Open AccessBlood Pressure and Cardiovascular Outcomes in Patients Taking Nonsteroidal Antiinflammatory Drugs
Author(s) -
Krum Henry,
Swergold Gary,
Gammaitoni Arnold,
Peloso Paul M.,
Smugar Steven S.,
Curtis Sean P.,
Brater D. Craig,
Wang Hongwei,
Kaur Amarjot,
Laine Loren,
Weir Matthew R.,
Can Christopher P.
Publication year - 2012
Publication title -
cardiovascular therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 46
eISSN - 1755-5922
pISSN - 1755-5914
DOI - 10.1111/j.1755-5922.2011.00283.x
Subject(s) - medicine , etoricoxib , diclofenac , blood pressure , heart failure , placebo , rofecoxib , clinical endpoint , cardiology , randomized controlled trial , anesthesia , cyclooxygenase , alternative medicine , pathology , biochemistry , chemistry , enzyme
SUMMARY Introduction: The increased thrombotic cardiovascular (CV) risk in trials of cyclo‐oxygenase‐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 Trialists’ 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 BP‐elevating effects of these agents, although such analyses, i.e., from randomized controlled trials, are unable to definitively exclude such a relationship.