Abstract

Background: Ambient air pollution is an established cardiovascular risk factor; however, its impact on long-term outcomes after coronary artery bypass grafting (CABG) remains insufficiently defined. We aimed to evaluate whether chronic exposure to air pollutants may influence long-term mortality following surgical revascularization. Methods: In this multicenter retrospective cohort study, 1033 consecutive patients undergoing CABG with BIMA (bilateral internal mammary arteries) grafting were analyzed with a median follow-up of 8.1 years. Individual exposure to nitrogen dioxide (NO2), particulate matter ≤10 μm (PM10), and ≤2.5 μm (PM2.5) was estimated based on residential data. Multivariable Cox proportional hazards models were used to assess associations with long-term mortality. Model performance was evaluated using receiver operating characteristic (ROC) analysis, while incremental prognostic value was quantified using net reclassification improvement (NRI) and integrated discrimination improvement (IDI). Kaplan–Meier analyses were performed using data-driven thresholds and model-based risk stratification. Results: During follow-up, 220 deaths (21.1%) occurred. In multivariable analysis, both NO2 and PM10 were associated with increased mortality (NO2: HR 2.70 per 10 μg/m3, 95% CI 2.03–3.59; PM10: HR 2.73 per 10 μg/m3, 95% CI 1.94–3.83; both p < 0.001), whereas PM2.5 was not significant. The clinical model demonstrated moderate discrimination (AUC 0.73), which improved significantly after inclusion of pollution variables (AUC 0.84; ΔAUC 0.11). Reclassification analysis showed substantial improvement (NRI 0.42, p < 0.001; IDI 0.11, p < 0.001). Kaplan–Meier analysis confirmed enhanced risk stratification, with a hazard ratio of 2.70 for the clinical model and 7.02 for the combined clinical and pollution model (both p < 0.001). Conclusions: In this retrospective cohort of patients undergoing CABG with BIMA grafting, higher long-term residential exposure to NO2 and PM10 was associated with greater all-cause mortality after adjustment for measured clinical and procedural factors. These findings support further investigation of environmental exposure as a prognostic marker in surgically treated coronary disease, pending external validation and more granular control for contextual confounding. These findings suggest that environmental exposure may represent a relevant component of long-term risk stratification, although confirmation in large-volume cohorts is required.

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