Reduced cytokines release and myocardial damage in coronary artery bypass patients due to L-arginine cardioplegia supplementation.

Abstract

Recently, L-arginine has been added to cardioplegia to limit myocardial ischemic damage. The mechanism of action is related to the production of nitric oxide, with vasodilatation and reduction of endothelial dysfunction. Our prospective randomized study on coronary artery bypass patients investigates the effect of L-arginine on myocardial stress as expressed by myocardial cytokines release and myocardial ischemia in terms of troponin T concentration. Coronary artery surgery patients were randomly assigned to receive 7.5 g L-arginine in 500 mL of cardioplegic solution (group A). Group B was used as control. Cold blood 4:1 anterograde and retrograde cardioplegia with warm induction was administered. Blood samples were collected from the retrograde coronary sinus catheter to determine interleukin-2 receptor, interleukin-6, and tumor necrosis factor levels. Serum samples at different time points were also analyzed to measure myocardial ischemia markers. Hemodynamic and echocardiographic evaluations were obtained perioperatively. Sixty-five patients were enrolled (group A, treated with L-arginine, n = 33; group B, control, n = 32). Wedge pressure and intensive care unit stay were significantly reduced in group A (p = 0.023 and p = 0.03, respectively). Cytokines levels were lower in group A, with a significance for interleukin-6 (p = 0.026); troponin T was reduced in treated patients (0.33 versus 0.57 ng/mL at 18 hours: p = 0.009). Coronary artery surgery patients benefit from L-arginine cardioplegia supplementation in terms of reduced inflammatory reaction, limitation of myocardial ischemia, and better hemodynamic performance. Moreover, a clinical advantage is evident in terms of a shorter intensive care unit stay in patients treated with L-arginine.