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Torsade De Pointes' Ventricular Tachycardia NICHOLAS G Postgraduate Medical Journal (November 1979) 55, 832-835 Postgrad Med J: first published as 10.1136/pgmj.55.649.832 on 1 November 1979. Downloaded from Iatrogenic 'torsade de pointes' ventricular tachycardia NICHOLAS G. KOUNIS M.D. Chest Branch, East Birmingham Hospital, Birmingham, England Summary (Krikler and Curry, 1976) myocardial ischaemia Three patients who developed a distinctive form of (Prinzmetal's variant angina, myocardial infarction), ventricular tachycardia with oscillating QRS axis, electrolytic deficits (hypokalaemia, hypomagnes- while they were receiving drugs known to prolong aemia), acquired heart disease (myocarditis, coron- the repolarization time are described. In one of the ary arteriosclerosis), slow basic rhythm (sino-atrial patients suffering from psychiatric illness and receiving disease, high degree AV block), electrical ventricular psychotropic drugs the arrhythmia was fatal. It is stimulation and congenital disorders with deafness postulated that the tendency to this arrhythmia was (Jervell-Lange-Nielsen syndrome, Romano-Ward- augmented by repeated electric counter shocks and Barlow syndrome) with apparent (or only after negative bathmotropic drugs. Functional factors may exercise as a forme fruste) QT prolongation (Bernuth contribute to the pathogenesis ofthis arrhythmia which et al., 1973). seems to constitute an entity. The following report emphasizes the iatrogenicProtected by copyright. nature of the arrhythmia which can have a fatal Introduction outcome. Paroxysmal ventricular tachycardia in which the QRS axis oscillates over runs of 3 to 20 beats with Case reports definite changes in the direction has been recently Patient I recognized as the result of pharmacological overdose A 68-year-old man was admitted for investigation or side effects of certain drugs (Fazzini, Marchi of his fainting attacks. He had suffered from chronic and Pucci, 1973, 1975; Krikler and Curry, 1976a, bronchitis for 10 years and had had a myocardial b). This arrhythmia constitutes a distinctive type of infarction 2 years before. His fainting attacks started ventricular tachycardia with the accepted term from 2 months before admission when the only medication the French literature of torsade de pointes ventricular was prenylamine lactate tablets 60 mg thrice daily tachycardia (Krikler and Curry, 1976a, b). It is for his angina. A general practitioner who examined caused by prolonged myocardial repolarization time him during one of these episodes, prescribed slow manifested by prolongation of QT or QU interval release isoprenaline tablets 30mg thrice daily http://pmj.bmj.com/ (Bens et al., 1973; Fazzini et al., 1975), which favours because of his slow heart rate following the episode. a state of asynchronous depolarization (Han et al., Although prenylamine had been discontinued, the 1966) and encourages re-entry processes (Raynaud patient continued to have fainting attacks (more et al., 1969; Evans et al., 1976). often now, 3 to 4 times daily) while he was taking The drugs which, so far, have been implicated to isoprenaline for the next 7 days. On admission and induce torsade de pointes ventricular tachycardia during a routine electrocardiogram he fainted owing are cardioactive agents such as quinidine (Rainier- to runs of torsade de pointes ventricular tachycardia Pope et al., 1962; Seizer and Wray, 1964), procain- (Fig. 1). The ECG revealed prolonged Q-T interval on September 26, 2021 by guest. amide (McCord and Taguchi, 1951; Castellanos and (QTc 0.75 s), increased ventricular ectopic activity Salhanick, 1967), and lignocaine (Krikler and and prominent U waves. Successive treatment with Curry, 1976a), antianginal drugs such as prenyl- bolus lignocaine, followed by intravenous infusion, amine (Puritz et al., 1977) and amiodarone (Bens quinidine sulphate tablets 200 mg 4 times daily, et al., 1973), psychotropic agents (Fowler et al., and repeated (18) DC countershocks, although 1976), such as phenothiazines (chlorpromazine, initially successful, seemed to worsen the condition thioridazine, trifluoperazine, mesoridazine) and and made the episodes more frequent. Chest X-ray, tricyclic antidepressants (amitriptyline, imipramine, ECG electrolytes and urinary catecholamines were protriptiline, nortriptyline,) diuretics, corticosteroids normal. Cardiac screening revealed systolic expan- and glycyrrhizin (Bens et al., 1973), which induce sion at cardiac apex consistent with a ventricular hypokalaemia. Torsade de pointes can complicate aneurysm. Electrophysiological studies showed 0032-5473/79/1100-0832 $02.00 ( 1979 The Fellowship of Postgraduate Medicine Case reports 833 Postgrad Med J: first published as 10.1136/pgmj.55.649.832 on 1 November 1979. Downloaded from I .~~~~~~~~~~~~~~~~~~~~~~ FIG. 1. Routine electrocardiogram showing torsade de pointes in leads III and V2. Protected by copyright. prolonged repolarization time, increased ventricular countershocks aggravated the situation. Transvenous ectopic activity to stimuli during the refractory ventricular pacing was introduced but it provoked period and normal SA and AV nodal studies. The ventricular tachycardia culminating in ventricular arrhythmia finally was suppressed with mexiletine fibrillation which did not respond to DC counter- without any sequelae. shocks and the patient died. Post-mortem examina- tion revealed no gross or microscopic cardiac Patient 2 abnormality and histology of the conducting A 63-year-old woman with a 10-year history of system showed normal SA and AV nodes with depression was admitted to hospital after an normal common and bifurcated bundle of His. episode of syncope. The patient was receiving thioridazine hydrochloride tablets 50 mg 4 times Patient 3 daily and amitriptyline hydrochloride tablets 25 A 51-year-old man was admitted to hospital with mg thrice daily at the time of syncope. She gave a severe retrosternal pain and a diagnosis of antero- 2-year history of syncopal attacks but these were septal myocardial infarction was made. The patient http://pmj.bmj.com/ thought to be due to vertebro-basilar insufficiency. was taking, at the time of admission, prednisolone There was no past history of cardiac disease. On tablets 5 mg daily for his bronchial asthma and admission, a routine ECG (Fig. 2) revealed markedly frusemide 40 mg daily for congestive cardiac failure. prolonged Q-T interval (QTc 0'80 s). Clinical exam- The prednisolone tablets had been taken contin- ination revealed no abnormality. Chest X-ray, uously for the last 5 years and the frusemide tablets electrolytes, cardiac enzymes, echocardiogram, for the last one year. Two hours after admission he plasma cortisol and peripheral blood counts were developed acute left ventricular failure and he was on September 26, 2021 by guest. normal. Two days after admission she experienced treated with frusemide 80 mg i.v. and venesection. 2 syncopal attacks accompanied by weakness, He improved thereafter but the following day he dizziness, nausea and vomiting. Electrocardiographic developed 18 episodes of ventricular tachycardia monitoring revealed runs of ventricular tachycardia resembling the torsade de pointes. The plasma resembling the torsade de pointes form. A bolus potassium was 3 mmol/l on admission and 2-8 injection of 100 mg of lignocaine abolished the mmol/l the following day during the attacks of arrhythmias, but while she was on lignocaine infusion arrhythmia. Careful examination of his ECG the arrhythmia reappeared. Treatment with procain- showed U wave accentuation and QT and QU amide hydrochloride 500 mg 4 times daily did not prolongation (QTc 0.78 s). Chest X-ray, echocardio- affect the runs of torsade de pointes and it looked gram, plasma cortisol, urinary potassium excretion likely that quinidine and repeated direct current and peripheral blood counts were normal. His Postgrad Med J: first published as 10.1136/pgmj.55.649.832 on 1 November 1979. Downloaded from Case reports FIG. 2. Electrocardiogram showing marked prolongation of Q-T interval in patient 2. Protected by copyright. arrhythmia was successfully treated with lignocaine with meperidine, hydroxyzine, atropine, morphine and the hypokalaemia with potassium chloride in- and curare and during treatment with trifluoperazine fusion (64 mmol in 24 hr) and spironolactone (Reynolds and Vander Ark, 1976), ventricular tablets 25 mg 4 times daily. No further sequelae arrhythmias have appeared during the transient were noticed during his stay in hospital and after prolongation of QT interval, but they did not his discharge. recur when the QT interval became normal. The long QT interval and the arrhythmias disappeared when Discussion the drug was discontinued. The cases described developed repeated attacks Electrolytic disturbance and especially hypo- of ventricular tachycardia while receiving anti- kalaemia increases the ectopic activity and decreases anginal, psychotropic, inducing hypokalaemia and the conduction velocity in AV node (Curry et al., negative bathomotropic agents. Two of these 1976). This presumably induced the torsade de patients had suffered from ischaemic heart disease pointes in the third patient. The presence of U http://pmj.bmj.com/ also. In all patients the arrhythmia seemed to be waves in the described patients was due to hypo- aggravated by the repeated direct current counter- kalaemia, phenothiazines and negative batho- shocks. In one of the patients histological examina- motropic drug administration. However, in hypo- tion of the conducting system failed to reveal any calcaemia, which is not
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