Atrial Fibrillation and Subclinical Thyroid Dysfunction: Revisiting an Underrecognized Association - A Narrative Review

Subclinical thyroid disease, defined by abnormal thyroid-stimulating hormone (TSH) with normal thyroid hormone levels, is common and may be an underrecognized contributor to atrial fibrillation (AF). This narrative review summarizes current evidence on how mild thyroid dysfunction influences AF risk and highlights practical implications for clinical management, drawing on mechanistic studies, observational epidemiology, and major guideline recommendations addressing subclinical hyperthyroidism, subclinical hypothyroidism, and cardiac rhythm outcomes. Subclinical hyperthyroidism shows a consistent association with increased AF risk. Proposed mechanisms include thyroid hormone–mediated changes in cardiac electrophysiology, increased adrenergic sensitivity, and atrial structural and electrical remodeling. Current American Thyroid Association and European Thyroid Association guidance supports treating higher-risk patients, particularly those older than 65 years or with cardiovascular comorbidities, when TSH is below 0.1 mIU/L. In contrast, evidence linking subclinical hypothyroidism to AF is weak. Although it has traditionally been associated with bradyarrhythmias, newer studies suggest a possible modest increase in AF risk. Treatment decisions for subclinical hypothyroidism are more nuanced, with the strongest consensus favoring therapy when TSH exceeds 10.0 mIU/L, while lower-level elevations generally require individualized assessment. Overall, subclinical thyroid dysfunction, especially subclinical hyperthyroidism, appears meaningfully related to AF risk, but important evidence gaps remain, including limited large-scale trial data showing that treatment prevents AF. Because subclinical thyroid disease and AF both increase with age, management should be individualized according to age, TSH severity, cardiovascular risk, and comorbidities.