QT Prolongation and Torsade de Pointes Ventricular Tachycardia Produced by Ketanserin

A 65-year-old man with arterial hypertension received oral treatment with Ketanserin, a new drug, during a period of five months. He developed marked QT interval prolongation and have several Stokes-Adams attacks. A Holter recording obtained during one of these episodes showed torsade de pointes ventricular tachycardia. The arrhythmias occurred during maximum QT interval prolongation, The correlation between Ketanserin and QT interval prolongation was evaluated by using several Holter studies during administration and withdrawal of the drug. The effect of Ketanserin on the QTc interval was analyzed retrospectively in six patients who had been taking the drug orally. Following a period of four to eight months, the QTc interval was prolonged by the drug (5 to 31%, mean 17%) in five patients. We conclude that torsade de pointes is a potential hazard of long-term treatment with Ketanserin.     

Torsade de pointes as a complication of brainstem encephalitis

A case of brainstem encephalitis complicated by torsade de pointes is described. The possible occurrence of ventricular arrhythmias may contribute to the mortality in this condition. We recommend the admission of patients with brainstem encephalitis to an intensivve care unit, for a period of electrocardiographic monitoring.

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Torsade de pointes as a complication of brainstem encephalitis

     

Propafenone-Induced Torsade de Pointes: Cross-Reactivity with Quinidine

A 77-year-oid/emale with new onset atrial fibrillation occurring in the absence of structural heart disease developed torsade de pointes during therapy with quinidine bisulfate 500 mg orally every 8 hours. Ten days after quinidine therapy had been discontinued she developed torsade de pointes while receiving propafenone 300 mg orally every 8 hours. This case demonstrates that propafenone may be associated with torsade de pointes and suggests a cross-reactivity between this effect and prior occurrence of torsade de pointes on Class IA antiarrhythmic drug therapy.     

Torsade de Pointes and Other Pause-Induced Ventricular Tachycardias: The Short-Long-Short Sequence and Early Afterdepolarizations

The early after depolarization, which is an interruption of repolarization, can evoke a second upstroke or a salvo of action potentials. It is suggested that the electrophysiological characteristics of the early after depolarization can produce a lengthening of the QT interval and that the second upstroke and salvo of activity that may follow, it can explain many features of torsade de pointes and of certain other ventricular tachycardias. The early after depolarization, torsade de pointes, and repetitive monomorphic idiopathic ventricular tachycardia are all induced hy bradycardia or by a preceding long RH interal. The R-on-T phenomenon is also discussed.     

Risk of Torsades de Pointes From Oral Erythromycin with Concomitant Carbimazole (Methimazole) Administration

There are many reports of intravenous erythromycin causing QT prolongation and torsades de pointes, but this complication is seldom ascribed to orally administered erythromycin, which is by far the most commonly prescribed route. This report describes a case of torsades de pointes associated with oral erythromycin as a result of a previously undescribed interaction with carbimazole, an antithyroid drug that is metabolized to the active drug methimazole, and the potential pharmacokinetic and pharmacodynamic mechanisms are highlighted.     

Inconsistent shock advisories for monomorphic VT and Torsade de Pointes – A prospective experimental study on AEDs and defibrillators

BackgroundCardiovascular disease and sudden cardiac arrest are the leading causes of death in the United States. Early defibrillation is key to successful resuscitation for patients who experience shockable rhythms during a cardiac arrest. It is therefore vital that the shock advisory of AEDs (automated external defibrillators) or defibrillators in AED mode be reliable and appropriate. The goal of this study was to better understand the performance of multiple lay-rescuer and hospital professional defibrillators in AED mode in their analysis of ventricular arrhythmias. The measurable objectives of this study sought to quantify:

• 1.No shock advisory for sinus rhythms at any rate.
• 2.Recognition and shock advisory for ventricular fibrillation (VF).
• 3.Recognition and shock advisory for monomorphic ventricular tachycardia (VT).
• 4.Recognition and shock advisory for Torsades de Pointes (TdP).

MethodsThis is a prospective evaluation of two AEDs and four semi-automatic, hospital professional defibrillators. This study represents post-marketing evaluation of FDA approved devices. Each defibrillator was connected to multiple rhythm simulators and presented with simulated ECG waveforms 20 consecutive times at various rates when possible.ResultsAll four defibrillators and both AEDs tested consistently recognized normal sinus rhythm (NSR) from all rhythm sources, and did not recommend a shock for NSR at any rate (from 80 to 220 bpm). All four defibrillators and both AEDs recognized VF from all rhythm sources tested and recommended a shock 100% of the time. Variations were found in the shock advisory rates among defibrillators when testing simulated VT heart rates at or below 150 bpm. One AED tested did not consistently advise a shock for monomorphic VT or TdP at any tested rate.ConclusionLay-rescuer AEDs and professional hospital defibrillators tested in AED mode did not reliably recommend a shock for sustained monomorphic VT or TdP at certain rates, despite the fact that it is a critical component of the currently recommended treatment. These findings require further examination of the risk benefit analysis of shocking or not shocking rhythms such as TdP or pulseless VT.     

Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia

We report a 68-year-old man who developed torsades de pointes ventricular tachycardia induced by combined use of mosapride and flecainide. He had a permanent pacemaker (DDD mode) implanted because of sick sinus syndrome (bradytachy syndrome) 6 years earlier. The patient had started taking mosapride for upper abdominal discomfort 2 weeks earlier. On admission, ECG showed prolongation of the QTc interval from 0.48 to 0.56 seconds and self-terminating torsades de pointes occurred. We considered that this proarrhythmia was induced by mosapride in combination with antiarrhythmic agents.     

New-onset QT prolongation and torsades de pointes accompanied by left ventricular dysfunction secondary to acute pancreatitis

A 70-year-old woman presented with acute pancreatitis and new-onset QT prolongation with subsequent torsades de pointes. Coronary catheterization was performed and was unremarkable. After persistent QT prolongation, despite temporary atrial pacing, a permanent dual chamber cardioverter defibrillator was implanted. In addition to the QT prolongation, significant depression in the left ventricular function was noted. Both resolved once the pancreatitis abated.     

高血压性脑室型丘脑出血的治疗

目的　探讨微创治疗对降低高血压性脑室型丘脑出血患者病死率和致残率的意义。方法　Ⅰ～Ⅲ级高血压性脑室型丘脑出血患者 76例 ,均行单侧脑室外引流和反复腰穿治疗。结果　存活 6 6例 ,其中6 7.1%恢复生活自理 ,死亡 10例 (13.2 % )。结论　以脑室外引流加腰穿微创治疗高血压性脑室型丘脑出血 ,可降低病死率、病残率。提出了单侧脑室引流 ,不可减压过快 ,引流时间应按需延长     

Nicorandil, a Potassium Channel Opener, Abolished Torsades de Pointes in a Patient with Complete Atrioventricular Block

TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular fibrillation. Nicorandil, a potassium channel opener, shortened the QT interval and abolished TdP. This may suggest that potassium channel opening drugs are clinically effective against TdP associated with bradycardia-dependent QT prolongation.     

Torsade de pointes induced by ioxaglate intracoronary injection in patients with pre‐existent drug‐induced QT prolongation: case reports and review of literature

We report two cases of torsade de pointes directly related to intracoronary contrast media injection in patients without previous history of neither arrhythmia nor syncope but chronically treated with a drug prolonging ventricular repolarization. We discussed the effects of the contrast medium used on repolarization and concluded that three suggestions may be highlighted from the case reports presented and from the literature: (i) a QT prolongation should be systematically searched before coronary angiography; (ii) it seems important to correct QT prolongation when it results from a reversible cause (such as drug‐induced) before nonurgent coronary angiography; and (iii) if there is no reversible cause explaining QT prolongation, contrast media should be used cautiously in such patient and nonionic iso‐osmolar contrast media should be preferred.     

Mechanisms in Adrenergic Dependent Onset of Torsades de Pointes

Pause dependent onset of torsades de pointes is characteristic in acquired long QT syndromes, and the probable mechanism is reentry facilitated by increased disparity of refractoriness following a long cycle. Adrenergic dependent onset is usual in familial long QT syndromes, and the mechanism is uncertain. In this study with a computer simulation of torsades de pointes, possible mechanisms of adrenergic dependent onset have been identified. Decreased refractory periods facilitated the initiation of torsades de pointes by permitting earlier premature excitation and allowing reentry in the presence of the shorter refractory period that had been further shortened by the earlier excitation. In addition, accelerating rate resulted in responses occurring in the presence of refractory periods set by the prior response so each response was premature with respect to the preceding one. The difference between cycle lengths and refractory period decreased with increasing rate leading to the functional block required for initiation of simulated torsades de pointes. Findings define possible mechanisms in which the adrenergic effects of reduced refractory period duration and increased rate may lead to the initiation of torsades de pointes.     

Torsades de Pointes from Terfenadine and Sotalol Given in Combination

A patient receiving sotalol developed recurrent torsades de pointes following the addition of terfenadine (Seldane) to her medical regimen. A 71-year-old woman with a history of atrial fibrillation successfully suppressed with sotalol, 80 mg bid, was started on terfenadine, 60 mg bid. Eight days later, she developed repeated self-terminating episodes of torsades de pointes. Sotalol and terfenadine were discontinued, and no further arrhythmia was observed after 72 hours of temporary pacing was discontinued.     

Adenosine Induced Torsades de Pointes in a Child with Congenital Long QT Syndrome

Torsades de pointes is a rare arrhythmia characterized by its bradycardia dependence and increased adrenergic discharge, whether it occurs as a congenital anomaly or as an acquired problem resuiting from drug intoxication or other conditions. There are no reliable tests to assess the propensity toward torsades de pointes or evaluate the efficacy of treatment in these patients. Adenosine can result in marked slowing of sinus and ventricular rate and leads to increased sympathic discharge when given intravenously. We induced torsades de pointes in a child with congenital long QT syndrome (Jervell-Lange-Nielsen syndrome) using 200 μg/kg IV adenosine bolus. Higher dosage of adenosine (600 μg/kg) did not lead to torsades de pointes after β blockade. Adenosine may induce torsades de pointes in patients with the long QT syndrome and may be used as a test to reproduce the clinical arrhythmia. Whether adenosine proves to be useful for assessing the efficacy of treatment will require extensive investigation in larger series of patients.     

Role of Early Afterdepolarization in Familial Long QTU Syndrome and Torsade de Pointes

Torsade de pointes (TdP) syncopal episodes were almost invariably precipitated by emotional stress or menstruation in a 17-year-old girl. V wave accentuation occurred during sinus rhythm without pauses in periods of heightened sympathetic tone. To examine the role of early afterdepolarization (EAD), monophasic action potentials were recorded during ventricular extrasystoles and TdP occurring spontaneously and induced by ventricular pacing. The effects of lidocaine, verapamil, propranolol, and epinephrine were assessed. Our data show that: (1) EAD plays a significant role in the genesis of familial long QTU syndrome and TdP; (2) rapid ventricular pacing causes postpause-dependent EADs, U waves, and TdP; and (3) EAD is enhanced by epinephrine infusion in the absence of pause, whereas EAD-triggered firing is inhibited by verapamil and propranolol but not by lidocaine.     

新生儿颅内出血90例观察与护理

目的:探讨新生儿颅内出血(ICH)患儿的护理方法及其效果.方法:对90例新生儿颅内出血患儿进行回顾性分析,总结其护理方法及效果.结果:本组90例,治愈78例(86.7%),死亡12例(13.3%).对治愈的78例随访3个月,70例(89.7%)精神、发育、运动、智力正常.结论:认真观察新生儿颅内出血患儿的生命体征、有无惊厥、意识和精神状态、囟门、摄入情况,采取吸氧并保持呼吸道通畅、降低颅内压、保持正常体温、营养支持、并发症的治疗等治疗护理措施,可提高ICH的治愈率,降低后遗症的发生率与病死率.     

Torsades de Pointes Ventricular Tachycardia Induced by Clarithromycin and Disopyramide in the Presence of Hypokalemia

We report a 76-year-Old woman who developed TdP ventricular tachycardia induced by combined use of clarithromycin and disopyramide. She had a history of myocardial infarction 5 years earlier and has taken disopyramide for supraventricular arrhythmias. In addition, she had taken clarithromycin for upper respiratory tract infection. On admission, an ECG showed prolongation of QTc interval to 0.71 seconds and self-terminating TdP occurred several times. Disopyramide was metabolized by the cytochrome enzyme CYP3A4 and clarithromycin competitively inhibits this enzyme, probably resulting in an increase in plasma concentration of disopyramide. We should consider this possibility when prescribing clarithromycin in combination with antiarrhythmic agent disopyramide.     

Torsade de pointes ventricular tachycardia during low dose intermittent dobutamine treatment in a patient with dilated cardiomyopathy and congestive heart failure

The authors describe the case of a 56-year-old woman with chronic, severe heart failure secondary to dilated cardiomyopathy and absence of significant ventricular arrhythmias who developed QT prolongation and torsade de pointes ventricular tachycardia during one cycle of intermittent low dose (2.5 mcg/kg per min) dobutamine. This report of torsade de pointes ventricular tachycardia during intermittent dobutamine supports the hypothesis that unpredictable fatal arrhythmias may occur even with low doses and in patients with no history of significant rhythm disturbances. The mechanisms of proarrhythmic effects of Dubutamine are discussed.