Document Detail

Interventricular coupling coefficients in a thick shell model of passive cardiac chamber deformation.
MedLine Citation:
PMID:  18365264     Owner:  NLM     Status:  MEDLINE    
Mechanical interplay between the adjacent ventricles is one of the principal modulators of physiopathological heart function, and the underlying mechanisms of interaction are only partially understood, hence hampering clinically useful interpretation of imaging data. In order to characterize the influence of chamber geometry on ventricular coupling, the ventricles and septum are modeled as portions of ellipsoidal shells, and configuration is derived as a function of pressure gradients by combining shell element equilibrium equations through static boundary conditions applied at the sulcus. Diastolic volume (v) surfaces are calculated as a function of pressure (p), contralateral pressure (clp) and intrathoracic pressure (p ( t )) and match literature data where available. Ventricular interaction is characterized in terms of partial derivatives in v-p-clp-p ( t ) space both under physiological and altered (selectively stiffened walls) conditions. The model allows prediction of diastolic ventricular v-p-clp-p ( t ) interplay in a variety of physiopathological circumstances.
N Toschi; M Guerrisi
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Publication Detail:
Type:  Journal Article     Date:  2008-03-26
Journal Detail:
Title:  Medical & biological engineering & computing     Volume:  46     ISSN:  1741-0444     ISO Abbreviation:  Med Biol Eng Comput     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-06-19     Completed Date:  2008-12-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7704869     Medline TA:  Med Biol Eng Comput     Country:  United States    
Other Details:
Languages:  eng     Pagination:  637-48     Citation Subset:  IM    
Sezione di Fisica Medica, Dipartimento di Biopatologia e Diagnostica per Immagini, Università Degli Studi di Roma Tor Vergata, Rome, Italy.
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MeSH Terms
Diastole / physiology
Heart / physiology*
Heart Septum / physiology
Models, Cardiovascular*
Stress, Mechanical
Ventricular Function*

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