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Bidirectional ventricular tachycardia (BDVT) is a well-known phenomenon since it was first described in 1922. Various mechanisms have been proposed for BDVT, including digitalis toxicity, hypokalemia, Anderson-Tawil syndrome, acute myocarditis, and catecholaminergic polymorphic ventricular tachycardia. It is characterized by rapid, wide complex electrocardiogram pattern with alternating QRS morphology and axis. The alternation of the QRS is usually right bundle branch block with 180° swings in the frontal plane axis or, less commonly, alternation of right bundle branch and left bundle branch forms. Most of the proposed mechanisms involve triggered activity or enhanced automaticity. We describe a unique BDVT, with characteristics of both re-entry and triggered activity, which terminated with a focal Rf lesion., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Fascicular arrhythmias encompass a wide spectrum of ventricular arrhythmias that depend on the specialized conduction system of the right and left ventricles. These arrhythmias include premature ventricular complexes, monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation. These arrhythmias may be organized by mechanism, including intrafascicular reentry, interfascicular reentry, and focal. Mapping and ablation of the fascicular system can result in high cure rates of debilitating and potentially life-threatening arrhythmias. When approaching these arrhythmias, careful consideration of the structure of the His Purkinje system as well as their electrophysiologic properties may help guide even the most complex of arrhythmias., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Optical mapping of cytosolic calcium transients in intact mammalian hearts is now possible using long-wavelength [Ca(2+)](i) indicators. We propose that beat-to-beat [Ca(2+)](i) transient alternans during ischemia may lead to spatial and temporal heterogeneity of calcium-activated membrane currents., Methods and Results: To test this hypothesis, isolated rabbit hearts were loaded with the fluorescent [Ca(2+)](i) indicator, rhod-2 AM, and imaged at 300 frames/sec during blood-perfused ischemic trials. High-quality [Ca(2+)](i) transients were recorded in each of 8 hearts.[Ca(2+)](i) transient alternans was never present in control records but occurred in each of the hearts during ischemia, with onset after 2 to 4 minutes. Alternans was confined to circumscribed regions of the heart surface 5 to 15 mm across. Multiple regions of alternans were found in most hearts, and regions that were out of phase with one another were found in 6 hearts. Quantitative maps of alternans were constructed by calculating an alternans ratio. This ratio behaved as a continuous variable that reached a maximum value in the center of the regions with alternans., Conclusions: These results demonstrate marked spatial heterogeneity of the [Ca(2+)](i) transient during the early phase of ischemia, which could produce electrical instability and arrhythmias in large mammalian hearts.

Purpose: To review the electropharmacology, clinical applications, side effects, and hemodynamic profile of intravenous amiodarone., Data Sources: The MEDLINE database was searched for English-language material, including reports of clinical trials and in vivo studies, review articles, and abstracts presented at national symposia, that was published between 1985 and 1996. Bibliographies of textbooks and articles were also examined., Study Selection: Studies that reported on the efficacy, toxicity, and hemodynamic profile of intravenous amiodarone and studies that examined the pharmacologic behavior of intravenous amiodarone in laboratory models were reviewed., Data Extraction: Study design and quality and relevant data on efficacy of suppression and treatment of arrhythmias with oral and intravenous amiodarone therapy, the reported mechanisms of antiarrhythmic effect, and hemodynamic changes seen with therapy were analyzed., Data Synthesis: Amiodarone is a unique antiarrhythmic agent that is now available in oral and intravenous forms in the United States. The use of intravenous amiodarone in the short-term treatment of life-threatening or hemodynamically unstable rhythm disturbances has generated much interest. Amiodarone has many electropharmacologic actions, some of which differ between the oral and intravenous forms. The wide clinical application of amiodarone includes treatment and prevention of supraventricular and ventricular arrhythmias and arrhythmias related to myocardial infarction. Intravenous amiodarone is effective for supraventricular and ventricular arrhythmias that are resistant to other antiarrhythmic agents. The effectiveness of intravenous amiodarone as short-term treatment also suggests that the drug has an important role in protocols of advanced cardiac life support. Intravenous amiodarone seems to have an overall favorable hemodynamic profile and does not produce many of the unwanted long-term side effects associated with oral therapy., Conclusion: Intravenous amiodarone shows much promise for the short-term treatment of unstable arrhythmias. Its favorable hemodynamic effects and minimal short-term side effects make it an attractive option in the management of cardiac arrhythmias.

Analysis of surface electrocardiograms from patients with long RP' tachycardia due to either atypical atrioventricular node reentrant tachycardia, permanent junctional reciprocating tachycardia, or low atrial tachycardia was performed. Although a negative P wave in the inferior leads is common to all 3 mechanisms, the results suggest that a positive or isoelectric P wave in electrocardiographic lead I strongly supports a diagnosis of atypical atrioventricular node reentrant tachycardia, whereas a negative or biphasic P wave in lead I argues against this mechanism.

To characterize the sequence of retrograde atrial activation in the presence of dual atrioventricular (AV) nodal pathways, we analyzed electrophysiologic data from seven patients in whom discontinuous AV nodal and ventriculoatrial conduction curves could be induced with programmed electrical stimulation. In all patients, electrograms of the high right atrium (HRA), lateral right atrium (LRA), low septal right atrium (SRA) and proximal coronary sinus (PCS) near the coronary sinus ostium were simultaneously recorded at a paper speed of 150-250 mm/sec. During programmed ventricular extrastimulation and incremental ventricular pacing, ventriculoatrial conduction via the fast AV nodal pathway resulted in SRA activation before PCS, HRA and LRA activation. However, the sequence of retrograde atrial activation abruptly changed with a shift from retrograde fast to retrograde slow AV nodal pathway conduction. Characteristically, during ventriculoatrial conduction via the slow AV nodal pathway, activation of the PCS preceded SRA activation by 5-20 msec and was accompanied by an alteration of the temporal relationship between HRA and LRA activation in all patients. These observations suggest that anatomically, the proximal common AV nodal pathway is a broad area that permits the slow AV nodal pathway to have a retrograde exit located posteriorly, inferiorly and to the left of that of the fast AV nodal pathway, and that the retrograde atrial activation sequence recorded during tachyarrhythmias should be determined with caution attempting to differentiate retrograde normal AV pathway from retrograde anomalous bypass tract conduction.

Interpretation of deflections presumably retrograde His bundle in origin has to be performed in context considering the coexisting changes in simultaneously recorded intracardiac and surface leads. His bundle electrocardiography thus conceived is helpful in the analysis of the runs of ectopic beats elicited by premature ventricular stimulation during the antecedent T wave in patients without coronary artery or primary myocardial disease. Identification of AV nodal echoes within the paroxysms as well as the subsequent runs of reciprocating tachycardias, was possible in patients with and without preexcitation, although a thorough study of these cases also requires recording of coronary sinus and low lateral right atrial electrograms. The behavior of the retrograde H deflection in respect to the first extra beat following the premature QRS complex helped in excluding bundle branch reentry. The latter is improbable in patients with 'complete' bundle branch block pattern, if extra beats show a contralateral bundle branch morphology. However, in absence of bundle branch block, retrograde H deflections were not helpful in elucidating the mechanisms of pacemaker-induced intraventricular (bundle branch, fasicular or vulnerability-related) reentry.

Twenty patients with the Wolff-Parkinson-White (WPW) syndrome and 1 or more episodes of symptomatic atrial fibrillation (AF) due to rapid anterograde bypass tract conduction underwent electrophysiologic testing. The mean ventricular rate during spontaneous AF was 242 +/- 56 beats/min (+/- standard deviation) and the shortest preexcited R-R interval was 194 +/- 40 ms. Six patients underwent surgical bypass tract ablation and 14 were treated medically, based on the results of electropharmacologic testing. Over a mean follow-up period of 35 +/- 19 months (+/- standard deviation), only 1 patient treated medically had a recurrence of minimally symptomatic AF. The successful chemoprophylaxis of symptomatic AF was associated with the inability to induce AF and atrioventricular reciprocating tachycardia during drug testing (7 patients) or with the induction of AF with a ventricular rate less than 200 beats/min and a shortest preexcited R-R interval of greater than 250 ms (7 patients). Electrophysiologic testing can identify a subgroup of patients with WPW and AF in whom medical therapy is a suitable alternative to bypass tract ablation.

Electrophysiologic and hemodynamic studies were performed before and after intravenous infusion of a new antiarrhythmic agent, propafenone, in 28 patients with recurrent ventricular tachycardia. Propafenone was given at a loading dose of 2 mg/kg in all patients. Subsequently, group A, the first 14 patients, received 1 mg/min and group B, the second 14 patients, received 2 mg/min continuous infusion. Propafenone exerted no effect on sinus nodal recovery time and sinoatrial conduction time, but significantly prolonged atrioventricular (AV) nodal and His-Purkinje conduction time and the QRS duration (respectively, 95 +/- 19, 48 +/- 10 and 120 +/- 23 ms before, and 110 +/- 28, 53 +/- 10 and 135 +/- 27 ms after; p less than 0.001). Propafenone did not change the mean arterial blood pressure but slightly increased right atrial, pulmonary artery and capillary wedge pressures resulting in mild depression of the cardiac index (2.6 +/- 0.8 liters/min per m2 before and 2.3 +/- 0.7 liters/min per m2 after; p less than 0.001). None of the patients were symptomatic from these changes. In group A, propafenone did not affect the inducibility of ventricular tachycardia except for one patient whose arrhythmia was sustained before and become nonsustained after propafenone. In group B, sustained ventricular tachycardia became noninducible in three patients and nonsustained in two patients, and nonsustained ventricular tachycardia became noninducible in one patient after propafenone. Therefore, an appropriate loading dose of intravenous propafenone such as 2 mg/kg followed by 2 mg/min infusion may be given safely and may suppress ventricular tachycardia. Propafenone may be a useful addition to currently available antiarrhythmic agents.

His bundle electrograms were recorded in 2 patients with ectopic beats arising in accessory atrioventricular tracts. Case 1 had Wolff-Parkinson-White (WPW) type A and a left-sided Kent tract with a short effective refractory period. Though ectopic impulse formation most probably occurred within the Kent tract itself, a vulnerability-related origin in the ventricular muscle close to the distal end of the Kent tract could not be excluded. In Case 2, with a Mahaim tract extending from His bundle to ventricles, there were three types of QRS morphologies resulting from : (a) atrioventricular conduction exclusively through the normal pathways; (b) atrioventricular conduction through both, normal pathway, and Mahaim tract; and (c) ectopic impulse formation in the Mahim tract. Specialized electrophysiological studies were essential to diagnose these unusual arrhythmias.

To assess the electrophysiologic characteristics of the excitable gap, 12 patients with orthodromic atrioventricular (AV) reciprocating tachycardia were studied. During tachycardia, 8 patients used a left-sided and 4 patients a right-sided anomalous bypass tract for retrograde conduction. QRS complex-synchronized single extrastimuli were delivered from high right atrium, right ventricular apex and coronary sinus, respectively, scanning the whole cycle length of tachycardia. An excitable gap was determined to be present if tachycardia resetting or tachycardia termination occurred. The duration of the excitable gap varied among different pacing sites and occupied 0 to 48% (mean 17 +/- 16) of basic tachycardia cycle length (240 to 480 ms, mean 327 +/- 70). Three patterns of tachycardia resetting were observed: the sum of coupling interval and return cycle being (1) less than a fully compensatory pause in 12 of 12 patients, (2) more than a fully compensatory pause in 5 of 12 patients and (3) equal to a fully compensatory pause in 2 of 12 patients, depending on extent of AV nodal conduction delay exhibited in return cycle. Tachycardia termination was possible when extrastimuli were delivered from right ventricular apex and coronary sinus but not from high right atrium, and only when basic tachycardia cycle length was greater than or equal to 290 ms in 7 of 12 patients. Tachycardia termination was accounted for by development of orthodromic conduction block in AV node in 7 of 7 patients and in bypass tract in 2 of 7 patients. Therefore, site of extra-stimulation and basic tachycardia cycle length affect electrophysiologic manifestations of excitable gap. Further, functional properties of the AV node influence patterns of tachycardia resetting and are primarily responsible for tachycardia termination during programmed single extrastimulation.

A false pattern of intermittent complete A-V block was seen in two asymptomatic patients when A-V dissociation was superimposed on a basic 2:1 A-V block. Although the conduction disturbance occurred at the A-V nodal level in both cases, in Case 2 it resembled A-V block due to bilateral or trifascicular disease. This arrhythmia was the end result of Type I (Wenckebach) block and apparently has a better prognosis than those emerging from a Type II (Mobitz) block.

Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.

His bundle electrograms were recorded during catheter insertion for prophylactic demand pacing in two patients with accelerated or nonaccelerated "atrioventricular (A-V) junctional" rhythms associated with A-V junctional Wenckebach periods. This appears to be the first published report of so-called A-V junctional Wenckebach periods in which the characteristic irregularities of the H-H intervals were recorded. Patient 1 had an additional area of "complete" anterograde A-V nodal (A-H) block. In Patient 2 the rate of impulse formation was consistent with nonparoxysmal A-V junctional tachycardia. The His bundle recordings were obtained in patients with digitalis toxicity and should be interpreted in the context. The integration of clinical and intracardiac findings with extrapolations from microelectrode and pharmacolic studies and with deductions from the clinical electrocardiograms suggests that the conduction disturbances probably occurred within the A-V node itself (in its AN region). This hypothesis implies that automaticity also originated in the A-V node because the site of impulse formation must have been proximal to the site of the Wenckebach periods. However, conclusive proof of of these postulates will require further studies with refined techniques.

His bundle and right ventricular apical electrograms were recorded in 18 patients with acute transmural myocardial infarction in whom catheter insertion was considered necessary for clinical reasons. The V-RVA and H-V intervals were of normal duration (5 to 30 and 35 to 55 msec, respectively) in five patients (Group 1) with persistently narrow (less than 100 msec) QRS complexes. In contrast, 13 patients (Group 2) who manifested a "complete" right bundle branch block pattern within 96 hours after admission had prolonged V-RVA intervals (range 50 to 80 msec, mean 59.2 msec) and H-V intervals that were at the upper limits of normal or prolonged (range 55 to 90 msec, mean 63 msec). In 6 of these 13 patients, the duration of the V-RVA interval became normal when the "complete" right bundle branch block pattern disappeared and was replaced by a "complete" left bundle branch block pattern in three patients and by narrow QRS complexes in the three other patients. This study showed that transmural myocardial infarction in itself did not increase the duration of the V-RVA interval even when "complete" left bundle branch block was present. Moreover, a prolonged V-RVA interval coexsting with a "complete" right bundle branch block pattern was not due to distal right bundle branch block but resulted from a conduction disturbance located in the proximal portions of the right bundle, or perhaps, even within the His bundle itself.

An unusual form of atrioventricular (A-V) nodal reentry is described as the underlying mechanism for incessant tachycardia in two children. During tachycardia a fast pathway was utilized for anterograde conduction and a slow pathway for retrograde conduction. This is the reverse of the usual form of A-V nodal reentrant tachycardia, in which the slow pathway is utilized for anterograde conduction and the fast pathway for retrograde conduction. One patient had a smooth ventriculoatrial (V-A) conduction curve demonstrating exclusive utilization of the slow pathway for retrograde conduction. The other had a discontinuous V-A conduction curve demonstrating failure of retrograde fast pathway conduction with resultant slow pathway conduction. In both cases the retrograde effective refractory period of the fast pathway was longer than that of the slow pathway, resulting in the establishment of this unusual reentry circuit. Both patients had a superior P axis with a P-R interval shorter than the R-P interval during tachycardia, features described in a significant number of children with incessant tachycardia. This unusual form of reentrant tachycardia can be suggested by its electrocardiographic pattern and is another mechanism for reentrant tachycardia not previously documented in children.

The incidence and significance of dual atrioventricular (A-V) nodal pathways are described in 78 children with associated congenital or acquired heart disease. None of these patients had clinical or electrocardiographic evidence of arrhythmia. Dual A-V nodal pathways were observed in 35 percent of the preoperative group and in 33 percent of the postoperative group. Despite this substrate for A-V nodal reentry, supraventricular tachycardia was neither induced during electrophysiologic evaluation nor did it develop clinically over a follow-up period of 1 month to 15 years. It is concluded that dual A-V nodal pathways are common and may be a benign finding in arrhythmia-free children with heart disease.

Atrioventricular nodal alternating Wenckebach periods were defined as episodes of 2:1 atrioventricular block in which there was a gradual increase in transmission intervals of conducted beats ending in two or three consecutively blocked atrial impulses. This is one of the mechanisms whereby 2:1 atrioventricular block progresses into 3:1 or 4:1 atrioventricular block. Alternating Wenckebach periods appear during rapid atrial pac,ng (even in the absence of depressed atrioventricular nodal function), provided that the atria can be captured at a rate fast enough to allow for the occurrence of this phenomenon. Treatment of atrial flutter with digoxin and quinidine produces alternating Wenckebach's periods, with associated electrocardiographic changes specific for the type of drug given. In patients with "atrial tachycardia with atrioventricular block" due to digitalis intoxication or with primary disease of the conducting system or with acute myocardial infarction, there are coexisting severe arrhythmias and clinical symptoms requiring almost immediate pharmacologic or electrical therapy. We conclude that atrioventricular nodal alternating Wenckebach's periods are common and frequentyly transient and that they occur in a variety of clinical conditions, most of which are benign; however, contrary to what is commonly accepted, some episodes appear in clinical settings requiring prompt pharmacologic or electrical treatment.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.

Advances in the area of clinical electrophysiology have allowed definition of the mechanisms of most forms of supraventricular tachyarrhythmias. Reentry, automaticity, and triggered activity are the three basic mechanisms. Treatment of the arrhythmias is based on frequency and hemodynamic severity. After accurate diagnosis, empirical therapy with currently available medications usually controls symptomatic supraventricular tachyarrhythmias. Nonpharmacologic therapy with permanent antitachycardia pacemakers, percutaneous catheter ablation, or surgery is indicated for selected patients with medically recalcitrant supraventricular tachyarrhythmia.

Beta-adrenoceptor-blocking agents reduce beta-adrenergic activity and depress sinoatrial and atrioventricular nodal conduction. These agents are thus useful for controlling supraventricular tachyarrhythmias. For the treatment of ventricular arrhythmias, beta-adrenoceptor-blocking agents possess antifibrillatory properties, depress diastolic depolarization of ectopic pacemaker activity, reduce electrical instability associated with prolongation of the QT interval, and are specifically effective in suppressing ventricular arrhythmias that are rate (tachycardia) dependent and/or caused by catecholamine-sensitive automaticity. Furthermore, beneficial hemodynamic effects of beta-adrenoceptor blockade on ischemic myocardium may also contribute to the antiarrhythmic potency of these agents.

To assess the effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability, the electrophysiologic properties of the atrium were studied before and during intravenous infusion of isoproterenol at 2 to 5 micrograms/min in 11 patients with paroxysmal supraventricular tachycardia exhibiting atrial latency during programmed atrial extrastimulation. In all patients, the isoproterenol infusion reduced the extent of maximum atrial latency (from 86 +/- 19 to 62 +/- 16 ms, p less than 0.001). This was accompanied by a significant shortening of both effective and functional refractory periods of the atrium (from 213 +/- 31 to 174 +/- 40 ms, p less than 0.005 and from 259 +/- 31 to 215 +/- 29 ms, p less than 0.001, respectively). The intra-atrial and interatrial conduction times were also significantly reduced (from 24 +/- 15 and 63 +/- 17 to 15 +/- 10 and 48 +/- 15 ms, p less than 0.005, respectively). In 3 patients with demonstrable atrial vulnerability, the isoproterenol infusion abolished the inducibility of repetitive atrial responses or atrial flutter, or both. Although the clinical significance of the suppressive action of beta-adrenergic stimulation on atrial vulnerability remains to be determined, the present study has demonstrated that beta-adrenergic stimulation significantly reduces atrial latency.

The sequence of retrograde atrial activation of premature ventricular beats was studied in 12 patients without pre-excitation syndrome. Forward and retrograde AV nodal conduction times were within normal limits. The septal low right atrial (LRA2) deflection was inscribed 25 to 55 ms (ave: 37.9 ms) before the low left atrial (LLA2) electrogram and 35 to 75 ms (ave: 53.7 ms) ahead of the high right atrial (HRA2) deflection. LLA2 preceded HRA2 in 8 patients, more or less coincided with HRA2 in 3 cases, and was inscribed 10 ms ahead in 1 patient. In all cases a decrease in the coupling (St1-St2) interval resulted in a proportional increase of the septal LRA1-LRA2, LLA1-LLA2, and HRA1-HRA2 intervals. Atrial echoes occurring in 3 cases had a sequence of arrival of excitation at the recording sites which was similar to the ones shown by the same patients during ventricular pacing. This is in keeping with the existence of an upper common pathway located above the area where functional longitudinal dissociation occurred. Thus, it is concluded that impulses emerging from the AV node in a retrograde direction reach the septal low right atrium before they activate the explored low left atrial sites, regardless as to whether they arise in the ventricles or in the atria.

Symptomatic bradycardia-independent atrioventricular block occurred in a patient with right bundle-branch block, left anterior hemiblock, and prolonged HV interval. The arrhythmia, triggered by a spontaneous or induced premature beats, appeared when the post-extrasystolic PP and HH intervals increased to a critical value. Reinitiation of atrioventricular conduction required the presence of ventricular escapes. Bradycardia-dependent atrioventricular block was related to either an enhanced or slightly rising slope of diastolic depolarization, or to a decrease in membrane responsiveness. The patient also, most probably, had tachycardia-dependent atrioventricular block. Both types of conduction disturbance occurred in the same part of the intraventricular conducting system, either in the low His bundle or left bundle-branch or its posteroinferior division. It is suggested that the electrophysiological study of cases with prolonged HV intervals should include procedures which can expose bradycardia-dependent atrioventricular block.

This report described initiation of A-V nodal reentrant tachyycardia in a patient with acute inferior myocardial infarction. The onset of tachycardia was preceded by an abortive A-V nodal Wenckebach periodicity. A-V nodal ischemia with or without vagotonia was implicated as the cause of induction of critical functional dissociation between the two A-V nodal conduction pathways. Since the tachycardia manifested its rate between 95-110 beats/min during the evolutionary phase of acute inferior myocardial infarction, it simulated, electrocardiographically, an accelerated A-V junctional rhythm. Analysis of the onset of tachcardia was of diagnostic importance.

During atrial extrastimulation, split His potentials, prolonged His-to-ventricular (H2V2) intervals and block distal to the His bundle deflection were observed in both preoperative and postoperative children with heart defects. His-Purkinje responses and refractoriness were identified in 31 of 78 (40%) pediatric patients (20 of 51 preoperative and 11 of 27 postoperative) during atrial extrastimulation coupled to sinus and/or paced cycle lengths. Split His potentials were found in 14 patients (eight preoperative and six postoperative) and His bundle relative refractory periods ranged from 250--490 msec. Prolonged H2V2 intervals were found in these and in an additional 16 patients (11 preoperative and five postoperative) and the relative refractory period of the His-Purkinje system ranged from 230--500 msec. Block distal to the His deflection occurred in seven patients (five preoperative and two postoperative) and the effective refractory period ranged from 230--510 msec. Split His potentials, long H2V2 intervals and block distal to the His bundle deflection produced by atrial extrastimulation were found in peroperative as well as postoperative children. These responses probably represent functional electrophysiologic characteristics of the pediatric cardiac conduction system.

Programmed stimulation was alternatively performed exclusively from the right ventricular endocardium, exclusively from the left ventricular epicardium and simultaneously from both ventricles in 8 patients who did not have coronary artery disease or bundle branch block. A specially constructed QRS triggered pacemaker, (with a refractory period of 260 msec and an escape interval of 800 msec) connected to the right ventricular and left ventricular electrodes, was used to perform simultaneous biventricular stimulation. The latter had no untoward effects and was not more dangerous than exclusive right ventricular, or exclusive left ventricular, stimulation. In 3 patients, pacemaker-induced repetitive firing occurred during right and left ventricular pacing. Persistence of this phenomenon (in these 3 patients) during simultaneous biventricular stimulation is in keeping either with a microreentry occurring in the vicinity of the electrodes or with a macroreentry involving the bundle branches. A more precise evaluation of the reentry circuit requires that left ventricular pacing be performed from an endocardial (rather than from an epicardial) site. This study suggests that the pulse generator described in the present communication can be used to produce simultaneous atrial and ventricular activation (or pacing) by connecting one pole to an atrial electrode and the other pole to a ventricular electrode. This modality of stimulation can be effective in preventing or abolishing some types of reciprocating atrioventricular tachycardias.

In an attempt to prevent recurrent reentrant supraventricular tachycardia, an experimentally designed new pacemaker has been developed. The pacemaker, when connected to both atrial and ventricular electrodes, is capable of sensing either an atrial or ventricular signal and, in turn, triggers simultaneous atrioventricular A-V) stimulation. Efficacy of this pacemake was tested in four patients with recurrent paroxysmal A-V nodal reentrant tachycardia during electrophysiologic studies. After connection of the electrodes to the new pacemaker, all atrial or ventricular premature stimuli elicited simultaneous A-V stimulation with resultant impulse collision in the A-V junction. Consequently, the reentrant tachycardia zone was completely abolished in all patients. This study has thus demonstrated the clinical feasibility of simultaneous A-V pacing to abolish the supraventricular tachycardia zone in man.

To define electrophysiologic properties and antiarrhythmic mechanisms of N-acetylprocainamide (NAPA), we studied 16 patients with symptomatic ventricular dysrhythmias. Electrophysiologic studies were performed before and after intravenous infusion of NAPA at 20 mg/kg over 20 minutes, achieving plasma concentrations of 24 +/- 3.2 to 35.5 +/- 4.5 micrograms/ml. NAPA did not significantly change sinus cycle length or atrioventricular (AV) conduction times (PA, AH, HV, and QRS), but it lengthened the QTc interval (p less than 0.001) during sinus rhythm. Programmed atrial stimulation revealed that NAPA had no discernible effects on AV nodal conduction; however, it exerted depressive effects on the His-Purkinje system in 9 of 16 patients. In 7 of 16 patients who manifested frequent ventricular premature beats (VPBs), NAPA abolished VPBs in only three of them; NAPA induced progressive prolongation of the premature coupling interval before complete abolition of VPBs. In 8 of 16 patients who had inducible repetitive ventricular response (RVR) because of reentry within the His-Purkinje system, NAPA narrowed or abolished the RVR zone in 3 patients and slowed the RVR rate with widening of the RVR zone in the remaining 5 patients. In 2 of 16 patients with slow ventricular tachycardia (VT), NAPA had no antiarrhythmic effects. By contrast, in the other 2 of 16 patients in whom sustained VT could be reproducibly elicited with programmed ventricular stimulation, NAPA slowed the rate of VT and suppressed VT inducibility. We conclude that electrophysiologic properties of NAPA are slightly different from those of procainamide and that NAPA is not uniformly effective for suppressing ventricular dysrhythmias, but its antiarrhythmic mechanisms are similar to those of procainamide.

To demonstrate the occurrence of concealed conduction in anomalous atrioventricular (AV) bypass tracts, 11 patients were selected for study. Two had a right-sided and nine had a left-sided bypass tract. Electrode catheters were placed in the right atrium, coronary sinus, AV junction and right ventricle. After every eighth atrial or ventricular driving beat (A1 or V1) at a constant cycle length, two successive atrial or ventricular premature beats (A2 and A3 or V2 and V3) were delivered. The A1A2 or V1V2 interval was fixed at 30 ms greater than the effective refractory period of the atrium or right ventricle, but less than the effective refractory period of the bypass tract in the anterograde or retrograde direction. This allows A2 or V2 to capture the atrium or ventricle, but not conduct in the bypass tract. The A3 or V3 was delivered from late diastole with a progressively shorter A2A3 or V2V3 interval until atrial or ventricular refractoriness was encountered. In the anterograde direction, the presence of A2 prevented A3 conduction in the bypass tract despite A1A3 intervals being longer than the anterograde effective refractory period of the bypass tract in 8 of the 11 patients. In the retrograde direction, the presence of V2 prevented V3 conduction in the bypass tract despite V1V3 intervals being longer than the retrograde effective refractory period of the bypass tract in 3 of the 11 patients. Thus, using the technique of programmed electrical stimulation, concealed conduction in anomalous AV bypass tracts can be demonstrated in both anterograde and retrograde directions.

Pseudo bundle branch block, a previously unreported arrhythmia produced by concealed premature impulses arising in the bundle branches, was seen in two patients with sick sinus node syndrome. Although concealed conduction was not apparent in either the surface or intracardiac leads, the latter were essential in localizing the site of manifest impulse formation. Patient 1, with left bundle branch extrasystoles, had pseudo bundle branch block and pseudo atrioventricular block that depended on the timing and extent of concealment of premature depolarization. Because of the coexisting sinus bradycardia in this patient, electrical stimulation and the recording of the right ventricular apical electrograms gave additional information that helped corroborate the postulated mechanisms. Patient 2 had right bundle branch extrasystoles with sinus beats that showed a right bundle branch block pattern possibly caused by pseudo bundle branch block. In this case the possibility that both the automaticity and the conduction disturbance had a mechanical origin could not be excluded.

Verapamil, a calcium channel blocking agent, has been demonstrated to have depressive effects on the atrioventricular (AV) node but not anomalous AV bypass tracts. Of 39 patients with AV reciprocating tachycardia utilizing left-sided bypass tracts for retrograde conduction, intravenous infusion of verapamil (0.15 mg/kg) terminated the tachycardia in 31 patients. Verapamil interrupted the tachycardia circuit by inducing retrograde conduction block in the bypass tract rather than the AV node in 5 of these 31 patients. Electrophysiologic studies in these five patients revealed that verapamil-induced conduction block in the bypass tract could be accounted for by two distinctly different mechanisms. In three patients, verapamil induced alternating slow and fast AV nodal conduction resulting in alternating long and short cycle lengths during the tachycardia; consequently, development of the Ashman phenomenon in the bypass tract terminated the tachycardia. In the remaining two patients, the bypass tract exhibited properties similar to those of the AV node; verapamil prolonged the effective refractory period of the bypass tract, thereby terminating the tachycardia. Thus, depending on the functional properties of the bypass tract, verapamil may interrupt an AV reciprocating tachycardia circuit by exerting either a direct or indirect depressive action on the bypass tract.

Intraventricular dissociation due to intraventricular block occurred in a patient with cardiac arrest due to massive cerebral hemorrhage. The electrocardiogram showed complete atrioventricular block with three different types of accelerated ventricular rhythm. The ectopic beats did not interfere with each other because of the existence of an area of complete block surrounding the areas in which impulse formation occurred. Hence, the corresponding QRS complexes did not result from depolarization of all the ventricular muscle mass but only of certain regions. The latter were large enough to produce ventricular complexes of enough size to be recorded at the body surface. This phenomenon is the clinical counterpart of the multiple isolated focal contractions which may be seen directly in the ventricules of dying hearts.

The electrocardiographic R-on-T phenomenon was observed in the absence of Wolff-Parkinson-White syndrome during recurrent episodes of supraventricular tachycardia (SVT) with rates between 240 to 275 per minute in a 5 year old boy. The rapid ventricular response during SVT corroborates the recent finding of a short refractory period of the A-V node in children. The demonstration of the R-on-T phenomenon in this child may be important in attempting to understand the pathogenesis of sudden death in children.

Invasive electrophysiological studies were performed in 2 symptomatic patients with recurrent arrhythmias in which impulse formation presumably occured within atrioventricular nodal bypass tracts. Case 1 had ectopic beats arising within, or close to, the upper end of a left-sided atrioventricular nodal bypass tract of the type described by Brechenmacher. In addition, this conduction was 'concealed' during sinus rhythm and right atrial pacing because the relatively prolonged right-to-left atrial conduction time allowed right atrial impulses to reach the His bundle via the atrioventricular node before they could do so through the atrioventricular nodal bypass tract. Case 2 had ectopic beats arising in a right-sided atrioventricular nodal bypass tract which did not conduct in either forward or retrograde directions, its presence being detected only when initiating impulses. However, it could not be determined whether this tract was an 'abnormal' atrio-His connection or a 'normal' transitional (atrio-atrioventricular nodal) tract. Though intracardiac studies complement body surface recordings, they should be interpreted with knowledge of their inherent limitations.

His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.

The various patterns resulting from stimulation through the catheter electrodes recording His bundle activity were evaluated in 30 patients using intracardiac electrograms from the right ventricular apex (RVA), posterosuperior wall of the left ventricle (LV), high right atrium (HRA) and left atrium (LA) in the vicinity of the coronary sinus. His bundle pacing was characterized by a QRS complex and stimulus (St)-V, St-RVA and St-LV intervals that equated the QRS configuration, H-V, H-RVA and H-LV intervals of sinus beats. Right septal pacing produced pattern of "complete" left bundle branch block (with normal electrical axis) associated with St-V intervals of 0 msec, and St-RVA and St-LV intervals of different duration from that of the H-RVA and H-LV intervals recorded during sinus rhythm. Fusion beats resulting from simultaneous activation of His bundle and right septal muscle were characterized by St-V intervals of 0 msec and St-RVA or St-LV intervals of similar duration to that of the H-RVA or H-LV intervals of sinus beats. Fusion QRS configuration depended on the type of ventricular complex present during sinus rhythm. Analysis of the retrograde atrial activation intervals permitted differentiation among impulse initiation at the low right atrium, His bundle or right septal muscle. Simultaneous recording of multiple atrial and ventricular electrograms has enhanced understanding of the complex patterns observed during attempted His bundle pacing in man.