Joint association of high-sensitivity C-reactive protein–triglyceride glucose index and coronary artery calcification with adverse outcomes in patients with coronary artery disease: a large-scale cohort study
Song Wen, Zhanyuan Chen, Rui Fu, Lingbing Meng, Bowen Li, Kefei DouBackground
The high-sensitivity C-reactive protein triglyceride glucose index (CTI) integrates metabolic dysregulation and systemic inflammation, whereas moderate-to-severe coronary artery calcification (MSCAC) reflects anatomic atherosclerotic burden. Whether CTI prognostic value varies by MSCAC status and whether these measures interact clinically remains unclear.
Methods
This prospective cohort study included 22 218 patients with angiography‑confirmed coronary artery disease (CAD) enrolled from January 2017 to December 2018, categorized by CTI median (≤9.08 vs. >9.08) and MSCAC presence. CTI was calculated as Ln(fasting glucose [mg/dl] × triglycerides [mg/dl])/2 + Ln(hs‑CRP [mg/L]) × 0.412. The primary endpoint was cardiovascular events; the secondary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE). Restricted cubic spline, Kaplan–Meier, and Cox regression analyses were applied.
Results
Each 1-unit CTI increase was associated with 15% higher cardiovascular event risk [hazard ratio: 1.15, 95% confidence interval (CI): 1.02–1.29] and 9% higher MACCE risk (hazard ratio: 1.09, 95% CI: 1.03–1.15). MSCAC independently conferred a 32% higher risk of cardiovascular events (hazard ratio: 1.32, 95% CI: 1.05–1.67) and 23% higher MACCE risk (hazard ratio: 1.23, 95% CI: 1.10–1.38). Patients with both elevated CTI and MSCAC had 66% increased cardiovascular event risk (hazard ratio: 1.66, 95% CI: 1.20–2.30) and 38% increased MACCE risk (hazard ratio: 1.38, 95% CI: 1.18–1.62) versus neither. No statistically significant additive or multiplicative interaction was detected.
Conclusion
In patients with CAD, elevated CTI and MSCAC independently portend adverse outcomes, and their coexistence identifies a particularly high‑risk phenotype. These findings support the complementary value of metabolic‑inflammatory and anatomic measures in risk stratification.