Factors influencing the contribution of myocardial laminar sheets to ventricular wall thickening

Abstract

The myocardium is composed of laminar sheets of myofibers (oriented at angle β from radial), which shear during systole and account for >50% of wall thickening (E33). The sheet strains (Ess, Enn, Esn) are related to wall thickening by E33 = Ess*cos2β + Enn*sin2β + 2*Esn*cosβ*sinβ. We hypothesized that the contribution of each term to wall thickening was determined primarily by anatomic structure, and independent of load. To test this hypothesis, we imaged transmural columns of beads implanted into the left ventricle of open‐chest dogs (n=15) using biplane cineradiography. Strains were expressed in terms of a histologically measured fiber‐sheet coordinate system. At 20% depth, the sheet extension (Ess) term was the primary contributor to end‐systolic wall thickening, with an average of 68%. At 52 and 81% depths, the sheet shear (Esn) term was the predominant factor, contributing 49 and 48% respectively. This transmural trend held during diastolic wall thinning (EDP from 3 to 18 mmHg), with Ess term = 78%, and Esn term = 79 and 127% corresponding to the 3 depths. Increasing afterload (LV pressure from 119 to 169 mmHg) also gave a similar transmural result. We conclude that the transmural deformation of the myocardial wall is a property of the local anatomical orientation, with laminar structures contribution similarly during diastole and systole with varying loads. Supported by NIH grant HL32583.