Are autoimmune diseases associated with increased odds of atrial fibrillation in adult outpatients?
Autoimmune diseases are modestly associated with an increased risk of atrial fibrillation, supporting the role of systemic inflammation in AF pathogenesis and highlighting the need for cardiovascular risk assessment in these patients.
Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice and is associated with considerable morbidity and mortality. Chronic systemic inflammation is increasingly recognized as a contributing factor in AF pathogenesis. Autoimmune diseases (AIDs), with their prototypical inflammatory conditions, may therefore be associated with AF. However, evidence from routine outpatient care regarding these potential associations across multiple AIDs remains limited. We aimed to examine whether autoimmune diseases are associated with increased odds of atrial fibrillation and to assess whether these associations differ between women and men. We conducted a retrospective 1:1 matched case-control study using data from the Disease Analyzer database (IQVIA). Adult patients with AF (2010–2024) were matched to AF-free controls based on age, sex, comorbidities, medication use and observation time. The presence of predefined AIDs prior to AF diagnosis was identified using ICD-10 codes. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) and sex-stratified data were analyzed. A total of 174,992 AF cases and 174,992 matched controls were included (mean age 74.0 years, 48% female). Overall, any AID was associated with AF (OR 1.12; 95% CI 1.09–1.15). Significant associations were observed for rheumatoid arthritis (OR 1.14; 95% CI 1.10–1.18), inflammatory bowel disease (OR 1.16; 95% CI 1.06–1.27), psoriasis (OR 1.10; 95% CI 1.05–1.15), and Graves’ disease (OR 1.29; 95% CI 1.18–1.41). Several AIDs were modestly associated with atrial fibrillation in routine outpatient care. Sex-stratified analyses suggested variation in point estimates for some associations, while interaction analyses showed limited evidence for true sex-specific effect modification. These findings support the role of systemic inflammation in AF pathogenesis and underscore the need for interdisciplinary cardiovascular risk assessment in patients with autoimmune conditions.
Sedighi et al. (Mon,) studied this question.