Comparison of Isovolumic Relaxation Time and Transmitral Flow Velocities With Time Constant of Isovolumic Relaxation

msec (p=0.04) with a concomitant decrease in IVRT from 74±18 to 38±8 msec (p=0.03). During decreased inotropy (by propranolol infusion) at constant preload, slowing of relaxation was indicated by an increase in T from 40±8 to 51±+13 msec (p=0.02) with a concomitant increase in IVRT from 71±+15 to 83+±21 msec (p<0.05). A significant correlation between changes in and changes in IVRT was found (r=0.66, p<0.001). In contrast, when left ventricular end-diastolic pressure was increased from 7±2 to 24±4 mmHg at constant inotropy, r increased from 47±f14 to 64±25 msec (p=0.03), whereas no change in IVRT was observed (76±+19 and 71±+19 msec, respectively). Aortic pressure was not significantly changed during any intervention, and heart rate was kept constant by pacing. Peak early transmitral velocity was unchanged by propranolol but increased during isoproterenol and saline infusion (p<0.001 and p<0.01, respectively). During volume loading, left atrial V wave pressure was a positive predictor (p=0.002) and r was a negative (p=0.06) predictor of the flow-adjusted transmitral flow velocity. Thus, IVRT reflected r during changing contractility at constant preload, but not during increasing preload. Prolongation of IVRT as a sign of slowing of relaxation during volume loading was counteracted by an earlier opening of the mitral valve caused by increasing atrial pressure, thus leaving IVRT unchanged. (Circulation 1990;81: 260-266)