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Double Ventricular Response to an Extrastimulus in a Patient with Triple Atrioventricular Pathways

1978; Elsevier BV; Volume: 74; Issue: 5 Linguagem: Inglês

10.1378/chest.74.5.593

1931-3543

João Pimenta, Manoel Miranda, Lélio A Silva,

Atrial Fibrillation Management and Outcomes

A patient with the Wolff-Parkinson-White Syndrome was studied through recordings of the intracardiac potentials and programmed atrial stimulation. During programmed atrial stimulation at progressively shorter coupling intervals (A1-A2 intervals), the His deflection was always recorded after the ventricular complex. Thus, at coupling intervals between 295 and 250 msec, there was a double ventricular response, one through the accessory pathway (QRS complex of the Wolff-Parkinson-White morphologic pattern) and the other by the normal atrioventricular pathway (normal QRS complex or with pattern of left bundle-branch block). At a coupling interval of 295 msec, the atrio-His (A-H) interval increased from 200 to 350 msec. This fact and the presence of two distinct A2-H2 intervals are suggestive of the existence of dual atrioventricular pathways, coexisting functionally with a lateral accessory bypass (Kent's bundle). A patient with the Wolff-Parkinson-White Syndrome was studied through recordings of the intracardiac potentials and programmed atrial stimulation. During programmed atrial stimulation at progressively shorter coupling intervals (A1-A2 intervals), the His deflection was always recorded after the ventricular complex. Thus, at coupling intervals between 295 and 250 msec, there was a double ventricular response, one through the accessory pathway (QRS complex of the Wolff-Parkinson-White morphologic pattern) and the other by the normal atrioventricular pathway (normal QRS complex or with pattern of left bundle-branch block). At a coupling interval of 295 msec, the atrio-His (A-H) interval increased from 200 to 350 msec. This fact and the presence of two distinct A2-H2 intervals are suggestive of the existence of dual atrioventricular pathways, coexisting functionally with a lateral accessory bypass (Kent's bundle). In spite of having been thoroughly studied through the recordings of the atrioventricular potentials and through atrial stimulation with the technique using extrastimuli, the Wolff-Parkinson-White syndrome (preexcitation syndrome) can still offer interesting aspects. Thus, a stimulus arising in the atrium or ventricle can be conducted by the accessory pathway or the normal pathway (or both) and produce arrhythmias, which are sometimes difficult to explain. This current report presents the findings in a case of Wolff-Parkinson-White syndrome with a lateral accessory pathway associated with a dual intranodal pathway, with a double ventricular response to a premature atrial depolarization.Case ReportA 45-year-old man who had diabetes that was controlled by administration of isophane insulin suspension (NPH insulin) had a routine electrocardiogram that showed patterns of the Wolff-Parkinson-White syndrome, type B; he had never had a crisis of tachycardia recorded electrocardiographically. With the patient's consent, he underwent an electrophysiologic study under local anesthesia. The His bundle was recorded by the technique described by Scherlag and associates,1Scherlag BJ Lau SH Helfant RH et al.Catheter technique for recording His bundle activity in man.Circulation. 1969; 39: 13-18Crossref PubMed Scopus (689) Google Scholar and the right atrium was scanned by the technique using extrastimuli.2Damato AN Lau SH Patton RD et al.A study of atrioventricular conduction in man using premature atrial stimulation and His bundle recordings.Circulation. 1969; 40: 61-69Crossref PubMed Scopus (43) Google Scholar The electrodes were connected to a multichannel oscilloscope-recorder (Electronics for Medicine DR-12) with surface electrocardiographic leads (leads 2 and V1) and were recorded on photographic paper at a paper speed of 100 mm/sec. The right atrium was paced by a programmed stimulator (designed by Mr. Percival Gomes Neto, engineer, and developed by Indústria de Aparelhos Médicos e Eletrônicos, Sao Paulo, Brazil); the stimulator delivered regular stimuli (E1) and extrastimuli (E2) manually, both with 2-msec duration and at twice the diastolic threshold. The right atrium was scanned by shortening the coupling interval of 20 msec and of 10 or 5 msec on several occasions. The patient was not receiving any cardioactive drug at the time of the study.FindingsThe atrial, His bundle, and ventricular responses due to sinus rhythm are designated as A, H, and V; those deflections elicited by E1 and E2 are designated as A1, H1, and V1 and as A2, H2, and V2, respectively. Under control conditions, there was sinus rhythm (Fig 1) of 88 beats per minute (A-A interval of 680 msec), with a P-R interval of 120 msec, a P-A interval of 40 msec, an A-H interval of 90 msec, an H-V interval of "minus" 10 msec, and a ventricular response of 100 msec, showing a delta wave. In these conditions the His deflection was recorded after the onset of the ventricular complex (after the delta wave); and under atrial stimulation at a driving cycle length that was higher than the sinus cycle, due to prolongation of the A-H interval, the His potential disappeared inside the ventricular inscription, making the analysis of normal atrioventricular conduction difficult with high rates, since the P-delta interval (P-D interval) remained unchanged but always showing patterns of the Wolff-Parkinson-White syndrome.The use of extrastimuli with progressively shorter coupling intervals showed preferential conduction by the accessory pathway, with V2 similar to V1 until an A1-A2 interval of 330 msec. At an A1-A2 interval of 320 msec, the H2 was recorded after V2, with A2-H2 interval of 120 msec. At a coupling interval of 310 msec, the same pattern occurred but with A2-H2 interval of 150 msec; and at an A1-A2 interval of 300 msec, the A2-H2 interval was 200 msec (H2 always after V2), with the A2-V2 interval fixed, which event is commonly observed in atrioventricular refractory studies (Fig 1).At a coupling interval between 295 and 280 msec (Fig 2), there were double ventricular responses, one with conduction along the accessory pathway (V2) and the other later (V3) with ventricular activation through the normal atrioventricular junction. Thus, at a coupling interval of 295 msec, the A2-H2 interval was 350 msec, the H2-V3 interval was 40 msec, and V3 was 70 msec, eliciting reciprocal atrial beats and a short run of supraventricular paroxysmal tachycardia that was quickly aborted. At a coupling interval between 295 and 270 msec, all A2-H2 intervals were increased; at coupling intervals between 270 and 250 msec, there was a ventricular response of the pattern of preexcitation and, following it, a ventricular activation with a morphologic pattern of complete left bundle-branch block. At a coupling interval of 260 msec, there was an A2-H2 interval of 250 msec, an H2-V3 interval of 60 msec, and V3 of 130 msec.Figure 2Tracings obtained with leads 2 and V1, high right atrium (RA), and His bundle electrogram (HBE), recorded simultaneously. A (top), At coupling interval of 300 msec, A2-H2 interval is 200 msec, with H2 after V2. B (middle), At A1-A2 interval of 295 msec, there is double ventricular response (V2 along anomalous pathway and V3 along normal atrioventricular pathway, with normal intraventricular conduction), with sudden increase in A2-H2 interval, reaching 350 msec. C (bottom), By shortening coupling interval (A1-A2 interval of 260 msec), A2-H2 interval becomes shorter (250 msec), and ventricular activation (Vs) shows left bundle-branch block.View Large Image Figure ViewerDownload (PPT)The effective refractory periods of the atrioventricular junction and the atria were 240 and 220 msec, respectively. It was not possible to evaluate the effective refractory period of the accessory pathway because it was shorter than the atrial one. This sequence shows a bypass, probably of the Kent type (fixed P-D interval under atrial pacing and extrastimulus), conducting preferentially by Kent's bundle and simultaneously through the normal pathway, proved by a coupling interval of 320 msec or shorter. At an A1-A2 interval of 295 msec, a double ventricular response and an unexpected increase of the A-H interval were already present. This fact and the presence of two distinct A2-H2 intervals suggest dual intranodal pathways.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar An alternative explanation is that A2 was blocked in the atrioventricular node, and the ventricular activation occurred totally through the accessory bypass, producing H2 retrogradely. This seems unlikely because the V2-H2 interval would be quite variable, and the atrial echo beat always appeared after V2 and was never recorded just after H2.DiscussionAs far as we know, the ventricular complexes in the Wolff-Parkinson-White syndrome result from the ventricular activation through the accessory bundle and the atrioventricular junctional pathway producing fusion beats. Thus, depending on the refractoriness of the atrioventricular junction and Kent's bundle, the syndrome has many degrees of fusion with morphologically different QRS complexes; this fact usually is observed in electrophysiologic studies using the technique of extrastimuli. Nevertheless, marked delays in normal atrioventricular conduction, enough to activate the His bundle after a ventricular depolarization, are unusual. Previously, three cases of double ventricular activation resulting from a premature atrial depolarization or during atrial fibrillation were reported, although in all cases the ventricular activation through the atrioventricular junction showed left bundle-branch block.4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google ScholarIn this case, with coupling intervals under 320 msec, because of the lengthening of the A-H interval, the His spike was recorded after V2 (morphologic pattern of preexcitation), not eliciting the ventricular response through the normal atrioventricular pathway, due to the absolute refractoriness of the ventricles. At a coupling interval of 295 msec, when the effective refractory period of the fast intranodal pathway had been reached, an unexpected prolongation of atrioventricular conduction occurred (A2-H2 interval of 350 msec), a sufficient time for ventricular repolarization (V2-V3 interval of 330 msec) due to the conduction through the slow pathway, producing two ventricular responses, one with preexcitation and the other with normal ventricular activation; although with a shorter coupling interval, V3 showed the pattern of left bundle-branch block.Grouleau et al,4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar Neuss et al,5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar and Josephson et al6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar postulated the occurrence of longitudinal dissociation between the accessory pathway and the atrioventricular junctional system, in order to explain the phenomenon, although such authors always recorded V3 with left bundle-branch block. In spite of the same event occurring in our patient, he still had beats with normal intraventricular conduction when the A-H interval increased from 200 to 350 msec (after scanning of the right atrium), an event that can be characteristically diagnosed as a dual intranodal pathway.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar Therefore, the normalization of ventricular activation through the normal pathway occurred when the slow pathway was utilized, with a V2-V3 interval of 330 msec, probably higher than the absolute refractory period of the left bundle. When there was left bundle-branch block, the V2-V3 interval was 250 msec. The reported authors4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar always obtained beats with left bundle-branch block because their patients probably did not have three atrioventricular pathways placed in parallel and because the conduction along the atrioventricular junction always reached the left bundle in the absolute refractory phase.Although it might be obtained with drugs, the normalization of the ventricular activation, in spite of being artificial, can help us to recognize electrocardiographic changes such as regions of necrosis, cardiac hypertrophies, disturbances in conduction, and ischemic abnormalities, which are usually obscured by preexcitation. The reciprocal atrial beat in this patient only occurred after ventricular activation by normal atrioventricular conduction, with retrograde conduction along the accessory pathway. Due to the delay in atrioventricular conduction, it becomes impossible for an extrastimulus to be conducted anterogradely by Kent's bundle and retrogradely by the normal pathway, since the His bundle is chronologically activated after the ventricular depolarization. In these cases, the low refractoriness of the accessory bundle "protects" against the development of paroxysmal tachycardia, because it keeps the ventricles in the refractory phase. The tachyarrhythmia can only be elicited through marked intranodal delays, but this is difficult to observe spontaneously, so that explains why this patient has three atrioventricular pathways and never showed a crisis of tachycardia. The references to multiple atrioventricular pathways have been frequent, but this seems to be the first recording of double ventricular activation with normal intraventricular conduction due to the delay in the slow pathway. In spite of having been thoroughly studied through the recordings of the atrioventricular potentials and through atrial stimulation with the technique using extrastimuli, the Wolff-Parkinson-White syndrome (preexcitation syndrome) can still offer interesting aspects. Thus, a stimulus arising in the atrium or ventricle can be conducted by the accessory pathway or the normal pathway (or both) and produce arrhythmias, which are sometimes difficult to explain. This current report presents the findings in a case of Wolff-Parkinson-White syndrome with a lateral accessory pathway associated with a dual intranodal pathway, with a double ventricular response to a premature atrial depolarization. Case ReportA 45-year-old man who had diabetes that was controlled by administration of isophane insulin suspension (NPH insulin) had a routine electrocardiogram that showed patterns of the Wolff-Parkinson-White syndrome, type B; he had never had a crisis of tachycardia recorded electrocardiographically. With the patient's consent, he underwent an electrophysiologic study under local anesthesia. The His bundle was recorded by the technique described by Scherlag and associates,1Scherlag BJ Lau SH Helfant RH et al.Catheter technique for recording His bundle activity in man.Circulation. 1969; 39: 13-18Crossref PubMed Scopus (689) Google Scholar and the right atrium was scanned by the technique using extrastimuli.2Damato AN Lau SH Patton RD et al.A study of atrioventricular conduction in man using premature atrial stimulation and His bundle recordings.Circulation. 1969; 40: 61-69Crossref PubMed Scopus (43) Google Scholar The electrodes were connected to a multichannel oscilloscope-recorder (Electronics for Medicine DR-12) with surface electrocardiographic leads (leads 2 and V1) and were recorded on photographic paper at a paper speed of 100 mm/sec. The right atrium was paced by a programmed stimulator (designed by Mr. Percival Gomes Neto, engineer, and developed by Indústria de Aparelhos Médicos e Eletrônicos, Sao Paulo, Brazil); the stimulator delivered regular stimuli (E1) and extrastimuli (E2) manually, both with 2-msec duration and at twice the diastolic threshold. The right atrium was scanned by shortening the coupling interval of 20 msec and of 10 or 5 msec on several occasions. The patient was not receiving any cardioactive drug at the time of the study.FindingsThe atrial, His bundle, and ventricular responses due to sinus rhythm are designated as A, H, and V; those deflections elicited by E1 and E2 are designated as A1, H1, and V1 and as A2, H2, and V2, respectively. Under control conditions, there was sinus rhythm (Fig 1) of 88 beats per minute (A-A interval of 680 msec), with a P-R interval of 120 msec, a P-A interval of 40 msec, an A-H interval of 90 msec, an H-V interval of "minus" 10 msec, and a ventricular response of 100 msec, showing a delta wave. In these conditions the His deflection was recorded after the onset of the ventricular complex (after the delta wave); and under atrial stimulation at a driving cycle length that was higher than the sinus cycle, due to prolongation of the A-H interval, the His potential disappeared inside the ventricular inscription, making the analysis of normal atrioventricular conduction difficult with high rates, since the P-delta interval (P-D interval) remained unchanged but always showing patterns of the Wolff-Parkinson-White syndrome.The use of extrastimuli with progressively shorter coupling intervals showed preferential conduction by the accessory pathway, with V2 similar to V1 until an A1-A2 interval of 330 msec. At an A1-A2 interval of 320 msec, the H2 was recorded after V2, with A2-H2 interval of 120 msec. At a coupling interval of 310 msec, the same pattern occurred but with A2-H2 interval of 150 msec; and at an A1-A2 interval of 300 msec, the A2-H2 interval was 200 msec (H2 always after V2), with the A2-V2 interval fixed, which event is commonly observed in atrioventricular refractory studies (Fig 1).At a coupling interval between 295 and 280 msec (Fig 2), there were double ventricular responses, one with conduction along the accessory pathway (V2) and the other later (V3) with ventricular activation through the normal atrioventricular junction. Thus, at a coupling interval of 295 msec, the A2-H2 interval was 350 msec, the H2-V3 interval was 40 msec, and V3 was 70 msec, eliciting reciprocal atrial beats and a short run of supraventricular paroxysmal tachycardia that was quickly aborted. At a coupling interval between 295 and 270 msec, all A2-H2 intervals were increased; at coupling intervals between 270 and 250 msec, there was a ventricular response of the pattern of preexcitation and, following it, a ventricular activation with a morphologic pattern of complete left bundle-branch block. At a coupling interval of 260 msec, there was an A2-H2 interval of 250 msec, an H2-V3 interval of 60 msec, and V3 of 130 msec.The effective refractory periods of the atrioventricular junction and the atria were 240 and 220 msec, respectively. It was not possible to evaluate the effective refractory period of the accessory pathway because it was shorter than the atrial one. This sequence shows a bypass, probably of the Kent type (fixed P-D interval under atrial pacing and extrastimulus), conducting preferentially by Kent's bundle and simultaneously through the normal pathway, proved by a coupling interval of 320 msec or shorter. At an A1-A2 interval of 295 msec, a double ventricular response and an unexpected increase of the A-H interval were already present. This fact and the presence of two distinct A2-H2 intervals suggest dual intranodal pathways.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar An alternative explanation is that A2 was blocked in the atrioventricular node, and the ventricular activation occurred totally through the accessory bypass, producing H2 retrogradely. This seems unlikely because the V2-H2 interval would be quite variable, and the atrial echo beat always appeared after V2 and was never recorded just after H2. A 45-year-old man who had diabetes that was controlled by administration of isophane insulin suspension (NPH insulin) had a routine electrocardiogram that showed patterns of the Wolff-Parkinson-White syndrome, type B; he had never had a crisis of tachycardia recorded electrocardiographically. With the patient's consent, he underwent an electrophysiologic study under local anesthesia. The His bundle was recorded by the technique described by Scherlag and associates,1Scherlag BJ Lau SH Helfant RH et al.Catheter technique for recording His bundle activity in man.Circulation. 1969; 39: 13-18Crossref PubMed Scopus (689) Google Scholar and the right atrium was scanned by the technique using extrastimuli.2Damato AN Lau SH Patton RD et al.A study of atrioventricular conduction in man using premature atrial stimulation and His bundle recordings.Circulation. 1969; 40: 61-69Crossref PubMed Scopus (43) Google Scholar The electrodes were connected to a multichannel oscilloscope-recorder (Electronics for Medicine DR-12) with surface electrocardiographic leads (leads 2 and V1) and were recorded on photographic paper at a paper speed of 100 mm/sec. The right atrium was paced by a programmed stimulator (designed by Mr. Percival Gomes Neto, engineer, and developed by Indústria de Aparelhos Médicos e Eletrônicos, Sao Paulo, Brazil); the stimulator delivered regular stimuli (E1) and extrastimuli (E2) manually, both with 2-msec duration and at twice the diastolic threshold. The right atrium was scanned by shortening the coupling interval of 20 msec and of 10 or 5 msec on several occasions. The patient was not receiving any cardioactive drug at the time of the study. FindingsThe atrial, His bundle, and ventricular responses due to sinus rhythm are designated as A, H, and V; those deflections elicited by E1 and E2 are designated as A1, H1, and V1 and as A2, H2, and V2, respectively. Under control conditions, there was sinus rhythm (Fig 1) of 88 beats per minute (A-A interval of 680 msec), with a P-R interval of 120 msec, a P-A interval of 40 msec, an A-H interval of 90 msec, an H-V interval of "minus" 10 msec, and a ventricular response of 100 msec, showing a delta wave. In these conditions the His deflection was recorded after the onset of the ventricular complex (after the delta wave); and under atrial stimulation at a driving cycle length that was higher than the sinus cycle, due to prolongation of the A-H interval, the His potential disappeared inside the ventricular inscription, making the analysis of normal atrioventricular conduction difficult with high rates, since the P-delta interval (P-D interval) remained unchanged but always showing patterns of the Wolff-Parkinson-White syndrome.The use of extrastimuli with progressively shorter coupling intervals showed preferential conduction by the accessory pathway, with V2 similar to V1 until an A1-A2 interval of 330 msec. At an A1-A2 interval of 320 msec, the H2 was recorded after V2, with A2-H2 interval of 120 msec. At a coupling interval of 310 msec, the same pattern occurred but with A2-H2 interval of 150 msec; and at an A1-A2 interval of 300 msec, the A2-H2 interval was 200 msec (H2 always after V2), with the A2-V2 interval fixed, which event is commonly observed in atrioventricular refractory studies (Fig 1).At a coupling interval between 295 and 280 msec (Fig 2), there were double ventricular responses, one with conduction along the accessory pathway (V2) and the other later (V3) with ventricular activation through the normal atrioventricular junction. Thus, at a coupling interval of 295 msec, the A2-H2 interval was 350 msec, the H2-V3 interval was 40 msec, and V3 was 70 msec, eliciting reciprocal atrial beats and a short run of supraventricular paroxysmal tachycardia that was quickly aborted. At a coupling interval between 295 and 270 msec, all A2-H2 intervals were increased; at coupling intervals between 270 and 250 msec, there was a ventricular response of the pattern of preexcitation and, following it, a ventricular activation with a morphologic pattern of complete left bundle-branch block. At a coupling interval of 260 msec, there was an A2-H2 interval of 250 msec, an H2-V3 interval of 60 msec, and V3 of 130 msec.The effective refractory periods of the atrioventricular junction and the atria were 240 and 220 msec, respectively. It was not possible to evaluate the effective refractory period of the accessory pathway because it was shorter than the atrial one. This sequence shows a bypass, probably of the Kent type (fixed P-D interval under atrial pacing and extrastimulus), conducting preferentially by Kent's bundle and simultaneously through the normal pathway, proved by a coupling interval of 320 msec or shorter. At an A1-A2 interval of 295 msec, a double ventricular response and an unexpected increase of the A-H interval were already present. This fact and the presence of two distinct A2-H2 intervals suggest dual intranodal pathways.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar An alternative explanation is that A2 was blocked in the atrioventricular node, and the ventricular activation occurred totally through the accessory bypass, producing H2 retrogradely. This seems unlikely because the V2-H2 interval would be quite variable, and the atrial echo beat always appeared after V2 and was never recorded just after H2. The atrial, His bundle, and ventricular responses due to sinus rhythm are designated as A, H, and V; those deflections elicited by E1 and E2 are designated as A1, H1, and V1 and as A2, H2, and V2, respectively. Under control conditions, there was sinus rhythm (Fig 1) of 88 beats per minute (A-A interval of 680 msec), with a P-R interval of 120 msec, a P-A interval of 40 msec, an A-H interval of 90 msec, an H-V interval of "minus" 10 msec, and a ventricular response of 100 msec, showing a delta wave. In these conditions the His deflection was recorded after the onset of the ventricular complex (after the delta wave); and under atrial stimulation at a driving cycle length that was higher than the sinus cycle, due to prolongation of the A-H interval, the His potential disappeared inside the ventricular inscription, making the analysis of normal atrioventricular conduction difficult with high rates, since the P-delta interval (P-D interval) remained unchanged but always showing patterns of the Wolff-Parkinson-White syndrome. The use of extrastimuli with progressively shorter coupling intervals showed preferential conduction by the accessory pathway, with V2 similar to V1 until an A1-A2 interval of 330 msec. At an A1-A2 interval of 320 msec, the H2 was recorded after V2, with A2-H2 interval of 120 msec. At a coupling interval of 310 msec, the same pattern occurred but with A2-H2 interval of 150 msec; and at an A1-A2 interval of 300 msec, the A2-H2 interval was 200 msec (H2 always after V2), with the A2-V2 interval fixed, which event is commonly observed in atrioventricular refractory studies (Fig 1). At a coupling interval between 295 and 280 msec (Fig 2), there were double ventricular responses, one with conduction along the accessory pathway (V2) and the other later (V3) with ventricular activation through the normal atrioventricular junction. Thus, at a coupling interval of 295 msec, the A2-H2 interval was 350 msec, the H2-V3 interval was 40 msec, and V3 was 70 msec, eliciting reciprocal atrial beats and a short run of supraventricular paroxysmal tachycardia that was quickly aborted. At a coupling interval between 295 and 270 msec, all A2-H2 intervals were increased; at coupling intervals between 270 and 250 msec, there was a ventricular response of the pattern of preexcitation and, following it, a ventricular activation with a morphologic pattern of complete left bundle-branch block. At a coupling interval of 260 msec, there was an A2-H2 interval of 250 msec, an H2-V3 interval of 60 msec, and V3 of 130 msec. The effective refractory periods of the atrioventricular junction and the atria were 240 and 220 msec, respectively. It was not possible to evaluate the effective refractory period of the accessory pathway because it was shorter than the atrial one. This sequence shows a bypass, probably of the Kent type (fixed P-D interval under atrial pacing and extrastimulus), conducting preferentially by Kent's bundle and simultaneously through the normal pathway, proved by a coupling interval of 320 msec or shorter. At an A1-A2 interval of 295 msec, a double ventricular response and an unexpected increase of the A-H interval were already present. This fact and the presence of two distinct A2-H2 intervals suggest dual intranodal pathways.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar An alternative explanation is that A2 was blocked in the atrioventricular node, and the ventricular activation occurred totally through the accessory bypass, producing H2 retrogradely. This seems unlikely because the V2-H2 interval would be quite variable, and the atrial echo beat always appeared after V2 and was never recorded just after H2. DiscussionAs far as we know, the ventricular complexes in the Wolff-Parkinson-White syndrome result from the ventricular activation through the accessory bundle and the atrioventricular junctional pathway producing fusion beats. Thus, depending on the refractoriness of the atrioventricular junction and Kent's bundle, the syndrome has many degrees of fusion with morphologically different QRS complexes; this fact usually is observed in electrophysiologic studies using the technique of extrastimuli. Nevertheless, marked delays in normal atrioventricular conduction, enough to activate the His bundle after a ventricular depolarization, are unusual. Previously, three cases of double ventricular activation resulting from a premature atrial depolarization or during atrial fibrillation were reported, although in all cases the ventricular activation through the atrioventricular junction showed left bundle-branch block.4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google ScholarIn this case, with coupling intervals under 320 msec, because of the lengthening of the A-H interval, the His spike was recorded after V2 (morphologic pattern of preexcitation), not eliciting the ventricular response through the normal atrioventricular pathway, due to the absolute refractoriness of the ventricles. At a coupling interval of 295 msec, when the effective refractory period of the fast intranodal pathway had been reached, an unexpected prolongation of atrioventricular conduction occurred (A2-H2 interval of 350 msec), a sufficient time for ventricular repolarization (V2-V3 interval of 330 msec) due to the conduction through the slow pathway, producing two ventricular responses, one with preexcitation and the other with normal ventricular activation; although with a shorter coupling interval, V3 showed the pattern of left bundle-branch block.Grouleau et al,4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar Neuss et al,5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar and Josephson et al6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar postulated the occurrence of longitudinal dissociation between the accessory pathway and the atrioventricular junctional system, in order to explain the phenomenon, although such authors always recorded V3 with left bundle-branch block. In spite of the same event occurring in our patient, he still had beats with normal intraventricular conduction when the A-H interval increased from 200 to 350 msec (after scanning of the right atrium), an event that can be characteristically diagnosed as a dual intranodal pathway.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar Therefore, the normalization of ventricular activation through the normal pathway occurred when the slow pathway was utilized, with a V2-V3 interval of 330 msec, probably higher than the absolute refractory period of the left bundle. When there was left bundle-branch block, the V2-V3 interval was 250 msec. The reported authors4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar always obtained beats with left bundle-branch block because their patients probably did not have three atrioventricular pathways placed in parallel and because the conduction along the atrioventricular junction always reached the left bundle in the absolute refractory phase.Although it might be obtained with drugs, the normalization of the ventricular activation, in spite of being artificial, can help us to recognize electrocardiographic changes such as regions of necrosis, cardiac hypertrophies, disturbances in conduction, and ischemic abnormalities, which are usually obscured by preexcitation. The reciprocal atrial beat in this patient only occurred after ventricular activation by normal atrioventricular conduction, with retrograde conduction along the accessory pathway. Due to the delay in atrioventricular conduction, it becomes impossible for an extrastimulus to be conducted anterogradely by Kent's bundle and retrogradely by the normal pathway, since the His bundle is chronologically activated after the ventricular depolarization. In these cases, the low refractoriness of the accessory bundle "protects" against the development of paroxysmal tachycardia, because it keeps the ventricles in the refractory phase. The tachyarrhythmia can only be elicited through marked intranodal delays, but this is difficult to observe spontaneously, so that explains why this patient has three atrioventricular pathways and never showed a crisis of tachycardia. The references to multiple atrioventricular pathways have been frequent, but this seems to be the first recording of double ventricular activation with normal intraventricular conduction due to the delay in the slow pathway. As far as we know, the ventricular complexes in the Wolff-Parkinson-White syndrome result from the ventricular activation through the accessory bundle and the atrioventricular junctional pathway producing fusion beats. Thus, depending on the refractoriness of the atrioventricular junction and Kent's bundle, the syndrome has many degrees of fusion with morphologically different QRS complexes; this fact usually is observed in electrophysiologic studies using the technique of extrastimuli. Nevertheless, marked delays in normal atrioventricular conduction, enough to activate the His bundle after a ventricular depolarization, are unusual. Previously, three cases of double ventricular activation resulting from a premature atrial depolarization or during atrial fibrillation were reported, although in all cases the ventricular activation through the atrioventricular junction showed left bundle-branch block.4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar In this case, with coupling intervals under 320 msec, because of the lengthening of the A-H interval, the His spike was recorded after V2 (morphologic pattern of preexcitation), not eliciting the ventricular response through the normal atrioventricular pathway, due to the absolute refractoriness of the ventricles. At a coupling interval of 295 msec, when the effective refractory period of the fast intranodal pathway had been reached, an unexpected prolongation of atrioventricular conduction occurred (A2-H2 interval of 350 msec), a sufficient time for ventricular repolarization (V2-V3 interval of 330 msec) due to the conduction through the slow pathway, producing two ventricular responses, one with preexcitation and the other with normal ventricular activation; although with a shorter coupling interval, V3 showed the pattern of left bundle-branch block. Grouleau et al,4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar Neuss et al,5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar and Josephson et al6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar postulated the occurrence of longitudinal dissociation between the accessory pathway and the atrioventricular junctional system, in order to explain the phenomenon, although such authors always recorded V3 with left bundle-branch block. In spite of the same event occurring in our patient, he still had beats with normal intraventricular conduction when the A-H interval increased from 200 to 350 msec (after scanning of the right atrium), an event that can be characteristically diagnosed as a dual intranodal pathway.3Denes P Wu D Dhingra R et al.Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia.Circulation. 1973; 48: 549-555Crossref PubMed Scopus (418) Google Scholar Therefore, the normalization of ventricular activation through the normal pathway occurred when the slow pathway was utilized, with a V2-V3 interval of 330 msec, probably higher than the absolute refractory period of the left bundle. When there was left bundle-branch block, the V2-V3 interval was 250 msec. The reported authors4Grouleau R Puech P Cabasson J et al.Particularités de la conduction auriculo-ventriculaire dans un syndrome de Wolff-Parkinson-White.Arch Mal Coeur. 1974; 67: 13-22PubMed Google Scholar, 5Neuss H Schlepper M Spies HF Double ventricular response to an atrial extrasystole in a patient with WPW syndrome type B.Eur J Cardiol. 1974; 2: 175-179Google Scholar, 6Josephson ME Seides SF Damato AN Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction.Am J Cardiol. 1976; 37: 1094-1096Abstract Full Text PDF PubMed Scopus (22) Google Scholar always obtained beats with left bundle-branch block because their patients probably did not have three atrioventricular pathways placed in parallel and because the conduction along the atrioventricular junction always reached the left bundle in the absolute refractory phase. Although it might be obtained with drugs, the normalization of the ventricular activation, in spite of being artificial, can help us to recognize electrocardiographic changes such as regions of necrosis, cardiac hypertrophies, disturbances in conduction, and ischemic abnormalities, which are usually obscured by preexcitation. The reciprocal atrial beat in this patient only occurred after ventricular activation by normal atrioventricular conduction, with retrograde conduction along the accessory pathway. Due to the delay in atrioventricular conduction, it becomes impossible for an extrastimulus to be conducted anterogradely by Kent's bundle and retrogradely by the normal pathway, since the His bundle is chronologically activated after the ventricular depolarization. In these cases, the low refractoriness of the accessory bundle "protects" against the development of paroxysmal tachycardia, because it keeps the ventricles in the refractory phase. The tachyarrhythmia can only be elicited through marked intranodal delays, but this is difficult to observe spontaneously, so that explains why this patient has three atrioventricular pathways and never showed a crisis of tachycardia. The references to multiple atrioventricular pathways have been frequent, but this seems to be the first recording of double ventricular activation with normal intraventricular conduction due to the delay in the slow pathway.