Effects of hydralazine on pressure-volume and stress-volume relations in congestive heart failure secondary to idiopathic dilated cardiomyopathy

Abstract

The mechanism by which hydralazine improves cardiac function in patients with heart failure is not well characterized. Hydralazine may improve left ventricular (LV) function by decreasing afterloading wall stress or by increasing myocardial contractility. The effect of intravenous hydralazine was assessed in 8 patients with severe idiopathic dilated cardiomyopathy. Hydralazine increased stroke volume index (from 24 ± 8 to 40 ± 9 ml/m 2, p < 0.01) and decreased systemic vascular resistance (from 1,603 ± 619 to 810 ± 317 dynes s cm −5, p < 0.01) and peak LV wall stress (from 476 ± 118 to 410 ± 68 kdynes/cm 2, p = 0.02). Two groups were defined by normal or high LV wall stress. Patients with high LV stress had higher LV end-diastolic pressure (38 ± 12 vs 17 ± 8 mm Hg, p < 0.01), LV end-diastolic volume index (184 ± 24 vs 149 ± 7 ml/m 2, p < 0.01) and systemic vascular resistance (1,423 ± 686 vs 846 ± 293 dynes s cm −5, p = 0.01). Hydralazine decreased stress more in these patients (−101 ± 57 vs −6 ± 9 kdynes/cm 2, p = 0.02), LV end-diastolic pressure (−12 ± 7 vs 2 ± 2 mm Hg, p = 0.02), systolic pressure (−15 ± 13 vs 3 ± 4 mm Hg, p = 0.03) and systemic vascular resistance (−1,053 ± 247 vs −363 ± 83 dynes s cm −5, p < 0.01) than in patients with normal LV stress. Decreased LV stress was caused by decreased systolic and diastolic pressures and/or volumes. Late systolic pressure-volume relations in patients with normal LV stress suggested increased myocardial contractility, but this was not confirmed by LV dP/dt. Hydralazine improves LV function in patients with dilated cardiomyopathy by reducing elevated LV wall stress, with little inotropic effect.