AUTHOR=Guo Hao-Yang , Wang Wei , Peng Hui , Yuan Hui 

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

JOURNAL=Frontiers in Immunology

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1017444

DOI=10.3389/fimmu.2022.1017444

ISSN=1664-3224

ABSTRACT=<sec><title>Background</title><p>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.</p></sec><sec><title>Methods</title><p>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.</p></sec><sec><title>Results</title><p>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, <italic>P</italic> = 0.017; weighted median, OR = 1.027, 95% CI: 1.006–1.049, <italic>P</italic> = 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, <italic>P</italic> = 0.921; weighted median, OR = 1.069, 95% CI: 0.855–1.338, <italic>P</italic> = 0.556) indicated that there was no causal association between genetic susceptibility to MI and an increased risk of RA.</p></sec><sec><title>Conclusion</title><p>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.</p></sec>