缺血后适应对接受急诊PCI治疗的STEMI患者细胞凋亡因子及心功能的影响
作者:
作者单位:

(南华大学附属长沙中心医院心内科,湖南省长沙市 410004)

作者简介:

徐海南,硕士研究生,研究方向为心血管内科,E-mail为3053923464@qq.com。

基金项目:

长沙市科技局项目(Kq1801143)


Effect of ischemic postconditioning on the response of apoptotic factors and cardiac function in patients with STEMI who received percutaneous coronary intervention
Author:
Affiliation:

Department of Cardiology, Changsha Central Hospital, Affiliated to University of South China, Changsha, Hunan 410004, China)

  • 摘要
  • | |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • | |
    摘要:

    目的 通过对急性ST段抬高型心肌梗死(STEMI)患者行急诊经皮冠状动脉介入治疗(PCI)前给予缺血后适应(IPOC)的处理,了解患者血清可溶性凋亡因子(sFas)及可溶性凋亡因子配体(sFasL)水平变化和术后1年内超声心动图下左心室射血分数(LVEF)的变化,探讨患者心功能的变化及其可能机制。方法 90例行急诊PCI的急性STEMI患者治疗前随机等分为常规PCI组、IPOC 45 s组以及IPOC 60 s组,常规PCI组开通梗死相关动脉(IRA)再灌注开始3 min内不施加任何干预;IPOC 45 s组在开通IRA后1 min内球囊在罪犯血管上游开始实施反复低压(4~6个标准大气压)充盈和回缩3次,每次持续45 s,IPOC 60 s组操作方法同IPOC 45 s组,每次持续60 s。检测患者术前及术后0 h、24 h、48 h血清sFas、sFasL水平,并随访1个月、3个月、6个月、1年内三组患者左心室射血分数(LVEF)变化情况。结果 三组患者的血清sFas、sFasL水平,在术前、术后0 h及术后24 h差异均无统计学意义(P>0.05);术后48 h,IPOC 60 s组和IPOC 45 s组患者血清sFas、sFasL水平较常规PCI组明显降低,且差异均有统计学意义(P<0.05);三组患者术后1周、术后1个月、术后3个月超声心动图下LVEF值,差异均无统计学意义(P>0.05),但术后6个月,IPOC 60 s组和IPOC 45 s组患者LVEF值均高于常规PCI组(P<0.05),术后1年IPOC 60 s组患者LVEF值仍高于常规PCI组(P<0.05)。结论 干预时限为60 s的缺血后适应能够明显改善STEMI患者心功能,其机制可能与IPOC能抑制心肌再灌注诱导的细胞凋亡有关。

    Abstract:

    Aim Patients with ST-elevation myocardial infarction (STEMI) were subjected to administer ischemic post-conditioning (IPOC) before conducting emergency treatment with percutaneous intervention (PCI). Changes in serum soluble apoptosis factor (sFas) and soluble apoptosis factor ligand (sFasL) and the left ventricular ejection fraction (LVEF) under echocardiography during the 1 postoperative year were investigated in patients, and changes in cardiac function in patients and the possible mechanisms were explored. Methods 90 patients with acute STEMI who underwent emergency PCI were randomly divided into three groups before treatment:routine PCI group, IPOC 45 s group and IPOC 60 s group. No intervention was given within 3 minutes after reperfusion of infarct-related artery (IRA) in routine PCI group. Within 1 minute after the opening of IRA, repeated low pressure (4~6 standard atmospheric pressure) filling and retraction of the balloon were performed at the upstream of the patient's blood vessels for 3 times, each time lasting 45 s. The operation method of the IPOC 60 s group was the same as that of the IPOC45 s group, lasting 60 s each time. The levels of serum sFas and sFasL were measured before operation and 0 h, 24 h and 48 h after operation, and the changes of LVEF in the three groups were followed up for 1 month, 3 months, 6 months and 1 year. Results There was no significant difference in serum sFas, sFasL level among the three groups before operation and 0 h, 24 h after operation (all P>0.05). 48 hours after operation, the serum sFas, sFasL level decreased significantly in the IPOC 60 s group and the IPOC 45 s group compared with the routine group (all P<0.05). There was no significant difference in LVEF values among the three groups at 1 week, 1 month and 3 months after operation(all P>0.05), but at 6 months after operation, the values of LVEF in IPOC 60 s group and IPOC 45 s group were higher than those in routine group. One year after operation, the value of LVEF in IPOC 60 s group was higher than that in routine group(P<0.05). Conclusion Ischemic postconditioning 60 s reperfusion therapy after ischemia can significantly improve cardiac function in STEMI patients, and the mechanism may be related to the inhibitory effect of IPOC on apoptosis induced by myocardial reperfusion.

    参考文献
    [1] Ibánez B, James S, Agewall S, et al.2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation.Rev Esp Cardiol (Engl Ed), 7,0(12):1082.
    [2] Verma S, Fedak PW, Weisel RD, et al.Fundamentals of reperfusion injury for the clinical cardiologist.Circulation, 2,5(20):2332-2336.
    [3] Zhao ZQ, Corvera JS, Halkos ME, et al.Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison with ischemic preconditioning.Am J Physiol Heart Circ Physiol, 3,5(2):H579-H588.
    [4] Thibault H, Piot C, Staat P, et al.Long-term benefit of postconditioning.Circulation, 8,7(8):1037-1044.
    [5] Mukherjee P, Jain M.Effect of ischemic postconditioning during primary percutaneous coronary intervention for patients with ST-segment elevation myocardial infarction:a single-center cross-sectional study.Ann Card Anaesth, 9,2(4):347-352.
    [6] Araszkiewicz A, Grygier M, Pyda M, et al.Ischemic postconditioning reduces infarct size and microvascular obstruction zone in acute ST-elevation myocardial infarction:a randomized study.Postepy Kardiol Interwencyjnej, 9,5(3):292-300.
    [7] 张苗苗, 王贵松.缺血后适应在临床中的应用及研究进展.中国动脉硬化杂志, 3,1(5):477-480.
    [8] 郑小芳, 吴黎明, 陈良龙.mitOKATP通道在瑞舒伐他汀联合缺血后处理减轻糖尿病小鼠心肌缺血再灌注损伤中的作用.中国动脉硬化杂志, 2,0(2):130-134.
    [9] Zhao WS, Xu L, Wang LF, et al.A 60-s postconditioning protocol by percutaneous coronary intervention inhibits myocardial apoptosis in patients with acute myocardial infarction.Apoptosis, 9,4(10):1204-1211.
    [10] Xing Z, Tang L, Huang J, et al.Effects of ischaemic postconditioning on outcomes of patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention:a Meta-analysis.BMJ Open, 9,9(3):e022509.
    [11] Jy H, Song YB, Kim EK, et al.Ischemic postconditioning during primary percutaneous coronary intervention:the effects of postconditioning on myocardial reperfusion in patients with ST-segment elevation myocardial infarction(POST)randomizedtrial.Circulation, 3,8(17):1889-1896.
    [12] Zhao ZQ.Postconditioning in reperfusion injury:a status report.Cardiovasc Drugs Ther, 0,4(3):265-279.
    [13] 中华医学会心血管病学分会.急性ST段抬高型心肌梗死诊断及治疗指南.中国心血管病杂志, 9,7(10):766-783.
    [14] Saraste A, Pulkki K, Kallajoki M, et al.Apoptosis in human acute myocardial infarction.Circulation, 7,5(2):320-323.
    [15] Cheng W, Kajstura J, Nitahara JA, et al.Programmed myocyte cell death affects the viable myocardium after infarction in rats.Exp Cell Res, 6,6(2):316-327.
    [16] Von Harsdorf R, Li PF, Dietz R.Signaling pathways in oxygen species-induced cardioomyocyte apoptosis.Circulation, 9,9(22):2934-2941.
    [17] Vinten-Johansen J.Involvement of neutrophils in the pathogenesis of lethal myocardial reperfusion injury.Cardiovasc Res, 4,1(3):481-497.
    [18] Kim JS, Jin Y, Lemasters JJ.Reactive oxygen species, but not Ca2+ overloading, trigger pH-and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia reperfusion.Am J Physiol Heart Circ Physiol, 6,0(5):H2024-H2034.
    [19] Zhou T, Chuang CC, Zuo L.Molecular characterization of reactive oxygen species in myocardial ischemia-reperfusion injury.Biomed Res Int, 5,5:864946.
    [20] Nie J, Duan Q, He M, et al.Ranolazine prevents pressure overload-induced cardiac hypertrophy and heart failure by restoring aberrant Na+ and Ca2+ handling.J Cell Physiol, 9,4(7):11587-11601.
    [21] Valls-Lacalle L, Barba I, Miró-Casas E, et al.Succinate dehydrogenase inhibition with malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition.Cardiovasc Res, 6,9(3):374-384.
    [22] Chang J, Zhang G, Zhang L, et al.High admission glucose levels increase Fas apoptosis and mortality in patients with acute ST-elevation myocardial infarction:a prospective cohort study.Cardiovasc Diabetol, 3,2:171.
    引证文献
引用本文

徐海南,邓平,蒋路平.缺血后适应对接受急诊PCI治疗的STEMI患者细胞凋亡因子及心功能的影响[J].中国动脉硬化杂志,2021,29(8):688~694.

复制
分享
文章指标
  • 点击次数:264
  • 下载次数: 619
历史
  • 收稿日期:2020-04-21
  • 最后修改日期:2020-06-12
  • 在线发布日期: 2021-08-10