The mechanism of action of aspirin--is there anything beyond cyclo-oxygenase?

Aspirin, today, is an established drug in the regime for the prevention of myocardial infarction, especially in high-risk groups. This use of aspirin has given it a new lease of life in its tenth decade of clinical use. Aspirin is probably the oldest synthetic drug in the Pharmacopoeias today; thus one would have imagined that understanding about the drug would have reached a zenith and if not, that at least there should be certainty about its mechanism of action. Most workers agree that aspirin inhibits the cyclo-oxygenase enzyme in the platelets leading to reduced formation of prostaglandin G2, the precursor of thromboxanes. This explanation does not appear to be complete, since the role of the platelet activating factor (PAF) seems to have been ignored. The precursor for PAF is the lysophospholipid that is almost always formed when membrane phospholipid breakdown takes place. Any effective antiplatelet drug would have to inhibit the formation and/or the action of PAF, if it were to prevent platelet aggregation. Alternatively, the pathophysiological role attributed to PAF is highly exaggerated and needs to be reassessed.