Blood pressure and cardiovascular outcomes in patients taking nonsteroidal antiinflammatory drugs

Henry Krum, Gary Swergold, Arnold Gammaitoni, Paul Peloso, Steven Smugar, Sean Curtis, D Craig Brater, Hongwei Wang, Amarjot Kaur, Loren Laine, Matthew Weir, Christopher Cannon

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18 Citations (Scopus)

Abstract

Introduction: The increased thrombotic cardiovascular (CV) risk in trials of cyclooxygenase- 2 (COX-2) inhibitors versus placebo, and the apparent similar risk with nonsteroidal antiinflammatory drugs (NSAIDs), may be related to their potential to elevate blood pressure (BP). Aims: We evaluated the relationship between baseline BP and change in BP on CV events (CVEs) in patients receiving NSAIDs or COX-2 inhibitors in the prospective randomized, double-blind, Multinational Etoricoxib and Diclofenac Arthritis Long-term Program (N = 34,701) comparing etoricoxib 60 or 90 mg or diclofenac 150 mg daily for a mean duration of 18 months. The main outcome measure was confirmed thrombotic CVEs. The Antiplatelet Trialistsa?? Collaboration endpoint, all-cause mortality, CV/congestive heart failure (CHF) mortality, and CHF incidence were similarly evaluated. Results: We found that baseline systolic BP (SBP) was associated with significantly higher risk of all events (P <0.001). Baseline diastolic BP (DBP) was inversely and significantly associated with risk of all events (P <0.001 to P = 0.016) except CV/CHF mortality (P = 0.054). There was no significant differential effect between etoricoxib and diclofenac in relation to CVEs, except for confirmed CHF, for which the risk was significantly higher with etoricoxib (P = 0.019). Only CHF risk (P = 0.020 for both SBP and DBP change), but not thrombotic endpoints, was significantly associated with change in BP from months 0 to 4. These findings were not meaningfully altered after covariate adjustment for baseline CV risk. Conclusions: Baseline BP, but not change in BP, was significantly associated with risk of thrombotic CVEs through 18 months. The CV risk of COX-2s and NSAIDs did not appear to be related to the BPelevating effects of these agents, although such analyses, i.e., from randomized controlled trials, are unable to definitively exclude such a relationship.
Original languageEnglish
Pages (from-to)342 - 350
Number of pages9
JournalCardiovascular Therapeutics
Volume30
Issue number6
DOIs
Publication statusPublished - 2012

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