右心室临时起搏抢救扭转型室速16例体会

由长Q—T间期综合征(LQTS)伴发的尖端扭转型室性心动过速(Tdp),是一种特殊表现的室性心动过速.发作时临床表现凶险,若不及时抢救,常危及生命.我们自1986年1月～1993年12月经静脉行紧急右心室临时起搏术抢救Tdp16例,取得较好疗效.现就治疗体会分析如下.1 临床资料1.1 一般资料 本组16例中,男5例,女11例.年龄17岁～78岁、平均年龄51岁.临床诊断:冠心病5例.先天性Q—T延长综合征3例、原发性扩张型心肌病2例,乐果中毒2例,风湿性心脏病、高血压性心脏病、病毒性心肌炎、慢性肾炎各1例.发作诱因:惊吓或情绪激动3例、低血钾8例.洋地黄中毒1例,其余原因不明.1.2 心电图表现Tdp发作间隙期:窦性心律伴频发室性早搏6例.窦性心动过缓伴室性早搏8例.Ⅲ°房室     

“快－慢”型室上性心律失常的射频导管消融治疗及随访

目的：探讨射频导管消融在治疗“快—慢”型室上性心律失常中的作用。方法：用射频导管消融的方法治疗了４例“快—慢”型室上性心律失常病人。结果：１９９１年１月至１９９６年１月间，对２４１例次各种快速性心律失常进行了射频导管消融治疗。其中４例为“快—慢”型室上性心律失常，２例为反复发作性房室结折返性心动过速（ＡＶＮＲＴ），终止时有长时间的心脏停搏并引起晕厥，原准备安装永久性心脏起搏器，ＡＶＮＲＴ根治后，由其引起的症状不复存在，电生理检查窦房结功能正常，故未安装起搏器；另２例均已植入永久性心脏起搏器，１例频繁发作快速心室率心房颤动并经常引起急性心功能不全，１例反复发作ＡＶＮＲＴ、心房扑动和心房颤动且有明显的症状，射频导管消融治疗后症状均消失，射频导管消融术对起搏器的功能无影响。３例平均随访３１±２个月，１例随访２个月未见并发症和临床症状复发。结论：射频导管消融法治疗“快—慢”型室上性心律失常具有重要的临床价值。     

为左上腔静脉永存合并右上腔静脉缺如患者植入起搏导线

目的 对左上腔静脉永存合并右上腔静脉缺如患者的心室起搏导线植入方法作初步探讨,方法 为3例病态窦房结综合征,2例三度房室阻滞患者植入VVI起搏系统,导线经左上腔静脉、冠状静脉窦、右心房、三尖瓣口而固定于右心室心尖部（4例）或至心大静脉远段（1例）,靠近心外膜左缘。结果 5例患者的导线均成功放置分别随访3个月-7年,起搏功能良好。结论 对左上腔静脉存伴右上腔静脉缺如患者植入心脏起搏系统,通过适当地操作,一般可将导线定侠于右心室心尖部;而经冠状静脉窦作左心室心外膜起搏亦是可以选择的。     

心内电击法阻断希氏束的动物实验研究

本文报道经皮穿刺股静脉由心内膜导管电极电击阻断希氏束的动物实验结果。14只狗用30—400瓦、秒电能通过负极对不同狗的希氏束分别进行非同步或同步电击。结果发现非同步电击可致室颤,而同步电击可安全有效地永久性阻断希氏束。本技术不仅可用以根治某些顽固性折返性室上性心动过速,且是目前形成完全性房室传导阻滞动物模型的最简易方法。     

三磷酸腺苷静注诊断10例隐性预激综合征

选择窦性心律时心电图无心室预激波(PEC)的44例阵发性室上速和6例仅有短PR间期者施行三磷酸腺苷(ATP)分级递增快速静注(ATP_Ⅳ)和诊断性电生理研究(DEPS)。结果:ATP_Ⅳ和DEPS分别揭示出隐性预激综合征(PE_L)10/50例和9/50例;ATP_Ⅳ揭示的10例PE_L中有6例在显示PEC前或中出现非预激搏动的房室结传导延缓或阻滞;ATP_Ⅳ未生严重并发症。提示(1)ATP_Ⅳ是诊断PE_L的一种简便、敏感和较安全的方法;(2)ATP_Ⅳ时PEC的揭示主要与ATP对房室结前向传导的负性变导性作用有关。     

Clinical and familial study of arrhythmogenic right ventricular cardiomyopathy

Objective　To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods　Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied. All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two-dimensional echocardiography (2-DE) and a signal averaging electrocardiogram. Programmed ventricular stimulation was performed in five patients. Results　All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2-DE. Fourteen persons had abnormal findings indicating ARVC. Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall. Twenty-five persons (seven patients and 18 family members) had abnormal findings in ECG. Positive ventricular late potential was recorded in 13 persons (six patients). Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients. Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS). Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle. Two members of one family died suddenly. One member was a dwarf with ARVC. Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients). Conclusion　Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC. The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle.     

房室结折返性心动过速时希—浦系统不应期的调整及其机制探讨

目的　阐明房室结折返性心动过速 (AVNRT)时希 -浦系统不应期的变化及可能机制。方法8例 AVNRT病人在射频消融前于高位右房 (HRA)常规行程序电刺激诱发心动过速并实时记录。结果　所有病人心动过速起始时均表现为房室 2∶ 1传导 ,其中 2例 2∶ 1阻滞点在希氏束以下部位 ,5例在希氏束以上部位 ,1例不明。房室 2∶ 1传导持续平均 14.0 3± 10 .0 3秒后转为房室 1∶ 1传导伴束支传导阻滞 ,其中 3例为右束支传导阻滞 ,3例为左束支传导阻滞 ,2例在不同的时间段分别为左束支和右束支传导阻滞。 1∶ 1房室传导伴束支传导阻滞平均持续 6 .87± 11.2 6秒后束支传导阻滞消失。结论　 AVNRT起始时希 -浦系统的不应期自动缩短使结室传导易化 ,这一机制是电重构机制 ,且常在 30～ 6 0秒之内完成。