From the Cardiology Division, Department of Medicine, University of
Connecticut, Farmington.
Correspondence to Arnold M. Katz, MD, Cardiology Division, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030-2249.
Only
a decade ago, end-stage heart failure was viewed as an irreversible
condition for which therapy could offer only transient
symptomatic relief. This led to a sense of hopelessness
that resembled the prevailing attitude toward coronary
occlusive disease 50 years ago, when atherosclerosis
was thought to be an inevitable feature of natural aging. In the case
of heart failure, as recently as the mid-1980s it was believed that
little could be done to improve the natural history in patients with
advanced chronic heart failure and a severely dilated ventricle. Yet
within a few years, work from unexpected directions demonstrated that
the progressive deterioration of the failing heart can be slowed and
prognosis improved.
The first class of drugs shown in large clinical trials to
improve prognosis in these patients was
vasodilators.1 Because unloading the failing
heart has an obvious energy-sparing effect and because virtually all
vasodilators alleviate symptoms over the short term, it came as a
surprise that not all of these drugs improve prognosis and that some
accelerate deterioration of the failing heart2
and shorten survival.3 4 5 6 Equally
counterintuitive was the finding that positive inotropic agents, which,
like vasodilators initially improve symptoms, also increase
mortality.7 8 Perhaps the most surprising finding
of the clinical trials in heart failure was that long-term
administration of ß-adrenergic receptor blockers, although they
initially worsen symptoms, reduce long-term morbidity and improve
survival.9 10 11 Taken together, these clinical
findings have led to a paradigm shift in our understanding of heart
failure, one that by highlighting long-term mortality as
This article has been cited by other articles:
© 1998 American Heart Association, Inc.
Editorials
Regression of Left Ventricular Hypertrophy
New Hope for Dying Hearts
Key Words: Editorials hypertrophy remodeling heart failure
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N. de Jonge, D. F. van Wichen, M. E. I. Schipper, J. R. Lahpor, F. H. J. Gmelig-Meyling, E. O. Robles de Medina, and R. A. de Weger
Left ventricular assist device in end-stage heart failure: persistence of structural myocyte damage after unloading: An immunohistochemical analysis of the contractile myofilaments
J. Am. Coll. Cardiol.,
March 20, 2002;
39(6):
963 - 969.
[Abstract]
[Full Text]
[PDF]
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