TORSADE-DE-POINTES COMPLICATING DRUG-TREATMENT OF LOW-MALIGNANT FORMSOF ARRHYTHMIA - 4 CASE-REPORTS

Citation
Ts. Faber et al., TORSADE-DE-POINTES COMPLICATING DRUG-TREATMENT OF LOW-MALIGNANT FORMSOF ARRHYTHMIA - 4 CASE-REPORTS, Clinical cardiology, 17(4), 1994, pp. 197-202
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
01609289
Volume
17
Issue
4
Year of publication
1994
Pages
197 - 202
Database
ISI
SICI code
0160-9289(1994)17:4<197:TCDOLF>2.0.ZU;2-D
Abstract
In patients with malignant ventricular anrhythmias, antiarrhythmic the rapy is known to carry a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or b enign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmia s, in whom anti-arrhythmic 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 an d sotalol in combination. In both patients Holter monitoring, 4-12 h a fter 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 e pisodes 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 treatme nt at a heart rate of 54 beats/min, a marked QT increase was associate d with the occurrence of repetitive episodes of polymorphic ventricula r tachycardia degenerating into ventricular fibrillation. None of the patients presented significant electrolyte abnormalities in the labora tory. A pathologic increase of the QTc-time was documented in Cases No . 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn af ter the proarrhythmic event and the patient became free of malignant t achyarrhythmias. Antiarrhythmic therapy also carries a considerable ri sk of proarrhythmia when ''benign'' cardiac arrhythmias are treated. T he risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Specia l attention should be paid to the selection of antiarrhythmic agents w hen used in combination.