Association between systemic lupus erythematosus and cardiovascular health based on genetic data.

IF 2.9 3区医学 Q2 RHEUMATOLOGY

Clinical Rheumatology Pub Date : 2025-06-01 Epub Date: 2025-05-03 DOI:10.1007/s10067-025-07396-x

Rui Wang, Xiao-Wei Cui, Miao Zhang, Jian Xu, Chan-Yuan Bu, Xiang-Yang Zhao

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引用次数: 0

Abstract

Objective: To investigate the genetic causal relationship between systemic lupus erythematosus (SLE) and cardiovascular diseases through Mendelian randomization (MR) analysis.

Methods: This study employed a two-sample bidirectional MR design. Data were sourced from publicly available genome-wide association study (GWAS) databases. A total of 482,911 European individuals diagnosed with SLE were selected, covering 24,198,877 single-nucleotide polymorphisms (SNPs), along with relevant GWAS summary data for cardiovascular diseases. Genetic variants were used as instrumental variables. The MR analysis was conducted using the TwoSampleMR R package, employing methods including inverse-variance weighting (IVW), weighted median, and MR-Egger to assess the causal relationships. Sensitivity analyses were also performed to verify result robustness.

Results: MR analysis indicated potential causal risk relationships between genetic predisposition to SLE and increased risk of pericarditis and peripheral artery disease (PAD). Conversely, reverse MR analyses did not demonstrate significant causal associations, with IVW estimates indicating no causal relationships between coronary artery disease (OR = 1.038, 95%CI 0.829-1.3, P = 0.745), dilated cardiomyopathy (OR = 1.044, 95%CI 0.907-1.203, P = 0.548), heart failure (OR = 0.991, 95%CI 0.729-1.348, P = 0.956), hypertrophic cardiomyopathy (OR = 0.958, 95%CI 0.896-1.024, P = 0.207), pericarditis (OR = 0.958, 95%CI 0.821-1.118, P = 0.589), or PAD (OR = 1.157, 95%CI 0.625-2.143, P = 0.642) and the risk of SLE.

Conclusions: This study utilizes MR analysis to reveal genetic causal relationships between SLE and cardiovascular complications, specifically pericarditis and PAD. These findings suggest that inflammation control in SLE patients may help prevent pericarditis while managing dyslipidemia could mitigate PAD risk. Key Points • This study utilizes MR analysis to reveal the causal relationships between SLE and conditions such as pericarditis and PAD from a genetic perspective. • It suggests that controlling inflammation in the treatment of SLE can prevent pericarditis, and managing abnormal lipid levels can reduce the risk of PAD.

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基于遗传数据的系统性红斑狼疮与心血管健康之间的关系

目的：通过孟德尔随机化（MR）分析，探讨系统性红斑狼疮（SLE）与心血管疾病的遗传因果关系。方法：本研究采用双样本双向磁共振设计。数据来源于公开的全基因组关联研究（GWAS）数据库。总共选择了482911名诊断为SLE的欧洲个体，涵盖了24198877个单核苷酸多态性（snp），以及心血管疾病的相关GWAS汇总数据。遗传变异被用作工具变量。磁共振分析采用TwoSampleMR软件包，采用反方差加权（IVW）、加权中位数和MR- egger等方法来评估因果关系。还进行了敏感性分析以验证结果的稳健性。结果：磁共振分析显示SLE的遗传易感性与心包炎和外周动脉疾病（PAD）风险增加之间存在潜在的因果风险关系。相反，反向MR分析并没有显示出显著的因果关系，IVW估计显示冠状动脉疾病（OR = 1.038, 95%CI 0.829-1.3, P = 0.745）、扩张型心肌病（OR = 1.044, 95%CI 0.907-1.203, P = 0.548）、心力衰竭（OR = 0.991, 95%CI 0.729-1.348, P = 0.956）、肥厚性心肌病（OR = 0.958, 95%CI 0.896-1.024, P = 0.207）、心包炎（OR = 0.958, 95%CI 0.821-1.118, P = 0.589）、PAD (OR = 1.157，95%CI为0.625-2.143,P = 0.642)与SLE风险之间的关系。结论：本研究利用MR分析揭示SLE与心血管并发症，特别是心包炎和PAD之间的遗传因果关系。这些发现表明，控制SLE患者的炎症可能有助于预防心包炎，而控制血脂异常可以降低PAD的风险。•本研究利用MR分析从遗传角度揭示SLE与心包炎、PAD等疾病之间的因果关系。•提示在SLE治疗中控制炎症可以预防心包炎，控制异常脂质水平可以降低PAD的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical Rheumatology 医学-风湿病学

CiteScore

6.90

自引率

2.90%

发文量

441

审稿时长

3 months

期刊介绍： Clinical Rheumatology is an international English-language journal devoted to publishing original clinical investigation and research in the general field of rheumatology with accent on clinical aspects at postgraduate level. The journal succeeds Acta Rheumatologica Belgica, originally founded in 1945 as the official journal of the Belgian Rheumatology Society. Clinical Rheumatology aims to cover all modern trends in clinical and experimental research as well as the management and evaluation of diagnostic and treatment procedures connected with the inflammatory, immunologic, metabolic, genetic and degenerative soft and hard connective tissue diseases.