Saphenous vein graft and nitric oxide: strategies to prevent graft failure and enhance patency in coronary artery bypass grafting.

Overview

abstract

Nitric oxide (NO) is a central regulator of vascular homeostasis and a key determinant of saphenous vein graft (SVG) outcomes in coronary artery bypass grafting (CABG). Endothelial dysfunction, driven by altered shear stress, oxidative stress, and cardiovascular risk factors, impairs NO production and release, contributing to SVG thrombosis, intimal hyperplasia, and atherosclerosis. SVG harvesting technique, storage, and intraoperative handling affects endothelial integrity, inflammatory response, and vascular remodeling, influencing arterialization, long-term patency, and clinical outcomes. Preservation of perivascular adipose tissue (PVAT) during vein harvesting enhances NO bioavailability, reduces inflammation and oxidative stress, and supports graft adaptation. Internal thoracic artery (ITA) grafts provide durable patency, survival benefit, and NO-mediated vasoprotection, improving SVG function and mitigating maladaptive remodeling. Graft configuration further determines SVG adaptation. ITA-composite SVGs confer continuous NO exposure, promote arterial-like remodeling, and attenuate low shear stress. Optimal secondary prevention, including antiplatelet therapy, statins and lifestyle modifications further preserves endothelial function and reduces SVG failure. Targeting NO through surgical technique, graft configuration, and pharmacologic intervention represents a unifying strategy to enhance SVG performance, arterialization, and long-term outcomes, addressing the current limitation of SVG in CABG.