(Circulation. 1999;99:600-604.)
© 1999 American Heart Association, Inc.
Editorial |
Function of the Cardiac Myocyte in the Conundrum of End-Stage, Dilated Human Heart Failure
From Temple University School of Medicine (S.R.H.), Department of Physiology, Philadelphia, Pa, and Laboratory of Cardiovascular Science (E.G.L.), Gerontology Research Center, Baltimore, Md.
Correspondence to Edward G. Lakatta, MD, Laboratory of Cardiovascular Science, Gerontology Research Center, 5600 Nathan Shock Dr, Baltimore, MD 21224. E-mail lakattae@grc.nia.nih.gov
Key Words: Editorials • myocardium • sarcoplasmic reticulum • heart failure
Chronic heart failure is a phenotype that marks the final common pathway in a diversity of specific cardiovascular disease states, eg, severe coronary ischemia and myocardial infarction, and chronic hypertension, or it can be idiopathic in nature. A trilogy of clinical signs that includes reduced systolic myocardial function, increased diastolic filling pressure, and an increased likelihood for the occurrence of cardiac arrhythmias is eventually accompanied by a markedly dilated heart. The specific role of cardiac myocyte dysfunction in progressive cardiac dilatation that heralds the end stage of chronic heart failure is 1 facet of the conundrum of the end-stage dilated heart. In this issue of Circulation, Hasenfuss et al1 have studied cardiac muscle isolated from the left ventricle of end-stage, dilated cardiomyopathic hearts removed from patients and cardiac muscle from control, non–heart-failure organ donors in an attempt to discover mechanisms that may underlie cardiomyocyte dysfunction in chronic end-stage heart failure.
See p 641
As a platform for the discussion of their study, let us first
acknowledge that a plethora of hypotheses, in addition to progressive
myocyte dysfunction, have been put forth to explain the progressive
functional demise and cardiac remodeling and dilatation that
characterize end-stage heart failure. These hypotheses were originally
cast from observations in heart failure in animal models, including
those resulting from chronic experimental mechanical (pressure or
volume) overload or chronic ischemia and those resulting from
naturally occurring heart failure in specific genetic strains of
rodents (eg, the Syrian hamster; the old, spontaneously hypertensive,
obese, or diabetic
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