索他洛尔致尖端扭转性室性心动过速一例

患者女性 ,47岁 ,因胸闷、心悸 2周入院。体格检查 :血压 130 /70ｍｍＨｇ(1ｍｍＨｇ =0 133ｋＰａ) ,神志清楚 ,口唇无紫绀 ,无颈静脉怒张 ,心率 83次 /ｍｉｎ ,心律不齐 ,可闻早搏3～ 5次 /ｍｉｎ ,未闻及心脏杂音 ,肝、脾未触及 ,双下肢无浮肿。实验室检查 :血清钾 4 6ｍｍｏｌ/Ｌ ,血清镁 0 95ｍｍｏｌ/Ｌ ,血清氯、钠、钙均正常。心电图示 :窦性心律 ,频发室性早搏 ,ＱＴｃ间期 0 44ｓ(图 1Ａ)。 2 4ｈ动态心电图示 :窦性心律 ,频发室性早搏 176 81次 /2 4ｈ。超声心动图示心脏各房室内径大小正常 ,左心室后壁及室间隔均不厚 ,左心…     

Torsade de pointes induced by N-acetylprocainamide

N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide. Initial evaluation with an intravenous infusion of NAPA indicated a favorable antiarrhythmic response. The QTC interval was prolonged, but the 2.4 ms/microgram per ml incremental QTC interval lengthening caused by NAPA was not greater than usual. During subsequent oral therapy with NAPA, torsade de pointes developed at plasma levels of this drug that appeared to be well tolerated during the initial evaluation.     

Torsade de pointes induced by citalopram and amiodarone

Long QT syndrome (LQTS) is a disorder of myocardial repolarization characterized by a prolonged QT interval on the electrocardiogram (ECG). This disorder is associated with an increased risk of torsade de pointes (TdP). We report a case of TdP induced by citalopram, a selective serotonin reuptake inhibitor (SSRI), taken in conjunction with amiodarone.     

Torsade de pointes

The polymorphic ventricular tachycardia torsade de pointes can occur in the congenital long QT syndromes or as a consequence of therapy with QT-prolonging drugs. The latter can include not only antiarrhythmic drugs such as quinidine, but also a number of drugs which are not usually considered to have major cardiovascular effects: these include nonsedating antihistamines, such as terfenadine; antibiotics such as erythromycin; and neuroleptics such as thioridazine. The electrocardiographic hallmark of both the congenital and acquired forms of the long QT syndrome is marked QT(U) lability, particularly as a function of heart rate. The underlying mechanism is thought to be triggered activity arising as a consequence of early afterdepolarizations. An understanding of the basic mechanism has led to an understanding of the effective forms of therapy, which include maneuvers to include the heart rate (pacing, isoproterenol) as well as maneuvers which may not necessarily alter the QT interval but may prevent the arrhythmia (magnesium, beta blockers). Intensive study of the clinical features and basic mechanisms underlying torsade de pointes has led to the definition of a new mechanism for cardiac arrhythmias; understanding such mechanisms may ultimately lead to the development of safer antiarrhythmic therapy.     

Torsade de pointes

The evaluation of syncope in severe aortic stenosis usually requires intense work-up. Mechanical obstruction should not always be implicated as the underlying cause of syncope. Syncope at rest may be rarely associated with ventricular arrhythmias. We present a patient with severe aortic stenosis who experienced syncopal events due to torsade de pointes.     

Torsade de pointes

Prolonged QT or QU intervals can be caused by a variety of conditions which include drugs, electrolyte imbalance, and acquired and congenital diseases. This finding is associated with life-threatening ventricular arrhythmias that, at times, have unusual morphologies characteristically named "torsade de pointes." Treatment, when iatrogenic, is obvious--when due to acute acquired diseases, therapy is supportive until the acute phase passes. In congenital prolonged QT syndromes, primidone (Mysoline) recently has been found to be successful in long-term management.     

Torsade de pointes

Torsade de pointes ventricular tachyarrhythmia in the long QT syndrome is a prime example of how molecular biology, ion channel, and cellular and organ physiology, coupled with clinical observations, promise to be the future paradigm for advancement of medical knowledge. Both the congenital and the acquired long QT syndrome are caused by abnormalities (intrinsic, acquired, or both) of the ionic currents underlying ventricular repolarization. In this review, the continually unraveling molecular biology of congenital long QT syndrome is discussed. The various pharmacologic agents associated with the acquired long QT syndrome are listed. Although it is difficult to predict which patients are at risk for torsade de pointes, careful assessment of the risk to benefit ratio is important before prescribing drugs known to cause QT prolongation. The in vivo electrophysiologic mechanism of torsade de pointes in the long QT syndrome is described, using as a paradigm the anthopleurin-A canine model, a surrogate for LQT3. The characteristic association of torsade de pointes with T-wave alternans and short-long cardiac sequences is discussed, with emphasis on electrophysiologic mechanisms. Finally, the expanding knowledge of genetic mutations other than long QT syndrome associated with polymorphic ventricular tachyarrhythmia is emphasized.     

Torsade de pointes induced by short-term oral amiodarone therapy.

Although amiodarone appears to have few pro-arrhythmic effects, torsade de pointes (TdP) has been observed during long-term drug administration, usually in conjunction with electrolyte disturbances, a change in drug dosage, or concomitant drug therapy. We report two cases of amiodarone-induced TdP shortly after administration of a low dose of oral amiodarone, in the absence of predisposing factors.     

Methadone-induced Torsade de pointes tachycardias

Methadone is a synthetic opioid frequently used in drug maintenance programs for heroin addicts. It prolongs the QT-interval and is mainly metabolized by the isoenzyme CYP3A4 of the hepatic cytochrome-P450-system, which is used by numerous other QT-prolonging agents. Its most severe side effect is the development of life-threatening Torsade de pointes ventricular tachycardia in the setting of a prolonged QT-interval. Since drug addicts are prone to concomitant medical conditions requiring additional medication as well as to continued abuse of cocaine, they are at higher risk for developing this major complication of methadone therapy. Before subjecting patients on methadone to other drugs, the QT-interval should be determined and it should be ascertained whether the new agent has the property to prolong the QT-interval or is metabolised by the cytochrome-P450 system.     

Torsade de pointes induced by quinidine: a case treated successfully with verapamil

The Authors report a case of incessant torsade de pointes, associated with QT prolongation, due to the proarrhythmic effect of quinidine, which was successfully treated with i.v. verapamil. The arrhythmia occurred after oral administration of quinidine polygalacturonate (550 mg + 275 mg + 275 mg over a 4-hour period) for the conversion of atrial fibrillation in a 41-year-old woman with mild mitral stenosis and regurgitation. Verapamil was administered as an i.v. bolus (5 mg at a rate of 1 mg/min) and with in four minutes the arrhythmia disappeared. The electrophysiological mechanisms of torsade de pointes and the potential role of Ca+(+)-channel-blocking agents in its treatment are briefly discussed.     

Torsade de pointes induced by terfenadine in a patient with long QT syndrome

Torsade de pointes is a form of polymorphic ventricular tachycardia that is associated with prolongation of the QT interval. Although torsade de pointes is found in many clinical settings, it is mostly drug induced. Similar problems have been described with nonsedating H₁-receptor antagonists, such as astemizole and terfenadine. Terfenadine is a widely used antihistamine. The authors report a case of torsade de pointes in a patient with a possible congenital sporadic form of QT interval prolongation who was receiving a therapeutic dose of terfenadine.     

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.     

Torsade de pointes induced by hypocalcemia in a postoperative patient with thyrotoxicosis.

A 29-year-old woman with a long-term history of Graves' disease was admitted for thyroidectomy. Torsade de pointes occurred after the subtotal thyroidectomy. The level of her serum calcium was lower than normal. After administration of calcium gluconate intravenously, torsade de pointes disappeared and was no longer recorded. It is assumed that her torsade de pointes was caused by hypocalcemia as a complication of subtotal thyroidectomy.