The use of aspirin in medicine dates at least as far back as Hippocrates who found analgesic effects for the extract (salicin) of white willow bark.1 Aspirin irreversibly inactivates platelet cyclooxygenase, preventing platelets from synthesizing thromboxane A2, a potent vasoconstrictor and promoter of platelet aggregation. Aspirin also has anti-inflammatory and vasodilatory effects that may be important.
Aspirin use is recommended for the secondary prevention of cardiovascular disease (CVD) in patients with prior CVD because it decreases the risk of CVD events and mortality in clinical trials of men and women with CVD.2 The 2009 meta-analysis by the Antithrombotic Trialists' (ATT) collaboration analyzed individual participant data from 16 secondary prevention trials (17 000 individuals; 3306 CVD events).2 Compared with placebo, aspirin resulted in an approximate 10% relative risk (RR) reduction of CVD mortality and total mortality and an approximate 20% RR reduction of CVD events (absolute risk reduction, 6.7% vs 8.2%), with similar reduction in coronary events and ischemic stroke. Aspirin also increased the RR of gastrointestinal tract (GI) bleeding and hemorrhagic stroke, with the majority of hemorrhagic strokes occurring in patients with a history of ischemic stroke or transient cerebral ischemia. Because ischemic stroke is much more common than hemorrhagic stroke, the absolute benefit was greater than the absolute risk of aspirin, with a net RR reduction of total stroke.
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