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Excessive QT interval prolongation (long QT syndrome) is an increasingly recognised cause of malignant ventricular tachyarrhythmias, including torsades de pointes. Various mechanisms may cause the net increase of inward transmembrane ion currents underlying tor-sades de pointes. 1 In congenital long QT syndrome, torsades de pointes usually follows from increased adrenergic tone; in acquired long QT syndrome, torsades de pointes is associated with bradycardia. Torsades de pointes has been reported during AV block associated bradycardia. 2 This report demonstrates torsades de pointes suppression by atropine in a patient with bradycardia secondary to high grade AV block.
Case report
A 67 year old woman with a history of chronic atrial fibrillation was admitted for asthma cardiale. She took no medication. There was no family history of long QT syndrome. The ECG showed atrial fibrillation with a ventricular rate of 150-180 beats/min without ischaemia. The QT interval was 0.25 s and the rate corrected (Bazett) QT interval (QTc) 0.45. Laboratory analysis showed normokalaemia and minimal myocardial damage (creatine kinase MB 8.4 μg/l exceeded our laboratory's normal level of 7). We administered furosemide, nitroprusside, acenocoumarol, and digoxin. Ventricular rate slowed to 80-90 beats/min. However, after two days, excessively prolonged RR intervals, which were terminated by escape beats with a right bundle branch block morphology, suggested impending total AV block. Furthermore, there was a severe...