尖端扭转型室性心动过速的近代进展

尖端扭转型室性心动过速(Torsade de pointes,TdP)是一种介于室性心动过速(室速)和心室纤颤(室颤)之间的特殊类型的室速。近年来对TdP的命名、分类、发生机理及治疗均有新的认识。 一、概述 TdP早在50年前已被描述,但皆被误诊为室颤。Schwartz在1949年首先指出其发作的特点为短暂性,且可自行消失,因而称之为“短暂性室颤”。以后又由其     

房室传导阻滞伴扭转型室性心动过速,心室停搏1例

患者男性 ,５０岁。因反复心悸、晕厥、抽搐发作３年余 ,再发０．５ｈ入院。体检 :ＢＰ测不到。神志清。心界不大 ,心率２０～３１次／ｍｉｎ ,心音强弱不一。Ｘ线胸片示 :心影大小正常。临床诊断 :心律失常 ,阿＿斯综合征 ,间歇性预激综合征。１９９６年１月晕厥时心电图检查 (图１Ａ)示 :窦性心律 ,完全性左束支传导阻滞。动态心电图检查除左束支传导阻滞外未发现其他异常。１９９９年２月９日１５∶４５急诊体检时突然晕厥、抽搐。即查心电图 (图１Ｂ)示 :ＱＲＳ波群宽大畸形 ,主波方向时上时下 ,心室率２００～３００次／ｍｉｎ ,为尖端…     

低血钾致三度房室传导阻滞、尖端扭转型室性心动过速1例

患者女性，90岁。因腹胀、食欲减退半月，咳嗽、胸闷1周入院。有慢性支气管炎、原发性高血压及胆结石病史。否认黑嚎、晕厥史。体检：T36℃，BP240／60mmHg。神志清。心界不大，心率43次／min，心律齐，未闻及杂音。双肺闻干湿性哕音。     

完全性电交替合并尖端扭转型室性心动过速1例

患者女 ,73岁。临床诊断 :急性前间壁心肌梗死 ,肺癌晚期 ,肺心病 ,咯血。心率 13 0次 /ｍｉｎ ,血压 176/111ｍｍＨｇ ,呼吸急促 ,两肺布满干湿罗音和哮鸣音。心电图诊断 :窦性心动过速 ,频发多源性室早 (ＰＶＳ) ,反复发作短阵性尖端扭转型室速 (ＴＤＰ) ,急性期前间壁心肌梗死 ,完全性电交替 ,图中窦性心律 13 3次 /ｍｉｎ ,呈ＱＲＳ型 ,显示 2∶1完全性电交替。上行终末部及下行起始部可见ＴＤＰ ,频发多源性ＰＶＳ。图 1　完全性交替合并尖端扭转型室性心动过速讨论　本图粗看杂乱无章 ,但仔细分析可得出上述结果 ,临床上少见。出现完…     

女性是尖端扭转型室性心动过速的独立危险因素

本文总结了女性作为尖端扭转型室性心动过速的独立危险因素的临床和 动物实验依据，并探讨其影响因素及其可能的作用机制。     

女性是尖端扭转型室性心动过速的独立危险因素

本文总结了女性作为尖端扭转型室性心动过速的独立危险因素的临床和动物实验依据，并探讨其影响因素及其可能的作用机制。     

尖端扭转型室性心动过速24例分析

尖端扭转型室性心动过速（Tdp）是一种特殊类型致命快速室性心律失常Ⅲ,若不及时正确救治,常危及生命。现将我院近几年收治的Tdp24例临床作一分析。     

尖端扭转型室性心动过速38例分析

目的：分析38例尖端扭转型室性心动过速的发病原因,临床,心电图特点,抢救措施及结果：方法：按其心电图特点,临床表现,发病原因,发病机制的不同,采取不同的急救措施,结果：抢救成功28例（74．2％）,死亡10例（25．8％）,结论：尖端扭转型室性心动过速的发生机制较复杂,病因甚多,异丙基肾上腺素效果较好,心室起搏特别是抗快速心律失常起搏器,埋藏式自动心脏复律除颤器为发作频繁,持续时间长,有阿－斯氏征发作,心脏停搏危险开辟了新的治疗途径。     

尖端扭转型室性心动过速的实验模型

自 196 6年Ｄｅｓｓｅｒｔｅｎｎｅ首先描述尖端扭转型室性心动过速 (Ｔｏｒｓａｄｅｄｅｐｏｉｎｄｅｓ ,ＴｄＰ)以来 ,心脏电生理学者不断建立和完善ＴｄＰ实验模型以探索其发生机制。由于多种药物包括抗心律失常药都可引起ＱＴ间期延长导致ＴｄＰ ,所以建立ＴｄＰ模型也用以研究药物的促心律失常作用。目前实验模型由最初的在体模型逐渐发展到离体模型 ,以及计算机模拟模型。本文就这三种实验模型的进展进行综述。1　在体动物模型1.1　 慢性Ⅲ度房室阻滞 (ＡＶＢ)犬模型　利用化学药物或电灼伤造成犬Ⅲ度ＡＶＢ后 4～ 8周进行实验 ,主要…     

合并完全性房室阻滞的肾上腺能依赖性尖端扭转性室性心动过速二例

长QT综合征（long QT syndrome,LQTS）是一类可能发生恶性心律失常的综合征,分为先天性及获得性两大类型。既往曾经有学者认为多数先天性LQTS其尖端扭转性室性心动过速（torsades de pointes，TdP）发作多表现肾上腺能依赖性，而获得性LQTS及先天性LQTS3则表现为长间歇依赖性。近年的研究表明不少LQl、s病例同时存在长间歇依赖及肾上腺能依赖等特性的重叠交叉。本院自1999年以来收治2例合并完全性房室阻滞的LQTS，其TdP发作表现出典型肾上腺能依赖的特性，现报告如下。     

Torsade de pointes during loading with amiodarone

Torsade de pointes represents a potential complication of chronicamiodarone therapy. Several reports have emphasized the needfor a loading dose in order to achieve therapeutic blood levelsrapidly. We report a case of torsade de pointes following asingle oral dose of amiodarone (1400 mg or 30 mg kg^–1)administered after short intravenous loading for preventionof paroxysmal atrial flutter. Torsades de pointes were precededand associated with marked QT prolongation and bradycardia.This report suggests that careful monitoring of patients undergoingoral amiodarone loading is necessary.     

Familial inducible torsade de pointes with normal QT interval

A familial presentation of torsade de pointes is described.The propositus had recurrent syncope, documented torsade depointes, a normal Q-T, and close coupled premature ventricularbeats initiating the paroxysmal arrhythmia. The mother had sporadicsyncope without documented torsade de pointes, a normal Q-T,and closely coupled premature ventricular beats. Electrophysiologicalstudies demonstrated reproducible inducible torsade de pointestachycardia in both patients. Serial drug testing in both revealedsuppression of induced torsade de pointes with oral propranolol.Chronic oral propranolol resulted in clinical cure in both patients.     

Long QT syndrome and torsade de pointes in transient left ventricular apical ballooning syndrome

A recently reported cardiac syndrome of reversible left ventricular apical ballooning, also called Takotsubo cardiomyopathy or ampulla cardiomyopathy, clinically resembles acute myocardial infarction and presents with chest pain, anterior electrocardiographic changes and minimal elevation of cardiac enzymes in absence of myocardial ischemia or injury. Left ventricular function recovers completely in days to weeks. This syndrome is likely a non-ischemic, metabolic-dependent syndrome caused by stress-induced activation of the cardiac adrenoceptors, and results in markedly abnormal ventricular repolarization. Reported here is a case of left ventricular apical ballooning syndrome with QT interval prolongation in a young man who developed torsade de pointes and experienced aborted sudden cardiac death. Patient had a complete recovery of cardiac function and normalization of QT interval in a few days. The syndrome of transient left ventricular apical ballooning could be considered among the causes of long QT syndrome and torsade de pointes.     

Torsade de pointes associated with bradycardia and takotsubo cardiomyopathy

Two cases of torsade de pointes associated with bradycardia and takotsubo cardiomyopathy are reported. In both cases, atrioventricular block preceded the occurrence of takotsubo cardiomyopathy. Bradycardia-induced QT interval prolongation seemed to be amplified by the occurrence of takotsubo cardiomyopathy, resulting in torsade de pointes. Temporary ventricular pacing at a high rate decreased the QT interval and prevented the recurrence of torsade de pointes. Because atrioventricular block recurred or persisted even after the resolution of takotsubo cardiomyopathy, the patients received permanent pacemakers.     

Torsades de pointes during complete atrioventricular block: Genetic factors and electrocardiogram correlates

INTRODUCTION:

Atrioventricular (AV) block is infrequently associated with QT prolongation and torsades de pointes (TdP). It was hypothesized that patients with AV block-mediated QT-related arrhythmia may have latent congenital long QT syndrome or a vulnerable genetic polymorphism.

METHODS:

Eleven patients with complete AV block and TdP were prospectively identified. Patients underwent assessment, resting electrocardiography and telemetry at baseline, during AV block and pre-TdP. Genetic testing of KCNH2, KCNQ1, KCNE1, KCNE2 and SCN5A was performed. Thirty-three patients with AV block without TdP were included for comparison.

RESULTS:

Genetic variants were identified in 36% of patients with AV block and TdP. Patients with AV block who developed TdP had significantly longer mean (± SD) corrected QT intervals (440±93 ms versus 376±40 ms, P=0.048) and T_peak to T_end (T_p-T_e) intervals (147±25 ms versus 94±25 ms, P=0.0001) than patients with AV block alone. In patients with a genetic variant, there was a significant increase in T_p-T_e intervals at baseline, in AV block and pre-TdP compared with those who were genotype negative. A personal or family history of syncope or sudden death was more likely observed in patients with a genetic variant.

CONCLUSIONS:

TdP in the setting of AV block may be a marker of an underlying genetic predisposition to reduced repolarization reserve. The T_p-T_e interval at baseline, in AV block and pre-TdP may predict a genetic mutation or polymorphism compromising repolarization reserve. Patients with TdP in the setting of AV block represent a phenotypic manifestation of latent congenital long QT syndrome.     

LQT2模型尖端扭转型室性心动过速的发生机制

目的探讨LQT2模型早期后除极(EAD)、跨壁折返以及尖端扭转型室性心动过速(Tdp)的发生机制。方法采用冠状小动脉灌注兔左室心肌楔形组织块标本,应用浮置玻璃微电极动作电位及ECG同步记录技术,以IKr阻断剂d-sotalol作为工具药模拟LQT2,并与延迟整流钾电流IK阻滞剂azimilide对比,观察两者对兔心内膜和外膜层心肌细胞动作电位时程(APD)、跨壁复极离散度(TDR)、EAD、R-on-T早搏和Tdp的作用。结果d-sotalol和azimilide均显著延长心内膜和外膜层心肌细胞APD和QT间期;d-sotalol显著增加TDR,诱发EAD、R-on-T早搏和自发性Tdp的发生率分别为7/7,7/7和3/7;azimilide不增加TDR和不形成跨壁折返,但可诱发EAD和R-on-T早搏。结论通过冠状小动脉灌注兔左室心肌组织块LQT2模型,发现整体心室肌组织在QT延长的条件下,2相EAD是触发并引起Tdp的机制;TDR增加是产生EAD和形成折返的基础。     

Suppression of amiodarone-induced torsade de pointes by landiolol in a patient with atrial fibrillation-mediated cardiomyopathy

An elderly Japanese woman developed acute decompensated heart failure caused by persistent atrial fibrillation (AF) and left ventricular systolic dysfunction. Approximately 6 days after starting intravenous administration of amiodarone (600 mg/day) for maintaining sinus rhythm after cardioversion of AF, electrocardiograms revealed a prolonged QT interval associated with torsade de pointes (TdP). The amiodarone-induced TdP disappeared after intravenous administration of landiolol plus magnesium and potassium, without discontinuation of amiodarone or overdrive cardiac pacing, although the prolonged QT interval persisted. To the best of our knowledge, this is the first report that landiolol could be effective for amiodarone-induced TdP.     

Langendorff逆灌流制备特非那丁诱发尖端扭转室性心动过速模型

目的对临床易发尖端扭转型室性心动过速(TDP)的情况进行模拟,利用Langendorff逆灌流技术灌注离体兔心,研究特非那丁促TDP的机制。方法烧灼法制备Ⅲ°房室传导阻滞离体兔心模型,应用不同浓度的特非那丁低钾镁台氏液,利用Langendorff逆灌流技术灌注兔心,以不同周长起搏,利用慢频率和刺激周长骤变方法诱发早期后除极(EADs)、TDP。结果基础台氏液和低钾镁台氏液(MT)灌流下均未见EADs、TDP;各浓度特非那丁低钾镁台氏液灌流都可延长QT间期和单向动作电位复极达90%时限(MAPD90),10/18例记录到EADs,起搏周长1 400~2 400 ms。10/18例诱发出TDP,7/18例经过刺激周长骤变诱发出TDP,以300~2 300 ms为多(6/18例),MT+特非那丁浓度8×10-6mmol/L时诱发TDP频率最高,为66.7%。结论在离体兔心,特非那丁MT灌注呈浓度及频率依赖性延长MAPD90;EAD及其引起的触发活动(TA)是诱发TDP的基础。     

Suppression of amiodarone‐induced torsade de pointes by landiolol in a patient with atrial fibrillation‐mediated cardiomyopathy

An elderly Japanese woman developed acute decompensated heart failure caused by persistent atrial fibrillation (AF) and left ventricular systolic dysfunction. Approximately 6 days after starting intravenous administration of amiodarone (600 mg/day) for maintaining sinus rhythm after cardioversion of AF, electrocardiograms revealed a prolonged QT interval associated with torsade de pointes (TdP). The amiodarone‐induced TdP disappeared after intravenous administration of landiolol plus magnesium and potassium, without discontinuation of amiodarone or overdrive cardiac pacing, although the prolonged QT interval persisted. To the best of our knowledge, this is the first report that landiolol could be effective for amiodarone‐induced TdP.