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

IF 3.9 2区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Jie Li, Ben Ma, Qin Fang, Jing Wang, Yang Sun, Hu Ding, Yan Wang
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引用次数: 0

Abstract

Background: It 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.

Methods: A 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.

Results: Compared 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.

Conclusions: Our 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.

脂蛋白(a)摩尔浓度比基因变异更能预测中国汉族冠状动脉疾病的风险和严重程度。
背景:脂蛋白(a)升高[Lp(a)]是冠状动脉疾病(CAD)的重要危险因素。血浆Lp(a)水平是由基因决定的,在不同种族、地区和个体之间差异很大。然而,目前对Lp(a)相关遗传变异的研究大多集中在高加索人群。我们的研究旨在测试汉族人群中LPA基因变异、Lp(a)浓度和CAD之间的关系。方法:选取同济医院行冠状动脉造影的患者3779例。TaqMan探针实时定量聚合酶链反应(qPCR)检测LPA Kringle IV型2 (KIV-2)拷贝,TaqMan探针基因分型分析检测LPA基因15个单核苷酸多态性(snp)。LPA遗传风险评分(GRS)基于与Lp(a)相关的7个snp计算。LPA遗传变异与Lp(a)和CAD的关系分别采用线性回归分析和Logistic回归分析进行评估。结果:与Lp(a)的第一个四分位数相比,第四个四分位数显示出与CAD的显著关联[比值比(OR): 2.08, 95%置信区间(CI): 1.67-2.59, p]结论:我们的研究结果表明,LPA遗传变异可以影响Lp(a)水平,但不超过Lp(a)摩尔浓度有效地预测CAD的发病率和严重程度,突出了Lp(a)检测和管理的重要性。
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来源期刊
Lipids in Health and Disease
Lipids in Health and Disease 生物-生化与分子生物学
CiteScore
7.70
自引率
2.20%
发文量
122
审稿时长
3-8 weeks
期刊介绍: Lipids in Health and Disease is an open access, peer-reviewed, journal that publishes articles on all aspects of lipids: their biochemistry, pharmacology, toxicology, role in health and disease, and the synthesis of new lipid compounds. Lipids in Health and Disease is aimed at all scientists, health professionals and physicians interested in the area of lipids. Lipids are defined here in their broadest sense, to include: cholesterol, essential fatty acids, saturated fatty acids, phospholipids, inositol lipids, second messenger lipids, enzymes and synthetic machinery that is involved in the metabolism of various lipids in the cells and tissues, and also various aspects of lipid transport, etc. In addition, the journal also publishes research that investigates and defines the role of lipids in various physiological processes, pathology and disease. In particular, the journal aims to bridge the gap between the bench and the clinic by publishing articles that are particularly relevant to human diseases and the role of lipids in the management of various diseases.
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