Brain Perfusion, Cognitive Functions, and Vascular Age in Middle Aged Patients With Essential Arterial Hypertension

Parfenov, V. А.; Остроумова, Т. М.; Perepelova, E. M.; Perepelov, V. A.; Кочетков, А. И.; Остроумова, О Д

doi:10.18087/cardio.2018.5.10117

Cited by 8 publications

(11 citation statements)

References 24 publications

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“…Along with other studies, the results of our open comparative clinical trial confirm the association between EH, cognitive decline, and diminished CBF 150. We enrolled untreated middle-aged patients with stage 1 and 2 EH, and evaluated cerebral perfusion using the arterial spin-labeling technique.…”

Section: Vascular Cognitive Impairment Pathophysiological Mechanismssupporting

confidence: 78%

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Parfenov¹,

Остроумова²,

Остроумова³

et al. 2019

NDT

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Vascular cognitive impairment (VCI) and vascular dementia are the most common forms of cognitive disorder associated with cerebrovascular disease and related to increased morbidity and mortality among the older population. Growing evidence suggests the contribution of blood-pressure variability, cardiac arrhythmia, hyperactivation of the renin–angiotensin–aldosterone system, endothelial dysfunction, vascular remodeling and stiffness, different angiopathies, neural tissue homeostasis, and systemic metabolic disorders to the pathophysiology of VCI. In this review, we focus on factors contributing to cerebrovascular disease, neurovascular unit alterations, and novel approaches to cognitive improvement in patients with cognitive decline. One of the important factors associated with the neuronal causes of VCI is the S100B protein, which can affect the expression of cytokines in the brain, support homeostasis, and regulate processes of differentiation, repair, and apoptosis of the nervous tissue. Since the pathological basis of VCI is complex and diverse, treatment affecting the mechanisms of cognitive disorders should be developed. The prospective role of a novel complex drug consisting of released–active antibodies to S100 and to endothelial NO synthase in VCI treatment is highlighted.

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Section: Vascular Cognitive Impairment Pathophysiological Mechanismssupporting

confidence: 78%

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Parfenov¹,

Остроумова²,

Остроумова³

et al. 2019

NDT

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“…Thirteen of the 27 added cross-sectional studies investigated patients without cognitive impairment including patients with varying degrees of WMH burden, 7, 16, 22, 23 hypertensive patients with and without SVD, 6, 24, 25 individuals with Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy (CADASIL), 26 cognitively normal older subjects 14, 27 and patients with ischaemic stroke. 28 Two of these 13 studies investigated the effect of blood pressure reduction on CBF in SVD, from which only baseline data on CBF and WMH burden, prior to any treatment, were extracted.…”

Section: Resultsmentioning

confidence: 99%

“…Fifteen studies used ASL 6-8, 10, 14, 15, 19, 20, 25, 27, 30, 32, 34-36 , 3 used CT perfusion 18, 28, 29 , 2 used dynamic susceptibility contrast (DSC) MRI 9, 37 , one study each used SPECT 21 , phase contrast MRI 22 , CT angiography/digital subtraction angiography, 31 PET, 23 and a combination of CT and DSC MRI 12 . Five studies used transcranial Doppler ultrasound 16, 17, 24, 26, 33 .…”

Section: Resultsmentioning

confidence: 99%

“…We included 34 cross-sectional studies ( n =2180) in this updated meta-analysis, of which 24 had been previously identified. 3 The 10 newly identified studies covered 4 brain regions, including mean global CBF, 18, 21, 22, 25 mean basal ganglia blood flow, 23 total grey matter 6, 20 and centrum semiovale 23 (Figure 2). We extracted data on CBF velocity, as measured from the middle cerebral artery (vMCA) 16, 24, 26 and included this under a new subgroup in the meta-analysis.…”

Section: Resultsmentioning

confidence: 99%

“…40 One cross-sectional study ( n =73) found cerebral perfusion was lower in patients with hypertension, with or without WMH, than in healthy controls, though sample size was limited. 25 Meanwhile diabetes has been linked to increased blood viscosity and a reduction in deformability of erythrocytes proportional to the degree of microvascular complications; 41 white matter CBF is also lower in patients with type 2 diabetes than in controls. 42 As such, controlling for cardiovascular risk factors is crucial in avoiding potential confounds.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Associations between white matter hyperintensity burden, cerebral blood flow and transit time in small vessel disease: an updated meta-analysis

Stewart

Stringer

Shi

et al. 2020

Preprint

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Cerebral small vessel disease is a major contributor to stroke and dementia, characterised by white matter hyperintensities (WMH) on neuroimaging. WMH are associated with reduced cerebral blood flow (CBF) cross-sectionally, though longitudinal associations remain unclear. We updated a 2016 meta-analysis, identifying 30 studies, 27 cross-sectional (n=2956) and 3 longitudinal (n=440), published since 2016. Cross-sectionally, we meta-analysed 10 new studies with 24 previously reported studies, total 34 (n=2180), finding lower CBF to be associated with worse WMH burden (mean global CBF: standardised mean difference: -0.45, 95% confidence interval (CI): -0.64,-0.27). Longitudinally, the association of baseline CBF with WMH progression varied: the largest study (5 years, n=252) found no associations, while another small study (4.5 years, n=52) found that low CBF in the periventricular WMH penumbra predicted WMH progression. We could not meta-analyse longitudinal studies due to different statistical and methodological approaches. We found lower CBF within WMH compared to normal appearing white matter (novel meta-analysis; 5 cross-sectional studies; n=295; SMD: -1.51, 95% CI: -1.94,-1.07). These findings highlight that relationships between resting CBF and WMH are complex and that more longitudinal studies analysing regional CBF and subsequent WMH change are required to determine the role of CBF in small vessel disease progression.

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Vascular cognitive impairment – Past, present, and future challenges

Badji,

Youwakim,

Cooper

et al. 2023

Ageing Research Reviews

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Brain Perfusion, Cognitive Functions, and Vascular Age in Middle Aged Patients With Essential Arterial Hypertension

Cited by 8 publications

References 24 publications

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Associations between white matter hyperintensity burden, cerebral blood flow and transit time in small vessel disease: an updated meta-analysis

Vascular cognitive impairment – Past, present, and future challenges

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