Arteriolosclerosis Differs from Venular Collagenosis in Relation to Cerebrovascular Parenchymal Damages: An Autopsy-based Study
Yuan Cao1, Mei-Ying Huang1, Chen-Hui Mao1, Xue Wang2, Yuan-Yuan Xu2, Xiao-Jing Qian2, Chao Ma2, Wen-Ying Qiu2, Yi-Cheng Zhu1
1Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 2Human Anatomy, Histology and Embryology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College
Objective:
We aimed to investigate the associations between microvascular injuries, including arteriolosclerosis and venular collagenosis, and related parenchymal damages in aging brains, to investigate the underlying correlations.
Background:
Cerebrovascular parenchymal damage is prevalent in aging brains; however, its vascular etiology has not been fully elucidated. In addition to the underlying role of sclerotic arterioles, the correlation between collagenized venules has not been clarified.
Design/Methods:
We evaluated arteriolosclerosis and venular collagenosis in seven regions from 27 autopsy cases with no history of stroke or brain tumor. The correlations between the ratio of arteriolosclerosis, venular collagenosis, and the severity of cerebrovascular parenchymal damage, including lacunes, microinfarcts, myelin loss, and parenchymal and perivascular hemosiderin deposits, were assessed.
Results:
Arteriolosclerosis and venular collagenosis became more evident with age. Arteriolosclerosis was associated with lacunes (p = 0.004) and brain parenchymal hemosiderin deposits in the superior frontal cortex (p = 0.024) but not with leukoaraiosis severity. Venular collagenosis was not associated with the number of lacunes or hemosiderin, while white matter generally became paler with severe venular collagenosis in the periventricular (β = -0.430, p = 0.028) and deep white matter (β = -0.437, p = 0.025).
Conclusions:
Our findings imply an important role for venular lesions in relation to microvessel-related parenchymal damage which is different from that for arteriolosclerosis. Different underlying mechanisms of both cerebral arterioles and venules require further investigation.