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Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction

BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide associat...

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Autores principales: Guo, Hao-Yang, Wang, Wei, Peng, Hui, Yuan, Hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755576/
https://www.ncbi.nlm.nih.gov/pubmed/36532051
http://dx.doi.org/10.3389/fimmu.2022.1017444
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author Guo, Hao-Yang
Wang, Wei
Peng, Hui
Yuan, Hui
author_facet Guo, Hao-Yang
Wang, Wei
Peng, Hui
Yuan, Hui
author_sort Guo, Hao-Yang
collection PubMed
description BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide association study summary datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using inverse-variance weighted (IVW), weighted median, MR-Egger regression, simple mode, and weighted mode methods. RESULTS: The MR results for the causal effect of RA on MI (IVW, odds ratio [OR] = 1.041, 95% confidence interval [CI]: 1.007–1.076, P = 0.017; weighted median, OR = 1.027, 95% CI: 1.006–1.049, P = 0.012) supported a causal association between genetic susceptibility to RA and an increased risk of MI. MR results for the causal effect of MI on RA (IVW, OR = 1.012, 95% CI: 0.807–1.268, P = 0.921; weighted median, OR = 1.069, 95% CI: 0.855–1.338, P = 0.556) indicated that there was no causal association between genetic susceptibility to MI and an increased risk of RA. CONCLUSION: Bidirectional TSMR analysis supports a causal association between genetic susceptibility to RA and an increased risk of MI but does not support a causal association between genetic susceptibility to MI and an increased risk of RA.
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spelling pubmed-97555762022-12-17 Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction Guo, Hao-Yang Wang, Wei Peng, Hui Yuan, Hui Front Immunol Immunology BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide association study summary datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using inverse-variance weighted (IVW), weighted median, MR-Egger regression, simple mode, and weighted mode methods. RESULTS: The MR results for the causal effect of RA on MI (IVW, odds ratio [OR] = 1.041, 95% confidence interval [CI]: 1.007–1.076, P = 0.017; weighted median, OR = 1.027, 95% CI: 1.006–1.049, P = 0.012) supported a causal association between genetic susceptibility to RA and an increased risk of MI. MR results for the causal effect of MI on RA (IVW, OR = 1.012, 95% CI: 0.807–1.268, P = 0.921; weighted median, OR = 1.069, 95% CI: 0.855–1.338, P = 0.556) indicated that there was no causal association between genetic susceptibility to MI and an increased risk of RA. CONCLUSION: Bidirectional TSMR analysis supports a causal association between genetic susceptibility to RA and an increased risk of MI but does not support a causal association between genetic susceptibility to MI and an increased risk of RA. Frontiers Media S.A. 2022-12-02 /pmc/articles/PMC9755576/ /pubmed/36532051 http://dx.doi.org/10.3389/fimmu.2022.1017444 Text en Copyright © 2022 Guo, Wang, Peng and Yuan https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Guo, Hao-Yang
Wang, Wei
Peng, Hui
Yuan, Hui
Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title_full Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title_fullStr Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title_full_unstemmed Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title_short Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
title_sort bidirectional two-sample mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755576/
https://www.ncbi.nlm.nih.gov/pubmed/36532051
http://dx.doi.org/10.3389/fimmu.2022.1017444
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