Effects of chronic supraventricular pacing tachycardia on relaxation rate in isolated cardiac muscle cells

Chronic supraventricular pacing tachycardia (SVT) causes abnormalities in both ventricular and cellular relaxation. The mechanisms causing these abnormalities have not been fully determined. To examine two of the possible mechanisms, a decrease in restoring force or an impairment of the intrinsic myocardial relaxation process, cardiocytes were enzymatically isolated from the left ventricle of pigs subjected to left atrial pacing at 240 beats/min for 3 wk and normal control pigs. SVT caused a decrease in the extent of cardiocyte shortening and the velocity of cardiocyte lengthening. To determine whether the changes in the relaxation velocity merely reflected a concomitant decrease in the extent of cardiocyte shortening (and a resultant decrease in restoring forces) or, in addition, reflected impairment in intrinsic relaxation properties, the relation between cardiocyte relaxation velocity and cardiocyte shortening extent was examined. There was a direct relation between relaxation velocity and shortening extent in both control and SVT cardiocytes. However, SVT decreased the relaxation velocity at any common extent of shortening and decreased the slope of the direct relation (slope 5.91 in control vs. 3.51 s-1 in SVT, P < 0.05). Therefore, these data suggested that SVT caused a primary impairment in the intrinsic myocardial relaxation process independently of a decrease in restoring force.