TRANSVERSE-SHEAR ALONG MYOCARDIAL CLEAVAGE PLANES PROVIDES A MECHANISM FOR NORMAL SYSTOLIC WALL THICKENING

Recent studies in humans acid other species show that there is substan tial transverse shear strain in the left ventricular myocardium, and o thers have shown transverse myocardial laminae separated by cleavage p lanes. We proposed that cellular rearrangement based on shearing along myocardial cleavage planes could account for >50% of normal systolic wall thickening since <50% can be explained by increases in myocyte di ameter, To test this hypothesis, we measured strains at two sites with different cleavage-plane anatomy in eight open-chest dogs. Columns of radiopaque markers were implanted in the left ventricular anterior fr ee wall and septum. Markers were tracked with biplane cineradiography, and strains were quantified by using finite deformation techniques. H earts were perfusion-fixed with glutaraldehyde, and cleavage-plane ori entations at the bead sites were measured in three orthogonal planes. At subendocardial sites of the anterior left ventricular wall, where t he cleavage planes approach the endocardium obliquely from the apical side of the surface normal in the longitudinal-radial plane (-67+/-11 degrees), systolic longitudinal-radial transverse shear (E(23)) was po sitive (0.14+/-0.08). At the septal sites where the subendocardial cle avage planes approach the endocardium obliquely from above the surface normal (44+/-12 degrees), E(23) was negative (-0.12+/-0.08). The diff erences in cleavage-plane angle and E(23) at the two sites were each h ighly significant (P<.0005). At both sites, the transverse shear strai n accompanied substantial systolic wall thickening at the subendocardi um (anterior, E(33)=0.44+/-0.16; septum, E(33)=0.22+/-0.14). These dat a are not representative of the behavior in midwall and outer wall sit es, where cleavage-plane orientation was not consistently different nt between anterior left ventricle and septum. Our data indicate that re arrangement of myocytes by slippage along myocardial cleavage planes i s in the correct direction end of sufficient. magnitude in the subendo cardium (inner third) to account for a substantial proportion (>50%) o f systolic wall thickening. Furthermore, three-dimensional reconstruct ion of the myocardial laminae and local comparison with maximum strain vectors indicate that for the inner third of the ventricular wall the maximum shear deformation is a result of relative sliding between myo cardial laminae.