RELATION OF REGIONAL CROSS-FIBER SHORTENING TO WALL THICKENING IN THEINTACT HEART - 3-DIMENSIONAL STRAIN ANALYSIS BY NMR TAGGING

Background The mechanism by which small amounts of myofiber shortening lead to extensive wall thickening is unknown. When isolated fibers sh orten, they thicken in the two orthogonal directions. In situ fibers, however, vary in their orientation through the wall, and each is tethe red to near or distant neighbors, which allows shortening to occur bot h in the direction of the fibers and also perpendicular to them. This ''cross-fiber'' shortening may enable the wall to shorten in two direc tions and thereby thicken extensively in the third. Methods and Result s Nuclear magnetic resonance tagging is a noninvasive method of labeli ng and tracking myocardium of the entire heart in three dimensions tha t does not interfere with myocardial motion. To investigate the presen ce and importance of cross-fiber shortening in the intact left ventric le, 10 closed-chest dogs were studied by nuclear magnetic resonance ta gging. Five short-axis and four long-axis images were acquired to reco nstruct 32 cubes of myocardium in each dog at end diastole and end sys tole. Pathological dissection was performed to determine the fiber dir ection at the epicardium, midwall, and endocardium of each cube. Strai n was computed from the three-dimensional cube coordinates in the fibe r and cross-fiber directions for epicardial and endocardial surfaces, and thickening of the full wall and its epicardial and endocardial hal ves was determined. Shear deformations were also calculated. Fiber str ain at the epicardium and endocardium was -6.4+/-0.7% and -8.5+/-0.6% (mean+/-SEM), respectively (difference, P>.05). Cross-fiber strain at epicardium and endocardium was -0.6+/-0.5% and -25+/-0.6%, respectivel y (difference, P<.05). Thickening of the full wall reached 32.5+/-1.0% , composed of epicardial thickening of 25.5+/-0.6% and endocardial thi ckening of 43.3+/-1.0% (difference, P<.05). Fiber/cross-fiber shear st rain was small (<3%). Significant regional differences were present in all strains. A significant correlation was found between the extents of regional thickening and cross-fiber shortening. Conclusions Cross-f iber shortening at the endocardium, therefore, far exceeds cross-fiber shortening at the epicardium and fiber shortening at both epicardium and endocardium. Since no active shortening can occur locally in the c ross-fiber direction, the extensive endocardial cross-fiber shortening must result from interaction with differently aligned fibers at a dis tance. The correlation between regional thickening and cross-fiber sho rtening supports the hypothesis that this interaction is the mechanism for amplifying small amounts of fiber shortening to cause extensive e ndocardial thickening.