AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 289: H8-H16, 2005; doi:10.1152/ajpheart.01303.2004
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INVITED REVIEW

Does load-induced ventricular hypertrophy progress to systolic heart failure?

Kambeez Berenji,1 Mark H. Drazner,1,3 Beverly A. Rothermel,1 and Joseph A. Hill1,2,3

3Donald W. Reynolds Cardiovascular Clinical Research Center and the Departments of 1Internal Medicine and 2Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas

Ventricular hypertrophy develops in response to numerous forms of cardiac stress, including pressure or volume overload, loss of contractile mass from prior infarction, neuroendocrine activation, and mutations in genes encoding sarcomeric proteins. Hypertrophic growth is believed to have a compensatory role that diminishes wall stress and oxygen consumption, but Framingham and other studies established ventricular hypertrophy as a marker for increased risk of developing chronic heart failure, suggesting that hypertrophy may have maladaptive features. However, the relative contribution of comorbid disease to hypertrophy-associated systolic failure is unknown. For instance, coronary artery disease is induced by many of the same risk factors that cause hypertrophy and can itself lead to systolic dysfunction. It is uncertain, therefore, whether ventricular hypertrophy commonly progresses to systolic dysfunction without the contribution of intervening ischemia or infarction. In this review, we summarize findings from epidemiologic studies, preclinical experiments in animals, and clinical trials to lay out what is known—and not known—about this important question.

congestive heart failure; eccentric hypertrophy; concentric hypertrophy; systolic dysfunction



Address for reprint requests and other correspondence: M. H. Drazner, Div. of Cardiology, Dept. of Internal Medicine, Univ. of Texas Southwestern Medical Center, Dallas, TX 75390-9047 (E-mail: mark.drazner{at}utsouthwestern.edu)




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