LAUSR

TO THE EDITOR: I thank you for the opportunity to respond to Munoz and colleagues’ comments and expand the discussion on our recently published paper (1). We pioneered the research on epicardial adipose tissue (2). In addition to its peculiar and unique anatomical, genetic, and biological properties and functions, epicardial fat has recently emerged as a modifiable and measurable cardiometabolic risk factor and well-responsive therapeutic target. Our most recent trial showed a rapid and large reduction (around 36%) of the ultrasound-measured epicardial fat thickness in type 2 diabetic subjects treated with additional liraglutide, a glucagon-like peptide 1 (GLP-1) analog, as compared to subjects on metformin monotherapy. Our study had the power to detect statistically significant differences in epicardial fat between the two arms. We acknowledged that our clinical trial had some limitations, as it was not a double-blinded placebo control study, the two groups were relatively imbalanced, and no other visceral fat markers were measured.