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1 Department of Biomedical Engineering, Washington University, St. Louis, Missouri 63110; 2 Department of Internal Medicine, Kansai Medical University, Kyoto, Japan; and Departments of 3 Bioengineering and 4 Medicine, University of California, San Diego, La Jolla, California 92093
Previous studies suggest that the laminar
architecture of left ventricular myocardium may be critical for normal
ventricular mechanics. However, systolic three-dimensional deformation
of the laminae has never been measured. Therefore, end-systolic finite strains relative to end diastole, from biplane radiography of transmural markers near the apex and base of the anesthetized open-chest canine anterior left ventricular free wall
(n = 6), were referred to
three-dimensional laminar microstructural axes reconstructed from
histology. Whereas fiber shortening was uniform [
0.07 ± 0.04 (SD)], radial wall thickening increased from base (0.10 ± 0.09) to apex (0.14 ± 0.13). Extension of the laminae transverse to the muscle fibers also increased from base (0.08 ± 0.07) to apex (0.11 ± 0.08), and interlaminar shear changed sign
[0.05 ± 0.07 (base) and 0.07 ± 0.09 (apex)],
reflecting variations in laminar architecture. Nevertheless, the apex
and base were similar in that at each site laminar extension and shear contributed ~60 and 40%, respectively, of mean transmural
thickening. Kinematic considerations suggest that these dual
wall-thickening mechanisms may have distinct ultrastructural origins.
cleavage planes; cardiac mechanics; finite strain; wall thickening; regional
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