Aspirin (acetylsalicylic acid) is a simple molecule first synthesized in Germany 150 years ago. Its pain-relieving properties were recognized and exploited commercially 100 years ago. In the last 50 years, aspirin has been shown to have remarkable antithrombotic benefits.
Aspirin's antithrombotic effect is mediated by inhibition of blood platelets. The drug blocks a platelet enzyme, cyclo-oxygenase, by acetylating the enzyme's active site. Inhibition of the enzyme blocks production of an important prothrombotic agent known as thromboxane A2. Thromboxane A2 causes activation and aggregation of platelets, which is an early step in thrombosis. Aspirin is more effective in preventing arterial thrombosis (myocardial infarction, stroke) than venous thrombosis (deep venous thrombosis, pulmonary embolism). The explanation for this difference seems to be that platelets play a larger role in causing arterial thrombosis.
Today, more potent platelet inhibitors than aspirin are available, but aspirin remains the most commonly used drug in this category and is still our most cost-effective antithrombotic drug. Aspirin (either 81 mg or 325 mg daily) is indicated in the following conditions:
- Unstable angina (acute coronary syndrome)
- Acute myocardial infarction
- Secondary prevention of myocardial infarction
- Secondary prevention of stroke (carotid or primary cerebrovascular disease)
- Prevention of peripheral arterial thrombosis