Munavvar Izhar

Effects of COX Inhibition on Blood Pressure and Kidney Function in ACE Inhibitor-Treated Blacks and Hispanics

Abstract—Cyclo-oxygenase (COX) inhibitors attenuate the antihypertensive effects of angiotensin-converting enzyme (ACE) inhibitors and reduce kidney function. The study tests the hypothesis that these two classes of drugs have similar effects on glomerular filtration rate (GFR) and 24-hour blood pressure. The primary endpoint was change in 24-hour systolic blood pressure. Using a randomized crossover design, 25 black and Hispanic hypertensive participants (mean age 58±3 years) with osteoarthritis were studied. All participants received an ACE inhibitor at baseline. Once systolic blood pressure was <140 mm Hg, either celecoxib 200 mg/d or diclofenac 75 mg twice daily for 4 weeks was started. After measurements were obtained, all participants underwent a 2-week washout period and crossed over to the other drug for 4 weeks. A significant difference in mean 24-hour systolic blood pressure was noted between groups at 4 weeks (+4.1±1.1 mm Hg diclofenac versus +0.6±0.6 mm Hg celecoxib; P =0.01). However, because celecoxib has duration of action shorter than 24 hours, we compared ambulatory values at celecoxib trough and peak activities. At peak, no difference in systolic blood pressure was noted between agents (+3.6±0.04 mm Hg diclofenac versus +4.2±1.9 mm Hg celecoxib; P =0.67). GFR was also differentially affected at 24 hours (−9.9±2.4 mL/min diclofenac versus −0.4±1.2 mL/min celecoxib; P =0.01). We conclude that diclofenac and celecoxib increase systolic blood pressure at peak levels; however, these agents differ in their 24-hour effects. Differences observed in blood pressure response between COX inhibitors may not be related in their sensitivity but rather their dosing frequency.

P-649: Prevalence and controll of cardiovascular risk factors in a tertiary hypertension clinic

according to the formula: LDL5CHL-(HDLcholesterol1 Triglicerides/5). All the patients did not assume any antidyslipidemic treatment. Mean sphygmomanometric blood pressure was: 150 1/-19/901/-10 mmHg; mean PP was: 60 1/-15 mm Hg and heart rate: 72 1/-12 beats/ min. Total-cholesterol, HDL-cholesterol, Triglicerides and LDL-cholesterol were: 2251/-37 mg/dl, 561/-15 mg/dl, 1431/-61 mg/dl and 1401/-34 mg/dl, respectively. A significant correlation was observed between PP and LDL-cholesterol (linear regression analysis; r 5 0.21, p,.02), whereas the correlation between PP and Total-cholesterol, and between PP and HDL-cholesterol did not reach a statistical significance (r5 0.17, p5.07; r5 0.13, p5.18, respectively). In conclusion, in the population studied of resistant hypertensive patients, the correlation found between pulse pressure and LDL-cholesterol suggests that, in presence of persistently elevated blood pressure, plasma lipids may influence the vascular stiffness, expressed by pulse pressure values. Possibly, the vascular alterations linked to dyslipidemia may account for resistence versus pharmacological therapy.