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Am J Physiol Heart Circ Physiol 289: H1234-H1241, 2005. First published May 6, 2005; doi:10.1152/ajpheart.00119.2005
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Transmural sheet strains in the lateral wall of the ovine left ventricle

Allen Cheng,1 Frank Langer,1 Filiberto Rodriguez,1 John C. Criscione,2 George T. Daughters,1,3 D. Craig Miller,1 and Neil B. Ingels, Jr.1,3

1Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford; 3Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of The Palo Alto Medical Foundation, Palo Alto, California; and 2Department of Biomedical Engineering, Texas A & M University, College Station, Texas

Submitted 7 February 2005 ; accepted in final form 26 April 2005

In an attempt to provide a better understanding of our finding that regions with contracting left ventricular myofibers need not develop a significant transmural systolic wall thickening gradient, the analytic approach of Costa et al. (Am J Physiol Heart Circ Physiol 276: H595–H607, 1999) was applied to the four-dimensional dynamic data obtained 1 and 8 wk after surgical implantation of transmural radiopaque beads in the lateral equatorial left ventricular wall in seven ovine hearts. Quantitative histology of tissue blocks demonstrated that fiber angles varied linearly across the wall in this region from –37° in the subepicardium to +18° in the subendocardium. Sheet angles exhibited a pleated-sheet behavior, alternating sign from subepicardium to subendocardium. From end diastole (reference configuration) to end systole (deformed configuration), fiber strain was uniformly negative, sheet extension and sheet thickening were uniformly positive, and sheet-normal shear contributed to wall thickening at all wall depths. Subepicardial radial wall thickening increased significantly from week 1 to week 8, with significant increases in the contributions from subepicardial sheet extension and sheet-normal shear. At 1 and 8 wk, the contribution of sheet-normal shear to wall thickening was substantial at all transmural depths; the contribution of sheet extension to wall thickening was greatest in the subepicardium and least in the subendocardium, and the contribution of sheet thickening to wall thickening was greatest in the subendocardium and least in the subepicardium. A mechanistic model is proposed that provides a working hypothesis that a selective decrease in subepicardial intercellular matrix stiffness is responsible for elimination of the transmural wall thickening gradient 1–8 wk after marker implantation surgery.

wall thickening; myocardium; systolic function


Address for reprint requests and other correspondence: N. B. Ingels, Jr., Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, 795 El Camino Real (Ames Bldg.), Palo Alto, CA 94301 (E-mail: ingels{at}stanford.edu)




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