Ventricular Extrastimulation Research Articles

The effects of premature stimulation of the His bundle on epicardial activation and body surface late potentials in dogs susceptible to sustained ventricular tachyarrhythmias.

Experiments were performed on 20 anesthetized dogs to determine the effects of premature stimulation of the His bundle on epicardial conduction and late potentials recorded on the body surface. Fifteen dogs underwent occlusion of the left anterior descending coronary for 2 hr followed by reperfusion, and five that did not undergo operation served as controls. Animals were studied 2 to 52 weeks after the induction of infarction, and four animals with infarction and four control animals exhibited no sustained arrhythmias in response to programmed ventricular extrastimulation. Five dogs with infarction and one control dog had ventricular fibrillation while the six remaining dogs had inducible sustained ventricular tachycardia. All animals with ventricular tachycardia had late potentials in the terminal portion of the signal-averaged body surface QRS complexes during sinus rhythm and QRS durations in the animals were 64 msec or greater. The voltage in the last 20 msec of the QRS complex was 13.5 microV or less and the duration of late activity below 30 microV was 18.2 msec or more. These values did not overlap values in animals with no inducible arrhythmias. Ventricular fibrillation was a nonspecific end point in these experiments and values overlapped those in animals with no arrhythmias and those with ventricular tachycardia. All animals with infarction and late potentials associated with their QRS complexes also had delayed and prolonged epicardial electrograms that extended into the time of the late potentials recorded from 45 standard sites in the infarcted regions. A single premature beat evoked by His bundle pacing (coupling interval of 192 to 270 msec) had no significant effect on late potentials or their relationship to epicardial activation in the area of infarct. However, changes in the durations of electrograms in response to premature beats were different in animals with infarction and ventricular tachycardia than in those with ventricular fibrillation. In animals with ventricular tachycardia, electrograms at 15 of 210 sites increased in duration by more than 10 msec while those at 61 of 210 sites decreased in duration. In animals with ventricular fibrillation, electrograms at 40 of 207 sites were of increased duration while those at 26 of 207 decreased. The decreases in duration were usually due to components of fractionated electrograms "dropping out" and likely represent local conduction block near the recording electrode.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of site of pacing on dispersion of refractoriness

The variation in dispersion of ventricular refractoriness with different sites of pacing was measured in 11 patients not taking antiarrhythmic drugs. Dispersion of refractoriness between 3 right ventricular sites was determined at constant paced cycle lengths (S 1S 1. Refractoriness to ventricular extrastimulation (S 2 using atrial pacing vs “clinical” pacing (drive or S 1 at the right ventricular apex) vs the conventional measurement of dispersion (S 1 at the site of S 2 was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S 2. Dispersion of ERP was always wider using clinical pacing (65.4 ± 26 ms [± standard deviation]) than atrial pacing or traditional drive (20.4 ± 14 and 19.1 ± 10 ms, p < 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 ± 35 vs 21.8 ± 14 and 17.3 ± 13, p < 0.011). In 2 patients with left bundle branch block these differences were most striking. Clinical pacing foreshortened FRP relative to ERP (FRP shorter than ERP by an average 12.5 ms at nonapical sites) but this did not induce tachycardias, perhaps because FRP was still longer than the shortest V 1V 2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p < 0.05). With atrial pacing there is less dispersion of refractoriness than with clinical ventricular pacing, although this difference is not appreciated when dispersion is measured in the conventional manner.

Electrophysiologic effects of ethmozin in patients with ventricular tachycardia

Ten patients with recurrent episodes of ventricular tachycardia (VT) had electrophysiologic studies in the basal state and on chronic oral ethmozin (12.1 ± 0.6 SE mg/kg/day). Ethmozin significantly prolonged the AH interval (basal: 75 ± 8 SE msec; ethmozin: 91 ± 10 msec, p < 0.05), the HV interval (51 ± 3; 66 ± 5 msec, p < 0.01), and the QRS duration (101 ± 4; 118 ± 4 msec, p < 0.001). Atrial and ventricular refractory periods and the corrected QT interval were not significantly affected by ethmozin. VT was induced in 7 of 10 patients in the basal state by means of programmed right ventricular extrastimulation or rapid burst ventricular pacing. On oral ethmozin nine patients had inducible VT. VT cycle length was consistently prolonged on ethmozin (250 ± 13; 326 ± 14 msec, p < 0.001). Four of the seven patients with VT on basal ambulatory monitoring had total abolition of spontaneous VT on ethmozin. Ethmozin failed to prevent induction of VT in most patients despite significant reductions in ventricular arrhythmia on ambulatory monitoring. Further studies comparing VT induction with ambulatory monitoring in patients on ethmozin are needed to confirm these findings and to define the clinical significance of this dissociation.

Responses of an AV universal (DDD) pulse generator (Cordis 233D) to programmed single ventricular extrastimuli.

To evaluate factors playing a role in initiation and perpetuation of pacemaker-mediated tachycardias (PMTs), 22 consecutive patients with symptomatic conduction disorders were studied after implantation of an AV universal (DDD) pulse generator (Cordis 233D). Patients were divided into two groups, depending upon the presence or absence of ventriculo-atrial (VA) conduction during electrophysiological study (EPS) performed before pacemaker implantation. PMTs could be initiated in six of eight patients of Group I and in none of 14 patients of Group II. Initiation and perpetuation of PMTs during DDD pacing were dependent upon the capacity of the patient to conduct ventricular premature beats (VPBs) and subsequent paced ventricular beats retrogradely to the atria, and upon three programmable parameters of the pulse generator (AV delay period, upper rate limit, tachycardia response). Programmed single ventricular extrastimulation demonstrated that: (1) merely the presence of VA conduction during EPS, although necessary, was not sufficient to induce PMTs after DDD pacemaker implantation; (2) VPBs introduced late rather than early in the cardiac cycle initiated PMTs in a different way; (3) the initiation of PMTs could be prevented during study by adjusting the programmable parameters (AV delay period, upper rate limit, tachycardia response); (4) one of the two available tachycardia responses of the pulse generator (gradual fall-back response) was able to terminate and initiate PMTs consistently. These observations helped in understanding the responses of the Cordis 233D pulse generator to ventricular premature beats. They indicate that additional refinement of the pulse generator is necessary to solve the problem of PMT.

Inducible polymorphous ventricular tachycardia following Mustard operation for transposition of the great arteries.

A 22-year-old woman with chronic atrial tachycardia following Mustard's operation for transposition of the great arteries presented with dizziness and ventricular tachycardia documented with dynamic 24-h electrocardiogram. During intracardiac electrophysiology study, programmed ventricular extrastimulation induced polymorphous ventricular tachycardia (torsades de pointes). This was prevented by intravenous administration of procainamide. We postulate that polymorphous ventricular tachycardia is a possible cause of death in patients with Mustard's operation. Postoperative electrophysiologic study may define those patients at risk to develop this potentially fatal arrhythmia.

Induction of clinical ventricular tachycardia using programmed stimulation: Value of third and fourth extrastimuli

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis, All patients received 1 to 4 extrastimuli (S 2, S 3, S 4 and S 5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S 2 or S 3 in 16 patients and by S 4 or S 5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), In 11 by S 2 or S 3 and in 13 by S 4 or S 5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S 4 and S 5 in the right ventricle increases the yield of inducible clinical VT compared with use of S 2 and S 3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.

Electrophysiologic mechanism of exercise-induced sustained ventricular tachycardia

To elucidate electrophysiologic mechanism of exercise-induced ventricular tachycardia (VT), electrophysiologic studies were performed in 12 patients in whom sustained VT had developed during treadmill exercise testing. Six patients had arteriosclerotic coronary heart disease, 3 had cardiomyopathy, and 3 had no clinical evidence of organic heart disease. All patients had had documented episodes of sustained VT related to exertion and had experienced dizziness, syncope, or both. In addition, 3 patients had had nonfatal cardiac arrest. Electrophysiologic studies provoked paroxysms of sustained VT identical to those observed during treadmill exercise testing in 10 patients and provoked ventricular flutter/fibrillation in 1. Seven patients had VT suggestive of a reentrant mechanism, as the VT could be readily initiated with programmed ventricular extrastimulation or terminated by ventricular overdrive pacing, or both. Three patients had VT suggestive of catecholamine-sensitive automaticity. The VT could not be initiated with programmed electrical stimulation, but it could be provoked by intravenous isoproterenol infusion; furthermore, the VT could not be terminated with ventricular overdrive pacing, but it could be abolished by discontinuing isoproterenol infusion. Reproduction of VT in these 10 patients allowed serial pharmacologic testing in selecting an effective antiarrhythmic regimen. Thus (1) exercise-induced VT can be caused by either reentry or catecholamine-sensitive automaticity, and (2) electrophysiologic studies are of use in defining the underlying mechanism of exercise-induced sustained VT.

Analysis of the re-entrant beat in response to the ventricular extrastimulation--using 10 polar electrode catheter.

The study of re-entry phenomenon during the right ventricular extrastimulus method was performed on 22 patients using 10 polar electrode catheter. Two to 4 spikes from the specialized conduction system were recorded in response to the premature extrastimulation (S2). By using this catheter, the catheter position was defined more clearly than the other reports. From the patterns and sequence of spikes in response to S2, the routes of impulse propagation were studied. In 17 cases whose patterns of spikes were different from those of antegrade conduction, the impulse from S2 seemed to be retrogradely conducted via the left bundle branch (LBB) to the branching portion and thereafter conducted bidirectionally both to His bundle (HB) and the right bundle branch (RBB) (HPS re-entry). In 6 cases whose patterns of spikes were similar to those of antegrade conduction, the impulse from S2 was retrogradely conducted via RBB to HB and turned in some portion above HB and antegradely traveled to the ventricle. In one case who was diagnosed as concealed WPW syndrome, the pattern of spikes showed 2 types of re-entry as described above. The mechanism of the ventricular re-entry was able to be classified into 2 types from the patterns and sequence of spikes in response to S2.

Sequence of retrograde atrial activation in patients with dual atrioventricular nodal pathways.

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.

Determinants of ventricular refractory periods in children with congenital heart disease: Effects of cycle length and age

Ventricular effective refractory periods (ERP) and functional refractory periods (FRP) were determined by programmed ventricular extrastimulation in 63 pediatric patients with a spectrum of congenital heart disorders. Of these 63 children (ages 8 months to 18 years), 38 were preoperative, 17 had repair of their cardiac lesion via right ventriculotomy, and eight were postoperative without a ventriculotomy. We demonstrated that there was a linear relationship between the cycle length and ventricular refractory periods. The regression equations 73 + 0.29 × cycle length (msec) for the ventricular ERP (msec) and 80 + 0.30 × cycle length (msec) for ventricular FRP (msec) were found to define the determined properties of ventricular refractory periods (VRP) in children. These VRP characteristics were independent of age in children less than 13 years of age.

Repetitive beating after single ventricular extrastimuli: Incidence and prognostic significance in patients with recurrent ventricular tachycardia

The incidence of repetitive ventricular beating in response to programmed single ventricular extrastimuli delivered during spontaneous rhythm was tabulated in 59 patients with recurrent ventricular tachycardia. Repetitive beating occurred in only nine patients (15 percent). The repetitive response seemed to be a result of bundle branch reentry in four subjects and possibly a result of other mechanisms in five. There was no difference in the incidence of repetitive beating or type of repetitive response in patients with and without ischemic heart disease. During an average patient follow-up period of 13.6 months, there were eight sudden and six nonsudden deaths. Life table analysis revealed a significantly greater incidence of sudden death in patients with ischemic than in patients with nonischemic heart disease. There was no significant difference in the incidence of sudden death in patients with and without repetitive beating. It is concluded that the repetitive response to single ventricular extrastimulation is infrequent in patients with recurrent ventricular tachycardia, and that repetitive beating is not a prognostic indicator or an indicator of vulnerability to ventricular tachycardia.

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Ventricular extrastimulation in the mitral valve prolapse syndrome. Evidence for ventricular reentry

Fourteen patients with mitral valve prolapse and essentially normal coronary arteries were evaluated for ventricular arrhythmias, utilizing programmed ventricular extrastimulation. Three were symptomatic with ventricular tachyarrhythmias. Application of appropriately timed ventricular extrasystoles initiated the tachyarrhythmias in these three patients. The remaining eleven mitral prolapse patients were apparently free of tachycardias. Repetitive ectopic beats were not induced by extrastimulation in these eleven patients. The initiation of ventricular tachyarrhythmias by extrastimulation suggests a reentrant mechanism for the ventricular ectopy of mitral valve prolapse.