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TRANSMURAL DEFORMATION

TRANSMURAL DEFORMATION
透壁变形
批准号:
3343950
负责人:
JAMES W COVELL
金额:
$19.27万
依托单位国家:
美国
项目类别:
财政年份:
1984
资助国家:
美国
项目状态:
已结题
起止时间:
1984-07-01 至 1990-06-30

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中文摘要
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英文摘要
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.
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