Obstructive sleep apnea and atrial fibrillation: insights from a bidirectional Mendelian randomization study

Lu Chen; Xingang Sun; Yuxian He; Yunlong Lu; Liangrong Zheng

doi:10.1186/s12920-022-01180-5

February 16, 2022BMC Medical GenomicsOpen Access

Obstructive sleep apnea and atrial fibrillation: insights from a bidirectional Mendelian randomization study

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Why the study?

Observational studies linking obstructive sleep apnea to atrial fibrillation might be confounded, leaving it unclear whether the relationship is causal.

Does genetically predicted obstructive sleep apnea increase the risk of atrial fibrillation?

Structured PICO

Does genetically predicted obstructive sleep apnea increase the risk of atrial fibrillation?

P

Population

Individuals from genome-wide association studies (GWAS) datasets for obstructive sleep apnea (OSA) and atrial fibrillation (AF)

I

Intervention

Genetically predicted obstructive sleep apnea (OSA)

C

Comparator

Genetically predicted absence of obstructive sleep apnea

O

Outcome

Risk of atrial fibrillation (AF)

This Mendelian randomization study provides genetic evidence supporting a causal role of obstructive sleep apnea in increasing the risk of atrial fibrillation.

Implication

Supports causal OSA-AF link genetically but not practice change; leaves open need for RCTs to confirm treatment effects.

Abstract

BACKGROUND: Observational studies have suggested that obstructive sleep apnea (OSA) is in relation to atrial fibrillation (AF); however, these studies might be confounded and whether the relationship is causal remains unclear. We conducted a bidirectional Mendelian randomization (MR) study to clarify the causal inference between OSA and AF. METHODS: Genetic instruments for OSA and AF were obtained from genome-wide association studies. The fixed-effects inverse-variance weighted (IVW) method was used as the main method, supplemented by several sensitivity analyses. For replication, another AF dataset was used to validate the causal effect of OSA on AF. Furthermore, multivariable MR analyses were performed to obtain direct estimates adjusting for potential confounders. RESULTS: ]. The results were consistent in MR sensitivity analyses as well as in replication analyses, and the significance remained after adjusting for potential confounders. In the reverse MR analyses, there was no causal effect of AF on OSA. CONCLUSIONS: Our study strengthened the causal evidence of genetically predicted OSA with a higher AF risk. Early screening and appropriate management of OSA might show anti-arrhythmic benefits.