Nonsteroidal Anti-Inflammatory Drugs
These agents are widely used for the control of pain in patients with arthritis. Because the widely use steroidal anti-inflammatory agents of the sixties and seventies (cortisone, prednisone) caused relief but long-term use produced serious adverse effects, nonsteroidal agents were heralded as the answer for a variety of arthritic disorders.
NSAIDs, however, cause the kidneys to retain sodium and water. This action may cause an increase in blood pressure. Also, an increase in sodium and water in the body increases the work of the heart and can precipitate heart failure in patients with a weak heart muscle (left ventricular dysfunction). Patients may experience increased shortness of breath and swelling of the ankles. These agents are well known to cause bleeding from the stomach.
Available NSAIDs used from the seventies include carprofen, diclofenac, fenoprofen, flurbiprofen, ibuprofen, indomethacin, ketoprofen, naproxen, piroxicam, sulindac, and tolmetin. Newer agents discovered in 1989 and introduced into medical practice in the early nineties block COX-2 and are called COX-2 inhibitors. These include celecoxib, meloxicam, rofecoxib parecoxib, and valdecoxib. It was speculated that these specific COX-2 inhibitors (selective NSAIDs) would be safer and cause less gastric bleeding than the old NSAIDs, and this is the main reason that COX-2 inhibitors are publicized as having advantages over NSAIDs.
- 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.