From Exposure to Outcome: Air Pollution-Induced Oxidative Stress as a Determinant of Early and Late Outcomes After Coronary Artery Bypass Grafting

Coronary artery bypass grafting (CABG) remains one of the most effective treatments for advanced coronary artery disease; however, substantial variability persists in both perioperative and long-term outcomes despite advances in surgical technique, myocardial protection, and risk stratification. Oxidative stress is a central mediator of tissue injury during cardiac surgery, contributing to ischemia–reperfusion injury, endothelial dysfunction, systemic inflammation, and postoperative organ complications. At the same time, chronic exposure to ambient air pollution has emerged as an important environmental determinant of cardiovascular disease through mechanisms that converge on many of the same redox-sensitive pathways. We propose the concept of environmental oxidative priming, whereby long-term exposure to particulate matter, nitrogen oxides, ozone, and other pollutants establishes a persistent state of endothelial dysfunction, mitochondrial impairment, chronic inflammation, nitric oxide depletion, and reduced antioxidant reserve before surgery. Within this framework, CABG represents a second oxidative challenge superimposed on a pre-existing environmentally conditioned phenotype. We discuss the mechanistic overlap between air pollution-induced cardiovascular injury and cardiac surgical stress and examine how this interaction may contribute to postoperative complications, graft adaptation, major adverse cardiovascular events, and long-term survival. Recognition of air pollution as a modifier of biological resilience provides a novel framework for understanding outcome heterogeneity after CABG and may support future precision-based risk stratification and preventive strategies.