Preferential action of mexiletine on central common pathway of reentrant ventricular tachycardia.

OBJECTIVES: The action of mexiletine on diseased myocardium was assessed in reentrant ventricular tachycardia (VT). BACKGROUND: Whether class Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been studied in humans. METHODS: In 10 consecutive patients (7 with a previous myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was measured from stimulus to the entrained electrogram at the exit from the presumed central common pathway (i.e., the earliest site of activation). Mexiletine at 125 to 250 mg was administered intravenously, and when VT with the same configuration was induced, the study was repeated. The action of mexiletine on the central common pathway was assessed from the changes in VT cycle length and orthodromic conduction time. The effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were compared between normal and diseased myocardium. RESULTS: Mexiletine prolonged the VT cycle length in all patients, from (mean +/- SD) 316 +/- 30 to 360 +/- 64 ms (mean change 20 +/- 7%, p < 0.001); during entrainment of VT, the orthodromic conduction time was prolonged, from 306 +/- 58 to 367 +/- 89 ms (mean change 18 +/- 9%, p < 0.001). These changes were highly correlated (r = 0.95, p < 0.001). QRS duration changed little (4 +/- 3%), and local conduction time showed no change. The duration of the fragmented electrogram width was prolonged by mexiletine: from 146 +/- 50 to 176 +/- 56 ms (mean change 23 +/- 8% during VT, p < 0.001). Only a slight change occurred in the effective refractory period, both at the pacing site and at the exit. CONCLUSIONS: Mexiletine caused little change in conduction time in normal myocardium but prolonged VT cycle length, orthodromic conduction time and duration of the local electrogram at the earliest site of activation of VT. From these findings, a preferential action of mexiletine on diseased myocardium was suggested but seemed to occur only at higher frequencies during tachycardia.

Mechanism of arrhythmogenicity of the short-long cardiac sequence that precedes ventricular tachyarrhythmias in the long QT syndrome.

OBJECTIVES: The purpose of this study was to investigate the electrophysiologic mechanism(s) that underlie the transition of one or more short-long (S-L) cardiac sequences to ventricular tachyarrhythmias (VTs) in the long QT syndrome. BACKGROUND: One or more S-L cardiac cycles, usually the result of a ventricular bigeminal rhythm, frequently precedes the onset of VT in patients with either normal or prolonged QT interval. Electrophysiologic mechanisms that underlie this relationship have not been fully explained. METHODS: We investigated electrophysiologic changes associated with the transition of a S-L cardiac sequence to VT in the canine anthopleurin-A model, a surrogate of LQT3. Experiments were performed on 12 mongrel puppies after administration of anthopleurin-A. Correlation of tridimensional activation and repolarization patterns was obtained from up to 384 electrograms. Activation-recovery intervals were measured from unipolar electrograms and were considered to represent local repolarization. RESULTS: We analyzed 24 different episodes of a S-L sequence that preceded VT obtained from 12 experiments. The VT followed one S-L sequence (five episodes), two to five S-L sequences (12 episodes) and more than five S-L sequences (seven episodes). The single premature ventricular beats coupled to the basic beats were consistently due to a subendocardial focal activity (SFA). There were two basic mechanisms for the development of VT after one or more S-L sequences: 1) in 10 examples of a S-L sequence due to a stable unifocal bigeminal rhythm, the occurrence of a second SFA, which arose consistently from a different site, infringed on the pattern of dispersion of repolarization (DR) of the first SFA to initiate reentrant excitation; 2) in the remaining 14 episodes of a S-L sequence, a slight lengthening (50 to 150 ms) in one or more preceding cycle lengths (CLs) resulted in alterations of the spatial pattern of DR at key sites to promote reentry. The lengthening of the preceding CL produced differentially a greater degree of prolongation of repolarization at midmyocardial and endocardial sites compared with epicardial sites with consequent increase of DR. The increased DR at key adjacent sites resulted in the development of de novo zones of functional conduction block and/or slowed conduction to create the necessary prerequisites for successful reentry. CONCLUSIONS: The occurrence of VT after one or more S-L cardiac sequences was due to well defined electrophysiologic changes with predictable consequences that promoted reentrant excitation.

Catheter ablation of ventricular tachycardia with radiofrequency currents, with special reference to the termination and minor morphologic change of reinduced ventricular tachycardia.

During catheter ablation with radiofrequency (RF) currents, the incidence of the termination of reentrant ventricular tachycardia (VT) during application of RF energy and the morphologic change of the reinduced VT were analyzed. Twenty-five patients (20 men and 5 women, aged 44 +/- 17 years) were studied. After induction of monomorphic sustained VT, the ablation site was determined by endocardial activation mapping, identification of isolated mid-diastolic potential, and pacing during tachycardia. Thirty-six monomorphic VTs were induced in 25 patients and terminated with programmed stimulation. The cycle length was 323 +/- 55 ms and all VTs were entrained with rapid ventricular pacing. The target site was the earliest site of activation of VT in 26 VTs in 16 patients, and the area of slow conduction in 10 VTs in 9 patients. VT was terminated soon after the application of RF currents in 33 VTs in 22 patients at 6.0 +/- 3.1 seconds, and VT was induced immediately after the cessation of RF currents in 11 patients. Of these, 4 patients with idiopathic left ventricular VT had an alternation in the QRS configuration before catheter ablation and required repeat ablation of the other VT morphology. In the other 7 patients, such morphology was not observed before ablation, but was observed in VT induced when the original VT was terminated. Repeated attempts of catheter ablation 2 to 9 times at the remapped site was, however, successful in 7 of 8 VTs.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of atropine on QT prolongation and torsade de pointes induced by intracoronary acetylcholine in the long QT syndrome.

We recently reported a marked QT prolongation and torsade de pointes (TDP) induced by an intracoronary acetylcholine (ACh) administration in patients with long QT syndrome, but the mechanism was not determined. In the present study, the effect of atropine on the ACh-induced QT prolongation and TDP was studied in long QT syndrome. Nine patients with congenital long QT syndrome were studied. ACh at doses of 20, 50, and 100 microg were injected in a stepwise manner into the left main coronary artery, and the changes in the QT interval were measured. In 4 of the 9 patients, ACh administration at a dose of 100 microg was repeated after an intravenous atropine administration at a dose of 0.5 mg. The QT intervals were measured using 12-lead electrocardiograms, and the data were compared before and after atropine administration. The coronary angiograms were normal and coronary spasm was not induced by ACh in all patients. The intracoronary administration of ACh at a dose of 100 microg significantly prolonged the corrected QT interval (QTc), from 511 +/- 26 to 629 +/- 40 ms (p <0.05). In 5 of the 9 patients, TDP was induced and was spontaneously terminated within 10 seconds (n = 4) or required direct-current shock (n = 1). After atropine administration, intracoronary ACh at the same dose resulted in no QT prolongation, and the QTc interval remained unchanged (525 +/- 29 vs 520 +/- 21 ms before and after atropine), and no TDP was induced. These findings indicate that the muscarinic receptor is involved in ACh-induced QT prolongation and TDP, both of which were prevented by the atropine administration.

Acetylcholine-induced prolongation of the QT interval in idiopathic long QT syndrome.

Intracoronary acetylcholine prolonged the QT interval in 5 patients with congenital long QT syndrome but not in subjects with normal QT intervals. Prolongation was not due to bradycardia or adrenergic drive, and atropine was suggested to attenuate the response.

Recovery of the right atrial effective refractory period after cardioversion of chronic atrial fibrillation.

The effective refractory period was shorter in patients with than without chronic atrial fibrillation (AF). The effective refractory period was prolonged, and at 12 and 24 hours after cardioversion of AF it was the same as the subjects without AF.

Spatial orientation of the reentrant circuit of idiopathic left ventricular tachycardia.

In 6 patients with idiopathic left ventricular VT, the spatial orientation of the reentrant circuit was estimated from the results of transient entrainment of VT with rapid pacing at different sites. The entrance to the area of slow conduction was located toward the outflow tract, whereas the exist was located at the apicoposterior area of the left interventricular septum.

Ventricular tachycardia initiated by high energy cardioversion in a patient with an implantable cardioverter defibrillator.

A transvenous implantable cardioverter defibrillator (ICD) was implanted into a 58 year old woman with idiopathic dilated cardiomyopathy who had drug refractory monomorphic ventricular tachycardia (VT). Antitachycardia pacing failed to terminate the VT; termination was attempted at 24 J, which was above the defibrillation threshold. When cardioversion at 24 J was delivered, VT with a different morphology and slower rate was reproducibly initiated. At 3 J, however, the original VT was successfully terminated without initiation of the slower VT. A new VT may be induced by high energy cardioversion. This may be a manifestation of the proarrhythmic potential of ICDs.

Bifid T waves induced by isoprenaline in a patient with Brugada syndrome.

A 41 year old man with incomplete right bundle branch block and persistent coved-type ST elevation in the right precordial leads during sinus rhythm had an episode of syncope while driving. He had never had syncope before and there was no family history of sudden cardiac death. Ventricular fibrillation was induced during electrophysiological study (EPS) by double extrastimuli applied to the right ventricle. Disopyramide was effective in preventing ventricular fibrillation during EPS. beta Adrenoceptor stimulation manifested bifid T waves and reduced ST segment elevation in right precordial leads. Simultaneously recorded monophasic action potential (MAP) duration at 90% repolarisation did not change in the right ventricular outflow tract, while it shortened in the left ventricular septum. These findings suggest that right precordial bifid T waves might result from relatively early repolarisation of the left ventricles. Moreover the gradient of action potential duration might explain the mechanism of ST segment abnormalities in a patient with Brugada syndrome.

Drug-induced narrowing of the width of the zone of entrainment as a predictor of the subsequent non-inducibility of reentrant ventricular tachycardia after an additional dose of an antiarrhythmic drug.

BACKGROUND: The efficacy of drugs used to treat inducible monomorphic sustained ventricular tachycardia (VT) has been assessed by investigating their ability to suppress inducibility, but the mechanism of the drug action remains to be determined. OBJECTIVES: To determine electrophysiological variables that predict inducibility, divided doses of class I antiarrhythmic drugs were given and their effects were analysed, particularly the ability of the final dose to suppress inducibility. METHODS: The excitable gap was estimated by the zone of entrainment, which was defined as the difference between the cycle length of VT and the longest paced cycle length that interrupted VT during entrainment of VT with rapid pacing at paced cycle lengths in decrements of 10 ms. The cycle length of VT, the block cycle length, and the zone of entrainment were measured in the drug free state and after intermediate and final doses of procainamide, disopyramide, cibenzoline, and mexiletine. RESULTS: Sustained monomorphic VT with a mean (SD) cycle length of 285 (43) ms was induced in 8 patients. It was entrained and interrupted at the block cycle length of 231 (31) ms. The width of the zone of entrainment was 54 (23) ms. In 8 studies VT was not inducible at final doses of procainamide in 4, cibenzoline in 1, and mexiletine in 3. In another 10 studies (procainamide in 4, disopyramide in 1, cibenzoline in 2, and mexiletine in 3), VT remained inducible at the intermediate dose and at the final dose. The cycle length of VT was prolonged to a similar degree in studies of effective and ineffective drugs, but the cycle length that blocked VT was longer at the intermediate dose of the effective drugs. Consequently, the width of the zone of entrainment was significantly narrowed at the intermediate dose of effective drugs and the width of the zone of entrainment was narrower than when ineffective drugs were given (22 (13) ms v 76 (18) or 75 (37) ms at the intermediate and final doses respectively (P < 0.02). CONCLUSION: Drugs that narrowed the zone of entrainment were associated with non-inducibility of VT after the final dose of the drug was given. The baseline variables did not predict the responses to class I antiarrhythmic drugs.

Radiofrequency catheter ablation for idiopathic right ventricular tachycardia with special reference to morphological variation and long-term outcome.

OBJECTIVE: To assess the long term outcome of radiofrequency (RF) catheter ablation for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle, with special reference to the morphological variation in the VT-QRS complexes. PATIENTS: 13 patients whose ventricular tachycardia was treated with RF ablation were followed up more than 18 months after RF ablation. RESULTS: Endocardial mapping revealed the various extensions of ventricular tachycardia origin (from 0.5 x 0.5 cm to 2.0 x 2.0 cm) in which the earliest local electrogram was recorded during ventricular tachycardia. In all five tachycardias from a relatively wider origin (more than 0.5 x 0.5 cm) and in four of eight from a narrow origin (< 0.5 x 0.5 cm), subtle morphological variation in the VT-QRS complexes was observed. In tachycardias with morphological variation, the local electrogram at the tachycardia origin also showed concomitant variation in morphology and activation sequence. Ventricular tachycardia from a narrow site was eliminated by RF ablation to the confined site, but a larger number of RF applications was required in tachycardias from a wider origin. All 13 tachycardias were successfully ablated by RF current, and during the follow up period of 28.2 (SD 7.2) months, recurrence was observed in only one patient who had a wider origin. CONCLUSIONS: Long term efficacy of RF ablation was excellent in idiopathic ventricular tachycardia originating from the outflow tract of the right ventricle. Subtle morphological variations were frequently observed in this type of ventricular tachycardia, and about half of them represented a relatively wider arrhythmogenic area.

Discrepant effects of mexiletine on cycle length of ventricular tachycardia and on the effective refractory period in the area of slow conduction.

OBJECTIVE: Monomorphic sustained ventricular tachycardia (VT) can often be entrained and interrupted at a critical paced cycle length. The aim was to evaluate a possible determinant of this phenomenon by observing the action of mexiletine on the critical paced cycle length and other variables. METHODS: Nine consecutive patients with symptomatic VT were studied. After induction of VT, the area of slow conduction was mapped as the earliest site of the activation or the site with mid-diastolic potential during the tachycardia. Rapid pacing was performed at a site distant from the tachycardia circuit to entrain the tachycardia, starting at a cycle length 10-20 ms shorter than the VT cycle length, and repeated after a decrement of the cycle length in steps of 10 ms to obtain the longest paced cycle length that interrupted the tachycardia: the block cycle length. The effective refractory period (ERP) was measured at the pacing site at which the myocardium was presumed to be normal and also in the area of slow conduction. The effects of mexiletine on the cycle length of VT, the block cycle length, and the ERP at two sites were obtained before and after mexiletine administration. The relation between the cycle length of VT and block cycle length and their changes were also analysed. RESULTS: 11 VTs with the same morphology were induced before and after mexiletine administration. The VT cycle length was prolonged by mexiletine from 309 (SD 53) to 361 (47) ms, and it was interrupted at block cycle lengths of 247 (37) and 307 (41) ms, respectively, the changes being 18 (12)% and 23 (8)% (both P < 0.001). All VTs were entrained, and during pacing at the block cycle length there was abrupt loss of fusion and change in the presystolic electrogram, always associated with interruption of VT on cessation of rapid pacing. A good correlation was observed between the VT cycle length and the block cycle length (r = 0.77 to 0.80). The ERP at the pacing site (normal myocardium) and in the area of slow conduction showed no significant change: 241 (21) v 240 (22) ms and 262 (9) v 252 (9) ms, respectively. The block cycle length was longer than the ERP after mexiletine administration: 362 (55) v 252 (9) ms (P < 0.02). CONCLUSIONS: Mexiletine prolonged the cycle length of VT and the VT-interrupting critical cycle length but not the ERP. The prolongation of the VT cycle length and the block cycle length by mexiletine seemed to be unrelated to the action potential duration, but related to depressed intercellular conduction.

Relation between bradycardia dependent long QT syndrome and QT prolongation by disopyramide in humans.

BACKGROUND: Recent molecular biological investigations have identified abnormal genes in familial forms of long QT syndrome, but in bradycardia dependent acquired long QT syndrome, no such genetic abnormality has yet been identified. OBJECTIVE: To investigate the relation between the responses of QT interval to pacing change and to disopyramide. METHODS: This study included 13 patients with bradyarrhythmia who had undergone pacemaker implantation. The patients were divided into two groups: group I (n = 8), patients with QT prolongation (QT interval > or = 500 ms) during bradycardia; group II (n = 5), patients without QT prolongation (QT interval < 500 ms) during bradycardia. The responses of QT interval caused by the change of pacing rate were determined and compared with the changes of the QT interval after disopyramide administration. RESULTS: The QT interval in group I was significantly longer than that in group II when the pacing rate was decreased from 110 to 50 beats/min: mean (SD) 451 (16) v 416 (17) ms at 90 beats/min (p = 0.0033), and 490 (19) v 432 (18) ms at 70 beats/min (p = 0.0002), respectively. The QT interval was prolonged significantly by disopyramide in both groups, but the change was more pronounced in group I than in group II: 78 (33) v 35 (10) ms (p < 0.05). CONCLUSIONS: This study suggests that the patients showing bradycardia dependent QT prolongation are also more markedly affected by disopyramide and that abnormal potassium channel may be the underlying mechanism.

Discrepancy between inducibility of ventricular tachycardia and activity of cardiac sarcoidosis. Requirement of defibrillator implantation for the inactive stage of cardiac sarcoidosis.

Monomorphic ventricular tachycardia (VT) developed in two patients with cardiac sarcoidosis. Before treatment with prednisolone, technetium or gallium scintigram revealed abnormal accumulation in the heart and bilateral hilar lymph nodes, but programmed electrical stimulation failed to induce VT in either case. Prednisolone was administered and the abnormal accumulation of the scintigra ms disappeared. However, VT became reproducibly inducible, and in one of the patients, transient entrainment was demonstrated in clinical VT morphology. Defibrillators were implanted in both patients. Some VTs associated with cardiac sarcoidosis are due to reentry, and inducibility of VT is not associated with the activity of cardiac sarcoidosis. Even though steroid therapy suppresses the activity of cardiac sarcoidosis, defibrillator implantation is necessary to prevent a possible arrhythmic event during the follow-up.

Radiofrequency current caused slowing of non-reentrant idiopathic right ventricular tachycardia originating from a wide arrhythmogenic area.

Radiofrequency catheter ablation was attempted in a patient with non-reentrant idiopathic right ventricular tachycardia (VT). Endocardial mapping indicated that the VT originated in the outflow tract of the right ventricle; however, an electrogram with an almost the identical activation time was recorded from an area extending to 1.0 x 2.0 cm. Each application of radiofrequency current within the area terminated VT, but a progressively slower VT with the same QRS configuration was induced until the area was covered by separate radiofrequency lesions. A progressive prolongation of VT cycle length might be related to a residual arrhythmogenic myocardium. Termination and slowing of the VT rate can be a hallmark of efficacy of each radiofrequency lesion.

Structure of the reentrant circuit of idiopathic left ventricular tachycardia: new insights into the role of the Purkinje network.

In idiopathic left ventricular tachycardia (ILVT), the reentrant circuit is considered to involve the Purkinje system, and the Purkinje potential (P-potential) appears to be a marker for successful ablation. However, the characteristics of the reentrant circuit in ILVT have not yet been defined. In 2 cases of ILVT, we performed detailed mapping along the left ventricular septum during VT and sinus rhythm. ILVTs were successfully ablated at the posteroapical area of the left ventricular septum where the high frequency P-potential was recorded and this portion was considered to be the exit site of the reentrant circuit. A small P-potential was also recorded at the portion proximal to the exit site, and it preceded the P-potential at the exit site. However, the local ventricular electrogram at the exit site preceded that at the proximal site during VT. Moreover, the small P-potential was orthodromically entrained by ventricular pacing from the proximal site. These findings suggest that the reentry circuit of ILVT appeared to have considerable size.

Intravenous administration of class I antiarrhythmic drugs induced T wave alternans in a patient with Brugada syndrome.

A 71-year-old man who experienced aborted sudden death was referred to our hospital. Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V1 to V3. Double ventricular extrastimuli at coupling intervals >180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V1 to V3, and visible T wave alternans was induced in leads V2 and V3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V2 and V3. Class I antiarrhythmic drug-related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.

Role of alpha1-blockade in congenital long QT syndrome: investigation by exercise stress test.

Beta-blockade is widely reported to reduce the incidence of syncope in 75-80% of patients with congenital long QT syndrome (LQTS). However, despite full-dose beta-blockade, 20-25% of patients continue to have syncopal episodes and remain at high risk for sudden cardiac death. In some patients refractory to beta-blockade, the recurrence of arrhythmias is successfully prevented by left stellate ganglionectomy, and also by labetalol, a nonselective beta-blockade with alpha1-blocking action. These observations suggest that not only beta-adrenoceptors, but also alpha1-adrenoceptors, play an important pathogenic role, especially under sympathetic stimulation, in LQTS. The clinical effects of alpha1-blockade in congenital LQTS were investigated in 8 patients with familial or sporadic LQTS. Two measurements of the QT interval were taken, from the QRS onset to the T wave offset (QT) and from the QRS onset to the peak of the T wave (QTp). Using the Bruce protocol, an exercise test was performed after administration of beta-blockade alone and again after administration of alpha1-blockade. The following were compared: (1) Bazzet-corrected QT (QTc) and QTp (QTpc) intervals in the supine and standing position before exercise and in the early recovery phase after exercise; and (2) the slopes (reflecting the dynamic change in the QT interval during exercise) of the QT interval to heart rate were obtained from the linear regression during the exercise test. In the supine position before exercise, there was no change in the QTc before or after the addition of alpha1-blockade (498+/-23 vs 486+/-23 ms [NS]). However, in the upright position before exercise and in the early recovery phase after exercise, QTc was significantly shortened from 523+/-21 to 483+/-22ms (p<0.01), and from 521+/-30 to 490+/-39ms (p<0.01), respectively, by alpha1-blockade. The QTpc was unchanged in any situation. Consequently, QTc-QTpc was significantly shortened by alpha1-blockade in the upright position before exercise and in the early recovery phase after exercise (131+/-36 to 105+/-37ms (p<0.05), and 132+/-29 to 102+/-31 ms (p<0.01), respectively). The slopes of the QT interval-heart rate relation by linear regression became significantly steeper from -2.23+/-0.38 to -2.93+/-0.76 (p<0.01) with the addition of alpha1-blockade. The findings suggest that the addition of alpha1-blockade attenuated the exercise-induced prolongation of the QT interval and that the rate adaptation of the QT interval to heart rate during exercise was improved. This indicates that additional treatment with alpha1-blockade may be beneficial to prevent cardiac events in LQTS patients in whom ventricular arrhythmia is resistant to beta-blockade.

AV nodal reentrant tachycardia with a bystander Mahaim fiber.

A 13 year old boy had a wide QRS complex tachycardia. A discontinuity in the AV nodal functional curve was observed in the electrophysiologic study. The AV internal was prolonged in association with progressive ventricular preexcitation. At maximal preexcitation, the HV interval was -20 msec and the QRS complex was identical to that seen during clinical tachycardia. No VA conduction was found and atrial premature beats did not affect the tachycardia. The His deflection was found at variable timing when tachycardia was induced. These findings confirmed that tachycardia originated within the AV node and was conducted to the ventricle over the Mahaim fiber. The short effective period of the Mahaim fiber had clinical significance since when atrial fibrillation developed, a rapid ventricular response was observed.

Alternation in the fusion complex during constant pacing of sustained ventricular tachycardia.

In a patient with sustained ventricular tachycardia (VT), we observed two different conduction times through the reentry circuit at the critical paced cycle length. The cycle length of the VT was 420 msec and overdrive pacing initially performed at a paced cycle length of 400 msec and repeated at decrements of 10 msec until the VT was interrupted at a paced cycle length of 320 msec. During rapid pacing, constant fusion and progressive fusion were confirmed. The first post-pacing return cycle was identical to each paced cycle length. The conduction time between the stimulus artifact and the orthodromically captured electrogram at the left ventricle was constant at 350 msec in each paced cycle length. However, only at a pacing cycle length of 360 msec two conduction times were alternatively observed, one of 350 msec and the other of 365 msec. When the conduction time changed from 350 msec to 365 msec, morphological alternation both in the surface QRS complex and in the orthodromically captured electrogram was evident. Dual slow pathways or a single slow pathway with plural exits from the reentry circuit is a likely mechanism of the alternation.