While present in many patients with heart failure and a normal ejection fraction the role of isolated impairments in active myocardial relaxation in the genesis of elevated filling pressures is not well characterized. Due to difficulties in determining the effect of prolonged myocardial relaxation in vivo, we used a cardiovascular simulated computer model. The effect of myocardial relaxation as assessed by tau (exponential time constant of relaxation) on pulmonary vein pressure (PVP) and left ventricular end diastolic pressure (LVEDP) was investigated over wide range of tau values (20-100msec) and heart rate (60-140bpm) while keeping end diastolic volume constant. Cardiac output (CO) was recorded over wide range of tau and heart rate while keeping PVP constant. The effect of systolic intervals was investigated by changing time to end systole at the same heart rate. At heart rate of 60bpm increases in tau form baseline value to extreme value of 100msec cause only minor increase in PVP of 3mmHg. In contrast at 120bpm the same increase in tau increase PVP by 23mmHg. Increase in filling pressures at high heart rates was attributable to incomplete relaxation. PVP-LVEDP gradient was not constant and increased with increasing tau and heart rate. Prolonged systolic intervals augmented the effects of tau on PVP. Impaired myocardial relaxation is an important determinate of PVP and cardiac output only during rapid heart rate and especially when combine with prolonged systolic intervals. These findings clarify the role of myocardial relaxation in the pathogenesis of elevated filling pressures characteristic of heart failure.