Obesity is a well known risk factor for cardiovascular diseases including cardiac arrhythmias, but the underlying mechanisms are not well elucidated. While body mass index (BMI) is the conventional clinical metric used for obesity classification, it may not account for the fat deposits directly on the heart, also called the epicardial fat. Given, the endocrine, autocrine, and paracrine functional profile of fat cells (adipocytes), it is possible that the cross talk between fat and cardiac tissue could play a role in arrhythmogenesis.
There are typically three main ingredients required to generate clinical arrhythmias including the arrhythmogenic substrate, the trigger factor, and the modulation factors. The arrhythmogenic substrate could be functional or structural. An example would be a tissue region that is in functional refractory period or there exists a non-conducting scar tissue. The arrhythmogenic triggers include enhanced automaticity or triggered beats such as early or late after depolarizations. The modulation factors include autonomic dysfunction, stress, hypoxia etc.
We are interested in exploring whether the accumulation of fat on the cardiac surface (epicardial adiposity) could modulate the arrhythmogenic substrate, the trigger factor, and/or the local autonomic regulation, and if so, what are the underlying molecular mechanisms?