Analysis of changes in annexin A2 and vascular endothelial cadherin in patients with cerebral infarction treated with emergency thrombolysis and the relationship with short-term progression
10.3760/cma.j.cn115455-20250123-00095
- VernacularTitle:急诊溶栓治疗的脑梗死患者膜联蛋白A2和血管内皮钙黏蛋白水平变化及与短期进展的关系
- Author:
Zuke XU
1
;
Ying LI
1
;
Yuanyuan LI
1
;
Yibo TIAN
1
;
Long LI
1
Author Information
1. 西安国际医学中心医院神经内科，西安 710100
- Publication Type:Journal Article
- Keywords:
Thrombolytic therapy;
Brain infarction;
Annexin A2;
Cadherin
- From:
Chinese Journal of Postgraduates of Medicine
2025;48(11):993-1000
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To Explore the changes of annexin A2 and vascular endothelial cadherin (VE-Cad) in patients with cerebral infarction (CI) undergoing emergency thrombolysis, and analyze their relationship with progression within 10 d.Methods:Using a prospective research method, 78 patients with CI were selected from October 2019 to June 2022 in Xi'an International Medical Center Hospital, and all patients were treated with emergency thrombolysis. The serum levels of annexin A2 and VE-Cad before and after thrombolysis were measured by enzyme-linked immunosorbent assay, and the National Institute stroke scale (NIHSS) was used to assess patients' neurologic impairment. The baseline data, imaging findings at admission and routine laboratory examination indexes were recorded. The progression within 10 d after thrombolysis was recorded. Pearson correlation analysis was used to analyze the correlation between annexin A2, VE-Cad and NIHSS score. Multivariate Logistic regression was used to analyze the independent risk factors of progression within 10 d after thrombolysis in patients with CI. The value of annexin A2 and VE-Cad in predicting the progression within 10 d after thrombolysis in patients with CI was evaluated by the receiver operating characteristics (ROC) curve. A restricted cubic spline model was drawn to evaluate the dose-response relationship between annexin A2, VE-Cad and the progression within 10 d after thrombolysis in patients with CI.Results:Compared with before thrombolysis, the annexin A2 after thrombolysis was significantly higher: (24.50 ± 3.27) μg/L vs. (20.86 ± 3.84) μg/L, the VE-Cad and NIHSS score were significantly lower: (4.72 ± 1.05) mg/L vs. (6.81 ± 1.31) mg/L and (8.64 ± 2.35) scores vs. (13.01 ± 2.86) scores, and there were statistical differences ( P<0.01). Before and after thrombolysis, Pearson correlation analysis result showed there was a negative correlation between annexin A2 and NIHSS score ( r =-0.796 and - 0.568, P<0.01), and a positive correlation between VE-Cad and NIHSS score ( r = 0.820 and 0.502, P<0.01). Among 78 patients with CI treated with emergency thrombolysis, 7 cases (8.97%) experienced progression within 10 d. There were statistical differences in hypertension, diabetes, hyperlipidemia, onset to thrombolysis time, infarct site, systolic blood pressure, triacylglycerol, high-density lipoprotein cholesterol, and the NIHSS score, annexin A2, VE-Cad before and after thrombolysis between patients with progression within 10 d after thrombolysis and patients without progression within 10 d after thrombolysis ( P<0.05 or <0.01); there were no statistical differences in gender composition, age, body mass index, coronary heart disease, atrial fibrillation, smoking, alcohol consumption, family history of stroke, carotid plaques, blood glucose, diastolic blood pressure, white blood cell count, platelet count, total cholesterol low-density lipoprotein cholesterol between the two groups ( P>0.05). After adjusting for hypertension, diabetes and hyperlipidemia, multivariate Logistic regression analysis result showed that the infarction site, onset to thrombolysis time, VE-Cad after thrombolysis and annexin A2 after thrombolysis were still independent factors of progression within 10 d after thrombolysis in patients with CI ( OR = 2.570, 2.496, 3.147 and 0.352; 95% CI 1.285 to 5.139, 1.303 to 4.781, 1.629 to 6.080 and 0.158 to 0.782; P<0.05 or <0.01). ROC curve analysis results showed that the area under the curve of annexin A2 combined with VE-Cad after thrombolysis to predict the progression within 10 d after thrombolysis in patients with CI was significantly larger than that of annexin A2 and VE-Cad after thrombolysis alone (0.898 vs. 0.822 and 0.799, χ2 = 2.17 and 1.98, P = 0.039 and 0.048). The optimal cutoff values of annexin A2 and VE-Cad after thrombolysis were <23.27 μg/L and >4.92 mg/L, with a sensitivity of 88.24%, and a specificity of 77.05%. The restricted cubic spline analysis result showed that the continuous changes in annexin A2 after thrombolysis were roughly negatively correlated with the progression within 10 d after thrombolysis in patients with CI ( OR = 0.720, 95% CI 0.561 to 0.930, P = 0.010), the continuous changes in VE-Cad after thrombolysis were roughly positively correlated with the progression within 10 d after thrombolysis in patients with CI ( OR = 1.450, 95% CI 1.126 to 1.188, P = 0.004). When annexin A2<23.80 ng/L and VE-Cad>5.25 mg/L after thrombolysis, the risk of progression within 10 d after thrombolysis in patients with CI significantly increased. Conclusions:The expression of annexin A2 increases and VE-Cad decreases after emergency thrombolysis in patients with CI, and the expression levels of both are closely related to the degree of neurologic impairment, and the risk of progression within 10 d after thrombolysis could be determined clinically by detecting their changes.
