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1 September 1994 | Volume 121 Issue 5 | Pages 363-371
Heart failure is a progressive condition with a 5-year survival of less than 50%. This poor prognosis, which can be reproduced by overloading the hearts of experimental animals, may reflect molecular abnormalities caused when overload stimulates adult cardiac myocytes to undergo hypertrophy. Because these terminally differentiated cells have little or no capacity to divide, hypertrophy represents an unnatural growth response; however, the mechanism by which overload shortens survival remains speculative. Modification of this unnatural growth response by converting enzyme inhibitors and nitrates, which have growth inhibitory as well as vasodilator effects, may contribute to the ability of these drugs to improve prognosis in patients with heart failure.
Author and Article Information
From the University of Connecticut School of Medicine, Farmington, Connecticut.
PERSPECTIVE
The Cardiomyopathy of Overload: An Unnatural Growth Response in the Hypertrophied Heart
Requests for Reprints: Arnold M. Katz, MD, Cardiology Division, University of Connecticut Health Center, Farmington, CT 06030-1305.
Acknowledgments: The author thanks the Class of 1996 of the University of Connecticut Schools of Medicine and Dental Medicine for their interest in and enthusiasm for his lectures on this topic, which led to the preparation of this article; and James B. Young, MD, who pointed out the contribution of Austin Flint to our understanding of the importance of cardiac hypertrophy.
Grant Support: In part by Program Project HL-33026 from the National Heart, Lung, and Blood Institute.
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