Circulation. 2005;111:2837-2849
doi: 10.1161/CIRCULATIONAHA.104.500546
doi: 10.1161/CIRCULATIONAHA.104.500546
(Circulation. 2005;111:2837-2849.)
© 2005 American Heart Association, Inc.
Basic Science for Clinicians |
Mechanisms and Models in Heart Failure
The Biomechanical Model and Beyond
From the Winters Center for Heart Failure Research, Department of Medicine, Baylor College of Medicine, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Tex (D.L.M.), and Division of Cardiology and Cardiovascular Institute, University of Colorado Health Science Center, Denver (M.R.B.).
Reprint requests to Douglas L. Mann, MD, Winters Center for Heart Failure Research, MS F524, 6565 Fannin, Houston, TX 77030. E-mail dmann@bcm.tmc.edu
Received August 25, 2004; revision received December 23, 2004; accepted January 19, 2005.
Key Words: drugs • infarction • inflammation • receptors, adrenergic, beta • cytokines
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure, no single conceptual paradigm for heart failure has withstood the test of time. Whereas clinicians initially viewed heart failure as a problem of excessive salt and water retention that was caused by abnormalities of renal blood flow (the "cardiorenal model"1), as physicians began to perform careful hemodynamic measurements, it also became apparent that heart failure was associated with a reduced cardiac output and excessive peripheral vasoconstriction. This latter realization led to the development of the "cardiocirculatory" or "hemodynamic" model for heart failure,1 wherein heart failure was thought to arise largely as a result of abnormalities of the pumping capacity of the heart and excessive peripheral vasoconstriction. However, although both the cardiorenal and cardiocirculatory models for heart failure explained the excessive salt and water retention that heart failure patients experience, neither of these models explained the relentless "disease progression" that occurs in this syndrome. Thus, although the cardiorenal models provided the rational basis for the use of diuretics to control the volume status of patients with heart failure, and the cardiocirculatory model provided the rational basis for the use of inotropes and intravenous vasodilators to augment cardiac output, these therapeutic strategies have not prevented heart failure from progressing, nor have they led to prolonged life for patients with moderate to severe heart failure.1,2
In the present review we will summarize recent advances in the field of heart failure, with a focus on the new
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