Total Cerebral Small Vessel Disease Score and Anthropometric Indices: A Population-Based Study in Older Adults of Amerindian Ancestry

2021 ◽  
pp. 1-4
Author(s):  
Oscar H. Del Brutto ◽  
Robertino M. Mera

A total of 590 older adults of Amerindian ancestry living in rural Ecuador received anthropometric measurements and a brain magnetic resonance imaging to estimate the total cerebral small vessel disease (cSVD) score. A fully adjusted ordinal logistic regression model, with categories of the total cSVD score as the dependent variable, disclosed significant associations between the waist circumference, the waist-to-hip, and the waist-to-height ratios – but not the body mass index (BMI) – and the cSVD burden. Indices of abdominal obesity may better correlate with severity of cSVD than the BMI in Amerindians. Phenotypic characteristics of this population may account for these results.

2015 ◽  
Vol 22 (11) ◽  
pp. 1482-1487 ◽  
Author(s):  
L. A. Zuurbier ◽  
M. A. Ikram ◽  
A. I. Luik ◽  
A. Hofman ◽  
E. J. W. Van Someren ◽  
...  

2021 ◽  
Vol 13 ◽  
Author(s):  
Arunima Kapoor ◽  
Aimée Gaubert ◽  
Anisa Marshall ◽  
Irene B. Meier ◽  
Belinda Yew ◽  
...  

Background: Cerebral small vessel disease (SVD) is associated with increased risk of stroke and dementia. Progressive damage to the cerebral microvasculature may also trigger angiogenic processes to promote vessel repair. Elevated levels of circulating endothelial progenitor cells (EPCs) and pro-angiogenic signaling proteins are observed in response to vascular injury. We aimed to examine circulating levels of EPCs and proangiogenic proteins in older adults with evidence of SVD.Methods: Older adults (ages 55–90) free of dementia or stroke underwent venipuncture and brain magnetic resonance imaging (MRI). Flow cytometry quantified circulating EPCs as the number of cells in the lymphocyte gate positively expressing EPC surface markers (CD34+CD133+CD309+). Plasma was assayed for proangiogenic factors (VEGF-A, VEGF-C, VEGF-D, Tie-2, and Flt-1). Total SVD burden score was determined based on MRI markers, including white matter hyperintensities, cerebral microbleeds and lacunes.Results: Sixty-four older adults were included. Linear regression revealed that older adults with higher circulating EPC levels exhibited greater total SVD burden [β = 1.0 × 105, 95% CI (0.2, 1.9), p = 0.019], after accounting for age and sex. Similarly, a positive relationship between circulating VEGF-D and total SVD score was observed, controlling for age and sex [β = 0.001, 95% CI (0.000, 0.001), p = 0.048].Conclusion: These findings suggest that elevated levels of circulating EPCs and VEGF-D correspond with greater cerebral SVD burden in older adults. Additional studies are warranted to determine whether activation of systemic angiogenic growth factors and EPCs represents an early attempt to rescue the vascular endothelium and repair damage in SVD.


2019 ◽  
Vol 15 ◽  
pp. P1190-P1190
Author(s):  
Mozhu Ding ◽  
Rui Wang ◽  
Gregoria Kalpouzos ◽  
Kristina Johnell ◽  
Laura Fratiglioni ◽  
...  

Stroke ◽  
2021 ◽  
Author(s):  
Mozhu Ding ◽  
Rui Wang ◽  
Grégoria Kalpouzos ◽  
Erika J. Laukka ◽  
Yuanjing Li ◽  
...  

Background and Purpose: Cerebral small vessel disease, as a potential mechanism underlying the association between atrial fibrillation (AF) and dementia, remains poorly investigated. In this cohort study, we sought to examine the association between AF and cerebral small vessel disease markers among older adults. Methods: Data on 336 participants (age ≥60 years, mean 70.2 years; 60.2% women) free of dementia, disability, and cerebral infarcts were derived from the population-based Swedish National Study on Aging and Care in Kungsholmen. Structural brain magnetic resonance imaging examinations were performed at baseline (2001–2004) and follow-ups (2004–2007 and 2007–2010). Magnetic resonance imaging markers of cerebral small vessel disease included perivascular spaces, lacunes, and volumes of white matter hyperintensities, lateral ventricles, and total brain tissue. AF was assessed at baseline and follow-ups through clinical examinations, electrocardiogram, and medical records. Data were analyzed using linear mixed-effects models. Results: At baseline, 18 persons (5.4%) were identified to have prevalent AF and 17 (5.6%) developed incident AF over the 6-year follow-up. After multivariable adjustment, AF was significantly associated with a faster annual increase in white matter hyperintensities volume (β coefficient=0.45 [95% CI, 0.04–0.86]) and lateral ventricular volume (0.58 [0.13–1.02]). There was no significant association of AF with annual changes in perivascular spaces number (β coefficient=0.53 [95% CI, −0.27 to 1.34]) or lacune number (−0.01 [−0.07 to 0.05]). Conclusions: Independent of cerebral infarcts, AF is associated with accelerated progression of white matter lesions and ventricular enlargement among older adults.


2015 ◽  
Vol 36 (1) ◽  
pp. 72-94 ◽  
Author(s):  
Anna Poggesi ◽  
Marco Pasi ◽  
Francesca Pescini ◽  
Leonardo Pantoni ◽  
Domenico Inzitari

The term cerebral small vessel disease (SVD) refers to a group of pathologic processes with various etiologies that affect small arteries, arterioles, venules, and capillaries of the brain. Magnetic resonance imaging (MRI) correlates of SVD are lacunes, recent small subcortical infarcts, white-matter hyperintensities, enlarged perivascular spaces, microbleeds, and brain atrophy. Endothelial dysfunction is thought to have a role in the mechanisms leading to SVD-related brain changes, and the study of endothelial dysfunction has been proposed as an important step for a better comprehension of cerebral SVD. Among available methods to assess endothelial function in vivo, measurement of molecules of endothelial origin in peripheral blood is currently receiving selective attention. These molecules include products of endothelial cells that change when the endothelium is activated, as well as molecules that reflect endothelial damage and repair. This review examines the main molecular factors involved in both endothelial function and dysfunction, and the evidence linking endothelial dysfunction with cerebral SVD, and gives an overview of clinical studies that have investigated the possible association between endothelial circulating biomarkers and SVD-related brain changes.


Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Robert M Bryan ◽  
Sharon C Phillips ◽  
David J Durgan

In recent years, it has become apparent that the gut microbiome can influence the functioning and pathological states of organs and systems throughout the body. In this study we tested the hypothesis that the gut microbiome has a major role in the cascade of pathological events, including inflammation and hypertension, leading to the onset of cerebral small vessel disease (CSVD). To test this hypothesis, we used an animal model for hypertensive CSVD, the spontaneously hypertensive stroke prone rat (SHRSP). At birth, SHRSP pups were placed with foster dams of the SHRSP strain or dams of the WKY strain, the control strain that does not develop hypertensive CSVD. Similarly, WKY pups were placed with dams of the same or opposite strain. The rationale for cross fostering is that gut microbiomes are shaped by environmental bacteria of the foster dam and the nesting surroundings. Analysis of the bacterial genera in feces using 16S rRNA analysis demonstrated that the gut microbiome in the rat pups was strongly influenced by the foster dam. SHRSP offspring fostered on WKY dams had systolic blood pressures (SBPs) that were significantly decreased by 26 mmHg (P<0.001, N=5-7/group) at 20 weeks, compared to SHRSP offspring fostered on SHRSP dams. Similarly, WKY offspring fostered on SHRSP dams had significantly increased SBP compared to WKY offspring fostered on WKY dams, although the magnitude of SBP change was not as robust (9 mmHg, P<0.05, N=6-8/group). At ~20 weeks of age, rats fostered on SHRSP dams showed increased expression of IL-1a, TLR-2, E-CAD, Muc-2, and Il-17a in ileum regardless of the strain of the offspring (N=6/group, P<0.05). Loss of blood-brain barrier (BBB) integrity, an early marker of CSVD onset, was assessed by extravasation of IgG, which is confined to the plasma space under normal conditions. Extravasation of IgG was increased four-fold in SHRSP fostered on SHRSP dams compared to WKY rats fostered on WKY dams; however, extravasation of IgG was decreased in SHRSP fostered on WKY dams by ~ 50% (P=0.005, N=5/group). These findings demonstrate that although SHRSP is a genetic model for CSVD, the makeup of the gut microbiota has a major influence on gut and brain physiology, and ultimately in shaping the phenotype and onset of CSVD.


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