The present study was designed to investigate the anisotropy of systolic chord shortening in the lateral, inferior, septal, and anterior regions of the human left ventricle. At the time of surgery, 12 miniature radlopaque markers were implanted into the left ventricular midwall of the donor heart in 15 cardiac transplant recipients. Postoperative biplane cineradiograms were computer-analyzed to yield the three-dimensional coordinates of these markers at 16.7-msec intervals. In each of the four left ventricular regions, chords were constructed from a central marker to outlying markers, and the percent systolic shortening of each chord was calculated. In each region, chord angles were measured with respect to the circumferential direction (positive angles counterclockwise) and each chord was assigned to one of four angular groups: I. oblique, -45±22.5° or 135±22.5°; II. circumferential, 0±22.5° or 180±22.5°; III. oblique, 45±22.5° or -135±22.5°; or IV. longitudinal, 90±22.5° or -90±22.5°. In the lateral, inferior, and septal regions, respectively, systolic shortening (mean± SD percent;) was significantly greater in Group I chords (19±5percent;, 17±5percent;, and 15±4percent;) than those in Group II (15±5percent;, 12±4percent;, and 11±4percent;), Group III (12±4percent;, 12±5percent;, and 11±4percent;), or Group IV (13±5percent;, 13±6percent;, and 12±5percent;). The anterior region was unique hi exhibiting equal shortening in both Group I and Group n chords (16±5percent;), although the shortening of these chords was significantly greater than that of Group III and Group IV (12±5percent;) in this region. A cylindrical mathematical model was developed to relate longitudinal, circumferential, and oblique systolic shortening to torsional deformation about the long axis of the left ventricle. Torsional deformations measured in these 15 hearts were of sufficient magnitude and correct sense to agree with model predictions. These data suggest that torsional deformations of the left ventricle are of fundamental importance in Unking the one-dimensional contraction of the helically wound myocytes to the three-dimensional anisotropic systolic shortening encountered in the transplanted human heart.