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1.
目的探讨病毒性心肌炎(VM)患儿急性期血清颗粒酶B(GrB)和可溶性FasL(sFasL)水平变化及其与心脏超声和心脏收缩功能的关系。方法采用ELISA方法检测60例VM和40例健康儿童血清GrB和sFasL水平,同时对VM患儿行心脏超声及心功能检查。测定心脏指数(CI)、射血分数(EF)、心轴缩短率(SF)、每搏指数(SI)、左室内径(LV)、左房内径(LA)、右室内径(RV)。结果VM组GrB和sFasL水平显著高于对照组(P均<0.01);VM患儿血清GrB与sFasL水平呈正相关(r=0.7608 P<0.05);VM组GrB和sFasL升高者,心脏超声检查示心脏扩大、心肌动度减弱和心功能下降发生率明显增加(P均<0.05)。结论血清GrB和sFasL可作为判断VM患儿心肌损害程度及评估心功能的辅助指标。  相似文献   

2.
目的 回顾性分析心肌炎患儿的首发临床症状、实验室检查等临床资料,探讨暴发性心肌炎的早期危险因素,为临床诊治提供指导.方法 收集23例临床诊断为暴发性心肌炎患儿的临床资料,并收集同期于本院诊断为普通心肌炎的30例患儿的临床资料,对两组患儿入院时首发临床症状、心电图、心脏超声及血清生化检查等各项指标进行回顾性分析,并进行多因素Logistic回归分析,筛选暴发性心肌炎的独立危险因素.结果 53例患儿中,死亡8例,均为暴发性心肌炎患儿;暴发性心肌炎组与普通心肌炎组首发临床症状差异有统计学意义(P<0.05);暴发性心肌炎组心脏超声收缩功能、左室射血分数、室壁运动障碍显著低于普通心肌炎组(P<0.05);暴发性心肌炎组 NT-proBNP、cTnⅠ、CK-MB显著高于普通心肌炎组(P<0.05);左室射血分数降低(OR=0.878,95%CI 0.797-0.967,P<0.05)、NT-proBNP升高(OR=1.120,95%CI 1.000-1.254,P<0.05)是暴发性心肌炎的独立危险因素.结论 暴发性心肌炎的临床表现多以心外症状起病,左室射血分数降低、NT-proBNP升高是暴发性心肌炎的独立危险因素.  相似文献   

3.
小儿扩张型心肌病与病毒性心肌炎的鉴别诊断   总被引:1,自引:0,他引:1  
对46例扩张型心肌病和112例病毒性心肌炎患儿的病程、症状、体征、心电图、心腔大小、心功能、心室收缩协调性、血抗CoxBIgM、抗心肌线粒体抗体、心肌酶进行了比较,发现上述指标对两种疾病的鉴别均无特异性。临床实践中必须综合上述指标,才能对扩张型心肌病和病毒性心肌炎进行正确的鉴别。上述指标中,病程长、病情重、心脏大、心功能差、心室收缩协调性差有助于扩张型心肌病的诊断;病程短、早搏、房室传导阻滞、抗CoxBIgM阳性、抗心肌抗体阳性、心肌酶增高,有助于病毒性心肌炎的诊断。  相似文献   

4.
目的 调查儿童暴发性心肌炎的临床特点及预后的影响因素,为临床诊治及预后评估提供参考。方法 回顾性分析24例暴发性心肌炎患儿的临床资料。根据患儿预后分为存活组(n=12)和死亡组(n=12)。应用logistic回归分析筛选出影响暴发性心肌炎患儿预后的危险因素。结果 24例暴发性心肌炎患儿中,入院首发症状为消化系统症状者14例,神经系统症状12例,呼吸系统症状1例,循环系统症状2例。入院时血清肌酸激酶MB同工酶、肌钙蛋白I、脑钠肽水平均升高;左室射血分数减低22例(92%);心胸比值增大10例;Ⅲ度房室传导阻滞8例,ST段改变11例,室性心律2例。死亡组患儿左室射血分数低于存活组(PPOR=7.418,P结论 儿童暴发性心肌炎临床特点缺乏特异性。左室射血分数减低是暴发性心肌炎患儿预后不良的危险因素。  相似文献   

5.
目的探讨病毒性心肌炎(VM)患儿TNFα的变化及维生素E、C的干预作用。方法将31例VM患儿随机分为A组16例,予抗感染、营养心肌药物及对症治疗;B组15例,在A组治疗基础上加用维生素E胶囊50mg/d口服,维生素C注射液100mg/(kg·d)静脉点滴,疗程均为1个月,采用ELISA双抗体夹心法测定VM患儿及健康儿童外周血清TNFα含量,采用美国贝克曼公司生产的CX7型全自动化分析仪测定31例VM心肌酶。结果VM组TNFα水平显著高于健康儿童(P<0.01),VM组TNFα升高者其各项心肌酶异常百分数均显著增高(P均<0.05);B组TNFα水平较A组显著下降(P<0.05)。结论TNFα参与VM发生发展的病理生理过程,检测血清TNFα水平有助于VM的诊断、病情判断和预后,维生素E、C可降低VM患儿血清TNFα的水平。  相似文献   

6.
目的:探讨血清超氧化物歧化酶(SOD)活力与抗心磷脂抗体(ACA)在小儿病毒性心肌炎(VM)的关系。方法:SOD活力检测应用化学比色法,ACA测定采用ELISA法,62例VM儿治疗前后均同时测定SOD活力和ACA,并与40名健康儿童进行对照。结果:VM儿治疗前血清SOD活力显著降低,ACA阳性率明显增高,ACA阳性的血清SOD活力显著低于ACA阴性者(P均<0.05);治疗后血清SOD活力增高,ACA阳性率下降,与治疗前相比均有显著意义(P均<0.05)。结论:血清SOD活力和ACA均参与了小儿VM的发病过程,两者呈负相关。  相似文献   

7.
γ干扰素、肿瘤坏死因子α在病毒性心肌炎时变化及意义   总被引:5,自引:0,他引:5  
目的 探讨γ干扰素(IFN-γ)、肿瘤坏死因子α(TNF-α)在病毒性心肌炎(VM)发病中的作用。方法 通过检测VM患儿外周血IFN-γ、TNF-α丙二醛(MDA)、超氧化物歧化酶(SOD)、心肌酶的含量,分析IFN-γ、 TNF-α与MDA、SOD、心肌酶的关系。结果 VM组患儿IFN-γ、TNF-α含量均显著高于健康儿童(P<0.01); IFN-γ、TNF-α升高者的血清SOD活力低于IFN-γ、TNF-α正常者,MDA含量高于IFN-γ、TNF-α正常者(P <0.01);IFN-γ、TNF-α升高者各项心肌酶异常百分数均增高(P<0.05);IFN-γ、TNF-α与SOD、MDA及CK-MB 密切相关(P<0.001)。结论 IFN-γ、TNF-α参与VM的发病;检测VM患儿IFN-γ、TNF-α的含量有助于VM的诊 断、判断病情和预后。  相似文献   

8.
小儿暴发性心肌炎危险因素分析   总被引:6,自引:0,他引:6       下载免费PDF全文
目的:通过对小儿病毒性心肌炎临床表现、体征以及实验室检查指标等方面进行回顾性分析研究,以探讨小儿暴发性心肌炎的危险因素。方法:收集临床诊断为病毒性心肌炎患儿资料71例,分为暴发性心肌炎组(n=16)和非暴发性心肌炎组(n=55),采用χ2检验或t检验对两组患儿入院时的临床表现、心电图、心脏B超与血清生化检查等各项指标进行回顾性分析,对有统计学意义的相关因素,进行logistic多元回归分析,研究暴发性心肌炎的独立高危因素。结果:暴发性心肌炎组死亡率远高于非暴发性心肌炎组(50% vs 0%)。急性病毒性心肌炎患儿入院时血压降低、血清CK-MB水平升高、cTnI阳性、心电图QRS波时限延长、ST段改变、完全性房室传导阻滞、完全性左束支传导阻滞,以及左室射血分数和左室短轴缩短率降低与心肌炎暴发阶段密切相关。QRS波群时限延长(OR=1.139;CI=1.014~1.279; P<0.05)和左心室射血分数降低(OR=0.711;CI=0.533~0.949;P<0.05)是小儿暴发性心肌炎的独立阳性预测因素。结论:暴发性心肌炎死亡率高。入院时QRS波群时限延长和左心室射血分数降低是小儿暴发性心肌炎的独立危险因素。[中国当代儿科杂志,2009,11(8):627-630]  相似文献   

9.
目的 观察儿童少年期原发性高血压左室结构及心功能的变化,对高血压患儿靶器官异常进行评估.方法 应用超声心动图对47例儿童少年期原发性高血压患儿和62名健康体查者进行检查,测量其心脏结构和功能改变.结果 高血压组舒张末期室间隔厚度(IVST.D)、舒张末期左室后壁厚度(LVPWT.D)、舒张末期左室内径(LVED.D)、收缩末期左室内径(LVES.D)、左室质量(LVM)、左室质量指数(LVMI)较正常组显著增高(P均<0.01),射血分数(EF)、左室短轴缩短率(FS)较正常组降低(P<0.05).舒张早期充盈峰速度(E峰)较正常组下降,但差异无统计学意义(P>0.05),舒张晚期充盈峰速度(A峰)上升(P<0.05),E/A显著下降(P<0.01).11 例患儿存在左室肥厚(LVH),出现心脏构型改变.结论 在儿童少年期原发性高血压病中,作为病变累及的靶器官心脏存在结构和功能的异常改变.  相似文献   

10.
对152例心肌炎患儿行24小时Holter监测,并与常规心电图、心肌酶及心功能进行对比性探讨。结果提示:Holter心律失常检出率82.9%明显高于心电图51.3%;24小时早搏总数多于14400次者,心脏指数(CI)及射血分数(EF)均受影响;CK-MB增高者发生室速或室上速的机会多;Holter对捕捉一过性及复杂性心律失常有重要作用。对较严重潜在威胁生命的心律失常有提示预后及预防猝死的价值。  相似文献   

11.
目的:近年研究发现硫化氢(H2S)在血管活性调节、炎症反应、细胞增殖凋亡、缺血再灌注、氧化应激等方面起重要作用,而在心肌炎发病机制中也存在这些基本的病理生理过程,因此本研究检测胱硫醚-γ-裂解酶(CSE)/H2S通路在小鼠病毒性心肌炎中的表达。方法:6周龄近交系雄性Balb/c小鼠随机分为对照组 (n=25)和病毒性心肌炎组 (n=30),分别给予PBS和10-5.69TCID50/mL CVB3 0.1 mL注射,第4和10天各随机取10只小鼠处死并取血和心脏标本,检测血清H2S和心肌H2S生成活性,心肌常规苏木素 伊红染色,免疫组化检测CSE蛋白表达。结果:在急性病毒性心肌炎小鼠模型中,血清H2S及心肌H2S生成活性较对照组升高(P<0.05),心肌CSE蛋白表达亦增加(P<0.05)。结论:在急性小鼠CVB3心肌炎中CSE和其下游产物H2S水平上调,CSE/ H2S通路表达上调可能通过多个环节参与疾病的发病。[中国当代儿科杂志,2010,12(9):744-748]  相似文献   

12.
This study was conducted to assess the use of the serum cardiac troponin T (cTnT) level as a noninvasive indicator to differentiate acute myocarditis and chronic dilated cardiomyopathy in pediatric patients. Myocarditis and dilated cardiomyopathy are clinically difficult to differentiate. Endomyocardial biopsy proved to be quite useful. However, the nature of the procedure--invasiveness, time-consuming, and limited sensitivity--caused some concerns, especially in pediatric patients. Hence, we attempted to find an alternative method that could give a prompt diagnosis of acute myocarditis. Twenty cases with clinically suspected myocarditis or dilated cardiomyopathy and a control group of 21 cases with moderate left-to-right shunt and congestive heart failure were recruited. History, physical examination, electrocardiogram, chest roentgenogram, echocardiogram, cTnT, creatine kinase MB isoenzyme (CK-MB mass), and/or endomyocardial biopsy were compared. The gold standard used to diagnose myocarditis is endomyocardial biopsy (Dallas criteria) and/or recovery from cardiovascular problems within 6 months of follow-up. Ten patients were diagnosed as having myocarditis (group 1) and 10 with chronic dilated cardiomyopathy (group 2). The control group of 21 cases was designated as group 3. The median serum cTnT levels were 0.088 (0.04-3.11), 0.010 (0.010-0.990), and 0.010 (0.010-0.550) ng/ml in groups 1, 2, and 3, respectively. The mean CK-MB mass level for groups, 1, 2, and 3 were 18.35 (7.14-70.00), 4.80 (0.54-108.00), and 2.26 (0.95-7.06) ng/ml. The study showed that both the cTnT and CK-MB mass levels were significantly higher in group 1 than either group 2 or group 3. Histopathology was studied in 9 cases. In 2 of 5 cases and in all 4 cases in group 1 and group 2 histopathology was pathologically proved. Levels of cTnT and CK-MB were significantly higher for myocarditis than for dilated cardiomyopathy and left-to-right shunt with CHF. Further study is needed to assess the optimum cTnT level for differentiating both conditions.  相似文献   

13.
Enterovirus infections in neonates are difficult to diagnose. Diphasic pattern and possibly fatal myocarditis must be anticipated. CASE REPORT: A 14-day-old girl had presented a heart failure after an initial episode of gastroenteritis and supraventricular tachycardia. Investigation demonstrated global myocardial dysfunction. Diagnosis of neonatal enterovirus myocarditis was made by polymerase chain reaction detection of viral genome. Heart failure was controlled with medical treatment. CONCLUSION: Enterovirus myocarditis is typically a biphasic illness. Rapid diagnosis of enteroviral infection in neonatal period may be made by polymerase chain reaction detection of viral genome. There is anecdoctal evidence that immunoglobulin infusions may improve outcome.  相似文献   

14.
病毒性心肌炎患儿微小病毒B19感染的研究   总被引:1,自引:1,他引:1  
目的探讨病毒性心肌炎患儿微小病毒B19(HPV B19)感染的状况及其相关性。方法应用巢式聚合酶链反应法对60例病毒性心肌炎患儿(观察组)及30例健康体检儿童(对照组)血浆中微小病毒B19-DNA进行检测,并对观察组中HPV B19-DNA检测阳性与阴性两组中血CK、CK-MB及心功能指标进行比较。结果观察组B19-DNA检测阳性率为26.7%(16/60例),对照组B19-DNA检测均为阴性,两组比较差异有显著性(P〈0.01)。观察组中HPV B19-DNA检测阳性与阴性的两组中血CK、CK—MB值差异无显著性(P〉0.05)。心功能指标LVSF比较差异有显著性(P〈0.01),SV比较差异亦有显著性(P〈0.05)。结论小儿病毒性心肌炎与HPV B19感染有关,HPV B19可能是小儿病毒性心肌炎主要病原之一;HPV B19感染所致小儿病毒性心肌炎的心功能改变中左室功能受累程度较重。  相似文献   

15.
目的探讨心肌肌钙蛋白Ⅰ(cTnI)、肌酸激酶同工酶(CK-MB)和高敏C反应蛋白(hs-CRP)联合检测对病毒性心肌炎(VMC)的诊断价值。方法将114例患儿分为病毒性心肌炎组、疑似心肌炎组及非心肌炎组,所有患儿入院次日晨空腹采静脉血,分别测定cTnI、CK-MB和hs-CRP三个指标。结果病毒性心肌炎组的cTnI和CK-MB阳性率及hs-CRP的测定值均显著高于非心肌炎组(P<0.01);病毒性心肌炎组cTnI和CK-MB阳性率与疑似心肌炎组比较差异无统计学意义(P>0.05);病毒性心肌炎组与疑似心肌炎组及非心肌炎组hs-CRP测定值比较差异有统计学意义(P<0.01)。单个指标cTnI、CK-MB和hs-CRP诊断VMC的灵敏度依次为cTnI(81.4%)>CK-MB(71.2%)>hs-CRP(62.7%),特异度为hs-CRP(81.8%)>cTnI(50.9%)>CK-MB(43.6%)。三项指标联合检测对VMC诊断的特异度(85.5%)分别高于应用cTnI、CK-MB和hs-CRP单一指标。结论联合应用cTnI、CK-MB和hs-CRP进行检测,能更准确诊断VMC,为建立一种联合检测以提高对VMC的诊断提供理论依据。  相似文献   

16.
目的探讨心肌炎患儿免疫功能的改变。方法应用单克隆抗体夹心酶联免疫吸附试验(ELISA)法对30例病毒性心肌炎急性期患儿可溶性白细胞介素2受体(sIL-2R)进行检测,并与22例健康儿童对照进行比较。结果病毒性心肌炎患儿血清sIL-2R水平明显升高,为632.56±293.45U/ml,在急性期病人中,病程小于1个月者与病程2~6个月者血清sIL-2R无显著性差异。当病毒感染时,机体免疫功能处于紊乱状态,随着病程的延长,病情的迁延不愈,血清sIL-2R一直处于高水平状态。sIL-2R升高可使白细胞介素2(IL-2)产生受体抑制,从而进一步加重机体的免疫功能紊乱。结论动态观察血清sIL-2R水平对判定病情变化和预后有意义,亦可评估机体的免疫状态。  相似文献   

17.
Background: Epidemics of enterovirus 71 infection have caused the death of many children throughout the world. Rhombencephalitis, brain stem encephalitis, and heart failure were present in all of the fatal cases. However, no evidence of myocarditis was noted in the heart specimens, and the mechanism of heart failure remains unknown. Aims: To characterise the presentation of cardiac complications in children with enterovirus rhombencephalitis and discuss its pathogenesis. Methods: Ninety one consecutive patients with enterovirus rhombencephalitis underwent echocardiography. Of these, 17 patients (nine male, eight female; median age 14 months, range 4–57 months) with left ventricular dysfunction were studied. Results: Tachycardia was noted in all patients and systemic hypertension in 12. Muscle-brain fraction of creatine kinase was >5% in 14 patients. Plasma norepinephrine and epinephrine levels were significantly raised in the three patients in whom these were analysed. Electrocardiographic abnormalities were noted in eight patients. Pulmonary oedema was complicated in 15 patients. The initial ejection fraction of the left ventricle was 22–58% (mean 37%, SD 11%). All patients deteriorated to hypotensive shock within 12 hours and 13 died. Heart specimens from seven patients showed no evidence of myocarditis, but significant coagulative myocytolysis, myofibrillar degeneration, and cardiomyocyte apoptosis were observed. Conclusions: Acute heart failure was noted in 19% of patients with enterovirus rhombencephalitis, which had a fatality rate of 77%. It was not caused by myocarditis but possibly by neurogenic cardiac damage.  相似文献   

18.
BACKGROUND: Epidemics of enterovirus 71 infection have caused the death of many children throughout the world. Rhombencephalitis, brain stem encephalitis, and heart failure were present in all of the fatal cases. However, no evidence of myocarditis was noted in the heart specimens, and the mechanism of heart failure remains unknown. AIMS: To characterise the presentation of cardiac complications in children with enterovirus rhombencephalitis and discuss its pathogenesis. METHODS: Ninety one consecutive patients with enterovirus rhombencephalitis underwent echocardiography. Of these, 17 patients (nine male, eight female; median age 14 months, range 4-57 months) with left ventricular dysfunction were studied. RESULTS: Tachycardia was noted in all patients and systemic hypertension in 12. Muscle-brain fraction of creatine kinase was >5% in 14 patients. Plasma norepinephrine and epinephrine levels were significantly raised in the three patients in whom these were analysed. Electrocardiographic abnormalities were noted in eight patients. Pulmonary oedema was complicated in 15 patients. The initial ejection fraction of the left ventricle was 22-58% (mean 37%, SD 11%). All patients deteriorated to hypotensive shock within 12 hours and 13 died. Heart specimens from seven patients showed no evidence of myocarditis, but significant coagulative myocytolysis, myofibrillar degeneration, and cardiomyocyte apoptosis were observed. CONCLUSIONS: Acute heart failure was noted in 19% of patients with enterovirus rhombencephalitis, which had a fatality rate of 77%. It was not caused by myocarditis but possibly by neurogenic cardiac damage.  相似文献   

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