Key result
Genetically predicted sleep-disordered breathing loses its association with AFib after adjusting for BMI.
Why the study?
It remains unclear whether the association between OSA and AF is causal or mediated by shared comorbidities like obesity, as observational studies are conflicting and prone to confounding.
Is the association between sleep-disordered breathing and atrial fibrillation causal or mediated by obesity?
Observational (n=537,409)
Is the association between sleep-disordered breathing and atrial fibrillation causal or mediated by obesity?
Odds Ratio: 2.09 (95% CI 1.1–3.98)
p-value: p=0.03
Elevated BMI appears to be a causal risk factor for atrial fibrillation independent of sleep-disordered breathing, suggesting the SDB-AF association is largely mediated by obesity.
Suggests obesity mediates the sleep-disordered breathing–atrial fibrillation link; leaves open independent causal effects and requires trial confirmation.
It remains unclear whether the association between obstructive sleep apnoea (OSA), a form of sleep-disordered breathing (SDB), and atrial fibrillation (AF) is causal or mediated by shared co-morbidities such as obesity. Existing observational studies are conflicting and limited by confounding and reverse causality. We performed Mendelian randomisation (MR) to investigate the causal relationships between SDB, body mass index (BMI) and AF. Single-nucleotide polymorphisms associated with SDB (n = 29) and BMI (n = 453) were selected as instrumental variables to investigate the effects of SDB and BMI on AF, using genetic association data on 55,114 AF cases and 482,295 controls. Primary analysis was conducted using inverse-variance weighted MR. Higher genetically predicted SDB and BMI were associated with increased risk of AF (OR per log OR increase in snoring liability 2.09 (95% CI 1.10–3.98), p = 0.03; OR per 1-SD increase in BMI 1.33 (95% CI 1.24–1.42), p < 0.001). The association between SDB and AF was not observed in sensitivity analyses, whilst associations between BMI and AF remained consistent. Similarly, in multivariable MR, SDB was not associated with AF after adjusting for BMI (OR 0.68 (95% CI 0.42–1.10), p = 0.12). Higher BMI remained associated with increased risk of AF after adjusting for OSA (OR 1.40 (95% CI 1.30–1.51), p < 0.001). Elevated BMI appears causal for AF, independent of SDB. Our data suggest that the association between SDB, in general, and AF is attributable to mediation or confounding from obesity, though we cannot exclude that more severe SDB phenotypes (i.e., OSA) are causal for AF.
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Ardissino et al. (2022) conducted an observational in Atrial Fibrillation (n=537,409). Sleep-disordered breathing and Body Mass Index was evaluated on Atrial fibrillation (OR 2.09, 95% CI 1.10-3.98, p=0.03). Genetically predicted sleep-disordered breathing was associated with atrial fibrillation (OR 2.09; 95% CI 1.10-3.98), but this association was lost after adjusting for BMI (OR 0.68; P=0.12).
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