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=Volume 10 - 2019 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 prospective cohort study from the China National Stroke Registry 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 multivariate logistic regression. Results: A total of 1135 patients with SAO stroke and 1125 dICH patients were included for analyses. Generally, patients with SAO stroke were more likely to be male (odds ratio [OR] 0.74, confidence interval [CI] 0.58-0.94) and have diabetes (0.30, 0.22-0.40), higher atherogenic lipid profiles, higher body mass index (BMI) (0.96, 0.94-0.99), higher WHtR (waist-height ratio) (0.12, 0.03-0.48), higher platelet (PLT) count (0.84, 0.77-0.91), and higher proportion of abnormal estimated glomerular filtration rate (eGFR﹤90, ml/min/1.73m2) (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 [WBC count]: 1.61, 1.48-1.76; high sensitivity C-reactive protein [hs-CRP]: 2.07, 1.36-3.16) and high-density lipoprotein-c (HDL-c) (1.57, 1.25-1.98). Conclusions: The risk profile between SAO stroke and dICH were different. Furthermore, despite of traditional indexes, WHtR, PLT count, inflammation levels, lipid profile and eGFR also play important roles in driving arteriolosclerosis into opposite ends.