Endless loop tachycardia started by an atrial premature complex in a patient with a dual chamber pacemaker

In a patient with a dual chamber pacemaker that senses in both the atrium and ventricle (VDD, DDD), a ventricular depolarization temporally displaced from a P wave can cause retrograde atrial activation and initiate an endless loop pacemaker-mediated tachycardia. A case in which an endless loop tachycardia was initiated by an end-diastolic atrial premature complex is reviewed. Retrograde conduction occurred because of the change in the temporal relation of atrial sensing and atrioventricular (AV) node depolarization. The implanted pacemaker did not have the capability of atrial refractory programmability. Atrial refractory interval extension, which occurs in this model after a ventricular premature complex to protect against a retrograde P wave, was not invoked since the tachycardia was begun by an atrial rather than a ventricular premature complex. The tachycardia was controlled by shortening the programmable AV delay. The mechanism of tachycardia induction and its management are outlined. Atrial refractory programmability is required in all VDD or DDD pacemakers.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

The mechanisms of exercise provocation of supraventricular tachycardia

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.     

Implantable automatic scanning pacemaker for termination of supraventricular tachycardia

Thirteen patients suffering from reentrant supraventricular tachycardia have undergone implantation of a scanning extrastimulus pacemaker. This pacemaker is fully implanted and automatic, and it requires no external control device to activate or control it. The pacemaker is activated when tachycardia occurs. After four cycles an extrastimulus is induced with a preset coupling time from a sensed intracardiac potential, and every four cycles thereafter a further extrastimulus occurs, but on each occasion there is a decrement in coupling cycle by 6 ms until 90 ms of the cardiac cycle has been scanned by extrastimuli. When necessary, two extrastimuli can be introduced with a fixed but preset coupling time between them. Every four beats two extrastimuli are induced but the coupling time between the spontaneous cardiac potential and the first stimulus is decreased by 6 ms until 90 ms of the cardiac cycle has been scanned. The coupling time between the two stimuli is fixed throughout the scan. When termination of tachycardia occurs the successful timing variables are retained in the pacemaker memory so that at the onset of the next episode of tachycardia these settings are used first. Pacemaker pulse width, sensitivity, tachycardia trigger rate, coupling intervals for both stimuli and the use of single or double extrastimuli are all programmable transcutaneously.Three patients required single, and seven patients double ventricular premature stimuli; three patients required double atrial premature stimuli for termination of tachycardia. Despite frequent attacks of tachycardia before implantation, only two patients had a sustained attack of tachycardia after pacemaker implantation.     

Pacing techniques in the management of supraventricular tachycardias. Part 1. The use of high frequency stimulation (HFS) in the management of paroxysmal supraventricular tachycardia.

Using techniques for programmed electrical stimulation of the heart, seven patients with paroxysmal supraventricular tachycardia have been studied and shown to have a reciprocal mechanism as the most likely basis for the tachycardia. In four patients it was found that the tachycardia could be terminated by single right atrial premature beats and in three patients two right atrial premature beats were required. A variable zone for tachycardia termination was found when single or double stimuli were used and so a system for introducing high frequency stimuli at 100 or 1000 stimuli/sec for a given duration is described. Using this system a wider range of the cardiac cycle could be covered, thereby increasing the likelihood of producing correctly timed premature beats. The results of using this system are presented and its practical usage discussed.     

Prevention of Tachycardia Initiation by Programmed Stimulation

A 20-year-old female with a left-sided concealed atrioventricular accessory pathway was studied during programmed stimulation to investigate the mechanisms of prevention of tachycardia by timed stimulation of the ventricle after a tachycardia initiating atrial extrastimulus. After the atrial tachycardia initiation zone was determined, the prvention zone of the ventricular stimulus was determined for each initiating interval. Two different prevention mechanisms were found, one whereby the ventricular depolarization was blocked retrogradely in the accessory pathway and another whereby the ventricular depolarization was conducted over the accessory pathway to the atrium but subsequently blocked anterogradely in the AV node. The preventive zone timed from the last ventricular complex to the ventricular stimulus was always greater than 30 msec whereby the minimum preventive internal was determined by the ventricular refractory period. This could be of value when such a preventive algorithm is incorporated into a dual-chamber antitachycardia pacemaker. Knowing the exact mechanisms by which the prevention occurs allows one to predict how tachycardia can be prevented when the atrial extra beat originates from a different site and when the parameters of the heart are changed due to changes in antonomic tone or catecholamine level.     

Intravenous flecainide acetate for supraventricular tachycardias

Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty-three patients with paroxysmal Supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.     

Surgical alternatives for supraventricular tachycardias

Since Sealy's pioneering surgical intervention for Wolff-Parkinson-White syndrome, surgical electro-physiologic interventions have been developed for all supraventricular arrhythmias. The surgical rationales are based on the site of origin of the arrhythmic mechanism and the associated pathology that characterizes the “arrhythmogenic substrate.”

The Wolff-Parkinson-White syndrome is characterized by an accessory atrioventricrdar (AV) connection distinct from the AV node—His bundle system. It is associated with AV reentrant tachycardia or atrial fibrillation, or both, with fast ventricular responses through the accessory pathway. The current surgical management involves ablation of the accessory pathway using either an endocardial or an epicardial approach. Surgical ablation is associated with high efficiency and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or the Mahaim fiber.

AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoabladon of the arrhythmogenic substrate located in the coronary sinus orifice region. The chronotropic atrial function, abolished by incessant or paroxysmal idiopathic atrial fibrillation, can be restored using the corridor operation (sinus node-AV node insulation). The success of surgical intervention in atrial tachycardias is uncertain, but it may be an option in selected patients with resistant atrial tachycardias.     

Complete abolition of the reentrant supraventricular tachycardia zone using a new modality of cardiac pacing with simultaneous atrioventricular stimulation

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 pacemaker was tested in four patients with recurrent paroxysmal A-V nodal reentrant tachycardia during electrpphysiologic 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.     

Termination of pacemaker-mediated tachycardia by adenosine

A 30-year-old woman was referred for follow-up right- and left-heart catheterization 4 years after cardiac transplantation. She had an implanted epicardial pacemaker for bradycardia; this was programmed to the DDD mode. At the time of her catheterization, as a pigtail catheter was pulled back across the aortic valve, runs of premature ventricular complexes occurred and tachycardia with ventricular pacing spikes and ventricular capture was initiated at a rate of 126 beats/min. Adenosine 6 mg was given intravenously through a femoral venous sheath and within 20 s the tachycardia broke. The tachycardia was consistent with pacemaker-mediated tachycardia (PMT), a circus movement tachycardia occurring when ventricular pacing causes retrograde atrial depolarization followed by triggering of ventricular pacing. With reprogramming of the pacemaker to an AV delay of 160 ms and a postventricular atrial refractory period of 300 ms, no further episodes of PMT have occurred. This case illustrates that intravenous adenosine can effectively terminate PMT by causing ventriculoatrial block, thus interrupting the reentrant circuit by eliminating retrograde atrial activation.     

Computer detection of premature ventricular complexes: A modified approach

The accuracy of a data reduction system for arrhythmia detection in identifying premature ventricular complexes was evaluated in continuous tape records of 30 patients in a coronary care unit. Computer analysis was performed with a Honeywell 316 digital computer. Threshold values for dominant complexes were automatically determined and recognition of premature ventricular complexes was based on differences in QRS configuration, timing and T wave configuration from the dominant complexes. Verification of the computer accuracy in detecting premature ventricular complexes was made with visual beat by beat inspection using a two channel strip chart recorder with simultaneous recording of the electrocardiogram and computer signal. This procedure allowed for exact beat to beat correlation and, thus, absolute determination of false positive and false negative identifications.From 0.5 to 6 continuous hours of monitoring per patient (average 3.5 hours) were analyzed for a total of 105 monitoring hours. The basic cardiac rhythms noted were normal sinus rhythm, sinus arrhythmia, sinus tachycardia, demand pacemaker rhythm, atrial fibrillation and atrioventricular (A-V) dissociation with junctional rhythm. Premature ventricular complexes were evident in 28 tapes (93 percent) including 12 (43 percent) with multifocal premature ventricular complexes and 3 (11 percent) with ventricular tachycardia. The visual count of premature ventricular complexes totaled 7,921. Of these, 7,542 (95 percent) were properly classified by the computer. The total computer count was 8,717, representing a 13 percent false positive and 5 percent false negative identification rate. The false positive identifications of premature ventricular complexes occurred during periods of 10 seconds or more of continuous noise artifact and in the presence of atrial premature complexes conducted aberrantly. When these sections of tape were excluded, the computer had a less than 2 percent false negative and 3 percent false positive rate of identification of premature ventricular complexes.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Electrophysiologic effects of intravenous diltiazem in patients with recurrent supraventricular tachycardias

The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.     

Usefulness of the pre-excitation index to determine the mechanism of supraventricular paroxysmal tachycardia and the location of the anomalous pathway

To evaluate the preexcitation index in determinate the mechanism of paroxysmal supraventricular tachycardia and localize accessory pathway, fifty nine patients with clinical and electrocardiographic supraventricular tachycardia were analyzed. There were thirty eight patients (64.4%) with orthodromic AV reentry using an accessory pathway for retrograde conduction and 21 patients (35.6%) with typical AV nodal reentrant tachycardia. Preexcitation of the atrium during tachycardia by premature ventricular complex at a time when anterograde His bundle activation was present in 30 o 38 (79%) patients with AV reentry while only 8 of 21 (38%) patients with AV nodal reentry demonstrated preexcitation during tachycardia. There was no significant difference between left and right accessory pathways and in mean tachycardia cycle length between the two groups. However, atrioventricular reentry demonstrated atrial preexcitation during tachycardia more frequently than AV nodal reentry. In conclusion, our findings show that the preexcitation index is a useful method for determinate the mechanism of supraventricular tachycardia and to localize accessory pathways.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.     

Subcostal M-mode echocardiography of the right atrial wall in the diagnosis of cardiac arrhythmias

The M-mode echocardiogram of the right atrial (RA) wall can be easily recorded in each person from the subcostal location. In a normal RA wall motion pattern, atrial contraction is represented by a markedly prominent posterior motion. The presence or absence of atrial contractions in the subcostal RA wall echocardiogram, their amplitude, and their timing may help in the diagnosis of cardiac arrhythmias with the simultaneously recorded non-diagnostic electrocardiogram. Flat and hidden P waves can be accurately identified throughout the cardiac cycle. It is possible to distinguish between atrial, ventricular, and nodal premature beats and to recognize atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia, paroxysmal atrial tachycardia with block, atrioventricular (AV) nodal tachycardia, and supraventricular tachycardias with aberrant ventricular conduction. The diagnosis of wandering pacemaker, AV dissociation, sinoatrial block, and AV block is facilitated. On the basis of study of 60 patients with various rhythm disturbances, it was concluded that analysis of the subcostal RA wall echocardiogram is a new, helpful noninvasive approach in the diagnosis of cardiac arrhythmias.     

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Atrioventricular (AV) conduction, ventriculoatrial (VA) conduction, and the mechanism of tachycardia, were studied by programmed electrical stimulation before and after the administration of verapamil, in 10 patients with paroxysmal re-entrant supraventricular tachycardia. In 7 patients the tachycardia circuit was confined to the AV node. In 3 patients an accessory pathway conducting only in the ventriculoatrial direction was used during tachycardia. When administered intravenously during tachycardia, verapamil terminated the arrhythmia in 9 patients. Verapamil lengthened the effective and the functional refractory period of the AV node and the AV nodal transmission time in all patients in whom this could be studied. As a result of these changes, it was not possible to initiate tachycardia in 3 patients. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in 5 patients, and increased in 2 patients. In 6 of these 7 patients the tachycardia zone shifted to longer premature beat intervals. Verapamil resulted in slowing of the heart rate during tachycardia. Apart from slowing in heart rate during tachycardia and termination of tachycardia after intravenous verapamil, the 3 patients with an accessory pathway showed no beneficial effect of verapamil on the mechanism of initiation of tachycardia. Five patients were restudied after 2 to 3 weeks of oral administration of verapamil. Though less, effects were similar to those obtained after intravenous administration.     

Computer detection of atrioventricular dissociation from surface electrocardiograms during wide QRS complex tachycardias

Differentiation of wide QRS complex tachycardias on surface electrocardiograms is difficult for physicians and computers due in part to their inability to identify atrial activity, specifically atrioventricular (AV) dissociation. We studied 20 examples of AV associated rhythms and 17 examples of AV dissociated ventricular tachycardia. We applied an algorithm consisting of subtraction of a mean beat from each individual beat in leads II and V1 to generate remainder electrocardiograms. The remainder electrocardiograms were visually inspected for the presence of P wave candidates and then autocorrelated. AV dissociated P wave candidates were evident on visual inspection of remainder electrocardiograms in none of 20 AV associated and 15 of 17 AV dissociated rhythms. Atrial cycle length and the presence of AV dissociation were automatically detected by applying a peak selection algorithm to the autocorrelation function. AV association was detected in all 20 AV associated rhythms and AV dissociation was detected for 11 of 17 AV dissociated rhythms (sensitivity 65%, specificity 100%, positive and negative predictive accuracy 100%, 77%). The correlation coefficient of detected vs true atrial cycle length for the 11 correctly detected AV dissociated rhythms was r = .98. Visual inspection of the remainder electrocardiograms along with the original electrocardiogram may increase the ease with which human readers can identify the presence of AV dissociation and thus diagnose ventricular tachycardia. Computer diagnosis of wide QRS complex tachycardias should be significantly improved by use of this algorithm.     

Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.