AUTHOR=Chen Zimo , Mo Jinglin , Xu Jie , Qin Haiqiang , Zheng Huaguang , Pan Yuesong , Meng Xia , Jing Jing , Xiang Xianglong , Wang Yongjun
TITLE=Risk Profile of Ischemic Stroke Caused by Small-Artery Occlusion vs. Deep Intracerebral Hemorrhage
JOURNAL=Frontiers in Neurology
VOLUME=10
YEAR=2019
URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2019.01213
DOI=10.3389/fneur.2019.01213
ISSN=1664-2295
ABSTRACT=Background: Small-artery occlusion (SAO) subtype accounts for a quarter of the cases of ischemic stroke and is mainly caused by pathological changes in cerebral small vessels, which also involve in deep intracerebral hemorrhage (dICH). However, the factors that drive some cases to SAO and others to dICH remained incompletely defined.
Material and Methods: This study is a cross-sectional study from the China National Stroke Registry that included consecutive patients with ischemic stroke or intracerebral hemorrhage between August 2007 and September 2008. We compared the risk profile between the two subgroups using multivariable logistic regression.
Results: A total of 1,135 patients with SAO stroke and 1,125 dICH patients were included for analyses. Generally, patients with SAO stroke were more likely to be male (odds ratio = 0.74, confidence interval = 0.58–0.94) and have diabetes (0.30, 0.22–0.40), higher atherogenic lipid profiles, higher body mass index (0.96, 0.94–0.99), higher waist/height ratio (0.12, 0.03–0.48), higher platelet count (0.84, 0.77–0.91), and higher proportion of abnormal estimated glomerular filtration rate (<90, ml/min/1.73 m2) (0.77, 0.62–0.95). Conversely, patients with dICH were more likely to have higher blood pressure parameters, inflammation levels (white blood cell count: 1.61, 1.48–1.76; high sensitivity C-reactive protein: 2.07, 1.36–3.16), and high-density lipoprotein-c (1.57, 1.25–1.98).
Conclusions: The risk profile between SAO stroke and dICH were different. Furthermore, despite of traditional indexes, waist/height ratio, platelet count, inflammation levels, lipid profile, and estimated glomerular filtration rate also play important roles in driving arteriolosclerosis into opposite ends.