小儿病毒性心肌炎的临床诊断与治疗

目的探讨小儿病毒性心肌炎患者的诊断以及治疗,提高患儿的治愈率。方法选取我院2013年9月~2015年9月收治的病毒性心肌炎患儿17例作为研究对象,对所有患儿的临床资料进行回顾性分析,分析诊断情况以及治疗情况,观察疗效。结果所有病毒性心肌炎患儿完成治疗后,在患儿17例中,显效8例,有效8例,无效1例,治疗总有效率为94.12%。结论针对小儿病毒性心肌炎患儿,进行早期诊断,实施对症治疗,能有效促进患儿的康复,显著提高患儿的生活质量。     

儿童病毒性心肌炎与心脏神经症心率变异性比较观察

目的探讨儿童病毒性心肌炎与心脏神经症心率变异性(HRV)变化的临床意义。方法对病毒性心肌炎16例、心脏神经症32例、对照组20例进行心率变异性时域分析。结果与心脏神经症组及对照组比较,病毒性心肌炎组SDNNindex(71.50±22.33ms)、rMSSD(58.06±16.94ms)、PNN50(27.38%±10.07%)明显增高(P<0.01);心脏神经症组与对照组心率变异性比较差异无显著性意义。结论病毒性心肌炎患儿迷走神经张力增高,交感神经张力降低;而心脏神经症患儿未出现与病毒性心肌炎相似的表现。     

外周血微小RNA-216a与小儿病毒性心肌炎的相关性研究

背景病毒性心肌炎主要由柯萨奇病毒B3(CVB3)感染引起,而微小RNA(miRNAs)与CVB3感染密切相关,因此明确miRNAs与小儿病毒性心肌炎的关系可能为临床诊治小儿病毒性心肌炎患儿提供新思路。目的探讨外周血miRNA-216a与小儿病毒性心肌炎的相关性。方法选取2018年1月—2019年1月哈尔滨医科大学附属第四医院收治的疑似病毒性心肌炎患儿38例,其中确诊为病毒性心肌炎患儿30例(观察组),另选取同期体检健康儿童30例作为对照组。比较两组儿童外周血miRNA-216a表达量及血清心肌肌钙蛋白I(c TnI)、肌酸激酶同工酶(CK-MB)水平,外周血miRNA-216a表达量与病毒性心肌炎患儿住院时间、急性生理学及慢性健康状况评分系统Ⅱ(APACHEⅡ)评分及血清cTnI、CK-MB水平间的相关性分析采用Pearson相关分析;绘制受试者工作特征(ROC)曲线以评价外周血miRNA-216a表达量及血清cTnI、CK-MB水平对小儿病毒性心肌炎的诊断价值。结果 (1)观察组患儿外周血miRNA-216a表达量及血清cTnI、CK-MB水平高于对照组(P0.05)。(2)Pearson相关分析结果显示,外周血miRNA-216a表达量与病毒性心肌炎患儿住院时间(r=0.409)、APACHEⅡ评分(r=0.607)及血清cTnI(r=0.491)、CK-MB(r=0.472)水平呈正相关(P0.05)。(3)ROC曲线显示,外周血miRNA-216a表达量诊断小儿病毒性心肌炎的曲线下面积(AUC)为0.662,血清cTnI水平为0.705,血清CK-MB水平为0.678。结论外周血miRNA-216a表达量与小儿病毒性心肌炎及其病情严重程度、心肌损伤程度有关,且其对小儿病毒性心肌炎的诊断价值与血清cTnI、CK-MB水平相似。     

小儿病毒性心肌炎的护理方法分析与研究

目的分析小儿病毒性心肌炎的护理方法。方法选择2015年5月~2016年2月小儿病毒性心肌炎患儿60例并随机分组。常规组进行常规护理,优质组则进行优质护理。比较两组病毒性心肌炎缓解率;住院时间、家长满意度评价、护理质量评分。结果优质组病毒性心肌炎缓解率高于常规组(P0.05);优质组住院时间、家长满意度评价、护理质量评分优于常规组(P0.05)。结论小儿病毒性心肌炎进行优质护理可有效缓解患儿不良情绪,提升护理服务质量,提升家长满意度,缩短住院时间,值得推广。     

护理干预对小儿重症病毒性脑炎合并心肌炎的效果观察

目的分析护理干预对小儿重症病毒性脑炎合并心肌炎的效果。方法选取2013年1月~2014年2月我院收治的重症病毒性脑炎合并心肌炎患儿80例,随机分为观察组和对照组,对照组采用常规护理,观察组采用护理干预,比较两组患儿护理后临床症状恢复时间。结果观察组重症病毒性脑炎合并心肌炎患儿护理后临床症状恢复时间优于对照组患儿,差异有统计学意义(P0.05)。结论护理干预对小儿重症病毒性脑炎合并心肌炎具有良好的护理效果。     

小儿病毒性心肌炎的观察与护理

目的观察小儿病毒性心肌炎的护理措施及效果。方法选择2013年5月~2015年5月我院收治的小儿病毒性心肌炎患儿60例作为研究对象,将其随机分成对照组与实验组,各30例,对照组采用一般护理,实验组采用系统性护理,观察两组护理效果。结果实验组患儿治疗依从性为93.33%,明显高于对照组患儿的70.00%,且两组护理满意评分及心电图恢复时间比较,差异均有统计学意义(P0.05)。结论针对病毒性心肌炎患儿采用系统性护理的护理效果明显,能缓解患儿临床症状,提高患儿的治疗依从性及家属的满意度。     

小儿病毒性心肌炎护理体会

目的探讨36例小儿病毒性心肌炎的护理体会。方法选取2013年6月~2014年6月我院收治的患有病毒性心肌炎的患儿36例作为研究对象,给予患儿综合性护理,观察患儿的效果。结果经过综合护理后,显效26例,总有效率为97.22%。结论小儿病毒性心肌炎经过综合护理后,效果显著改善,值得广泛应用。     

丙种球蛋白治疗小儿病毒性心肌炎疗效观察

病毒性心肌炎是儿科常见病 ,且病死率和致残率相对较高 ,严重威胁患儿身心健康。目前 ,对病毒性心肌炎的治疗尚缺乏有效而特异的药物。 1 992年国外动物实验证实 ,人血静脉用丙种球蛋白 ( IVIG)对病毒性心肌炎有治疗作用[1] ,1 998年国内动物实验也证实了丙种球蛋白对病毒性心肌炎心肌细胞有保护及治疗作用[2 ] ,然而临床将丙种球蛋白用于治疗病毒性心肌炎的报道较少。我们试用 IVIG治疗病毒性心肌炎患儿 36例 ,并进行了观察。现报告如下。1　资料与方法1 .1　临床资料　将 2 0 0 0年 3月至 2 0 0 2年 2月收治的临床诊断为病毒性心肌炎…     

17例小儿重症病毒性心肌炎随访观察

目的观察重症病毒性心肌炎患儿的预后。方法对17例重症病毒性心肌炎患儿进行3个月至7年的随访。结果17例患儿痊愈9例,恢复迁延4例,死亡2例,转变为扩张型心肌病2例。结论小儿重症病毒性心肌炎给予及时有效治疗预后较好。影响预后的因素是多方面的,早期应用激素可改变预后。     

大剂量高浓度维生素C治疗病毒性心肌炎疗效观察

大剂量高浓度维生素Ｃ治疗病毒性心肌炎疗效观察山东省千佛山医院（２５００１４）姚慧徐海燕我们采用大剂量高浓度维生素Ｃ治疗病毒性心肌炎，取得了满意疗效。临床资料：本组１８例患儿按九省市小儿病毒性心肌炎会议制定的标准诊断，其中心肌炎急性期１６例，疑似病毒性...     

Increased severity of viral myocarditis in mice lacking lymphocyte maturation

The role of lymphocytes in the pathogenesis of viral myocarditis is controversial. To better understand how lymphocyte maturation controls a virus-induced myocarditic process, a murine model of viral myocarditis was utilized. Encephalomyocarditis virus (EMCV) was inoculated intraperitoneally into three kinds of mice; virus-susceptible C57BL/6, virus-resistant 129/SV and recombination activity gene (RAG)-2 knockout 129/SV mice. The RAG2 participate in the maturity of T and B lymphocytes. Survival rate, heart weight (HW), HW to body weight (BW) ratio, viral genome, cardiac inflammation and myocardial necrosis were evaluated after EMCV (500 plaque forming unit/mouse) inoculation. On post-inoculation day 10, the survival rate of C57BL/6, 129/SV and RAG2 knockout mice were 42, 90 and 0%, respectively. Myocardial viral titer was significantly (P<0.05) higher in C57BL/6 and RAG2 knockout mice than in 129/SV mice. In situ hybridization demonstrated the EMCV genome in the myocardium of RAG2 knockout and C57BL/6 mice, but not in 129/SV mice. At day 8, HW and HW/BW ratios were elevated (P<0.05) in RAG2 knockout mice as well as C57BL/6 mice compared with 129/SV mice. Myocardial necroses were more severe in RAG2 knockout mice than in wild-type 129/SV mice. In conclusion, matured lymphocytes protect the development of viral myocarditis which includes viral replication and myocardial apoptosis.     

过敏性紫癜急性期患儿淋巴细胞凋亡特征的研究

为探讨过敏性紫癜(HSP)患儿急性期外周血淋巴细胞凋亡特征及其与T淋巴细胞免疫应答活性的相关性，选择HSP患儿及健康儿童各33例(HSP组及对照组)，分别应用形态法、间接免疫荧光法检测外周血淋巴细胞凋亡率、T淋巴细胞亚群及CD^ 23细胞百分率。结果HSP组急性期外周血淋巴细胞培养前及培养、48小时凋亡率均显著高于对照组(P均＜O．01)，外周血CD^ 4细胞百分率及CD^ 4／CD^ 4均明显低于对照组(P＜O.01，P＜0．05)；培养48小时CD^ 25细胞百分率显著低于对照组(P＜O．01)；培养48小时淋巴细胞凋亡率与CD^ 25细胞百分率呈负相关(P＜0．05)。认为HSP患儿外周血淋巴细胞凋亡过度，此与其T淋巴细胞免疫应答活性低下关系密切。     

中药芪芍五味合剂对病毒性心肌炎小鼠心肌细胞凋亡和坏死的影响

取 2 4 0只 4周龄 Balb/ c雄性小鼠 ,随机等分为 6组 (每组 4 0只 ) ,即 :正常对照组 (A组 )、中药对照组 (B组 )、病毒对照组 (C组 )、中药治疗组 (D组 )、维生素 C治疗组 (E组 )、病毒唑治疗组 (F组 )。 A、B两组每只小鼠均腹腔接种 0 .1ml不含病毒的 Eagle's液 ,C～F组每只小鼠服腔接种 0 .1ml10 7.5TCID/ ml的柯萨奇 B3(CVB3)病毒液。根据分组分别给予不同的药物治疗。结果 :病毒性心肌炎时心肌细胞的凋亡率和坏死率均显著增加。心肌细胞凋亡高峰在CVB感染后 7～ 10天 ,而心肌坏死高峰出现在 CVB3感染后 14天 ,并且与组织形态学观察一致。应用中药黄芪、赤芍治疗后 ,心肌细胞凋亡率和坏死率均显著降低 (P <0 .0 5 ) ,维生素 C和病毒唑均可降低心肌细胞坏死率 ,但对心肌细胞凋亡影响不大。 CVB感染 3～ 7天内 ,各感染组心肌细胞凋亡率和坏死率均与心肌内病毒滴度呈正相关 (r =0 .76、P <0 .0 1,r=0 .5 4、 P <0 .0 5 ) ;而感染 10～ 30天 ,凋亡率及坏死率与病毒含量无相关性。各感染组心肌细胞凋亡率与坏死率均与心肌病理积分呈正相关 (r=0 .5 5、P <0 .0 5 ,r=0 .76、P<0 .0 1)。中药黄芪、赤芍、五味子可明显减轻病毒性心肌炎小鼠的病理损害程度 ,显著降低病毒性心肌炎心肌细胞凋亡率和坏死率 ,对     

病毒性心肌炎与扩张型心肌病心肌线粒体DNA缺失的定量分析

目的对比研究病毒性心肌炎(VMC)与扩张型心肌病(DCM)患者活检心肌组织线粒体DNA(mtDNA)缺失突变情况及其与外周淋巴细胞mtDNA缺失程度的相关性.方法用定量PCR法检测20例VMC患者、12例DCM患者心肌细胞及其外周血淋巴细胞mtDNA4977碱基对(mtDNA4977)和mtDNA7436碱基对(mtDNA)缺失率.取12例健康意外死亡者心肌和23例献血员外周血淋巴细胞作正常对照.结果正常对照者、VMC和DCM患者心肌细胞均存在mtDNA4977及mtDNA7436缺失,合计缺失率分别为0.175%、0.385%和3.004%;外周淋巴细胞mtDNA缺失程度与心肌细胞呈一致性改变,且有良好的相关性(r=0.960,P＜0.001).结论mtDNA缺失可能是VMC发病及其向DCM演变的一个重要心肌损伤机制;外周淋巴细胞在研究心肌细胞mtDNA缺失中的作用值得进一步探讨.     

Enteroviral and Immune Mediated Myocarditis in SCID mice

Severe combined immune deficiency (SCID) mice have been used as an animal model to study both the direct cytopathic effect of enteroviruses on the heart in the absence of an effective immune system and to investigate the role of immune mediated processes in the pathogenesis of human myocarditis. The infection of SCID mice with coxsackievirus B3 resulted in severe myocarditis with very high titers of the virus in the myocardium and severe necrosis of myocytes. This direct cytopathic effect caused an impairment of the myocardial function and resulted in a high mortality rate of the infected animals. For the study of the immune mechanisms in human myocarditis, peripheral blood leukocytes of patients with myocarditis, having an impaired left ventricular function without viral persistence in the myocardium, were transferred into SCID mice. As controls peripheral blood leukocytes of normal donors were used. At 60 days after transfer, human immunoglobulines could be demonstrated in the peripheral blood of the SCID mice, however, human autoantibodies against the adenine nucleotide translocator, a myocardial autoantigen, were only present in the animals receiving peripheral blood leukocytes from patients with myocarditis. Cellular infiltrates of human leukocytes in the myocardium and an impaired left ventricular function were also only observed in animals reconstituted with peripheral blood leukocytes from patients. These effects were T cell dependent as shown by differential transfer. These results are of interest for the treatment of human myocarditis, suggesting the avoidance of an immunosuppressive therapy in acute or chronic myocarditis with viral persistence to prevent a direct cytopathic effect in the absence of an effective immune system. However, in the setting of a chronic, (auto-)immunological myocarditis with the proven absence of entero- or adenoviral sequences an immunomodulatory therapy seems to be effective and safe.     

Cellular and molecular bases for the immunopathology of the myocardial cell damage involved in acute viral myocarditis with special reference to dilated cardiomyopathy.

Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of the myocardial cell damage involved in viral myocarditis. To investigate the cellular and molecular bases of both target cells and effector cells for cell-mediated cytotoxicity involved in viral myocarditis and dilated cardiomyopathy, we first examined the expression of major histocompatibility complex (MHC) antigens and a cell adhesion molecule, intercellular adhesion molecule-1 (ICAM-1) in myocardial cells of a murine model of viral myocarditis and in patients with acute myocarditis and dilated cardiomyopathy. Secondly, we analyzed the characteristics of the infiltrating cells in the heart, especially the expression of a cytolytic factor, perforin. We found that Coxsackievirus B3 (CVB3)-induced murine acute myocarditis resulted in enhanced expression of MHC (class I) antigens and ICAM-1 on myocardial cells, and that perforin was abundantly expressed in NK (natural killer)-like large granular lymphocytes (LGL), which represent the main infiltrating cell type in the early stage. Immunoelectron microscopic study showed killer cells directly damaging cardiac myocytes by the release of perforin. Perforin was also expressed in the infiltrating cells in the heart of a patient with acute myocarditis. Both MHC antigens and ICAM-1 were clearly expressed in the hearts of patients with acute myocarditis and dilated cardiomyopathy. These data provided direct evidence that cell-mediated cytotoxicity plays a critical role in the myocardial cell damage involved in viral myocarditis.     

实验性病毒性心肌炎病程中穿孔素表达水平的变化及其与心肌损害的关系

目的探讨病毒性心肌炎（ＶＭＣ）发病过程中，心肌炎症细胞中穿孔素（ＰＦＰ）表达水平的动态变化及其与心肌病变的关系。方法采用半定量ＲＴ－ＰＣＲ及免疫组化方法，检测小鼠ＶＭＣ各时期心肌炎症细胞的ＰＦＰｍＲＮＡ及其抗原表达水平，并检查心肌病理变化及半定量分析其程度，统计学分析ＰＦＰ表达水平的动态变化与心肌病变程度的演变的相关性。结果（１）感染后０～１０天，ＰＦＰｍＲＮＡ及抗原的表达水平逐渐升高，心肌病变以炎症细胞浸润及心肌坏死为主并逐渐加重，１０～１５天ＰＦＰ表达水平最高，上述心肌病变也最严重，２０天以后ＰＦＰ逐渐下降，心肌炎症细胞浸润及坏死逐渐减轻，代之以成纤维细胞增生、胶原纤维沉积及心肌纤维化等；（２）在小鼠心肌炎发病过程中，ＰＦＰ抗原表达水平的变化与心肌病变积分的变化呈显著正相关（ｒ＝０．９５，Ｐ＜０．０５）。结论ＰＦＰ介导的细胞毒作用可能是ＶＭＣ中心肌损害的主要机制之一。     

Role of Fas/FasL pathway in the activation of infiltrating cells in murine acute myocarditis caused by Coxsackievirus B3

OBJECTIVES: This study was designed to investigate the roles of Fas/FasL pathway in myocardial damage in murine acute myocarditis caused by Coxsackie virus B3 (CVB3). BACKGROUND: Cardiac myocyte apoptosis rarely occurs in murine acute myocarditis caused by CVB3. Fas/FasL belong to the tumor necrosis factor receptor/ligand superfamily of costimulatory molecules and are known to play a critical role in the induction of apoptosis, as well as in the cytotoxicty mediated by T-cells and natural killer cells. METHODS: We first analyzed the expression of Fas on cardiac myocytes in vivo and in vitro. Second, we examined the development of myocardial damage, in C3H/He mice treated with an anti-FasL monoclonal antibody (mAb), and in C3H/He-lpr/lpr mice and C3H/He-gld/gld mice infected with CVB3. Third, to investigate the effects of anti-FasL mAb treatment on the activation of the infiltrating cells, we examined the expression of interferon (IFN)-gamma and interleukin (IL)-2 as activation markers in the heart of mice by semiquantitative polymerase chain reaction. RESULTS: Fas was markedly induced on cardiac myocytes with acute myocarditis. Myocardial inflammation was decreased in mice treated with anti-Fas L mAb, C3H/He-lpr/lpr mice and C3H/He-gld/gld mice. Anti-FasL mAb-treatment also decreased the expression of IFN-gamma, IL-2, inducible nitric oxide synthase and CVB3 genomes in myocardial tissue. CONCLUSIONS: Our findings strongly suggested that the Fas/FasL pathway played a critical role in the development of massive myocardial necrosis through activation of infiltrating cells, and raise the possibility of immunotherapy by blocking the Fas/FasL pathway to prevent myocardial damage and improve the prognosis of patients with viral myocarditis.     

病毒性心肌炎患者心肌细胞线粒体DNA缺失的定量分析

为探讨病毒性心肌炎 (VMC)患者心肌细胞线粒体 DNA(mt NDA)缺失突变情况及意义 ,用定量 PCR法检测 2 0例 VMC患者心肌细胞及其外周血淋巴细胞 mt DNA4 977碱基对 (mt DNA4 977)和 mt DNA74 36 碱基对 (mt D-NA74 36 )缺失率。取 10例健康意外死亡者心肌和 2 0例献血员外周血淋巴细胞作正常对照。结果显示 ,正常对照者和 VMC患者心肌细胞均存在 m t DNA4 977及 mt DNA74 36缺失 ,合计缺失率分别为 0 .176 %、0 .384 % ,二者差异显著 ,P<0 .0 5 ;VMC患者外周淋巴细胞 mt DNA缺失程度与心肌细胞呈一致性改变 ,且有良好的相关性 (r=0 .92 0 ,P<0 .0 0 1)。提示 mt DNA缺失可能是 VMC发病过程中重要的心肌损伤机制 ;外周淋巴细胞在研究心肌细胞 mt DNA缺失中的作用值得进一步探讨     

鼠巨细胞病毒感染BALB/c小鼠心肌炎模型的建立

目的:建立鼠巨细胞病毒(MCMV)感染心肌炎动物模型。方法:用巨细胞病毒经腹腔注射感染BALB/c小鼠。结果:MCMV感染小鼠心肌炎发病率为69.4%,死亡高峰在感染后7～14d,死亡率为11.11%;44.5%的感染鼠出现心外膜炎。MCMV感染的第7天,心肌细胞出现肿胀、变性,血管周围有大量炎症细胞灶性浸润;第14天,可见单个心肌细胞核固缩、溶解,心肌细胞小灶性坏死、崩解,周围见单核细胞、淋巴细胞浸润;病变于感染后7～14d达高峰,第14天后开始减轻。MCMV感染小鼠全部心肌病变积分均≤2分,属轻度心肌炎改变;心电图的改变率达50%。结论:该心肌炎动物模型为探讨病毒性心肌炎的发病机制、转归及抗病毒药物的筛选提供了有力的工具。