Author + information
- Received January 24, 1995
- Revision received June 1, 1995
- Accepted June 7, 1995
- Published online November 1, 1995.
- Bella Koifman, MD,
- Yoram Wollman, PhD,
- Natalie Bogomolny, MD,
- Tamara Chernichowsky, MSc,
- Ariel Finkelstein, MD,
- Gary Peer, MD,
- Jack Scherez, BSc,
- Miriam Blum, MD,
- Shlomo Laniado, MD,
- Adrian Iaina, MD and
- Gad Keren, MD, FACC*
- ↵*Address for correspondence:Dr. Gad Keren, Department of Cardiology, Tel Aviv Medical Center, 6 Weizman Street, Tel Aviv. Israel. 64239.
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 a 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 a 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 a 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 a 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/NO3increased 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 a beneficial hemodynamic and possibly therapeutic profile.
This study was supported in part by Grant 3150 from the Israel Ministry of Health, Jerusalem, Israel.
- Received January 24, 1995.
- Revision received June 1, 1995.
- Accepted June 7, 1995.
- American College of Cardiology