Numerous trials and meta-analyses have shown a strong obesity paradox in atrial fibrillation (AFib), in which overweight and obese patients with AFib tend to have a better prognosis than normal or underweight patients. Despite this, recent evidence found that weight loss, physical activity and exercise, and increases in cardiorespiratory fitness (CRF) help with the primary prevention and reduction of AFib recurrences, according to a state-of-the-art review published October 9 in the Journal of the American College of Cardiology.

The prevalence of AFib in adults is expected to increase by nearly three-fold over the next 30 years, from 5.2 million to 12.1 million affected people in the U.S. alone, causing experts to categorize this as an AFib epidemic. Meanwhile, evidence shows an association between the increasing obesity epidemic and an increase in the risk of developing AFib. Additionally, in recent epidemiological studies, obesity has emerged as an independent risk factor for AFib.

Professor Carl Lavie et al., examined special issues regarding AFib in obesity and the interrelation between these disorders and the prevalence of cardiovascular disease events.

In exploring the relation of left atrial (LA) remodeling and altered LA function to AFib in obesity, the authors note LA enlargement to be present in nearly all obese patients in postmortem studies. Previous studies also found LA size to be an independent predictor of AFib, and obesity to be more a potent predictor of LA enlargement than hypertension.

Regarding the relation between fat and AFib, multiple controlled studies demonstrated an association between pericardial fat and AFib; however, fat deposits in direct contact with LA myocardium (EAT) have shown a higher likeliness in the development of AFib. Meanwhile, studies have associated obesity with increased pericardial fat volumes. “In summary, the paracrine effects of excessive fat (particularly EAT) in obese patients, in association with modulation of the autonomic nervous system may serve as triggers for the development of AFib and contribute to its severity,” the authors write.

The authors also highlight the complexity of pathophysiological mechanisms linking obesity and AFib, emphasizing they are not yet completely understood. These mechanisms include dysregulation in domains such as hemodynamics, neurohumoral, inflammatory, metabolic, adipokines and autonomics, and a combination of these mechanisms ultimately contribute to the initiation and maintenance of AFib in obese atria.

“Although future studies are needed to determine the clinical relevance of this phenomenon, the current evidence from weight-loss intervention studies … argue that the obesity paradox should not be used as a rationale against aggressive lifestyle risk factor modification, including weight loss for management of AFib patients,” state the study authors.

Specifically, while weight gain is associated with increased risk of AFib, intentional weight loss results in a favorable impact on the epidemiology of AFib, reducing symptom burden and severity, EAT, and LA volumes and left ventricular wall thickness. The authors suggest conducting future studies to determine if these strategies can decrease the long-term risk of mortality, stroke and heart failure hospitalization.

Higher CRF levels have also been associated with greater arrhythmia-free survival in patients with existing AFib, as well as a lower risk of AFib recurrence and symptom burden. Aerobic interval training was also found to significantly lower burden of AFib over a short-term follow-up period.

“Future large randomized controlled trials are needed to determine if the beneficial effects of exercise in AFib patients in the short-term may translate into favorable CVD outcomes in the long-term follow-up,” the authors concluded.