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Background-The present study examined pacing site-dependent changes in QT interval and transmural dispersion of repolarization (TDR) and their potential role in the development of torsade de pointes (TdP). Methods and Results-In humans, the QT interval, JT interval, and TDR were measured in 29 patients with heart failure during right ventricular endocardial pacing (RVEndoP), biventricular pacing (BiVP), and left ventricular epicardial pacing (LVEpiP). In animal experiments, pacing site-dependent changes in ventricular repolarization were examined with a rabbit left ventricular wedge preparation in which action potentials from endocardium and epicardium could be simultaneously recorded with a transmural ECG. In humans, LVEpiP and BiVP led to significant QT and JT prolongation. LVEpiP also enhanced TDR. Frequent R-on-T extrasystoles generated by BiVP and LVEpiP but completely inhibited by RVEndoP occurred in 4 patients, of whom 1 developed multiple episodes of nonsustained polymorphic ventricular tachycardia and another suffered incessant TdP. In rabbit experiments, switching from endocardial to epicardial pacing produced a net increase in QT interval and TDR by 17Ϯ5 and 22Ϯ5 ms, respectively (nϭ6, PϽ0.01), without parallel increases in ventricular transmembrane action potential durations. Epicardial pacing facilitated transmural propagation of early afterdepolarization, leading to the development of R-on-T extrasystoles and TdP in the presence of action potential duration-prolonging agents. Conclusions-LVEpiP

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Witnessed sudden cardiac death due to paroxysmal atrioventricular (AV) block during ambulatory monitoring occurred in a 56‐year‐old female with primary conduction system disease. The control tracings showed right bundle branch block. Holter recordings obtained during the fatal event revealed paroxysmal complete AV block followed by ventricular asystole of approximately 13 seconds which, in turn, preceded the emergence of a slow idioventricular rhythm. The patient was definitely alive 5 minutes and 10 seconds following the onset of the AV block (since she activated the event marker in the recorder twice) and, possibly, 8 minutes later. Complete AV block persisted until the cessation of all cardiac activity, which took place 47 minutes following the occurrence of AV block. It is very likely that this patient could have been resuscitated in a city having a rapidly responding rescue squad.

A 6-year-old female with congenital long QT syndrome (LQTS) presented to the hospital with recurrent syncope. She had frequent episodes of Torsade de pointes (TdP) that occurred at night during the hospital stay. The Figure shows interesting recordings from her telemetry monitor. In panel A, on first glance, the patient seemed to be in sinus bradycardia with a heart rate (HR) of 48 beats per minute (bpm) with abnormally long QT interval of 840 ms and bifid T waves. After a closer look, it became clear that the patient was actually in 2:1 AV block with P wave marching out regularly at a rate of 96 bpm, and ventricular rate was 48 bpm. When every other P wave arrived at the His-Purkinje system or ventricular myocytes, most likely they were still repolarizing and hence refractory, so the electrical impulse failed to propagate from the atria to the ventricles. When QT interval abbreviated to 680 ms due to spontaneous variation, refractory period of ventricular tissue shortened, thereby impulse was able to conduct normally (Panel B). With a HR of 125 bpm and rate-dependent shortening in the QT interval (Panel C), the T waves completely engulfed the P waves. The location of 2:1 AV block in this case is unlikely to be at the AV node, but it is rather at the His-Purkinje system or ventricular myocytes. Moreover, block is unlikely to be Figure.related to a disease of conduction system but is simply due to physiological block related to prolonged refractoriness as evident in panel B, where AV block disappears with abbreviation of QT interval. The 2:1 AV block related to conduction system abnormality has been reported in some infants with congenital LQTS, and many of these infants required permanent pacemaker implantation. 1 Our patient received an implantable cardioverter-defibrillator that was also programmed to prevent bradycardia. Reference