Evidence map›Paper›PMID 41944283›Full record

SynthesisClinical cardiology2026

Lipoprotein(a) and the Risk of Heart Failure: A Dose-Response Meta-Analysis.

Yongmei He, Jun Liu, Jingwei Zhuang, Hongjia Hu

Abstract readMeta-AnalysisReview
In one paragraph

Synthesis in Clinical cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Yongmei HeDepartment of Endocrinology, Pengzhou People's Hospital, Pengzhou, China.ORCID https://orcid.org/0009-0007-2236-9115
Jun LiuDepartment of Endocrinology, Pengzhou People's Hospital, Pengzhou, China.
Jingwei ZhuangDepartment of Endocrinology, Pengzhou People's Hospital, Pengzhou, China.
Hongjia HuDepartment of Endocrinology, Pengzhou People's Hospital, Pengzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipoprotein(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.

methodsA 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.

resultsFive 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.

conclusionsElevated Lp(a) is associated with an increased HF risk in a nonlinear pattern, with risk escalation slowing at higher concentrations.

Indexed as

Heart FailureLipoprotein(a)BiomarkersGlobal HealthHumansIncidencePrognosisRisk AssessmentRisk FactorsBiomarkersLipoprotein(a)LPA protein, humandose‐responseheart failureincidencelipoprotein(a)meta‐analysis

Identifiers

PMID41944283
PMCPMC13054834

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.