The Role of Highly inflamed Epicardial Adipose Tissue in the Development of Atrial Fibrillation

Project Abstract My long-term goal is to be a clinical-translational research scientist focused on developing effective therapies for patients with cardiovascular disease. My background in the development and physiology of adipose tissue as well as clinical training in cardiovascular medicine have motivated me to better understand the molecular mechanisms by which epicardial adipocytes influence the development of atrial fibrillation. I proposed to conduct a prospective clinical investigation to test the hypothesis that adipocytes are recruiting myeloid cells to the myocardium to increase vulnerability for postoperative AF. The specific aims of the parent K23 proposal are: Aim 1. Characterize transcriptomic profiles of epicardial adipocytes and determine circulating levels of adipose-derived chemokines Aim 2. Determine the relationship between inflammation in epicardial adipose tissue and left atrial function as assessed by echocardiographic parameters, including left atrial volume index, left atrial function index and left atrial mechanical dispersion. Aim 3. Examine the relationship between inflammation in epicardial adipose tissue and incident postoperative AF after coronary artery bypass graft surgery I am seeking an administrative supplement to the parent K23 award to provide bioinformatic support for analyzing single nuclei RNA sequencing and proteomics datasets to better understand the molecular mediators of inflammation and identify new treatments for postoperative AF.