Tissue structure and ventricular wall mechanics.

Considering that the left ventricle is a thick-walled body that maintains its volume while reducing intracavitary volume by two thirds, it should come as no surprise that the ventricular wall thickens during systole and that there is a transmural gradient in wall thickening. Wall thickening on the inner wall may exceed values of 40% measured by a variety of techniques. These values far exceed the 8% diameter increase estimated by simple conservation of volume in an individual myocyte shortening by 15%. Physiologists have long understood that changes in the macrostructure of the wall (cellular rearrangement) must account for the difference between wall thickening and estimates of cell thickening.1 Reorientation of laminae or sheets of muscle cells has been proposed to account for this change in macrostructure.2,3 The dichotomy between wall thickening and estimated change in myocyte diameter has been elegantly framed by Cheng et al4 in this issue of Circulation, which shows nearly identical transmural fiber shortening at 2 ventricular sites, with very different wall thickening in the ovine ventricle. Similar data have been shown for other species.5,6 However, the data presented by Cheng et al4 provide strong evidence that the cellular rearrangements are different at the 2 sites. Cheng et al4 used a method developed by Costa et al5 in which regional histological measurements of muscle fiber and sheet orientations were used to resolve 3-dimensional transmural strain distributions obtained from implanted arrays of radiopaque markers into components. These components were defined by local axes that are parallel to the fibers, transverse to the fibers in the sheet plane, and transverse to the sheets. Wall thickening then can be resolved into components of sheet motion. Costa et al5 and Takayama et al6 reported that the interlaminar shear-strain term (Esn) and the sheet extension term (Ess) were chiefly responsible for the additional wall thickening not explained by myofiber shortening, and that this result was similar at 2 sites within the dog left ventricle. Cheng et al4 have shown that Esn is similar at 2 sites but provide evidence for very different roles for Ess and the sheet-thickening term (Enn) at the 2 sites in the ovine heart. Cheng et al4 found that on the subendocardium, where most wall thickening is generated, the most significant differences between the 2 regions was in sheet thickening (Enn) and shearing within the sheet planes rather than across them (Efs), and a loss of sheet extension (Ess). However, in the dog heart, Ess is a major component of wall thickening at both sites measured. These data, taken with the differences in the role of sheet thickening and sheet extension and compared with studies in the dog, further support the concept proposed by Cheng et al4 that there are large regional and speciesspecific differences in the mechanism by which fiber shortening is amplified to produce wall thickening. As pointed out by Cheng et al,4 these differences may be important in the response of the ventricular wall to disease. For example, fibrosis that primarily affects connections between myocytes might be expected to preferentially affect deformation within myocardial laminae (Efs, Ess, Enn).