Mechanisms
Lp(a) at or above 30 mg/dL plus carotid plaque together carry a 4.18-fold ASCVD risk over 11.5 years in 5,471 participants (J Am Heart Assoc 2024)
Original title: Independent Relationship of Lipoprotein(a) and Carotid Atherosclerosis With Long-Term Risk of Cardiovascular Disease
This study followed 5,471 participants without baseline cardiovascular disease (mean age 60.0 years, 48.4% men) for a median 11.5 years, during which 539 incident ASCVD events occurred (8.4 per 1,000 person-years). Overall, 7.6% had Lp(a) at or above 50 mg/dL. Lp(a) was independently associated with long-term ASCVD, coronary events, and ischaemic stroke risk; participants with Lp(a) at or above 50 mg/dL had a 62% higher ASCVD risk than those below 10 mg/dL (95% CI 1.19-2.21), with a 10-year cumulative incidence of 11.7%, an association that held even after adjusting for prevalent carotid plaque. Participants with both Lp(a) at or above 30 mg/dL and prevalent carotid plaque had a 4.18-fold higher ASCVD risk than those with neither. Elevated Lp(a) independently predicts long-term ASCVD risk, and this risk is substantially amplified when atherosclerotic plaque is already present.
Original abstract
Background: Lipoprotein(a) (Lp(a)) is considered to be a causal risk factor of atherosclerotic cardiovascular disease (ASCVD), but whether there is an independent or joint association of Lp(a) and atherosclerotic plaque with ASCVD risk remains uncertain. This study aims to assess ASCVD risk independently or jointly conferred by Lp(a) and carotid atherosclerotic plaque.
Methods And Results: A total of 5471 participants with no history of cardiovascular disease at baseline were recruited and followed up for ASCVD events (all fatal and nonfatal acute coronary and ischemic stroke events) over a median of 11.5 years. Independent association of Lp(a), or the joint association of Lp(a) and carotid plaque with ASCVD risk, was explored using Cox proportional hazards models. Overall, 7.6% of the participants (60.0±7.9 years of age; 2649 [48.4%] men) had Lp(a) ≥50 mg/dL, and 539 (8.4/1000 person-years) incident ASCVD events occurred. Lp(a) concentrations were independently associated with long-term risk of total ASCVD events, as well as coronary events and ischemic stroke events. Participants with Lp(a) ≥50 mg/dL had a 62% higher risk of ASCVD incidence (95% CI, 1.19-2.21) than those with Lp(a) <10 mg/dL, and they exhibited a 10-year ASCVD incidence of 11.7%. This association exists even after adjusting for prevalent plaque. Moreover, participants with Lp(a) ≥30 mg/dL and prevalent plaque had a significant 4.18 times higher ASCVD risk than those with Lp(a) <30 mg/dL and no plaque.
Conclusions: Higher Lp(a) concentrations are independently associated with long-term ASCVD risk and may exaggerate cardiovascular risk when concomitant with atherosclerotic plaque.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.