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

> **NIH NIH K23** · UNIV OF MASSACHUSETTS MED SCH WORCESTER · 2022 · $162,000

## Abstract

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 propose 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 my 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 a K23 Mentored Patient-Oriented Career Development Award from the National Heart Lung and
Blood Institute allow me the opportunities to expand my skills in clinical research methodologies, bioinformatics
and biostatistics and enable me to be a translational scientist. The training plan in this proposal takes
advantage of coursework and a strong mentoring team (Drs. McManus, Fitzgerald, and Corvera) with broad
expertise (atrial fibrillation, innate immunity, adipocyte biology and clinical research methodologies) to fill key
gaps in my previous training to advance my career goals. This proposal is among the first to explore the
mechanism by which myeloid cells are recruited to the myocardium. This work will provide novel insights into
the association between epicardial adipose tissue, inflammation and postoperative AF. The recruitment of
inflammatory cells is key to the subsequent immune-mediated dysregulation of the electrical properties in
cardiomyocytes and the downstream fibrotic processes. Understanding the molecular mediators of
inflammation will identify new treatments for postoperative AF.

## Key facts

- **NIH application ID:** 10526040
- **Project number:** 1K23HL161432-01A1
- **Recipient organization:** UNIV OF MASSACHUSETTS MED SCH WORCESTER
- **Principal Investigator:** Khanh-Van Thi Tran
- **Activity code:** K23 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $162,000
- **Award type:** 1
- **Project period:** 2022-09-01 → 2027-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10526040

## Citation

> US National Institutes of Health, RePORTER application 10526040, The Role of Highly inflamed Epicardial Adipose Tissue in the Development of Atrial Fibrillation (1K23HL161432-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10526040. Licensed CC0.

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