Torsade de pointes caused by high-dose intravenous haloperidol in cardiac patients

Intravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high-dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high-dose intravenous haloperidol therapy have appeared. The present report describes three patients with definite haloperidol-induced QTc prolongation and torsade. In each case, QTc prolongation preceded the arrhythmia and disappeared following the discontinuation of haloperidol. Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high-dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life-threatening complication of high-dose intravenous haloperidol.     

Torsade de pointes due to coxsackie B3 myocarditis

Viral myocarditis may present with a variety of electrocardiologic aberrations. Torsade de pointes, a potentially malignant ventricular arrhythmia associated with prolongation of the QT interval has not been described in patients with acute viral myocarditis. This report details this finding in a patient with coxsackie B3 myocarditis in whom symptomatic torsade de pointes was documented.     

家族性长QTU综合征伴发扭转型室速的电生理机制及电药理评价

本文采用新型接触电极观察三种药物对家族性长QTU综合征患者的早期后除极、U波及室性心律失常的作用,发现维拉帕米及普萘洛尔有效,而利多卡因则无效,并提示早期后除极与本病扭转室速的发病有关．     

A Low Incidence of Proarrhythmia Using Low-Dose Amiodarone

The incidence of proarrhythmia with antiarrhythmic agents is reported to be 2%-23%, depending on the agent, definition of proarrhythmia, method of assessment, and severity of underlying rhythm disturbance. Several case reports of amiodarone-induced proarrhythmia have appeared; however, its prevalence and clinical significance have not been adequately defined. In our series of 107 patients with potentially lethal ventricular arrhythmias, amiodarone was administered as a 5-mg/kg bolus infusion, followed by 600–800 mg/day for 7–10 days. A mean daily maintenance dose of 270 mg/day was given for an average of 15 months (range <57). Proarrhythmia was defined by the method of Morganroth as: (1) a three- to tenfold increase in VPC frequency, (2) a marked increase in VT rate, or (3) the development of new sustained VT/VF or torsade de pointes. Bradyarrhythmias, conduction delays, and out-of-hospital sudden death were not included by definition. Baseline 24-hour-Holter monitoring revealed 449 ± 685 VPCs/hr, 740 ± 584 couplets/24 hr, and 61 ± 685 episodes of nonsustained VT/24 hr. Proarrhythmia occurred in three patients (2.8%). Two of these episodes occurred during the first week of treatment and resolved without dosage adjustment. These episodes included a 4.7- and 5.1-fold increase in VPC frequency. The other proarrhythmic event was a case of torsade de pointes that occurred after 12 months of treatment and required acute intervention and withdrawal of amiodarone. In conclusion, low-dose amiodarone appears to have a low potential for proarrhythmia and compares favorably with other agents in this regard, perhaps owing to its unique electrophysiologic properties.     

Individual patterns of QT/RR relationship

In clinical practice, an imprecision introduced by ad hoc selected heart rate correction formula of the QTinterval is unlikely to lead to erroneous conclusions if all borderline cases are carefully considered. On thecontrary, in clinical investigations (e.g., studies of drug effects) the over- or undercorrection of QTcmay lead to significant and systematic bias with both false positive and false negative findings.None of the previously published global heart rate correction formulae has been universallysuccessful because the QT/RR relationship is different between different subjects and a formula that correctsthe QT interval for heart rate acceptably in one individual may be very misleading in another individual.Moreover, it has been recently established that the QT/RR patterns not only exhibit a substantialinter-subject variability but also a high intra-subject stability. Thus, in precise investigations, individualQT/RR relationship should be first established in each subject and subsequently translated into individualheart rate correction formula.     

Prolonged Asymptomatic Torsade de Pointes

Torsade de pointer is often associated with syncope, particularly when prolonged. We report a cane of prolonged asymptomatic torsade de pointes in a 68-year-old woman being treated with quinidine gluconate for paroxysmal atrial fibrillation. Ambulatory monitoring obtained one week after an increase in the daily qninidine dosage demonstrated one minute of polymorphous ventricular tachycardia. The patient remained entirely asymptomatic throughout the time of the arrhythmia. Therefore, a lack of symptoms in patients at risk for torsade de pointes may not exclude the presence of this arrhythmia.     

Q-T prolongation and torsades de pointes in a patient with subarachnoid hemorrhage

An extreme Q-T prolongation in a patient with subarachnoid hemorrhage was observed. Multiple torsades de pointes occurred. Lidocaine, metoprolol, and atropine were not effective in controlling the arrhythmia, whereas shortening the Q-T interval by intravenous administration of orciprenaline or overdrive ventricular pacing was successful. The occurrence of T wave alternations was a sign of increased sympathetic activity.     

获得性长QT综合征的心电图分析

目的探讨获得性QT间期延长（LQTS）伴尖端扭转型室速（TdP）的心电图特征、相关病因及诱因。方法选取获得性LQTS伴Tdp发作住院患者19例,观察其QT、QTc间期和TdP发作特征。结果 19例患者QTc间期变动在0.49-0.87s（平均0.63±0.09s）,伴随T波电交替4例,Niagara瀑布样T波3例,Tdp触发方式和发作时间不同。相关诱因和病因包括电解质紊乱8例,缓慢性心律失常7例,药物过量4例。15例患者抢救成功,4例发生院内死亡。结论 LQTs伴Tdp起病急骤,院内死亡率高,了解其心电图特点、相关诱因及其危险因素,及时防范,对于减少院内心脏恶性事件的发生意义重大。     

Torsade de pointes tachycardia as a rare manifestation of acute enteroviral myocarditis

A patient with cardiac arrest and documented torsade de pointes ventricular tachycardia is presented in whom acute coxsackievirus B2 myocarditis was identified as the most likely underlying cardiac condition. This case shows that torsade de pointes may occur as a rare manifestation of viral myocarditis. Serial serological tests and endomyocardial biopsies may be helpful in establishing a diagnosis in such patients.


Keywords: torsade de pointes; ventricular tachycardia; viral myocarditis     

A practical approach to torsade de pointes

The term torsade de pointes refers to polymorphic ventricular tachycardia that occurs in the setting of an abnormally long QT interval. While the most common cause is treatment with QT prolonging drugs, torsade de pointes also occurs in the congenital long QT syndromes and in the setting of acquired heart block or severe electrolyte disturbance, notably hypokalemia. Among QT prolonging drugs that cause torsade de pointes, both antiarrhythmics and “noncardioactive” drugs have been recognized. The electrocardiographic features of torsade de pointes include labile QT intervals, prominent U waves, and a “pause-dependent” onset of the arrhythmia. Treatment consists of recognition of the syndrome, correction of underlying electrolyte abnormalities, and withdrawal of any offending drugs. Magnesium, isoproterenol, or cardiac pacing provides specific antiarrhythmic therapy in torsade de pointes.     

Biventricular pacing and QT interval prolongation

Introduction: The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB).
Methods and Results: One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 ± 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 ± 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 ± 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 ± 9 ms during BiV pacing vs 178 ± 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 ± 34 ms with BiV pacing versus 445 ± 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 ± 9 ms vs 320 ± 20 ms, P < 0.0001). During a mean follow-up of 24 ± 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued.
Conclusion: Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.     

Torsade de pointes due to prenylamine controlled by lignocaine

Four patients are described with prenylamine toxicity. Thesepatients developed life-threatening ventricular arrhythmiasdue to QT prolongation. The ventricular arrhythmias includingpolymorphous ventricular tachycardia (‘torsade de pointes’)responded immediately to lignocaine administration. We stressthe need of a careful follow-up in older patients who receiveprenylamine.     

Cellular Basis for Complex T Waves and Arrhythmic Activity Following Combined IKr and IKs Block

INTRODUCTION: A growing number of cardiomyopathies have been shown to result in a reduction in both I(Kr) and I(Ks) yet little is known about the electrophysiologic and ECG characteristics of combined I(Kr) and I(Ks) block. METHODS AND RESULTS: To address this gap in our knowledge, transmembrane action potentials (APs) from epicardial, M, and endocardial cells were recorded simultaneously, together with a transmural ECG from arterially perfused canine left ventricular wedge preparations exposed to combined I(Kr) (d-sotalol; 100 micromol/L) and I(Ks) (chromanol 293B; 30 to 60 micromol/L) block. Under baseline conditions, the T wave was typically upright; epicardium repolarized first, coinciding with the peak of the T wave, and the M cells repolarized last, coinciding with the end of the T wave (T(end)). Complex (inverted, biphasic, and triphasic) T waves developed following combined I(Kr) and I(Ks) block. M and epicardial APs prolonged dramatically, so that the endocardial AP was now the earliest to repolarize, coinciding with the first nadir of the complex T wave. In the case of biphasic/triphasic or inverted T waves, Tend coincided with repolarization of either M or epicardial cells, whichever was the last to repolarize. QT intervals prolonged from 286+/-13 msec up to 744+/-148 msec and transmural dispersion of repolarization (TDR) increased from 33+/-10 msec up to 244+/-71 msec. Early afterdepolarizations (EADs) developed in M and epicardial cells, evoking extrasystoles that precipitated polymorphic ventricular tachycardia. Acceleration-induced EADs and T wave alternans also were observed. CONCLUSION: Combined I(Kr) and I(Ks) block gives rise to inverted, biphasic, and triphasic T wave morphologies, a dramatic increase in TDR, and a high incidence of EADs. The diversity of T wave morphologies derives from a preferential AP prolongation of different transmural layers leading to variation in the predominance of voltage gradients on either side of the M cell region. Our study provides direct evidence linking EADs that arise in ventricular epicardial and M cells to the triggered beats that precipitate polymorphic ventricular tachycardia. Our results also suggest possible guidelines for the estimation of TDR from complex T waves appearing in the precordial leads of the surface ECG.     

Alcoholic liver cirrhosis complicated with torsade de pointes during plasma exchange and hemodiafiltration

Received: March 8, 2000 / Accepted: October 20, 2000     

Torsade de pointes complicating drug treatment of low-malignant forms of arrhythmia: Four case reports

In patients with malignant ventricular arrhythmias, antiarrhythmic therapy is known to carry a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias, in whom antiarrhythmic therapy was used and resulted in documented ventricular fibrillation or torsade de pointes. In Cases No. 1 and 2, atrial fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-12 h after conversion to sinus rhythm, documented the spontaneous occurrence of torsade de pointes degenerating into ventricular fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient suffering dilative cardiomyopathy. After 6 days of treatment at a heart rate of 54 beats/min, a marked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillation. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of the QTc-time was documented in Cases No. 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyarrhythmias. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when “benign” cardiac arrhythmias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection of antiarrhythmic agents when used in combination.