Database : MEDLINE
Search on : Cerebral and Small and Vessel and Diseases [Words]
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  1 / 2001 MEDLINE  
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[PMID]: 29438074
[Au] Autor:Benjamin P; Trippier S; Lawrence AJ; Lambert C; Zeestraten E; Williams OA; Patel B; Morris RG; Barrick TR; MacKinnon AD; Markus HS
[Ad] Address:From the Department of Radiology, Imperial College NHS Trust, London, United Kingdom (P.B.); Atkinson Morley Regional Neuroscience Centre, St George's University Hospitals NHS Foundation Trust, London, United Kingdom (S.T., A.D.M.); Neuroscience Research Centre, Institute of Molecular and Clinical S
[Ti] Title:Lacunar Infarcts, but Not Perivascular Spaces, Are Predictors of Cognitive Decline in Cerebral Small-Vessel Disease.
[So] Source:Stroke;49(3):586-593, 2018 03.
[Is] ISSN:1524-4628
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Cerebral small-vessel disease is a major cause of cognitive impairment. Perivascular spaces (PvS) occur in small-vessel disease, but their relationship to cognitive impairment remains uncertain. One reason may be difficulty in distinguishing between lacunes and PvS. We determined the relationship between baseline PvS score and PvS volume with change in cognition over a 5-year follow-up. We compared this to the relationship between baseline lacune count and total lacune volume with cognition. In addition, we examined change in PvS volume over time. METHODS: Data from the prospective SCANS study (St Georges Cognition and Neuroimaging in Stroke) of patients with symptomatic lacunar stroke and confluent leukoaraiosis were used (n=121). Multimodal magnetic resonance imaging was performed annually for 3 years and neuropsychological testing annually for 5 years. Lacunes were manually identified and distinguished from PvS. PvS were rated using a validated visual rating scale, and PvS volumes calculated using T1-weighted images. Linear mixed-effect models were used to determine the impact of PvS and lacunes on cognition. RESULTS: Baseline PvS scores or volumes showed no association with cognitive indices. No change was detectable in PvS volumes over the 3 years. In contrast, baseline lacunes associated with all cognitive indices and predicted cognitive decline over the 5-year follow-up. CONCLUSIONS: Although a feature of small-vessel disease, PvS are not a predictor of cognitive decline, in contrast to lacunes. This study highlights the importance of carefully differentiating between lacunes and PvS in studies investigating vascular cognitive impairment.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1161/STROKEAHA.117.017526

  2 / 2001 MEDLINE  
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[PMID]: 29311265
[Au] Autor:Duperron MG; Tzourio C; Sargurupremraj M; Mazoyer B; Soumaré A; Schilling S; Amouyel P; Chauhan G; Zhu YC; Debette S
[Ad] Address:From the Inserm, Bordeaux Population Health Research Center (M-G.D., C.T., M.S., A.S., S.S., G. C., S.D.) and Institut des Maladies Neurodégénératives, CNRS-CEA UMR 5293 (B.M.), University of Bordeaux, France; Pole de santé publique (C.T.) and Department of Neurology (S.D.), Centre Hospitalier Unive
[Ti] Title:Burden of Dilated Perivascular Spaces, an Emerging Marker of Cerebral Small Vessel Disease, Is Highly Heritable.
[So] Source:Stroke;49(2):282-287, 2018 02.
[Is] ISSN:1524-4628
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: The genetic contribution to dilated perivascular space (dPVS) burden-an emerging MRI marker of cerebral small vessel disease-is unknown. We measured the heritability of dPVS burden and its shared heritability with other MRI markers of cerebral small vessel disease. METHODS: The study sample comprised 1597 participants from the population-based Three City (3C) Dijon Study, with brain MRI and genome-wide genotyping (mean age, 72.8±4.1 years; 61% women). dPVS burden and lacunar brain infarcts were rated on a semiquantitative scale, whereas an automated algorithm generated white matter hyperintensity volume (WMHV). We estimated dPVS burden heritability and shared heritability with WMHV and lacunar brain infarcts using the genome-wide complex trait analysis tool, on unrelated participants, adjusting for age, sex, intracranial volume, and principal components of population stratification. RESULTS: dPVS burden was significantly correlated with WMHV and lacunar brain infarcts, the strongest correlation being found between WMHV and dPVS in basal ganglia. Heritability estimates were h =0.59±0.24 ( =0.007) for dPVS burden, h =0.54±0.24 ( =0.010) for WMHV, and h =0.48±0.81 ( =0.278) for lacunar brain infarcts. We found a nonsignificant trend toward shared heritability between dPVS and WMHV (r =0.41±0.28; =0.096), which seemed driven by dPVS in basal ganglia (r =0.72±0.61; =0.126) and not dPVS in white matter (r =-0.10±0.36; =0.393). A genetic risk score for WMHV based on published loci was associated with increased dPVS burden in basal ganglia ( =0.031). CONCLUSIONS: We provide evidence for important genetic contribution to dPVS burden in older community-dwelling people, some of which may be shared with WMHV. Differential heritability patterns for dPVS in white matter and basal ganglia suggest at least partly distinct underlying biological processes.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1161/STROKEAHA.117.019309

  3 / 2001 MEDLINE  
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[PMID]: 29351598
[Au] Autor:Frösen J; Joutel A
[Ad] Address:Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio University Hospital, Kuopio 70029, Finland.
[Ti] Title:Smooth muscle cells of intracranial vessels: from development to disease.
[So] Source:Cardiovasc Res;114(4):501-512, 2018 Mar 15.
[Is] ISSN:1755-3245
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cerebrovascular diseases that cause ischaemic or haemorrhagic stroke with subsequent loss of life or functional capacity due to damage of the brain tissue are among the leading causes of human suffering and economic burden inflicted by diseases in the developed world. Diseases affecting intracranial vessels are significant contributors to ischaemic and haemorrhagic strokes. Brain arteriovenous malformations, which are a collection of abnormal blood vessels connecting arteries to veins, are the most common cause of intracranial haemorrhage in children and young adults. Saccular intracranial aneurysms, which are pathological saccular dilations mainly occurring at bifurcations of the large intracranial arteries near the circle of Willis, are highly prevalent in the middle-aged population, causing significant anxiety and concern; their rupture, although rare, is a significant cause of intracranial haemorrhage in those past middle age that is associated with a very sinister prognosis. Cerebral small-vessel disease, which comprise all pathological processes affecting vessels <500 microns in diameter, account for the majority of intracerebral haemorrhages and ∼25% of ischaemic strokes and 45% of dementias in the elderly. In this review, we summarize the developmental, structural, and functional features of intracranial vessels. We then describe the role of smooth muscle cells in brain arteriovenous malformations, intracranial aneurysms, and small-vessel diseases, and discuss how the peculiar ontogeny, structure, and function of intracranial vessels are related to the development of these diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1093/cvr/cvy002

  4 / 2001 MEDLINE  
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[PMID]: 29247143
[Au] Autor:Banerjee G; Wilson D; Ambler G; Osei-Bonsu Appiah K; Shakeshaft C; Lunawat S; Cohen H; Yousry T; Lip GYH; Muir KW; Brown MM; Al-Shahi Salman R; Jäger HR; Werring DJ; CROMIS-2 Collaborators
[Ad] Address:From the UCL Stroke Research Centre (G.B., D.W., K.O.-B.A., C.S., S.L., M.M.B., D.J.W.) and Lysholm Department of Neuroradiology and the Neuroradiological Academic Unit (T.Y., H.R.J.), Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, and the National Hospital for Neurology
[Ti] Title:Cognitive Impairment Before Intracerebral Hemorrhage Is Associated With Cerebral Amyloid Angiopathy.
[So] Source:Stroke;49(1):40-45, 2018 01.
[Is] ISSN:1524-4628
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Although the association between cerebral amyloid angiopathy (CAA) and cognitive impairment is increasingly recognized, it is not clear whether this is because of the impact of recurrent intracerebral hemorrhage (ICH) events, disruptions caused by cerebral small vessel damage, or both. We investigated this by considering whether cognitive impairment before ICH was associated with neuroimaging features of CAA on magnetic resonance imaging. METHODS: We studied 166 patients with neuroimaging-confirmed ICH recruited to a prospective multicentre observational study. Preexisting cognitive impairment was determined using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Magnetic resonance imaging markers of cerebral small vessel disease, including CAA, were rated by trained observers according to consensus guidelines. RESULTS: The prevalence of cognitive impairment before ICH was 24.7% (n=41) and, in adjusted analyses, was associated with fulfilling the modified Boston criteria for probable CAA at presentation (odds ratio, 4.01; 95% confidence interval, 1.53-10.51; =0.005) and a higher composite CAA score (for each point increase, odds ratio, 1.42; 95% confidence interval, 1.03-1.97; =0.033). We also found independent associations between pre-ICH cognitive decline and the presence of cortical superficial siderosis, strictly lobar microbleeds, and lobar ICH location, but not with other neuroimaging markers, or a composite small vessel disease score. CONCLUSIONS: CAA (defined using magnetic resonance imaging markers) is associated with cognitive decline before symptomatic ICH. This provides evidence that small vessel disruption in CAA makes an independent contribution to cognitive impairment, in addition to effects due to brain injury caused directly by ICH. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02513316.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Process
[do] DOI:10.1161/STROKEAHA.117.019409

  5 / 2001 MEDLINE  
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[PMID]: 29244126
[Au] Autor:Moulignier A; Savatovsky J; Assoumou L; Lescure FX; Lamirel C; Godin O; Valin N; Tubiana R; Canestri A; Roux P; Sadik JC; Salomon L; Abrivard M; Katlama C; Yazdanpanah Y; Pialoux G; Girard PM; Costagliola D; MicroBREAK Study Group
[Ad] Address:Fondation Adolphe de Rothschild, Department of Neurology, Paris.
[Ti] Title:Silent Cerebral Small-Vessel Disease Twice as Prevalent in Middle-Aged Well-Controlled cART-Treated HIV-Infected Individuals Than HIV-Uninfected Individuals.
[So] Source:Clin Infect Dis;, 2017 Dec 13.
[Is] ISSN:1537-6591
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Silent cerebral small-vessel disease (CSVD) is defined as white matter hyperintensities, silent brain infarction or microbleeds. CSVD is responsible for future vascular events, cognitive impairment, frailty and shorter survival. CSVD prevalence among middle-aged persons living with well-controlled HIV infection (PLHIVs) is unknown. Methods: ANRS EP51 MicroBREAK (NCT02082574) is a cross-sectional study with prospective enrollment of treated PLHIVs, ≥50 years old with viral load controlled for ≥12 months, and frequency age- and sex-matched HIV-uninfected controls (HUCs). It was designed to estimate CSVD prevalence on 3T MRI (3D FLAIR, DWI and T2*), as diagnosed by 2 blinded neuroradiologists. A logistic-regression model was used to assess the impact of HIV on CSVD after adjustment for traditional risk factors. Results: Between June 2013 and May 2016, 456 PLHIVs and 154 HUCs were recruited. Respective median ages were 56 and 58 years (P=0.001), among whom 84.9% and 77.3% (P=.030) were men. CSVD was detected in 51.5% of PLHIVs and 36.4% of HUCs with an adjusted odds ratio (aOR) of 2.3. The HIV impact differed according to age, with aOR values of 5.3, 3.7 and 1.0 for age groups <54, 54-60 and >60 years, respectively (P=.022). Older age, hypertension or lower CD4-cell nadir was independently associated with a higher risk of CSVD among PLHIVs. Conclusions: HIV is an independent risk factor for CSVD. Despite sustained immunovirological control, the CSVD prevalence was twice as high among middle-aged PLHIVs than HUCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/cid/cix1075

  6 / 2001 MEDLINE  
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[PMID]: 29331631
[Au] Autor:Rodrigues MA; Samarasekera N; Lerpiniere C; Humphreys C; McCarron MO; White PM; Nicoll JAR; Sudlow CLM; Cordonnier C; Wardlaw JM; Smith C; Al-Shahi Salman R
[Ad] Address:Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK.
[Ti] Title:The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy: model development and diagnostic test accuracy study.
[So] Source:Lancet Neurol;17(3):232-240, 2018 Mar.
[Is] ISSN:1474-4465
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Identification of lobar spontaneous intracerebral haemorrhage associated with cerebral amyloid angiopathy (CAA) is important because it is associated with a higher risk of recurrent intracerebral haemorrhage than arteriolosclerosis-associated intracerebral haemorrhage. We aimed to develop a prediction model for the identification of CAA-associated lobar intracerebral haemorrhage using CT features and genotype. METHODS: We identified adults with first-ever intracerebral haemorrhage diagnosed by CT, who died and underwent research autopsy as part of the Lothian IntraCerebral Haemorrhage, Pathology, Imaging and Neurological Outcome (LINCHPIN) study, a prospective, population-based, inception cohort. We determined APOE genotype and radiologists rated CT imaging appearances. Radiologists were not aware of clinical, genetic, and histopathological features. A neuropathologist rated brain tissue for small vessel diseases, including CAA, and was masked to clinical, radiographic, and genetic features. We used CT and APOE genotype data in a logistic regression model, which we internally validated using bootstrapping, to predict the risk of CAA-associated lobar intracerebral haemorrhage, derive diagnostic criteria, and estimate diagnostic accuracy. FINDINGS: Among 110 adults (median age 83 years [IQR 76-87], 49 [45%] men) included in the LINCHPIN study between June 1, 2010 and Feb 10, 2016, intracerebral haemorrhage was lobar in 62 (56%) participants, deep in 41 (37%), and infratentorial in seven (6%). Of the 62 participants with lobar intracerebral haemorrhage, 36 (58%) were associated with moderate or severe CAA compared with 26 (42%) that were associated with absent or mild CAA, and were independently associated with subarachnoid haemorrhage (32 [89%] of 36 vs 11 [42%] of 26; p=0·014), intracerebral haemorrhage with finger-like projections (14 [39%] of 36 vs 0; p=0·043), and APOE É›4 possession (18 [50%] of 36 vs 2 [8%] of 26; p=0·0020). A prediction model for CAA-associated lobar intracerebral haemorrhage using these three variables had excellent discrimination (c statistic 0·92, 95% CI 0·86-0·98), confirmed by internal validation. For the rule-out criteria, neither subarachnoid haemorrhage nor APOE É›4 possession had 100% sensitivity (95% CI 88-100). For the rule-in criteria, subarachnoid haemorrhage and either APOE É›4 possession or finger-like projections had 96% specificity (95% CI 78-100). INTERPRETATION: The CT and APOE genotype prediction model for CAA-associated lobar intracerebral haemorrhage shows excellent discrimination in this cohort, but requires external validation. The Edinburgh rule-in and rule-out diagnostic criteria might inform prognostic and therapeutic decisions that depend on identification of CAA-associated lobar intracerebral haemorrhage. FUNDING: UK Medical Research Council, The Stroke Association, and The Wellcome Trust.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Data-Review

  7 / 2001 MEDLINE  
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[PMID]: 28469098
[Au] Autor:Fang XJ; Yu M; Wu Y; Zhang ZH; Wang WW; Wang ZX; Yuan Y
[Ad] Address:Department of Neurology, Peking University First Hospital, Beijing 100034, China.
[Ti] Title:Study of Enhanced Depth Imaging Optical Coherence Tomography in Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy.
[So] Source:Chin Med J (Engl);130(9):1042-1048, 2017 May 05.
[Is] ISSN:0366-6999
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:BACKGROUND: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary small artery disease caused by NOTCH3 gene mutation. We performed enhanced depth imaging optical coherence tomography (EDI-OCT) to evaluate the retinal vessel changes in CADASIL patients and assessed their consonance with brain magnetic resonance imaging (MRI) findings. METHODS: Of 27 genetically confirmed patients and an equal number of controls were recruited at the Peking University First Hospital from January 2015 to August 2016. All patients underwent 7T-MRI of the brain. Fazekas score, number of small infarcts and microbleeds were evaluated. All patients and controls underwent EDI-OCT to measure subfoveal choroidal thickness (SFCT), inner and outer diameters as well as arterial and venous wall thickness, and arterial venous ratio of the inner (AVRin) and outer diameters (AVRout). The relation between retinal vessel changes and Fazekas scores, numbers of small infarcts, or microbleeds was analyzed. Paired t-test was used to compare the SFCT and retinal vessel measurement data between patients and controls. Spearman's correlation was used to investigate the correlation between retinal vessel changes and MRI lesions. RESULTS: In CADASIL patients, mean SFCT (268.37 ± 46.50 µm) and mean arterial inner diameter (93.46 ± 9.70 µm) were significantly lower than that in controls (P < 0.001,P = 0.048, respectively). Mean arterial outer diameter (131.74 ± 10.87 µm), venous inner (128.99 ± 13.62 µm) and outer diameter (164.82 ± 14.77 µm), and mean arterial (19.13 ± 1.85 µm) and venous (17.91 ± 2.76 µm) wall thickness were significantly higher than that in controls (P = 0.023,P = 0.004,P < 0.001,P < 0.001, respectively). Arterial inner diameter (rs= -0.39, P= 0.044), AVRin (rs= -0.65,P < 0.001), and AVRout (rs= -0.56, P= 0.002) showed a negative correlation with the number of small infarcts. Venous inner diameter (rs = 0.46, P= 0.016) showed a positive correlation with the number of small infarcts. Venous inner diameter (rs = 0.59, P= 0.002), outer diameter (rs = 0.47, P= 0.017), showed a positive correlation with the number of cerebral microbleeds (CMBs). AVRin (rs= -0.52, P= 0.007) and AVRout (rs= -0.40, P= 0.048) showed a negative correlation with the number of CMBs. CONCLUSIONS: Measurement of retinal vessels using EDI-OCT correlates moderately well with MRI parameters. EDI-OCT might be a useful evaluation tool for CADASIL patients.
[Mh] MeSH terms primary: Leukoencephalopathies/pathology
Magnetic Resonance Imaging/methods
Tomography, Optical Coherence/methods
[Mh] MeSH terms secundary: Adult
Brain/metabolism
CADASIL
Cerebral Infarction/pathology
Female
Humans
Male
Middle Aged
Mutation
Receptor, Notch3/genetics
Retinal Vessels/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptor, Notch3)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:170505
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.204935

  8 / 2001 MEDLINE  
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[PMID]: 29459517
[Au] Autor:Seto-Yukimura R; Ogawa E; Hisamatsu T; Torii S; Shiino A; Nozaki K; Fujiyoshi A; Miura K; Nakano Y; Ueshima H; SESSA Research Group
[Ad] Address:Division of Respiratory Medicine, Department of Internal Medicine, Shiga University of Medical Science.
[Ti] Title:Reduced Lung Function and Cerebral Small Vessel Disease in Japanese Men: the Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA).
[So] Source:J Atheroscler Thromb;, 2018 Feb 16.
[Is] ISSN:1880-3873
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:AIM: We aimed to investigate the association between reduced lung function and cerebral small vessel diseases via cranial magnetic resonance imaging (MRI) in the cross-sectional study of the general Japanese population. METHODS: We recruited participants aged ≥40 years from the general population of a single city in Japan. We clarified the comorbidities and treatments, smoking habits, second-hand smoke exposure, current alcohol consumption, education level, exercise habits, and occupation. The pulmonary function test was performed to assess the forced expiratory volume in 1 second (FEV ) % predicted and forced vital capacity (FVC) % predicted values. Cranial MRI was performed to evaluate the white matter lesions (WMLs) and lacunar infarcts. We examined the association of the WMLs and lacunar infarcts with a 1-standard deviation (SD) lower in the FEV % predicted and FVC % predicted, on the basis of the smoking status. RESULTS: A total of 473 men were examined. The association of WMLs and lacunar infarcts with the spirometry-based indices were significant only in never smokers. The association between lung function impairment and cerebral small vessel disease did not change after further adjusting for second-hand smoke exposure. CONCLUSION: In a community-based sample of Japanese men, we found an association between reduced lung function and WMLs and lacunar infarcts in never smokers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:Publisher
[do] DOI:10.5551/jat.42127

  9 / 2001 MEDLINE  
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[PMID]: 29459114
[Au] Autor:Song TJ; Chang Y; Kim AR; Kim Y; Kim YJ
[Ad] Address:Department of Neurology, College of Medicine, Ewha Womans University, Seoul, Korea.
[Ti] Title:High dietary glycemic load was associated with the presence and burden of cerebral small vessel diseases in acute ischemic stroke patients.
[So] Source:Nutr Res;, 2017 Dec 27.
[Is] ISSN:1879-0739
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cerebral small vessel diseases (SVDs) are closely associated with stroke. Elevated postprandial blood glucose is also an important risk factor for stroke. Dietary glycemic load (GL) and glycemic index (GI) are frequently used as markers of postprandial blood glucose response used as an estimator of the overall glycemic effect of the diet. We hypothesized that high dietary GL or GI will be associated with presence of cerebral SVDs in patients with acute ischemic stroke. We prospectively included 263 patients who had experienced first-ever symptomatic cerebral infarction within 7 days after symptom onset and who submitted a fully filled-in semi-quantitative food frequency questionnaire. The dietary GL and GI values of food were constructed through an International table based on glucose. The presence and burden of high-grade white matter hyperintensities (HWMHs), cerebral microbleeds (CMBs), high-grade perivascular spaces (HPVSs) and asymptomatic lacunar infarctions (ALIs) were investigated. Mean age of the total patient population was 65.4 ± 11.7 years. After adjusting for age, sex, and variables with P < .1 in univariate analysis, high dietary GL was independently associated with an increased risk of presence of HWMHs (odds ratio (OR) (95% confidence interval (CI)) comparing the top quartile with the bottom quartile: 3.31 (1.37-7.98); P (for trend) = .006), CMBs (OR (95% CI): 3.06 (1.06-8.85); P = .032), PVSs (OR (95% CI): 3.24 (0.75-13.90); P = .039), and ALIs (OR (95% CI): 2.44 (0.97-6.13); P = .037). In conclusion, high dietary GL was associated with the presence and burden of cerebral SVDs in patients with acute cerebral infarction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:Publisher

  10 / 2001 MEDLINE  
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[PMID]: 29451817
[Au] Autor:Thorin-Trescases N; de Montgolfier O; Pinçon A; Raignault A; Caland L; Labbé P; Thorin E
[Ad] Address:Montreal Heart Institute, Canada.
[Ti] Title:The impact of pulse pressure on cerebrovascular events leading to age-related cognitive decline.
[So] Source:Am J Physiol Heart Circ Physiol;, 2018 Feb 16.
[Is] ISSN:1522-1539
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aging is a modern concept: human life expectancy has more than doubled in less than 150 years in Western countries. Longer lifespan, however, reveals age-related diseases, including cerebrovascular diseases. The vascular system is a prime target of aging: the "wear and tear" of large elastic arteries exposed to a life-long pulsatile pressure causes arterial stiffening by fragmentation of elastin fibers and replacement by stiffer collagen. This arterial stiffening increases in return the amplitude of the pulse pressure (PP), its wave penetrating deeper into the microcirculation of low resistance, high flow organs such as the brain. Several studies have associated peripheral arterial stiffness responsible for the sustained increase in PP, with brain microvascular diseases such as cerebral small vessel disease, cortical gray matter thinning, white matter atrophy and cognitive dysfunction in older individuals and prematurely in hypertensive and diabetic patients. The rarefaction of white matter is also associated with middle cerebral artery pulsatility that is strongly dependent on PP and artery stiffness. Pulse pressure and brain damage are likely associated, but the sequence of mechanistic events is not established. Elevated PP promotes endothelial dysfunction that may slowly develop in parallel with the accumulation of pro-inflammatory senescent cells and oxidative stress, generating cerebrovascular damage and remodeling, as well as brain structural changes. We review data suggesting that age-related increased peripheral artery stiffness may promote the penetration of a high PP to cerebral microvessels, likely causing functional, structural, metabolic and hemodynamic alterations that could ultimately promote neuronal dysfunction and cognitive decline.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:Publisher
[do] DOI:10.1152/ajpheart.00637.2017


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