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(Circulation. 2004;110:2559-2561.)
© 2004 American Heart Association, Inc.

Editorial

Cellular Basis for Therapeutic Choices in Heart Failure

Lionel H. Opie, MD

From the Hatter Institute for Cardiology Research, University of Cape Town, Cape Town, South Africa.

Correspondence to Dr Lionel H. Opie, Hatter Institute for Cardiology Research, Chris Barnard Building, Cape Heart Center Faculty of Health Sciences, University of Cape Town, 7925 Observatory, Cape Town, South Africa. E-mail opie@capeheart.uct.ac.za

Key Words: Editorials • heart failure • angiotensin • renin • receptors, adrenergic, beta

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Stop it at the start; it’s late for medicine to be prepared when disease has grown strong through long delays.

— —Ovid, Remedia Amoris

A crucial experimental study in 1985 showed that the angiotensin-converting enzyme inhibitor (ACEi) captopril did more than reduce the after- and preload on the heart in failure; captopril also improved remodeling by lessening the degree of left ventricular (LV) dilation.¹ A series of powerful clinical studies starting in 1987 established the crucial role of ACE inhibition in severe heart failure such that it almost became unethical to test other modalities of heart failure therapies except as add-on therapies. Thus, it was difficult to know whether the advent of the angiotensin II subtype I receptor blockers (ARBs) brought improvement beyond those of standard ACEi therapy. The most practical approach was to add an ARB such as valsartan to the therapeutic regimen of patients, 86% of whom were already receiving an ACEi.² In the small non-ACEi group, valsartan appeared to be even more effective, but the limited size of the group made it difficult to be sure. Furthermore, the addition of valsartan to the small number of patients already being treated with ACEi and ß-blockade appeared to be harmful. These defects have been remedied by another ARB, candesartan, which was evaluated in the Candesartan in Heart Failure Assessment of Reduction in Mortality and morbidity (CHARM) series of studies. The study by Young et al³ represents the effects of candersartan versus placebo given to a prespecified subgroup of patients . . . [Full Text of this Article]

Related Article:

Mortality and Morbidity Reduction With Candesartan in Patients With Chronic Heart Failure and Left Ventricular Systolic Dysfunction: Results of the CHARM Low-Left Ventricular Ejection Fraction Trials

James B. Young, Mark E. Dunlap, Marc A. Pfeffer, Jeffrey L. Probstfield, Alain Cohen-Solal, Rainer Dietz, Christopher B. Granger, Jaromir Hradec, Jerzy Kuch, Robert S. McKelvie, John J.V. McMurray, Eric L. Michelson, Bertil Olofsson, Jan Ostergren, Peter Held, Scott D. Solomon, Salim Yusuf, Karl Swedberg for the Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) Investigators and Committees
Circulation 2004 110: 2618-2626. [Abstract] [Full Text]

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