DRUG-INDUCED TORSADE-DE-POINTES - INCIDENCE, MANAGEMENT AND PREVENTION

被引:67
作者
FABER, TS
ZEHENDER, M
JUST, H
机构
[1] Innere Medizin III, Medizinische Universitätsklinik Freiburg, Freiburg, 79106
关键词
D O I
10.2165/00002018-199411060-00007
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Torsade de pointes is a particular form of polymorphic ventricular tachycardia causing few haemodynamic symptoms, but carries a poor prognosis because of recurrence and sudden death in up to 31% of patients. A wide range of agents have been shown to aggravate and even to cause torsade de pointes by prolonging the QT interval or increasing QT dispersion. For the majority of substances the incidence of torsade de pointes remains unclear, but is of the order of 3 to 15% for a wide range of agents. Elicitation of proarrhythmia by drug-induced QT prolongation is mainly based on increased cellular excitability and/or abnormal dispersion of ventricular repolarisation. Torsade de pointes has been shown to be related to bradycardia-dependent early after-depolarisations and/or increased dispersion of repolarisation. Clinically, patients with predisposing factors prior to medication should be considered at risk of drug-mediated proarrhythmic therapy. During this phase, QT interval measurement and assessment of the QTc time should be performed frequently. Phases of bradycardia or occurrence of ventricular extra beats with a long coupling interval may be of help to identify patients at high risk of proarrhythmic events. As a first attempt in managing this arrhythmia, magnesium sulphate has been shown to be effective in many patients. In case of recurrence of torsade de pointes, the use of a temporary pacemaker with pacing at about 100 to 120 beats/min is the therapy of choice until the causative agent has been completely eliminated.
引用
收藏
页码:463 / 476
页数:14
相关论文
共 152 条
[1]  
Dessertenne F., Un chapitre nouveau d’electrocardiographic: les variations progressives de l’amplitude de l’electrocardio-gramme, Actual Cardiol Angiol Int, 15, (1966)
[2]  
Dessertenne F., La tachycardia ventriculaire a deux foyers opposes variable, Arch Mal Coeur Vaiss, 59, (1966)
[3]  
Sasyniuk B.I., Valois M., Toy W., Recent advances in understanding the mechanisms of drug-induced torsades de pointes arrhythmias, Am J Cardiol, 64, 20, pp. 29J-32J, (1989)
[4]  
Abildskov J.A., Effects of activation sequence on local recovery of ventricular excibility in the dog, Circ Res, 38, (1976)
[5]  
Abildskov J.A., The ventricular gradient and repolarization, Jpn Heart J, 27, pp. 197-204, (1986)
[6]  
Day C.P., McComb J.M., Campbell R.W.F., QT dispersion: an indication of arrhythmia risk in patients with long QT intervals, Br Heart J, 63, (1990)
[7]  
Hii J.T.Y., Wyse D.G., Gillis A.M., Et al., Precordial QT interval dispersion as a marker of torsade de pointes. Disperate effects of class la antiarrhythmic drugs and amiodarone, Circulation, 86, (1992)
[8]  
Bonatti V., Rolli A., Botti G., Recordings of monophasic action potentials of the right ventricle in long QT syndromes complicated by severe ventricular arrhythmias, Eur Heart J, 4, (1983)
[9]  
Singh B.N., When is QT prolongation antiarrhythmic and when is it proarrhythmic?, Am J Cardiol, 63, (1989)
[10]  
Selzer A., Wray H.W., Quinidine syncope. Paroxysmal ventricular fibrillation occurring during treatment of chronic atrial arrhythmias, Circulation, 30, pp. 17-26, (1964)