Smoking increased death risk after CABG nearly 3-fold (HR 2.87), while exercise reduced risk of HF (HR 0.85) and death (HR 0.83); glycemic control and genetics also predicted outcomes.
Do clinical, lifestyle, and genetic risk factors predict long-term outcomes (MI, PCI, HF, and death) in patients after coronary artery bypass grafting?
Impaired glycemic control, systemic inflammation, elevated Lp(a), genetic factors, and smoking are significant predictors of worse long-term outcomes after CABG, highlighting the need for aggressive, multifactorial secondary prevention.
Absolute Event Rate: 0% vs 0%
Abstract Background Despite advances in surgical techniques and perioperative management, long-term outcomes following coronary artery bypass grafting (CABG) remain high with increased risk of myocardial infarction (MI), percutaneous coronary intervention (PCI), heart failure (HF), and death. Multiple clinical, lifestyle, and genetic risk factors drive the risk of coronary artery disease (CAD), but their relative impact on long-term outcomes after CABG remains poorly understood. Purpose This study investigates the association of clinical, lifestyle, and genetic risk factors with four major adverse outcomes following CABG. Methods A total of 11,625 patients who underwent CABG and had available clinical, lifestyle, and genetic data were included from the UK Biobank. The incidence of four outcomes occurring after CABG (MI, PCI, HF, and all-cause mortality) was identified through linked hospital records, procedural codes, and mortality registries. The association of multiple clinical, genetic, and lifestyle factors with these outcomes were evaluated using Cox proportional hazards models. Results Among 11,625 CABG patients (at mean age 62.41±9.35 years, 83.2% male), the median follow-up was 9.25 (IQR: 3.64–15.64) years. The incidence of MI was 12.7% (n=1,481), PCI 11.21% (n=1,303), HF 17.1% (n=1,986), and all-cause mortality 19.9% (n=2,317). Older age at CABG was associated with higher risk of MI, HF, and death, and lower risk of PCI; and there were no differences by sex (Fig 1). When evaluating clinical risk factors, type 2 diabetes was associated with death (HR 1.49, 95% CI 1.22-1.81); HbA1c was associated with MI (HR/SD 1.13, 95% CI 1.04-1.22), HF (HR/SD 1.20, 95% CI 1.13-1.29) and death (HR/SD 1.23, 95% CI 1.15-1.30); BMI was associated with HF (HR/SD 1.25, 95% CI 1.16-1.35) and death (HR/SD 1.11, 95% CI 1.03-1.20); Lp(a) was associated with PCI (HR/SD 1.24, 95% CI 1.13-1.35) and HF (HR/SD 1.10, 95% CI 1.02-1.18) (Fig 2A). Elevated hsCRP was associated with increased risk of HF (HR/SD 1.16, 95% CI 1.07-1.24) and death (HR/SD 1.19, 95% CI 1.12-1.27). CAD polygenic risk score (PRS) was associated with PCI (HR/SD 1.12, 95% CI 1.03-1.23) (Fig 2B), and presence of large clonal haematopoiesis of indeterminate potential (CHIP) was associated with HF (HR 1.45, 95% CI 1.04-2.03) and death (HR 1.52, 95% CI 1.16-1.99). Among lifestyle factors, smoking was the strongest predictor of poor outcomes (HR of 1.33 for MI, 1.80 for HF, and 2.87 for death), and exercise was protective for HF and death (HR 0.85 and 0.83, respectively). Conclusion Impaired glycaemic control, systemic inflammation, elevated Lp(a), and genetic factors were key predictors of worse long-term outcomes after CABG. Smoking was the most significant lifestyle factor, while exercise conferred protection. These findings highlight the importance of a multifactorial approach to post-CABG risk assessment and may help guide secondary prevention strategies.
Lambermont et al. (Sat,) reported a other. Smoking increased death risk after CABG nearly 3-fold (HR 2.87), while exercise reduced risk of HF (HR 0.85) and death (HR 0.83); glycemic control and genetics also predicted outcomes.