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contributor authorJack D. Lemmon
contributor authorAjit P. Yoganathan
date accessioned2017-05-09T00:01:51Z
date available2017-05-09T00:01:51Z
date copyrightAugust, 2000
date issued2000
identifier issn0148-0731
identifier otherJBENDY-25902#297_1.pdf
identifier urihttp://yetl.yabesh.ir/yetl/handle/yetl/123343
description abstractA computational model that accounts for blood–tissue interaction under physiological flow conditions was developed and applied to a thin-walled model of the left heart. This model consisted of the left ventricle, left atrium, and pulmonary vein flow. The input functions for the model included the pulmonary vein driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The Immersed Boundary Method was used for the interaction of the tissue and blood in response to fluid forces and changes in tissue pathophysiology, and the fluid mass and momentum conservation equations were solved using Patankar’s Semi-Implicit Method for Pressure Linked Equations (SIMPLE). This model was used to examine the flow fields in the left heart under abnormal diastolic conditions of delayed ventricular relaxation, delayed ventricular relaxation with increased ventricular stiffness, and delayed ventricular relaxation with an increased atrial contraction. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions, and to the results from simulations of normal diastolic function in this model 1. Cases involving impairment of diastolic function were modeled with changes to the input functions for fiber relaxation/contraction of the chambers. The three cases of diastolic dysfunction investigated agreed with the changes in diastolic flow fields seen clinically. The effect of delayed relaxation was to decrease the early filling magnitude, and this decrease was larger when the stiffness of the ventricle was increased. Also, increasing the contraction of the atrium during atrial systole resulted in a higher late filling velocity and atrial pressure. The results show that dysfunction can be modeled by changing the relationships for fiber resting-length and/or stiffness. This provides confidence in future modeling of disease, especially changes to chamber properties to examine the effect of local dysfunction on global flow fields. [S0148-0731(00)00104-7]
publisherThe American Society of Mechanical Engineers (ASME)
titleComputational Modeling of Left Heart Diastolic Function: Examination of Ventricular Dysfunction
typeJournal Paper
journal volume122
journal issue4
journal titleJournal of Biomechanical Engineering
identifier doi10.1115/1.1286559
journal fristpage297
journal lastpage303
identifier eissn1528-8951
keywordsForce
keywordsPressure
keywordsFlow (Dynamics)
keywordsFluids
keywordsFibers
keywordsRelaxation (Physics)
keywordsBlood
keywordsDiseases
keywordsStiffness
keywordsComputer simulation
keywordsEngineering simulation
keywordsFunctions
keywordsInflow AND Biological tissues
treeJournal of Biomechanical Engineering:;2000:;volume( 122 ):;issue: 004
contenttypeFulltext


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