ABSTRACT
Platelets play a key role in arterial thrombosis (Fig. 1), where platelet activation and aggregation are the proximate events associated with acute coronary syndromes (ACS), stroke, and peripheral artery disease (PAD) (1-7). Platelet adhesion to injured vascular endothelium leads to platelet activation, which is further amplified by various platelet agonists, including arachidonic acid, thromboxane A2, adenosine disphosphate (ADP), thrombin, serotonin, and collagen (6-8). Aspirin was the first antiplatelet drug to provide insight into the role of platelets in health and disease (7,9). Since its development in 1899 and subsequent elucidation of mechanism of action, thromboxane A2 blockade has been one of the most well-known antiplatelet paradigms (9). Aspirin inhibits the formation of thromboxane by irreversibly inhibiting COX-1 via acetylation of the serine-529 peptide, the requisite site for the formation of thromboxane from arachidonic acid. It was not until the late 1970s that aspirin was widely recognized for its therapeutic benefit in cardiovascular disease (3,10). Aspirin is known to reduce the risk of myocardial infarction (MI), lower the risk of developing ischemic stroke, and decrease mortality in patients with vascular disease (11). Aspirin is presently recommended for the management of acute MI and unstable angina and is an effective therapeutic agent for secondary prevention of ischemic events (Fig. 2) (12,13).
