Key result
Impaired CYP2C19 metabolism is linked to ~29% higher odds of multi-vessel CAD.
Why the study?
Multi-vessel coronary artery disease confers poor clinical outcomes, and CYP2C19 participates in lipid metabolism and inflammatory regulation, which may relate to variations in coronary lesion severity.
Are CYP2C19 polymorphisms and metabolic comorbidities associated with multi-vessel coronary artery disease in patients with CAD?
Cross-Sectional (n=4,124)
No
Are CYP2C19 polymorphisms and metabolic comorbidities associated with multi-vessel coronary artery disease in patients with CAD?
Odds Ratio: 1.285 (95% CI 1.095–1.508)
p-value: p=0.002
Impaired CYP2C19 metabolic phenotypes and traditional metabolic comorbidities are independently associated with the presence of multi-vessel coronary artery disease, highlighting the role of genetic susceptibility in severe CAD.
CYP2C19 poor metabolizer status may refine multivessel CAD risk stratification; leaves open prospective validation before clinical adoption.
Background: Multi-vessel coronary artery disease (MVCD), defined as stenosis affecting ≥ 2 major coronary arteries, confers poor clinical outcomes in patients with coronary artery disease (CAD). Cytochrome P450 2C19 (CYP2C19) CYP2C19 participates in lipid metabolism and inflammatory regulation, which may be associated with individual variations in the severity of coronary artery lesions. This study aimed to explore the clinical and genetic factors associated with MVCD focusing on CYP2C19 polymorphisms and chronic metabolic diseases. Methods: This single‑center cross‑sectional study enrolled 4124 patients with angiographically confirmed CAD, who were divided into single‑vessel CAD (n=846) and MVCD (n=3278) groups. Baseline clinical data and CYP2C19 genotypes were collected. The chi-square test, Hardy-Weinberg equilibrium test, and logistic regression analyses were performed for statistical evaluation. Results: Higher prevalences of hypertension, type 2 diabetes mellitus, and dyslipidemia were observed in MVCD patients. CYP2C19*2 (rs4244285, 681G>A) and *3 (rs4986893, 636G>A) allele frequencies were markedly elevated in the MVCD group. Logistic regression analysis confirmed that hypertension (odds ratio (OR)=1.485, 95% confidence interval (CI): 1.267‑1.740, p < 0.001), T2DM (OR=2.441, 95% CI: 2.006‑2.970, p < 0.001), dyslipidemia (OR=1.313, 95% CI: 1.097‑1.572, p =0.003), and CYP2C19 poor metabolizer (*2/*2, *2/*3 and *3/*3 genotypes) status (OR=1.744, 95% CI: 1.360‑2.237, p < 0.001) was independently associated with MVCD. The combined impaired CYP2C19 metabolic phenotype (intermediate (*1/*2 and *1/*3 genotypes) plus poor metabolizers) was also independently correlated with MVCD (adjusted OR=1.285, 95% CI: 1.095– 1.508, p =0.002). Conclusion: Clinical metabolic comorbidities and the combined impaired CYP2C19 metabolic phenotype are associated with MVCD. These findings may provide valuable reference for risk assessment of severe CAD.
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Cai et al. (2026) conducted a cross-sectional in Coronary artery disease (CAD) (n=4,124). Impaired CYP2C19 metabolic phenotype (intermediate and poor metabolizers) vs. Extensive metabolizer phenotype was evaluated on Multi-vessel coronary artery disease (MVCD) (OR 1.285, 95% CI 1.095-1.508, p=0.002). Impaired CYP2C19 metabolic phenotypes (intermediate and poor metabolizers) were independently associated with multi-vessel coronary artery disease (OR 1.285), alongside hypertension, T2DM, and dyslipidemia.
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