How does aspirin prevent thromboembolism / heart attack? Antiplatelete action of aspirin:
A thrombus is formed due to platelete aggregation. And platelete aggragation is mediated by a prostaglandin called thromboxane A2 (TX A2). As aspirin inhibits prostaglandin systhesis by inhibiting the COX enzyme, no thromboxane is produced.
So since there is no TX A2, there is no platelete aggragation and no thrombus or embolus formation.
This is particularly important in heart patients suffering from myocardial infarction. They have to take 75 mg of aspirin for life long to prevent myocardial infarction.
Why low dose of aspitin (75 mg/day) is sufficient to prevent platelete aggragation?
The half life a platelets is around 8-11 days. Aspirin inhibits the cycloxygenase enzyme inside the platelets for their entire lifespan (ie 8-11 days). And platelets have no mechanism for synthesis of new cycloxygenase enzyme. That means there is no way of forming new thromboxane A2 to cause platelete aggregation. So low dose (75mg/day) of aspirin is sufficient to prevent platelete aggration.
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