LAUSR

The Manitoba Follow-Up Study first identified obesity as a risk factor for AF over 20 years ago (3). Since then, numerous studies have shown that obesity increases the likelihood of AF development (4). Weight loss, whether as part of a structured risk-factor intervention program (5) or as a result of bariatric surgery (6), reduces AF risk. Preclinical studies have suggested a variety of potential mediating mechanisms for the AF-promoting effects of obesity. In a genetic rat model of leptin-deficient obesity, ventricular diastolic dysfunction predisposes to left-atrial dilation that mediates AF promotion (7). Sheep with obesity due to overfeeding develop atrial electrophysiological, electroanatomic, and structural remodeling, along with increased occurrence and sustainability of AF (8). Furthermore, there is evidence that adipocytes produce biologically active molecules that directly promote the development of