Heart disease, aspirin, and fish oil.

T he antithrombotic action of aspirin depends on inhibition of cyclooxygenase activity' in platelets, thereby reducing thromboxane A2 formation and consequently, their aggregability. In 1978, two important concepts on eicosanoid formation were presented. The first2 was that the vascular wall could utilize endoperoxides released by adhering platelets for the formation of prostacyclin. The second3 proposed that eicosapentaenoic acid (EPA) from oily fish or fish oil could, through the formation of the active analogue of prostacyclin, prostaglandin 13 but inactive thromboxane A3, produce an antithrombotic state that protects against cardiovascular disease. Over the last decade, both