Torsade de pointes (TdP) syncopal episodes were almost invariably precipitated by emotional stress or menstruation in a 17-year-old girl. U wave accentuation occurred during sinus rhythm without pauses in periods of heightened sympathetic tone. To examine the role of early afterdepolarization (EAD), monophasic action potentials were recorded during ventricular extrasystoles and TdP occurring spontaneously and induced by ventricular pacing. The effects of lidocaine, verapamil, propranolol, and epinephrine were assessed. Our data show that: (1) EAD plays a significant role in the genesis of familial long QTU syndrome and TdP; (2) rapid ventricular pacing causes postpause-dependent EADs, U waves, and TdP; and (3) EAD is enhanced by epinephrine infusion in the absence of pause, whereas EAD-triggered firing is inhibited by verapamil and propranolol but not by lidocaine.

The hemodynamic responses of atrial (AP), atrioventricular sequential (AVP) and ventricular pacing (VP) were compared to sinus rhythm (SR) in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg), mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm-5), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrioventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were: (Chart: See text) The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p less than 0.01) and systemic vascular resistance (SVR) (p less than 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p less than 0.05).

Early Afterdepolarizations in Long QTU Syndrome. Torsade de pointes‐induced syncopal episodes were almost invariably precipitated by emotional stress or menses in a 17‐year‐old female. U wave accentuation occurred during periods of heigbtened sympathetic tone. To document tbe role of early afterdepolarizations (EADs), monopbasic action potentials were recorded during ventricular extrasystoles and torsade de pointes occurring spontaneously and induced by ventricular pacing in tbe control state and after intravenous lidocaine. The effects of verapamil, propranolol, and epinephrine were observed. Our data show that: (1) EADs may play a significant role in the genesis of familial long QTU syndrome and torsade de pointes; (2) a faster ventricular pacing rate for a longer duration is related to tbe emergence of subsequent pause‐dependent EADs, U waves, and torsade de pointes; (3) atrial pacing with Wenckebach block can provoke large postpause U waves, thus eliciting dual ventricular tachycardia; (4) EADs are enhanced by epinepbrine infusion in the absence of pause; and (5) EAD‐triggered firing is inhibited by verapamil and propranolol but not by lidocaine. (J Cardiovasc Electrophysiol. Vol. 3, pp. 431–436, October 1992)

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