Oral L-arginine in patients with coronary artery disease on medical management

Background-Vascular nitric oxide (NO) bioavailability is reduced in patient s with coronary artery disease (CAD). We investigated whether oral L-argini ne, the substrate for NO synthesis, improves homeostatic functions of the v ascular endothelium in patients maintained on appropriate medical therapy a nd thus might be useful as adjunctive therapy. Methods and Results-Thirty CAD patients (29 men; age, 67+/-8 years) on appr opriate medical management were randomly assigned to L-arginine (9 g) or pl acebo daily for 1 month, with crossover to the alternate therapy after 1 mo nth off therapy, in a double-blind study. Nitrogen oxides in serum las an i ndex of endothelial NO release), flow-mediated brachial artery dilation las an index of vascular NO bioactivity), and serum cell adhesion molecules la s an index of NO-regulated markers of inflammation) were measured at the en d of each treatment period. L-Arginine significantly increased arginine lev els in plasma (130+/-53 versus 70+17 mu mol/L, P<0.001) compared with place bo. However, there was no effect of L-arginine on nitrogen oxides (19.3+/-7 .9 versus 18.6+/-6.7 mu mol/L, P=0.546), on flow-mediated dilation of the b rachial artery (11.9+/-6.3% versus 11.4+/-7.9%, P=0.742), or on the cell ad hesion molecules E-selectin (47.8+/-15.2 versus 47.2+/-14.4 ng/mL, P=0.601) , intercellular adhesion molecule-1 (250+/-57 versus 249+/-57 ng/mL, P=0.86 2), and vascular cell adhesion molecule-1 (567+/-124 versus 574+/-135 ng/mL , P=0.473). Conclusions-Oral L-arginine therapy does not improve NO bioavailability in CAD patients on appropriate medical management and thus may not benefit thi s group of patients.