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Original article
Vasa vasorum and plaque progression, and their response to atorvastatin in a rabbit model of atherosclerosis: contrast-enhanced ultrasound imaging and intravascular ultrasound study
  1. Jinwei Tian1,2,
  2. Sining Hu1,
  3. Yanli Sun1,
  4. Huai Yu1,2,
  5. Xue Han3,
  6. Wen Cheng3,
  7. Xiang Ban4,
  8. Shaosong Zhang5,
  9. Bo Yu1,2,
  10. Ik-Kyung Jang6
  1. 1The Key Laboratories of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang, China
  2. 2Cardiology Division, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China
  3. 3Ultrasound Department, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China
  4. 4Pathology Department, Harbin Medical University, Harbin, Heilongjiang, China
  5. 5LightLab Imaging/St. Jude Medical Westford, Boston, Massachusetts, USA
  6. 6Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Dr Bo Yu, The Key Laboratories of Myocardial Ischaemia, Chinese Ministry of Education, Cardiology Division, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China; yubodr{at}


Objectives To serially investigate the relationship between vasa vasorum (VV) proliferation and plaque progression in vivo, and the effects of atorvastatin on VV and atherosclerosis as assessed by contrast-enhanced ultrasound (CEUS) and intravascular ultrasound (IVUS) imaging.

Methods Carotid atherosclerosis was induced in rabbits with a high-cholesterol diet for 20 weeks and balloon injury. At week 16, following the imaging of the right common carotid arteries by CEUS and IVUS, 20 rabbits were randomised into a control or atorvastatin group (2 mg/kg/day). At week 20, CEUS and IVUS were repeated. Normalised maximal video-intensity enhancement (MVE) was calculated to quantify the density of VV. Plaque volume was determined by IVUS.

Results When compared with the control group, lipid levels were not significantly lower following 4 weeks of atorvastatin administration. The increases in the normalised MVE over time were greater in the control group than in the atorvastatin group (p=0.001). The increase in plaque volume from 16 to 20 weeks was significantly greater in the control group than in the atorvastatin group (p=0.001). There was a positive relationship between changes in normalised MVE and plaque volume (r=0.72, p=0.002).

Conclusions There was a positive correlation between VV density and plaque progression. Atorvastatin significantly inhibits the development of adventitial VV and progression of atherosclerosis independent of lowering the cholesterol level.

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