Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion

The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37°C) ischemic arrest, isovolumic developed pressure, and dP/dt(max) during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (P(ed)) increased 37.0 ± 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27°C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (~ 100% of control), less elevation of P(ed) (21.4 ± 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.