Antiplatelet therapy, including aspirin and complementary agents targeting various signaling pathways, is central to the treatment and prevention of cardiovascular disease.
Reinforces guideline-directed antiplatelet use in CVD; leaves open optimization of multi-pathway regimens in high-risk subgroups.
Platelet activation and aggregation are considered to be central to arterial thrombus formation. Antiplatelet therapy is therefore important for both the treatment and prevention of cardiovascular disease. Aspirin, the most widely used antiplatelet agent, inhibits platelet cyclo-oxygenase and the conversion of arachidonic acid to the potent platelet agonist thromboxane A(2) but does not prevent platelet activation occurring via various signalling pathways that are independent of thromboxane A(2) release. Therefore a number of other compounds have been developed to complement aspirin's beneficial effect. These include the thienopyridines (clopidogrel and ticlopidine), dipyridamole, and the alpha(IIb)beta(3) (glycoprotein IIb/IIIa) receptor inhibitors.
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Behan et al. (2004) studied this question.
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