Document Detail

Does load-induced ventricular hypertrophy progress to systolic heart failure?
MedLine Citation:
PMID:  15961379     Owner:  NLM     Status:  MEDLINE    
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.
Kambeez Berenji; Mark H Drazner; Beverly A Rothermel; Joseph A Hill
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  289     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-06-17     Completed Date:  2005-08-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H8-H16     Citation Subset:  IM    
Div. of Cardiology, Dept. of Internal Medicine, Univ. of Texas Southwestern Medical Center, Dallas, TX 75390-9047, USA.
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MeSH Terms
Blood Volume*
Cardiac Output, Low / etiology*,  physiopathology*
Cardiomegaly / complications*,  etiology*
Heart Ventricles
Hypertension / complications*

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