OBJECTIVE Left ventricular (LV) hypertrophy is associated with increased diastolic chamber stiffness early after aortic valve replacement for valve stenosis. Enoximone, a phosphodiesterase III inhibitor, has been shown to improve myocardial contractility and relaxation when administered as a single dose after cardiac surgery. The present study investigated, by analysis of transmitral flow velocity patterns and end-diastolic pressure-area relations, whether enoximone administered before aortic valve surgery has an effect on LV diastolic properties. METHODS Prospective, randomized study. METHODS Referral center for cardiothoracic surgery at a university hospital. METHODS Thirty-four patients undergoing aortic valve replacement for aortic stenosis. METHODS Patients in the enoximone group (n = 17) received a bolus dose of 0.35 mg/kg (0.15 mg/kg before aortic cross-clamping and 0.2 mg/kg added to the cardioplegic solution). Individual pressure-area relations (pulmonary capillary wedge pressure v left ventricular end-diastolic area) were obtained by using volume loading by leg elevation before and after surgery with closed chest. RESULTS The pressure-area relation on the pressure-area plot was shifted to the left after surgery, indicating decreased LV diastolic distensibility in the enoximone and control groups and providing evidence of decreased LV diastolic function. Indices of LV diastolic chamber stiffness, LV operating stiffness (K(LV)) derived from the deceleration time of early ventricular filling, and the constant of chamber stiffness (beta) derived from pressure-area relations were not different after enoximone treatment. Systolic LV function was unaltered after cardiac surgery in both groups. Analysis of changes in transmitral flow patterns identified an increased atrial filling fraction in enoximone-treated patients, suggesting increased atrial systolic function. The unaltered systolic pulmonary venous flow velocity compared with the decrease in the control group after volume loading further supports preservation of left atrial reservoir function with enoximone in the absence of evidence for decreased LV stiffness. CONCLUSIONS Preemptive enoximone did not change LV diastolic function based on diastolic filling patterns or LV stiffness indices (K(LV) and beta) derived from Doppler early filling deceleration time and pressure-area relations. Doppler data suggested improvement of left atrial systolic function and preservation of left atrial reservoir function with enoximone.