Relation between transmural deformation and local myofiber direction in canine left ventricle.

Abstract

To determine the relation between local myofiber anatomy and local deformation in the wall of the left ventricle, both three-dimensional transmural deformation and myofiber orientation were examined in the anterior free wall of seven canine left ventricles. Deformation was measured by imaging columns of implanted radiopaque markers with high-speed, biplane cineradiography (16 mm, 120 frames/sec). Hearts were fixed at end diastole and sectioned parallel to the local epicardial tangent plane to determine the transmural distribution of fiber directions at the site of strain measurement. The principal direction of deformation associated with the greatest shortening was compared with the local fiber direction in the outer (21 ± 8 % of the wall thickness from the epicardium) and inner (65 ±9%) halves of the wall. Although the fiber direction varied substantially with depth from the epicardium, the principal direction did not. In the outer half of the wall, fiber direction averaged-8 ± 24°, while the principal direction averaged-33 ±24° from circumferential (counterclockwise angles are positive). In the inner half, fiber direction averaged 69 ±10°, while the principal direction averaged-22 ±21°. Therefore, while fiber and principal directions were not substantially different hi the outer half, the greatest shortening occurred orthogonally to the fiber direction hi the inner half. Normal and shear strains measured in a cardiac coordinate system (circumferential, longitudinal, and radial coordinates) were rotated (transformed) to "fiber" coordinates hi both halves of the wall. In the outer half, normal strains observed in the fiber (-0.09 ±0.04) and cross-fiber (-0. 0 4 ±0.04) directions were not significantly different (paired t test, p<0.05). In the inner half, more than twice as much strain occurred in the cross-fiber (-0.17 ± 0.03) than in the fiber direction (-0.06 ± 0.06). Moreover, the only shear strain that remained substantial after transformation was transverse shear in the plane of the fiber and radial coordinates. These results suggest that both reorientation and cross-sectional shape changes of myofibers or the interstitium may contribute to the large wall thickenings observed during contraction, particularly in the inner hah* of the ventricular wall. (Circulation Research 1988;63:550-562) T he way in which myofibers lying at different depths in the heart wall and having different orientations interact during contraction is not known. It is well known, however, that there is an extensive collagenous network surrounding the myocyte and collagen struts between myocytes. 12 Moreover, the direction of the myofibers, which varies continuously with depth spanning more than 100° across the anterior free wall of the canine left ventricle, 34 is neither altered by large changes in ventricular mass or shape 3 nor affected greatly by

Contribution of laminar myofiber architecture to load-dependent changes in mechanics of LV myocardium

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Functional Recovery of Subepicardial Myocardial Tissue in Transmural Myocardial Infarction After Successful Reperfusion

“…24,25 The technique allows precise quantification of complex 3D motion and deformation patterns, and the results correspond very well with those obtained by invasive methods that use metallic markers sewn in the myocardium. 12,26,27 Variability percentages were small and comparable with previous reports that used MR imaging to quantify LV parameters. 28 So although there is ample evidence to support the intrinsic accuracy of the technique, the limitations of the present study are introduced by the need to match MRI and PET data and the imprecision of matching serial MRI studies.…”

Left Ventricular Torsional Mechanics in Uncomplicated Pregnancy

“…34, 9, 543-548 (2011) stores potential energy in both intra-and extracellular structures. 26,27 This stored energy is then released during diastolic untwisting and contributes to the formation of an intraventricular suction gradient that facilitates LV inflow. 28 -30 Numerous studies have suggested that LV Tor adaptively changes in response to ventricular loading conditions.…”