(Circulation. 2000;102:484.)
© 2000 American Heart Association, Inc.
Editorial |
From the Division of Cardiology, University of Colorado Health Sciences Center, Denver, CO 80262
Correspondence to Michael R. Bristow, MD, PhD, the Division of Cardiology, University of Colorado Health Sciences Center, Denver, CO 80262.
Key Words: Editorials heart failure receptors, adrenergic, beta hemodynamics
The success of ß-blocking agents in treating mild to
moderate heart failure has generated a debate over whether the salutary
results are strictly a class effect caused by
ß1-adrenergic receptor antagonism or if
additional pharmacological properties of some compounds increase the
efficacy inherent in all agents that block
ß1-receptors. The diverse adrenergic receptor
activities of ß-blocking agents that have been used successfully to
treat chronic heart failure, the emerging role of the various
adrenergic receptor pathways in the mediation of
cardiomyopathic phenotypes in model systems
(recently reviewed in Circulation1 ), and the
vigor of pharmaceutical company scientific marketing all contribute to
the legitimacy and decibel level of the discussion. The original,
largely theoretical arguments2 3 4 have led to increasingly
more rigorous tests of the hypothesis that clinically important
differences exist among these agents. In this issue of
Circulation, Metra et al5 report the
largest of these tests to date. They provide a direct comparison of the
of the ß1-adrenergic-receptorselective,
"second generation" ß-blocker metoprolol with the nonselective
ß/
-blocker, "third generation" compound carvedilol.
Metra et al5 measured left ventricular
(LV) functional and hemodynamic effects in 150 subjects
with heart failure who were prospectively randomized 1:1 to the
recommended doses of each agent. Previous, smaller studies had reported
either subtle differences in favor of carvedilol4 6 or no
difference7 between the 2 agents. Their data5
indicate that compared with metoprolol, carvedilol provides, as
expected, a greater degree of ß-blockade. Also, as expected and as
previously reported in individual clinical trials,8 9
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