Myocardial fiber orientation undergoes an orderly transition from epicardium to endocardium in the left ventricle. In the anterior free wall midwall fibers course in a generally circumferential direction and fibers on the endocardium and epicardium are oriented more longitudinally. At the apex and base, fiber direction changes more rapidly and adjacent valve rings influence local myofiber direction. How fibers at different depths and ventricular sites interact to produce local deformation is not fully understood. It will be the general objective of these studies to define the relationship between fiber direction and local deformation. We have developed a method a measure three- dimensional finite deformations from biplane radiographic images of implanted markers demarcating small volumes of myocardium. Initial studies in the free wall indicate substantial interaction between adjacent fibers, i.e., principal strains increase with depth, significant transverse shear accompanies normal strains, and the orientation of the first principal axis (direction of greatest shortening) varies transmurally much less than fiber direction. Moreover, strain direction can be modified substantially by epicardial activation and may not be colinear with local fiber direction. These findings refute the theory that myocardium deforms as a set of noninteracting nested membranes, each with its own preferred orientation. The magnitudes of the transverse shears and directions of the principal strains observed demand either cellular rearrangements out of the epicardial tangent plane as proposed by Spotnitz or cellular shape changes to account for the deformations and the wall thickening not explained by cell diameter changes occurring during systole. The studies in the present proposal are directed at quantitating the myofiber anatomy can account for the observed transmural deformation and should provide new insight into the mechanism of ventricular wall thickening. Further studies are planned on the effects of chronic increases in loading conditions on transmural deformation.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL032583-06
Application #
3343955
Study Section
Cardiovascular Study Section (CVA)
Project Start
1984-07-01
Project End
1990-06-30
Budget Start
1989-07-01
Budget End
1990-06-30
Support Year
6
Fiscal Year
1989
Total Cost
Indirect Cost
Name
University of California San Diego
Department
Type
Schools of Medicine
DUNS #
077758407
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Howard, Elliot J; Kerckhoffs, Roy C P; Vincent, Kevin P et al. (2013) Myofiber prestretch magnitude determines regional systolic function during ectopic activation in the tachycardia-induced failing canine heart. Am J Physiol Heart Circ Physiol 305:H192-202
Ashikaga, Hiroshi; Omens, Jeffrey H (2012) In vivo validation of longitudinal-circumferential area change ratio to estimate myofiber shortening in the heart. IEEE Trans Biomed Eng 59:1391-7
Chuang, Joyce S; Zemljic-Harpf, Alice; Ross, Robert S et al. (2010) Determination of three-dimensional ventricular strain distributions in gene-targeted mice using tagged MRI. Magn Reson Med 64:1281-8
Kerckhoffs, Roy C P; Omens, Jeffrey H; McCulloch, Andrew D et al. (2010) Ventricular dilation and electrical dyssynchrony synergistically increase regional mechanical nonuniformity but not mechanical dyssynchrony: a computational model. Circ Heart Fail 3:528-36
Raskin, Anna M; Hoshijima, Masahiko; Swanson, Eric et al. (2009) Hypertrophic gene expression induced by chronic stretch of excised mouse heart muscle. Mol Cell Biomech 6:145-59
Ashikaga, Hiroshi; van der Spoel, Tycho I G; Coppola, Benjamin A et al. (2009) Transmural myocardial mechanics during isovolumic contraction. JACC Cardiovasc Imaging 2:202-11
Campbell, Stuart G; Howard, Elliot; Aguado-Sierra, Jazmin et al. (2009) Effect of transmurally heterogeneous myocyte excitation-contraction coupling on canine left ventricular electromechanics. Exp Physiol 94:541-52
Coppola, B A; Omens, J H (2009) Use of Larger Species such as Dog and Pig as Model Systems to Study Cardiac Disease. Drug Discov Today Dis Models 5:195-200
Kerckhoffs, Roy C P; McCulloch, Andrew D; Omens, Jeffrey H et al. (2009) Effects of biventricular pacing and scar size in a computational model of the failing heart with left bundle branch block. Med Image Anal 13:362-9
Coppola, Benjamin A; Omens, Jeffrey H (2008) Role of tissue structure on ventricular wall mechanics. Mol Cell Biomech 5:183-96

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