Among 764 HFpEF patients without pre-existing atrial fibrillation followed for a median 5.81 years in a Hong Kong registry, each 10 mL/m² increase in left atrial volume index (LAVI) raised incident AF risk by 8% (HR 1.08; 95% CI 1.06–1.11). Patients in the highest LAVI tertile faced 78% greater cause-specific AF risk (HR 1.78; 95% CI 1.28–2.49) even after competing-risk adjustment for death. Risk was nonlinear — spline analysis revealed accelerating excess risk at higher LAVI values — and was most concentrated in the first year of follow-up.
HFpEF and atrial fibrillation form a notoriously vicious cycle: atrial pressure overload promotes structural remodeling that begets arrhythmia, which then worsens diastolic filling. This analysis adds mechanistic granularity by showing that LAVI's prognostic signal is partially — but not fully — mediated by hemodynamic markers (E/e' ratio, pulmonary artery systolic pressure), implying an independent structural contribution. The first-year concentration of risk is clinically actionable, potentially justifying intensified rhythm monitoring immediately after HFpEF diagnosis in patients with marked left atrial enlargement. Limitations include the observational, single-center registry design and reliance on documented AF diagnoses, which may undercount paroxysmal events. Generalizability beyond a Chinese cohort warrants caution. As a preprint not yet peer-reviewed, findings require independent validation before informing clinical protocols. Still, the competing-risk methodology is rigorous, and this work meaningfully extends the structural-phenotyping framework for HFpEF risk stratification.
