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. 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.

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. With small-size multiprogrammable units, arrhythmias may be treated by changing parameters non-invasively. By temporary inhibition, one may analyze the underlying rhythm and pacemaker dependency. In patients without chronic atrial flutter/fibrillation who require pacing and possibly tachyarrhythmia control, our experience with multiprogrammable "non-committed" AV sequential pacing has been very satisfactory. The evolution toward newer pacing modes which provide atrial sensing and tracking (DDD), and thus preserve AV synchrony over a wider range of atrial rates, may contribute even further to successful patient management. This may be applicable to pediatric patients as well.

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. No immediate postoperative complications occurred after implantation. Furthermore, during the follow-up periods (4 to 20 months), clinical assessment, ambulatory (Holter) monitoring and invasive (as well as noninvasive) evaluations have confirmed continuous effectiveness in recognizing and automatically terminating the tachycardias. Late pacemaker system malfunction has not occurred. The frequency of the tachycardias and the dosage of concomitantly-administered antiarrhythmic medications were significantly reduced. Furthermore, preliminary studies performed in our laboratory suggest that DVI,MN pacemakers may also be useful in certain types of intra-atrial reentry tachycardias coexisting with sinus node dysfunction.

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. In addition, burst ventricular pacing, performed while this atrial tachyarrhythmia was present, initiated and subsequently terminated a ventricular tachycardia with similar characteristics to the one occurring spontaneously. The double (atrial and ventricular) tachycardias described in this communication were different from those previously reported in that the arrhythmias were not due to digitalis toxicity, but resulted from the modality of ventricular stimulation performed in a patient who had the specific type of cardiomyopathy seen in the chronic stage of Chagas' disease.

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. In 12 patients with malfunctioning QRS-inhibited (VVI) pacemakers, an abnormally-prolonged pacemaker refractory period was equivalent to intermittent parasystole with phase 3 protection; and non-sensing during the terminal portions of the cycle was the iatrogenic counterpart of intermittent parasystole with phase 4 protection. Premature beats occurring within the periods of phase 3 and phase 4 protection were "encompassed" by ectopic intervals equalling the ectopic cycle length, or twice the ectopic cycle length. Therefore, they were manifested differently from the "decelerating" and "accelerating" phases of modulation since premature beats occurring during the letter phases may be encompassed by ectopic intervals which are longer and shorter, respectively, than the ectopic cycle length. Because in previous reports the search for these phenomena was based on premises established "a priori," future studies should be designed to analyze tracings of "group beating" where no previous conclusions have been reached.

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. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-"distal" His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the "proximal" His bundle was stimulated. In these two patients, having as "common denominators" short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possible due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the "slow" nodal pathway.