Improvement of cardiac performance by intravenous infusion of l-arginine in patients with moderate congestive heart failure

Objectives. The aim of this study was to evaluate the hemodynamic effect of l-arginine infusion in patients with congestive heart failure. Background. Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from l-arginine. Our hypothesis was that administration of l-arginine in patients with congestive heart failure may increase nitric oxide production and have beneficial hemodynamic effect. Methods. Twelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction <35%) were given 20 g of l-arginine by intravenous infusion over 1 h at constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated. Results. One hour of infusion of l-arginine resulted in significant increase in stroke volume (from 68 ± 18 ml to 76 ± 23 ml [mean ± SD], p = 0.014) and cardiac output (from 4.07 ± 1.22 liters/min to 4.7 ± 1.42 liters/min, p = 0.006) without change in heart rate. Mean arterial blood pressure decreased (from 102 ± 11 mm Hg to 89 ± 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of l-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during l-arginine administration (from 13.28 ± 0.42 ml/min to 29.97 ± 1.09 ml/min, p < 0.001). Conclusions. Infusion of l-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting beneficial hemodynamic and possibly therapeutic profile.