Abstract
Acute interventions may shift the left ventricular diastolic pressure-volume curve in man, but the mechanism is unclear. Methoxamine hydrochloride was given to 7 patients without coronary disease to raise mean arterial pressure 25-35 mmHg. High fidelity left ventricular pressures were recorded simultaneously with single plane cineventriculography and pressure-volume curves were constructed before and during methoxamine infusion. Methoxamine significantly increased left ventricular end-diastolic pressure (12 .+-. 1 vs. 25 .+-. 1 mmHg), left ventricular minimal diastolic pressure (6 .+-. 1 vs. 15 .+-. 2 mmHg), right atrial pressure (5 .+-. 1 vs. 9 .+-. 1 mmHg), left ventricular end-diastolic volume (185 .+-. 32 vs. 207 .+-. 37 ml), left ventricular end-systolic volume (72 .+-. 19 vs. 93 .+-. 25 ml) and left ventricular mass (168 .+-. 17 vs. 187 .+-. 18 g), while left ventricular wall thickness changed little (8.5 .+-. 0.6 vs. 8.7 .+-. 0.5 mm). In each patient the diastolic pressure-volume curve was shifted upward and left ventricular pressure was higher for any given volume with methoxamine. Serial ventriculograms in 5 subjects who did not receive methoxamine showed no shift. Since methoxamine has no effect on the myocardium and since the subjects had no evidence of left ventricular ischemia, it is unlikely that the changes in the pressure-volume curve are caused by intrinsic changes in myocardial properties. Viscous properties cannot solely account for the observations, since the diastolic filling rate was altered only in the first 1/3 of diastole. The increase in left ventricular wall mass suggests that acute increases in systemic arterial pressure may augument left ventricular stiffness by coronary vascular engorgement and an erectile effect on the myocardium. Pericardial restriction and changes in right ventricular loading may contribute to acute shifts in the left ventricular diastolic pressure-volume curve.