血清4种生化指标与心肌梗死预后相关性分析

摘要/Abstract

摘要： 目的：探讨急性心肌梗死（AMI）患者血清4种生化因子，血管内皮生长因子B（VEGF-B）、白细胞介素-32（IL-32）、蛋白相关磷脂酶A2（Lp-PLA2）及儿茶酚抑素（CST）与AMI预后相关性。方法：收集我院急性冠脉综合征患者294例，其中AMI患者189例，不稳定心绞痛（UA）患者105例，记录一般情况并测定血清中VEGF-B、Lp-PLA2、CST、IL-32水平变化，同时评估AMI组患者各期心功能指标，对AMI患者随访6个月发生心脏主要不良事件（MACE）情况，探讨上述4种生化因子与AMI预后关系。结果：对AMI组及UA组（对照组）治疗前后进行对比，治疗前两组血清VEGF-B无明显差异（P＞0.05），与UA组相比，AMI组Lp-PLA2、CST均较高（P＜0.05），IL-32在UA组高于AMI组（P＜0.05）；治疗后两组患者血清各指标无明显差异（P＞0.05）。心功能各期对比发现VEGF-B在KiliipⅠ-Ⅳ间无明显差异（P＞0.05）；Lp-PLA2、CST水平在各组间随着心功能恶化呈上升趋势；IL-32含量随心功能恶化而降低。随访终止时AMI患者总MACE发生率为42.33%。预后不良组患者入院时血清中VEGF-B、IL-32明显低于预后良好组（P＜0.05），Lp-PLA2、CST显著高于预后良好组（P＜0.05）。结论：AMI与UA时由于心肌细胞缺氧受损或死亡，患者体内各种生化因子会发生不同变化。这些不同变化可能与应激及炎症反应有关，随着心功能的变化各指标变化趋势不同，提示4种指标对AMI严重程度有一定指导意义，且对AMI预后评估具有一定价值。CST、Lp-PLA2水平越高提示预后不良，VEGF-B、IL-32与预后MACE发生率呈负相关。

Abstract: Objective：To investigate the correlation between serum four biochemical factors(vascular endothelial growth factor B， interleukin-32， lipoprotein-associated phospholipase A2 and catestatin) and prognosis of acute myocardial infarction（AMI） in patients with AMI.Methods： Comprehensive collection of 294 cases of acute coronary syndrome patients in our hospital， including 189 cases of AMI patients， 105 UA patients， record the general condition and determine serum VEGF-B， Lp-PLA2， CST， IL-32 level. AMI group were assessed at the same time the index of heart function and AMI patients were followed up 6 months of occurrence of major adverse cardiac events to investigate the correlation between these four kinds of biochemical factors and prognosis of AMI. Results： There was no significant difference in serum VEGF-B between the two groups before and after treatment(P>0.05). Compared with UA group， Lp-PLA2 and CST in AMI group were higher than those in UA group(P<0.05). IL-32 was higher in UA group than in AMI group(P<0.05). There was no significant difference in serum between the two groups(P>0.05). The comparison of cardiac function showed that there was no significant difference in VEGF-B between Kiliip Ⅰand IV(P>0.05)； the levels of Lp-PLA2 and CST showed an upward trend with the deterioration of cardiac function in all groups； IL-32 content decreased with the deterioration of heart function. At the end of follow-up， the incidence of total MACE in patients with AMI was 42.33%. The serum levels of VEGF-B and IL-32 in patients with poor prognosis were significantly lower than those in the good prognosis group(P<0.05)， Lp-PLA2 and CST were significantly higher than those in the patients with good prognosis(P<0.05).Conclusion： In AMI and UA， due to hypoxia damage or death， various biochemical factors in patients will have different changes. These changes may associated with stress and inflammatory response， along with the changes of cardiac function indexes of different trends， suggesting that the four indexes have certain guiding significance for the severity of AMI， and have value for the evaluation of the prognosis of AMI. The higher the CST， Lp-PLA2 level indicates poor prognosis， VEGF-B， IL-32 and incidence of prognosis MACE was negatively correlated.

许涛. 血清4种生化指标与心肌梗死预后相关性分析[J]. .

xutao. Correlation Analysis between Four Biochemical Indexes of Serum and Prognosis of Myocardial Infarction[J]. .

参考文献

[1] 金捷.微处理器控制的植入式心脏起搏器专用电路研制 [J].中国医疗器械信息,2003,9(5):11-13.
[2] Kirchberger I, Heier M, Kuch B, et al. Presenting symptoms of myocardial infarction predict short-and long-term mortality:The MONICA/KORA Myocardial Infarction Registry [J]. Am Heart J,2012, 164(6): 856-861.
[3] Armas NB, Ortega YY, Suárez R, et al. Early acute myocardial infarction mortality in cuba, 1999-2008 [J]. MEDICC Rev, 2012, 14(4): 19-25.
[4] American Hear Association.2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science.Circulation,2010+122:$639—946.
[5] Erhardt L,Herlitz J,Bossaert L,et a1.Task force on the management of chest pain.EurHearl J,2002,23:1153—1176.
[6] Yao HC,Liu T,Meng XY,eI al. Effect of basic fibroblast growth factor the myocardial expression of hypoxia-inducible factor-1α and vascular endothelial growth factor following acute myocardial infarction [J].Heart Lung Circ,2013;22(11);946-51.
[7] Lee S,Kim JH,Kim H,et al.Activation of the interleukin-32 proinflammatory pathway in response to human papillomavirus infection and over-expressionof interleukin-32 controls the expression of the humanpapillomavirus oncogene[J].Immunology,2011,132(3) :410－420.
[8] Choi JD,Bae SY,Hong JW,et al.Identification of the most active interleukin－32 isoform[J].Immunology,2009,126(4) :535－542.
[9] 安新,高利常,孙太起,等. IL-32、MMP-13及IL-10在类风湿关节炎中的表达及意义研究［J/CD］.中华临床医师杂志( 电子版),2013,7(20) :9089．
[10] Moon YM,Yoon BY,Her YM,et al.L-32 and IL-17 interact and have the potential to aggravate osteoclastogenesis in rheumatoid arthritis[J].Arthritis Ｒes Ther,2012,14(6):Ｒ246.
[11] 宁长青,冯伟,刘益杰,等.IL-17与类风湿性关节炎的研究进展[J].中国中医骨伤科杂志,2013,21(9) :67-69.
[12] 陈家林. 血清IL-32与急性心梗患者预后的相关性分析[J]. 安徽医药,2016,(03):512-515.
[13] 宋　强,雍海溟,张水华,等畅血管内皮生长因子Ｂ生物学功能的研究进展[J].医学研究生学报,2012,25(7):774-7.
[14] Devaux Y,Azuaje F,Vausort M,et al.Integrated protein network and microarray analysis to identify potential biomarkers after myocardial infarction[J].Funct Integr Genomics,2010,(3):329-37.
[15] Mahapatra N R,Mahata M,Mahata S K,et al.The chromogranin A fragment catestatin:specificity,potency and mechanism to inhibit exocytotic secretion of multiple catecholamine storage vesicle cotransmitters[J].J Hypertens,2006,24(5):895-904.
[16] Theurl M,Schgoeo W,Albrecht K,et al.The neuropeptide catestatin acts as a novel angeogenic cytokine via a basic fibroblast growth factor-dependent mechanism[J].Circulation Research,2010,107（11）：1326-1335.
[17] Lavi S, Mc Connell JP, Prasad A, et al. Local production of lipoprotein-associated phospholipase A2 and lysophosphatidylcholine in the coronary circulation: association with early coronary atherosclerosis and endothelial dysfunction in Humans. Circulation,2012;115:2715-2721.
[18] Robert S, Rosenson, Diana M, Stafforini. Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associated phospholipase A2. Journal of lipid research, 2012;53:1767-1782.
[19] Winkler K, Winkelmann B R, Schamagl H, et al. Platelet-activating factor accttylyhdrolase activity indicates angiographic coronary artery disease independently of systemic inflammation and other risk factors :the Ludwigshafen Risk and Cardiovascular Health Study. Circulation, 2005;111:980-987.
[20] 张振,王海斌,王国龙,陈月婷. Lp-PLA2预测急性心梗患者PCI预后的价值[J].临床心电学杂志,2015,(06):410-415.

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