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Lipoprotein(a) and extent of coronary artery disease in patients undergoing PCI

Oct 2026 · European Heart Journal · Vol 47 · 0 citations

TL;DR

A clear dose–response relationship was observed, with progressively higher odds of multivessel CAD across increasing Lp(a) quartiles, underscoring the contribution of Lp(a) to residual atherosclerotic risk beyond traditional cardiometabolic factors.

Abstract

Lipoprotein(a) [Lp(a)] has emerged as an independent contributor to residual atherosclerotic cardiovascular risk. However, its association with angiographic disease burden among patients undergoing percutaneous coronary intervention (PCI) remains incompletely characterized. To evaluate the relationship between Lp(a) levels and coronary artery disease (CAD) extent, and to determine whether Lp(a) independently predicts multivessel CAD (MVD). During a 6-month period, we analyzed 260 consecutive patients undergoing PCI at our tertiary center. Cardiovascular risk factors, lipid profile, C-reactive protein (CRP), and HbA1c were recorded. Coronary angiography was used to classify patients into single vessel disease (SVD) or MVD. Lp(a) levels were assessed at index presentation. Group comparisons were performed using non-parametric testing. Multivariable logistic regression was conducted to identify independent predictors of MVD, adjusting for age, hypertension, HbA1c, lipid markers, CRP, and Lp(a). Among the cohort, patients with MVD were older [69 (58-77) vs 63 (55-74) years, p=0.01] and exhibited higher Lp(a) levels [Figure 1, 19 (9-40) vs 9 (8-20) mg/dL, p=0.001] and HbA1c [6.2 (5.9-7.0) vs 5.9 (5.6-6.3), p<0.001]. CRP was also elevated in MVD [3.6 (1.5-7.4) vs 2.1 (1-4.8) mg/L, p=0.005]. LDL-C and triglycerides did not differ significantly between groups. In multivariable analysis (Figure 2), Lp(a) remained independently associated with MVD (OR 1.20 per 10 mg/dL increase, 95% CI 1.05-1.38, p=0.009), alongside age (OR 1.04 per year, p=0.039) and HbA1c (OR 1.50 per 1% increase, p=0.034). CRP showed a borderline association (p=0.094).When modeled categorically, a clear dose-response relationship was observed across increasing Lp(a) quartiles. Compared with patients in the lowest quartile, those in the intermediate and highest quartiles had progressively higher odds of MVD (OR 3.8 and OR 5.1, respectively, global p=0.002). In a trend analysis, each increment in Lp(a) quartile was associated with nearly a twofold increase in odds of MVD (OR 1.98, 95% CI 1.28-3.07, p=0.002), confirming a graded association independent of traditional risk factors. In this contemporary PCI cohort, elevated Lp(a) levels were independently associated with greater angiographic coronary disease burden. A clear dose–response relationship was observed, with progressively higher odds of multivessel CAD across increasing Lp(a) quartiles. This association persisted after adjustment for age, glycemic status, and inflammatory markers, underscoring the contribution of Lp(a) to residual atherosclerotic risk beyond traditional cardiometabolic factors. These findings support routine assessment of Lp(a) in patients undergoing PCI and highlight its potential role as a determinant of coronary disease complexity.Figure 1Figure 2

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