Afterload, activation sequence, inotropism, and extent of shortening affect the time constant (T) of left ventricular (LV) isovolumic pressure decay, yet it is unknown if they modify peak lengthening velocity of the LV minor axis [(dD/dt)/D]. Accordingly, we studied their effects on (dD/dt)/D, measured by sonomicrometry, in nine anesthetized open-chest dogs during atrial pacing at 2 Hz. Afterload was increased 20-40 mmHg by 1) constricting the ascending aorta and 2) occluding the descending aorta for four beats. Activation was altered by right ventricular pacing. These interventions, plus constriction of venae cavae, were studied during four inotropic states. Aortic stenosis increased (dD/dt)/D (P less than 0.05), whereas occlusion of the descending aorta, vena caval constriction, and right ventricular pacing decreased (dD/dt)/D (P less than 0.05). Left atrial pressure was constant except during vena caval constriction. Alterations in inotropic state modified (dD/dt)/D (P less than 0.001). Extent of shortening and (dD/dt)/D were directly related (r = 0.80, P less than 0.001). Changes in (dD/dt)/D and T were inversely related (r = 0.70, P less than 0.001), and alterations in the interval from -dP/dtpeak to the end of rapid filling were directly related to changes in T (r = 0.75, P less than 0.001). We conclude that (dD/dt)/D can be modified by systolic and diastolic load perturbations, activation sequence, and inotropic interventions. These effects relate to changes in extent of shortening, time course of inactivation, or both.