scholarly journals Cerebral small vessel disease and heart rate variability: A quest for nontraditional risk factors

Author(s):  
Aleksandra M. Pavlovic
2021 ◽  
Author(s):  
Miaoyi Zhang ◽  
Huan Yu ◽  
Weijun Tang ◽  
Ding Ding ◽  
Jie Tang ◽  
...  

Abstract Background To assess heart rate variability(HRV) among patients with arteriosclerotic cerebral small vessel disease (CSVD) by comparing with control subjects, and to determine whether HRV parameters were related to structural alterations in brain regions involved in autonomic regulation among CSVD patients. MethodsWe consecutively recruited subjects aged between 50 and 80 years who visited the Sleep Center of Huashan Hospital from September 1, 2018 to August 31, 2019. Brain magnetic resonance imaging(MRI) was scanned before enrollment. 63 patients were assigned to the arteriosclerotic CSVD group and 46 to the control group. Polysomnography and synchronous analyses of HRV were performed. Multivariable binary logistic regression was used to identify the relationship between HRV parameters and CSVD. A number of 24 CSVD patients and 21 control participants further underwent three-dimensional brain volume scan, and the voxel based morphometry (VBM) analysis was used to identify gray matter atrophy.ResultsLower standard deviation of normal-to-normal intervals(SDNN, OR=0.943, 95% CI 0.903 to 0.985, P=0.009) and higher ratio of low to high frequency power (LF/HF, OR=4.372, 95% CI 1.033 to 18.508, P=0.045) during the sleep period were associated with CSVD, independent of traditional cerebrovascular risk factors and sleep disordered breathing. Based on VBM results, SDNN during the awake time (b=0.544, 95% CI 0.211 to 0.877, P=0.001) and the sleep period(b=0.532, 95% CI 0.202 to 0.862, P=0.001) were both positively related with gray matter thickness within the right inferior frontal gyrus only among CSVD patients.ConclusionsDecreased nocturnal HRV may be associated with arteriosclerotic CSVD independent of traditional cerebrovascular risk factors and sleep disordered breathing. The structural atrophy of some brain regions associated with cardiac autonomic regulation sheds light on the potential relationship.Trial registration Trial registration number: ChiCTR1800017902.Date of registration: 2018-08-20


Stroke ◽  
2019 ◽  
Vol 50 (9) ◽  
pp. 2486-2491 ◽  
Author(s):  
Oscar H. Del Brutto ◽  
Robertino M. Mera ◽  
Aldo F. Costa ◽  
Pablo R. Castillo

2018 ◽  
Vol 314 (6) ◽  
pp. H1117-H1136 ◽  
Author(s):  
Dana R. Jorgensen ◽  
C. Elizabeth Shaaban ◽  
Clayton A. Wiley ◽  
Peter J. Gianaros ◽  
Joseph Mettenburg ◽  
...  

Aging in later life engenders numerous changes to the cerebral microvasculature. Such changes can remain clinically silent but are associated with greater risk for negative health outcomes over time. Knowledge is limited about the pathogenesis, prevention, and treatment of potentially detrimental changes in the cerebral microvasculature that occur with advancing age. In this review, we summarize literature on aging of the cerebral microvasculature, and we propose a conceptual framework to fill existing research gaps and advance future work on this heterogeneous phenomenon. We propose that the major gaps in this area are attributable to an incomplete characterization of cerebrovascular pathology, the populations being studied, and the temporality of exposure to risk factors. Specifically, currently available measures of age-related cerebral microvasculature changes are indirect, primarily related to parenchymal damage rather than direct quantification of small vessel damage, limiting the understanding of cerebral small vessel disease (cSVD) itself. Moreover, studies seldom account for variability in the health-related conditions or interactions with risk factors, which are likely determinants of cSVD pathogenesis. Finally, study designs are predominantly cross-sectional and/or have relied on single time point measures, leaving no clear evidence of time trajectories of risk factors or of change in cerebral microvasculature. We argue that more resources should be invested in 1) developing methodological approaches and basic science models to better understand the pathogenic and etiological nature of age-related brain microvascular diseases and 2) implementing state-of-the-science population study designs that account for the temporal evolution of cerebral microvascular changes in diverse populations across the lifespan.


2019 ◽  
Author(s):  
Guanxi Xiao ◽  
Rosie Kumar ◽  
Yutaro Komuro ◽  
Jasmine Burguet ◽  
Visesha Kakarla ◽  
...  

AbstractCerebral small vessel disease and resulting white matter pathologies are worsened by cardiovascular risk factors including obesity. The molecular changes in cerebral endothelial cells caused by chronic cerebrovascular risk factors remain unknown. We developed a novel approach for molecular profiling of chronically injured cerebral endothelial cells using cell-specific translating ribosome affinity purification (RiboTag) with RNA-seq in Tie2-Cre:RiboTag mice. We used this approach to identify the transcriptome of white matter endothelial cells after the onset of diet-induced obesity (DIO). DIO induces an IL-17B signaling pathway that acts on the cerebral endothelia through IL-17Rb to increase levels of both circulating CXCL5 and local endothelial expression of CXCL5 in both the DIO mouse model and in humans with imaging or pathologic evidence of cerebral small vessel disease. In the white matter, endothelial CXCL5 acts as a chemoattractant and promotes the association of oligodendrocyte progenitor cells (OPCs) with cerebral endothelia increasing vessel-associated OPC cell number and triggers OPC gene expression programs regulating migration and chemokine receptor activation. Targeted blockade of IL-17B with peripheral antibody administration reduced the population of vessel-associated OPCs by reducing endothelial CXCL5 expression. CXCL5-mediated sequestration of OPCs to white matter vasculature impairs OPC differentiation after a focal white matter ischemic lesion. DIO promotes a unique white matter endothelial-to-oligodendrocyte progenitor cell signaling pathway that compromises brain repair after stroke.


2019 ◽  
Vol 67 (4) ◽  
pp. 1209-1219 ◽  
Author(s):  
Bibek Gyanwali ◽  
Muhammad Amin Shaik ◽  
Boon Yeow Tan ◽  
Narayanaswamy Venketasubramanian ◽  
Christopher Chen ◽  
...  

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