Lp(a) of 30 mg/dL or above predicts MACE in both primary and secondary prevention, 51,934-subject Taiwanese study confirms the threshold (Eur J Prev Cardiol 2025)

Original title: Clinical Significance of Elevated Lipoprotein(a) in Primary and Secondary Prevention: A Multi-institutional Study

Eur J Prev Cardiol · 22 October 2025 · 8

Chen DY, Tsai ML, Hsieh MJ, Chang CY, Chen TH, Chen SW, Chu PH, Hsieh IC, Hung KC, Wen MS, Chen CC

This retrospective analysis drew on 51,934 subjects from the Chang Gung Research Database in Taiwan (2004-2019), comprising 49,363 individuals without prior ASCVD and 2,571 with established ASCVD, to test whether the 30 mg/dL Lp(a) cutoff predicts major adverse cardiovascular events (MACE) in both groups. Over a mean 6.6-year follow-up (median Lp(a) 9.6 mg/dL, IQR 4.6-18.5), Lp(a) of 30 mg/dL or above independently predicted higher MACE risk both in ASCVD-free individuals (adjusted subdistribution hazard ratio 1.24, 95% CI 1.07-1.43) and in those with established ASCVD (aSHR 1.36, 95% CI 1.07-1.74), with restricted cubic spline analysis showing progressive risk elevation beyond the threshold in both groups. This large East Asian dataset supports 30 mg/dL as a workable Lp(a) cutoff for risk stratification across both primary and secondary prevention settings.

Original abstract

Aims: Recent evidence suggests that elevated lipoprotein(a) [Lp(a)] contributes to atherosclerotic cardiovascular disease (ASCVD). The predictive value of specific Lp(a) cutoff points of 30 mg/dL remains to be established. This study investigated the relationship between Lp(a) concentrations and cardiovascular outcomes in Taiwanese individuals, stratified by pre-existing ASCVD status.

Methods: We conducted a retrospective analysis of 51,934 subjects from the Chang Gung Research Database (January 2004 to June 2019), comprising 49,363 individuals without ASCVD and 2,571 with established ASCVD. The primary outcome was major adverse cardiovascular events (MACEs), encompassing acute myocardial infarction, ischemic stroke, revascularization procedures, peripheral arterial interventions, and cardiovascular mortality. Individuals were followed until their last visit to our institutions or December 31, 2019.

Results: During a mean follow-up of 6.6 years (standard deviation: 5.0 years), the study population demonstrated a median Lp(a) of 9.6 mg/dL (interquartile range: 4.6-18.5). In ASCVD-free individuals, Lp(a) concentrations ≥30 mg/dL were associated with increased MACE risk (adjusted subdistribution hazard ratio [aSHR]: 1.24; 95% confidence interval [CI]: 1.07-1.43). Similarly, in the ASCVD cohort, elevated Lp(a) predicted higher MACE occurrence (aSHR: 1.36; 95% CI: 1.07-1.74). Restricted cubic spline analysis confirmed a progressive risk elevation beyond the 30 mg/dL threshold in both groups.

Conclusions: Lp(a) levels ≥30 mg/dL independently predicted adverse cardiovascular outcomes, regardless of baseline ASCVD status. This threshold appears suitable for cardiovascular risk stratification in both primary and secondary prevention settings.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.