HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/5/H1994    most recent 00326.2004v1 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 ISI 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 ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Ashikaga, H. Articles by Covell, J. W. Search for Related Content PubMed PubMed Citation Articles by Ashikaga, H. Articles by Covell, J. W.

Time-dependent remodeling of transmural architecture underlying abnormal ventricular geometry in chronic volume overload heart failure

Departments of Medicine and Bioengineering, University of California, San Diego, La Jolla, California 92093

Submitted 13 April 2004 ; accepted in final form 30 June 2004

To test the hypothesis that the abnormal ventricular geometry in failing hearts may be accounted for by regionally selective remodeling of myocardial laminae or sheets, we investigated remodeling of the transmural architecture in chronic volume overload induced by an aortocaval shunt. We determined three-dimensional finite deformation at apical and basal sites in left ventricular anterior wall of six dogs with the use of biplane cineradiography of implanted markers. Myocardial strains at end diastole were measured at a failing state referred to control to describe remodeling of myofibers and sheet structures over time. After 9 ± 2 wk (means ± SE) of volume overload, the myocardial volume within the marker sets increased by >20%. At 2 wk, the basal site had myofiber elongation (0.099 ± 0.030; P < 0.05), whereas the apical site did not [P = not significant (NS)]. Sheet shear at the basal site increased progressively toward the final study (0.040 ± 0.003 at 2 wk and 0.054 ± 0.021 at final; both P < 0.05), which contributed to a significant increase in wall thickness at the final study (0.181 ± 0.047; P < 0.05), whereas the apical site did not (P = NS). We conclude that the remodeling of the transmural architecture is regionally heterogeneous in chronic volume overload. The early differences in fiber elongation seem most likely due to a regional gradient in diastolic wall stress, whereas the late differences in wall thickness are most likely related to regional differences in the laminar architecture of the wall. These results suggest that the temporal progression of ventricular remodeling may be anatomically designed at the level of regional laminar architecture.

heart failure; fiber; myocardial lamina; finite deformation

This article has been cited by other articles:

				J. W. Covell Tissue Structure and Ventricular Wall Mechanics Circulation, August 12, 2008; 118(7): 699 - 701. [Full Text] [PDF]

				R. M. Setser, N. G. Smedira, M. L. Lieber, E. D. Sabo, and R. D. White Left ventricular torsional mechanics after left ventricular reconstruction surgery for ischemic cardiomyopathy. J. Thorac. Cardiovasc. Surg., October 1, 2007; 134(4): 888 - 896. [Abstract] [Full Text] [PDF]

				P. A. Helm, L. Younes, M. F. Beg, D. B. Ennis, C. Leclercq, O. P. Faris, E. McVeigh, D. Kass, M. I. Miller, and R. L. Winslow Evidence of Structural Remodeling in the Dyssynchronous Failing Heart Circ. Res., January 6, 2006; 98(1): 125 - 132. [Abstract] [Full Text] [PDF]

				H. Ashikaga, J. W. Covell, and J. H. Omens Diastolic dysfunction in volume-overload hypertrophy is associated with abnormal shearing of myolaminar sheets Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2603 - H2610. [Abstract] [Full Text] [PDF]