伊布利特致尖端扭转性室性心动过速一例

患者女性，65岁，心悸1d于2004年11月1日13：30入院。既往史：冠心病病史4年；乳腺癌术后6个月，化疗3次。入院时查体：体温36．7℃，脉搏120次／min，呼吸18次／min，血压140／100mmHg（1mmHg=0．133kPa），神志清楚，双肺未闻及干湿哕音，右胸部见-20cm手术疤痕，心界叩诊略向左大，心率150次／min，心律绝对不规则，心音强弱不等，各瓣膜听诊区未闻及杂音。心电图示：心房颤动（房颤），心电轴左偏，室性早搏，T波改变，QTc=430ms（图1a）。患者人院后15：20给予富马酸伊布利特（河北联合制药股份有限公司生产，批号：040401）1mg，溶于0．9％氯化钠溶液20ml内10min静脉注射。15：30患者心电图示：房颤，心电轴左偏，室性早搏，短阵室性心动过速（室速），T波改变，QTc=470ms（图1b）。15：40富马酸伊布利特重复给药1次（同前）。15：50心电图示：窦性心律，心电轴左偏，P波改变，T波改变，QTc=500ms（图1C）。患者无不良主诉。16：30患者突然出现气短、抽搐和意识不清，心电监护显示尖端扭转性室速（图2）。立即给予150J同步直流电复律1次，转复为窦性心律，并给予利多卡因50mg静脉注射。血钾4．1mmol／L，血钠140．1mmol／L。此后至17：00给予利多卡因、硫酸镁、氯化钾持续静脉滴注，在此期间出现3次尖端扭转性室速，每次均以舒张晚期室性早搏诱发，均给予同步直流电复律转复，发作问期QTc为520～600ms（图1d）。18：00给予美托洛尔5mg溶于5％葡萄糖20ml中静脉推注。18：10美托洛尔重复给药1次（同前）。18：40给予美托洛尔50mg口服。在给予美托洛尔过程中患者血压、心率均在正常范围，无明显波动。19：00心电图示：窦性心律，QTc=540ms。     

伊布利特转复房颤致尖端扭转型室性心动过速1例

1 临床资料 女性,52岁,因"间断心悸4年,加重1d"于2012年10月7日入院.患者4年来间断心悸,症状发作时于外院行心电图示"房颤".入院1d前无明显诱因再发心悸,伴胸闷憋气、乏力、大汗,不能平卧入睡,为进一步诊治入院.既往高血压6年,高脂血症2年.入院查体:脉搏100次/min,血压150/90mmHg(1mmHg=0.133kPa),不能平卧,颈静脉无怒张,双肺底可闻及少量吸气末细湿啰音,心尖搏动位于第V肋间左锁骨中线外0.5cm,心界向左下扩大,心率134次/min,心律不齐,S1强弱不等,P2＜A2,各瓣膜听诊区未闻及病理性杂音,肝、脾肋下未触及,双下肢不肿.     

抗心律失常肽对低钾低镁条件下伊布利特致尖端扭转性室性心动过速的影响

目的探讨缝隙连接开放剂抗心律失常肽(AAP10)对低钾、低镁条件下伊布利特致尖端扭转性室性心动过速(TdP)及心肌电不稳定性的影响。方法 54只日本长耳大白兔随机制备成左室楔形心肌块模型,随机分为对照组、低钾低镁组、伊布利特组、低钾低镁伊布利特组和AAP10干预组。对照组灌流正常台氏液,低钾低镁组灌流低钾低镁台氏液,伊布利特组灌流浓度2mg/l的伊布利特,低钾低镁伊布利特组灌流溶有同浓度伊布利特的低钾低镁台氏液,AAP10组给予AAP10干预的条件后灌流溶有伊布利特的低钾低镁台氏液。比较各组早期后除极(EAD)、R on T室性早搏和TdP的发生情况,以及QT间期、T波顶点到终点距离(Tp-e)和Tp-e/QT的变化。结果与对照组比较,低钾低镁伊布利特组QT间期、Tp-e和Tp-e/QT延长,EAD、R on T室性早搏、TdP的发生率明显增多。AAP10干预组,TdP、QT间期、Tp-e和Tp-e/QT比低钾、低镁伊布利特组显著减少。结论 AAP10可能通过开放缝隙连接减少跨壁复极离散度,从而起到预防伊布利特在低钾、低镁条件下的致TdP的作用。     

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     

阿司咪唑中毒致尖端扭转性室性心动过速一例

患者女性 ,5 0岁 ,因突发胸闷、心悸并晕厥 1次急诊入院 ,入院前 4ｈ误服大剂量阿司咪唑 (息斯敏 ,3ｍｇ× 85片 )2 5 5ｍｇ。入院时体格检查 :神志清醒 ,血压 12 0 /70ｍｍＨｇ(1ｍｍＨｇ =0 133ｋＰａ) ,心率 72次 /ｍｉｎ ,心电图示频发多源性室性早搏 (室早 )、ＱＴ间期延长 (0 6 4ｓ)、短阵多形室性心动过速 (室速 )。患者有慢性过敏性鼻炎病史 ,无心脏病史。入院后立即予以洗胃、利尿、吸氧、静脉注射利多卡因并维持静脉滴注以及补镁补钾治疗 ,心电监护示室性早搏明显减少 ,但ＱＴ间期长。入院后第 6ｈ患者小便时再发晕厥 1次 ,心电…     

变异型心绞痛致尖端扭转性室性心动过速1例

患者,女,40岁。主因头晕3年,胸闷、胸痛1个月,加重6d,于2006年4月5日入院。该患者3年前无诱因出现头晕、头痛,诊断为高血压,血压最高160/120mmHg(1mmHg=0.133kPa),口服北京降压0号、牛黄降压丸等药。1个月前出现活动后胸闷、胸痛,持续1~2min自行缓解,未诊治。6d前上述症状加重,休息时可出现胸闷、胸痛、出汗,多于凌晨发作,持续1~5min,含服速效救心丸好转,每日发作1~2次,无晕厥及意识障碍。否认糖尿病史、吸烟史及猝死家族史。否认奎尼丁、胺碘酮等用药史。体检:BP150/100mmHg。神志清楚。双肺呼吸音清。HR86次/min,律齐,未闻及杂音。腹…     

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…     

起搏器感知不良致尖端扭转性室性心动过速一例

患者男性 ,80岁。十二年前因“心房颤动伴Ⅲ度房室阻滞”在外院安置心脏ＶＶＩ起搏器 (ＣＰＩ,ＡＳＴＲＡＴ6)。 2 0 0 0年 2月 2日起反复出现头晕、胸闷。 2月 3日症状加重并多次出现短暂意识丧失伴四肢抽搐、小便失禁 ,每次持续约半分钟自行缓解。来院就诊后 ,又有类似发作 2次 ,每次发作时意识丧失 ,测血压为零 ,心电图示尖端扭转性室性心动过速(ＴＤＰ)、心室颤动 (简称室颤 ) ,起搏器感知不良 (见附图 )。给予 30 0Ｊ电击除颤 2次成功 ,其间ＴＤＰ发生时曾予利多卡因静脉推注无效。之后再次发生ＴＤＰ ,予静脉推注硫酸镁终止 ,并静脉滴…     

12例尖端扭转性室性心动过速临床分析

尖端扭转性室性心动过速(Torsades de pointes,Tdp)是一种恶性程度较高的多形性室性心动过速,临床并非少见,极易导致晕厥和心室颤动,严重威胁患者生命,正确及时识别和处理极为重要。本文回顾性分析12例TDP患者,分析其临床特征,以寻找影响其发作及终止的相关因素,目     

成功抢救尖端扭转性室性心动过速1例报告

<正> 病例报告 男,88岁,因“头部外跌伤后疼痛伴间歇性抽搐17小时”于1999年3月23日入院.患者于入院前17小时突然昏倒,头部受伤,随后出现间歇性抽搐多次,急诊入院.家庭史:无同样病史者.体检:神清,反应迟钝,右额部有长约5cm头皮裂口.已缝合,心界向左下扩大约2cm,心音强弱不一,双肺呼吸音增粗.神经系统检查无定位症状.6次查血钾、钠、氯、钙正常.X光胸片示靴形心,心胸比率0.65,主动脉粥状钙化斑.心电显示Ⅲ度房室传导阻滞,心室率平均42次/min,频发性多形性室性期前收缩,伴有尖端扭转性室性心动过速(Torsade de     

Amiodarone-induced torsades de pointes

Five cases of amiodarone-induced syncope due to torsades depointes or ventricular fibrillation are described. Amiodaronewas used for recurrent supraventricular tachycardia in fourcases and frequent ventricular extra systoles complicating congenitalQT prolongation in the remaining case. Each was associated witha marked prolongation in the QTc interval following amiodarone.Three cases had had a previous history of life-threatening ventriculararrhythmias secondary to anti-arrhythmic drugs. Hypokalemiamay have been a contributory factor in two. The clinical features,predisposing factors, and treatment are discussed.     

Terminology of torsades de pointes

Marked prolongation of the QT interval may be associated with life-threatening ventricular tachycardia. The ventricular tachycardia has a polymorphous appearance and is usually induced by antiarrhythmic drugs. This peculiar type of ventricular tachycardia was termed by Desserstenne torsades de pointes because of its twisting ORS axis. The main reason to give this entity a special name that differentiates it from other types of ventricular tachycardia is the unique therapeutic approach to its treatment. Torsades de pointes can be suppressed by interventions that shorten the QT interval by increasing the heart rate, such as ventricular or atrial pacing, isoproterenol infusion, or atropine. Recently intravenous magnesium was also shown to be extremely effective. If torsades de pointes is treated as a conventional ventricular tachycardia by drugs that may further prolong the QT interval, it may lead to fatal results. To draw the attention of physicians to this unusual form of ventricular tachycardia, we suggest that the term torsades de pointes be kept. This specific diagnosis will hopefully guide the treating physician in selecting the appropriate mode of therapy.     

Ketoconazole induced torsades de pointes without concomitant use of QT interval-prolonging drug

Ketoconazole is not known to be proarrhythmic without concomitant use of QT interval-prolonging drugs. We report a woman with coronary artery disease who developed a markedly prolonged QT interval and torsades de pointes (TdP) after taking ketoconazole for treatment of fungal infection. Her QT interval returned to normal upon withdrawal of ketoconazole. Genetic study did not find any mutation in her genes that encode cardiac IKr channel proteins. We postulate that by virtue of its direct blocking action on IKr, ketoconazole alone may prolong QT interval and induce TdP. This calls for attention when ketoconazole is administered to patients with risk factors for acquired long QT syndrome.     

Suppression of torsades de pointes by atropine

A 67 year old woman with a history of chronic atrial fibrillation presented with asthma cardiale. She took no medication and there was no family history of long QT syndrome. She was treated with furosemide, nitroprusside, acenocoumarol, and digoxin. Two days later excessively prolonged RR intervals, which were terminated by escape beats with a right bundle branch block morphology, suggested impending total AV block. There was also severe QT (0.48 s) and QTc (0.56) interval prolongation with bizarre inverted TU waves and multifocal premature ventricular complexes within the U waves. The patient experienced angina pectoris followed by episodes of torsades de pointes, which were interpreted as the result of bradycardia, and the bradycardia as the result of high grade AV block induced by increased vagal tone caused by ischaemia in the presence of digoxin intoxication (serum digoxin was 2.5 µg/l). Subsequent atropine infusion sped up the ventricular rate and shortened the QT (0.39) and QTc (0.51) intervals. Digoxin was replaced by metoprolol to control ventricular rate and angina pectoris. Within days, QT and QTc intervals became normal and the U waves disappeared. Neither torsades de pointes nor angina pectoris recurred. Based on a review of the literature, it is suggested that the electrophysiological mechanism of this effect is not only an increase of the heart rate, but also a direct action of muscarinic receptor antagonism on Purkinje cells and ventricular refractoriness.

Keywords: torsades de pointes;  long QT syndrome;  atropine;  AV block     

A patient with "atrial torsades de pointes"

A patient with long QT syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP durations in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of "atrial torsades de pointes" in a patient.     

苯妥因钠治疗尖端扭转型室性心动过速的临床观察

目的 通过静脉注射苯妥因钠治疗尖端扭转型室性心动过速（TDP），对其治疗作用、副作用进行观察。方法 尖端扭转型室性心动过速病人6例（男性1例，女性5例，年龄49－74岁），给苯妥因钠125－500mg静脉注射。结果 苯妥因钠静脉注射治疗尖端扭转型室速疗效确切，且对三种类型的TDP均有效。结论 提示苯妥因钠是治疗尖端扭转型室速的方法之一。     

QT prolongation and torsades de pointes: the sole manifestation of coronary artery disease

We describe a case of torsades de pointes as the sole manifestation of coronary artery disease, a presentation not previously reported to our knowledge.     

When an ICD is not the answer... hypothyroidism-induced cardiomyopathy and torsades de pointes

Introduction: An increasing number of patients with left ventricular (LV) dysfunction are referred for placement of an implantable cardioverter‐defibrillator (ICD). Case Report: A 78‐year‐old female with fatigue, palpitations, and presyncope was referred for consideration of an ICD because of a cardiomyopathy and nonsustained ventricular tachycardia (VT). Her evaluation revealed severe hypothyroidism, marked QT prolongation, and episodes of torsades de pointes. With levothyroxine therapy, her ventricular arrhythmias rapidly abated, with subsequent normalization of LV function and the QT interval. Conclusions: This report highlights the critical importance of detecting hypothyroidism as an unusual cause for reversible cardiomyopathy and ventricular arrhythmias.