ABSTRACT
Aspirin (acetylsalicyl acid, ASA) is well known as the “reference” anti-platelet drug. It acts as an irreversible inhibitor of cyclooxygenase, an enzyme involved in the synthesis of thromboxane A2 (Fig. 14.1), an important amplifier of platelet aggregation [10]. Aspirin is the first discovered member of the class of drugs known as nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin has been used for over a century to treat fundamental signs of inflammation (heat, redness, swelling, and pain), whereas recently it has been shown to prevent myocardial infarction, stroke, and additionally there is evidence that a daily intake of aspirin reduces the risk of cancer [11]. Other NSAIDs failed to show a protective effect on myocardial infarction in a large observational study [12]. A reason might be that platelets are not able to resynthesize cyclooxygenase causing an inhibition for as long as the platelet circulates, while other NSAIDs bind and inhibit COX-isoenzymes reversible. Numerous large-scale clinical trials and meta-analyses have consistently demonstrated the benefit of low doses of aspirin as a secondary prevention measure for recurrent ischemic events in patients with various manifestations of atherothrombotic disease [13, 14].
