Abstract
The epidemics of obesity and diabetes mellitus are associated with an increased incidence of both atrial fibrillation (AF), the most common sustained arrhythmia in adults, and sudden cardiac death (SCD). Obesity and DM are known to have adverse effects on cardiac structure and function. The pathologic mechanisms are thought to involve cardiac tissue remodeling, metabolic dysregulation, inflammation, and oxidative stress. Clinical data suggest that left atrial size, epicardial fat pad thickness, and other modifiable risk factors such as hypertension, glycemic control, and obstructive sleep apnea may mediate the association with AF. Data from human atrial tissue biopsies demonstrate alterations in atrial lipid content and evidence of mitochondrial dysfunction. With respect to ventricular arrhythmias, abnormalities such as long QT syndrome, frequent premature ventricular contractions, and left ventricular hypertrophy with diastolic dysfunction are commonly observed in obese and diabetic humans. The increased risk of SCD in this population may also be related to excessive cardiac lipid deposition and insulin resistance. While nutritional interventions have had limited success, perhaps due to poor long-term compliance, weight loss and improved cardiorespiratory fitness may reduce the frequency and severity of AF.