NSAIDS AND INCREASED BLOOD-PRESSURE - WHAT IS THE CLINICAL-SIGNIFICANCE

Several randomised studies have demonstrated that various nonsteroidal antiinflammatory drugs (NSAIDs) elevate blood pressure in normotensiv e and hypertensive individuals; however, these data have been contradi cted by numerous negative studies. Two meta-analyses have demonstrated that, after pooling data drawn from published reports of randomised t rials of younger adults, NSAID use produces a clinically significant i ncrement in mean blood pressure of 5mm Hg, most marked in patients wit h controlled hypertension. Stratification by NSAID type revealed that piroxicam, naproxen and indomethacin had the greatest, and sulindac th e smallest, presser effect. These data were supported by 2 large commu nity studies involving elderly patients. Recent NSAID users had a 1.7- fold higher risk of requiring the initiation of antihypertensive thera py compared with nonusers; NSAID users also had a 40% increased risk o f receiving a diagnosis of hypertension compared with nonusers. It is vital to determine the nature of the association in the elderly, 12 to 15% of whom are concurrently receiving an NSAID and an antihypertensi ve agent. Importantly, a 5 to 6mm Hg increase in diastolic blood press ure maintained over a few years may be associated with a 67% increase in total stroke risk and a 15% increase in coronary heart disease even ts. While the mechanism(s) remain speculative, salt and water retentio n through several factors operating in parallel, coupled with increase d total peripheral vascular resistance, via increased renal endothelin -l synthesis, are potentially important. Clinicians should strive to a void excessive use of NSAID treatment and consider well-tolerated ther apeutic alternatives, including simple analgesics and physical therapy . For patients who require concomitant NSAID and antihypertnesive trea tment, physicians should be aware that indomethacin, naproxen and piro xicam may be associated with a greater presser effect than many other NSAIDs, and that antagonism of P-blockers may be greater than that of vasodilators (including ACE inhibitors and calcium antagonists) and di uretics. Finally, the progress of each patient should be monitored by careful blood pressure measurement, particularly during the period of initiation of NSAID therapy.