Epidemiology
Elevated Lp(a) does not predict new or progressing coronary calcium, large 41,929-person Korean cohort finds, challenging a common risk-marker assumption (Eur J Prev Cardiol 2025)
Original title: Elevated lipoprotein(a) is not linked to coronary artery calcification incidence or progression
This longitudinal cohort study followed 41,929 Korean adults aged 30 or older with baseline Lp(a) and coronary artery calcium (CAC) by multi-detector CT, split into baseline CAC of zero (n = 32,338) and CAC above zero (n = 9,591), to test whether Lp(a) predicts CAC incidence and progression. Among those with baseline CAC of zero over a median 4.04-year follow-up, neither Lp(a) quintile nor clinical category was associated with incident CAC (HR for highest vs. second quintile 0.998, 95% CI 0.90-1.10; HR for 100 mg/dL or above vs. below 30 mg/dL, 0.83, 95% CI 0.57-1.23). Among those with baseline CAC above zero over a median 3.78-year follow-up, CAC progression did not differ materially across Lp(a) categories either. The authors conclude elevated Lp(a) is not associated with new-onset or progressing coronary calcium, suggesting its atherogenic effect may act through pathways other than calcification.
Original abstract
Aims: Lipoprotein(a) [Lp(a)] is a genetically determined, independent risk factor for atherosclerotic cardiovascular disease. However, its role in coronary artery calcification (CAC) remains unclear. We aimed to determine whether Lp(a) levels are associated with the incidence and progression of CAC.
Methods And Results: We conducted a longitudinal cohort study (2015-22) of 41 929 adults (aged ≥30 years) who underwent baseline Lp(a) measurement and CAC assessment via multi-detector computed tomography. Participants were stratified into those with baseline CAC = 0 (n = 32 338) and CAC > 0 (n = 9591). Outcomes were analysed according to Lp(a) quintiles and clinically relevant categories (<30, 30-50, 50-100, ≥ 100 mg/dL). Cox proportional hazards models estimated hazard ratios (HRs) for incident CAC (CAC > 0) among those with CAC = 0 (median follow-up, 4.04 years). Linear mixed-effects models evaluated CAC progression among those with CAC > 0 (median follow-up, 3.78 years). All models were adjusted for cardiovascular risk factors. Among participants with CAC = 0 (mean age, 40.94 ± 5.81 years; 85.69% men), neither Lp(a) quintiles nor clinical categories were significantly associated with incident CAC [HR for highest vs. second quintile: 0.998 (95% confidence interval, CI, 0.90-1.10); HR for ≥100 vs. <30 mg/dL: 0.83 (95% CI, 0.57-1.23)]. Among those with CAC > 0 (mean age, 45.99 ± 7.20 years; 94.90% men), CAC progression did not differ materially across Lp(a) quintiles or clinical thresholds.
Conclusion: Elevated Lp(a) levels were not associated with new-onset CAC or progression of existing CAC in this large longitudinal cohort.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.