Submitted on February 7, 2005
Accepted on April 26, 2005
Transmural Sheet Strains in the Lateral Wall of the Ovine Left Ventricle
Allen Cheng1*, Frank Langer1, Filiberto Rodriguez1, John C Criscione2, George T Daughters3, D. Craig Miller1, and Neil B Ingels, Jr.3
1 Department of Cardiovascular and Thoracic Surgery, Stanford University, Stanford, CA, USA
2 Department of Biomedical Engineering, Texas A&M University, College Station, TX, USA
3 Department of Cardiovascular and Thoracic Surgery, Stanford University, Stanford, CA, USA; Department of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, CA, USA
* To whom correspondence should be addressed. E-mail: allencheng{at}stanford.edu.
In an attempt to provide a better understanding of our finding that regions with contracting LV myofibers need not develop a significant transmural systolic wall thickening gradient, the analytical approach of Costa et al. (Am J Physiol 1999;276:H595) was applied to the 4-D dynamic data obtained 1- and 8- weeks after surgical implantation of transmural radiopaque beads in the lateral equatorial LV wall in 7 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 ED (reference configuration) to ES (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 both 1- and 8- weeks, 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 from 1- to 8-weeks after marker implantation surgery.
