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Differential distribution of vasa vasorum in different vascular beds in humans

Heike A Hildebrandt1, Mario Gossl, Dallit Mannheim

  • 1Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA.

Atherosclerosis
|October 26, 2007
PubMed

Insights

Vasa vasorum (VV) density is higher in coronary arteries than peripheral ones, suggesting a link between VV and atherosclerosis susceptibility in different human vascular beds.

Area of Science:

  • Vascular Biology
  • Cardiovascular Pathology
  • Medical Imaging

Background:

  • Vasa vasorum (VV) are small blood vessels supplying the outer wall of large arteries.
  • VV are increasingly recognized for their role in the pathogenesis of atherosclerosis.
  • Understanding VV distribution is crucial for elucidating arterial disease mechanisms.

Purpose of the Study:

  • To quantify and compare vasa vasorum density across different human arterial beds.
  • To investigate the relationship between vasa vasorum density and atherosclerosis distribution.
  • To explore the association of VV density with inflammatory markers and collagen content.

Main Methods:

  • Analysis of 42 human arteries (coronary, renal, femoral) using 3D micro-computed tomography (micro-CT).
  • Calculation of VV density, endothelial-surface-fraction, and vascular-area-fraction.
  • Histological staining for endothelial cells, macrophages (CD68), VEGF, and collagen.

Main Results:

  • Coronary arteries exhibited significantly higher VV density compared to renal and femoral arteries.
  • Higher VV density correlated positively with CD68-positive cells and VEGF immunoreactivity.
  • VV density showed a negative correlation with collagen I content.

Conclusions:

  • Human coronary arteries possess a greater density of vasa vasorum than peripheral arteries.
  • This finding supports the hypothesis that VV density influences arterial susceptibility to atherosclerosis.
  • VV distribution may be a key factor in the differential vulnerability of arteries to atherosclerotic disease.
Abstract

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