Blood Pressure Destabilization on Nonsteroidal Antiinflammatory Agents

Abstract

It has been conventional wisdom for some time now that nonsteroidal antiinflammatory drugs (NSAIDs), whether selective for inhibition of cyclooxygenase 2 (COX-2) or nonselective, increase blood pressure (BP) or interfere with BP control and that acetaminophen should not have this effect.1,–,4 Controlled clinical trials have shown that NSAIDs have heterogeneous effects on clinic and 24-hour BP in normotensive and hypertensive subjects.3 The inhibition of COX-2 by NSAIDs results in decreased actions of both vasodilatory and natriuretic prostaglandins.3 In most individuals, homeostasis of plasma volume is reestablished by small, nearly undetectable increases in BP,5 whereas in patients with impaired excretory function, more substantial volume retention occurs that may be associated with hypertension, edema, and congestive heart failure.3,5 Article see p1789 Before 2002, little was known about the effects of NSAIDs on 24-hour BP in patients with arthritis who also had hypertension and/or vascular diseases.6,–,8 Because ambulatory BP has improved reproducibility compared with clinic measurements, detection of small but clinically meaningful differences in drug treatment groups9,10 is more likely to occur. Ambulatory monitoring also allows improved evaluation of pharmacodynamic effects of any drug, including the NSAIDs.6,7 For example, in the Celecoxib Rofecoxib Efficacy and Safety in Comorbidities Evaluation Trial (CRESCENT), destabilization of systolic BP control occurred for ≈18 of the 24 hours after dosing of rofecoxib at standard osteoarthritis doses of 25 mg each morning.8 In contrast, no changes from baseline in 24-hour systolic BP were observed with celecoxib or naproxen at …