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Lack of Deleterious Interaction Between Angiotensin Receptor Blockers and ß-Blockers in the Treatment of Patients With Heart Failure

Department of Biomedical Science, Center of Excellence, Florida Atlantic University, Boca Raton, Florida, Department of Medicine, University of Miami School of Medicine, Miami, Florida, Department of Epidemiology and Public Health, University of Miami School of Medicine, Miami, Florida, PROFCHHMD{at}prodigy.net

Magda Kowalczykowski

Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts

Danielle Hollar, PhD

Department of Biomedical Science, Center of Excellence, Florida Atlantic University, Boca Raton, Florida, Department of Medicine, University of Miami School of Medicine, Miami, Florida

The Valsartan-Heart Failure trial formulated the hypothesis that combination therapy with angiotensin-converting enzyme inhibitors and ß-blockers with an angiotensin-receptor blocker had a deleterious interaction. Furthermore, the Food and Drug Administration (FDA)-approved heart failure indication for valsartan included the statement that concomitant use of an angiotensin-converting enzyme inhibitor, a ß-blocker was not recommended. The Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM)-Added and the VALsartan In Acute Myocardial Infarction Trial (VALIANT) provide reassuring evidence to support concomitant use of angiotensin-receptor blockers, angiotensin-converting enzyme inhibitors, and ß-blockers. The FDA-approved heart failure indication for candesartan included the statement of additive benefits with angiotensin-converting enzyme inhibitors and ß-blockers and led to a change in the valsartan label. These considerations have great clinical and public health importance given the increasing numbers of patients with heart failure, their high morbidity and mortality, and the relatively limited number of effective drug therapies

Key Words: congestive heart failure • cardiovascular pharmacology • secondary prevention

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 11, No. 2, 149-152 (2006)
DOI: 10.1177/1074248406289916


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