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.
Recent studies have suggested that ibuprofen may interfere with the cardioprotective effects of aspirin on the cardiovascular system. Thus, patients with cardiovas¬cular disease who require aspirin therapy should not be using NSAIDs concomitantly.
A. Effects on Prostacyclin
Normal formation of prostacyclin (PGI 2), a vasodilator and potent platelet inhibitor, is increased mainly through COX-2. NSAIDs and COX-2 inhibitors (selective NSAIDs) block prostacyclin production in vessel walls. Prostacyclin prevents platelet aggregation and cardiac arrhythmias. It keeps the arteries dilated and the arterial walls ‘‘clean.’’ PGI 2 may limit the extent of platelet adhesion and activation at sites of atherothrombotic disease. COX-2 inhibitors are potent prostacyclin inhibi¬tors and increase cardiovascular atherothrombotic events. To reemphasize, selective inhibitors of cycolooxgenase, COX-2 inhibitors depress prostacylin but not COX-1– derived thromboxane A2. Thus, the harmful effects of thromboxane A2 are exaggerated by COX-2 inhibitors; this action predisposes cardiovascular patients to stroke and myocardial infarction. See Figure 1. It is not surprising, therefore, that in 2004, warnings as to dangers of COX-2 inhibitors were publicized.

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