Last update:
16-Jun-2006

Aspirin reduces the possibility of serious atherothrombotic vascular events and death in a broad category of high risk patients by about one quarter. Aspirin has remained an enigmatic drug; not only does it present with new benefits for treating an ever-expanding list of apparently unrelated diseases, but also aspirin enhances understanding of the nature of the disease processes. Originally, the beneficial effects of aspirin were shown to stem from its inhibition of cyclooxygenase-derived prostaglandins and its direct platelet inhibitory function. In recent years however, the hypothesis has been raised that the mechanisms by which aspirin acts as a protective anti-ischemic agent exceed the inhibition of platelet thromboxane A2 synthesis only. Accumulating evidence suggests that aspirin may have additional biological effects on the vasculature that contribute to the reduction of ischemic cardiovascular events. In addition to inhibiting cyclooxygenase activity, aspirin can also inhibit proinflammatory signaling pathways, gene expression and other factors distinct from eicosanoid biosynthesis that control inflammation, as well as enhancing the synthesis of endogenous protective anti-inflammatory factors. In conclusion there is considerable evidence for multifactorial, or pleiotropic, effects of aspirin, and the main question is whether, for the prevention of cardiovascular events, other effects of aspirin could be just as important, or even more important, than its inhibition of platelet aggregation.

Key words: Aspirin, Cardiovascular diseases, Cyclooxygenases, Endogenous anti-inflammatory factors.