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J Thorac Cardiovasc Surg 2001;122:421-423
© 2001 The American Association for Thoracic Surgery
Editorials |
From the Department of Medicine, Divisions of Circulatory Physiology and Cardiology, Columbia University, New York, NY.
Received for publication March 20, 2001. Accepted for publication March 27, 2001. Address for reprints: Daniel Burkhoff, MD, PhD, Department of Medicine, Divisions of Circulatory Physiology and Cardiology, Columbia University, 812 Black Building, 650 W 168th St, New York, NY 10032.
See related article on page 482.
Laplace's law, which can be used to estimate myocardial wall stress (
) from intraventricular pressure (LVP), radius of curvature (R), and wall thickness (h), has long been recognized as a fundamental physical principle in understanding cardiac function in health and disease:
= LVP · R/h. On the basis of this law, the enlarged chamber radius of the chronically failing heart exposes myocytes to increased systolic wall stress. This leads to cellular and chamber hypertrophy, which, in an adaptive process, acts to renormalize wall stress.
1 As the chamber continues to dilate over time, the limits of hypertrophy appear to be reached so that wall stress ultimately increases. This increased afterload further impairs the ability of the already weakened myocytes to shorten, and cardiac performance deteriorates. Globally referred to as ventricular remodeling, this process is partially preventable and reversible as demonstrated in studies of angiotensin-converting enzyme inhibitors,
2 ß-blockers,
3 and during hemodynamic unloading by prolonged support with a left ventricular assist device.
4
Several surgical therapies, such as the Myocor ventricular shape change device (Myocor, Inc, Plymouth, Minn), described in this issue by McCarthy and colleagues,
5 are being developed for treating heart failure by physically remodeling the dilated heart. Stress reduction via Laplace's
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J. Thorac. Cardiovasc. Surg. 2001 122: 482-490.
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