Sinus and Atrioventricular
Nodal Reentrant Tachycardia
in the Same Patient
KARLEN
L.
PAULAY,
JEREMY
N.
RUSKIN,
ANTHONY
Staten
N.
MD
Sinus and atrioventricular
MD
DAMATO,
(A-V)
nodal reentry
are shown to coexist
in
the same patient, and the following conclusions are drawn: (1) Reentry at one nodal site may mask reentry at the other nodal site, (2) concealed reentry at either site may become manifest reentry under the appropriate conditions, (3) manifest sinus nodal reentry may alternate with manifest A-V nodal reentry, and (4) a Wenckebach type phenomenon manifest in the A-V node and concealed in the sinus node may in some instances be the basis for coexistent sinus and A-V nodal reentry in man.
MD
island, New York
As suggested in 1943 by Barker et al.,l supraventricular tachycardia may be due to reentry in either the atrioventricular (A-V)2,3 or sinus4m H nodes. It has recently been shown that in A-V nodal reentrant tachycardia, atria1 activation is initiated low in the atrium, in the region of the A-V node, and in sinus nodal reentrant tachycardia, atria1 activation is initiated high in the atrium, in the region of the sinus node. Thus, the atria1 activation sequence in A-V nodal reentry may be referred to as a “low-high” sequence and the atria1 activation sequence in sinus nodal reentry as a “high-low” sequence. Since reentry in the A-V node should not preclude reentry in the sinus node it was reasonable to expect that occasionally sinus nodal and A-V nodal reentry might coexist in the same patient and become manifest at different times. This report describes such an event and proposes the following: (1) Sinus and A-V nodal reentry may coexist in the same patient, (2) reentry at either site may mask reentry at the other site, (3) concealed reentry at either site may become manifest reentry under the appropriate conditions, (4) manifest sinus nodal reentry may alternate with manifest A-V nodal reentry, and (5) a Wenckebach type phenomenon manifest in the A-V node and concealed in the sinus node may in some instances be the basis for coexistent sinus and A-V nodal reentry in man. Methods
From the Cardiopulmonary Laboratory, U. S. Public Health Service Hospital, Staten Island, N. Y. This work was supported in part by the Bureau of Medical Services, U. S. Public Health Service Project Py 75-1 and Project HE 1253604 from the National Heart and Lung Institute, National Institutes of Health, Bethesda, Md. Manuscript accepted October 23, 1974. Address for reprints: Anthony N. Damato, MD, Cardiopulmonary Laboratory, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.
810
November
1975
The American
The patient was a 69 year old man with a documented 3 year history of paroxysmal supraventricular tachycardia. When supraventricular tachycardia was first noted September 15, 1970 (Fig. l), negative P waves in the inferior leads suggested that the basis for the tachycardia might be A-V nodal reentry. Electrophysiologic studies performed at that time confirmed this clinical impression. During sinus rhythm the P waves were positive in the inferior leads (middle panel, Fig. 1). During the next 3 years the patient experienced several attacks of supraventricular tachycardia that were terminated either by carotid sinus massage or by direct-current cardioversion. Digoxin and quinidine were relatively ineffective in controlling these attacks. Because of the more recent, observation that at times supraventricular tachycardia in this patient was associated with upright P waves in the inferior leads (right panel, Fig. I ), repeat electrophysiologic studies were performed to delineate further the nature of his tachycardia.
Journal of CARDIOLOGY
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38
SINUS AND A-V
Cardiac catheterization: Right heart catheterization was performed with the patient in the postabsorptive, nonsedated state after informed consent was obtained. The patient was not receiving cardioactive medication, and maintenance digoxin therapy (0.25 mg, daily) had been discontinued 4 days before study. The recording and stimulation techniques that were used have previously been described in detail.g A quadripolar catheter was positioned in the high right atrium so that the proximal pair of electrodes lay at the junction of the superior vena cava and right atrium in the region of the sinus node. Stimuli were delivered to the high right atrium by way of the distal pair of electrodes, and atria1 activity from the region of the sinus node was recorded by the proximal pair of electrodes. Another quadripolar catheter positioned in the proximal coronary sinus was used to deliver stimuli to the coronary sinus region by way of the distal pair of electrodes and to record atria1 activity from the coronary sinus region by the proximal pair of electrodes. A tripolar catheter positioned across the tricuspid valve recorded activity from the bundle of His and the low atria1 septum in the region of the A-V node. Stimuli were delivered both continuously and by the extrastimulus methodlo with use of a programmed digital stimulator and a battery-powered pacemaker. Electrocardiographic leads I, II and VI, atria1 electrograms, His bundle electrograms and time marks at 10 and
B.
s-s
L2
AR
NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
i_ I
136
126
FIGURE 1. Electrocardiographic records taken during episodes of supraventricular tachycardia (left and right) and during sinus rhythm (middle). The arrows denote the inverted P waves during A-V nodal reentrant tachycardia (September 15. 1970) and the upright P waves during sinus rhythm (September 20, 1970) and sinus nodal reentrant tachycardia (October 7. 1973). A premature ventricular contraction is recorded on October 7, 1973. AR = atrial rate (beats/ min).
340
FIGURE 2. A-V nodal reentrant tachycardia (A) and sinus nodal reentrant tachycardia (B) after the abrupt termination of high right atrial pacing at a rate of 176Imin (cycle length 340 msec). The rapid deflections in this and subsequent records have been retouched for the purpose of reproduction. See text. CS = coronary sinus: HBE = His bundle electrogram; HRA = high right atrium: S = stimulus; TL = time lines at 10 and 100 msec.
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NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
100 msec were observed on a switched beam oscilloscope and recorded on magnetic tape. The records were subsequently transferred from tape to photographic paper at a paper speed of 150 mm/set.
Results Coexisting sinus and A-V nodal reentrant tachycardia: In the supine resting position the patient had normal sinus rhythm with occasional atria1 and ventricular premature beats. After the abrupt termination of continuous atria1 pacing at rates up to 145/min sinus rhythm returned. However, at pacing rates greater than 145/min the abrupt termination of pacing was followed either by sinus rhythm or by supraventricular tachycardia. The tachycardia elicited was of two different types (Fig. 2). In panel A, during atria1 pacing at a rate of 176/min, the A-H interval progressively increases from 230 to 270 msec. After the last paced beat the A-H interval increases suddenly to 455 msec and is followed by sustained tachycardia at a regular rate of approximately 160/min. A low-high atria1 activation sequence and negative P waves in lead II were recorded during the tachycardia. The progressive increase in A-V nodal delay, low-high atria1 activation sequence and P wave configuration all suggest that the basis of the tachycardia in panel A is A-V nodal reentry.” In Figure 2B, during atria1 pacing at the same rate
TL
(176/min), a progressive increase in the A-H interval also occurs; however, pacing is discontinued when the A-H interval has increased to only 240 msec. After termination of pacing at this point, sustained tachycardia at a regular rate of approximately 118/min is observed. A high-low atria1 activation sequence and upright P waves in lead II were recorded during the tachycardia. The similarity of the upright P waves in lead II and the atria1 activation sequence recorded during the tachycardia to the sinus P waves and atrial activation sequence recorded during sinus rhythm (Fig. 3, panel A at left) suggests that the basis of the tachycardia in panel B is sinus nodal reentry.4 Both sinus and A-V nodal reentrant tachycardias were sustained and could be initiated and terminated by rapid atria1 pacing from either the high right atrium or coronary sinus region. The change from sinus rhythm to sinus nodal reentry, from sinus nodal reentry to A-V nodal reentry and from A-V nodal reentry back to sinus rhythm is shown in selected portions from a continuous record in Figure 3. In panel A, after delivery of stimuli to the right atrium at a rate of 187/min, an A-V nodal Wenckebach phenomenon appears with dropped beats noted at the end of panel A and after the fourth A deflection in panel B. Pacing is terminated when the A-H interval is 230 msec. In this patient A-V nodal reentry was never observed when the A-H in-
A’
-1
CONTINUOUS
+
FIGURE 3. Selected portions of a continuous record are shown in panels A and B (this page) and C to E (next page). In A and B, atrial pacing associated with A-V nodal Wenckebach cycles is followed by a sinus nodal reentrant tachycardia when pacing is abruptly terminated (B). In C, atrial pacing changes the sinus nodal reentrant tachycardia to an A-V nodal reentrant tachycardia. Atrial pacing initiated in D then terminates this A-V nodal reentrant tachycardia in E. The open arrow denotes an atrial premature contraction. Abbreviations as in Figure 2. See text.
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terval was less than 300 msec. The sustained high-low tachycardia that follows the termination of pacing is consistent with sinus nodal reentry. In panel C, atria1 pacing at the same site and rate is terminated after an increase in the A-H interval to 380 msec. The sustained low-high tachycardia that follows the termination of pacing is consistent with A-V nodal reentry. Pacing resumes during A-V nodal reentry (panel D) and when pacing is terminated (panel E) sinus rhythm is restored. The open arrow indicates a premature atria1 beat. The atria1 depolarization pattern for the sinus beats after the tachycardia differs somewhat from that observed for sinus beats before the tachycardia and can be explained by a shift in sinus nodal pacemaker site after the tachycardia. Initiation of A-V nodal reentry: A-V nodal reentry was observed only during rapid continuous atria1 pacing and not during premature atria1 stimulation.
NDDAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
This finding is related to the dependence of the initiation of A-V nodal reentry upon achievement of a requisite degree of A-V nodal conduction delay.ll In this patient an A-H interval exceeding 300 msec was necessary for A-V nodal reentry to occur. This requisite degree of A-V nodal delay was not observed during coupled premature atria1 stimulation (Fig. 4). In the top panel of Figure 4, basic pacing stimuli are applied to the right atrium at a cycle length of 600 msec. A premature stimulus (Ss) is coupled to the 10th basic paced beat at an Si-Sz interval of 280 msec. The A-H intervals of the basic drive and premature beats are 120 (Al-Hi) and 175 (AZ-HZ) msec, respectively, and A-V nodal reentry does not occur. An increase in the AZ-HZ interval is not seen when Si-Sz is decreased by 10 msec (bottom panel), since Sz then falls within the atria1 refractory period and atria1 capture does not occur.
Ll L2 Vl
I-IRA
IIBE
TL
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NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
FIGURE 4. The failure of premature atrial stimulation to achieve the requisite degree of A-V nodal conduction delay necessary for A-V nodal reentry is shown in the upper panel. When the coupling is decreased by 10 msec (lower panel), S2 falls within the atrial refractory period and atrial capture does not occur. Abbreviations as in Figure 2. See text
A repeat electrophysiologic stud?, was performed ‘L weeks later when plasma quinidine and digoxin levels were within the therapeutic range: 4.0 mg/liter and 2.2 ng/liter, respectively. At this time A-V nodal reentry was not seen although the A-H interval increased to 500 msec during atria1 pacing with the Wenckebach phenomenon. Sinus nodal reentry was observed for only one or two beats and sustained sinus nodal reentrant tachycardia was not seen. Discussion Concept of dual nodes: This patient
pathways
in sinus
and
A-V
demonstrates t,hat sinus nodal and A-V nodal reentrant tachycardias may be present at different times in the same patient. A possible explanation of the findings in this study is based upon the concept that the sinus and A-V nodes can become functionally divided int,o two or more interconnecting pathways with differing refractory periods. Such a concept of dual pathways has been applied to the A-V node. l2 If such a concept could he applied to the sinus node as well, then the mechanism for sinus and A-V nodal reentry observed in this
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1975
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study could be schematically Figure 5.
depicted
as shown in
In Figure 5, panels A to E, stimuli (S) are delivered to the right atrium (RA) during rapid continuous atria1 pacing. In panel A, the wave front of atria1 depolarization arrives at the sinus and A-V nodes and engages two functionally differing pathways, a and h. At both nodes pathway b is considered to have a longer effective refractory period than pathway a. In the sinus node the impulses traversing pathways a and b are shown to collide* with the result that the two wave fronts become extinguished. In the A-V node a similar collision of impulses occurs; however, the impulse traversing pathway a also continues t.o propagate down to the bundle of His and ventricles. The standard electrocardiographic pattern for lead II (L2) is shown at the bottom of the figure. After the next stimulus (panel B) slowing of some degree occurs in both the a and b pathways. Because of conduction delay along pathway a in the A-V node, the P-R (or A-H) interval increases, as shown in lead II. With the next stimulus, panel C, further Alternatively, impulse propagation along pathway b may decrement and fail before collision actually occurs, but then refractoriness along pathway b would block further retrograde impulse propagation.
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SINUS AND A-V
NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
SN
RA
AVN
L2 FIGURE 5. A possible mechanism reentrant
tachycardia
for sinus and A-V nodal during atrial pacing. See text.
slowing occurs. In panels A to C the progressive slowing of conduction in the A-V node is manifested by a progressive prolongation of the P-R (or A-H) interval. However, a similar progressive slowing of conduction in the sinus node is concealed. In panel D, the approaching wave front fails to enter pathway b in the sinus node because of refractoriness at that site. The impulse slowly traverses pathway a, arrives at pathway b (depicted as a line to the right of b) when it has partially recovered and then reenters the atrium as a sinus nodal echo beat shown as P’ in lead II. If the atria1 echo beat reexcites pathway a (dotted horizontal arrow) then a sustained sinus nodal reentrant tachycardia may develop. Alternatively, panel C may proceed to panel E if the block in pathway b occurs in the A-V node before it occurs in the sinus node. In this case, an A-V nodal echo beat depicted as P” in lead II will be recorded. If the atria1 echo beat reenters pathway a (dotted arrow) then sustained A-V nodal reentry tachycardia may develop. The dotted arrow in panels D and E is depicted as lying outside the sinus and A-V nodes for the purpose of diagrammatic simplicity only. intranodal
Concepts of manifest and concealed reentry: The concepts of (1) manifest A-V nodal and concealed sinus nodal Wenckebach phenomena, and (2) manifest and concealed reentry13J4 could explain many of the observations in this study. For example, Figure 3 may be explained as follows: In panels A and B of Figure 3 a concealed Wenckebach type phenomenon is occurring in the sinus node. When pacing is terminated (middle portion of panel B) at the appropriate time in the sinus nodal Wenckebach cycle sinus nodal reentry tachycardia becomes manifest. The interval of 545 msec between the last paced beat and the first reentrant beat represents the time required for the first echo beat to traverse the reentrant pathway. Sinus nodal reentry is concealed during pacing because of the relatively short cycle length (320 msec) of stimulation. A-V nodal reentry is not observed during atria1 pacing for a similar reason. If
pacing had been terminated when the A-H interval had increased to 375 msec in panel A, A-V nodal reentry would probably have been seen. Since the requisite degree of A-V nodal delay has not yet occurred when pacing is terminated in panel B, A-V nodal reentry is not seen. If the periodicity of the Wenckebach phenomenon in the sinus and A-V nodes is different then, depending on when pacing is terminated, one will see either sinus nodal reentry (panel B), A-V nodal reentry (panel C), or neither (panel E). The response to termination of pacing in panel E is what would be expected if pacing were discontinued immediately after panel C in Figure 5.
A-V nodal Wenckebach phenomenon: Of special clinical diagnostic importance is the observation that when the A-V nodal Wenckebach phenomenon precedes the initiation of supraventricular tachycardia the tachycardia may be either of the A-V nodal or of the sinus nodal reentrant type. In the case of sinus nodal reentrant tachycardia the A-V nodal Wenckebath phenomenon is incidental and occurs simply because of rapid atria1 pacing. However, in the case of A-V nodal reentrant tachycardia the magnitude of A-V nodal delay is critical. Masking of A-V nodal reentry by sinus nodal reentry: The sudden and significant increment in the A-V nodal conduction time that immediately preceded A-V nodal reentry in this patient resembled the phenomenon described in a recent report by Denes et a1.15 These investigators postulated that th6 A-V node behaved as if it were divided (anatomically or functionally) into two pathways: one pathway with relatively fast conduction and a long effective refractory period and the other pat.hway with relatively slow conduction and a short refractory period. Echo beats were noted when conduction failed along the fast pathway, which then became available for retro-
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NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
grade propagation of an impulse back to the atria. The sudden and significant increment in the A-V nodal conduction time from 270 to 455 msec in Figure 2, panel A, delays the appearance of the first echo beat after pacing is terminated. Because of this delay A-V nodal reentry is not seen until 620 msec after the last paced beat. Thus, it is possible to understand how sinus nodal reentry in some instances might mask A-V nodal reentry in this patient since in panel B only 520 msec elapses from the last paced beat to the onset of the first sinus nodal reentrant beat. This sinus nodal reentrant beat could then enter the A-V node and interrupt potential reentry from that site by colliding with the returning wave front. A-V nodal reentry would then remain absent since the requisite degree of A-V nodal conduction delay would not
occur in the presence of the relatively slow rate ( 12O/min) of the sinus nodal reentrant tachycardia. Effect of digoxin and quinidine: The failure to demonstrate A-V nodal reentry and sustained sinus nodal reentry at a time when plasma levels of digoxin and quinidine were at therapeutic levels may have clinical importance. Although it is tempting to speculate that digoxin blocked A-V nodal reentry and quinidine blocked sinus nodal reentry,ls it is recognized that both drugs may have blocked reentry at both sites. Acknowledgment We gratefully acknowledge the technical assistance of Mary Vecchione, the secretarial help of Anne Mazzella and the photographic services of Kenneth Donohue.
References 1. Barker PS, Wilson FN, Johnston FD: The mechanism of auricular paroxysmal tachycardia. Am Heart J 26:435-445, 1943 2. Bigger JT Jr, Goidreyer BN: The mechanism of supraventricular tachycardia. Circulation 42:673-688, 1970 3. Goldreyer BN, Bigger JT Jr: Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43: 15-26, 1971 4. Pauiay KL, Varghese PJ, Damato AN: Sinus node reentry: an in vivo demonstration in the dog. Circ Res 32:455-463. 1973 5. Pauiay KL, Varghese PJ, Damato AN: Atriai rhythms in response to an early atrial premature depolarization in man. Am Heart J 85:323-331, 1973 6. Weisfogei GM, Batsford WP, Josephson ME, et al: Sinus node reentrant tachycardia in man. Circulation 48:Suppl iV:IV-122. 1973 7. Naruia OS: Sinus node re-entry: a mechanism for supraventricuiar tachycardia. Circulation 50:1114-l 128, 1974 8. Wu D, Amat-Y-Leon F, Denes P, et al: Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 5 1:234-243, 1975 9. Gallagher JJ, Damaio AN, Varghese PJ, et al: Localization of an area of maximum refractoriness or “gate” in the ventricular specialized conduction system of man. Am Heart J 84:310-320, 1972
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10. Krayer 0, Mandoki JJ, Mendez C: Studies on veratrum alkaloids. XVI. The action of epinephrine and of veratramine on the functional refractory period of the auriculo-ventricular transmission in the heart-lung preparation of the dog. J Pharmacol Exp Ther 103:412-419, 1951 11. Goidreyer BN, Damato AN: The essential role of atrioventricuiar conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43:679-687, 1971 12. Mender C, Moe GK: Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 19:378393, 1966 13. Damato AN, Varghese PJ, Lau SH, et al: Manifest and concealed reentry: a mechanism of A-V nodal Wenckebach phenomenon. Circ Res 30:283-292, 1972. 14. Gallagher JJ, Damato AN, Varghese PJ, et al: Manifest and concealed reentry: a mechanism of A-V nodal Wenckebach in man. Circulation 47:752-757, 1973 15. Denes P, Wu D, Dhingra RC, et al: Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 48549-555, 1973 16. Pauiay KL, Weisfogei GM, Damato AN: Sinus nodal reentry. Effect of quinidine. Am J Cardiol 33:617-622, 1974
Volume 36
Nodal Reentrant Tachycardia
in the Same Patient
KARLEN
L.
PAULAY,
JEREMY
N.
RUSKIN,
ANTHONY
Staten
N.
MD
Sinus and atrioventricular
MD
DAMATO,
(A-V)
nodal reentry
are shown to coexist
in
the same patient, and the following conclusions are drawn: (1) Reentry at one nodal site may mask reentry at the other nodal site, (2) concealed reentry at either site may become manifest reentry under the appropriate conditions, (3) manifest sinus nodal reentry may alternate with manifest A-V nodal reentry, and (4) a Wenckebach type phenomenon manifest in the A-V node and concealed in the sinus node may in some instances be the basis for coexistent sinus and A-V nodal reentry in man.
MD
island, New York
As suggested in 1943 by Barker et al.,l supraventricular tachycardia may be due to reentry in either the atrioventricular (A-V)2,3 or sinus4m H nodes. It has recently been shown that in A-V nodal reentrant tachycardia, atria1 activation is initiated low in the atrium, in the region of the A-V node, and in sinus nodal reentrant tachycardia, atria1 activation is initiated high in the atrium, in the region of the sinus node. Thus, the atria1 activation sequence in A-V nodal reentry may be referred to as a “low-high” sequence and the atria1 activation sequence in sinus nodal reentry as a “high-low” sequence. Since reentry in the A-V node should not preclude reentry in the sinus node it was reasonable to expect that occasionally sinus nodal and A-V nodal reentry might coexist in the same patient and become manifest at different times. This report describes such an event and proposes the following: (1) Sinus and A-V nodal reentry may coexist in the same patient, (2) reentry at either site may mask reentry at the other site, (3) concealed reentry at either site may become manifest reentry under the appropriate conditions, (4) manifest sinus nodal reentry may alternate with manifest A-V nodal reentry, and (5) a Wenckebach type phenomenon manifest in the A-V node and concealed in the sinus node may in some instances be the basis for coexistent sinus and A-V nodal reentry in man. Methods
From the Cardiopulmonary Laboratory, U. S. Public Health Service Hospital, Staten Island, N. Y. This work was supported in part by the Bureau of Medical Services, U. S. Public Health Service Project Py 75-1 and Project HE 1253604 from the National Heart and Lung Institute, National Institutes of Health, Bethesda, Md. Manuscript accepted October 23, 1974. Address for reprints: Anthony N. Damato, MD, Cardiopulmonary Laboratory, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.
810
November
1975
The American
The patient was a 69 year old man with a documented 3 year history of paroxysmal supraventricular tachycardia. When supraventricular tachycardia was first noted September 15, 1970 (Fig. l), negative P waves in the inferior leads suggested that the basis for the tachycardia might be A-V nodal reentry. Electrophysiologic studies performed at that time confirmed this clinical impression. During sinus rhythm the P waves were positive in the inferior leads (middle panel, Fig. 1). During the next 3 years the patient experienced several attacks of supraventricular tachycardia that were terminated either by carotid sinus massage or by direct-current cardioversion. Digoxin and quinidine were relatively ineffective in controlling these attacks. Because of the more recent, observation that at times supraventricular tachycardia in this patient was associated with upright P waves in the inferior leads (right panel, Fig. I ), repeat electrophysiologic studies were performed to delineate further the nature of his tachycardia.
Journal of CARDIOLOGY
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38
SINUS AND A-V
Cardiac catheterization: Right heart catheterization was performed with the patient in the postabsorptive, nonsedated state after informed consent was obtained. The patient was not receiving cardioactive medication, and maintenance digoxin therapy (0.25 mg, daily) had been discontinued 4 days before study. The recording and stimulation techniques that were used have previously been described in detail.g A quadripolar catheter was positioned in the high right atrium so that the proximal pair of electrodes lay at the junction of the superior vena cava and right atrium in the region of the sinus node. Stimuli were delivered to the high right atrium by way of the distal pair of electrodes, and atria1 activity from the region of the sinus node was recorded by the proximal pair of electrodes. Another quadripolar catheter positioned in the proximal coronary sinus was used to deliver stimuli to the coronary sinus region by way of the distal pair of electrodes and to record atria1 activity from the coronary sinus region by the proximal pair of electrodes. A tripolar catheter positioned across the tricuspid valve recorded activity from the bundle of His and the low atria1 septum in the region of the A-V node. Stimuli were delivered both continuously and by the extrastimulus methodlo with use of a programmed digital stimulator and a battery-powered pacemaker. Electrocardiographic leads I, II and VI, atria1 electrograms, His bundle electrograms and time marks at 10 and
B.
s-s
L2
AR
NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
i_ I
136
126
FIGURE 1. Electrocardiographic records taken during episodes of supraventricular tachycardia (left and right) and during sinus rhythm (middle). The arrows denote the inverted P waves during A-V nodal reentrant tachycardia (September 15. 1970) and the upright P waves during sinus rhythm (September 20, 1970) and sinus nodal reentrant tachycardia (October 7. 1973). A premature ventricular contraction is recorded on October 7, 1973. AR = atrial rate (beats/ min).
340
FIGURE 2. A-V nodal reentrant tachycardia (A) and sinus nodal reentrant tachycardia (B) after the abrupt termination of high right atrial pacing at a rate of 176Imin (cycle length 340 msec). The rapid deflections in this and subsequent records have been retouched for the purpose of reproduction. See text. CS = coronary sinus: HBE = His bundle electrogram; HRA = high right atrium: S = stimulus; TL = time lines at 10 and 100 msec.
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NODAL REENTRANT TACHYCARDIA-PAULAY
ET AL.
100 msec were observed on a switched beam oscilloscope and recorded on magnetic tape. The records were subsequently transferred from tape to photographic paper at a paper speed of 150 mm/set.
Results Coexisting sinus and A-V nodal reentrant tachycardia: In the supine resting position the patient had normal sinus rhythm with occasional atria1 and ventricular premature beats. After the abrupt termination of continuous atria1 pacing at rates up to 145/min sinus rhythm returned. However, at pacing rates greater than 145/min the abrupt termination of pacing was followed either by sinus rhythm or by supraventricular tachycardia. The tachycardia elicited was of two different types (Fig. 2). In panel A, during atria1 pacing at a rate of 176/min, the A-H interval progressively increases from 230 to 270 msec. After the last paced beat the A-H interval increases suddenly to 455 msec and is followed by sustained tachycardia at a regular rate of approximately 160/min. A low-high atria1 activation sequence and negative P waves in lead II were recorded during the tachycardia. The progressive increase in A-V nodal delay, low-high atria1 activation sequence and P wave configuration all suggest that the basis of the tachycardia in panel A is A-V nodal reentry.” In Figure 2B, during atria1 pacing at the same rate
TL
(176/min), a progressive increase in the A-H interval also occurs; however, pacing is discontinued when the A-H interval has increased to only 240 msec. After termination of pacing at this point, sustained tachycardia at a regular rate of approximately 118/min is observed. A high-low atria1 activation sequence and upright P waves in lead II were recorded during the tachycardia. The similarity of the upright P waves in lead II and the atria1 activation sequence recorded during the tachycardia to the sinus P waves and atrial activation sequence recorded during sinus rhythm (Fig. 3, panel A at left) suggests that the basis of the tachycardia in panel B is sinus nodal reentry.4 Both sinus and A-V nodal reentrant tachycardias were sustained and could be initiated and terminated by rapid atria1 pacing from either the high right atrium or coronary sinus region. The change from sinus rhythm to sinus nodal reentry, from sinus nodal reentry to A-V nodal reentry and from A-V nodal reentry back to sinus rhythm is shown in selected portions from a continuous record in Figure 3. In panel A, after delivery of stimuli to the right atrium at a rate of 187/min, an A-V nodal Wenckebach phenomenon appears with dropped beats noted at the end of panel A and after the fourth A deflection in panel B. Pacing is terminated when the A-H interval is 230 msec. In this patient A-V nodal reentry was never observed when the A-H in-
A’
-1
CONTINUOUS
+
FIGURE 3. Selected portions of a continuous record are shown in panels A and B (this page) and C to E (next page). In A and B, atrial pacing associated with A-V nodal Wenckebach cycles is followed by a sinus nodal reentrant tachycardia when pacing is abruptly terminated (B). In C, atrial pacing changes the sinus nodal reentrant tachycardia to an A-V nodal reentrant tachycardia. Atrial pacing initiated in D then terminates this A-V nodal reentrant tachycardia in E. The open arrow denotes an atrial premature contraction. Abbreviations as in Figure 2. See text.
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terval was less than 300 msec. The sustained high-low tachycardia that follows the termination of pacing is consistent with sinus nodal reentry. In panel C, atria1 pacing at the same site and rate is terminated after an increase in the A-H interval to 380 msec. The sustained low-high tachycardia that follows the termination of pacing is consistent with A-V nodal reentry. Pacing resumes during A-V nodal reentry (panel D) and when pacing is terminated (panel E) sinus rhythm is restored. The open arrow indicates a premature atria1 beat. The atria1 depolarization pattern for the sinus beats after the tachycardia differs somewhat from that observed for sinus beats before the tachycardia and can be explained by a shift in sinus nodal pacemaker site after the tachycardia. Initiation of A-V nodal reentry: A-V nodal reentry was observed only during rapid continuous atria1 pacing and not during premature atria1 stimulation.
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This finding is related to the dependence of the initiation of A-V nodal reentry upon achievement of a requisite degree of A-V nodal conduction delay.ll In this patient an A-H interval exceeding 300 msec was necessary for A-V nodal reentry to occur. This requisite degree of A-V nodal delay was not observed during coupled premature atria1 stimulation (Fig. 4). In the top panel of Figure 4, basic pacing stimuli are applied to the right atrium at a cycle length of 600 msec. A premature stimulus (Ss) is coupled to the 10th basic paced beat at an Si-Sz interval of 280 msec. The A-H intervals of the basic drive and premature beats are 120 (Al-Hi) and 175 (AZ-HZ) msec, respectively, and A-V nodal reentry does not occur. An increase in the AZ-HZ interval is not seen when Si-Sz is decreased by 10 msec (bottom panel), since Sz then falls within the atria1 refractory period and atria1 capture does not occur.
Ll L2 Vl
I-IRA
IIBE
TL
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FIGURE 4. The failure of premature atrial stimulation to achieve the requisite degree of A-V nodal conduction delay necessary for A-V nodal reentry is shown in the upper panel. When the coupling is decreased by 10 msec (lower panel), S2 falls within the atrial refractory period and atrial capture does not occur. Abbreviations as in Figure 2. See text
A repeat electrophysiologic stud?, was performed ‘L weeks later when plasma quinidine and digoxin levels were within the therapeutic range: 4.0 mg/liter and 2.2 ng/liter, respectively. At this time A-V nodal reentry was not seen although the A-H interval increased to 500 msec during atria1 pacing with the Wenckebach phenomenon. Sinus nodal reentry was observed for only one or two beats and sustained sinus nodal reentrant tachycardia was not seen. Discussion Concept of dual nodes: This patient
pathways
in sinus
and
A-V
demonstrates t,hat sinus nodal and A-V nodal reentrant tachycardias may be present at different times in the same patient. A possible explanation of the findings in this study is based upon the concept that the sinus and A-V nodes can become functionally divided int,o two or more interconnecting pathways with differing refractory periods. Such a concept of dual pathways has been applied to the A-V node. l2 If such a concept could he applied to the sinus node as well, then the mechanism for sinus and A-V nodal reentry observed in this
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study could be schematically Figure 5.
depicted
as shown in
In Figure 5, panels A to E, stimuli (S) are delivered to the right atrium (RA) during rapid continuous atria1 pacing. In panel A, the wave front of atria1 depolarization arrives at the sinus and A-V nodes and engages two functionally differing pathways, a and h. At both nodes pathway b is considered to have a longer effective refractory period than pathway a. In the sinus node the impulses traversing pathways a and b are shown to collide* with the result that the two wave fronts become extinguished. In the A-V node a similar collision of impulses occurs; however, the impulse traversing pathway a also continues t.o propagate down to the bundle of His and ventricles. The standard electrocardiographic pattern for lead II (L2) is shown at the bottom of the figure. After the next stimulus (panel B) slowing of some degree occurs in both the a and b pathways. Because of conduction delay along pathway a in the A-V node, the P-R (or A-H) interval increases, as shown in lead II. With the next stimulus, panel C, further Alternatively, impulse propagation along pathway b may decrement and fail before collision actually occurs, but then refractoriness along pathway b would block further retrograde impulse propagation.
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SN
RA
AVN
L2 FIGURE 5. A possible mechanism reentrant
tachycardia
for sinus and A-V nodal during atrial pacing. See text.
slowing occurs. In panels A to C the progressive slowing of conduction in the A-V node is manifested by a progressive prolongation of the P-R (or A-H) interval. However, a similar progressive slowing of conduction in the sinus node is concealed. In panel D, the approaching wave front fails to enter pathway b in the sinus node because of refractoriness at that site. The impulse slowly traverses pathway a, arrives at pathway b (depicted as a line to the right of b) when it has partially recovered and then reenters the atrium as a sinus nodal echo beat shown as P’ in lead II. If the atria1 echo beat reexcites pathway a (dotted horizontal arrow) then a sustained sinus nodal reentrant tachycardia may develop. Alternatively, panel C may proceed to panel E if the block in pathway b occurs in the A-V node before it occurs in the sinus node. In this case, an A-V nodal echo beat depicted as P” in lead II will be recorded. If the atria1 echo beat reenters pathway a (dotted arrow) then sustained A-V nodal reentry tachycardia may develop. The dotted arrow in panels D and E is depicted as lying outside the sinus and A-V nodes for the purpose of diagrammatic simplicity only. intranodal
Concepts of manifest and concealed reentry: The concepts of (1) manifest A-V nodal and concealed sinus nodal Wenckebach phenomena, and (2) manifest and concealed reentry13J4 could explain many of the observations in this study. For example, Figure 3 may be explained as follows: In panels A and B of Figure 3 a concealed Wenckebach type phenomenon is occurring in the sinus node. When pacing is terminated (middle portion of panel B) at the appropriate time in the sinus nodal Wenckebach cycle sinus nodal reentry tachycardia becomes manifest. The interval of 545 msec between the last paced beat and the first reentrant beat represents the time required for the first echo beat to traverse the reentrant pathway. Sinus nodal reentry is concealed during pacing because of the relatively short cycle length (320 msec) of stimulation. A-V nodal reentry is not observed during atria1 pacing for a similar reason. If
pacing had been terminated when the A-H interval had increased to 375 msec in panel A, A-V nodal reentry would probably have been seen. Since the requisite degree of A-V nodal delay has not yet occurred when pacing is terminated in panel B, A-V nodal reentry is not seen. If the periodicity of the Wenckebach phenomenon in the sinus and A-V nodes is different then, depending on when pacing is terminated, one will see either sinus nodal reentry (panel B), A-V nodal reentry (panel C), or neither (panel E). The response to termination of pacing in panel E is what would be expected if pacing were discontinued immediately after panel C in Figure 5.
A-V nodal Wenckebach phenomenon: Of special clinical diagnostic importance is the observation that when the A-V nodal Wenckebach phenomenon precedes the initiation of supraventricular tachycardia the tachycardia may be either of the A-V nodal or of the sinus nodal reentrant type. In the case of sinus nodal reentrant tachycardia the A-V nodal Wenckebath phenomenon is incidental and occurs simply because of rapid atria1 pacing. However, in the case of A-V nodal reentrant tachycardia the magnitude of A-V nodal delay is critical. Masking of A-V nodal reentry by sinus nodal reentry: The sudden and significant increment in the A-V nodal conduction time that immediately preceded A-V nodal reentry in this patient resembled the phenomenon described in a recent report by Denes et a1.15 These investigators postulated that th6 A-V node behaved as if it were divided (anatomically or functionally) into two pathways: one pathway with relatively fast conduction and a long effective refractory period and the other pat.hway with relatively slow conduction and a short refractory period. Echo beats were noted when conduction failed along the fast pathway, which then became available for retro-
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grade propagation of an impulse back to the atria. The sudden and significant increment in the A-V nodal conduction time from 270 to 455 msec in Figure 2, panel A, delays the appearance of the first echo beat after pacing is terminated. Because of this delay A-V nodal reentry is not seen until 620 msec after the last paced beat. Thus, it is possible to understand how sinus nodal reentry in some instances might mask A-V nodal reentry in this patient since in panel B only 520 msec elapses from the last paced beat to the onset of the first sinus nodal reentrant beat. This sinus nodal reentrant beat could then enter the A-V node and interrupt potential reentry from that site by colliding with the returning wave front. A-V nodal reentry would then remain absent since the requisite degree of A-V nodal conduction delay would not
occur in the presence of the relatively slow rate ( 12O/min) of the sinus nodal reentrant tachycardia. Effect of digoxin and quinidine: The failure to demonstrate A-V nodal reentry and sustained sinus nodal reentry at a time when plasma levels of digoxin and quinidine were at therapeutic levels may have clinical importance. Although it is tempting to speculate that digoxin blocked A-V nodal reentry and quinidine blocked sinus nodal reentry,ls it is recognized that both drugs may have blocked reentry at both sites. Acknowledgment We gratefully acknowledge the technical assistance of Mary Vecchione, the secretarial help of Anne Mazzella and the photographic services of Kenneth Donohue.
References 1. Barker PS, Wilson FN, Johnston FD: The mechanism of auricular paroxysmal tachycardia. Am Heart J 26:435-445, 1943 2. Bigger JT Jr, Goidreyer BN: The mechanism of supraventricular tachycardia. Circulation 42:673-688, 1970 3. Goldreyer BN, Bigger JT Jr: Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43: 15-26, 1971 4. Pauiay KL, Varghese PJ, Damato AN: Sinus node reentry: an in vivo demonstration in the dog. Circ Res 32:455-463. 1973 5. Pauiay KL, Varghese PJ, Damato AN: Atriai rhythms in response to an early atrial premature depolarization in man. Am Heart J 85:323-331, 1973 6. Weisfogei GM, Batsford WP, Josephson ME, et al: Sinus node reentrant tachycardia in man. Circulation 48:Suppl iV:IV-122. 1973 7. Naruia OS: Sinus node re-entry: a mechanism for supraventricuiar tachycardia. Circulation 50:1114-l 128, 1974 8. Wu D, Amat-Y-Leon F, Denes P, et al: Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 5 1:234-243, 1975 9. Gallagher JJ, Damaio AN, Varghese PJ, et al: Localization of an area of maximum refractoriness or “gate” in the ventricular specialized conduction system of man. Am Heart J 84:310-320, 1972
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10. Krayer 0, Mandoki JJ, Mendez C: Studies on veratrum alkaloids. XVI. The action of epinephrine and of veratramine on the functional refractory period of the auriculo-ventricular transmission in the heart-lung preparation of the dog. J Pharmacol Exp Ther 103:412-419, 1951 11. Goidreyer BN, Damato AN: The essential role of atrioventricuiar conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43:679-687, 1971 12. Mender C, Moe GK: Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 19:378393, 1966 13. Damato AN, Varghese PJ, Lau SH, et al: Manifest and concealed reentry: a mechanism of A-V nodal Wenckebach phenomenon. Circ Res 30:283-292, 1972. 14. Gallagher JJ, Damato AN, Varghese PJ, et al: Manifest and concealed reentry: a mechanism of A-V nodal Wenckebach in man. Circulation 47:752-757, 1973 15. Denes P, Wu D, Dhingra RC, et al: Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 48549-555, 1973 16. Pauiay KL, Weisfogei GM, Damato AN: Sinus nodal reentry. Effect of quinidine. Am J Cardiol 33:617-622, 1974
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