemic attacks. Aspirin, the combination of aspirin and dipyridamole, and ticlopidine have all been shown to be useful in reducing the frequency of secondary stroke events. Clopidogrel has been shown to reduce the frequency of secondary vascular ischemic events when stroke, myocardial infarction, and peripheral arterial disease are considered together. Unfortunately, all antithrombotic agents carry a potential risk for inducing symptomatic intracerebral hemorrhage during ischemic stroke. The mechanism by which this may happen with antiplatelet agents has not yet been determined. As in other areas of stroke treatment, it is the balance between efficacy in reduction of symptomatic thrombotic events and the risk for hemorrhage that will define benefit.
Footnotes
Series editor: J. Donald Easton MD
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