scholarly journals Risk of vascular events or death in different manifestations of cerebral small vessel disease: a 2-year follow-up study with a control group

2017 ◽  
Author(s):  
Jacek Staszewski ◽  
Renata Piusińska-Macoch ◽  
Bogdan Brodacki ◽  
Ewa Skrobowska ◽  
Katarzyna Macek ◽  
...  

Background and PurposeNatural course of cerebral small vessel disease (CSVD) has not yet been thoroughly studied. The aim of the single center study was to establish risk of vascular events or death in different manifestations of CSVD.Methods150 consecutive, functionally independent patients with marked MRI features of CSVD and with recent lacunar stroke (n=52, LS), 20 with deep hemorrhagic stroke (HS), 28 with vascular parkinsonism (VaP), 50 with vascular dementia (VaD) and 55 controls (CG) with high atherothrombotic risk free of cerebrovascular events were prospectively recruited and followed for 24 months.ResultsMean age and sex distribution were similar in CSVD and CG but patients with CSVD were less likely to have CAD (19% vs 40%, p=0,02) and tended to have higher prevalence of diabetes (54% vs 37%, p=0,11). The risk of vascular events or death was increased in any patients with moderate to severe white matter lesions at baseline MRI (HR 2,0; 95%CI 0,85-7,2), in CSVD (4,56; 95%CI 1,3-14,9) vs CG, regardless of its clinical manifestation: LS or HS (HR 4,70; 95%CI 1,3-16,2) and VaD or VaP (HR 4,59; 95%CI 1,3-15,7).ConclusionsPatients with symptomatic CSVD regardless of the clinical (acute or chronic) manifestation had more than fourfold the risk of vascular events or death in 24 months of observation compared with controls with high atherothrombotic risk free of cerebrovascular events.

Heliyon ◽  
2017 ◽  
Vol 3 (11) ◽  
pp. e00455 ◽  
Author(s):  
Jacek Staszewski ◽  
Renata Piusińska-Macoch ◽  
Bogdan Brodacki ◽  
Ewa Skrobowska ◽  
Katarzyna Macek ◽  
...  

2020 ◽  
Vol 5 (3) ◽  
pp. 297-308
Author(s):  
Joanna Wardlaw ◽  
Philip M W Bath ◽  
Fergus Doubal ◽  
Anna Heye ◽  
Nikola Sprigg ◽  
...  

Background Small vessel disease causes a quarter of ischaemic strokes (lacunar subtype), up to 45% of dementia either as vascular or mixed types, cognitive impairment and physical frailty. However, there is no specific treatment to prevent progression of small vessel disease. Aim We designed the LACunar Intervention Trial-2 (LACI-2) to test feasibility of a large trial testing cilostazol and/or isosorbide mononitrate (ISMN) by demonstrating adequate participant recruitment and retention in follow-up, drug tolerability, safety and confirm outcome event rates required to power a phase 3 trial. Methods and design LACI-2 is an investigator-initiated, prospective randomised open label blinded endpoint (PROBE) trial aiming to recruit 400 patients with prior lacunar syndrome due to a small subcortical infarct. We randomise participants to cilostazol v no cilostazol and ISMN or no ISMN, minimising on key prognostic factors. All patients receive guideline-based best medical therapy. Patients commence trial drug at low dose, increment to full dose over 2–4 weeks, continuing on full dose for a year. We follow-up participants to one year for symptoms, tablet compliance, safety, recurrent vascular events, cognition and functional outcomes, Trails B and brain MRI. LACI-2 is registered ISRCTN 14911850, EudraCT 2016–002277-35. Trial outcome: Primary outcome is feasibility of recruitment and compliance; secondary outcomes include safety (cerebral or systemic bleeding, falls, death), efficacy (recurrent cerebral and cardiac vascular events, cognition on TICS, Trails B) and tolerability. Summary LACI-2 will determine feasibility, tolerability and provide outcome rates to power a large phase 3 trial to prevent progression of cerebral small vessel disease.


2013 ◽  
Author(s):  
Medhat M. Riad ◽  
Bram Platel ◽  
Frank-Erik de Leeuw ◽  
Nico Karssemeijer

2021 ◽  
Vol 13 ◽  
Author(s):  
Yangyi Fan ◽  
Ming Shen ◽  
Yang Huo ◽  
Xuguang Gao ◽  
Chun Li ◽  
...  

Background: Cerebral small vessel disease (cSVD) and neurodegeneration are the two main causes of dementia and are considered distinct pathological processes, while studies have shown overlaps and interactions between the two pathological pathways. Medial temporal atrophy (MTA) is considered a classic marker of neurodegeneration. We aimed to investigate the relationship of total cSVD burden and MTA on MRI using a total cSVD score and to explore the impact of the two MRI features on cognition.Methods: Patients in a memory clinic were enrolled, who underwent brain MRI scan and cognitive evaluation within 7 days after the first visit. MTA and total cSVD score were rated using validated visual scales. Cognitive function was assessed by using Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scales. Spearman's correlation and regression models were used to test (i) the association between MTA and total cSVD score as well as each cSVD marker and (ii) the correlation of the MRI features and cognitive status.Results: A total of 312 patients were finally enrolled, with a median age of 75.0 (66.0–80.0) years and 40.7% (127/312) males. All of them finished MRI and MMSE, and 293 subjects finished MoCA. Of note, 71.8% (224/312) of the patients had at least one of the cSVD markers, and 48.7% (152/312) of them had moderate–severe MTA. The total cSVD score was independently associated with MTA levels, after adjusting for age, gender, years of education, and other vascular risk factors (OR 1.191, 95% CI 1.071–1.324, P = 0.001). In regard to individual markers, a significant association existed only between white matter hyperintensities and MTA after adjusting for the factors mentioned above (OR 1.338, 95% CI 1.050–1.704, P = 0.018). Both MTA and total cSVD score were independent risk factors for MMSE ≤ 26 (MTA: OR 1.877, 95% CI 1.407–2.503, P < 0.001; total cSVD score: OR 1.474, 95% CI 1.132–1.921, P = 0.004), and MoCA < 26 (MTA: OR 1.629, 95% CI 1.112–2.388, P = 0.012; total cSVD score: OR 1.520, 95% CI 1.068–2.162, P = 0.020). Among all the cSVD markers, microbleed was found significantly associated with MMSE ≤ 26, while no marker was demonstrated a relationship with MoCA < 26.Conclusion: Cerebral small vessel disease was related to MTA in patients of a memory clinic, and both the MRI features had a significant association with cognitive impairment.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ilse M. J. Kant ◽  
◽  
Henri J. M. M. Mutsaerts ◽  
Simone J. T. van Montfort ◽  
Myriam G. Jaarsma-Coes ◽  
...  

2020 ◽  
Author(s):  
Xuemei Chen ◽  
Lin Wang ◽  
Junying Jiang ◽  
Yuanyuan Gao ◽  
Rui Zhang ◽  
...  

Abstract Objective: As one of the Magnetic resonance imaging (MRI) makers of cerebral small vessel disease (SVD), increasing evidences have showed that white matter hyperintensity (WMH) can predict the short-term outcome of acute ischemic stroke (AIS). It is unclear that whether neuroimaging markers of SVD are also associated with short-term outcomes of minor cerebrovascular events. In the present study, We investigate neuroimaging markers of SVD in order to explore their roles in prediction of short-term outcome in patients with minor cerebrovascular events. Methods: Consecutive first-ever stroke patients(n=546)from the Affiliated Jiangning Hospital of Nanjing Medical University were enrolled. A total of 388 patients were enrolled according to minor cerebrovascular events definition and exclusion criteria. MRI scans were performed within seven days of stroke onset, and then neuroimaging markers of SVD including WMH, lacunes, cerebral microbleeds (CMB), and perivascular spaces (PVS) , SVD burden scores were assessed. We completed baseline characteristics and evaluated the relationships of short-term outcomes to SVD neuroimaging markers and SVD scores. The 90-day modified Rankin Scale (mRS) was thought as primary outcome and was dichotomized as good functional outcome (mRS 0-1) and poor outcome (mRS 2-6). Secondary outcomes were stroke progression and stroke recurrence. Results: Higher age, National Institutes of Health Stroke Scale (NIHSS) upon admission, lipoprotein-associated phospholipase A2 (LP-PLA2) and lacunes, Fazekas score were correlated with poor functional outcome (P<0.05), But after adjusting for confounding variables, among the neuroimaging markers of cerebral small vessel disease, only Fazekas score (OR, 1.343; 95% confidence interval, 1.020-1.770; P=0.036) was found to be associated with poor outcome at 90 days. Higher Fazekas and SVD scores were not associated with stroke progression or stroke recurrence. Conclusion: WMH can predict the poor functional outcome of minor cerebrovascular events. Adding other neuroimaging markers of SVD and total SVD burden score, however, does not improve the prediction,which indicated WMH can as neuroimaging markers for guiding the treatment of minor cerebrovascular events.


2021 ◽  
Vol 17 (S1) ◽  
Author(s):  
Eric de Silva ◽  
Carole H Sudre ◽  
Jo Barnes ◽  
Marzia Antonella Scelsi ◽  
Andre Altmann

2019 ◽  
Vol 47 (1-2) ◽  
pp. 55-67 ◽  
Author(s):  
Renyuan Liu ◽  
Wenhui Wu ◽  
Qing Ye ◽  
Yucheng Gu ◽  
Junhui Zou ◽  
...  

Objective: To explore the within- and between-network patterns of the default mode network (DMN), the frontoparietal control network (FPCN), and the dorsal attention network (DAN) in cerebral small vessel disease (CSVD) with and without cognitive impairment (CI). Methods: Twenty CSVD with CI subjects, 21 CSVD without CI subjects, and 25 healthy elderly controls were recruited. The within- and between-network patterns of the networks were identified based on resting-state functional magnetic resonance imaging data. Results: Compared with the control group, both the CSVD with CI group and the CSVD without CI group displayed decreased within-network function of the DMN and lower negative connectivity between the DMN and other networks (i.e., DMN and DAN, DMN and FPCN), whereas the CSVD with CI group additionally showed within- and between-network alterations of the FPCN (i.e., increased within-network function of the FPCN and lower negative connectivity between the FPCN and the DMN). Furthermore, these alterations of the FPCN were correlated with the cognitive function of CSVD subjects. Interestingly, the between-network connectivity of the FPCN and the DMN was negatively correlated with deep white matter hyperintensities (DWMH) volume in CSVD subjects. Conclusion: These findings suggest that cognitive alterations of CSVD subjects may be mainly regulated by the FPCN that correlates with DWMH burden, and shed light on the investigation of surrogate markers of CSVD.


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