Comparative impact of local and systemic inflammation on vessel-oriented outcomes following PCI in coronary artery disease
Z Ye, K DouAbstract
Background
Inflammation influences outcomes after percutaneous coronary intervention (PCI). However, the relative impact of local coronary inflammation versus systemic inflammation on vessel-oriented outcomes remains unclear. This study aimed to compare their prognostic value for vessel-oriented composite endpoints (VOCE) in patients with coronary artery disease (CAD) undergoing PCI.
Methods
In 2,075 CAD patients undergoing PCI with pre-procedural coronary CT angiography, pericoronary fat attenuation index (FAI) in major coronary vessels were quantified. Systemic inflammation was evaluated by high-sensitivity CRP (hs-CRP). Multivariable Cox analyses, restricted cubic splines, Kaplan–Meier analyses were used. Subgroup analyses were conducted. VOCE was analyzed including vessel-related cardiac death, vessel-related myocardial infarction (nonprocedural) and targeted vessel revascularization (TVR).
Results
Over median 3 years follow-up, 126 target vessels (4.9%) experienced VOCE. After multivariable adjustment, local inflammation (FAI-LAD, FAI-LCX, FAI-RCA, FAI-MAX, FAI-MEAN, FAI-MIN) was independently associated with VOCE. XGBoost identified FAI-MAX as the most important local predictor (SHAP value 1.44 for VOCE). Patients with combined high local (FAI-MAX ≥-70.00HU) and high systemic inflammation had the highest risk (VOCE: HR 4.23, 95% CI 2.44-7.33; both P<0.001). Notably, high local inflammation with low systemic inflammation conferred greater risk than low local with high systemic inflammation for VOCE (FAI-targeted for HR 1.66 vs. 1.20). Integration of FAI with hs-CRP significantly improved prognostic prediction over either marker alone (AUC 0.711 for FAI-MAX + hs-CRP vs. 0.589 for hs-CRP alone, DeLong P<0.05).
Conclusion
In CAD patients after PCI, local coronary inflammation (FAI-MAX and FAI-targeted) may demonstrate a stronger and more direct association with adverse outcomes than systemic inflammation. Integrating both improves risk stratification, supporting inflammation-guided management in CAD.