丙种球蛋白治疗小儿急性病毒性心肌炎合并完全性房室传导阻滞的临床观察

目的探讨丙种球蛋白治疗小儿急性病毒性心肌炎合并完全性房室传导阻滞(CAVB)的临床疗效。方法选取病毒性心肌炎合并CAVB患儿80例,采取随机数字表法分为常规组与丙种球蛋白组,每组各40例,对比两组患儿临床疗效、治疗前后外周血T细胞亚群变化、心肌酶谱变化、症状消失时间、心肌酶恢复时间、心电图恢复正常时间。结果丙种球蛋白组的总有效率(95.00%)高于常规组(80.00%),差异具有统计学意义(P0.05)。两组治疗后与治疗前相比CD3+升高、CD4+降低、CD8+升高、CD4+/CD8+降低,肌酸激酶(CK)、肌酸激酶同工酶MB(CKMB)、乳酸脱氢酶(LDH)降低,且治疗后丙种球蛋白组与常规组上述指标改善更加显著,差异具有统计学意义(P0.05)。丙种球蛋白组与常规组相比症状消失时间、心肌酶恢复时间、心电图恢复正常时间均明显缩短,差异具有统计学意义(P0.05)。结论丙种球蛋白治疗小儿急性病毒性心肌炎合并CAVB的临床效果显著。     

小儿心肌炎后的完全性房室传导阻滞

小儿完全性房室传导阻滞(CAVB)是先天的或是后天获得的,后天获得的CAVB最常见的病因是心脏手术后,偶见于心肌炎患者。 该文阐述小儿心肌炎后获得性非手术创伤性CAVB的病因、自然病程和预后。 病例和方法 该文收集了1990年6月～     

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…     

小儿完全性房室传导阻滞30例临床分析

本文报道小儿完全性房室传导阻滞(CAVB)30例。对诊断、影响预后因素、治疗原则尤其对安装起搏器指征作了讨论。     

丙种球蛋白治疗病毒性心肌炎30例临床分析

目的观察丙种球蛋白静脉注射对小儿病毒性心肌炎的疗效。方法 60例病毒性心肌炎患儿随机分成治疗组与对照组,各30例。对照组常规给予能量合剂、辅酶Q10、维生素C、维生素E等;治疗组在常规治疗基础上加用大剂量人血丙种球蛋白静脉滴注。结果应用丙种球蛋白1周后,血清IgG,IgM显著增高,IgA增高不明显,T、B淋巴细胞增生较治疗前明显提高。临床症状、心电图、心肌酶谱、平均住院日期缩短均优于对照组。结论常规治疗基础上静注丙种球蛋白能提高病毒性心肌炎治疔效果。     

大剂量激素治疗病毒性心肌炎并发房室(窦房)传导阻滞的疗效分析

大剂量激素治疗病毒性心肌炎并发房室（窦房）传导阻滞的疗效分析王惠政（宁波市第一医院３１５０１０）关键词心肌炎，病毒性房室传导阻滞地塞米松我们对１９８７年～１９９５年本院收治的急性病毒性心肌炎并发Ⅲ°（高度）房室传导阻滞（ＡＶＢ）２１例和２∶１窦房传导...     

小儿完全性房室传导阻滞

完全性房室传导阻滞（ＣＡＶＢ）又称三度房室传导阻滞,是指由于房室传导系统房室结的绝对不应期异常延长,致所有来自心房的激动都不能下传至心室,形成完全性房室分离的现象,是儿科常见的缓慢性心律失常之一。ＣＡＶＢ可表现为一过性、间歇性或持久性。１病因１．1 先天性ＣＡＶＢ 小儿时期,尤其是婴幼儿以先天性ＣＡＶＢ居多。其发生可能与以下因素有关：①母亲孕期患结缔组织病（如系统性红斑狼疮等）,血清中的抗体通过胎盘与胎儿心脏传导组织发生病理性免疫反应,引起炎症、变性及纤维化;②房室传导系统胚胎发育畸形、缺损,如先…     

病毒性心肌炎致高度房室传导阻滞1例

患者女性,14岁。因发作性头晕、恶心3d。晕厥5次。于2004年5月8日入院。查体：血压105／60mmHg,精神差。心率52次／min,心律不齐,心前区可闻及海鸥鸣样杂音。24h动态心电图(图1)示：窦性心律、高度房室传导阻滞,室内传导阻滞,偶发室早,ST改变。高度房室传导阻滞表现为窦性P波以2：1～7：1,甚至偶有10：1的比例下传心室。QRS波时限延长,长间歇有94次。晕厥发作2次,心室停搏均可达28s。     

Complete atrioventricular block in experimental murine myocarditis

BACKGROUND: There were few reports on the pathological characteristics of the conduction system in myocarditis. This study was aimed to clarify the pathological characteristics of complete atrioventricular (AV) block in myocarditis. METHODS AND RESULTS: We studied serial electrocardiograms in experimental myocarditis in mice and also examined their cardiac pathology. After taking baseline electrocardiograms, mice were inoculated intraperitoneally with the encephalomyocarditis virus. Electrocardiograms were serially recorded until day 360. Serial electrocardiograms revealed the appearance of complete AV block. Myocardial lesions were found in the hearts of mice with these ectopic beats. Mononuclear cell infiltrations into the His bundle and necrotic lesions of the conduction system were found in 10.7% (18/168) of mice with complete AV block. However, 17.3% (29/168) of mice showed no evident pathological lesions except the edematous changes of AV node. CONCLUSIONS: The appearance of complete AV block in myocarditis may suggest not only significantly comparable pathological lesions of the conduction system but also the trivial edematous changes; in clinical settings, in the former case, permanent pacing therapy is necessary, and in the latter case, the disease may be transient and could be recovered from complete AV block. This study may shed light on the pathological characteristics of complete AV block in myocarditis.     

Complete atrioventricular block persisting after regression of infectious myocarditis

Atrioventricular block is usually transient during the course of infectious myocarditis. We report the case of a patient presenting with complete infra-hisian atrioventricular block occurring in the setting of infectious myocarditis and in whom a pacemaker should be finally implanted. Borderline serologies for picornavirus were present 6 weeks later. Complete atrioventricular block persisted during the two years of follow-up despite otherwise complete regression of the myocarditis. We then discuss the main features of conduction disturbances complicating infectious myocarditis, including a list as complete as possible of all the causal agents possibly involved.     

Complete atrioventricular block associated with toxoplasma myocarditis.

Myocarditis has been described during and after a wide variety of infectious agents: viral, rickettsial, bacterial, protozoal, and metazoal diseases may cause cardiac inflammation. We report a case of toxoplasma myocarditis in a young healthy man.     

老年急性前壁心肌梗死并发房室传导阻滞患者临床研究

完全性房室传导阻滞(complete atrioventricularblock,CA-VB)是急性心肌梗死(AMI)的常见并发症,急性下壁心肌梗死(inferior wall myocardial infarction,IWMI)CA-VB的发生率是急性前壁心肌梗死(anteriorwall myocardial infarction,AWMI)的2~4倍,且临床表现不同[1]。为比较老年     

临时起搏在急性病毒性心肌炎合并Ⅲ度房室传导阻滞的应用分析

目的通过对15例合并Ⅲ度房室传导阻滞(ⅢoAVB)的急性病毒性心肌炎的临床特征辅助检查,临时起搏治疗和转归的分析,总结临时起搏的作用。方法分析15例合并Ⅲ度房室传导阻滞的急性病毒性心肌炎患者应用临时起搏后的治疗效果。结果15例患者接受临时起搏治疗后能恢复窦性心律,临时起搏留置时间2～13d。结论急性病毒性心肌炎合并Ⅲ度房室传导阻滞时应及时使用临时起搏并辅以其他治疗,可在较短时间内恢复窦性心律。     

Long-term follow up of children with congenital complete atrioventricular block and the impact of pacemaker therapy.

AIMS: This study assessed survival, morbidity and impact of pacemaker (PM) therapy in children with Congenital Complete Atrioventricular Block (CCAVB). METHODS AND RESULTS: Data of 32 children, diagnosed as showing CCAVB at a median age of 0.4 years (range foetal-10 years), were retrospectively analysed. For comparison of clinical data patients were separated into two groups: CCAVB without structural heart disease (group 1; n = 23) and with structural heart disease (group 2; n = 9). Median follow-up time was 10.2 years. Pacemakers (PM) were implanted in 17 group 1 and all group 2 children. Frequency of PM therapy, age and symptoms before PM implantation did not differ significantly between the groups. Indications for PM implantation were bradycardia in 15, decreased exercise tolerance in 6, syncope in 3 and heart failure in 2 children. PM system related complications occurred in 11/26 (42%) children. Although 1 child died due to PM exit block no further CCAVB related symptoms were recorded in children with PM. CONCLUSION: PM therapy reduces mortality and morbidity in children with CCAVB when compared with natural history data. Although children with PM are free from CCAVB related symptoms limited morbidity remains due to PM system related complications.     

急性心肌梗死并发房室传导阻滞的临床分析

目的探讨急性心肌梗死(AMI)患者发生房室传导阻滞(AVB)的临床特点。方法采用非创伤性心电监测法监测122例心肌梗死患者AVB的发生率及其对药物治疗反应、演变过程和最终预后。结果 122例AMI患者中20例发生AVB(16.4%)。17例发生于下/后心肌梗死者,3例发生于前壁/广泛前壁心肌梗死者。按AVB发生的不同时期分为早发组(发病8 h内,n=8)和晚发组(发病8 h后,n=12),晚发组并发症显著高于早发组(25﹪vs 83.3﹪,P<0.05);早发组对阿托品或山莨菪碱治疗反应较好(P<0.05);早发组Ⅲ度AVB 7例、Ⅱ度AVB 1例,持续时间短。晚发组Ⅰ度AVB 5例、Ⅱ度AVB 6例、Ⅲ度AVB 1例,持续时间长;早发组住院期间死亡1例、晚发组死亡5例,有显著差异(P<0.05)。结论 AMI病人中下/后壁心肌梗死易并发AVB;8 h之内发生的AVB以Ⅲ度AVB为主,早期发生的AVB患者预后好。     

Acute myocarditis associated with transient marked myocardial thickening and complete atrioventricular block

A 17-day-old male infant with acute myocarditis developed complete heart block and cardiogenic shock. In addition, extensive concentric thickening of the left ventricular walls and diminution of the ventricular cavity were demonstrated by serial echocar-diography. The echocardiographic findings mimicked a nonobstructive hypertrophic cardiomyopathy. However, the wall thickness gradually returned to normal, coincident with clinical improvement. This unusual myocardial thickening may have resulted from myocardial edema or cellular infiltration. Its relationship to high-dose steroid therapy is unclear.     

病毒性心肌炎患儿心肌酶改变及其与心功能关系的研究

为探讨病毒性心肌炎（VM）患儿心肌酶改变及其与心功能的关系,测定了112例VM患儿的心肌酶、心功能,并分析两者之间的关系。结果VM患儿五项心肌酶均显著高于健康儿童,经综合治疗1个月后,心肌酶指标均显著下降,且VM患儿CKMB增高者中心脏收缩功能降低者显著多于CKMB正常者。认为VM患儿心肌酶增高,部分VM患儿心功能降低,心功能降低与CKMB增高有关。