NSAID use and BP in treated hypertensives: a retrospective controlled observational study

Abstract

The objective of this study was to investigate the association between NSAID use and blood pressure (BP) among a sample of treated hypertensive patients. A controlled observational study was designed in UK primary care setting. Patients with diagnosed hypertension and currently being prescribed antihypertensive medication registered with four general practices, comparing patients also prescribed NSAIDs (exposed) to those not prescribed NSAIDs (unexposed). Majority of the patients were elderly. Systolic and diastolic pressure were the outcome measures. Data were collected for 184 NSAID users and 762 nonusers with a mean age of 68 years. There was no difference in either systolic (adjusted difference 1.9 mmHg, 95% CI À0.7 to 4.5, P ¼ 0.15) or diastolic (adjusted difference 1.0 mmHg, 95% CI À0.3 to 2.3, P ¼ 0.15) blood pressure. There was no evidence of any interactions according to categories of age, sex, or number of antihypertensive drugs prescribed. Among NSAID users, there was no evidence of any differences in blood pressure according to NSAID type or dose. In conclusion we found no evidence for an association between NSAID usage and BP control in known hypertensive patients receiving antihypertensive medication in primary care. The reported association between NSAID use and BP control appears much less substantial than has been previously suggested.

The effect of non-steroidal anti-inflammatory drugs and other commonly used non-narcotic analgesics on blood pressure level in adults

“…There is consistent evidence from case reports [23,24], observational studies [8,9,[13][14][15][16][17] and clinical trials [10][11][12][18][19][20][21][22] of an association between NSAID use and increased blood pressure in both normotensive and hypertensive adults. What is less consistent is the evidence concerning the magnitude of the blood pressure change.…”

“…Two studies have reported blood pressure increases of þ10/þ7 mmHg [21] and þ12/þ5 mmHg [22] after the addition of NSAIDs to antihypertensive therapy. Two meta-analyses have reported much smaller increases in mean arterial pressure of þ3.4 mmHg [11] and þ5.4 mmHg [12] and several studies have reported blood pressure increases of only þ2/þ1 mmHg [17][18][19]. Some of this variation may be explained by patient characteristics, including age and renal function [4], but blood pressure response may also vary with NSAID type [11,12] and concurrent antihypertensive treatment [12,[19][20][21][22].…”

“…More clinical data were available in a retrospective observational study involving four general practices in the UK [17]. Using computer-based records and case notes, 184 hypertensive patients on prescribed NSAIDs (82% for muscloskeletal disease) were matched for age and sex with 762 hypertensive patients not on prescribed NSAIDs.…”

“…The shortcomings include the fact that most of the studies were small and short term and hence were underpowered to detect blood pressure differences [11,12]. In addition, different methods have been used to report blood pressure changes, including mean arterial pressure [11,12], systolic and diastolic blood pressure [10,[17][18][19][20][21][22][23][24] and incidence of hypertension [8,9,13,14]. This has been compounded by direct comparisons between NSAID studies reporting change in mean arterial blood pressure with reviews of cardiovascular outcome data based on diastolic blood pressure [12].…”

“…It is certainly biologically plausible that NSAIDs cause raised blood pressure by blocking synthesis of prostaglandins that regulate vascular tone and sodium excretion [4][5][6][7]. While much has been published in the literature concerning the possible association between NSAIDs and risk of hypertension, controversy continues about the magnitude of the blood pressure change and whether the risks are similar for all NSAID users [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]. This uncertainty arises from a number of factors related to shortcomings in the design and conduct of the reported studies which have generated inconsistent and unreliable results.…”