Local vs systemic inflammation and outcomes after percutaneous coronary intervention

BACKGROUND AND AIMS: Inflammation influences outcomes after percutaneous coronary intervention (PCI) in coronary artery disease (CAD). This study aimed to evaluate the relative and combined prognostic value of local coronary inflammation, and systemic inflammation for adverse outcomes. METHODS: In a prospective cohort of 1,987 patients with CAD undergoing PCI, local inflammation, quantified by the pericoronary fat attenuation index (FAI), and systemic inflammation, measured by high-sensitivity C-reactive protein (hs-CRP), were assessed. The patient-level primary endpoint was major adverse cardiovascular events (MACE) including all-cause mortality, non-fatal myocardial infarction, and unplanned repeat revascularization. The vessel-level endpoint was the vessel-oriented composite endpoint (VOCE). RESULTS: Over a median 3-year follow-up, 164 patients (8.3%) experienced MACE and 118 of 2,436 vessels (4.8%) experienced VOCE. Extreme Gradient Boosting with SHAP analysis ranked FAI-MAX as the most important local inflammatory feature for both MACE and VOCE. High FAI-MAX (? -70 HU) was strongly associated with MACE (HR 3.25, 95% CI 2.29-4.61) and VOCE (HR 3.15, 95% CI 2.06-4.82). Patients with high FAI-MAX and elevated hs-CRP had the highest risk (MACE HR 4.00, 95% CI 2.47-6.32; VOCE HR 4.15, 95% CI 2.37-7.25). High local inflammation with low systemic inflammation conferred substantially greater risk than the converse phenotype (MACE HR 2.88, 95% CI 1.85-4.49 vs 1.09, 95% CI 0.55-1.85; VOCE HR 2.64, 95% CI 1.55-4.50 vs 1.08, 95% CI 0.55-2.13). Addition of both markers significantly improved model discrimination compared with either alone (DeLong P < 0.05). In sensitivity analysis excluding revascularization, the advantage of isolated high FAI-MAX was attenuated, while the dual-high phenotype remained significant. CONCLUSIONS: Local coronary inflammation shows a stronger association with adverse outcomes after PCI than systemic inflammation. Integrating both markers improves risk stratification and may support inflammation-guided management in patients with CAD.