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An overview of commonly used antiplatelet agents.

Several agents inhibiting platelet function are commonly used in clinical practice, each having a unique mechanism of action. The complex cascade of events ultimately resulting in thrombus formation has several areas that pharmacologic agents can affect. The resultant effects range from being relatively non-specific with aspirin, ticlopidine, and clopidogrel to being specific with the glycoprotein IIb/IIIa receptor antagonists such that platelet aggregation will be inhibited irregardless of the metabolic pathway responsible for initiating aggregation. The clinical indications for these agents are vast, as platelet aggregation has been widely implicated in cardiovascular events. The degree of platelet inhibition is related to the frequency of bleeding. Aspirin is a relatively weak inhibitor of platelet function, ticlopidine has been said to have moderate activity, while the glycoprotein IIb/IIIa receptor antagonists are the most potent inhibitors of platelet aggregation. As our knowledge of the mechanisms of platelet aggregation expands, so will our treatment regimens. Clearly, we will await the results of future clinical trials to further define the role of antiplatelet agents.