Correlation of Adventitial Vasa Vasorum with Intracranial Atherosclerosis: A Postmortem Study.
- Author:
Lu ZHENG
1
;
Wen Jie YANG
;
Chun Bo NIU
;
Hai Lu ZHAO
;
Ka Sing WONG
;
Thomas Wai Hong LEUNG
;
Xiang Yan CHEN
Author Information
- Publication Type:Original Article
- Keywords: Atherosclerosis; Angiogenesis; Vasa vasorum
- MeSH: Arteries; Atherosclerosis; Autopsy; Basilar Artery; Brain; Cerebral Arteries; Constriction, Pathologic; Humans; Intracranial Arteriosclerosis*; Middle Cerebral Artery; Phenobarbital; Vasa Vasorum*; Vertebral Artery
- From:Journal of Stroke 2018;20(3):342-349
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND AND PURPOSE: Vasa vasorum (VV) have been believed to be rare or non-existent in small-caliber intracranial arteries. In a series of human cerebral artery specimens, we identified and examined the distribution of VV in association with co-existing intracranial atherosclerosis. METHODS: We obtained cerebral artery specimens from 32 consecutive autopsies of subjects aged 45 years or above. We scrutinized middle cerebral artery (MCA), vertebral artery (VA), and basilar artery (BA) for the presence of adventitial VV. We described the distribution of VV, and the characteristics of co-existing atherosclerotic lesions. RESULTS: Among 157 intracranial arteries, adventitial VV were present in 74 of the 157 specimens (47%), involving MCA (n=13, 18%), BA (n=14, 19%), and VA (n=47, 64%). Although qualitatively these 74 adventitial VV distributed similarly in arteries with or without atherosclerotic lesions (disease-free arteries n=4/8; arteries of pre-atherosclerosis n=17/42; and arteries of progressive atherosclerosis n=53/107), the presence of adventitial VV in intracranial VA was associated with a heavier plaque load (1.72±1.66 mm2 vs. 0.40±0.32 mm2, P < 0.001), severer luminal stenosis (25%±21% vs. 12%±9%, P=0.002), higher rate of concentric lesions (79% vs. 36%, P=0.002), and denser intraplaque calcification (44% vs. 0%, P=0.003). Histologically, intracranial VA with VV had a larger diameter (3.40±0.79 mm vs. 2.34±0.58 mm, P < 0.001), thicker arterial wall (0.31±0.13 mm vs. 0.23±0.06 mm, P=0.002), and a larger intima-media (0.19±0.09 mm vs. 0.13± 0.04 mm, P=0.003) than VA without VV. CONCLUSIONS: Our study demonstrated the distribution of adventitial VV within brain vasculature and association between vertebral VV and progressive atherosclerotic lesions with a heavier plaque load and denser intraplaque calcification.
