Document Detail


Myocardial mechanics in cardiomyopathies.
MedLine Citation:
PMID:  25081406     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Cardiomyopathies are a heterogeneous group of diseases that can be phenotypically recognized by specific patterns of ventricular morphology and function. The authors summarize recent clinical observations that mechanistically link the multidirectional components of left ventricular (LV) deformation with morphological phenotypes of cardiomyopathies for offering key insights into the transmural heterogeneity of myocardial function. Subendocardial dysfunction predominantly alters LV longitudinal shortening, lengthening and suction performance and contributes to the phenotypic patterns of heart failure (HF) with preserved ejection fraction (EF) seen with hypertrophic and restrictive patterns of cardiomyopathy. On the other hand, a more progressive transmural disease results in reduction of LV circumferential and twist mechanics leading to the phenotypic pattern of dilated cardiomyopathy and the clinical syndrome of HF with reduced (EF). A proper characterization of LV transmural mechanics, energetics, and space-time distributions of pressure and shear stress may allow recognition of early functional changes that can forecast progression or reversal of LV remodeling. Furthermore, the interactions between LV muscle and fluid mechanics hold the promise for offering newer mechanistic insights and tracking impact of novel therapies.
Authors:
Karen Modesto; Partho P Sengupta
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Publication Detail:
Type:  Journal Article     Date:  2014-03-11
Journal Detail:
Title:  Progress in cardiovascular diseases     Volume:  57     ISSN:  1873-1740     ISO Abbreviation:  Prog Cardiovasc Dis     Publication Date:    2014 Jul-Aug
Date Detail:
Created Date:  2014-08-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376442     Medline TA:  Prog Cardiovasc Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  111-24     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2014 Elsevier Inc. All rights reserved.
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