The axisymmetric model described represents myocardial tissue as a spongy anisotropic viscoelastic material. It includes torsion around the axis of symmetry of the ventricle, transmural variation of fiber angle, and redistribution of intracoronary blood in the myocardial wall. In simulations, end-systolic principal strains were equal to 0.45, -0.01, and -0.24 at two-thirds of the wall thickness from the epicardium and 0.26, 0.00, and -0.19 at one-third of the wall thickness from the epicardium. The direction of maximal shortening varied by less than 30 degrees from epicardium to endocardium, whereas fiber direction varied by greater than 100 degrees from epicardium to endocardium. During a normal cardiac cycle peak, equatorial intramyocardial pressure differed by less than 5% from peak intraventricular pressure. When redistribution of intracoronary blood in the ventricular wall was suppressed, peak equatorial intramyocardial pressure was found to exceed peak intraventricular pressure by greater than 30%. Simulated contraction of an unloaded left ventricle (left ventricular pressure = 0 kPa) produced similar magnitude for systolic intramyocardial pressures as the normal cardiac cycle. Transmural systolic fiber stress distribution was very sensitive to the chosen transmural fiber angle distribution.