Identification of the Slow Conduction Zone in Idiopathic Left Ventricular Tachycardia

The mechanism of verapamil sensitive idiopathic left ventricular tachycardia (ILVT) is considered to be reentry. However, the nature of the reentry circuit, including the location of the slow conduction zone, is unclear. We sought the local electrical activity that would reflect slow conduction by precise mapping around the tachycardia exit (TE) in nine patients with ILVT (mean age, 28 ± 10 years) undergoing radiofrequency catheter ablation (RFCA). The TE was defined as the earliest discrete spiky potential (SP) recorded during the tachycardia, or as a complete configuration-matched pacemap 12-lead electrocardiogram (ECG). In all patients, the TE was located at the mid or inferior distal portion of the septum. The SP at the TE preceded the surface QRS by 20 ± 9 ms. The pacemap score at the TE was 11.4 ± 0.6 points. In three patients, fractionated potentials (FP) were recorded during the tachycardia. The onset of the FP preceded the surface QRS by 47 ± 8 ms and was earlier than the SP at the TE (P < 0.01). The sites where an FP was detectable were restricted to a small area, and were at a distance of 14 ±4 mm from the TE. The direction of the FP site from the TE was more basal in two patients and inferior in one, Pacemap ECGs at the sites with an FP showed poor matching (9 ± 1 points), presumably because of predominant capture of the local ventricular muscle rather than an electrically isolated reentry circuit. Successful RFCA was achieved at the site of the FP in all three patients in which one was recorded, and at the TE in the other six patients. The FP, which has been shown to reflect the slow conduction of the ventricular tachycardia circuit in structural heart disease, was also detected in ILVT in the present study, and it is likely to reflect electrical excitation of the distal rim of the slow conduction zone.     

Radiofrequency Catheter Ablation of the Slow Reentrant Pathway of Sustained Ventricular Tachycardia

The article reports the cases of two patients with severe coronary artery disease and associated recurrent sustained ventricular tachycardia successfully treated with radiofrequency catheter ablation. In the first patient, two different types of ventricular tachycardia (one incessant) were eliminated. In all procedures, an area of slow conduction critical for tachycardia maintenance was localized by endocardial mapping techniques. Radiofrequency energy delivered to this area could permanently modify the anatomical substrate of the arrhythmia. After single follow-ups of 19, 14, and 13 months regarding the arrhythmic entities, the patients are well and free from spontaneous recurrences.     

Ventricular Tachycardia with Alternate Ventriculo-atrial Wenckebach Conduction Due to Two-level Block

A 54-year-old patient was studied because of ventricular tachycardia following an inferior myocardial infarction. During one episode of non-sustained ventricular tachycardia a 9:4 alternating ventriculo-atrial Wenckebach block was noted. This was based upon a 2:1 block between the ventricles and the bundle of His and a 5:4 Wenckebach block between the bundle of His and the atria. Our study shows that alternate Wenckebach periods during ventriculo-atrial conduction may be caused by two or more levels of block in the ventriculo-atrial conduction system.     

Conductive Property of the Zone of Slow Conduction of Reentrant Ventricular Tachycardia and Its Relation to Pacing Induced Terminability

In order to assess the functional characteristics of the zone of slow conduction of reentrunt VT, rapid pacing was performed to entrain VT. The orthodromic conduction time was measured as the interval between the stimulus and the orthodromically captured electrogram recorded distal to the zone of slow conduction, hut not precisely at the exit point, and its response to rapid pacing was evaluated. In 32 of 33 consecutive patients, rapid pacing was performed to entrain VT. Of these, rapid pacing was repeated in 28 patients at 3–10 cycle lengths in steps of 10 msec before VT was terminated, or rapid pacing produced an acceleration of the rate. A pacing induced prolongation of the orthodromic conduction time (slowed conduction) was observed in 16 (57.1%) patients and in another 12 (42.9%) patients, the conduction time was constant. The pacing induced termination was observed in 93.8% of VT with slowed conduction and in 50% of VT with constant conduction, and the difference was significant (P < 0.05). There was no difference in the cycle length of VT or the shortest paced cycle length between VT with and without slowed conduction. The zone of slow conduction in human VT showed different conductive properties and VT with slowed conduction was associated with an easier and safer terminability with rapid pacing. The fact might be useful in selecting patients for antitachycardia pacing.     

Conductive Properties of the Reentrant Pathway of Ventricular Tachycardia During Entrainment From Outside and Within the Zone of Slow Conduction

Ventricular tachycardia (VT) was entrained with rapid ventricular pacing outside and within the zone of slow conduction (SCZ), and the conductive properties of the reentrant pathway were compared between the two pacing sites. Underlying heart diseases were old myocardial infarction (n = 2), postoperative tetralogy of Fallot (n = 1) or double outlet of the right ventricle (n = 1), dilated cardiomyopathy (n = 1), and pulmonary regurgitation of unknown cause (n = 1). Rapid pacing was continued for 5–10 seconds, and the time interval from paced stimulus to the entrained electrogram at the exit from SCZ (St-Ex) or to the QRS complex (St-QRS) was measured. Rapid pacing was performed at three or more cycle lengths after a decrement in steps of 10 msec. During rapid pacing outside of SCZ and entrainment of VT, constant fusion and progressive fusion were observed, and St-Ex and St-QRS showed the same response pattern: either a frequency dependent prolongation in 4 of 7 VTs or a constant time interval in the others VTs. When rapid pacing was attempted within SCZ, the response of the time intervals from paced site to the QRS (St-QRS) was the same as those observed during pacing outside SCZ except for one VT. In VT with repaired tetralogy of Fallot, the frequency dependent prolongation was observed during pacing from outside of SCZ but not within SCZ. Diseased myocardium extending widely into the outflow tract of the right ventricle may be responsible for the frequency dependent prolongation of St-Ex. In conclusion, the conductive property of the reentrant pathway might be assessed by observing the response patterns of St-Ex or St-QRS interval during transient entrainment of VT outside of SCZ, but exceptions may exist.     

Two Different Reentrant Circuits of Ventricular Tachycardia in a Patient with an Extensive Anterior Infarction: Evaluation Using Electrical Catheter Ablation Techniques

Two morphologically distinct sustained ventricular tachycardias were initiated by programmed stimulation during attempted catheter ablation in a patient with an old anterior myocardial infarction. Right bundle branch block configuration of ventricular tachycardia, which was identical to the spontaneously occurring tachycardia, was initiated and displayed fragmented mid-diastolic potential at the apicolateral left ventricular site. Evidence of a critical slow conduction area was observed during delivery of electrical stimuli to this area. Following a 150-joule electrical shock delivered to this area, right bundle branch block pattern of ventricular tachycardia was no longer inducible but a new sustained monomorphic ventricular tachycardia with left bundle branch block pattern was initiated. The mid-diastolic fragmented activity at the ablation site became electrical activation of bystander area that was not participating in the left bundle branch block type of the ventricular tachycardia circuit. The critical slow conduction area was identified at the apicoseptal left ventricular site that was separated more than 5 cm from the ablation site. We speculate that two morphologically distinct sustained monomorphic ventricular tachycardias may be due to two different reentrant circuits and not the different expression of the same circuit.     

Endocardial Catheter Ablation for Refractory Ventricular Tachycardia Associated with Coronary Artery Disease

Percutaneous endocardial electrode catheter ablation using stored direct current (DC) electrical energy was performed in five patients with recurrent ventricular tachycardia (VT) refractory to many antiarrhythmic drugs, including amiodarone. All had prior myocardial infarction and poor left ventricular function with ejection fractions ranging from 20% to 40%. Endocardial catheter and pace mappings were used to localize the earliest site of activation during VT. Under general anesthesia, two to six shocks with 200 to 300 joules DC energy per shock were delivered to the localized sites. Immediate complications included ventricular fibrillation in one patient, transient QRS complex widening in two patients, transient complete AV block with persistent first-degree AV block in one patient, and transient asystole in two patients. None had inducible VT immediately following ablation, or 4 to 6 days later; none had evidence of intracardiac clot by two-dimensional (2D) echocardiography on the third to fifth day. Peak creatine kinase ranged from 189 to 1610 IU/L with 9% to 18% MB fraction. During a follow-up of 6 to 30 months, three patients had no recurrence of VT. Two patients had recurrent VT with a slower rate, which was controlled with antiarrhythmic drugs. None had worsening of congestive heart failure. Two patients died of nonarrhythmic causes. We conclude that nonsurgical endocardial ablation of VT with an electrode catheter is effective for the treatment of refractory VT in selected patients with coronary artery disease.     

Reproducibility of Electrophysiological Testing During Antiarrhythmic Therapy for Ventricular Arrhythmias Unrelated to Coronary Artery Disease

Although electrophysiological studies are commonly used in the management of patients with ventricular tachycardia (VT), the reproducibility of these studies during therapy has not been established in patients in whom VT is associated with conditions other than coronary artery disease. Therefore, we performed confirmation studies during drug therapy in 60 patients (mean age 48 ± 18 years; 41 male) with sustained ventricular arrhythmias induced during initial study to assess the reproducibility of drug effect. The stimulation protocol used included the serial introduction of up to three premature ventricular stimuli during sinus rhythm and with ventricular pacing at two pacing rates. Rapid ventricular pacing techniques were also used. Antiarrhythmic drug efficacy was confirmed in 78% of patients. Sustained VT was induced at repeat electrophysiological study in 18% of patients daring antiarrhythmic therapy that had been felt to be effective on the basis of a single drug study. We conclude that electrophysiological study results during antiarrhythmic therapy exhibit significant day-to-day variability. Sustained VT can be induced during antiarrhythmic therapy previously determined to be effective by electrophysiological techniques in many patients.     

Demonstration of Entrainment and Presence of Slow Conduction During Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

During VT in two cases with arrhythmogenic right ventricular dysplasia, entrainment criteria, constant fusion beats except for the last entrainment beat, progressive fusion, and a localized conduction block associated with interruption of VT, were demon strated with rapid ventricular pacing performed during VT. Furthermore, a long conduction interval was present during entrainment from the pacing site to the earliest activation site during VT. indicating the presence of a slow conduction area. VT in these cases was, thus, due to reentry with an area of slow conduction within the circuit.     

Comparison of Spectral Temporal Mapping to the Time Domain Signal-Averaged Electrocardiogram in Normal Subjects and in Patients with Coronary Artery Disease and Sustained Ventricular Tachycardia

Spectral temporal mapping is a new form of analysis for signal-averaged electro-cardiography, which has the goal of improving the sensitivity and specificity of traditional time domain analysis. Our objective in this study was to determine the effectiveness of one form of spectral temporal mapping, in the face of conflicting results that have so far been reported with this approach. We prospec-tively performed both spectral temporal mapping and time domain analysis on 50 patients with a history of coronary artery disease and inducible sustained monomorphic ventricular tachycardia (Group 1) and on 25 normal subjects with normal electrocardiograms and no history of heart disease (Group 2). We found that for the 40 Group 1 patients without bundle branch block (Group lA), the sensitivity of spectral temporal mapping was lower than that for time domain analysis (45% vs 80%, P < 0.005). The results of spectral temporal mapping for Group lA patients were similar to that for all of Group 1. The sensitivity of spectral temporal mapping was 60% (n = 10) for patients with bundle branch block (Group IB). The specificity noted in Group 2 was 88% by each means of analysis; however, no one In Group 2 had an abnormal finding by time domain and spectral temporal mapping. Attempts to optimize the criteria for an abnormal spectral analysis did not identify criteria that were superior to those currently in use. We conclude that spectral temporal mapping using Haberl's method is inferior to time domain analysis in identifying patients with sustained ventricular tachycardia, but may be of value in conjunction with the traditional approach in identifying normal subjects.     

Ventricular Tachycardia in a Patient with Primary Hyperparathyroidism

We present a case of primary hyperparathyroidism with hypercalcemia in a patient who had spontaneous attacks of ventricular tachycardia. Right ventricular burst pacing reproducibly induced ventricular tachycardia in the electrophysiological laboratory after intravenous administration of calcium-gluconate, and verapamil could terminate the tachycardia. After resection of the parathyroid adenoma, the calcium level was restored to normal, and ventricular tachycardia did not occur again during the follow-up period,     

Septal Origin of Sustained Ventricular Tachycardia in a Patient with Right Ventricular Outflow Tract Obstruction After Correction of Tetralogy of Fallot

Right ventricular hypertension and ventricular arrhythmias are risk factors for sudden death after correction of tetralogy of Fallot, but sustained ventricular tachycardia has been reported only in patients without residual hemodynamic abnormalities. A patient with right ventricular hypertension and hypotensive ventricular tachycardia tolerated the arrhythmia better after relief of right ventricular outflow tract obstruction. This case provides insight into the relationship between hemodynamic abnormalities and the clinical consequences of arrhythmias. To our knowledge, it is the first report of ventricular tachycardia originating in scar adjacent to the ventricular septal defect patch after correction of tetralogy of Fallot.     

Ventricular Tachycardia in Healing Canine Myocardial Infarction: Evidence for Multiple Reentrant Mechanisms

Prior studies have demonstrated that unimorphic VT, sometimes due to epicardial reentry, can be induced in healing canine MI; however, the characterization of the types of reentry involved has differed among prior studies. The purpose of this study was to further characterize the spectrum of epicardial reentrant circuits during induced VT in experimental canine MI. Experimental MI was created by total occlusion of the LAD in dogs. Five days later, programmed stimulation was used to induce VT, which was mapped on the epicardium using a combination of vector and isochronol techniques. Pathological analysis was used to determine regions of transmural MI. Epicardial reentrant circuits were identified in eight dogs. The mean cycle length of induced VT was 212 ± 32 ms. In 3 of 8 experiments, a region of transmural MI was present, which formed at least a portion of a central zone of block around which reentrant impulses circulated. In five experiments, reentry was functional in nature, although the characteristics of the region of functional conduction block were variable. Long lines of functional block, short lines of block with slow conduction transverse to fiber orientation, and leading circle reentry were each observed in different experiments. Although a zone of slow conduction was identified in seven of the experiments, slow conduction transverse to fiber orientation appeared crucial in maintaining reentry in only three experiments. Multiple reentrant mechanisms of VT may be present in this single canine infarction model. Although a zone of slow conduction is usually present, the characteristics of the region of block are highly variable. However, epicardial reentry accounted for only a minority of induced arrhythmia episodes.     

Monomorphic Right Ventricular Tachycardia in a Patient with Mitral Valve Prolapse

A patient with mitral valve prolapse and symptomatic ventricular ectopy underwent an electrophysiological study during which a sustained monomorphic ventricular tachycardia with a left bundle branch block/right axis deviation morphology was induced. This morphology was replicated by pace mapping at the right ventricular outflow tract. To the best of our knowledge, this finding has not been previously described and suggests that the association between ventricular arrhythmias and mitral valve prolapse may not necessarily be causal.     

Differentiation of Sinus Tachycardia From Ventricular Tachycardia with 1:1 Ventriculoatrial Conduction in Dual Chamher Implantable Cardioverter Defibrillators: Feasibility of a Criterion Based on the Atrioventricular Interval

Tachycardia discrimination in future implantable cardioverter defibrillators (ICDs) is likely to be enhanced by the addition of an atrial sensing/pacing lead. However, differentiation of sinus tachycardia (ST) from ventricular tachycardia (VT) with 1:1 VA conduction will remain problematic. We assessed the use of the AV interval as a potential criterion for correctly differentiating ST from VT. Incremental V pacing at the right ventricular (HV) apex served as a “VT” model in each of 41 patients with 1:1 VA conduction to pacing cycle lengths ≤ 450 msec. High right atrial and RV apical electrograms during normal sinus rhythm (NSR) and during incremental V pacing were digitized (simulating ICD sensing). From these signals, AV interval versus pacing cycle length plots were computer generated to identify crossover cycle lengths, each defined as the cycle length at which the AV interval during V pacing equals the AV interval during NSR. At cycle lengths longer than the crossover value, the AV interval during “VT” exceeds the AV interval during NSR. In contrast, the AV interval during ST is physiologically shorter than the AV interval during NSR. Thus, ST can be readily differentiated from “VT” over a range of cycle lengths greater than the crossover value. The overall mean calculated crossover cycle length was 371 ± 52 msec. In 11 patients paced multiple times, each crossover cycle length was reproducible (mean coefficient of variation was 1.2%± 0.9% per patient). AV intervals measured at the RV apex were also analyzed with incremental V pacing during catecholamine stimulation (isoproterenol, n = 5) and during alternate site “VT” (RV outflow tract [n = 8] and left ventricle [n = 2]). In all these cases, the new “VT” plots of AV interval versus pacing cycle length coincided with or fell to the left of those obtained during control RV apical pacing and recording (i.e., these AV interval values crossed the NSR baseline at cycle lengths ≤ the crossover cycle length). Thus, the cycle length range for recognizable differentiation of ST from “VT” remained valid. The data suggest that the described AV interval criterion relying on the crossover cycle length: (1) is a promising approach to improve differentiation of ST from relatively slow VTs with 1:1 VA conduction, and (2) can readily be automated in future dual chamber ICDs, given its computational simplicity.     

Programmable External Automatic Antitachycardia Pacing as a Bridge to Definitive Therapy in Patients with Recurrent Sustained Ventricular Tachycardia

The efficacy and safety of external programmable automatic antitachycardia pacemakers (ATPs) used in the critical care setting for recurrent sustained monomorphic ventricular tachycardia (VT) was evaluated. Ten patients who had failed a mean of 4.0 +/- 1.4 antiarrhythmic medications (range 2-7) and who had previously required electrical cardioversion for VT were enrolled. Prior to ATP use, successful overdrive pacing termination of VT was demonstrated in all patients. Intertach (Intermedics, Inc.; n = 9) and Orthocor II (Cordis, Inc.; n = 1) ATPs were attached to temporary bipolar transvenous or epicardial pacing leads. Mean patient age was 66.4 +/- 11.5 years, and mean left ventricular ejection fraction was 22 +/- 7.5%. At the time of initial ATP use, mean VT cycle length was 347 +/- 88 msec (range 280-550 msec). A burst scanning antitachycardia pacing algorithm was used in each patient; one patient was also treated with a fixed rate burst adapted to VT cycle length. The duration of ATP use ranged from 2-25 days (median 5), successfully terminating greater than 3,369 VT episodes (median 3, range 0 to greater than 3,103 episodes per-patient). Two episodes of ATP induced rate acceleration occurred, each successfully terminated by the ATP. Only two patients required external cardioversion during ATP use, one for primary ventricular fibrillation and one for rapid polymorphic VT associated with antiarrhythmic drug withdrawal. ATPs also provided antibradycardia pacing and allowed for serial programmed ventricular stimulation. No complications were associated with transvenous catheter or ATP use.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unusual Mechanism of PR Interval Variation and Nonreentrant Supraventricular Tachycardia as Manifestation of Simultaneous Anterograde Fast and Slow Conduction Through Dual Atrioventricular Nodal Pathways

Noninvasive recordings in a 69-year-old woman showed two distinct PR intervals of about 0.21 and 0.58 s, suggestive of dual AV nodal conduction. Various unusual mechanisms of transition from short to long and from long to short conduction intervals and phenomena of concealed conduction were due to the presence of two functionally separated intranodal pathways. Refractoriness of the slow pathway was associated with bradycardia. Episodes of tachycardia exhibited a one-to-two relationship between P-waves and ventricular activations as a consequence of simultaneous anterograde fast and slow conduction leading to double ventricular responses to single P-waves.     

Nonreentrant Supraventricular Tachycardia Due to Simultaneous Conduction Over Fast and Slow AV Node Pathways: Successful Treatment with Radiofrequency Ablation

A 55-year-old woman with frequent problematic supraventricular tachycardia is presented. The tachycardia was irregular with predominately normal QRS morphology and was refractory to multiple antiarrhythmic drugs. At electrophysiology study, the tachycardia was inducible with atrial or ventricular extrastimuli and dual pathways were observed. In contrast to the situation usually seen with dual atrioventricular node physiology, the slow pathway had a longer effective refractory period than the fast pathway and reentrant tachycardia was not induced. Simultaneous conduction over the fast and slow pathways during sinus rhythm was shown to be the mechanism for clinical tachycardia. The tachycardia was successfully treated using radiofrequency ablation of the slow pathway.     

Initiation of Ventricular Tachycardia by Interruption of Pacemaker-Mediated Tachycardia in a Patient with a Dual-Chamber Implantable Cardioverter Defibrillator

A 74-year-old man with a dual-chamber implantable cardioverter defibrillator implanted 3 years before experienced multiple ventricular tachycardias (VTs). All episodes were initiated by pacemaker-mediated tachycardia (PMT) that was either stopped by atrial undersensing or the tachycardia termination algorithm of the device. After the termination of PMT, two rapid ventricular paced beats, the first initiated by artificial triggering and the second due to retrograde conduction of the first one, initiated VT that was successfully terminated by antitachycardia pacing or a direct current shock of the device . All episodes revealed this pattern of initiation with a short-long-short ventricular sequence inducing VT.     

The Comparative Predictive Accuracy of Spectral Turbulence Analysis and Time-Domain Analysis for Sustained Monomorphic Ventricular Tachycardia in Postinfarction Patients with Conduction Defects

Signal-averaged electrocardiograms obtained in 86 postinfarction patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or intraventricular conduction defect (IVC-D), underwent time-domain analysis (TDA) and spectral turbulence analysis (STA) to determine which approach provided the more effective marker for patients with sustained monomorphic ventricular tachycardia. TDA parameters included the root mean square value of the last 40 ms of the vectormagnitude complex and the duration of the low amplitude signal below 40 μV STA utilized a summation lead (X + Y + Z) and quantitated four parameters: interslice correlation mean, interslice correlation standard deviation, low slice correlation ratio, and spectral entropy. High-pass filters of 40 Hz and 25 Hz were used to study the total patient population with noise levels ≤1 μV and a subset of 67 patients with noise levels ≤ 0.5 μV, The techniques compared their effectiveness as measured by their positive predictive values (PPV), negative predictive values (NPV), sensitivity (Sn), and specificity (Sp). In RBBB, STA was uniformly a more powerful tool utilizing either filter at both noise levels. In LBBB, STA was consistently more powerful at both noise levels at 40 Hz and, generally, more powerful at 25 Hz with isolated exceptions. In conduction defects in which QRS was > 100 ms but < 120 ms, TDA was equal to or more effective than STA, with the exception of PPV and Sp at 40 Hz at 1-μV noise level and the Sp at 0.5 μV. The addition of ejection fraction data to STA score resulted in further overall improvement in performance, but above conclusions were unchanged.