Atrioventricular Nodal Reentry in the WolffParkinson-White Syndrome* William] . Mandel, M.D.; 00 Michael M . Laks, M.D., F.C.C.P.; and Kanii Obayashi, M.D.
Wolff, Parkinson, and White, in their initial description of the syndrome that bears their names, emphasized the association of tachycardias with the electrocardiographic abnormality. Subsequent investigations have identified, both anatomically and electrophysiologically, that dual pathways of atrioventricular (A V) conduction exist. Furthermore, experimental and clinical evidence has stressed that the mechanism of tachycardia production in the syndrome appears to be reentry utilizing these
dual pathways. However, recent studies have emphasized that other mechanisms of tachycardia production may be responsible for the arrhythmias seen in this syndrome. The present report identifies that A V nodal reentry may be the sole mechanism for tachycardia induction in the Wolff-Parkinson-White (WPW) syndrome. This finding may be of great clinical significance in light of the availability of surgical therapy for WPW patients with intractable arrhythmias.
In 1930, Wolff, Parkinson, and White first described the clinical significance of the syndrome which bea;s their names. 1 This entity is characterized by the presence of a short P-R interval, wide QRS complex, and repeated episodes of supraventricular tachyarrhythmias. The generally accepted mechanism responsible for tachycardia initiation in this syndrome is reentry utilizing both atrioventricular ( AV) nodal and bypass tract ( s ) .2•5 Nevertheless, recent work by Rosen 6 has suggested that AV nodal reentry alone may be responsible for the supraventricular tachyarrhythmias seen in this syndrome. However, the impact of Rosen's study was limited because of assumptions posed by the author in light of the limitations in the available electrophysiologic data. It is the purpose of this study to report an investigation defining more clearly the role of AV nodal reentry as a mechanism for reciprocating tachycardias in the WolH-Parkinson-White ( WPW) syndrome.
syncope; tachyarrhythmias were not, however, documented by routine electrocardiographic studies. The patient was admitted for electrophysiologic evaluation, which included AV conduction studies utilizing methods previously described.7 Briefly, these studies involved, after obtaining informed consent, His bundle recordings, high right atrial recordings, atrial and ventricular pacing, and AV and ventriculoatrial (VA) refractory-period measurements using the extra stimulus technique. All records were obtained utilizing a multichannel oscilloscopic recorder. Three standard ECG leads, a high right atrial electrogram, and a His bundle electrogram were recorded. The AV refractory periods were measured at four basic pacing rates.
CASE REPORT AND METHODS
An 18-year-old man was first discovered to have the WPW syndrome one month prior to admission. The past history was significant in that the patient complained of recent onset of repeated episodes of palpitations, lightheadedness, and near °From the Department of Cardiology, Cedars-Sinai Medical Center; the Department of Cardiology, Harbor General Hospital; and the Department of Medicine, University of California, Los Angeles. This study was supported in part by USPHS grant no. 14682. 00 Milly Factor Clinical Investigator of the Western Cardiac Foundation. Manuscript received January 30; revision accepted March 14. Reprint requests: Dr. Mandel, Department of Cardiology, Cedars-Sinai Medical Center, 4833 Fountain Avenue, Los Angeles 90054
CHEST, 68: 3, SEPTEMBER, 1975
RESULTS
Control Recordings In the control state the patient demonstrated alternation between conduction with normal ventricular activation and ventricular preexcitation (Fig 1 ) . With ventricular preexcitation the delta wave preceded the inscription of the His spike (Fig 1 ).
Atrial Pacing Atrial pacing at increasing heart rates 110/min) produced 1:1 conduction utilizing only the AV conducting pathway (Fig 2). Progressive atrio-His (A-H) interval prolongation was observed with increasing atrial pacing rates, with anterograde AV block observed at a pacing rate of 170/min (Fig 2; Table I).
(2
Atrioventricular Refractory-Period Measurements Atrioventricular refractory-period measurements were obtained at basic cycle lengths of 70/min, 90/min, 110/min and 130/min. The WPW com-
ATRIOVENTRICULAR NODAL REENTRY IN WPW SYNDROME 321
A I'-~-
J,.. II
+
I
...J.A
..,.....
-J.,...
tNR
tNL
tNF
j_
.J_
'-'5
Vs
Ill
.JJ
~
'2
~
\\
r ~u
~ v..
8 ~-
~
..M..
-r-
,_..
II
Ill
tNR
tNL
tNF
J....,
.J....,
I
j_
-l....
v..
'-'5
Vs
I
Jv L \\
AEG ___:;
'2
~
~
• HY:.c·
A
HBE
.....
I
1'w;, .
LI
I
'
;
•
Ln Lm 1. Standard ECG and His bundle recordings obtained in control state. Left-hand panel (A ) shows standard 12-lead ECG during normal ventricular activation and intracardiac recordings with, from top to bottom, high right atrial electrogram ( AEG), His bundle electrogram ( HBE), and standard ECG leads 1, 2, and 3. Upper portion of right-hand panel (B) shows standard ECG recording during anomalous ventricular activation. Bottom portion of panel shows intracardiac recordings obtained during ventricular preexcitation. FIGURE
plexes were only observed at basic cycle lengths of 70/min and 90/min and only with coupling intervals equal to or greater than 440 msec (Fig 3A). Atrial effective refractory period, measured at basic cycle lengths of 70/min and 90/min, was 270 and 255 msec, respectively. All AV refractory-period responses were of type 1 configuration (Fig 3A) .8
Ventricular Pacing Ventricular pacing at 90/min produced 1:1 VA conduction with a conduction time of 163 msec. At rates equal to or greater than 110/ min, VA conduction block was observed ( Fig 4).
V entriculoatrial Refractory Periods Ventriculoatrial refractory periods were assessed using the extrastimulus technique at a basic cycle length of 90/min and demonstrated an effective refractory period of 540 msec (Fig 3B). No episodes of supraventricular tachycardia could be initiated with right ventricular premature stimulation.
Tachycardia Induction Utilizing the atrial extrastimulus technique and a basic cycle length of 130/min, reciprocating tachycardias could be initiated with coupling intervals of 255 to 280 msec and a low-to-high right atrial activation sequence (Fig 5). At no other coupling intervals were echo beats initiated. 322 MANDEL, LAKS, OBAYASHI
DISCUSSION
Tachyarrhythmias in man can be considered to be related to two basic mechanisms, reentry or ectopy. 9 One clinical situation in which reentry is clearly accepted as the mechanism for the development of tachyarrhythmias is the WPW syndrome; dual pathways of conduction have been identified electrophysiologically and anatomically. 2 •5 •7 •1(}. 15 Previous studies have defined the onset of tachyarrhythmias and activation sequence during tachyarrhythmia induction in the WPW syndrome, confirming reentry utilizing both the normal AV nodal and bypass tract pathways. 2• 7· 1(}.13.16-19 Table l-Progre..ive A.-H Interval Prolongation with lncreaaing A.Jrial Pacing Rate• Interval A-H
H-v•
WPW
Control 67/min
70
40
+
Pacing 90/min
125
40
+
I 10/min
135
40
±
130/min
140
40
!50/min
145
40
170/min
!55**
40
Heart Rate
*H-V, His-ventricle. **2 :1 conduction.
CHEST, 68: 3, SEPTEMBER, 1975
90/min
AEG
110/min
r. ~~
,.,
HBE
I
L:t
:
LII
~
Lm
~ t----
lsec
170/min
150/min
r
AEG
t
HBE LI Ln Lm
FrcuRE 2. Right atrial pacing. Four panels demonstrate effects of increasing right atrial pacing rates (90/min, 110/min, 150/min, and 170/min) on AV conduction. From top to bottom in each panel are high right atrial electrogram ( AEG), His bundle electrogram ( HBE), and standard ECG leads 1, 2, and 3. Note presence of anomalous ventricular activation at 90/min. At 110/min, there is alternating anomalous conduction and normal ventricular activation. At rates up . to 150/min, only nonnal ventricular activation was observed. Lower right-hand panel demonstrates development of anterograde AV block at pacing rate of 170/min; site of block was within AV node.
A) 600
500
HIH2
msec
.,
B)
AVRP
90/min
VARP 90/min
700
0
•• • •
0 0
.-
600
0
OWPN
500
400
IERP • 540 msec I
ERP • 265 msec FRP • 450 msec
IATRIAL ERP·~ - i
300
300
400
A1A2
msec
500
600
'!'.
•
eRSR
./
400
500
400
V1V2
600
700
msec
FIGU!lE 3. Atrioventricular nodal anterograde and retrograde refractory period detem1inations. Left-hand panel (A) displays points obtained during anterograde AV refractory-period measurements using extrastimulus technique (open circles, complexes with anomalous AV conduction; solid circles, complexes with normal ventricular activation). Horizontal axis identifies A1A" coupling interval; vertical axis identifies H 1 H~ response. Boxes identify effective ( ERP) and functional ( FRP) refractory periods of AV node as well as atrial effective refractory period ( ERP). Right-hand panel (B) shows results obtained during determination of VA refractory periods. Horizontal ax1s idPntifies V 1V" coupling interval; vertical axis identifies high right atrial A 1A2 responsP. EffPctive refractory period ( ERP) is identified in box.
CHEST, 68: 3, SEPTEMBER, 1975
ATRIOVENTRICULAR NODAL REENTRY IN WPW SYNDROME 323
90/min
AEG LI
110/min
il63l A*
Ln Lm FIGURE 4. Effect of right ventricular pacing on VA conduction. Left-hand panel shows effect of ventricular pacing at rate of 90/min. From top to bottom are high right atrial electrogram ( AEG) and standard ECG leads 1, 2, and 3. Number in box identifies VA conduction time. Right-hand panel shows results obtained during ventricular pacing at rate of 110/min. There is 2 : 1 VA conduction time of 210 msec.
Nevertheless, it is conceivable that the supraventricular tachycardias seen in the WPW syndrome need not occur because of a reciprocating mechanism utilizing this dual anatomic pathway concept. It is possible that ectopic pacemakers may occur or that a reciprocating mechanism may be responsible due to sinus-to-atrial reentry or AV nodal reentry. In the previous study of Rosen, 6 an AV nodal reentry mechanism was considered to be operative, but limited electrophysiologic data necessitated the use of assumptions by this author which detracted from the impact of his observations. We agree with Dr. Rosen that AV nodal reentry may be responsible for some of the tachyarrhythmias seen in the WPW syndrome. To consider AV nodal reentry as a mechanism of supraventricular tachycardia in the WPW syndrome, one must show that ( 1) the bypass tract fails to conduct anterograde at a rate in excess
of the spontaneous tachycardia rate, ( 2) the echo zone occurs at a shorter coupling interval than the bypass refractory period, ( 3) retrograde bypass conduction fails at rates less than observed during supraventricular tachycardia, and ( 4) bypass refractoriness is prolonged in excess of the supraventricular tachycardia cycle length. Our present data support the fact that, in this patient, the bypass tract electrophysiologic properties both in the anterograde and retrograde fashion would not sustain conduction at a rate in excess of 110/min. The electrophysiologic findings seen with premature atrial stimulation, culminating in the repeated episodes of supraventricular tachycardia, demonstrated characteristics which are in keeping with Goldreyer and Bigger's observations in patients with paroxysmal atrial tachycardia.20 The electrophysiologic observations are in concert with pioneering studies by
FIGURE 5. Induction of supraventricular tachycardia. Left-hand portion identifies eleetrogr
Wolff, Parkinson, and White, in their initial description of the syndrome that bears their names, emphasized the association of tachycardias with the electrocardiographic abnormality. Subsequent investigations have identified, both anatomically and electrophysiologically, that dual pathways of atrioventricular (A V) conduction exist. Furthermore, experimental and clinical evidence has stressed that the mechanism of tachycardia production in the syndrome appears to be reentry utilizing these
dual pathways. However, recent studies have emphasized that other mechanisms of tachycardia production may be responsible for the arrhythmias seen in this syndrome. The present report identifies that A V nodal reentry may be the sole mechanism for tachycardia induction in the Wolff-Parkinson-White (WPW) syndrome. This finding may be of great clinical significance in light of the availability of surgical therapy for WPW patients with intractable arrhythmias.
In 1930, Wolff, Parkinson, and White first described the clinical significance of the syndrome which bea;s their names. 1 This entity is characterized by the presence of a short P-R interval, wide QRS complex, and repeated episodes of supraventricular tachyarrhythmias. The generally accepted mechanism responsible for tachycardia initiation in this syndrome is reentry utilizing both atrioventricular ( AV) nodal and bypass tract ( s ) .2•5 Nevertheless, recent work by Rosen 6 has suggested that AV nodal reentry alone may be responsible for the supraventricular tachyarrhythmias seen in this syndrome. However, the impact of Rosen's study was limited because of assumptions posed by the author in light of the limitations in the available electrophysiologic data. It is the purpose of this study to report an investigation defining more clearly the role of AV nodal reentry as a mechanism for reciprocating tachycardias in the WolH-Parkinson-White ( WPW) syndrome.
syncope; tachyarrhythmias were not, however, documented by routine electrocardiographic studies. The patient was admitted for electrophysiologic evaluation, which included AV conduction studies utilizing methods previously described.7 Briefly, these studies involved, after obtaining informed consent, His bundle recordings, high right atrial recordings, atrial and ventricular pacing, and AV and ventriculoatrial (VA) refractory-period measurements using the extra stimulus technique. All records were obtained utilizing a multichannel oscilloscopic recorder. Three standard ECG leads, a high right atrial electrogram, and a His bundle electrogram were recorded. The AV refractory periods were measured at four basic pacing rates.
CASE REPORT AND METHODS
An 18-year-old man was first discovered to have the WPW syndrome one month prior to admission. The past history was significant in that the patient complained of recent onset of repeated episodes of palpitations, lightheadedness, and near °From the Department of Cardiology, Cedars-Sinai Medical Center; the Department of Cardiology, Harbor General Hospital; and the Department of Medicine, University of California, Los Angeles. This study was supported in part by USPHS grant no. 14682. 00 Milly Factor Clinical Investigator of the Western Cardiac Foundation. Manuscript received January 30; revision accepted March 14. Reprint requests: Dr. Mandel, Department of Cardiology, Cedars-Sinai Medical Center, 4833 Fountain Avenue, Los Angeles 90054
CHEST, 68: 3, SEPTEMBER, 1975
RESULTS
Control Recordings In the control state the patient demonstrated alternation between conduction with normal ventricular activation and ventricular preexcitation (Fig 1 ) . With ventricular preexcitation the delta wave preceded the inscription of the His spike (Fig 1 ).
Atrial Pacing Atrial pacing at increasing heart rates 110/min) produced 1:1 conduction utilizing only the AV conducting pathway (Fig 2). Progressive atrio-His (A-H) interval prolongation was observed with increasing atrial pacing rates, with anterograde AV block observed at a pacing rate of 170/min (Fig 2; Table I).
(2
Atrioventricular Refractory-Period Measurements Atrioventricular refractory-period measurements were obtained at basic cycle lengths of 70/min, 90/min, 110/min and 130/min. The WPW com-
ATRIOVENTRICULAR NODAL REENTRY IN WPW SYNDROME 321
A I'-~-
J,.. II
+
I
...J.A
..,.....
-J.,...
tNR
tNL
tNF
j_
.J_
'-'5
Vs
Ill
.JJ
~
'2
~
\\
r ~u
~ v..
8 ~-
~
..M..
-r-
,_..
II
Ill
tNR
tNL
tNF
J....,
.J....,
I
j_
-l....
v..
'-'5
Vs
I
Jv L \\
AEG ___:;
'2
~
~
• HY:.c·
A
HBE
.....
I
1'w;, .
LI
I
'
;
•
Ln Lm 1. Standard ECG and His bundle recordings obtained in control state. Left-hand panel (A ) shows standard 12-lead ECG during normal ventricular activation and intracardiac recordings with, from top to bottom, high right atrial electrogram ( AEG), His bundle electrogram ( HBE), and standard ECG leads 1, 2, and 3. Upper portion of right-hand panel (B) shows standard ECG recording during anomalous ventricular activation. Bottom portion of panel shows intracardiac recordings obtained during ventricular preexcitation. FIGURE
plexes were only observed at basic cycle lengths of 70/min and 90/min and only with coupling intervals equal to or greater than 440 msec (Fig 3A). Atrial effective refractory period, measured at basic cycle lengths of 70/min and 90/min, was 270 and 255 msec, respectively. All AV refractory-period responses were of type 1 configuration (Fig 3A) .8
Ventricular Pacing Ventricular pacing at 90/min produced 1:1 VA conduction with a conduction time of 163 msec. At rates equal to or greater than 110/ min, VA conduction block was observed ( Fig 4).
V entriculoatrial Refractory Periods Ventriculoatrial refractory periods were assessed using the extrastimulus technique at a basic cycle length of 90/min and demonstrated an effective refractory period of 540 msec (Fig 3B). No episodes of supraventricular tachycardia could be initiated with right ventricular premature stimulation.
Tachycardia Induction Utilizing the atrial extrastimulus technique and a basic cycle length of 130/min, reciprocating tachycardias could be initiated with coupling intervals of 255 to 280 msec and a low-to-high right atrial activation sequence (Fig 5). At no other coupling intervals were echo beats initiated. 322 MANDEL, LAKS, OBAYASHI
DISCUSSION
Tachyarrhythmias in man can be considered to be related to two basic mechanisms, reentry or ectopy. 9 One clinical situation in which reentry is clearly accepted as the mechanism for the development of tachyarrhythmias is the WPW syndrome; dual pathways of conduction have been identified electrophysiologically and anatomically. 2 •5 •7 •1(}. 15 Previous studies have defined the onset of tachyarrhythmias and activation sequence during tachyarrhythmia induction in the WPW syndrome, confirming reentry utilizing both the normal AV nodal and bypass tract pathways. 2• 7· 1(}.13.16-19 Table l-Progre..ive A.-H Interval Prolongation with lncreaaing A.Jrial Pacing Rate• Interval A-H
H-v•
WPW
Control 67/min
70
40
+
Pacing 90/min
125
40
+
I 10/min
135
40
±
130/min
140
40
!50/min
145
40
170/min
!55**
40
Heart Rate
*H-V, His-ventricle. **2 :1 conduction.
CHEST, 68: 3, SEPTEMBER, 1975
90/min
AEG
110/min
r. ~~
,.,
HBE
I
L:t
:
LII
~
Lm
~ t----
lsec
170/min
150/min
r
AEG
t
HBE LI Ln Lm
FrcuRE 2. Right atrial pacing. Four panels demonstrate effects of increasing right atrial pacing rates (90/min, 110/min, 150/min, and 170/min) on AV conduction. From top to bottom in each panel are high right atrial electrogram ( AEG), His bundle electrogram ( HBE), and standard ECG leads 1, 2, and 3. Note presence of anomalous ventricular activation at 90/min. At 110/min, there is alternating anomalous conduction and normal ventricular activation. At rates up . to 150/min, only nonnal ventricular activation was observed. Lower right-hand panel demonstrates development of anterograde AV block at pacing rate of 170/min; site of block was within AV node.
A) 600
500
HIH2
msec
.,
B)
AVRP
90/min
VARP 90/min
700
0
•• • •
0 0
.-
600
0
OWPN
500
400
IERP • 540 msec I
ERP • 265 msec FRP • 450 msec
IATRIAL ERP·~ - i
300
300
400
A1A2
msec
500
600
'!'.
•
eRSR
./
400
500
400
V1V2
600
700
msec
FIGU!lE 3. Atrioventricular nodal anterograde and retrograde refractory period detem1inations. Left-hand panel (A) displays points obtained during anterograde AV refractory-period measurements using extrastimulus technique (open circles, complexes with anomalous AV conduction; solid circles, complexes with normal ventricular activation). Horizontal axis identifies A1A" coupling interval; vertical axis identifies H 1 H~ response. Boxes identify effective ( ERP) and functional ( FRP) refractory periods of AV node as well as atrial effective refractory period ( ERP). Right-hand panel (B) shows results obtained during determination of VA refractory periods. Horizontal ax1s idPntifies V 1V" coupling interval; vertical axis identifies high right atrial A 1A2 responsP. EffPctive refractory period ( ERP) is identified in box.
CHEST, 68: 3, SEPTEMBER, 1975
ATRIOVENTRICULAR NODAL REENTRY IN WPW SYNDROME 323
90/min
AEG LI
110/min
il63l A*
Ln Lm FIGURE 4. Effect of right ventricular pacing on VA conduction. Left-hand panel shows effect of ventricular pacing at rate of 90/min. From top to bottom are high right atrial electrogram ( AEG) and standard ECG leads 1, 2, and 3. Number in box identifies VA conduction time. Right-hand panel shows results obtained during ventricular pacing at rate of 110/min. There is 2 : 1 VA conduction time of 210 msec.
Nevertheless, it is conceivable that the supraventricular tachycardias seen in the WPW syndrome need not occur because of a reciprocating mechanism utilizing this dual anatomic pathway concept. It is possible that ectopic pacemakers may occur or that a reciprocating mechanism may be responsible due to sinus-to-atrial reentry or AV nodal reentry. In the previous study of Rosen, 6 an AV nodal reentry mechanism was considered to be operative, but limited electrophysiologic data necessitated the use of assumptions by this author which detracted from the impact of his observations. We agree with Dr. Rosen that AV nodal reentry may be responsible for some of the tachyarrhythmias seen in the WPW syndrome. To consider AV nodal reentry as a mechanism of supraventricular tachycardia in the WPW syndrome, one must show that ( 1) the bypass tract fails to conduct anterograde at a rate in excess
of the spontaneous tachycardia rate, ( 2) the echo zone occurs at a shorter coupling interval than the bypass refractory period, ( 3) retrograde bypass conduction fails at rates less than observed during supraventricular tachycardia, and ( 4) bypass refractoriness is prolonged in excess of the supraventricular tachycardia cycle length. Our present data support the fact that, in this patient, the bypass tract electrophysiologic properties both in the anterograde and retrograde fashion would not sustain conduction at a rate in excess of 110/min. The electrophysiologic findings seen with premature atrial stimulation, culminating in the repeated episodes of supraventricular tachycardia, demonstrated characteristics which are in keeping with Goldreyer and Bigger's observations in patients with paroxysmal atrial tachycardia.20 The electrophysiologic observations are in concert with pioneering studies by
FIGURE 5. Induction of supraventricular tachycardia. Left-hand portion identifies eleetrogr
