• Liming Cao, Yi Guo, and Zhishan Zhu.
• Department of neurology, The First Affiliated Hospital of Jinan University, Guang zhou, China; Department of Neurology, The 3rd Affiliated Hospital of Shenzhen University, Shenzhen City, China. Electronic address: caolm-2007@163.com.
• J Stroke Cerebrovasc Dis. 2019 Jul 1; 28 (7): 1816-1823.

ObjectiveTo study the inflammatory mechanism of hyperhomocysteinemia on large-artery atherosclerosis based on hypersensitive C-reactive protein in patients.MethodsIn all, 153 inpatients and 1357 physical examinees were selected. The levels of homocysteine were compared between the carotid/intracranial artery stenosis group and the nonstenosis group, between the carotid artery unstable plaque group and the nonplaque group, and between the intima-media thickness (IMT) greater than or equal to 1 group and the normal IMT group. The hypersensitive C-reactive protein levels were compared between the lacunar infarction (LI) group and the nonstroke control group and between the unstable plaque group and the nonplaque group.ResultsHomocysteine level was significantly higher in the carotid/intracranial artery stenosis group than in the nonstenosis group, in the LI group than in the inpatient nonstroke group, and in the IMT greater than or equal to 1 group than in the normal IMT group. The hypersensitive C-reactive protein level was significantly higher in the LI group than in the nonstroke group and in the unstable plaque group than in the nonplaque group.ConclusionsHyperhomocysteinemia may aggravate the development of IMT, carotid atherosclerotic plaque instability, and carotid/intracranial artery stenosis by increasing inflammation, ultimately leading to the occurrence of LI. Hyperhomocysteinemia-induced inflammation mechanism warrants further study.Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

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