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替格瑞洛对不稳定型心绞痛择期PCI患者血清炎性因子及MMP-9、sICAM-1、tPAI-1的影响

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目的 研究替格瑞洛对不稳定型心绞痛(UAP)择期经皮冠状动脉介入治疗(PCI)患者
血清炎性因子及基质金属蛋白酶-9(MMP-9)、可溶性细胞间粘附分子-1(sICAM-1)、1型组织纤
溶酶原激活物抑制剂(tPAI-1)的影响。方法 选取2015年1月~2017年12月就诊于湖北医药学院附属国
药东风总医院心血管内科的UAP患者114例,依据随机数字表法分为替格瑞洛组(57例)与对照组(57
例)。对照组行常规治疗+氯吡格雷治疗,替格瑞洛组行常规治疗+替格瑞洛治疗。观察两组PCI中冠
状动脉(冠脉)血流及急性血栓形成情况和PCI前后心绞痛得分;检测血清心肌肌钙蛋白I(CTnI)、
肌酸激酶同功酶(CK-MB)、心肌型脂肪酸结合蛋白(H-FABP)等心肌损伤指标,血清MMP-9、
sICAM-1、tPAI-1等表达水平;并随访PCI后1年内主要不良心血管事件(MACE)发生情况。结果 替
格瑞洛组术中慢血流或无复流发生率(0.00%)低于对照组(7.02%,P<0.05)。PCI后,替格瑞洛组
西雅图心绞痛问卷(SAQ)不同维度评分及总分均高于对照组(P<0.05)。PCI后,替格瑞洛组CTnI、
CK-MB、H-FABP、MMP-9、sICAM-1、tPAI-1均低于对照组(P均<0.05)。PCI后1年内,替格瑞洛组
MACE发生率低于对照组(1.75% vs. 12.28%,P<0.05)。结论 替格瑞洛可改善UAP择期PCI患者冠脉血
流,缓解其心绞痛,清除炎性因子,抑制MMP-9、sICAM-1、tPAI-1生成,MACE发生率低。

Abstract:

Objective To study the influence of ticagrelor on serum inflammatory factors and mitochondrial
membrane potential-9 (MMP-9), soluble intercellular adhesion molecule-1 (sICAM-1), type-1 plasminogen
activator inhibitor (tPAI-1) in patients with unstable angina pectoris (UAP) undergone elective PCI. Methods UAP
patients (n=114) were chosen from Guoyao Dongfeng General Hospital affiliated to Hubei University of Medicine
from Jan. 2015 to Dec. 2017, and divided, according to random digital table, into ticagrelor group and control group
(each n=57). The control group was given routine therapy and clopidogrel and ticagrelor group was given routine
therapy and ticagrelor. The coronary artery flow and acute thrombosis during PCI, and angina pectoris scores
before and after PCI were observed in 2 groups. The levels of serum cardiac troponin I (cTnI), creatine kinase-
MB isoenzyme (CK-MB), heart-type fatty acid-binding protein (H-FABP), MMP-9, sICAM-1 and tPAI-1 were
detected. The incidence of major adverse cardiovascular events (MACE) was followed up after PCI for 1 y. Results
The incidence rate of coronary slow flow or no-reflow was lower in ticagrelor group (0.00%) than that in control
group (7.02%, P<0.05). The scores and total score of Seattle Angina Questionnaire (SAQ) at different dimensions
were higher in ticagrelor group than those in control group after PCI (P<0.05). The levels of CTnI, CK-MB, H-FABP,
MMP-9, sICAM-1 and tPAI-1 were all lower in ticagrelor group than those in control group after PCI (all P<0.05).
The incidence rate of MACE was lower in ticagrelor group than that in control group (1.75% vs. 12.28%) within 1
y after PCI (P<0.05). Conclusion Ticagrelor can improve coronary artery flow, relieve angina pectoris, eliminate
inflammatory factors, inhibit the productions of MMP-9, sICAM-1, tPAI-1 and reduce MACE incidence in patients
with UAP undergone selective PCI.

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