Platelet activation and inhibition in unstable coronary syndromes.
Platelet activation occurs episodically in unstable angina, as reflected by enhanced thromboxane metabolite excretion, and most episodes can be suppressed by low-dose aspirin. Biochemical evidence of platelet activation and electrocardiographic evidence of myocardial ischemia are often temporally dissociated, thus suggesting the likely involvement of different triggers. Aspirin is effective in reducing the short-term and long-term risks of myocardial infarction and death by 40-60%, in a dose-independent fashion consistent with the saturability of platelet cyclo-oxygenase inhibition at low doses. Suppression of platelet thromboxane synthesis by aspirin and the blockade of platelet adenosine diphosphate receptors by ticlopidine or clopidogrel appear to have a similar impact on limiting the risk of a thrombotic outcome of plaque fissuring, thereby suggesting combined strategies for future studies.
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Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia 19104-6100, USA.
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D000789:Angina, Unstable / Q000188:drug therapy / Q000503:physiopathology*; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy; D015539:Platelet Activation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D013928:Thromboxane A2 / Q000378:metabolism; D013988:Ticlopidine / Q000627:therapeutic use
D010975:Platelet Aggregation Inhibitors; D013928:Thromboxane A2; D013988:Ticlopidine; D001241:Aspirin