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The prognosis for patients with acute type B aortic dissection is bleak and determined primarily by dissection-related and patient-specific risk factors, which do not appear to be readily modifiable.

Background— Better understanding of the precise 3-dimensional geometric changes of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation (CIMR) is needed in order to devise better surgical repair techniques. We hypothesized that changes after inferior myocardial infarction would be different in hearts that developed CIMR compared with those that did not. Methods and Results— Twenty-four sheep underwent coronary snare and marker placement (annulus, papillary muscles, and anterior and posterior leaflets). After 8 days, cinefluoroscopy provided 3-dimensional marker data, and snare occlusion of obtuse marginal branches created inferior myocardial infarction, including the posterior papillary muscle. After 7 weeks, the 16 surviving animals were studied again and grouped by mitral regurgitation grade (≥ 2+, n=10 versus ≤ 1+, n=6). End-systolic mitral annulus dimensions, components of papillary muscle and leaflet displacement, were calculated. After inferior myocardial infarction, total displacement of the posterior papillary muscle from the midseptal annulus (“saddle horn”) was greater in CIMR(+) animals: 6.5±3.2 versus 3.1±2.7 ( P =0.02), with the posterior papillary muscle moving more laterally (6.8±3.4 versus 2.5±3.5 mm, P =0.01). Increase in mitral annular septal-lateral diameter was greater in animals with CIMR (4.9±2.7 versus 2.3±2.0, P =0.02), and apical displacement of the posterior leaflet (PL) margin was also greater in the CIMR(+) group (1.7±1.0 versus 0.3±0.5, P =0.01). Conclusions— The CIMR(+) group had greater septal-lateral annular dilatation, lateral posterior papillary muscle displacement, and apical PL restriction, indicating that these associated geometric alterations may be important in the pathogenesis of CIMR. Treatment of CIMR should address both annular septal-lateral dilatation and lateral displacement of the posterior papillary muscle.

Laminar, or sheet, architecture of the left ventricle (LV) is a structural basis for normal systolic and diastolic LV dynamics, but transmural sheet orientations remain incompletely characterized. We directly measured the transmural distribution of sheet angles in the ovine anterolateral LV wall. Ten Dorsett-hybrid sheep hearts were perfusion fixed in situ with 5% buffered glutaraldehyde at end diastole and stored in 10% formalin. Transmural blocks of myocardial tissue were excised, with the edges cut parallel to local circumferential, longitudinal, and radial axes, and sliced into 1-mm-thick sections parallel to the epicardial tangent plane from epicardium to endocardium. Mean fiber directions were determined in each section from five measurements of fiber angles. Each section was then cut transverse to the fiber direction, and five sheet angles (β) were measured and averaged. Mean fiber angles progressed nearly linearly from −41° (SD 11) at the epicardium to +42° (SD 16) at the endocardium. Two families of sheets were identified at approximately +45° (β + ) and −45° (β − ). In the lateral region (n = 5), near the epicardium, sheets belonged to the β + family; in the midwall, to the β − family; and near the endocardium, to the β + family. This pattern was reversed in the basal anterior region (n = 4). Sheets were uniformly β − over the anterior papillary muscle (n = 2). These direct measurements of sheet angles reveal, for the first time, alternating transmural families of predominant sheet angles. This may have important implications in understanding wall mechanics in the normal and the failing heart. Keywords cardiac microstructure; sheets LEFT VENTRICULAR (LV) myofibers are connected by an extensive extracellular collagen matrix (3) to form myolaminar "sheets," two-to-four cells thick, which are also interconnected Copyright © 2005 by a collagen network (16). This sheet architecture has been proposed as an anatomic basis for myofiber rearrangement throughout the cardiac cycle (17,22), and sheet deformation is thought to underlie LV mechanics during contraction (6) and relaxation (2).The three-dimensional geometry of fibers and sheets is critical. Maximum contraction of fibers that lie in planes tangent to the epicardial surface is only 15% along their long axis (21); yet LV ejection fractions of 60% and systolic radial wall thickening of 40% are typically observed. The helical arrangement of the fibers may account for some of this disparity (20), but an additional important mechanism appears to be sheet deformation (19,22). Laminar shear, extension, and thinning or thickening are thought to contribute to wall thickness changes (6,7,24).Fiber orientation, which can be measured directly, has been found in several species to vary from approximately −60° at the epicardium to +60° at the endocardium (4,10,12,14,23,28). Until recently, however, sheet orientation could only be inferred indirectly from the directions of fiber and cleavage planes from three orthogonal views (6). Recently, our group and Ashi...

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