Impact of raised body mass index on bi-atrial structure, function, and electrophysiology in patients with atrial fibrillation
N Bodagh, V Vigneswaran, A Gharaviri, I Kotadia, M Klis, S Niederer, A Von Kietzell, K Maciunas, A Chiribiri, N Grubb, S Haldar, M O'neill, S E WilliamsAbstract
Background
A raised body mass index (BMI) is an established risk factor for both the development of atrial fibrillation and arrhythmia recurrence following catheter ablation. Raised BMI has been associated with electrophysiological remodelling, but most evidence has been derived from animal models or human studies limited to the left atrium. An improved understanding of the impact of raised BMI on bi-atrial structure, function, and electrophysiology in humans could help to elucidate the mechanisms responsible for the increased risk of arrhythmia recurrence following catheter ablation in patients with high BMI.
Aim
To study the impact of raised BMI on bi-atrial structure, function, and electrophysiology in patients with atrial fibrillation.
Methods
A multicentre, prospective observational cohort study was conducted in patients undergoing atrial fibrillation ablation. Pre-procedural assessment of atrial structure and function was performed using cardiac magnetic resonance imaging (MRI), and intra-procedural assessment of electrophysiological function was performed using bi-atrial electroanatomic mapping and electrophysiological testing (Figure 1). Patients with BMI ≥27 kg/m² were identified from the cohort and matched 1:1 to a control group with BMI <27 kg/m² using propensity scores based on age, sex, atrial fibrillation type, heart failure, hypertension, stroke/TIA, diabetes and vascular disease.
Results
A total of 42 patients were included and divided into two groups: raised BMI (n=21) and reference (n=21). Body mass index was 31.4 ±4.9 kg/m2 in the raised BMI group and 24.1 ±2.1kg/m2 in the reference group. Left atrial ERP was significantly shorter in raised BMI patients compared with the reference group (230ms [IQR 200–240] vs 270ms [IQR 230–280], p=0.034). Similarly, right atrial ERP was significantly shorter amongst raised BMI patients (225ms [IQR 210–252.5] vs 250ms [IQR 240–280], p = 0.040) (Figure 2). No significant differences were observed in bi-atrial volume, ejection fraction, MRI-defined fibrosis, voltage, conduction velocity or wave collision percentage.
Conclusions
In this cohort, raised BMI was associated with shorter bi-atrial ERP, independent of measurable structural or functional remodelling. This bi-atrial electrical remodelling may contribute in part to the higher risk of arrhythmia recurrence following catheter ablation in patients with raised BMI. These findings suggest that a raised BMI may initially induce electrical rather than structural atrial changes, representing a potentially reversible stage before the development of structural or functional atrial effects. Early weight reduction may help reverse high BMI-related electrical remodelling and improve outcomes following catheter ablation.