Abstract 14355: Metabolic Dysregulation and Incident Atrial Fibrillation in Older Adults

Abstract

Introduction: Obesity and dysmetabolism are major risk factors for atrial fibrillation (AF). Fasting and post-load levels of glucose and non-esterified fatty acids (NEFA) reflect different facets of metabolic regulation, but their contributions to AF risk have not been studied simultaneously in prior studies. We assessed fasting and post-load glucose and NEFA in an older cohort to identify their independent associations with new-onset AF, and secondarily with baseline ECG parameters known to be markers of AF risk. Methods: This study focused on participants from the community-based Cardiovascular Health Study who were free of prevalent AF and had serum collected in the fasting state and after an oral glucose tolerance test. Maximal p wave duration and p wave terminal force in V1 (PTFV1) were measured from 12-lead ECG. Associations were evaluated with linear regression for ECG parameters, and Cox regression for AF. Results: The study included 1,877 participants (age 77.7±4.4). After adjustment, both fasting and post-load glucose, but not NEFA, were positively associated with higher PTFV1. When fasting and post-load glucose were entered together, only the relationship for the latter remained significant (63 μV*ms greater PTFV1 per SD increment in post-load glucose [p=0.028]). During median follow-up of 11.4 years, 717 cases of incident AF occurred. Post-load glucose, but not fasting glucose or either NEFA measure, showed an association with incident AF (adj. HR per SD=1.11 [95% CI=1.02, 1.21], p=0.017). There was significant interaction by sex (p=0.015). The positive relationship of post-load glucose with AF was observed in women (adj. HR per SD=1.21 [1.09, 1.35], p<0.001), but not men (adj. HR per SD=0.97 [0.85, 1.12], p=0.714). Conclusions: Among older adults, post-load glucose, but not fasting glucose or NEFA measures, was positively associated with incident AF, with consistent findings for PTFV1 on baseline ECG. The relationship with AF appeared specific to women. Because post-load glucose is a marker of both pancreatic β-cell insufficiency and skeletal muscle decline, these findings suggest that interventions to address such tissue-organ dysfunction in older women might prevent AF in this high-risk population.