Abstract
The ischemic insult due to experimental embolization of coronary artery has consistently resulted in a depression of the ventricular function manifested by the conventional hemodynamic variables. In those animals which survived the initial catastrophy, circulatory manifestation of the myocardial failure could be no more seen in these standard parameters, which were considered to allow assessment of the pump action of the loading heart but not the intrinsic property of muscle mechanics. Application of force-velocity relation to ischemic heart disease has been criticized for the series elastic modulus is assumed to differ in those hearts with structural alterations. However, on the basis of the proof in the literature that the active stiffness cannot be affected in the subacute stage of myocardial infarction15. Velocity of the contractile element (Vce) was calculated using the same coefficient of series elasticity for four weeks after the embolization. Vmax determined by extrapolation of stress-velocity curve to zero stress offered constant evidence of impaired myocardial function, and good correlation was observed between the morphological alteration and the decrement of the value of Vmax in observation at four week interval. Consequently, Vmax can be regarded as one which directly expresses a contractile state of the myocardium in quantitative terms.
