Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study

BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Shuo Huang [verfasserIn] Fugang Huang [verfasserIn] Chunyun Mei [verfasserIn] Fengyuan Tian [verfasserIn] Yongsheng Fan [verfasserIn] Jie Bao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke

Übergeordnetes Werk:	In: Frontiers in Cardiovascular Medicine - Frontiers Media S.A., 2015, 9(2022)
Übergeordnetes Werk:	volume:9 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fcvm.2022.896499

Katalog-ID:	DOAJ079350917

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520			\|a BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.
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allfields	10.3389/fcvm.2022.896499 doi (DE-627)DOAJ079350917 (DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d DE-627 ger DE-627 rakwb eng RC666-701 Shuo Huang verfasserin aut Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system Fugang Huang verfasserin aut Chunyun Mei verfasserin aut Fengyuan Tian verfasserin aut Yongsheng Fan verfasserin aut Yongsheng Fan verfasserin aut Jie Bao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.896499 kostenfrei https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
spelling	10.3389/fcvm.2022.896499 doi (DE-627)DOAJ079350917 (DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d DE-627 ger DE-627 rakwb eng RC666-701 Shuo Huang verfasserin aut Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system Fugang Huang verfasserin aut Chunyun Mei verfasserin aut Fengyuan Tian verfasserin aut Yongsheng Fan verfasserin aut Yongsheng Fan verfasserin aut Jie Bao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.896499 kostenfrei https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfields_unstemmed	10.3389/fcvm.2022.896499 doi (DE-627)DOAJ079350917 (DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d DE-627 ger DE-627 rakwb eng RC666-701 Shuo Huang verfasserin aut Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system Fugang Huang verfasserin aut Chunyun Mei verfasserin aut Fengyuan Tian verfasserin aut Yongsheng Fan verfasserin aut Yongsheng Fan verfasserin aut Jie Bao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.896499 kostenfrei https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfieldsGer	10.3389/fcvm.2022.896499 doi (DE-627)DOAJ079350917 (DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d DE-627 ger DE-627 rakwb eng RC666-701 Shuo Huang verfasserin aut Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system Fugang Huang verfasserin aut Chunyun Mei verfasserin aut Fengyuan Tian verfasserin aut Yongsheng Fan verfasserin aut Yongsheng Fan verfasserin aut Jie Bao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.896499 kostenfrei https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfieldsSound	10.3389/fcvm.2022.896499 doi (DE-627)DOAJ079350917 (DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d DE-627 ger DE-627 rakwb eng RC666-701 Shuo Huang verfasserin aut Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs. systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system Fugang Huang verfasserin aut Chunyun Mei verfasserin aut Fengyuan Tian verfasserin aut Yongsheng Fan verfasserin aut Yongsheng Fan verfasserin aut Jie Bao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.896499 kostenfrei https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
language	English
source	In Frontiers in Cardiovascular Medicine 9(2022) volume:9 year:2022
sourceStr	In Frontiers in Cardiovascular Medicine 9(2022) volume:9 year:2022
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Frontiers in Cardiovascular Medicine
authorswithroles_txt_mv	Shuo Huang @@aut@@ Fugang Huang @@aut@@ Chunyun Mei @@aut@@ Fengyuan Tian @@aut@@ Yongsheng Fan @@aut@@ Jie Bao @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	793951607
id	DOAJ079350917
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ079350917</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502082812.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230307s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3389/fcvm.2022.896499</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ079350917</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ77983ea1e3e9406f87c3cdce4b9acd0d</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Shuo Huang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">systemic lupus erythematosus</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cardiovascular disease</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">coronary artery disease</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">myocardial infarction</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">atrial fibrillation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ischemic stroke</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" 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callnumber-first	R - Medicine
author	Shuo Huang
spellingShingle	Shuo Huang misc RC666-701 misc systemic lupus erythematosus misc cardiovascular disease misc coronary artery disease misc myocardial infarction misc atrial fibrillation misc ischemic stroke misc Diseases of the circulatory (Cardiovascular) system Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study
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topic_title	RC666-701 Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study systemic lupus erythematosus cardiovascular disease coronary artery disease myocardial infarction atrial fibrillation ischemic stroke
topic	misc RC666-701 misc systemic lupus erythematosus misc cardiovascular disease misc coronary artery disease misc myocardial infarction misc atrial fibrillation misc ischemic stroke misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc systemic lupus erythematosus misc cardiovascular disease misc coronary artery disease misc myocardial infarction misc atrial fibrillation misc ischemic stroke misc Diseases of the circulatory (Cardiovascular) system
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title	Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study
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title_full	Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study
author_sort	Shuo Huang
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author_browse	Shuo Huang Fugang Huang Chunyun Mei Fengyuan Tian Yongsheng Fan Jie Bao
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title_sort	systemic lupus erythematosus and the risk of cardiovascular diseases: a two-sample mendelian randomization study
callnumber	RC666-701
title_auth	Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study
abstract	BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.
abstractGer	BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.
abstract_unstemmed	BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.
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title_short	Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study
url	https://doi.org/10.3389/fcvm.2022.896499 https://doaj.org/article/77983ea1e3e9406f87c3cdce4b9acd0d https://www.frontiersin.org/articles/10.3389/fcvm.2022.896499/full https://doaj.org/toc/2297-055X
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In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986–1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982–1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982–1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984–1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949–1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964–1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968–1.096, p-value = 0.352]. 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Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study

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