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Review Article
Mechanisms of Disease
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Volume 358:1370-1380 March 27, 2008 Number 13
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Cardiac Plasticity
Joseph A. Hill, M.D., Ph.D., and Eric N. Olson, Ph.D.

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The heart is capable of remodeling in response to environmental demands, and a variety of stimuli can induce it to grow or shrink (Figure 1). Exercise, pregnancy, and postnatal growth promote physiologic growth of the heart, whereas neurohumoral activation, hypertension, and myocardial injury can cause pathologic hypertrophic growth. In contrast to physiologic growth, hypertrophic growth can increase the risk of heart failure and malignant arrhythmia. Atrophy of the heart is a complication of protracted bed rest, prolonged weightlessness during space travel, and mechanical unloading with a ventricular assist device.

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Figure 1. Conditions Leading to Remodeling of the Heart and Resulting . . . [Full Text of this Article]

 
Dynamics of Myocardial Growth

Changing Ideas about Cardiac Hypertrophy

The Hypertrophic Phenotype

Contrasting Phenotypes of Cardiac Growth

Functional Decompensation in Pathologic Cardiac Hypertrophy

Myocardial Atrophy

Signal Transduction in Cardiac Growth

Cardiac Plasticity in Heart Disease

Prospects for Therapy

Limitations and Perspective


Source Information

From the Donald W. Reynolds Cardiovascular Clinical Research Center (J.A.H., E.N.O.); and the Departments of Internal Medicine (Cardiology) (J.A.H.) and Molecular Biology (J.A.H., E.N.O.), University of Texas Southwestern Medical Center, Dallas.

Address reprint requests to Dr. Hill at the Division of Cardiology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd., NB11.200, Dallas, TX 75390-8573, or at joseph.hill@utsouthwestern.edu.




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