Effect of epicardial or biventricular pacing to prolong QT interval and increase transmural dispersion of repolarization: does resynchronization therapy pose a risk for patients predisposed to long QT or torsade de pointes?

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.

Death due to paroxysmal atrioventricular block during ambulatory electrocardiographic monitoring.

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.

Management of tachyarrhythmias with dual-chamber pacemakers.

Multiprogrammable dual-demand AV sequential (DVI, MN) pacemakers were implanted in twenty-three patients (in one of them a DVI, MN unit was used as a VVI, MN with the aid of an atrial plug) with supraventricular tachycardias after electrophysiological studies revealed a great variety of AV reentry circuits. The latter included tachycardias involving accessory pathways of the Kent type, manifest or concealed Wolff-Parkinson-White syndromes, nodo-ventricular (Mahaim) tracts, "enhanced" AV node (or extra AV nodal) pathways and dual AV pathways. In addition, multiprogrammable "non-committed" AV sequential (DVI, MN and DDD, M) pacemakers were permanently implanted to treat different forms of ventricular tachyarrhythmias that included: torsade de pointes in the Romano-Ward syndrome and Chagas' cardiomyopathy, ventricular tachycardia which is bradycardia-dependent (in Chagas' cardiomyopathy) and reciprocal beats induced by, and producing severe hemodynamic derangements in a patient with a conventional VVI unit.

Treatment of drug resistant A-V reciprocating tachycardias with multiprogrammable dual demand A-V sequential (DVI,MN) pacemakers.

Programmable dual A-V sequential demand (DVI,MN) pacemakers were implanted in eight patients with recurrent or incessant, drug-refractory, A-V reciprocating tachycardias. This was done after intracardiac studies had identified a variety of electrogenetic mechanisms which include tachycardias involving Kent bundles, (manifest or concealed Wolff-Parkinson-White syndrome), nodoventricular (Mahaim) fibers, enhanced A-V node pathways (Lown-Ganong-Levine syndrome), and dual intranodal pathways. The antitachycardia features of the pacemaker were evaluated during the electrophysiological studies.

His bundle recordings in double tachycardias not due to digitalis intoxication.

Electrophysiological studies were performed in a patient with chronic chagasic cardiomyopathy, recurrent sustained ventricular tachycardia, and a history (without electrocardiographic documentation) of paroxysmal atrial flutter. Ventriculoauricular conduction occurred during short bursts of ventricular pacing. Moreover, the retrograde P of ectopic ventricular beats which appeared after pacing was stopped precipitated an atrial tachyarrhythmia with an irregular atrial rate.

Electronic pacemaker models of parasystole. With special reference to artificial intermittent parasystole with phase 3 and phase 4 protection and to parasystolic modulation.

This study deals with a method of analysis of artificial pacemaker function which can be used to understand the electrocardiographic manifestations of some spontaneous rhythms. The modes of operation of 11 normally-functioning QRS-inhibited (VVI) pacemakers resembled those of spontaneous automatic nonprotected (nonparasystolic) rhythms. The function of 11 continuous asynchronous (fixed rate or VOO) pacemakers was similar to that of continuous-parasystolic rhythms.

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of Wolff-Parkinson-White Syndrome.

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus.