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J Vasc Surg. 2004 Sep;40(3):529-35.

Adventitial vasa vasorum heterogeneity among different vascular beds.

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Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.



Different vascular beds show substantial variation in their susceptibilities for development of vascular disease like atherosclerosis, and thereby exhibit a variety of different clinical presentations. Yet, the underlying mechanism of this heterogeneity is not well defined. Recent evidence suggests a role for the vasa vasorum (VV) in vascular disease. We hypothesized that there is a differential distribution structure of adventitial VV in different vascular beds. Hence, the current study was designed to characterize and compare the structure of the adventitial VV in the coronary and the peripheral circulation.


Samples of vessels from different vascular beds were obtained from 6 female crossbred domestic pigs. The samples were scanned using micro-computed tomography, and the images reconstructed and analyzed to characterize VV architecture, including vessel wall area, VV count, VV density, intravessel spatial distribution, mean diameter of first- and second-order VVs and the ratio of second- to first-order VVs.


There were significant differences in VV density among different vascular beds. Density was highest in coronary arteries (2.91 +/- 0.26 vessels/mm2, P <.05, vs renal, carotid, and femoral arteries), intermediate in renal arteries (1.45+/- 0.22 vessels/mm2, P <.05, vs femoral artery) and carotid arteries (0.64 +/- 0.08 vessels/mm2, P <.05, vs femoral artery), and lowest in femoral arteries (0.23 +/- 0.05 vessels/mm2 ). A similar pattern for the ratio of second- to first-order VV was also observed. Random intravessel spatial distribution of VVs was seen in all vascular beds.


The current study demonstrates a differential structure of the adventitial VV in different vascular beds. This intra- and intervessel heterogeneity in VV anatomy is a phenotypic variability that might determine a differential local response to systemic risk factors and, thereby, variable propensity for vascular disease among different vascular beds.

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