Prestroke Statins, Progression of White Matter Hyperintensities, and Cognitive Decline in Stroke Patients with Confluent White Matter Hyperintensities

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• 作者：Yunyun Xiong (1) (2)
  Adrian Wong (4)
  Margherita Cavalieri (5)
  Reinhold Schmidt (5)
  Winnie W. C. Chu (3)
  Xinfeng Liu (1)
  Ka Sing Wong (2)
  Vincent Mok (2)
  
• 关键词：Statins ; White matter hyperintensities ; Stroke ; Cognitive decline
• 刊名：Neurotherapeutics
• 出版年：2014
• 出版时间：July 2014
• 年：2014
• 卷：11
• 期：3
• 页码：606-611
• 全文大小：144 KB
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• 作者单位：Yunyun Xiong (1) (2)
  Adrian Wong (4)
  Margherita Cavalieri (5)
  Reinhold Schmidt (5)
  Winnie W. C. Chu (3)
  Xinfeng Liu (1)
  Ka Sing Wong (2)
  Vincent Mok (2)
  
  1. Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, People’s Republic of China
  2. Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region, People’s Republic of China
  4. Department of Psychological Studies and Center for Psychosocial Health and Aging, The Hong Kong Institute of Education, Taipo, Hong Kong Special Administrative Region, People’s Republic of China
  5. Department of Neurology, Medical University Graz, Graz, Austria
  3. Department of Radiology and Organ Imaging, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region, People’s Republic of China
  
• ISSN：1878-7479

文摘

Cerebral white matter hyperintensities (WMH) are a consequence of cerebral small vessel disease. Statins have been shown to reduce recurrent stroke among patients with various stroke subtypes, including lacunar stroke, which also arises from small vessel disease. In this study, we investigated the hypothesis that prestroke statin use would reduce the progression of WMH and/or cognitive decline among stroke patients with confluent WMH. Patients (n--00) were participants of the VITAmins To Prevent Stroke magnetic resonance imaging substudy. All patients had confluent WMH on magnetic resonance imaging at baseline. Eighty-one patients completed the 2-year follow-up. We assessed general cognition and executive function using the mini-mental state examination and Mattis dementia rating scale–initiation/perseveration subscale, respectively. We compared the change in volume of WMH and cognition between prestroke statin use and prestroke nonstatin use groups. We also evaluated the effects of prestroke statin use on incident lacunes and microbleeds. The prestroke statin use group (n--1) had less WMH volume progression (1.54?±-.52?cm3 vs 5.01?±-.00?cm3, p--.02) compared with the prestroke nonstatin use group (n--0). Multivariate linear regression modeling identified prestroke statin use as an independent predictor of WMH progression (β-?-.31, p--.008). Prestroke statin use was also associated with less decline (Mattis dementia rating scale–initiation/perseveration subscale; β--.47, p--.001). No association was observed with changes in mini-mental state examination scores. There were no between group differences on incident lacunes or incident microbleeds. Prestroke statin use may reduce WMH progression and decline in executive function in stroke patients with confluent WMH.