Circulation, Vol 89, 1174-1182, Copyright © 1994 by American Heart Association
FE Rademakers, WJ Rogers, WH Guier, GM Hutchins, CO Siu, ML Weisfeldt, JL Weiss and EP Shapiro
BACKGROUND: The mechanism by which small amounts of myofiber shortening
lead to extensive wall thickening is unknown. When isolated fibers shorten,
they thicken in the two orthogonal directions. In situ fibers, however,
vary in their orientation through the wall, and each is tethered to near or
distant neighbors, which allows shortening to occur both in the direction
of the fibers and also perpendicular to them. This "cross-fiber" shortening
may enable the wall to shorten in two directions and thereby thicken
extensively in the third. METHODS AND RESULTS: Nuclear magnetic resonance
tagging is a noninvasive method of labeling and tracking myocardium of the
entire heart in three dimensions that does not interfere with myocardial
motion. To investigate the presence and importance of cross-fiber
shortening in the intact left ventricle, 10 closed-chest dogs were studied
by nuclear magnetic resonance tagging. Five short-axis and four long-axis
images were acquired to reconstruct 32 cubes of myocardium in each dog at
end diastole and end systole. Pathological dissection was performed to
determine the fiber direction at the epicardium, midwall, and endocardium
of each cube. Strain was computed from the three- dimensional cube
coordinates in the fiber and cross-fiber directions for epicardial and
endocardial surfaces, and thickening of the full wall and its epicardial
and endocardial halves was determined. Shear deformations were also
calculated. Fiber strain 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%, respectively (difference, P < .05). Thickening of the
full wall reached 32.5 +/- 1.0%, composed of epicardial thickening of 25.5
+/- 0.6% and endocardial thickening of 43.3 +/- 1.0% (difference, P <
.05). Fiber/cross-fiber shear strain 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-fiber 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 cross-fiber direction, the extensive endocardial
cross-fiber shortening must result from interaction with differently
aligned fibers at a distance. The correlation between regional thickening
and cross-fiber shortening supports the hypothesis that this interaction is
the mechanism for amplifying small amounts of fiber shortening to cause
extensive endocardial thickening.
ARTICLES
Relation of regional cross-fiber shortening to wall thickening in the intact heart. Three-dimensional strain analysis by NMR tagging
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Md.
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