22. European Stroke Conference 457 Small vessel stroke and white matter disease A study of endothelial dysfunction in relation to diffusion tensor imaging whole brain histo-gram analysis and clinical picture in CADASIL F. Pescini1, G. Chiti2, L.N. Mazzoni3, L. Fedeli4, S. Busoni5, A.M. Gori6, B. Giusti7, F. Cesari8, M. Moretti9, S. Chiti10, L. Ciolli11, R. Valenti12, S. Nannucci13, L. Pantoni14, D. Inzitari15 1Department of Neurologic and Psychiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY1, 1Department of Neurologic and Psychi-atric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY2, Health Physics Unit, Azienda Ospedaliero Universitaria Careggi, Florence, ITALY3, Health Physics Unit, Azienda Ospedaliero Universitaria Careggi, Florence, ITALY4, Health Physics Unit, Azienda Ospedaliero Universitaria Careggi, Florence, ITALY5, Dep of Medical and Surgical Critical Care, Atherothrombotic Diseases Center, University of Florence and Azienda Ospedaliero Universi-taria Careggi, Florence, ITALY6, Dep of Medical and Surgical Critical Care, Atherothrombotic Dis-eases Center, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, IT-ALY7, Dep of Medical and Surgical Critical Care, Atherothrombotic Diseases Center, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY8, Department of Radiol-ogy, Neuroradiology Unit, Azienda Ospedaliero Universitaria Careggi, , ITALY9,Department of Ra-diology, Azienda Ospedaliero Universitaria Careggi, Florence, ITALY10, Department of Neurologic and Psychiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY11, Department of Neurologic and Psychiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY12, Department of Neurologic and Psy-chiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY13, Department of Neurologic and Psychiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY14, Department of Neurologic and Psychiatric Sciences, University of Florence and Azienda Ospedaliero Universitaria Careggi, Florence, ITALY15 Background: Endothelial dysfunction (ED) could have a role in modulating phenotype in CADA-SIL. Microstructural brain alterations may be evaluated by diffusion tensor imaging (DTI) and are associated with white matter changes (WMC) on conventional MRI and cognitive decline. Methods: We studied the associations between ED biomarkers, cognitive performances, apparent diffusion coefficient (ADC) and fractional anisotropy (FA) whole brain histograms in 23 CADASIL patients. Endothelial progenitor cells (EPCs) (positive for CD34/KDR, CD133/KDR, CD34/CD133/KDR) and circulating progenitor cells (CPCs) (positive for CD34, CD133, CD34/CD133) were measured in peripheral blood by flow cytometry. Serum von Willebrand factor and thrombomodulin levels were measured by ELISA. A cognitive battery was applied. ADC and FA maps were generated from DTI data and examined in the whole brain excluding cerebellum, brainstem and cerebrospinal fluid. WMC severity was evaluated applying the Fazekas scale on FLAIR sequences. Results: We found significant associations between lower CPCs levels and higher mean-ADC (p=0.004), lower mean- FA (p=0.006), higher Fazekas score (p=0.05) and worse cognitive performances. Higher mean-ADC and lower mean-FA correlated with worse cognitive performances and higher Fazekas score. Age correlated with all the previous variables. CADASIL patients with history of stroke had significantly higher mean age, lower CPCs levels, higher mean-ADC and lower mean-FA than patients without stroke. Analogous differences were found for patients with Fazekas score ≥4 vs. patients with Faze-kas score <3. No association was found between the other ED markers and DTI data. Conclusion: Pluripotent CPCs levels were related with age and more severe clinical and neuroimaging pictures. Moreover, we confirm the association between both visible (on conventional MRI) WMC and mi-crostructural brain damage (on DTI) and cognitive performances. 530 © 2013 S. Karger AG, Basel Scientific Programme 458 Small vessel stroke and white matter disease EFFECT OF ATORVASTATIN ON THE LEVEL OF CIRCULATING ENDOTHELIAL PROGENITOR CELLS IN ACUTE LACUNAR STROKE L. Anatskaia1, N. Goncharova2, G. Khulup3 The Republic Research &Practical Center of Neurology and Neurosurgery, Minsk, BELAR-US1, The Republic Research & Production Center for Transfusiology and Medical Biotechnologies, Minsk, BELARUS2, The Republic Research & Production Center for Transfusiology and Medical Biotechnologies , Minsk, Belarus, Minsk, BELARUS3 Background and Purpose: Endothelial progenitor cells (EPCs) promote angiogenesis of small cere-bral vessels and could save as a marker of neovascularization after lacunar stroke. Several experi-mental and clinical studies have suggested, that statins mobilize EPCs after stroke. We aimed to de-termine numbers of circulating EPCs in acute lacunar infarctions (LI) resulting from cerebral small vessel disease (CSVD). Methods: The level of circulating EPCs (expression markers: CD31/CD34/ CD146, CD31/CD34/CD144, CD31/CD34/KDR, CD31/CD34/FLT1, CD36/CD34, CD31/vWF/ CD34, CD31/CD133/CD34, CD31/CD45/CD34) were examined using flow cytometry at 48 hours and after 7 days of treatment in control group of patients with LS and CSVD receiving standard therapy without Atorvastatin (n =22, a mean age of 62,2 ±15,4 years), and in main group of patients with LS and CSVD (n=17, a mean age of 61,2±17,6 years) treated with Atorvastatin 20 мг, once in 20 healthy volunteers. Results: An increased levels of cell, bearing the earliest EPCs markers KDR+, CD144+, р<0,05 after 7 days of atorvastatin treatment were reviled in main group of patints. Reduction in the number of cells bearing CD36 + and vWF + markers, p <0.05, on the 7th day of atorvastatin treatment compared to the results of free atorvastatin therapy, indirectly reflected the de-cline tendency to thrombosis due to endothelial repair and angiogenesis. After atorvastatin treatment CD34+ expression level according to MIF value was increasing at 1.3 times, р<0,001.The increase in the proportion of EPCs with the phenotype of CD34+CD146+ end CD34+CD144+, p<0.05, after 7 days of atorvastatin treatment may indicate an increase in the degree of functional activity of the EPCs involved in ndothelial repair and angiogenesis. Conclusion: The results of our study indicate the high potential of atorvastatin in the mobilization of EPCs in acute LS resulting from CSVD and stimulation endothelial repair and angiogenesis. The study of individual subgroups of EPCs may be-come the basis for understanding the processes of endothelial dysfunction and recovery after acute lacunar stroke resulting from CSVD.
Karger_ESC London_2013
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