Study of the Inflammatory Mechanisms in Hyperhomocysteinemia on Large-Artery Atherosclerosis Based on Hypersensitive C-Reactive Protein—A Study from Southern China

OBJECTIVE: To study the inflammatory mechanism of hyperhomocysteinemia on large-artery atherosclerosis based on hypersensitive C-reactive protein in patients. METHODS: In 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. RESULTS: Homocysteine 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. CONCLUSIONS: Hyperhomocysteinemia 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.