The older agents (NSAIDs) inhibit COX-1, but the inhibition is not permanent and they partially block COX-2. In contrast, aspirin permanently and irreversibly acetylates and blocks cyclooxygenase, therefore preventing the production of platelet thromboxane A2. The latter is a powerful platelet-aggregating agent that forms clots (thrombi). Aspirin, thus prevents platelet-derived throm¬bosis that is involved in the causation of myocardial infarction and stroke.
NSAIDs clearly do not have this cardioprotective benefit of the wonder drug, aspirin; (see Figure 1). Aspirin, (acetylsalicylic acid) irreversibly acetylates the enzyme cycolooxygenase, an enzyme necessary for the conversion of platelet arachidonic acid to thromboxane A2, a power¬ful platelet aggregating agent and vasoconstrictor. This beneficial effect is not provided by NSAIDs or COX-2 inhibitors (see the chapter entitled Aspirin for Heart Disease) and the newer agents, unfortunately, appear to increase the risk of cardiovascular thrombotic events.

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• I. ADVERSE CARDIOVASCULAR EFFECTS
  All NSAIDs significantly inhibit the beneficial effects of several drugs, including furosemide, hydrochlorothiazide, other thiazide diuretics, ACE inhibitors, and angiotensin receptor blockers. Aspirin is a weak NSAID that does not cause sodium and water retention, increased blood pressure, or heart failure, but it can interfere with the effectiveness of ACE inhibitors.
• BIBLIOGRAPHY
  Belton, O., and Fitzgerald, D. Cyclooxygenase-2 inhibitors and atherosclerosis. J. Am. Coll. Cardiol., 41:1820–2, 2003.