Evidence map›Paper›PMID 39953584›Full record

ArticleLipids in health and disease2025

Lipoprotein(a) molar concentrations rather than genetic variants better predict coronary artery disease risk and severity in Han Chinese population.

Jie Li, Ben Ma, Qin Fang, Jing Wang, Yang Sun, Hu Ding, Yan Wang

Abstract read
In one paragraph

Article in Lipids in health and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

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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

4 citing papers in PubMed.

  1. Review
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  4. ThebioRxiv : the preprint server for biology · 2025
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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

7 authors.

Jie LiDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Ben MaDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qin FangDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jing WangDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yang SunDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Hu DingDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. huding@tjh.tjmu.edu.cn.
Yan WangDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. newswangyan@126.com.

Funding

National Key Research and Development Program of China 2022YFE0209900
6 · The paper itself

Abstract

backgroundIt is well established that increased lipoprotein(a) [Lp(a)] is a significant risk factor for coronary artery disease (CAD). Plasma Lp(a) levels are genetically determined and vary widely between different races, regions and individuals. However, most studies on Lp(a) associated genetic variants have focused on the Caucasian population currently. Our study aimed to test the associations among LPA genetic variants, Lp(a) concentrations, and CAD in a Han Chinese cohort.

methodsA total of 3779 patients undergoing coronary angiography were recruited from Tongji Hospital. LPA Kringle IV type 2 (KIV-2) copies were detected using TaqMan probe real-time quantitative polymerase chain reaction (qPCR) analysis and fifteen single nucleotide polymorphisms (SNPs) within the LPA gene were detected using TaqMan probe genotyping analysis. LPA genetic risk score (GRS) was computed based on seven SNPs associated with Lp(a). Associations of LPA genetic variants with Lp(a) and CAD were evaluated using linear regression analyses and Logistic regression analyses, respectively.

resultsCompared with the first quartile of Lp(a), the fourth quartile exhibited a significant association with CAD [odds ratio (OR): 2.08, 95% confidence interval (CI): 1.67-2.59, p < 0.001], multivessel CAD [OR: 2.54, 95% CI: 2.06-3.12, p < 0.001], and high Gensini scores [OR: 2.17, 95% CI: 1.77-2.66, p < 0.001] after multivariable adjustment for cardiovascular risk factors. Both LPA GRS and KIV-2 quartiles were associated with Lp(a) concentrations (both p for trend < 0.001). However, after false discovery rate (FDR) correction, there were no significant associations of LPA genetic variants with CAD, multivessel CAD or high Gensini scores.

conclusionsOur findings indicate LPA genetic variants can affect Lp(a) levels, but do not exceed Lp(a) molar concentrations to predict CAD incidence and severity usefully, highlighting the importance of Lp(a) detection and management.

Indexed as

Coronary Artery DiseaseLipoprotein(a)AgedChinaCoronary AngiographyEast Asian PeopleFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsLipoprotein(a)LPA protein, humanEpidemiologyGenetic risk scoreGeneticsKringle IV type 2 copiesLPA geneSingle nucleotide polymorphism

Identifiers

PMID39953584
PMCPMC11827131

What Socratic holds

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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 Socratic graph.