Atrial Fibrillation in Diabetes: Epidemiology, Mechanisms and Integrated Management

Atrial fibrillation (AF) and diabetes mellitus frequently coexist and together define a high-risk cardiometabolic phenotype. Diabetes is associated with an increased incidence of AF, although this relationship is strongly influenced by obesity, hypertension, chronic kidney disease (CKD), heart failure (HF), sleep-disordered breathing, and broader metabolic risk clustering. Once AF develops, diabetes is associated with greater thromboembolic and HF risk, impaired quality of life, cognitive vulnerability, and excess mortality. These adverse outcomes may be partly explained by a multidimensional atrial substrate, described here within the conceptual framework of diabetic atrial cardiomyopathy, in which hyperglycaemia, insulin resistance, glycaemic variability, oxidative stress, inflammation, autonomic dysfunction, microvascular disease, lipotoxicity, and epicardial adipose tissue dysfunction may contribute to atrial fibrosis, electrical heterogeneity, impaired calcium handling, mitochondrial injury, and mechanical dysfunction. Collectively, these abnormalities may facilitate AF initiation, persistence, progression, and recurrence after rhythm-control interventions. Management should therefore extend beyond rhythm control and anticoagulation alone. In individuals at increased risk of AF, priorities include cardiometabolic optimization, treatment of obesity, hypertension, CKD, HF, and sleep apnoea, lifestyle intervention, and selective rhythm surveillance. In subclinical AF, decisions regarding anticoagulation should account for AF burden, thromboembolic and bleeding risk, renal function, frailty, and patient preference. In established AF, stroke prevention, symptom-directed rate or rhythm control, cardiometabolic therapy, and longitudinal reassessment remain central. This narrative review integrates the epidemiology, mechanisms, and management of AF in diabetes across the continuum from AF risk to subclinical and clinical disease.