(Circulation. 1995;91:2504-2507.)
© 1995 American Heart Association, Inc.
Articles |
Structural Basis for Heart Failure
Ventricular Remodeling and Its Pharmacological Inhibition
From the Cardiovascular Division, Department of Medicine, University of Minnesota Medical School (Minneapolis).
Correspondence to Jay N. Cohn, MD, Cardiovascular Division, University of Minnesota Medical School, Box 508 UMHC, 420 Delaware St SE, Minneapolis, MN 55455.
Key Words: heart failure • clinical trials • editorials • pharmacology
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Introduction |
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The syndrome of heart failure has traditionally been viewed as a functional disorder precipitated by impaired left ventricular pump performance. The classification into systolic and diastolic dysfunction has emphasized the functional distinction between abnormalities in contraction and relaxation. Recently, however, attention has been directed toward the possibility that the systolic dysfunction, which has been thought to be related to contractile failure, could be a consequence of a structural increase in ventricular chamber volume. This construct would revise the conventional view—contractile failure leads to chamber dilatation—with a more anatomic basis for heart failure: Chamber dilatation occurs as an early response that results in the reduced wall motion that is mandated to generate a normal stroke volume from a large ventricular end-diastolic volume. This structural alteration is not necessarily related to the underlying etiological cardiac pathology but rather represents an intrinsic morphological change that progresses over time in response to an initiating event. The term "remodeling" often is used to address these structural changes and may be best defined as a change in chamber volume and shape not related to a preload-mediated increase in sarcomere length.
In this issue of Circulation, Greenberg and his SOLVD
colleagues1 revisit the remodeling issue in chronic heart
failure with echocardiographic data collected in the long-term trial of
enalapril versus placebo in both symptomatic and asymptomatic patients
with left ventricular remodeling. Patients were selected for this study
on the basis of an ejection fraction of 
35%. At the time the study
was designed, this low ejection
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