Effect of tirofiban-assisted endovascular intervention on neurological function in patients with acute ischemic stroke

doi:10.3760/cma.j.issn.1007-1245.2024.13.004

Abstract

Abstract:

Objective　To investigate the effect of tirofiban-assisted endovascular intervention on neurological function in patients with acute ischemic stroke (AIS). Methods　Eighty-six patients with AIS treated at Department of Intervention, Baoji City People's Hospital from January 2020 to October 2023 were selected for the randomized controlled trial. The patients were randomly divided into a control group and an observation group by the random number table method, with 43 cases in each group. There were 25 males and 18 females in the control group; they were (60.33±6.13) years old. There were 26 males and 17 females in the observation group; they were (59.48±5.29) years old. The control group took endovascular intervention; in addition, the observation group took tirofiban (treated for 2 weeks). The treatment efficacies, neurological function scores [National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS)], neurotrophic indicators [brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and serum CNS-specific protein （S100β)], platelet function markers (platelet aggregation, adhesion rates, and maximum aggregation time), and oxidative and inflammatory markers [glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA), and C-reactive protein (CRP)] were compared between the two groups by the independent sample t test and χ² test. Results　After two weeks' treatment, the total effictive rate in the observation group higher than that in the control group [81.40% (35/43) vs. 60.47% (26/43)], with a statistical difference between the two groups (χ² =4.568, P<0.05). The scores of NIHSS and mRS in the observation group were lower than those in the control group [(7.48±1.35) vs. (9.68±1.89) and (1.69±0.24) vs. (2.06±0.23)], with statistical differences (t=6.211 and 7.299; both P<0.05). The levels of S100β, BDNF, and NGF in the observation group were better than those in the control group [(0.37±0.06) μg/L vs. (0.46±0.09) μg/L, (43.97±7.92) μg/L vs. (37.14±6.87) μg/L, and (99.38±12.73) ng/L vs. (86.47±9.56) ng/L], with statistical differences (t=5.456, 4.272, and 5.318; all P<0.05). The platelet aggregation rate, adhesion rate, and maximum aggregation time in the observation group were lower than those in the control group [(26.74±4.93)% vs. (32.64±5.26)%, (32.35±4.86)% vs. (38.26±5.38)%, and (147.35±21.83) s vs. (163.67±22.67) s], with statistical differences (t=5.367, 5.345, and 3.400; all P<0.05). The levels of GSH-Px, SOD, MDA, and CRP in the observation group were better than those in the control group [(168.97±24.73) U/L vs. (140.68±20.59) U/L, (86.36±12.79) U/mL vs. (75.21±11.47) U/mL, (4.89±1.35) μmol/L vs. (6.82±1.63) μmol/L, and (9.36±3.25) mg/L vs. (12.18±4.75) mg/L], with statistical differences (t=5.765, 4.256, 5.980, and 3.213; all P<0.05). There were no statistical differences in bleeding, symptomatic intracerebral hemorrhage, recurrence, and mortality between the two groups (all P>0.05). Conclusion　Tirofiban-assisted endovascular intervention for patients with AIS can significantly increase the overall treatment efficacy, their neurological function scores, and promote their neurological function recovery, and is safe.

Key words:

Tirofiban, Endovascular intervention, Acute ischemic stroke, Neurological function

摘要：

目的　探讨替罗非班辅助血管内介入治疗术对急性缺血性脑卒中（acute ischemic stroke，AIS）患者神经功能的影响。方法　采用前瞻性研究，研究对象为2020年1月至2023年10月在宝鸡市人民医院介入科接受治疗的86例AIS患者。按照随机数字表法分为两组，对照组43例，男25例，女18例，年龄（60.33±6.13）岁，接受血管内介入治疗术；观察组43例，男26例，女17例，年龄（59.48±5.29）岁，在对照组的基础上配合替罗非班治疗（治疗2周）。比较疗效，治疗前、治疗2周后的神经功能评分［美国国立卫生研究院脑卒中量表（NIHSS）和Rankin量表（mRS）］、神经功能指标［脑源性神经营养因子（BDNF）、神经生长因子（NGF）和中枢神经特异性蛋白（S100β）］、血小板功能指标（血小板聚集率、血小板黏附率和最大聚集时间）和氧化及炎症指标［谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）、丙二醛（MDA）和C反应蛋白（CRP）］，记录随访3个月的复发、死亡及治疗过程中各类出血情况。组间比较采用独立样本t检验、χ²检验。结果　治疗2周后，观察组总有效率为81.40%（35/43），高于对照组的60.47%（26/43），差异有统计学意义（χ²=4.568，P<0.05）；观察组NIHSS和mRS评分低于对照组［（7.48±1.35）分比（9.68±1.89）分、（1.69±0.24）分比（2.06±0.23）分］，差异均有统计学意义（t=6.211、7.299，均P<0.05）；观察组S100β水平低于对照组［（0.37±0.06）μg/L比（0.46±0.09）μg/L］，血清BDNF和NGF水平高于对照组［（43.97±7.92）μg/L比（37.14±6.87）μg/L、（99.38±12.73）ng/L比（86.47±9.56）ng/L］，差异均有统计学意义（t=5.456、4.272、5.318，均P<0.05）；观察组血小板聚集率、血小板黏附率和最大聚集时间均低于或短于对照组［（26.74±4.93）%比（32.64±5.26）%、（32.35±4.86）%比（38.26±5.38）%、（147.35±21.83）s比（163.67±22.67）s］，差异均有统计学意义（t=5.367、5.345、3.400，均P<0.05）；观察组GSH-Px和SOD水平均高于对照组［（168.97±24.73）U/L比（140.68±20.59）U/L、（86.36±12.79）U/mL比（75.21±11.47）U/mL］，MDA和CRP水平均低于对照组［（4.89±1.35）μmol/L比（6.82±1.63）μmol/L、（9.36±3.25）mg/L比（12.18±4.75）mg/L］，差异均有统计学意义（t=5.765、4.256、5.980、3.213，均P<0.05）。随访3个月，两组所有出血、症状性颅内出血、复发和病死率比较，差异均无统计学意义（均P>0.05）。结论　替罗非班辅助血管内介入治疗能显著提高AIS患者的治疗总有效率，改善其神经功能评分，有效促进患者神经功能恢复，且安全性良好。

关键词:

替罗非班, 血管内介入治疗, 急性缺血型脑卒中, 神经功能

Bai Zhangyong, Pu Xiaolong, Yang Liying.

Effect of tirofiban-assisted endovascular intervention on neurological function in patients with acute ischemic stroke [J]. International Medicine and Health Guidance News, 2024, 30(13): 2130-2135.

柏杖勇蒲晓龙杨丽英.

替罗非班辅助血管内介入治疗术对AIS患者神经功能的影响 [J]. 国际医药卫生导报, 2024, 30(13): 2130-2135.

References

[1] 徐倩倩,钱旭东,孙凡,等. 血清胱抑素C水平与急性缺血性脑卒中后抑郁共病状态的关系[J]. 中国现代医学杂志,2023,33(14):64-69. DOI:10.3969/j.issn.1005-8982.2023.14.011.
[2] 余青龙,刘玉鹏,任娟. ASPECTS评分联合D-二聚体、Hcy对急性缺血性脑卒中患者溶栓近期预后的预测价值分析[J]. 中国现代医学杂志,2022,32(13):1-7. DOI:10.3969/j.issn.1005-8982.2022.13.001.
[3] 丁伟莉,王天宇,陈青,等. 急性缺血性卒中血管内介入治疗术后即刻及24h双能CT检查对脑出血转化评估的作用[J]. 中国脑血管病杂志,2023,20(4):223-229. DOI:10.3969/j.issn.1672-5921.2023.04.002.
[4] 陈晓辉,吕在刚,高宗恩. 对比剂对缺血性脑血管病患者血管内介入治疗术后肾功能的影响[J]. 中国脑血管病杂志,2016,13(12):629-633. DOI:11.3969/j.issn.1672-5921.2016.12.003.
[5] 何菲,张天聪,陈丹,等. 显微三维成像技术分析替罗非班抑制血小板黏附聚集的量效关系[J]. 分析化学,2022,50(2):244-252. DOI:10.19756/j.issn.0253-3820.210671.
[6] 林兆信,陈海云,王景,等. 替罗非班对急性脑梗死患者静脉溶栓后血小板参数的影响[J]. 中国临床药理学杂志,2023,39(16):2292-2296. DOI:10.13699/j.cnki.1001-6821. 2023.16.003.
[7] 朱存良,易芳芳,谭若利,等. 替罗非班与丁苯酞联合治疗对发病24 h内未行溶取栓治疗的急性缺血性脑卒中的疗效影响[J]. 临床和实验医学杂志,2023,22(3):254-257. DOI:10.3969/j.issn.1671-4695.2023.03.008.
[8] 中华医学会神经病学分会,中华医学会神经病学分会脑血管病学组. 中国急性缺血性脑卒中诊治指南2018[J]. 中华神经科杂志,2018,51(9):666-682. DOI:10.3760/cma.j.issn.1006-7876.2018.09.004.
[9] 夏宪军,鲍正社. 依达拉奉右莰醇对急性脑梗死患者神经功能、氧化应激及炎性因子的影响[J]. 湖南师范大学学报(医学版),2022,19(2):133-136. DOI:10.3969/j.issn.1673-016X.2022.02.037.
[10] 童艳飞,张佩兰. NIHSS评分≥15分且发病时间≤4.5 h的重型脑梗死患者静脉溶栓的疗效观察[J]. 实用医学杂志,2016,32(5):812-815. DOI:10.3969/j.issn.1006-5725. 2016.05.038.
[11] 刘爱芹,岳冬雪,张津溶,等. 不同mRS评分的急性缺血性脑卒中患者血清PTX3、GAL3、Npt水平[J]. 中国老年学杂志,2021,41(21):4617-4619. DOI:10.3969/j.issn.1005-9202.2021.21.005.
[12] Stegner D, Klaus V, Nieswandt B. Platelets as modulators of cerebral ischemia/reperfusion injury[J]. Front Immunol, 2019,10:2505. DOI: 10.3389/fimmu.2019.02505.
[13] Alquisiras-Burgos I, Aguilera P. Involvement of glucose transporter overexpression in the protection or damage after ischemic stroke[J]. Neural Regen Res, 2022,17(4):783-784. DOI: 10.4103/1673-5374.322456.
[14] Zhao Y, Zhang X, Chen X, et al. Neuronal injuries in cerebral infarction and ischemic stroke: from mechanisms to treatment (Review)[J]. Int J Mol Med, 2022,49(2):15. DOI: 10.3892/ijmm.2021.5070.
[15] Wang Z, He D, Zeng YY, et al. The spleen may be an important target of stem cell therapy for stroke[J]. J Neuroinflammation, 2019, 16(1):20. DOI: 10.1186/s12974-019-1400-0.
[16] 张艾嘉,王爽,王萍,等. 缺血性脑卒中的病理机制研究进展及中医药防治[J]. 中国实验方剂学杂志,2020,26(5):227-240. DOI:10.13422/j.cnki.syfjx.20200538.
[17] 赵英喆,王晓莉,吕娥,等. 二十二碳六烯酸治疗缺血性脑卒中的机制研究进展[J]. 医学临床研究,2021,38(9):1281-1284. DOI:10.3969/j.issn.1671-7171.2021.09.001.
[18] Su Z, Ye Y, Shen C, et al. Pathophysiology of ischemic stroke: noncoding RNA role in oxidative stress[J]. Oxid Med Cell Longev, 2022,2022:5815843. DOI: 10.1155/2022/5815843.
[19] Wu L, Xiong X, Wu X, et al. Targeting oxidative stress and inflammation to prevent ischemia-reperfusion injury[J]. Front Mol Neurosci, 2020,13:28. DOI: 10.3389/fnmol.2020.00028.
[20] Jayaraj RL, Azimullah S, Beiram R, et al. Neuroinflammation: friend and foe for ischemic stroke[J]. J Neuroinflammation, 2019,16(1):142. DOI: 10.1186/s12974-019-1516-2.
[21] Pawluk H, Woźniak A, Grześk G, et al. The role of selected pro-inflammatory cytokines in pathogenesis of ischemic stroke[J]. Clin Interv Aging, 2020,15:469-484. DOI: 10.2147/CIA.S233909.
[22] Shah FA, Kury LA, Li T, et al. Polydatin attenuates neuronal loss via reducing neuroinflammation and oxidative stress in rat MCAO models[J]. Front Pharmacol, 2019,10:663. DOI: 10.3389/fphar.2019.00663.
[23] Joundi RA, Smith EE, Yu AYX, et al. Temporal and age-specific trends in acute stroke incidence: a 15-year population-based study of administrative data in Ontario, Canada[J]. Can J Neurol Sci, 2021,48(5):685-689. DOI: 10.1017/cjn.2020.257.
[24] Ospel JM, van der Lugt A, Gounis M, et al. A clinical perspective on endovascular stroke treatment biomechanics[J]. J Biomech, 2021,127:110694. DOI: 10.1016/j.jbiomech.2021.110694.
[25] Yang M, Huo X, Miao Z, et al. Platelet glycoprotein IIb/IIIa receptor inhibitor tirofiban in acute ischemic stroke[J]. Drugs, 2019,79(5):515-529. DOI: 10.1007/s40265-019-01078-0.
[26] RESCUE BT Trial Investigators; Qiu Z, Li F, et al. Effect of intravenous tirofiban vs placebo before endovascular thrombectomy on functional outcomes in large vessel occlusion stroke: the RESCUE BT randomized clinical trial[J]. JAMA, 2022,328(6):543-553. DOI: 10.1001/jama.2022.12584.
[27] Sun C, Li X, Zhao Z, et al. Safety and efficacy of tirofiban combined with mechanical thrombectomy depend on ischemic stroke etiology[J]. Front Neurol,2019,10:1100. DOI: 10.3389/fneur.2019.01100.
[28] Pan X, Zheng D, Zheng Y, et al. Safety and efficacy of tirofiban combined with endovascular treatment in acute ischaemic stroke[J]. Eur J Neurol, 2019,26(8):1105-1110. DOI: 10.1111/ene.13946.
[29] 张力维,李德鑫,王义成,等. 颈动脉斑块SMI分级联合血清超敏C-反应蛋白在急性缺血性脑卒中风险评估中的应用价值[J]. 河北医科大学学报,2023,44(3):329-333. DOI:10.3969/j.issn.1007-3205.2023.03.017.
[30] Lucci C, Cosentino N, Genovese S, et al. Prognostic impact of admission high-sensitivity C-reactive protein in acute myocardial infarction patients with and without diabetes mellitus[J]. Cardiovasc Diabetol, 2020,19(1):183. DOI: 10.1186/s12933-020-01157-7.