Publication

Statins Reduce Epicardial Adipose Tissue Attenuation Independent of Lipid Lowering: A Potential Pleiotropic Effect

Downloadable Content

Persistent URL
Last modified
  • 05/21/2025
Type of Material
Authors
    Paolo Raggi, Emory UniversityVaruna Gadiyaram, Emory UniversityChao Zhang, Emory UniversityZhengjia Chen, Emory UniversityGary Lopaschuk, University of AlbertaArthur Stillman, Emory University
Language
  • English
Date
  • 2019-06-18
Publisher
  • Wiley Open Access: Creative Commons Attribution Non-Commercial
Publication Version
Copyright Statement
  • © 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 2047-9980
Volume
  • 8
Issue
  • 12
Start Page
  • e013104
End Page
  • e013104
Abstract
  • Background: High epicardial adipose tissue (EAT) attenuation (Hounsfield units [HUs]) on computed tomography is considered a marker of inflammation and is associated with an increased risk of cardiovascular events. Statins reduce the volume of EAT, but it is unknown whether they affect EAT HUs. Methods and Results: We reviewed the chest computed tomographic scans of 420 postmenopausal women randomized to either 80 mg of atorvastatin or 40 mg of pravastatin daily and rescanned after 1 year to measure change in coronary artery calcium score. EAT HUs were measured near the proximal right coronary artery and remote from any area of coronary artery calcium. Computed tomographic images were also queried for subcutaneous adipose tissue (SubQ) attenuation (HUs) change over time. The mean patients’ age was 65±6 years. The baseline EAT HU value was higher than the SubQ HU value (−89.4±24.0 HU versus −123.3±30.4 HU; P<0.001). The EAT HU value decreased significantly in the entire cohort (−5.4±29.7 HU [−6% change]; P<0.001), but equally in the patients given atorvastatin and pravastatin (−6.35+31 HU and −4.55+28 HU; P=0.55). EAT HU change was not associated with change in total cholesterol, low-density lipoprotein cholesterol, coronary artery calcium, and EAT volume (all P=not significant). Change in high-density lipoprotein cholesterol was marginally associated with EAT HU change (P=0.07). Statin treatment did not induce a change in SubQ HUs. Conclusions: Statins induced a decrease in EAT HUs over time, independent of intensity of low-density lipoprotein cholesterol lowering. The positive effect on EAT and the neutral effect on SubQ suggest that statins induced a decrease in metabolic activity in EAT by reduction in cellularity, vascularity, or inflammation. The clinical significance of the observed change in EAT HUs remains to be demonstrated.
Author Notes
  • Correspondence to: Paolo Raggi, MD, PhD, Mazankowski Alberta Heart Institute, University of Alberta, 11220 83rd Ave, Ste 5A9-014, Edmonton, Alberta, Canada T6G 2B7. E-mail: raggi@ualberta.ca
Keywords
Research Categories
  • Biology, Biostatistics
  • Health Sciences, General

Tools

Relations

In Collection:

Items