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(Circulation. 2008;118:713-721.)
© 2008 American Heart Association, Inc.

Heart Failure

Heterogeneity of Left Ventricular Wall Thickening Mechanisms

Allen Cheng, MD; Tom C. Nguyen, MD; Marcin Malinowski, MD; George T. Daughters, MS; D. Craig Miller, MD; Neil B. Ingels, Jr, PhD

From the Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford (A.C., T.C.N., M.M., G.T.D., D.C.M., N.B.I.), and the Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto (G.T.D., N.B.I.), Calif.

Correspondence to Neil B. Ingels, Jr, PhD, Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, 795 El Camino Real (Ames Bldg), Palo Alto, CA 94301. E-mail ingels{at}stanford.edu

Received October 9, 2007; accepted June 6, 2008.

Background— Myocardial fibers are grouped into lamina (or sheets) 3 to 4 cells thick. Fiber shortening produces systolic left ventricular (LV) wall thickening primarily by laminar extension, thickening, and shear, but the regional variability and transmural distribution of these 3 mechanisms are incompletely understood.

Methods and Results— Nine sheep had transmural radiopaque markers inserted into the anterior basal and lateral equatorial LV. Four-dimensional marker dynamics were studied with biplane videofluoroscopy to measure circumferential, longitudinal, and radial systolic strains in the epicardium, midwall, and endocardium. Fiber and sheet angles from quantitative histology allowed transformation of these strains into transmural contributions of sheet extension, thickening, and shear to systolic wall thickening. At all depths, systolic wall thickening in the anterior basal region was 1.6 to 1.9 times that in the lateral equatorial region. Interestingly, however, systolic fiber shortening was identical at each transmural depth in these regions. Endocardial anterior basal sheet thickening was >2 times greater than in the lateral equatorial region (epicardium, 0.16±0.15 versus 0.03±0.06; endocardium, 0.45±0.40 versus 0.17±0.09). Midwall sheet extension was >2 times that in the lateral wall (0.22±0.12 versus 0.09±0.06). Epicardial and midwall sheet shears in the anterior wall were 2 times higher than in the lateral wall (epicardium, 0.14±0.07 versus 0.05±0.03; midwall, 0.21±0.12 versus 0.12±0.06).

Conclusions— These data demonstrate fundamentally different regional contributions of laminar mechanisms for amplifying fiber shortening to systolic wall thickening. Systolic fiber shortening was identical at each transmural depth in both the anterior and lateral LV sites. However, systolic wall thickening of the anterior site was much greater than that of the lateral site. Fiber shortening drives systolic wall thickening, but sheet dynamics and orientations are of great importance to systolic wall thickening. LV wall thickening and its clinical implications pivot on different wall thickening mechanisms in various LV regions. Attempts to implant healthy contractile cells into diseased hearts or to surgically manipulate LV geometry need to take into account not only cardiomyocyte contraction but also transmural LV intercellular architecture and geometry.

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CLINICAL PERSPECTIVE

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