Right ventricular endocardial monophasic action potential recordings were obtained in a patient with a qunidine-induced long QTU interval and polymorphic ventricular tachycardia of the torsade de pointes type. The recording showed a deflection on phase 3 repolarization characteristic of early afterdepolarization. The early afterdepolarization was synchronous with the U wave in surface electrocardiographic leads and there was a strong correlation between the amplitude of both waves. A strong correlation was also present between the cardiac cycle length and the U wave amplitude with larger amplitudes after longer cycles. Ventricular ectopic beats occurred only after long cycle lengths and seemed to arise close to the peak of the U wave and early afterdepolarization. However, there was no correlation between the amplitude of the U wave or early afterdepolarization and the occurrence of ectopic beats. Rapid ventricular pacing resulted in suppression of the ectopic rhythm associated with suppression of both the U wave and the early afterdepolarization. This case provides the first evidence to suggest that a quinidine-induced long QTU interval and torsade de pointes may be related to bradycardia-dependent early afterdepolarizations, although other factors may be involved in triggering the arrhythmia.

The AFFIRM Study enrolled 4060 predominantly elderly patients with atrial fibrillation to compare ventricular rate control with rhythm control. The patients in the AFFIRM Study were representative of patients at high risk for complications from atrial fibrillation, which indicates that the results of this large clinical trial will be relevant to patient care.

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SUMMARY The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos >two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index < 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients.The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.The initiation of ventricular arrhythmia by supraventricular extrasystoles is uncommon."2 The initiation of ventricular fibrillation by supraventricular extrasystoles in patients with acute myocardial infarction has been rarely reported.34 To assess the role of supraventricular extrasystoles in the initiation of ventricular fibrillation in patients with acute myocardial infarction we critically analysed the mode of initiation of the tachycardia in 72 consecutive patients in whom the onset of one or more episodes of ventricular fibrillation was recorded.

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