Why the study?
Although elevated Lp(a) is considered a causal cardiovascular risk factor, its independent contribution to CAD beyond traditional risk factors and lipid parameters in contemporary clinical practice remains uncertain.
Does lipoprotein(a) independently predict coronary artery disease after adjustment for traditional cardiovascular risk factors in patients referred for cardiovascular assessment?
Does lipoprotein(a) independently predict coronary artery disease after adjustment for traditional cardiovascular risk factors in patients referred for cardiovascular assessment?
Answers are grounded in this paper and cite their sources.
In a registry cohort of 1,342 patients referred for cardiovascular evaluation, lipoprotein(a) did not independently predict coronary artery disease after adjusting for traditional risk factors and LDL-C.
Background Elevated lipoprotein(a) [Lp(a)] is considered a causal cardiovascular risk factor, yet its independent contribution to coronary artery disease (CAD) in contemporary clinical practice remains uncertain. Determining whether Lp(a) adds predictive value beyond established risk factors is essential for risk stratification and treatment decisions. Purpose To assess whether Lp(a) independently predicts CAD after adjustment for traditional cardiovascular risk factors and lipid parameters, including LDL-C and remnant cholesterol (REMN-C). Methods We evaluated 1,342 consecutive patients from the PMMHRI-Lp(a) Registry referred for cardiovascular assessment. CAD was defined clinically. Logistic regression assessed the association between Lp(a) (analyzed as a continuous variable) and CAD, adjusted for age, sex, diabetes, hypertension, LDL-C, and REMN-C. Model performance is reported using odds ratios (ORs) with 95% confidence intervals (CIs). Results Lp(a) levels did not differ significantly between CAD and non-CAD groups (p=0.087) (Figure 1). Lp(a) was not an independent predictor of CAD (OR 1.00 per 1 mg/dL; 95% CI 0.998–1.007; p = 0.34). Strong predictors included age (OR 1.05 per year; 95% CI 1.03–1.07), male sex (OR 1.77; 95% CI 1.14–2.74), and hypertension (OR 4.46; 95% CI 2.71–7.58). LDL-C was inversely associated with CAD (OR 0.99; p < 0.001), likely reflecting more intensive lipid-lowering therapy in patients with established disease. REMN-C was not associated with CAD (Figure 2). The model demonstrated good discrimination and internal consistency. Conclusions In this large clinical cohort, Lp(a) did not independently predict CAD after adjustment for traditional risk factors and LDL-C. These results suggest the clinical impact of Lp(a) may depend on additional modifiers and may be attenuated in populations receiving intensive lipid-lowering therapy. Prospective studies are needed to determine whether Lp(a)-lowering interventions significantly improve cardiovascular outcomes.
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Sosnowska et al. (2026) studied this question.
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