- Email: [email protected]
Retrograde Wenckebach conduction in atrioventricular bypass tracts: Further evidence for AV nodal-like conduction in accessory pathways
1074
Brief Communications
genesis of Prinzmetal’s 50:534,
American
variant form of angina. Circulation
1974.
Maseri A: The revival of coronary spasm. Am J Med 70:752, 1981. Brown G: Coronary vasospasm: Observations linking the clinical spectrum of ischemic heart disease to the dynamic pathology of coronary atherosclerosis. Arch Intern Med 141:716, 1981. Saphir 0, Gore I: Evidence for an inflammatory basis of coronary atherosclerosis in the young. Arch Path01 49:418, 1950. Kohchi K, Takebayashi S, Hiroki T, Nobuyoshi M: Significance of adventitial inflammation of the coronary artery in unstable angina: Results at autopsy. Circulation 7 1:709, 1985.
Retrograde Wenckebach conduction in atrioventricular bypass tracts: Further evidence for AV nodal-like conduction in accessory pathways Zhaowen Deng, M.D., Mark E. Rosenthal, M.D., Daniel S. Oseran, M.D., Eli S. Gang, M.D., William J. Mandel, M.D., and Thomas Peter, M.D. Los Angeles, Calif. Atrioventricular (AV) accessory pathways provide the anatomic substrate for the preexcitation syndromes and their various clinical presentations. In spite of intensive electrophysiological investigation, there are only a few reports of the cellular characteristics of accessorypathways in the literature. le2Available histologic data suggest From the Department Medical Center. Reprint Medical
of Medicine,
Division
of Cardiology,
requests: Thomas Center,
8700
Peter, M.D., Dept. of Cardiology, Beverly Blvd., Los Angeles, CA 90048.
(A)
Cedars-Sinai Cedars-Sinai
November, 1985 Heart Journal
that the majority of accessorypathways are composedof tiny threads of working myocardium connecting the atrium and the ventricle. Connections composedof Purkinje fibers have been described as well.‘,3 In accordance with these findings, accessory pathways have exhibited the electrophysiologic characteristics of tissue composed of “fast response”cells, in that conduction is usually “all or none” with little evidence of decremental conduction.4s5 In recent.years, there have been isolated reports of accessory pathways exhibiting unusual electrophysiologic properties which had previously been attributed only to tissue composedof “slow response” cells, typically found in the sinus and AV node. In this article we will report our findings in two patients with the Wolff-Parkinson-White syndrome who demonstrated retrograde Wenckebach conduction in an AV bypasstract. during routine electrophysiologic testing. Patient No. 1. E.D. was a 57-year-old woman who underwent electrophysiologic evaluation for recurrent episodesof supraventricular tachycardia. Her physical examination, chest,x-ray films, and echocardiogramwere within normal limits. A B-lead ECG demonstrated “type A” preexcitation. Electrophysiologic studies were performed with electrode catheters positioned in the high right atrium, His bundle region, coronary sinus, and right ventricular apex. Orthodromic supraventricular tachycardia was easily inducible with both atria1 and ventricular extrastimuli. Earliest retrograde activation during supraventricular tachycardia @VT) occurred in the distal coronary sinus,suggestinga left-sided accessorypathway (Fig. 1, A). This eccentric atria1 activation sequencewasidentical to that. seenduring right ventricular pacing. In addition, the tachycardia cycle length prolonged by 70 msec during spontaneous left bundle branch block, confirming the presenceof a left-sided bypasstract (Fig. 1, B). When incremental ventricular pacing was performed at a cycle
(6)
RVA -‘-,-Y/-v?-
1. Supraventricuiar tachycardia (SVT) demonstrating eccentric atria1 activation sequenceand lengthening of cycle length during left bundle branch block. Simultaneousrecordingsare shownfrom ECG leadsI, AVF, V1, and intracardiac electrogramsfrom the high right atrium (HRA), distal coronary sinus (CSd), and right ventricular apex (RVA). A, During SVT, the earliest site of retrograde atria1 activation is in the distal coronary sinus, establishingthe presenceof a left-sided accessorypathway. B, During SVT, left bundle branch aberration developed spontaneouslywith subsequentlengthening of the cycle length of the SVT aswell asventriculoatrial conduction time. This further confirms the presenceof a left-sided AV bypass tract. Abbreviations: A = atria1 electrogram; H = His electrogram; V = ventricular electrogram; BP = blood pressure. Fig.
"Ol"me Number
110 5
Brief Communications
1075
AVl= VI HRA HBE BP
csd
RVA
2. Retrograde Wenckebach conduction in the accessorypathway during right ventricular pacing. Simultaneous recordings are shown from ECG leadsI, AVF, and V,, as well as intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE), distal coronary sinus (CSd), and right ventricular apex (RVA). Fixed-rate right ventricular pacing is performed at a cycle length (S,S,) of 315 msec.The VA interval (measuredfrom the earliest site of right ventricular activation to the CSd atria1 electrogram) is shownto prolong from 165msecto 310 msecprior to VA conduction block. Note that there is no change in the atria1 activation sequence during this phenomenon. Abbreviations: A = atria1 electrogram; BP = blood pressure;V = ventricular electrogram; S, = stimulus artifact. Fig.
(B)
Fig. 3. Supraventricular tachycardia demonstrating eccentric retrograde atrial activation sequenceand atria1 preexcitation, with a premature ventricular depolarization. Simultaneousrecordingsare shownfrom ECG leadsI, AVF, and V1, and intracardiac electrogramsfrom the high right atrium (HRA), His bundle region (HBE), proximal coronary sinus (CSp), distal coronary sinus (CSd), and right ventricular apex (RVA). A, SVT demonstrating earliest retrograde atrial activation in the CSp. B, Introduction of a premature ventricular depolarization (arrow) causes atria1 preexcitation without a change in the retrograde atria1 activation sequence. This occurred at a time when the His-Purkinje system was refractory, thus confirming the presenceof a left-sided paraseptal bypasstract. Abbreviations: A = atria1 electrogram; H = His bundle electrogram; V = ventricular electrogram; S = stimulus artifact.
length of 315 msec,the patient demonstrated ventriculoatrial Wenckebach phenomenon,occurring in the accessory pathway (Fig. 2). Location of the conduction delay in the accessorypathway was confirmed by the fact that the retro-
grade atria1 activation sequenceremainedunchangedduring the Wenckebach phenomenon. In addition, the QRS morphology remainedconstant, suggestingthat conduction delay wasnot occurring in the ventricular myocardium.
1076
Brief Communications
American
November, 1985 Heart Journal
I AVF VI HRA HBE CSP
RVA
Fig. 4. Wenckebach-type retrograde conduction delay in the accessorypathway during right ventricular
pacing, Simultaneous recordings are shown from ECG leads I, AVF, V1, and intracardiac electrograms from the high right atrium (NRA), His bundle region (HBE), proximal coronary sinus (CSp), and right ventricular apex (RVA). Progressive prolongation in the ventriculoatrial (VA) conduction time is noted during fixed-rate ventricular pacing at a cycle length of 250 msec. VA time was determined using the ventricular and atrial electrogramsin the CSp tracing in order to eliminate intraventricular conduction delay asa causefor the Wenckebach conduction. Before actual VA block occurs, orthodromic SVT results (arrow). Abbreviations: A = atrial electrogram; H = His electrogram; V = ventricular electrogram; S = stimulus artifact.
Patient No. 2. H.K. wasa 49-year-old woman evaluated for recurrent SVT of 28 years’ duration. Prior cardiac workup had demonstrated mitral valve prolapse. A 12lead ECG showed no evidence of preexcitation. Electrophysiologic studies were performed in the usual manner, with the induction of sustained narrow QRS complex tachycardia via stimulation at the high right atrium, coronary sinus, and right ventricular apex. During the SVT, the retrograde activation sequencewas abnormal, with earliest atrial activation in the proximal coronary sinus (Fig. 3, A). Premature ventricular extrastimuli during SVT, at a time when the His-Purkinje system was refractory, caused atria1 preexcitation with the same retrograde atrial activation sequence(Fig. 3, B). During fixed-rate pacing from the right ventricular apex at a cycle length of 250 msec, progressiveprolongation of the ventriculoatrial (VA) conduction time via the accessorypathway was noted (Fig. 4). Intra-atria1 conduction delay was unlikely to account for this, since the earliest site of atrial activation was used to determine the VA interval. In addition, intraventricular conduction delay was unlikely, in that the interval between the right ventricular electrogram and that in the coronary sinus was constant. This report describestwo patients in whom AV nodelike conduction was demonstrated in AV accessorypathways. Both patients showed progressive prolongation of retrograde conduction in an accessorypathway with fixed-
rate ventricular pacing, a finding consistentwith Wenckebath-type conduction delay. This finding has been felt to be a property of slow response (i.e., calcium channel dependent) cells. The classic concept of AV accessory pathways as being composedof “fast response,” sodium channel dependent cells has been challenged recently by several investigators. In 1979, Klein, et ala6 reported evidence of decremental VA bypass tract conduction in responseto ventricular extrastimuli in three patients with the Wolff-Parkinson-White syndrome. Gillette et al7 describedfour patients with right-sided anterior accessory pathways with long antegrade conduction times and evidencesof decremental antegrade conduction during electrophysiologic study. Further, the group of patients with “permanent junctional reciprocating tachycardia (PJRT)” has been shown to exhibit decremental retrograde conduction in posterior septal accessorypathways during preoperative and intraoperative electrophysiologic study.8-10Recently, intravenous verapamil, a calcium channel blocking agent, has been reported to depressor block conduction in accessoryventricular pathways, thus giving further credenceto the concept that thesepathways were composed of AV nodal-like tissue and “slow response”cells.11-13 Although a histologic explanation for these interesting electrophysiologic properties is currently not available, it would appear that in someinstancesaccessoryAV path-
Volume Number
110 5
Brief
ways can be composedof tissue with properties similar to the AV node. Rare histopathologic reports of AV bypass tracts composedof cells resemblingthose of the AV node and sinus node have been published.K14In addition, it is possiblethat accessorypathway cells,normally capable of the so-called“fast response”via the sodium channel, may become partially depolarized via disease or concealed conduction and may convert to the calcium channel as a meansfor impulse conduction. This explanation has been used by El-Sherif et a1.15to explain Wenckebach type second-degreeAV block occurring in the His-Purkinje system. As an alternative explanation, GallagherI has proposedthat decremental retrograde conduction seenin the PJRT syndrome is the result of the tortuous geometric configuration of the pathway rather than of unique ionic properties. Further anatomic studies are neededto resolve this question. The potential importance of recognizing the heterogenous nature of accessoryAV pathways has both research and clinical implications. The role of AV nodal-like tissue in explaining the phenomenon of differential antegrade and retrograde conduction in accessorypathways remains to be explored. In addition, the application of therapy aimed at blocking the calcium channel might have a more prominent role in the therapy of patients discovered to have an accessorypathway possessingthese electrophysiologic properties. REFERENCES
1. Sherif L, Neufeld HN: The pre-excitation syndrome: Facts and theories. New York. 1978. Yorke Medical Books. a. 90. 2. Berker AE, ‘Anderson RH, Durrer D, Wellens HJJ: The anatomical substrates of Wolff-ParkinsonzWhite syndrome. Circulation 57:870, 1978. 3. Anderson RH, Berker AE: Gross anatomy and microscopy of the conducting system. In Mandel WJ, editor: Cardiac arrhythmias: Their mechanism, diagnosis and treatment. Philadelphia, 1980, J.B. Lippincott Co., p. 37. 4. Gallagher JJ, Pritchett ELC, Sealy WC, Kasell J, Wallace AG: The pre-excitation syndrome. Prog Cardiovasc Dis 20:285,
1978.
6. Prystowsky EN, Miles WM, Heger JJ, Zipes DP: Preexcitation syndrome. Med Clin North Am 66:831, 1984. 6. Klein GJ. Prvstowsky EN, Pritchett LC, Davis D, Gallagher JJ: Atypical patterns-of retrograde conduction over accessory atrioventricular pathways in the Wolff-Parkinson-White syndrome. Circulation 60:1477, 1979. 7. Gillette PC. Garson A. Coolev DA. McNamara DG: Prolonged and decremental antegrade conduction properties in right anterior accessory connections. AM HEART J 103:60, 1982. 8. Guarnieri ‘I’, Sealy WC, Kasell JH, German LD, Gallagher JJ: The nonpharmacologic management of the permanent form of junctional reciprocating tachycardia. Circulation 69:269, 1984. 9. Brugada P, Bar FW, Vanagt EJ, Friedman PL, Wellens HJJ: Observation in patients showing AV junctional echoes with a shorter P-R than R-P interval. Am J Cardiol 48:611, 1981. 10. Farre J, Ross D, Wiener I, Bar FW, Vanagt EJ, Wellens HJJ: Reciprocal tachycardias using accessory pathways with long conduction times. Am J Cardiol 44:1099, 1979. 11. Rosenthal ME, Oseran DS, Gang ES, Deng ZW, Mandel WJ, Peter T: Verapamil induced retrograde conduction block in a concealed atrioventricular bypass tract. Am J Cardiol55:122, 1985. 12. Tai DY, Chang MS, Svinarich JT, Chiang BN, Sung RJ:
Communications
1077
Mechanisms of verapamil-induced conduction block in anomalous atrioventricular bypass t,ract. ,J Am Co11 Cardiol 5:311,1985.
13. Horio Y, Matsuyama K, Morikami Y, Rokutanda M, Hirata A, Okumura K, Takaoka K, Uchida H, Kugiyama K, Araki S: Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-white syndrome. J Am Co11 Cardiol 4:186, 1984. 14. James TN, Puech P: De subitanesis mortibus. IX. Type A Wolff-Parkinson-White syndrome. Circulation 50:1264, 1974. 15. El-Sherif N, Scherlag BJ, Lazzara R: Pathophysiology 01 second-degree atrioventricular block: A unified hypothesis. Am J Cardiol 35421, 1975. 16. Gallagher JJ: Variants of pre-excitation: Update 1984. In Zipes DP, Jallife J editors: Cardiac electrophysiology and arrhythmias. New York, 1985, Grune CL Stratton Inc., p. 419.
Concealed
atrial quadrigeminy
Shinji Kinoshita, M.D., Fumihiko Okada, M.D., and Michimaro Okada, M.D. Sapporo, Japan The phenomena “concealed ventricular bigeminy and trigeminy” were originally reported by Satoh et al.’ in 1960. In the classicalform of concealed bigeminy,‘v2 the number of sinus QRS complexesintervening between two successivenoninterpolated extrasystoles is always odd, i.e., 2n - 1, where n is any positive integer. In the classical form of concealedtrigeminy, it is 3n - 1. Thereafter two variants of concealed ventricular quadrigeminy were reported by Levy et a1.3More recently, Aygen et a1.4 demonstrated the presenceof the classicalform of concealed ventricular quadrigeminy, in which the number of intervening sinus QRS complexes was 4n - 1. In some patients with atria1 extrasystoles, the presence of concealed bigemine6 and trigeminy5 has also been shown. However, concealedatrial quadrigeminy has not yet been documented. The present report is the first one on concealedatrial quadrigeminy. A continuous ECG recording was obtained from a 77-year-old man with essentialhypertension. During the recording the patient was not undergoing antiarrhythmic therapy. The ECG showed sinus rhythm, with complete right bundle branch block with frequent atria1 extrasystoles and occasionalventricular extraeystoles. Fig. 1 shows parts of the long continuous recording. In the strips, P, represents the ith P wave after the preceding atria1 extrasystole labeled A. In Fig. 1, every atria1 extrasystole (A) follows a P,,- 1 wave (P,, P, or P,,), where n is a positive integer; in other words, the number of P waves intervening between two successive atria1 extrasystoles (A) is always 4n - 1. Coupling intervals of the atria1 extrasystoles to the preceding P waves are considerably variable. However, no fusion P waves are seen, and the From Reprint Hokkaido
Health
Administration
Center,
Hokkaido
requests: Shinji Kinoshita, M.D., University, Sapporo OfiO, Japan.
Health
liniversits. Administration
Center.
Brief Communications
genesis of Prinzmetal’s 50:534,
American
variant form of angina. Circulation
1974.
Maseri A: The revival of coronary spasm. Am J Med 70:752, 1981. Brown G: Coronary vasospasm: Observations linking the clinical spectrum of ischemic heart disease to the dynamic pathology of coronary atherosclerosis. Arch Intern Med 141:716, 1981. Saphir 0, Gore I: Evidence for an inflammatory basis of coronary atherosclerosis in the young. Arch Path01 49:418, 1950. Kohchi K, Takebayashi S, Hiroki T, Nobuyoshi M: Significance of adventitial inflammation of the coronary artery in unstable angina: Results at autopsy. Circulation 7 1:709, 1985.
Retrograde Wenckebach conduction in atrioventricular bypass tracts: Further evidence for AV nodal-like conduction in accessory pathways Zhaowen Deng, M.D., Mark E. Rosenthal, M.D., Daniel S. Oseran, M.D., Eli S. Gang, M.D., William J. Mandel, M.D., and Thomas Peter, M.D. Los Angeles, Calif. Atrioventricular (AV) accessory pathways provide the anatomic substrate for the preexcitation syndromes and their various clinical presentations. In spite of intensive electrophysiological investigation, there are only a few reports of the cellular characteristics of accessorypathways in the literature. le2Available histologic data suggest From the Department Medical Center. Reprint Medical
of Medicine,
Division
of Cardiology,
requests: Thomas Center,
8700
Peter, M.D., Dept. of Cardiology, Beverly Blvd., Los Angeles, CA 90048.
(A)
Cedars-Sinai Cedars-Sinai
November, 1985 Heart Journal
that the majority of accessorypathways are composedof tiny threads of working myocardium connecting the atrium and the ventricle. Connections composedof Purkinje fibers have been described as well.‘,3 In accordance with these findings, accessory pathways have exhibited the electrophysiologic characteristics of tissue composed of “fast response”cells, in that conduction is usually “all or none” with little evidence of decremental conduction.4s5 In recent.years, there have been isolated reports of accessory pathways exhibiting unusual electrophysiologic properties which had previously been attributed only to tissue composedof “slow response” cells, typically found in the sinus and AV node. In this article we will report our findings in two patients with the Wolff-Parkinson-White syndrome who demonstrated retrograde Wenckebach conduction in an AV bypasstract. during routine electrophysiologic testing. Patient No. 1. E.D. was a 57-year-old woman who underwent electrophysiologic evaluation for recurrent episodesof supraventricular tachycardia. Her physical examination, chest,x-ray films, and echocardiogramwere within normal limits. A B-lead ECG demonstrated “type A” preexcitation. Electrophysiologic studies were performed with electrode catheters positioned in the high right atrium, His bundle region, coronary sinus, and right ventricular apex. Orthodromic supraventricular tachycardia was easily inducible with both atria1 and ventricular extrastimuli. Earliest retrograde activation during supraventricular tachycardia @VT) occurred in the distal coronary sinus,suggestinga left-sided accessorypathway (Fig. 1, A). This eccentric atria1 activation sequencewasidentical to that. seenduring right ventricular pacing. In addition, the tachycardia cycle length prolonged by 70 msec during spontaneous left bundle branch block, confirming the presenceof a left-sided bypasstract (Fig. 1, B). When incremental ventricular pacing was performed at a cycle
(6)
RVA -‘-,-Y/-v?-
1. Supraventricuiar tachycardia (SVT) demonstrating eccentric atria1 activation sequenceand lengthening of cycle length during left bundle branch block. Simultaneousrecordingsare shownfrom ECG leadsI, AVF, V1, and intracardiac electrogramsfrom the high right atrium (HRA), distal coronary sinus (CSd), and right ventricular apex (RVA). A, During SVT, the earliest site of retrograde atria1 activation is in the distal coronary sinus, establishingthe presenceof a left-sided accessorypathway. B, During SVT, left bundle branch aberration developed spontaneouslywith subsequentlengthening of the cycle length of the SVT aswell asventriculoatrial conduction time. This further confirms the presenceof a left-sided AV bypass tract. Abbreviations: A = atria1 electrogram; H = His electrogram; V = ventricular electrogram; BP = blood pressure. Fig.
"Ol"me Number
110 5
Brief Communications
1075
AVl= VI HRA HBE BP
csd
RVA
2. Retrograde Wenckebach conduction in the accessorypathway during right ventricular pacing. Simultaneous recordings are shown from ECG leadsI, AVF, and V,, as well as intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE), distal coronary sinus (CSd), and right ventricular apex (RVA). Fixed-rate right ventricular pacing is performed at a cycle length (S,S,) of 315 msec.The VA interval (measuredfrom the earliest site of right ventricular activation to the CSd atria1 electrogram) is shownto prolong from 165msecto 310 msecprior to VA conduction block. Note that there is no change in the atria1 activation sequence during this phenomenon. Abbreviations: A = atria1 electrogram; BP = blood pressure;V = ventricular electrogram; S, = stimulus artifact. Fig.
(B)
Fig. 3. Supraventricular tachycardia demonstrating eccentric retrograde atrial activation sequenceand atria1 preexcitation, with a premature ventricular depolarization. Simultaneousrecordingsare shownfrom ECG leadsI, AVF, and V1, and intracardiac electrogramsfrom the high right atrium (HRA), His bundle region (HBE), proximal coronary sinus (CSp), distal coronary sinus (CSd), and right ventricular apex (RVA). A, SVT demonstrating earliest retrograde atrial activation in the CSp. B, Introduction of a premature ventricular depolarization (arrow) causes atria1 preexcitation without a change in the retrograde atria1 activation sequence. This occurred at a time when the His-Purkinje system was refractory, thus confirming the presenceof a left-sided paraseptal bypasstract. Abbreviations: A = atria1 electrogram; H = His bundle electrogram; V = ventricular electrogram; S = stimulus artifact.
length of 315 msec,the patient demonstrated ventriculoatrial Wenckebach phenomenon,occurring in the accessory pathway (Fig. 2). Location of the conduction delay in the accessorypathway was confirmed by the fact that the retro-
grade atria1 activation sequenceremainedunchangedduring the Wenckebach phenomenon. In addition, the QRS morphology remainedconstant, suggestingthat conduction delay wasnot occurring in the ventricular myocardium.
1076
Brief Communications
American
November, 1985 Heart Journal
I AVF VI HRA HBE CSP
RVA
Fig. 4. Wenckebach-type retrograde conduction delay in the accessorypathway during right ventricular
pacing, Simultaneous recordings are shown from ECG leads I, AVF, V1, and intracardiac electrograms from the high right atrium (NRA), His bundle region (HBE), proximal coronary sinus (CSp), and right ventricular apex (RVA). Progressive prolongation in the ventriculoatrial (VA) conduction time is noted during fixed-rate ventricular pacing at a cycle length of 250 msec. VA time was determined using the ventricular and atrial electrogramsin the CSp tracing in order to eliminate intraventricular conduction delay asa causefor the Wenckebach conduction. Before actual VA block occurs, orthodromic SVT results (arrow). Abbreviations: A = atrial electrogram; H = His electrogram; V = ventricular electrogram; S = stimulus artifact.
Patient No. 2. H.K. wasa 49-year-old woman evaluated for recurrent SVT of 28 years’ duration. Prior cardiac workup had demonstrated mitral valve prolapse. A 12lead ECG showed no evidence of preexcitation. Electrophysiologic studies were performed in the usual manner, with the induction of sustained narrow QRS complex tachycardia via stimulation at the high right atrium, coronary sinus, and right ventricular apex. During the SVT, the retrograde activation sequencewas abnormal, with earliest atrial activation in the proximal coronary sinus (Fig. 3, A). Premature ventricular extrastimuli during SVT, at a time when the His-Purkinje system was refractory, caused atria1 preexcitation with the same retrograde atrial activation sequence(Fig. 3, B). During fixed-rate pacing from the right ventricular apex at a cycle length of 250 msec, progressiveprolongation of the ventriculoatrial (VA) conduction time via the accessorypathway was noted (Fig. 4). Intra-atria1 conduction delay was unlikely to account for this, since the earliest site of atrial activation was used to determine the VA interval. In addition, intraventricular conduction delay was unlikely, in that the interval between the right ventricular electrogram and that in the coronary sinus was constant. This report describestwo patients in whom AV nodelike conduction was demonstrated in AV accessorypathways. Both patients showed progressive prolongation of retrograde conduction in an accessorypathway with fixed-
rate ventricular pacing, a finding consistentwith Wenckebath-type conduction delay. This finding has been felt to be a property of slow response (i.e., calcium channel dependent) cells. The classic concept of AV accessory pathways as being composedof “fast response,” sodium channel dependent cells has been challenged recently by several investigators. In 1979, Klein, et ala6 reported evidence of decremental VA bypass tract conduction in responseto ventricular extrastimuli in three patients with the Wolff-Parkinson-White syndrome. Gillette et al7 describedfour patients with right-sided anterior accessory pathways with long antegrade conduction times and evidencesof decremental antegrade conduction during electrophysiologic study. Further, the group of patients with “permanent junctional reciprocating tachycardia (PJRT)” has been shown to exhibit decremental retrograde conduction in posterior septal accessorypathways during preoperative and intraoperative electrophysiologic study.8-10Recently, intravenous verapamil, a calcium channel blocking agent, has been reported to depressor block conduction in accessoryventricular pathways, thus giving further credenceto the concept that thesepathways were composed of AV nodal-like tissue and “slow response”cells.11-13 Although a histologic explanation for these interesting electrophysiologic properties is currently not available, it would appear that in someinstancesaccessoryAV path-
Volume Number
110 5
Brief
ways can be composedof tissue with properties similar to the AV node. Rare histopathologic reports of AV bypass tracts composedof cells resemblingthose of the AV node and sinus node have been published.K14In addition, it is possiblethat accessorypathway cells,normally capable of the so-called“fast response”via the sodium channel, may become partially depolarized via disease or concealed conduction and may convert to the calcium channel as a meansfor impulse conduction. This explanation has been used by El-Sherif et a1.15to explain Wenckebach type second-degreeAV block occurring in the His-Purkinje system. As an alternative explanation, GallagherI has proposedthat decremental retrograde conduction seenin the PJRT syndrome is the result of the tortuous geometric configuration of the pathway rather than of unique ionic properties. Further anatomic studies are neededto resolve this question. The potential importance of recognizing the heterogenous nature of accessoryAV pathways has both research and clinical implications. The role of AV nodal-like tissue in explaining the phenomenon of differential antegrade and retrograde conduction in accessorypathways remains to be explored. In addition, the application of therapy aimed at blocking the calcium channel might have a more prominent role in the therapy of patients discovered to have an accessorypathway possessingthese electrophysiologic properties. REFERENCES
1. Sherif L, Neufeld HN: The pre-excitation syndrome: Facts and theories. New York. 1978. Yorke Medical Books. a. 90. 2. Berker AE, ‘Anderson RH, Durrer D, Wellens HJJ: The anatomical substrates of Wolff-ParkinsonzWhite syndrome. Circulation 57:870, 1978. 3. Anderson RH, Berker AE: Gross anatomy and microscopy of the conducting system. In Mandel WJ, editor: Cardiac arrhythmias: Their mechanism, diagnosis and treatment. Philadelphia, 1980, J.B. Lippincott Co., p. 37. 4. Gallagher JJ, Pritchett ELC, Sealy WC, Kasell J, Wallace AG: The pre-excitation syndrome. Prog Cardiovasc Dis 20:285,
1978.
6. Prystowsky EN, Miles WM, Heger JJ, Zipes DP: Preexcitation syndrome. Med Clin North Am 66:831, 1984. 6. Klein GJ. Prvstowsky EN, Pritchett LC, Davis D, Gallagher JJ: Atypical patterns-of retrograde conduction over accessory atrioventricular pathways in the Wolff-Parkinson-White syndrome. Circulation 60:1477, 1979. 7. Gillette PC. Garson A. Coolev DA. McNamara DG: Prolonged and decremental antegrade conduction properties in right anterior accessory connections. AM HEART J 103:60, 1982. 8. Guarnieri ‘I’, Sealy WC, Kasell JH, German LD, Gallagher JJ: The nonpharmacologic management of the permanent form of junctional reciprocating tachycardia. Circulation 69:269, 1984. 9. Brugada P, Bar FW, Vanagt EJ, Friedman PL, Wellens HJJ: Observation in patients showing AV junctional echoes with a shorter P-R than R-P interval. Am J Cardiol 48:611, 1981. 10. Farre J, Ross D, Wiener I, Bar FW, Vanagt EJ, Wellens HJJ: Reciprocal tachycardias using accessory pathways with long conduction times. Am J Cardiol 44:1099, 1979. 11. Rosenthal ME, Oseran DS, Gang ES, Deng ZW, Mandel WJ, Peter T: Verapamil induced retrograde conduction block in a concealed atrioventricular bypass tract. Am J Cardiol55:122, 1985. 12. Tai DY, Chang MS, Svinarich JT, Chiang BN, Sung RJ:
Communications
1077
Mechanisms of verapamil-induced conduction block in anomalous atrioventricular bypass t,ract. ,J Am Co11 Cardiol 5:311,1985.
13. Horio Y, Matsuyama K, Morikami Y, Rokutanda M, Hirata A, Okumura K, Takaoka K, Uchida H, Kugiyama K, Araki S: Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-white syndrome. J Am Co11 Cardiol 4:186, 1984. 14. James TN, Puech P: De subitanesis mortibus. IX. Type A Wolff-Parkinson-White syndrome. Circulation 50:1264, 1974. 15. El-Sherif N, Scherlag BJ, Lazzara R: Pathophysiology 01 second-degree atrioventricular block: A unified hypothesis. Am J Cardiol 35421, 1975. 16. Gallagher JJ: Variants of pre-excitation: Update 1984. In Zipes DP, Jallife J editors: Cardiac electrophysiology and arrhythmias. New York, 1985, Grune CL Stratton Inc., p. 419.
Concealed
atrial quadrigeminy
Shinji Kinoshita, M.D., Fumihiko Okada, M.D., and Michimaro Okada, M.D. Sapporo, Japan The phenomena “concealed ventricular bigeminy and trigeminy” were originally reported by Satoh et al.’ in 1960. In the classicalform of concealed bigeminy,‘v2 the number of sinus QRS complexesintervening between two successivenoninterpolated extrasystoles is always odd, i.e., 2n - 1, where n is any positive integer. In the classical form of concealedtrigeminy, it is 3n - 1. Thereafter two variants of concealed ventricular quadrigeminy were reported by Levy et a1.3More recently, Aygen et a1.4 demonstrated the presenceof the classicalform of concealed ventricular quadrigeminy, in which the number of intervening sinus QRS complexes was 4n - 1. In some patients with atria1 extrasystoles, the presence of concealed bigemine6 and trigeminy5 has also been shown. However, concealedatrial quadrigeminy has not yet been documented. The present report is the first one on concealedatrial quadrigeminy. A continuous ECG recording was obtained from a 77-year-old man with essentialhypertension. During the recording the patient was not undergoing antiarrhythmic therapy. The ECG showed sinus rhythm, with complete right bundle branch block with frequent atria1 extrasystoles and occasionalventricular extraeystoles. Fig. 1 shows parts of the long continuous recording. In the strips, P, represents the ith P wave after the preceding atria1 extrasystole labeled A. In Fig. 1, every atria1 extrasystole (A) follows a P,,- 1 wave (P,, P, or P,,), where n is a positive integer; in other words, the number of P waves intervening between two successive atria1 extrasystoles (A) is always 4n - 1. Coupling intervals of the atria1 extrasystoles to the preceding P waves are considerably variable. However, no fusion P waves are seen, and the From Reprint Hokkaido
Health
Administration
Center,
Hokkaido
requests: Shinji Kinoshita, M.D., University, Sapporo OfiO, Japan.
Health
liniversits. Administration
Center.