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1 Department of Medicine and Bioengineering, University of California, San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: jcovell{at}ucsd.edu.
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 3D finite deformation at apical and basal sites in LV anterior wall of 6 dogs using 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 weeks (mean±SE) of volume overload, the myocardial volume within the marker sets increased by greater than 20%. At 2 weeks, the basal site had myofiber elongation (0.099±0.030, P<0.05), whereas the apical site did not (P=NS). Sheet shear at the basal site increased progressively toward the final study (0.040±0.003 at 2 weeks 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, while 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.
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