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A surprisingly large amount of non-aspirin nonsteroidal anti-inflammatory drug (NANSAID) usage occurs in the United States, with estimates of as many as 30 billion tablets consumed per year. Perhaps even more impressive is the idea that most of NANSAID usage is over-the-counter (OTC), the non-prescription type. Since prostaglandins play a role in blood pressure and in urinary sodium excretion, this raises some interesting questions about whether there are blood pressure consequences when using NANSAIDs; these agents affect prostaglandin activity. Common consumption by a patient could be overlooked easily on a chart-medication flowsheet because of common usage and OTC availability. The release of the selective cyclooxygenase-2 inhibitors (“coxibs”) and the recognition that these drugs may increase blood pressure in some patients adds to the importance of the issue of blood pressure responses to cyclooxygenase inhibition.

Substantial evidence supports a blood pressure increasing effect with NANSAIDs. As reviewed in two meta-analyses1,2 and in the pages of The Journal of Clinical Hypertension,3 the effect is about 5 mm Hg of mean arterial pressure increase. Although this is reported as an increase in “mean arterial pressure,” essentially all of the increase is in systolic blood pressure. Part of the problem in interpreting the literature is that many studies are done for a short period of time in normotensive subjects (and sometimes hypertensive subjects) who usually had no reason to take a NANSAID other than to participate in a clinical trial. These trials were often done to assess a safety issue, and blood pressure was either recorded as part of the total evaluation, or was the safety issue. Thus, the generalizability of these data to the care of a 65-year-old patient with predominantly systolic hypertension who takes a NANSAID for months to years is limited. Therefore some clinical judgment is needed, tailored to each case.

Although the average increase in systolic blood pressure is small (and smaller in normotensive than in hypertensive patients), we have all seen hypertensive patients who have a large rise in blood pressure, sometimes with peripheral edema from sodium retention. Much of the blood pressure increase appears to be sodium related, and the saltsensitive hypertensive seems to be the person most likely to experience a systolic blood pressure increase. These tend to be the older, the African-American, and the diabetic patients. As a result, greater caution and frequent blood pressure checks are warranted in these patients. No class of antihypertensive agent appears to be immune to the effects of NANSAIDs on blood pressure, but in one study calcium channel blocker-treated patients were less affected.4

Although the systolic effects of NANSAIDs are usually small, and we are still waiting for a clearer picture of the coxib (COX2-inhibitor) effects on blood pressure, it is important to keep in mind studies like those of Gurwitz et al.5 They showed that in an older (Medicare) population of patients who were not receiving antihypertensive therapy the likelihood that they would submit a new prescription for an antihypertensive increased if a NANSAID was prescribed. This possibility increased proportionately to the dose of the NANSAID. Caveat Prescriptor!

References

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  2. References
  • 1
    Pope JE, Anderson JJ, Felson DT. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Intern Med. 1993;153(4):477484.
  • 2
    Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure? A meta-analysis. Ann Intern Med. 1994;121(4):289300.
  • 3
    Brook RD, Kramer MB, Blaxall BC, et al. Nonsteroidal anti-inflammatory drugs and hypertension. J Clin Hypertens. 2000;2(5):319323.
  • 4
    Houston MC, Weir M, Gray J, et al. The effects of nonsteroidal anti-inflammatory drugs on blood pressures of patients with hypertension controlled by verapamil. Arch Intern Med. 1995;155(10):10491054.
  • 5
    Gurwitz JH, Avorn J, Bohn RL, et al. Initiation of antihypertensive treatment during nonsteroidal anti-inflammatory drug therapy. JAMA. 1994;272(10):781786.