阿魏酸钠对急性心肌梗死行直接PCI术患者心肌保护作用及其机制研究
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摘要
目的观察阿魏酸钠对急性心肌梗死行直接经皮冠状动脉介入治疗(PCI)术患者的心肌保护作用,并探讨其中机制。方法将2016年2月至2018年5月该科收治的62例急性ST段抬高型心肌梗死(STEMI)患者随机分为对照组及试验组,每组31例。2组患者均行PCI术及药物治疗,试验组加用阿魏酸钠,共治疗10d。治疗前后评估2组患者左心功能、校正的TIMI帧数(CTFC),血清人内皮素-1(ET-1)、一氧化氮(NO)、炎症因子、氧化应激水平,术后90d心脏不良事件发生率及药物不良事件发生率。结果 PCI术后,试验组CTFC低于对照组,差异有统计学意义(P<0.05)。治疗后,2组左心功能均较本组治疗前提高,其中试验组较对照组改善更明显,差异均有统计学意义(P<0.05)。治疗后,2组丙二醛、ET-1、肿瘤坏死因子-α、白细胞介素-6及超敏C-反应蛋白水平均较本组治疗前降低,而试验组较对照组降低更明显,差异均有统计学意义(P<0.05)。治疗后,2组谷胱甘肽过氧化物酶、超氧化物歧化酶、NO水平均较本组治疗前升高,而试验组较对照组上升更明显,差异均有统计学意义(P<0.05)。试验组术后90d心脏不良事件发生率低于对照组,差异有统计学意义(P<0.05)。2组患者均未出现药物相关不良事件。结论 STEMI患者在PCI术及药物治疗基础上加用阿魏酸钠具有良好的安全性,可改善冠状动脉微循环灌注及心脏功能,减少心脏不良事件发生,其机制与阿魏酸钠抑制炎症及氧化应激反应、改善血管内皮功能有关。
Objective To investigate the effects of Sodium ferulate injection on myocardial protection in patients with acute myocardial infarction undergoing primary PCI and to explore the mechanism.Methods A total of 62 STEMI patients who admitted to the department from February 2016 to May 2018 were randomly divided into control group and experimental group,31 in each group.PCI and drug therapy were performed in both groups,and sodium ferulate was added to the experimental group for 10 days.Before and after treatment,left ventricular function,corrected CTFC,serum ET-1,NO,inflammatory factors,oxidative stress level,and incidence of cardiac adverse events and adverse drug events 90 days after surgery were evaluated in the two groups.Results After PCI,the CTFC of the experimental group was lower than that of the control group,and the difference was statistically significant(P<0.05).After treatment,the left heart function of the two groups was improved compared with that before treatment,and the experimental group was further improved compared with the control group,with statistically significant differences(P<0.05).After treatment,the levels of malondialdehyde,et-1,tumor necrosis factor-α,interleukin-6 and hypersensitive C-reactive protein in the two groups were lower than those before treatment in the same group,while the levels in the experimental group were lower than those in the control group,with statistically significant differences(P<0.05).After treatment,the levels of glutathione peroxidase,superoxide dismutase and NO in the two groups were higher than those before treatment in the same group,while those in the experimental group were higher than those in the control group,the differences were statistically significant(P<0.05).The incidence of adverse cardiac events 90 days after surgery in the experimental group was lower than that in the control group,and the difference was statistically significant(P<0.05).No drug-related adverse events occurred in two groups.Conclusion STEMI patients treated with sodium ferulate on the basis of PCI and drug therapy have good safety,can improve coronary microcirculation perfusion and cardiac function,reduce adverse cardiac events,the mechanism is related to sodium ferulate inhibiting inflammation and oxidative stress reaction,improve vascular endothelial function.
Objective To investigate the effects of Sodium ferulate injection on myocardial protection in patients with acute myocardial infarction undergoing primary PCI and to explore the mechanism.Methods A total of 62 STEMI patients who admitted to the department from February 2016 to May 2018 were randomly divided into control group and experimental group,31 in each group.PCI and drug therapy were performed in both groups,and sodium ferulate was added to the experimental group for 10 days.Before and after treatment,left ventricular function,corrected CTFC,serum ET-1,NO,inflammatory factors,oxidative stress level,and incidence of cardiac adverse events and adverse drug events 90 days after surgery were evaluated in the two groups.Results After PCI,the CTFC of the experimental group was lower than that of the control group,and the difference was statistically significant(P<0.05).After treatment,the left heart function of the two groups was improved compared with that before treatment,and the experimental group was further improved compared with the control group,with statistically significant differences(P<0.05).After treatment,the levels of malondialdehyde,et-1,tumor necrosis factor-α,interleukin-6 and hypersensitive C-reactive protein in the two groups were lower than those before treatment in the same group,while the levels in the experimental group were lower than those in the control group,with statistically significant differences(P<0.05).After treatment,the levels of glutathione peroxidase,superoxide dismutase and NO in the two groups were higher than those before treatment in the same group,while those in the experimental group were higher than those in the control group,the differences were statistically significant(P<0.05).The incidence of adverse cardiac events 90 days after surgery in the experimental group was lower than that in the control group,and the difference was statistically significant(P<0.05).No drug-related adverse events occurred in two groups.Conclusion STEMI patients treated with sodium ferulate on the basis of PCI and drug therapy have good safety,can improve coronary microcirculation perfusion and cardiac function,reduce adverse cardiac events,the mechanism is related to sodium ferulate inhibiting inflammation and oxidative stress reaction,improve vascular endothelial function.
引文
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[8]颜斯亮.阿魏酸钠注射液的药理作用与临床应用研究进展[J].甘肃科技,2016,32(7):100-101.
[9]卓杨,殷兆芳,张阳,等.校正的TIMI帧数评估血栓抽吸在急性ST段抬高型心肌梗死中的疗效[J].中国医学前沿杂志:电子版,2014,6(12):36-39.
[10]SRIKANTH S,AMBROSE JA.Pathophysiology of coronary thrombus formation and adverse consequences of thrombus during PCI[J].Curr Cardiol Rev,2018,8(3):168-176.
[11]HEUSCH G.The Coronary Circulation as a Target of Cardioprotection[J].Circ Res,2016,118(10):1643-1658.
[12]QING Y,DONG X,HONGLI L,et al.Berberine promoted myocardial protection of postoperative patients through regulating myocardial autophagy[J].Biomed Pharmacother,2018,105:1050-1053.
[13]段启瑞,邱颐,王彩霞.炎症因子与缺血再灌注损伤研究进展[J].内蒙古医科大学学报,2016,38(2):181-184.
[14]MONTEZANO AC,DULAK-LIS M,T SIROPOULOU S,et al.Oxidative stress and human hypertension:vascular mechanisms,biomarkers,and novel therapies[J].Can J Cardiol,2015,31(5):631-641.
[15]BOGER RH,BODE-BOGER SM,FROLICH JC.The larginine nitric oxide pathway:role in atherosclerosis and therapeutic implications[J].Atherosclerosis,1996,127(1):1-11.
[2] GALASSO G,SCHIEKOFER S,D′ANNA C,et al.No-reflow phenomenon:pathophysiology,diagnosis,prevention,and treatment.A review of the current literature and future perspectives[J].Angiology,2014,65(3):180-189.
[3]毛丹.阿魏酸钠的临床应用进展[J].现代诊断与治疗,2014,25(18):4166-4169.
[4]中华医学会心血管病学分会,中华心血管病杂志编辑委员会.2015急性ST段抬高型心肌梗死诊断和治疗指南[J].中华心血管病杂志,2015,43(5):380-393.
[5] DING S,PU J,QIAO ZQ,et al.TIMI myocardial perfusion frame count:a new method to assess myocardial perfusion and its predictive value for short-term prognosis[J].Cardiovasc Interv,2010,75(5):722-732.
[6] AMIER RP,TEUNISSEN PF,MARQUES KM,et al.Invasive measurement of coronary microvascular resistance in patients with acute myocardial infarction treated by primary PCI[J].Heart,2014,100(1):13-20.
[7] HEUSCH G,SKYSCHALLY A,KLEINBONGARD P.Coronary microembolization and microvascular dysfunction[J].Int J Cardiol,2018,258:17-23.
[8]颜斯亮.阿魏酸钠注射液的药理作用与临床应用研究进展[J].甘肃科技,2016,32(7):100-101.
[9]卓杨,殷兆芳,张阳,等.校正的TIMI帧数评估血栓抽吸在急性ST段抬高型心肌梗死中的疗效[J].中国医学前沿杂志:电子版,2014,6(12):36-39.
[10]SRIKANTH S,AMBROSE JA.Pathophysiology of coronary thrombus formation and adverse consequences of thrombus during PCI[J].Curr Cardiol Rev,2018,8(3):168-176.
[11]HEUSCH G.The Coronary Circulation as a Target of Cardioprotection[J].Circ Res,2016,118(10):1643-1658.
[12]QING Y,DONG X,HONGLI L,et al.Berberine promoted myocardial protection of postoperative patients through regulating myocardial autophagy[J].Biomed Pharmacother,2018,105:1050-1053.
[13]段启瑞,邱颐,王彩霞.炎症因子与缺血再灌注损伤研究进展[J].内蒙古医科大学学报,2016,38(2):181-184.
[14]MONTEZANO AC,DULAK-LIS M,T SIROPOULOU S,et al.Oxidative stress and human hypertension:vascular mechanisms,biomarkers,and novel therapies[J].Can J Cardiol,2015,31(5):631-641.
[15]BOGER RH,BODE-BOGER SM,FROLICH JC.The larginine nitric oxide pathway:role in atherosclerosis and therapeutic implications[J].Atherosclerosis,1996,127(1):1-11.
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