Background: Stimulated endothelium-derived relaxing factor-mediated vasodilation and conduit artery distensibility are impaired in congestive heart failure (CHF). L-arginine could have a potentially beneficial role in CHF, acting through the nitric oxide (NO)-L-arginine pathway or by growth hormone increment.
Hypothesis: This study was undertaken to investigate the effects of L-arginine on heart rate, hemodynamics, and left ventricular (LV) function in CHF.
Methods: In seven patients (aged 39 +/- 8 years) with CHF, we obtained the following parameters using echocardiography and an LV Millar Mikro-Tip catheter simultaneously under four conditions: basal, during NO inhalation (40 ppm), in basal condition before L-arginine infusion, and after L-arginine intravenous infusion (mean dose 30.4 +/- 1.9 g).
Results: Nitric oxide inhalation increased pulmonary capillary wedge pressure from 25 +/- 9 to 31 +/- 7 mmHg (p < 0.05), but did not change echocardiographic variables or LV contractility by elastance determination. L-arginine decreased heart rate (from 88 +/- 15 to 80 +/- 16 beats/min, p<0.005), mean systemic arterial pressure (from 84 +/- 17 to 70 +/- 18 mmHg, p < 0.007), and systemic vascular resistance (from 24 +/- 8 to 15 +/- 6 Wood units, p<0.003). L-arginine increased right atrial pressure (from 7 +/- 2 to 10 +/- 3 mmHg, p<0.04), cardiac output (from 3.4 +/- 0.7 to 4.1 +/- 0.8 l/min, p < 0.009), and stroke volume (from 40 +/- 9 to 54 +/- 14 ml, p < 0.008). The ratios of pulmonary vascular resistance to systemic vascular resistance at baseline and during NO inhalation were 0.09 and 0.075, respectively, and with L-arginine this increased from 0.09 to 0.12.
Conclusion: L-arginine exerted no effect on contractility; however, by acting on systemic vascular resistance it improved cardiac performance. L-arginine showed a negative chronotropic effect. The possible beneficial effect of L-arginine on reversing endothelial dysfunction in CHF without changing LV contractility should be the subject of further investigations.