Lipoprotein(a) and the Risk of Heart Failure: A Dose-Response Meta-Analysis
He Y, Liu J, Zhuang J, Hu H
Clinical cardiology · 0 citas
Cómo se estudió
- Diseño
- Metaanálisis (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiación independiente
Según la declaración de financiación del texto completo.
Publicación
- Publicado
- 2026-04-01 · Clin Cardiol · vol. 49 · número 4 · pág. e70289
- Editorial
- Wiley
- Citado
- 0 citas · más que el 23% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 40 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Lipoproteins and Cardiovascular Health · Heart Failure Treatment and Management · Cardiovascular Health and Risk Factors
- Palabras clave
- lipoprotein(a), heart failure, heart failure risk, dose-response relationship, nonlinear relationship, cardiovascular risk factors, prospective cohort
- MeSH
- humans, lipoprotein(a), prognosis, incidence, risk assessment, risk factors, heart failure, global health, biomarkers
4 autores
- Yongmei He · autor de correspondencia
- Jianfeng Liu
- Jingwei Zhuang
- Hongjia Hu
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein implicated in cardiovascular disease, but its role in heart failure (HF) remains uncertain. Observational studies indicate a link between elevated Lp(a) and HF risk, but the dose-response relationship remains unexplored. This meta-analysis aimed to quantify the association between circulating Lp(a) levels and HF incidence.
Methods
A systematic search of PubMed, Embase, and Web of Science identified prospective cohort studies reporting hazard ratios (HRs) for HF incidence across different Lp(a) levels. A random-effects model was applied to pool effect estimates while accounting for heterogeneity, and restricted cubic splines assessed dose-response relationships.
Results
Five prospective cohort studies with 400 631 participants were included. During a mean follow-up duration of 11.0 years, 10 598 (2.6%) patients developed HF. A high Lp(a) level was associated with an increased HF risk (HR: 1.34, 95% CI: 1.14-1.59, p < 0.001), with moderate heterogeneity (I² = 69%). Subgroup analysis showed a stronger association in studies using an Lp(a) cutoff of ≥ 50 mg/dL (HR: 1.68) compared to those with a cutoff of < 50 mg/dL (HR: 1.16, p for subgroup difference < 0.01), which completely explained the heterogeneity. The dose-response analysis revealed a nonlinear association (p for non-linearity = 0.001). HF risk increased nearly linearly below 55 mg/dL, then slowed, and plateaued at 160 mg/dL.
Conclusions
Elevated Lp(a) is associated with an increased HF risk in a nonlinear pattern, with risk escalation slowing at higher concentrations.
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