Epidemiology
Elevated Lp(a) marks a high-risk phenotype in advanced coronary calcification, IVUS study of 292 (Int J Cardiol Cardiovasc Risk Prev 2026)
Original title: Elevated lipoprotein(a) and adverse outcomes in advanced coronary artery calcification: An intravascular ultrasound study
Retrospective IVUS study of 292 patients with confirmed advanced coronary artery calcification (CAC), stratified into elevated (50 mg/dL or more, n=77) or low (below 50, n=215) Lp(a) groups. The elevated-Lp(a) group had a greater incidence of aortic valve calcification (p<0.001) and constrictive vascular remodelling with smaller lumen and vessel dimensions on IVUS. Over a median 17.2-month follow-up, the elevated-Lp(a) group had a substantially higher MACE rate (37.7% vs 15.8%, adjusted HR 2.60, 95% CI 1.55-4.35, p<0.001), driven particularly by ischaemic stroke (adjusted HR 7.14) and in-stent restenosis (adjusted HR 2.78). The authors propose routine Lp(a) testing in patients with severe CAC to identify this high-risk phenotype, an ideal candidate population for emerging Lp(a)-lowering therapies.
Original abstract
Background: Coronary artery calcification (CAC) signifies advanced atherosclerosis and portends increased cardiovascular risk. Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerosis; however, its association with in vivo lesion morphology and clinical outcomes in patients with symptomatic, advanced CAC remains incompletely characterized.
Objective: This study aimed to investigate the association between elevated Lp(a) levels and both in vivo lesion morphology and clinical outcomes in this high-risk population.
Methods: In this retrospective cohort, 292 patients with intravascular ultrasound(IVUS)-confirmed CAC were stratified into elevated (≥50 mg/dL,n = 77) or low (<50 mg/dL,n = 215) Lp(a) groups. The primary endpoint was major adverse cardiovascular events (MACEs). Associations were assessed via multivariable Cox models adjusted for clinical covariates.
Results: Patients in the elevated Lp(a) group presented a greater incidence of aortic valve calcification (p < 0.001). IVUS revealed constrictive remodeling with a smaller lumen and vessel dimensions. During a median follow-up of 17.2 months, the elevated Lp(a) cohort had a significantly higher MACE rate (37.7% vs. 15.8%; adjusted hazard ratio [aHR] 2.60, 95% CI 1.55-4.35, p < 0.001). Elevated Lp(a) independently predicted increased risks of ischemic stroke (aHR 7.14) and in-stent restenosis (aHR 2.78).
Conclusion: In symptomatic patients with IVUS-confirmed CAC, elevated Lp(a) identifies a high-risk phenotype characterized by constrictive vascular remodeling and a markedly increased risk of MACEs, driven particularly by ischemic stroke and in-stent restenosis. These findings support the integration of routine Lp(a) testing into the risk stratification of patients with severe CAC, thereby identifying a precise high-risk phenotype that warrants intensified monitoring and represents an ideal target for emerging Lp(a)-lowering therapies.
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Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.