Elevated Lipoprotein-Associated Phospholipase A2 Is Associated With Intracranial Atherosclerosis.
Elevated Lipoprotein-Associated Phospholipase A2 Is Associated With Intracranial Atherosclerosis.
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DOI:
10.3389/fneur.2022.858302
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发表时间:
2022
影响因子:
3.4
通讯作者:
Cao, Guodong
中科院分区:
文献类型:
--
作者:
Wang, Yuan;Liu, Gang;Song, Haiqing;Cao, Catherine;Ji, Xunming;Cao, Guodong
关键词:
Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory factor in the pathogenesis of atherosclerotic plaque and is associated with an increased risk of ischemic stroke. Whether Lp-PLA2 is associated with stenosis subtypes in acute ischemic stroke (AIS) has not been investigated. A total of 126 eligible AIS patients were divided into four groups: (1) no cerebral artery stenosis (NCS); (2) intracranial artery stenosis (ICAS); (3) extracranial artery stenosis (ECAS); and (4) combined intracranial and extracranial artery stenosis (IECS). Associations between serum Lp-PLA2 levels and the stenosis subtypes were assessed. The ICAS group had a lower frequency of dyslipidemia as compared to the NCS group and the IECS group (35.3% vs. 70% vs. 71.8%, respectively, p = 0.001) and was more likely to be symptomatic than the ECAS group (76.5% vs. 43.8%, respectively, p = 0.014). Lp-PLA2 levels in the ICAS group were 112.2 ± 66.8 μg/L which are, higher than those in the NCS, ECAS, and IECS groups (81.7 ± 38.5, 106.1 ± 57.8, 89.3 ± 52.2 μg/L, respectively, p = 0.025). In the third and fourth quartiles of Lp-PLA2 levels, stenosis had occurred more frequently in the ICAS group than in the other three groups (third Q: 50.0% vs. 3.1% vs. 28.1% vs. 18.8%, p = 0.002; fourth Q: 48.4% vs. 16.1% vs. 25.8% vs. 9.7%, p = 0.014). Lp-PLA2 levels were higher in patients with more or severe stenosis in the ICAS group. Elevated Lp-PLA2 levels were differentially associated with increased risk in AIS patients with ICAS compared to those with ECAS or no stenosis. Lp-PLA2 may be a promising biomarker and potential therapeutic target for ICAS.
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8.3
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Meschia JF;Bushnell C;Boden-Albala B;Braun LT;Bravata DM;Chaturvedi S;Creager MA;Eckel RH;Elkind MS;Fornage M;Goldstein LB;Greenberg SM;Horvath SE;Iadecola C;Jauch EC;Moore WS;Wilson JA;American Heart Association Stroke Council;Council on Cardiovascular and Stroke Nursing;Council on Clinical Cardiology;Council on Functional Genomics and Translational Biology;Council on Hypertension
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8.3
作者:
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通讯作者:
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