Objectives Plaque neovascularisation and the extent of adventitial vasa vasorum (VV) is closely associated with vulnerability of atherosclerotic plaque. To rigorously 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 Thirty New Zealand white rabbits were fed a highcholesterol diet for a period of 20 weeks. At week 4, all rabbits underwent balloon injury of the right common carotid artery. At week 16, Standard B-mode ultrasound and CEUS and IVUS examinations were performed,to investigate the relationship between the extent of adventitial vasa vasorum and plaque volume in vivo. All rabbits were randomised into a control or atorvastatin group (2 mg/kg/day). At week 20, CEUS and IVUS examinations were repeated, and then all rabbits were sacrificed by an overdose of intravenous sodium pentobarbital. The sections were stained with HE, Masson, oil-O and immunostaining was performed with anti-CD31 antibody (1 : 10 dilution; Novus Biologicals Littleton Colorado USA) separately for the formation, volume , characterisation and quanti cation of neovessels of plaques. At weeks 0, 16 and 20, plasma lipid levels were determined by enzymatic assays of blood samples and recorded. The CEUS and IVUS images were analysed off-line by two blinded reviewers. All data analyses were performed using SPSS V. 19.0. A probability value <0.05 was considered statistically significant.

Results When compared with the control group, lipid levels were not significantly lower following 4 weeks of atorvastatin therapy. From 16 to 20 weeks the increase in plaque volume accessed by IVUS was obviously greater in the control group than in the atorvastatin group (p = 0.001). And the VV’s number and density increases were more in the control group than in the atorvastatin group (p = 0.001). And we pathologily confirmd the above results.

Conclusions Concludely, the study firstly assess the VV’s number and density is positively relateted to the the plaque volume by CEUS and IVUS examinations. This study also demonstrates that atorvastatin significantly inhibits VV independent of a reduction in the cholesterol level and delays the development of atherosclerosis, which is also confirmed pathologily.