Abstract 4363321: Association of Left Atrial Dysfunction With Ventricular Arrhythmias in the ARIC Study

Introduction: Left atrial (LA) myopathy indicated by worsening LA function has been well-established as a predictor of atrial fibrillation (AF) and other atrial arrhythmias. However, its association with ventricular arrhythmias remains unclear. Hypothesis: Higher LA function is associated with lower frequency of premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT). Methods: We included 2,074 ARIC participants without prevalent AF who had LA strain measurements at Visit 5 (2011-2013) and underwent 2-week continuous monitoring with Zio XT Patch at Visit 6 (2016-2017). LA reservoir, conduit, and contractile strain were measured by speckle-tracking echocardiography. Outcomes included PVC frequency (PVCs/hour) and NSVT episodes/day. Multivariable regression models adjusted for demographics, cardiovascular risk factors, medications, and cardiac structure/function. Results: The cohort included 2,074 participants with a mean age of 74±5 years; 58% were women and 23% were Black participants. Overall, median PVC frequency was 2.4/hour (IQR 0.4-15.8), and 605 participants (29.2%) experienced NSVT with a median frequency of 0.08 episodes/day (IQR 0.07-0.21). In fully adjusted models, higher LA function was consistently associated with less frequent ventricular arrhythmias. Specifically, each SD increment in LA reservoir strain was associated with 10.3% lower PVC frequency (p<0.01) and 9.8% lower NSVT frequency (p<0.01). Similarly, each SD increment in LA contractile strain was associated with 7.6% lower PVCs frequency (p=0.03) and 6.5% lower NSVT frequency (p=0.03). LA conduit strain showed similar but non-significant trends, with each SD increase associated with 5.4% lower PVCs frequency (p=0.13) and 5.6% lower NSVT frequency (p=0.06). Conclusion: Atrial myopathy indicated by lower LA function is independently associated with ventricular arrhythmias. These findings suggest LA myopathy may reflect global cardiac substrate changes that predispose to both atrial and ventricular arrhythmogenesis.