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| |  Calcium Channel Blockers May Be Antihypertensive Therapy Option for Patients With Osteoarthritis: Presented at ACC By Mike Fillon CHICAGO -- April 1, 2008 -- A new study shows that the antihypertensive effect of calcium channel blockers (CCB) does not diminish when patients are also taking nonsteroidal anti-inflammatory drug (NSAID) therapy, and CCBs maintain their efficacy better than other antihypertensive drug classes when coadministered with NSAIDs. Results of the study were presented here on March 31 at the 57th Annual Meeting of the American College of Cardiology (ACC 2008) and were published in a supplement to the March 11 issue of the Journal of the American College of Cardiology. Previous studies have shown that NSAIDs can blunt the effects of antihypertensive medications to varying degrees depending on the antihypertensive drug class, according to lead author Henry Krum, PhD, Chair, Therapeutics, Professor of Medicine and Director, National Health and Medical Research Council Centre of Clinical Research Excellence in Therapeutics, Department of Epidemiology and Preventive Medicine and Department of Medicine, Monash University, Melbourne, Australia. Specifically, mechanistic studies suggested that NSAIDs appear to attenuate the blood pressure-lowering effects of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, central alpha-agonists and alpha-blockers, vasodilators, and to a lesser extent, diuretics, but they have little effect on the antihypertensive effects of CCBs. It has been postulated that this NSAID effect may work, at least in part, by prostaglandin inhibition caused by the blockage of the cyclooxygenase (COX) pathway, leading to reductions in renal blood flow and glomerular filtration rate, resulting in sodium retention, Dr. Krum said. "Because patients taking antihypertensives may be more likely to be salt-sensitive, such NSAID-related changes may have particularly evident effects on blood pressure," he noted in presenting the results of the post-hoc, multivariate analysis of the Multinational Etoricoxib and Diclofenac Arthritis Long-Term (MEDAL) Study. The analyses included subjects receiving etoricoxib 60 mg (n=6,769) or diclofenac 150 mg (n=6,700) daily for a mean duration of 20 months. Patients were evaluated for the differential effect of baseline antihypertensive therapy versus no antihypertensive therapy on the change from baseline in systolic blood pressure (SBP) at 4 months. The proportion of patients exceeding the predefined limits of change (PLoC) in SBP was also analysed. When adjusting for other risk factors, patients who were on multi-drug antihypertensive therapy at baseline achieved a significantly greater reduction in SBP at month 4 than patients not receiving antihypertensive medication at baseline. Use of renin-angiotensin monotherapy was also associated with a significant increase in SBP from baseline. CCB monotherapy was not associated with a significant change in SBP from baseline. Use of multi-drug therapy prior to enrolment in the study was significantly associated with the highest odds of exceeding SBP PLoC at any time during the study, compared with not receiving antihypertensive medication before study entry. Diuretic monotherapy and beta-blocker monotherapy use were also associated with significantly increased odds of exceeding SBP PLoC. Use of all other antihypertensive regimens was associated with numerically higher but nonsignificant odds of patients exceeding SBP PLoC. "As a result [of these findings], clinicians should consider the use of CCBs as a reasonable antihypertensive therapy option in patients with osteoarthritis and hypertension who require NSAID treatment," Dr. Krum concluded. Dr. Krum is also on the Advisory Board of Merck Research Laboratories, which provided funding for the MEDAL study. [Presentation title: Differential Effect of Baseline Antihypertensive Medications on Blood Pressure Changes in Patients With Osteoarthritis in the Multinational Etoricoxib and Diclofenac Arthritis Long-Term (MEDAL) Study: A Multivariate Analysis. Abstract 1036-321]
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