唐建琴
·论著·
血清超敏C反应蛋白、白介素6、肿瘤坏死因子α水平与持续性心房颤动并肺部感染患者左心房结构改变的关系研究
唐建琴
目的 分析血清超敏C反应蛋白(hs-CRP)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平与持续性心房颤动并肺部感染患者左心房结构改变的关系。方法 选取2014年6月—2015年6月成都市郫县中医医院内一科收治的持续性心房颤动患者150例作为房颤组,根据有无肺部感染分为肺部感染组54例,无肺部感染组96例;根据左心房内径(LAD)分为LAD>40 mm组92例和LAD≤40 mm组58例。选取同期在本院门诊体检的窦性心律者50例作为对照组。比较对照组与观察组受试者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标〔LAD、左心房后壁背向散射积分(IBS)及背向散射积分周期变化值(CVIB)〕,比较肺部感染组与无肺部感染组患者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标,比较LAD>40 mm组与LAD≤40 mm组患者血清hs-CRP、IL-6、TNF-α水平。结果 房颤组患者血清hs-CRP、IL-6、TNF-α水平及IBS高于对照组,LAD大于对照组,CVIB低于对照组(P<0.05)。肺部感染组患者血清hs-CRP、IL-6、TNF-α水平高于无肺部感染组(P<0.05);两组患者LAD、IBS、CVIB比较,差异无统计学意义(P>0.05)。LAD>40 mm组患者血清hs-CRP、IL-6、TNF-α水平高于LAD≤40 mm组(P<0.05)。结论 持续性心房颤动并肺部感染患者血清hs-CRP、IL-6、TNF-α水平升高,左心房增大并伴有心肌纤维化,hs-CRP、IL-6、TNF-α可能参与左心房结构改变过程。
心房颤动;肺部感染;炎性因子;左心房
唐建琴.血清超敏C反应蛋白、白介素6、肿瘤坏死因子α水平与持续性心房颤动并肺部感染患者左心房结构改变的关系研究[J].实用心脑肺血管病杂志,2016,24(10):15-18.[www.syxnf.net]
TANG J Q.Correlations between serum levels of hs-CRP,IL-6 and TNF-α and left atrium structure change of persistent atrial fibrillation patients complicated with pulmonary infection[J].Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease,2016,24(10):15-18.
心房颤动(atrial fibrillation)是心律失常的常见类型之一,老年人多发病及常见病,随着年龄增长其发病率呈升高趋势。冠心病是引发心房颤动的最常见疾病[1-2],部分冠心病患者甚至出现持续性心房颤动,同时易并发肺部感染[3-4]。临床研究显示,炎性因子所致的炎性反应可能参与心房颤动的发生过程,且肺部感染患者多种血清炎性因子水平出现异常升高[5-8]。本研究旨在分析血清超敏C反应蛋白(hs-CRP)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平与持续性心房颤动并肺部感染患者左心房结构改变的关系,并试着阐述炎性因子在持续性心房颤动并肺部感染患者左心房结构改变中的作用机制。
1.1 一般资料 选取2014年6月—2015年6月成都市郫县中医医院内一科收治的持续性心房颤动患者150例作为房颤组,根据有无肺部感染分为肺部感染组54例,无肺部感染组96例;根据左心房内径(LAD)分为LAD>40 mm组92例和LAD≤40 mm组58例。纳入标准:(1)结合病史及心电图检查等确诊为心房颤动,持续时间>7 d,符合持续性心房颤动诊断标准;(2)在纳入研究前未进行系统治疗;(3)停用抗心律失常药物超过2个t1/2。排除标准:(1)合并除肺部感染之外其他急慢性感染性疾病者;(2)急性心肌炎等可逆性病因所致心房颤动者;(3)有心脏手术史者;(4)其他疾病终末期者;(5)近1个月内有免疫抑制剂等抗炎药物治疗史者;(6)合并恶性肿瘤、免疫系统疾病及组织损伤性疾病者。选取同期在本院门诊体检的窦性心律者50例作为对照组,排除标准同房颤组。两组受试者性别、年龄、基础疾病及吸烟史阳性率比较,差异均无统计学意义(P>0.05,见表1),具有可比性。
1.2 方法
1.2.1 hs-CRP、IL-6、TNF-α检测方法 房颤组患者入院后第1天、对照组受试者体检当天均抽取空腹外周静脉血5 ml,静置4 h后3 000 r/min离心30 min,留取血清。采用免疫比浊法检测血清hs-CRP水平,采用双抗体酶联免疫吸附法检测血清IL-6、TNF-α水平,试剂盒均购自深圳晶美生物科技公司。
1.2.2 左心房结构指标测定方法 采用HP5500彩色多普勒超声诊断仪(飞利浦公司生产)测定两组受试者LAD,探头频率为2~4 MHz;测定左心房后壁背向散射积分(IBS)及背向散射积分周期变化值(CVIB)。
1.3 观察指标 比较对照组与房颤组受试者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标(LAD、IBS、CVIB),比较肺部感染组与无肺部感染组患者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标,比较LAD>40 mm组与LAD≤40 mm组患者血清hs-CRP、IL-6、TNF-α水平。
2.1 对照组与房颤组受试者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标比较 房颤组患者血清hs-CRP、IL-6、TNF-α水平及IBS高于对照组,LAD大于对照组,CVIB低于对照组,差异有统计学意义(P<0.05,见表2)。
2.2 肺部感染组与无肺部感染组患者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标比较 肺部感染组患者血清hs-CRP、IL-6、TNF-α水平高于无肺部感染组,差异有统计学意义(P<0.05);两组患者LAD、IBS、CVIB比较,差异无统计学意义(P>0.05,见表3)。
2.3 LAD>40 mm组与LAD≤40 mm组患者血清hs-CRP、IL-6、TNF-α水平比较 LAD>40 mm组患者血清hs-CRP、IL-6、TNF-α水平高于LAD≤40 mm组,差异有统计学意义(P<0.05,见表4)。
表4 LAD>40 mm组与LAD≤40 mm组患者血清hs-CRP、IL-6、TNF-α水平比较
表1 对照组与房颤组受试者一般资料比较〔n(%)〕
表2 对照组与房颤组受试者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标比较
表3 肺部感染组与无肺部感染组患者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标比较
血清及血浆中炎性反应标志物一般分为3类,包括急性时相蛋白、可溶性黏附因子和细胞因子,IL-6和TNF-α属于细胞因子,主要由单核细胞产生;hs-CRP属于急性时相蛋白,是非特异性炎性标志物,主要由肝细胞合成,由IL-6诱导产生,且其在机体炎症初期即可在血液中检测到[9]。IL-6的主要功能是调节机体免疫及代谢过程,其是多种病理过程中的主要递质,同时还可诱导TNF-α产生。LAD、IBS、CVIB均是与左心房结构变化相关的指标,LAD增大提示左心房增大,IBS和CVIB的变化主要与心肌胶原含量及心肌纤维化程度有关,当心肌出现胶原沉积及纤维化时会导致IBS升高及CVIB降低。
临床研究显示,心房颤动是心肌退化和纤维化的结果[5-7],且炎性反应可参与心房颤动的整个发病过程。冠心病的病理基础是冠状动脉粥样硬化,而在动脉粥样硬化斑块中一直存在无菌性炎性反应,可表现为hs-CRP、IL-6、TNF-α等炎性因子异常表达[10-12]。肺部感染以细菌感染多见,肺组织中大量中性粒细胞、单核巨噬细胞浸润可引起局部炎性因子大量释放,从而激活补体系统及免疫过程。心房颤动和肺部感染均可导致炎性因子异常表达,但炎性反应是否对心房颤动并肺部感染患者左心房结构产生影响目前研究报道较少。本研究结果显示,房颤组患者血清hs-CRP、IL-6、TNF-α水平及IBS高于对照组,LAD大于对照组,CVIB低于对照组,提示心房颤动患者存在炎性反应、左心房增大、心肌纤维化等;亚组分析结果显示,肺部感染组患者血清hs-CRP、IL-6、TNF-α水平高于无肺部感染组,两组患者LAD、IBS、CVIB间无差异,提示合并肺部感染的心房颤动患者机体内炎性反应过程可表现为急性反应,但肺部感染对左心房结构无影响,提示长期慢性炎性反应可能对左心房结构产生影响,但急性炎性反应对左心房结构影响轻微;进一步比较LAD>40 mm组与LAD≤40 mm组患者血清炎性因子水平发现,LAD>40 mm组患者血清hs-CRP、IL-6、TNF-α水平高于LAD≤40 mm组,推测炎性反应可能参与持续性心房颤动并肺部感染患者左心房结构改变过程。
综上所述,持续性心房颤动并肺部感染患者血清hs-CRP、IL-6、TNF-α水平升高,左心房增大并伴有心肌纤维化,hs-CRP、IL-6、TNF-α可能参与左心房结构改变过程。
本文无利益冲突。
[1]DE VOS C B,BREITHARDT G,CAMM A J,et al.Progression of atrial fibrillation in the REgistry on Cardiac rhythm disORDers assessing the control of Atrial Fibrillation cohort:clinical correlates and the effect of rhythm-control therapy[J].Am Heart J,2012,163(5):887-893.
[2]TORP-PEDERSEN C,CAMM A J,BUTTERFIELD N N,et al.Vernakalant:conversion of atrial fibrillation in patients with ischemic heart disease[J].Int J Cardiol,2013,166(1):147-151.
[3]GAMST J,CHRISTIANSEN C F,RASMUSSEN B S,et al.Pre-existing atrial fibrillation and risk of arterial thromboembolism and death following pneumonia:a population-based cohort study[J].BMJ Open,2014,4(11):e006486.
[4]ZHU J,ZHANG X,SHI G,et al.Atrial Fibrillation Is an Independent Risk Factor for Hospital-Acquired Pneumonia[J].PLoS One,2015,10(7):e0131782.
[5]GUO Y,LIP G Y H,APOSTOLAKIS S.Inflammation in atrial fibrillation[J].J Am Coll Cardiol,2012,60(22):2263-2270.
[6]DEWLAND T A,VITTINGHOFF E,HARRIS T B,et al.Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation:Results From the Health ABC Study (Health,Aging,and Body Composition)[J].JACC Clin Electrophysiol,2015,1(4):248-255.
[7]RICHTER B,GWECHENBERGER M,SOCAS A,et al.Markers of oxidative stress after ablation of atrial fibrillation are associated with inflammation,delivered radiofrequency energy and early recurrence of atrial fibrillation[J].Clin Res Cardiol,2012,101(3):217-225.
[9]MARROUCHE N F,WILBER D,HINDRICKS G,et al.Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation:the DECAAF study[J].JAMA,2014,311(5):498-506.
[10]INTERLEUKIN-6 RECEPTOR MENDELIAN RANDOMISATION ANALYSIS (IL6R MR)CONSORTIUM,SWERDLOW D I,HOLMES M V,et al.The interleukin-6 receptor as a target for prevention of coronary heart disease:a mendelian randomisation analysis[J].Lancet,2012,379(9822):1214-1224.
[11]赵伟,李婷婷,李莹.冠心病患者炎性因子水平与急性冠状动脉综合征的相关性分析[J].中华老年心脑血管病杂志,2014,16(2):207-208.
[12]TSIMIKAS S,DUFF G W,BERGER P B,et al.Pro-inflammatory interleukin-1 genotypes potentiate the risk of coronary artery disease and cardiovascular events mediated by oxidized phospholipids and lipoprotein (a)[J].J Am Coll Cardiol,2014,63(17):1724-1734.
(本文编辑:谢武英)
Correlations between Serum Levels of hs-CRP,IL-6 and TNF-α and Left Atrium Structure Change of Persistent Atrial Fibrillation Patients Complicated with Pulmonary Infection
TANGJian-qin.TheFirstDepartmentofInternalMedicine,theTraditionalChineseMedicineHospitalofPiCounty,Chengdu,Chengdu611730,China
Objective To analyze the correlations between serum levels of hs-CRP,IL-6 and TNF-α and left atrium structure change of persistent atrial fibrillation patients complicated with pulmonary infection.Methods From June 2014 to June 2015,a total of 150 patients with persistent atrial fibrillation were selected as case group in the First Department of Internal Medicine,the Traditional Chinese Medicine Hospital of Pi County,Chengdu,and they were divided into A1 group(complicated with pulmonary infection,n=54)and A2 group(did not complicate with pulmonary infection,n=96)according to the incidence of pulmonary infection,into B1 group(with LAD over 40 mm)and B2 group(with LAD equal or less than 40 mm)according to the LAD;and a total of 50 people with sinus rhythm who admitted to this hospital for physical examination were selected as control group at the same time.Serum levels of hs-CRP,IL-6 and TNF-α and left atrial structural parameters〔including LAD,integrated backscatter of left atrium posterior wall(IBS)and periodic change value of integrated backscatter(CVIB)〕 were compared between control group and case group,between A1 group and A2 group;meanwhile serum levels of hs-CRP,IL-6 and TNF-α were compared between B1 group and B2 group.Results Serum levels of hs-CRP,IL-6 and TNF-α,and IBS of case group were statistically significantly higher than those of control group,LAD of case group was statistically significantly larger than that of control group,while CVIB of case group was statistically significantly lower than that of control group(P<0.05).Serum levels of hs-CRP,IL-6 and TNF-α of A1 group were statistically significantly higher than those of control group(P<0.05);no statistically significant differences of LAD,IBS or CVIB was found between A1 group and A2 group(P>0.05).Serum levels of hs-CRP,IL-6 and TNF-α of B1 group were statistically significantly higher than those of B2 group(P<0.05).Conclusion Serum levels of hs-CRP,IL-6 and TNF-α of persistent atrial fibrillation patients complicated with pulmonary infection are significantly elevated,existing left atrial enlargement and myocardial fibrosis,hs-CRP,IL-6 and TNF-α may play important roles in the change of left atrium structure.
Atrial fibrillation;Pulmonary infection;Inflammatory factor;Left atrium
611730四川省成都市郫县中医医院内一科
R 541.75
A
10.3969/j.issn.1008-5971.2016.10.005
2016-07-15;
2016-10-13)