Combination of ACE inhibitor, angiotensin II receptor blocker beneficial for CHF

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Combination of ACE inhibitor, angiotensin II receptor blocker beneficial for CHF

WESTPORT, Sep 10 (Reuters Health) - In patients with congestive heart failure, an angiotensin-converting enzyme (ACE) inhibitor plus an angiotensin II receptor blocker may be more effective than either agent alone. That is one of the main findings of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study, published in the September 7th issue of Circulation: Journal of the American Heart Association.

After a 3-week run-in period, the RESOLVD investigators randomized 768 patients with symptomatic heart failure due to systolic dysfunction to 43 weeks of therapy with the angiotensin II blocker candesartan, the ACE inhibitor enalapril, or both.

Dr. R. S. McKelvie, of Hamilton General Hospital, Hamilton, Ontario, Canada, and the RESOLVD investigators report that candesartan alone was "...as effective, safe, and tolerable as enalapril." They also report that no significant between-group differences emerged in terms of exercise performance, functional class or quality of life.

The enalapril/candesartan combination was associated with a decrease in blood pressure and brain natriuretic peptide as well as a transient decrease in aldosterone, compared with treatment with either drug alone.

The investigators found that use of enalapril or candesartan alone appeared to negatively affect left ventricular volume. When the two drugs were combined, these changes were largely prevented.

Dr. Barry H. Greenberg, of the Heart Failure/Cardiac Transplantation Program at the University of California, San Diego Medical Center, says in an editorial that this is "[p]erhaps the most intriguing" finding of the RESOLVD Pilot Study and "deserves further attention."

According to Dr. Greenberg, the RESOLVD pilot findings imply that it may be time to reassess "..our concepts of the pathways through which [renin-angiotensin aldosterone system] activation leads to progressive [left ventricular] dysfunction and the mechanisms by which various drugs interrupt this process."