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This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/H1844    most recent 00961.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Dang, A. B. C. Articles by Ratcliffe, M. B. Search for Related Content PubMed PubMed Citation Articles by Dang, A. B. C. Articles by Ratcliffe, M. B.

Akinetic myocardial infarcts must contain contracting myocytes: finite-element model study

²Division of Cardiothoracic Surgery, Department of Surgery, ⁵Division of Cardiology, Department of Medicine, ³Department of Bioengineering, ⁶Department of Anesthesia, and ¹School of Medicine, University of California, San Francisco, and ⁴San Francisco Department of Veterans Affairs Medical Center, San Francisco, California; and ⁷Department of Cardiothoracic Surgery, University of Pennsylvania, Philadelphia, Pennsylvania

Submitted 16 October 2003 ; accepted in final form 9 December 2004

Infarcted segments of myocardium demonstrate functional impairment ranging in severity from hypokinesis to dyskinesis. We sought to better define the contributions of passive material properties (stiffness) and active properties (contracting myocytes) to infarct thickening. Using a finite-element (FE) model, we tested the hypothesis that infarcted myocardium must contain contracting myocytes to be akinetic and not dyskinetic. A three-dimensional FE mesh of the left ventricle was developed with echocardiographs from a reperfused ovine anteroapical infarct. The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction, and an elastance model for active fiber stress was incorporated. The diastolic stiffness (C) and systolic material property (isometric tension at longest sarcomere length and peak intracellular calcium concentration, T_max) of the uninfarcted remote myocardium were assumed to be normal (C = 0.876 kPa, T_max = 135.7 kPa). Diastolic and systolic properties of the infarct necessary to produce akinesis, defined as an average radial strain between –0.01 and 0.01, were determined by assigning a range of diastolic stiffnesses and scaling infarct T_max to represent the percentage of contracting myocytes between 0% and 100%. As C was increased to 11 times normal (C = 10 kPa) the percentage of T_max necessary for akinesis increased from 20% to 50%. Without contracting myocytes, C = 250 kPa was necessary to achieve akinesis. If infarct stiffness is <285 times normal, contracting myocytes are required to prevent dyskinetic infarct wall motion.

left ventricle; heart failure; dilated cardiomyopathy; remodeling; stress

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