Key result
Review details how obesity drives AF via atrial enlargement, pericardial fat, fibrosis, and inflammation.
Why the study?
Prevalence of atrial fibrillation and obesity has skyrocketed, but the pathogenesis linking obesity-related structural, hemodynamic, and electrical changes to atrial fibrillation warrants exploration.
This review highlights the pathophysiological mechanisms, including structural and inflammatory changes, linking obesity to the development and progression of atrial fibrillation.
Supports weight loss as AF prevention adjunct; leaves open validation of targeted anti-fibrotic therapies in trials.
In the past 40 years, the prevalence of atrial fibrillation and obesity have skyrocketed. It has long been established that obesity can lead to adverse cardiovascular outcomes due to its myriad of effects on cardiovascular architecture, cardiovascular hemodynamics, and electrical conduction interference. The goal of this article is to explore the pathogenesis of atrial fibrillation in obese patients and examine the role of atrial enlargement, increased adipose deposits surrounding the pericardium, interstitial fibrosis, and inflammation in the development and worsening of atrial fibrillation in obese patients.
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Upadhyay et al. (2023) conducted a review in Atrial Fibrillation and Obesity. This review explores the pathogenesis of atrial fibrillation in obese patients, examining the roles of atrial enlargement, pericardial adipose deposits, interstitial fibrosis, and inflammation.
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