Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is associated with increased risks of heart failure, stroke, and death.1 Despite its importance, current treatment approaches involving antiarrhythmic drugs and catheter ablation carry modest efficacy and significant risks.2 Development of new therapeutic strategies is desirable and may potentially be guided by known clinical risk factors for the arrhythmia. Epidemiologic studies have identified observational associations between multiple clinical conditions and AF, including hypertension, obesity, and thyroid dysfunction.3-5 Targeting biological pathways and lifestyle factors relevant to these conditions may serve as effective preventive therapy for AF; however, it is imperative to note that an observational association may not be reflective of a forward causal relationship. Attempting to decipher causality for observational associations is critical given that interventions on factors external to a causal pathway are less likely to achieve the desired effect on the outcome.
Roberts JD. Thyroid Function and the Risk of Atrial Fibrillation: Exploring Potentially Causal Relationships Through Mendelian Randomization. JAMA Cardiol. 2019;4(2):97–99. doi:10.1001/jamacardio.2018.4614
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