Arterial compliance is determined by structural factors, such as collagen and elastin, and functional factors, such as vasoactive neurohormones. To determine whether angiotensin II contributes to decreased arterial compliance in patients with heart failure, this study tested the hypothesis that administration of an angiotensin-converting enzyme inhibitor improves arterial compliance. Arterial compliance and stiffness were determined by measuring carotid artery diameter, using high-resolution duplex ultrasonography, and blood pressure in 23 patients with heart failure secondary to idiopathic dilated cardiomyopathy. Measurements were made before and after intravenous administration of enalaprilat (1 mg) or vehicle. Arterial compliance was inversely related to both baseline plasma angiotensin II ( r = −0.52; P = 0.015) and angiotensin-converting enzyme concentrations ( r = −0.45; P = 0.041). During isobaric conditions, enalaprilat increased carotid artery compliance from 3.0 ± 0.4 to 5.0 ± 0.4 × 10−10N−1· m4( P = 0.001) and decreased the carotid artery stiffness index from 17.5 ± 1.8 to 10.1 ± 0.6 units ( P = 0.001), whereas the vehicle had no effect. Thus angiotensin II is associated with reduced carotid arterial compliance in patients with congestive heart failure, and angiotensin-converting enzyme inhibition improves arterial elastic properties. This favorable effect on the pulsatile component of afterload may contribute to the improvement in left ventricular performance that occurs in patients with heart failure treated with angiotensin-converting enzyme inhibitors.
Inhibition of angiotensin converting enzyme with enalapril maleate in infants with congestive heart failure.
