Effects of asynchrony and anatomic structure on left ventricular mechanics
- Author(s): Coppola, Benjamin Anthony;
- et al.
It is now recognized that regional estimates of myocardial function are necessary to understand the underlying basis of global cardiac function. Moreover, these regional measures are more meaningful when expressed in terms of the muscle fiber architecture. In addition, myocardium has been shown to be a syncytium of myofibers organized into branching laminar "sheets", and recent evidence suggests that the sheet structure is important to systolic wall thickening. Therefore, we studied the regional mechanics of both the normal heart and a model of dyssynchronous activation, and related each to the local fiber and sheet structure. Regional deformation was assessed by implanting beads into the canine heart and imaging them with biplane cineradiography. After the functional data was acquired, fiber and sheet orientations were determined by histological sectioning. In the model of the dyssynchronous heart, myofibers in the late-activated region continued to stretch 44 ms after local tissue activation, and was associated with little stretching perpendicular to the fibers or shearing. Despite occurring primarily during isovolumic systole, this deformation differed markedly from what has been observed during passive inflation, reflecting the state of partial activation. In addition, this dyskinetic contraction did not alter the motion of myocardial sheets relative to wall motion. The relative contributions of sheet lengthening and shearing represented most of the overall wall thickening, and no acute interventions changed this relationship. Therefore, the structural architecture of the ventricular wall appears to be the dominant factor for its regional mechanical function. Using detailed histological measurements of the myocardial sheets, we attempted to derive a mathematical model coupling myofiber tension to active stress transmission through the myocardium. When simulating ventricular mechanics with a finite element model, it appears that a stress component transverse to the myofibers is necessary to replicate experimental measurements. However, the direction of transverse stress transmission is not bounded by the sheet orientation (i.e. only within sheets), so the mechanistic role of the sheets on active contraction remains unclear