Prognostic relevance of cortical superficial siderosis in cerebral amyloid angiopathy
Por:
Wollenweber, FA, Opherk, C, Zedde, M, Catak, C, Malik, R, Duering, M, Konieczny, MJ, Pascarella, R, Samoes, R, Correia, M, Marti-Fabregas, J, Linn, J, Dichgans, M
Publicada:
19 feb 2019
Resumen:
Objective To investigate the prognostic relevance of cortical superficial siderosis (cSS) in patients with cerebral amyloid angiopathy (CAA). Methods A total of 302 patients fulfilling clinical and imaging criteria for probable or possible CAA were enrolled into a prospective, multicenter cohort study and followed for 12 months. cSS was assessed on T2*/susceptibility-weighted imaging MRI. The predefined primary composite endpoint was incident stroke or death in patients with cSS compared to those without. Secondary analyses included cerebrovascular events and functional outcome measured by the modified Rankin Scale (mRS). Multiple regression analysis was performed to adjust for possible confounders. Results cSS prevalence was 40%. The primary endpoint occurred more frequently in patients with cSS (22%, 27/121) compared to those without (8%, 15/181, p = 0.001). Rates of CAA-related incident intracranial hemorrhage were 17% (cSS) and 4% (no cSS, p = 0.0003). The proportion of patients being functionally independent (mRS 0-2) 12 months from baseline were 59% (cSS) and 82% (no cSS, p = 0.00002). Presence of cSS was associated with the primary endpoint (adjusted odds ratio [OR] 1.2, 95% confidence interval [CI] 1.1-1.3, p = 0.0005), incident intracranial hemorrhage (adjusted OR 1.2, 95% CI 1.1-1.3, p = 0.0003), and less favorable outcome as assessed by the mRS (common OR 1.9, 95% CI 1.2-3.1, p = 0.009). Similar results were obtained in analyses restricted to patients with probable CAA and to patients with disseminated cSS (all p < 0.005). Conclusions Patients with cSS and suspected CAA are at high risk for CAA-related incident intracranial hemorrhage and poor functional outcome. Both the presence and extent of cSS have prognostic relevance and may influence clinical decision-making.
Filiaciones:
Wollenweber, FA:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Opherk, C:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
SLK Kliniken Heilbronn GmbH, Neurol Klin, Heilbronn, Germany
Zedde, M:
Arcispedale Santa Maria Nuova, Azienda Unita Sanit Locale IRCCS Reggio Emilia, Stroke Unit, Neurol Unit, Reggio Emilia, Italy
Arcispedale Santa Maria Nuova, Azienda Unita Sanit Locale IRCCS Reggio Emilia, Neuroradiol Unit, Reggio Emilia, Italy
Catak, C:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Malik, R:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Duering, M:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Konieczny, MJ:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Pascarella, R:
Arcispedale Santa Maria Nuova, Azienda Unita Sanit Locale IRCCS Reggio Emilia, Stroke Unit, Neurol Unit, Reggio Emilia, Italy
Arcispedale Santa Maria Nuova, Azienda Unita Sanit Locale IRCCS Reggio Emilia, Neuroradiol Unit, Reggio Emilia, Italy
Samoes, R:
Hosp Santo Antonio, Ctr Hosp Porto, Serv Neurol, Porto, Portugal
Correia, M:
Hosp Santo Antonio, Ctr Hosp Porto, Serv Neurol, Porto, Portugal
Marti-Fabregas, J:
Hosp Santa Creu & Sant Pau, Biomed Res Inst St Pau, IIB St Pau, Barcelona, Spain
Linn, J:
Univ Klinikum Carl Gustav Carus, Inst & Poliklin Neuroradiol, Dresden, Germany
LMU, Klinikum Univ Munchen, Dept Neuroradiol, Munich, Germany
Dichgans, M:
Ludwig Maximilians Univ Munchen, Univ Hosp, Inst Stroke & Dementia Res, Munich, Germany
Munich Cluster Syst Neurol SyNergy, Munich, Germany
German Ctr Neurodegenerat Dis DZNE, Munich, Germany
Green Published
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