THE JOURNAL OF CLINICAL HYPERTENSION VOL. IV NO. VI NOVEMBER/DECEMBER 2002436

A surprisingly large amount of non-aspirin non-steroidal anti-inflammatory drug (NANSAID)usage occurs in the United States, with estimates ofas many as 30 billion tablets consumed per year.Perhaps even more impressive is the idea that mostof NANSAID usage is over-the-counter (OTC), thenon-prescription type. Since prostaglandins play arole in blood pressure and in urinary sodium excre-tion, this raises some interesting questions aboutwhether there are blood pressure consequenceswhen using NANSAIDs; these agents affectprostaglandin activity. Common consumption by apatient could be overlooked easily on a chart-med-ication flowsheet because of common usage andOTC availability. The release of the selectivecyclooxygenase-2 inhibitors (‘coxibs”) and therecognition that these drugs may increase bloodpressure in some patients adds to the importanceof the issue of blood pressure responses tocyclooxygenase inhibition.

Substantial evidence supports a blood pressureincreasing effect with NANSAIDs. As reviewed intwo meta-analyses1,2 and in the pages of TheJournal of Clinical Hypertension,3 the effect isabout 5 mm Hg of mean arterial pressure increase.Although this is reported as an increase in “meanarterial pressure,” essentially all of the increase isin systolic blood pressure. Part of the problem ininterpreting the literature is that many studies aredone for a short period of time in normotensivesubjects (and sometimes hypertensive subjects)who usually had no reason to take a NANSAID

other than to participate in a clinical trial. Thesetrials were often done to assess a safety issue, andblood pressure was either recorded as part of thetotal evaluation, or was the safety issue. Thus, thegeneralizability of these data to the care of a 65-year-old patient with predominantly systolichypertension who takes a NANSAID for monthsto years is limited. Therefore some clinical judg-ment is needed, tailored to each case.

Although the average increase in systolic bloodpressure is small (and smaller in normotensive thanin hypertensive patients), we have all seen hyper-tensive patients who have a large rise in bloodpressure, sometimes with peripheral edema fromsodium retention. Much of the blood pressureincrease appears to be sodium related, and the salt-sensitive hypertensive seems to be the person mostlikely to experience a systolic blood pressure in-crease. These tend to be the older, the African-American, and the diabetic patients. As a result,greater caution and frequent blood pressure checksare warranted in these patients. No class of anti-hypertensive agent appears to be immune to theeffects of NANSAIDs on blood pressure, but inone study calcium channel blocker-treated patientswere less affected.4

Although the systolic effects of NANSAIDs areusually small, and we are still waiting for a clearerpicture of the coxib (COX2-inhibitor) effects onblood pressure, it is important to keep in mindstudies like those of Gurwitz et al.5 They showedthat in an older (Medicare) population of patientswho were not receiving antihypertensive therapythe likelihood that they would submit a new pre-scription for an antihypertensive increased if aNANSAID was prescribed. This possibilityincreased proportionately to the dose of the NAN-SAID. Caveat Prescriptor!

Non-Aspirin Nonsteroidal Anti-Inflammatory Drugs

Raymond R. Townsend, MD

From the Hypertension Program, Department of Medicine, University of Pennsylvania, Philadelphia, PAAddress for correspondence: Raymond R. Townsend, MD, University of Pennsylvania,210 White Building, Philadelphia, PA 19104

C o m m o n Q u e s t i o n s a n d A n s w e r s i n t h e M a n a g e m e n t o f H y p e r t e n s i o nR a y m o n d R . T o w n s e n d , M D , S e c t i o n E d i t o r

continued on page 440

THE JOURNAL OF CLINICAL HYPERTENSION VOL. IV NO. VI NOVEMBER/DECEMBER 2002440

REFERENCES

1 Pope JE, Anderson JJ, Felson DT. A meta-analysis of theeffects of nonsteroidal anti-inflammatory drugs on bloodpressure. Arch Intern Med. 1993;153(4):477–484.

2 Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure? A meta-analysis.Ann Intern Med. 1994;121(4):289–300.

3 Brook RD, Kramer MB, Blaxall BC, et al. Nonsteroidal

anti-inflammatory drugs and hypertension. J ClinHypertens. 2000;2(5):319–323.

4 Houston MC, Weir M, Gray J, et al. The effects of non-steroidal anti-inflammatory drugs on blood pressures ofpatients with hypertension controlled by verapamil. ArchIntern Med. 1995;155(10):1049–1054.

5 Gurwitz JH, Avorn J, Bohn RL, et al. Initiation of antihy-pertensive treatment during nonsteroidal anti-inflammato-ry drug therapy. JAMA. 1994;272(10):781–786.

Townsend (continued from page 436)