Explains the physiological basis for vasodilator therapy in heart failure, highlighting the inverse relationship between afterload and myocardial fiber shortening.
Experiments on isolated cardiac tissue have established that myocardial-fiber shortening is dependent on three factors: the preload, which determines the muscle fiber's end-diastolic length; the contractile or inotropic state of the myocardium; and the afterload (i.e., the myocardial systolic tension). At any level of the contractile state and preload, the extent of shortening varies inversely with the afterload: when afterload is progressively raised, an increasing proportion of the muscle's contractile activity is expended in the generation of tension, and a smaller fraction is expended in fiber shortening. Although the geometric arrangement of myocardial fibers is far more complex in the . . .
Eugene Braunwald (Thu,) studied this question.