- Email: [email protected]
Dual atrioventricular nodal pathways: A benign finding in arrhythmia-free children with heart disease
Dual Atrioventricular Nodal Pathways: A Benign Finding in Arrhythmia-Free Children With Heart Disease
ALFONSO CASTA, MD GRACE S. WOLFF, MD, FACC ASHOK V. MEHTA, MD DOLORES TAMER, MD, FACC OTTO L. GARCIA, MD, FACC ARTHUR S. PICKOFF, MD PEDRO L. FERRER, MD, FACC RUEY J. SUNG, MD, FACC HENRY GELBAND, MD, FACC Miami, Florida
The incidence and significance of dual atrioventricular (A-V) nodal pathways are described in 78 children with associated congenital or acquired heart disease. None of these patients had clinlcal or electrocardiographlc evidence of arrhythmia. Dual A-V nodal pathways were observed in 35 percent of the preoperative group and in 33 percent of the postoperative group. Desplte this substrate for A-V nodal reentry, supraventrtcular tachycardla was neither induced durlng electrophysiologlc evaluation nor did it develop clinically over a follow-up period of 1 month to 15 years. It is concluded that dual A-V nodal pathways are common and may be a benign finding in arrhythmia-free children with heart disease.
Moe et a1.l provided evidence in animals of dual atrioventricular (A-V) nodal conduction pathways when they demonstrated an abrupt increase in the A-V conduction time when the atria1 coupling interval was reduced. This resulted in discontinuous A-V conduction curves and implied the presence of parallel A-V conduction pathways with different electrophysiologic properties. Discontinuous A-V nodal conduction curves (Al-As and Hi-Hz) suggestive of the presence of dual A-V nodal pathways have been found in patients without supraventricular tachycardia213 and have been demonstrated as a common mechanism for supraventricular tachycardia in adults and children.2-10 Denes et a1.2 reported a 10 percent incidence rate of dual A-V nodal pathways in a mixed group of adults, most of whom had disease of the conduction system, whereas Thapar and Gillette3 reported an overall incidence rate of 46 percent in a group of children, most of whom were evaluated because of arrhythmias. This report describes the incidence of dual A-V nodal pathways in 78 preoperative and postoperative children with cardiac defects in whom there was no clinical or electrocardiographic evidence of arrhythmias; they were found in 35 percent of the preoperative group and 33 percent of the postoperative group. Our observations indicate that dual A-V nodal pathways are common in arrhythmia-free children with heart disease and probably represent functional properties of the human A-V node. Methods From the University of Miami School of Medicine, Departments of Pediatrics and Medicine, Miami, Fkxida. This study was supported in part by Grant 07436 from the National institutes of Health, Bethesda, Maryland, and the American Heart Association, Fiwida Afffliate, Miami. Florida. Manuscript received April 21, 1980; revised manuscript received June 24, 1980, accepted June 27, 1980. Address for reprints: Alfonso Casta, MD, Pediatric Cardiology, Department of Pediatrics, University of Miami, School of Medicine, P.O. Box 016820, Miami, Florida 33101.
Patients: Diagnostic cardiac catheterization and electrophysiologic studies were performed in 78 consecutive patients. The patients were classified into two groups. Group I consisted of 51 preoperative patients with the following heart
defects: secundum atria1 septal defect (lo), ventricular septal defect (ll), coarctation of the aorta (3), rheumatic heart disease (2), endocardial cushion defect (6), pulmonary valve stenosis (lo), aortic valve stenosis (2), tetralogy of
FaIlot (Z), corrected transposition of the great vessels (l), primary pulmonary hypertension (l), congenital mitral insufficiency (1) and myocarditis (1). One patient had a normal heart. The patients’ ages ranged between 10 months and
18 years. Group II consisted of 27 patients with repaired cardiac defects: tetralogy of Fallot (17), ventricular septal defect (3), endocardial cushion defect (3), transposition of the great vessels (l), subvalvular aortic stenosis (2) and double
December1990
The American Journal of CARDIOLOGY
Volume 46
1013
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
outlet right ventricle (1). The patients’ ages ranged between 2 and 18 years. The electrocardiograms in both groups revealed normal P-R intervals and no arrhythmias. Electrophysiologio studies: The 78 patients were premedicated with combinations of Demerole, Phenergane, Thorazine@ and Nembutale (49); Demerol, Phenergan and
Thorazine (26); Demerol and Nembutal(2); and general anesthesia (1). The electrophysiologic studies were conducted after completion of cardiac catheterization. A tripolar catheter was introduced percutaneously through the right femoral vein and positioned across the tricuspid valve for recording of the low septal right atrial and His bundle electrograms.ll A second
TABLE I Electrocardiographic and Electrophyslologic Data on 27 Children With Heart Defects and Dual A-V Nodal Pathways
Case
Sex & Age (yr)
Clinical Diagnosis
P-R
QRS
QRS Axis
Fast Pathway ERPiFRP
Slow Pathway ERPIFRP
Group I (preoperative) 1
F13
Rheumatic Ml
136
75
+50
2
M5
151
70
+45
3
F6
PS, rubella syndrome +PDA ASD(2”)
113
65
+75
4
Ml4
ASD(2”)
160
75
+120
5
M5%*
AS
156
60
+90
6
F3
VSD
159
70
+60
7
FlO
Syncope, normal heart
169
65
+60
6
Ml6
Coarctation of aorta
125
65
+60
9
Ml
VSD
70
135
+a0
10
F5
VSD
60
120
+60
11
F5
PS
95
140
+100
12
M4% 2
ASD(2’)
60
141
+60
13
F5%
Corrected TGV. VSD
65
166
+30
60
163
+90
100
136
+135
60
146
+75
100
173
+110
75
139
+60
14
M7%
15
M4%2
16
F17
17
Ml7
16
M4
PS, PPS Primary pulmonary hypertension Congenital mitral insufficiency PS VSD
S = ARl<275; P = 2401270 S = 26Oi360; P = 27OK360 S =*. P =‘240/<330 s = 3301565; P = 3iol460 s = 3ooi405; P = 3101395 S = 2201365; p =* S = 2601430; P = NR/NR S = NR/NR; P = 3201425 S = 2601315; P = NRINR s = 3401440; P = 3401415 S = AR/AR; P = 2701360 S = 2501400; P = 2501400 S = AR/AR; P = 2201340 s = 2601450; P = 300/440 s = 3401410; P = 2601410 S = ARIAR; P = 3601410 s = 3301340; P = 3501425 S = 2601355; P = 2601340
SP = ARIAR sPyARIAR; S =‘; P = ARIAR Sp=_2601660; S = 2501470; P = 2401465 S = NRINR; p=* S = NRINR; sps P L ARIAR S = <215/350; sp_T P L 3001430 S-; P = AR/AR S = AR/AR; P = ARIAR S-; P = AR/AR S = ARIAR; P = 2aol4io S = <270/>410; Sp_T P L 2701420 S = ARIAR; P = 3101555 s = 2401395; P = <260/365
Group II (postoperative) 19
F9
To F (4)+
134
120
+90
20
F5
To F (3)f
190
190
+120
21
F6
To F (2)+
149
100
+60
22
F5
To F (2)+
137
140
Indet.
23
M6
To F (2)+
160
120
Indet.
24
M6% 2
ECD
157
75
-45
25
FWW
Subaortic stenosis
26
M5%
(5)+ VSD (2%2)+
27
Ml7
(4)+
Subaortic stenosis (12)+
136
105
+75
142
100
+90
175
160
+10
s = 2951350; P = 3101370 sp==3 10/400; S = ;5/520. P = 3601446 s = 410/500; P = 4501510 S = 5701610; P = 5201590 S = 2601330; D = ?60lWU1 .S = 2’9013;;: P = 2901355 s = 3301445; P = 3301425 s = 3501490; P = 3501490
S = AR/AR; P = AR/AR S = AR/AR; p =* S = 3001665; P = 3501520 S = 4001525; Sp=4501600; PS = <260/<440; P = 2501420 S = AR/AR; P = AR/AR S = AR/AR; P = AR/AR s = 3401560; P = 3401550
Refractory periods were not determined. + Numbers in parentheses indicate number of years after operation. AR = limited by atrial refractoriness; AS = aortic stenosis; ASD(2’) = atrial septal defect (secundum); ECD = endocardial cushion defect; ERP = effective refractory period; FRP = functional refractory period; Indet. = indeterminate; Ml = mitral insufficiency; NR = not reached; P = atrial PPS = peripheral pulmonic stenosis; PS = vafvular pulrnoni~ paced cycle; P- = no dual pathways on paced rftythm; PDA = patent ductus artertt; stenosis; S = sinus cycle; S- = no dual pathways on sinus rhythm; TGV = transposition of the great vessels; To F = tetralogy of Fallot: VSD = ventricular septal defect. l
1614
December 1980
The American Journal of CARDIOLOGY
Volume 46
DUAL A-V NODAL PATHWAYS IN CHILDREN-CASTA
tripolar or tetrapolar catheter was introduced through the same femoral vein and positioned in the high right atrium for stimulation and for recording the high right atria1 electrogram. Surface electrocardiographic leads I, II, III or I, II and VI and intracardiac electrograms were recorded simultaneously on a multichannel photograpl$c recorder (Electronics for Medicine DR-12, White Plains, New York) with a pap& speed of 100 mm/s and filter settings of 40 to 500 hertz. Stimuli were delivered by a programmable digital stimulator (Medtronics model 5325 programmable stimulator) with a strength of twice diastolic threshold and a duration of 2 ms. Rapid atria1 pacing and programmed atria1 extrastimulation were performed in all patients. The atria1 and atrio-
ventricular (A-V) nodal refractory periods were determined utilizing the atrial extrastimulus technique.12 Coupling of an atria1 extrastimulus to both sinus and atria1 paced cycle lengths was performed in 61 of the 78 patients; coupling of the extrastimulus to sinus cycle length only or to an atria1 paced cycle length only was performed in 14 and 3 patients, respectively. Ventricular extrastimulation studies were performed in 54 patients and in the majority the extrastimulus was coupled to the sinus rhythm. The atria1 or ventricular test stimulus (Sp) was introduced after every eighth spontaneous or driven beat (Sl). The coupling interval was decreased by 10 to 20 ms decrements during both atria1 and ventricular extrastimulation. Definitions:HRA1, Al, HI and VI refer, respectively, to the high right atrial, low septal right atrial, His bundle and ventricular electrograms of spontaneous sinus or driven beats. HRA2, AZ, HS and VZ refer to the respective responses to the extrastimulus (SQ). Refractory periods and A-V conduction intervals were defined and measured as described by Denes et al l3 and Castellanos et al l4 respectively. The diagnosis of dual A-$ nodal pathways was based on the induction of discontinuous A-V nodal conduction curves (Al-A2 and HI-HZ) with programmed atria1 extrastimulation.2*6 The curve to the right of the discontinuity reflected fast A-V nodal pathway conduction, and to the left slow A-V nodal pathway conduction. The effective refractory period of the fast A-V nodal pathway was the longest AI-AZ interval that failed to conduct through the fast A-V nodal pathway, and its functional refractory period was the shortest HI-HZ interval on the fast A-V nodal pathway curve. The effective refractory period of the slow A-V nodal pathway was the longest Al-A2 interval that was not conducted through the slow A-V nodal pathway, and its functional refractory period was the shortest HI-HZ interval on the slow A-V nodal pathway curve. A-V nodal reentry was diagnosed by the occurrence of atrial echoes with a low to high atria1 activation sequence. The echo zone was defined as the zone within which atria1 extrastimuli induced atria1 echoes.15-l7 The critical A-H interval was the shortest AZ-HZ interval inducing an atria1 echo.‘8
Results Dual A-V nodal pathways were demonstrated in 27 (35 percent) of the 78 patients-18 (35 percent) of the 51 in the preoperative group and 9 (33 percent) of the 27 in the postoperative group. Of 27 patients who had dual atrioventricular (A-V) nodal pathways 24 were studied with the atria1 extrastimulus coupled to both sinus and paced rhythms. In 11 of these 24 patients dual A-V nodal pathways were documented during coupling
ET AL.
of the atrial extrastimulus to both sinus and paced atrial rhythms: in 7 during sinus rhythm only and in 6 during paced rhythm only. In 20 of the 27 patients with dual A-V nodal pathways, ventricular extrastimulation was performed. Ventriculoatrial (V-A) conduction was present in 10 patients, an incidence rate of 50 percent. The incidence rate of V-A conduction in patients without dual A-V nodal pathways was 49 percent. The effective and functional refractory periods of the fast A-V nodal pathway ranged between 220 and
570 and 270 and 610 ms, respectively, whereas the effective and functional refractory periods of the slow A-V nodal pathway ranged between 240 and 450 and 350 and 665 ms, respectively (Table I). Accurate measurement of the refractory periods of the slow A-V nodal pathway was limited by atria1 refractoriness in 12 patients. The effective and functional refractory periods of the fast A-V nodal pathway in the preoperative group were 287 f 42 and 398 f 61 ms, respectively. The effective and functional refractory periods of the fast A-V nodal pathway in the postoperative group was 345 f 80 and
.
1
SllUSCl430
460
.
=
. .
=: 420 t
.
.
.
330
.
02 . O. DZIB 2111.
225-215
.
.
l
,
OL,
250 c
. l
0
280
250
.
300 350 A$2 [mcc]
100
450
500
FIGURE 1. Patient 19. A-V conduction curves (AlA and HIHe; AlA;! and A2H2) during atrial extrastimulation coupled to sinus rhythm. The average sinus cycle length (CL) is 530 ms. Note discontinuity due to a sudden increase in atrioventricular (A-V) nodal conduction time (A2H2) at a coupling interval of 295 ms. In this and subsequent figures closed circler represent responses wlthout atrial echoes; open clrcfes represent responses with atrial echoes. The effective and functional refractuy pe&ds of the fast pathway were 295 and 350 ms, respectively. The effective and functiil refractory periods of the slow pathway were limited by atrial refractoriness. The echo zoned ranged between 225 and 215 ms. Sustained supraventricular tachycardia was not induced.
December 1980
The American Journal of CARDK)LOGY
Volume 46
1015
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
fractory periods of the fast A-V nodal pathway were 310 and 370 ms, respectively. The measurement of the refractory periods of the slow A-V nodal pathway was also limited by atrial refractoriness.This was the only patient in whom atrial echoes were elicited. Sustained A-V nodal reentrant tachycardia could not be elicited in any patient. Figure 3 demonstrates the electrophysiologic tracings from Patient 3 (Table I) during atria1extrastimulus coupled to a paced cycle length of 490 ms. Electrocardiographic leads I, II, III and His bundle electrograms are shown. In panel A, an atrial premature beat at a coupling interval (Ai-Az) of 250 ms results in an Az-Hz of 160 ms. In panel B, an atrial premature beat at a coupling interval (AI-AZ) of 240 ms prolongs the A-H interval to 230 ms, resulting in discontinuous A-V nodal conduction curves.
. . . .
.
The sudden increase or jump in A-V conduction time (As-Hz) resulting when conduction failed in the fast A-V nodal pathway and shifted to the slow A-V nodal pathway ranged between 40 and 185 ms in the entire group.
.
100 t
l*
Discussion
00. .
L, II
200
250
300 350 A,A2[msec]
I
400
450
508
FIGURE 2. Patient 19. A-V conduction curves (AtAs and HtHs; AlA and AsH2) during atrial extrastimulation coupled to a high right atrial pacing cycle length of 500 ms. Note discontinuity due to a sudden increase in A-V nodal conduction time (AsH2) at a coupling interval (A1A2) of 310 ms. The effective and functional refractory periods of the fast pathway were 310 and 370 ms, respectively. The effective and functional refractory periods of the slow pathway were limited by atrial refractoriness. The echo zone ranged between 250 and 2 10 ms. Sustained supraventricular tachycardia was not induced.
427 f 83 ms, respectively. Slow A-V nodal pathway refractory periods were limited by atrial refractoriness in the majority of patients. Representative cases: Figure 1 demonstrates the induction of discontinuous A-V nodal conduction curves (Ai-Az and Hi-Hz; Ai-A2 and AZ-Hz) in Patient 19 (Table I) during atrial extrastimulation coupled to sinus rhythm. The average sinus cycle length was 530 ms. At a coupling interval (Ai-Az) of 295 ms there was a sudden prolongation in the Az-Hs interval of 55 ms resultingin discontinuous A-V nodal conduction curves. The echo zone could be defined between coupling intervals (Ai-Az) of 225 and 215 ms. Sustained A-V nodal reentry was not induced. The effective and functional refractory periods of the fast A-V nodal pathway were 295 and 350 ms, respectively. The measurement of the refractory periods of the slow A-V nodal pathway was limited by atria1refractoriness. The echo zone was narrowerduring atrial extrastimulationcoupled to sinus rhythm than during that coupled to paced rhythm (Fig. 2). Figure 2 demonstrates the induction of discontinuous A-V nodal conduction curves (Ai-Az and Hi-Hz; Ai-Az and Az-Hz) in this patient during atrial pacing. The paced atrial cycle length (Si-Sz) is 500 ms. At a coupling interval (Al-As) of 310 ms there was sudden prolongation in the As-Hz interval of 50 ms resulting in discontinuous A-V nodal conduction curves. The echo zone could be defined between coupling intervals (AI-AZ) of 250 and 210 ms. The effective and functional re-
1016
December 1960
The American Journal of CARDIOLOGY
Mechanism of supraventricular tachycardia: Atrioventricular nodal reentry is a common cause of supraventricular tachycardia in adultseJa*2o and chil-
drens~8J0and electrophysiologic studies have confirmed that dual atrioventricular (A-V) nodal pathways are a frequent underlying mechanism for supraventricular tachycardia.2,3s-10 The slow-fast form of A-V nodal reentrant tachycardia involves a slow A-V nodal pathway for anterograde conduction and a fast A-V nodal pathway for retrograde conduction.lgJO However, the fast-slow form utilizes a fast A-V nodal pathway for anterograde conduction whereas retrograde conduction occurs through a slow A-V nodal pathway.7Jgp20 Both forms of A-V nodal reentry have been demonstrated in children.317,8Studies in adults have primarily involved patients with conduction disease. Denes et a1.g found a 10 percent incidence rate (41 of 397 patients) of dual A-V nodal pathways in a group of such patients, but 16 (39 percent) of the 41 patients had no history of palpitations or supraventricular tachycardia. This benignity appears to apply to pediatric patients aa well. Therefore, dual A-V nodal pathways are common in both adults and children. Incidence of dual A-V nodal pathways: Both DuBrow et allo and Thapar and Gillette3 have reported the presence of dual A-V nodal pathways in arrhythmia-free children. Of 61 children studied by Thapar and Gillette3 the majority had some rhythm disorder, but 17 children with a cardiac defect without arrhythmia demonstrated a 29 percent incidence of dual A-V nodal pathway conduction before surgery. This is in agreement with our findings of a 35 percent incidence rate in an unselected group of preoperative and postoperative patients (35 percent in the former group alone and 33 percent in the latter group alone). This high incidence rate of dual A-V nodal pathways may be related to the significantly shorter atria1 and A-V nodal refractory has been sugperiods in children.21*22 It gested3p2a,24that these electrophysiologic changes cor-
Volume 46
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
PACED CL490
I
-
-500 mfec-
I
-556
me-
FIGURE 3. Patient 3. His bundle electrogram during atrial extrastimulation coupled to a paced cycle length (CL) of 490 ms. Electrocardiographic leads I, II and Ill and His bundle electrogram (HBE) are shown. Sf and Sp represent atrial pacing and premature stimuli, respectively. A,, HI and VI represent the low right atrium, His bundle and ventricular electrogram during pacing. As, H2 and V2 represent the responses to a premature atrial extrastimulus (Ss). A, at a coupling interval (AtAs) of 250 ms the A&f2 interval is 160 ms. 6, at a coupling interval (AtA*) of 240 ms the A2H2 interval prolongs to 230 ms resulting in discontinuous A-V nodal conduction curves.
with maturational histologic changes. In addition, Sapire et a1.25 have demonstrated that meperidine (Demerol), promethazine (Phenergan) and chlorpromazine (Thorazine) shorten A-V nodal refractory periods. These medications, by their shortening effect on refractory periods, may unmask the presence of dual A-V nodal pathways by allowing conduction at shorter coupling intervals when the slow A-V nodal pathway is utilized for conduction after the fast A-V nodal pathway refractory period has been reached. In general, atria1 paced rhythm decreases atria1 refractoriness and prolongs the refractory periods of the fast A-V pathway by shortening the atiial cycle length.13 Therefore, dual A-V nodal pathway conduction is expected to be observed more frequently during atria1 paced rhythm than during sinus rhythm. The finding that such conduction occurred during sinus rhythm but not during atria1 paced rhythm in seven of our patients was unusual. In four patients (Cases 2,4,15 and 23) we could attribute this finding to paradoxical shortening of the effective refractory period of the fast A-V nodal pathway induced by atria1 pacing. This would prevent exposure of dual A-V nodal pathways because the fast A-V nodal pathway is used at both long and short coupling intervals. This shortening of the refractory period of the fast A-V nodal pathway with atria1 pacing is the expected response of atrial and His-Purkinje tissue and is unusual in A-V nodal tissue.13
relate
Incidence of supraventricular tachycardk of
cidence of echoes is probably a reliable finding because more than half of our patients had high right atria1 recordings, and the atria1 electrograms were clearly discernible. The failure to induce sustained supraventricular tachycardia may be explained by this absence of atria1 echoes.g Supraventricular tachycardia has not been observed clinically in any of our patients during a follow-up period of 1 month to 15 years. Whether dual A-V nodal pathways will persist with maturation in an individual patient cannot be predicted from our data because only two children have had sequential electrophysiologic studies; both children demonstrated dual pathways before and 2 years after surgery. Although the substrate exists for A-V nodal reentry, the initiation of sustained supraventricular tachycardia depends on an interplay of many factors. These include the presence or absence of atria1 or ventricular extrasystoles and alterations in the functional properties of each A-V nodal pathway in relation to age, cycle length, autonomic tone and medications. In our patients the interplay of these factors was not synchronized for reentrant tachycardia. Therefore, dual A-V nodal pathways are a common and frequently a benign electrophysiologic phenomenon in children and may represent normal functional characteristics of the human A-V node. Acknowledgment
None
our patients had sustained A-V nodal reentrant tachycardia during electrophysiologic studies and only one patient (Case 19) had atria1 echoes. This small in-
We gratefully acknowledge the technical assistance of Ralph Portuondo and Francisco Garcia-Montes and the secretarial assistance of Diane McMullen.
December 1980
The American Journal of CARDIOLDDV
Volume 48
1017
DUAL A-V NODAL PATHWAYS IN CHILDREN-CASTA
ET AL.
References 1. 2.
3.
4.
5. 6.
7.
6. 9.
10.
11.
12.
13.
Mx GK,Preston JB, Burlington H. Physiologic evidence for a dual A-V transmission system. Circ Res 19564357-75. Denes P, Wu D, Dhlngra R, Amat-y-Leon F, Wyndham C, Rosen KM. Dual atrioventricular nodal pathways. A common electrophysiological response. Br Heart J 1975;37: 1069-76. Thapar MK, Glllette PC. Dual atrioventricular nodal pathways: a common electrophysiologic response in children. Circulation 1979;60:1369-74. Wu D, Denes P, Dhlngra R, Pletras RJ, Rosen KM. New manifestations of dual A-V nodal pathways. Eur J Cardiol 1975;2: 459-66. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol 1974;33:291-4. Denes P, Wu D, Dhlngra RC, Chuqulmla R, Rosen KM. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 1973;46:549-55. Wolff GS, Sung RJ, Plckoff A, et al. The fast-slow form of atrioventricular nodal reentrant tachycardia in children. Am J Cardiol 1979;43:1161-6. Gillette PC. The mechanisms of supraventricular tachycardia in children. Circulation 197&54:133-g. Denes P, Wu D, Amat-y-Leon F, Dhtngra R, Wyndmn CR, Rosen KM. The determinants of atrioventricular nodal reentrance with premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 1977;58:253-9. DuBrow IW, Fisher EA, Hastrelter AR. Dual A-V node pathways (D) with and without paroxysmal supraventricular tachycardia (PSVT) in pediatric cardiology (abstr). American Academy of Pediatrics 46th Annual Meeting, October 13-16, 1979. Scharlag BJ, Lau SH, Helfanf RH, Berkowitz WD, Stein E, Damato AN. Catheter technique for recording His bundle activity in man. Circulation 1969;39:13-16. Sung RJ, Castellanos A, Mallon SM, Gelband H, Mendoza I, Myerberg RJ. Mode of initiation of reciprocating tachycardla during programmed ventricular stimulation in the Wolff-Parkinson-White syndrome. With reference to various patterns of ventriculoatrial conduction. Am J Cardiol 1977;40:24-31. Denes P,Wu D, Dhlngra R, Pletras RJ, Rosen KM. The effects of
1016
December 1960
The American Journal of CARDIOLOGY
14.
15. 16. 17. 16.
19.
20.
21.
22.
23. 24. 25.
cycle length on cardiac refractory periods in man. Circulation 1974;49:32-41. Castellanos A Jr, Castlllo CA, Agha AS, Tessler M. His bundle electrograms in patients with short PR intervals, narrow QRS complexes, and paroxysmal tachycardias. Circulation 1971;43: 667-76. Msndez C, Moe GK. Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 1968;19:376-93. Bigger JT Jr, Goldreyer BN. The mechanism of supraventricular tachycardia. Circulation 1970;42:673-66. Goldreyer BN, Bigger JT Jr. Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 1971;43: 15-26. Goldreyer BN, Damato AN. The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 1971;43:679-67. Wu D, Denes P, Amat-y-Leon F, Wyndham CRC, Dhlngra R, Rosen KM. An unusual variety of atrioventricular nodal reentry due to retrograde dual atrioventricular nodal pathways. Circulation 1977:56:50-g. Sung RJ, Styperek JL, Myerburg RJ, Castellanos A. Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man. Am J Cardiol 1976;42:404-15. DuBrow IW, Fisher EA, Amat-y-Leon F, et al. Comparison of cardiac refractory periods in children and adults. Circulation 1975;51:465-91. DuBrow IW, Fisher EA, Denes P, Hasbelter AR. The influence of age on cardiac refractory periods in man. Pedlatr Res 197610: 135-g. James TN. Cardiac conduction system: fetal and postnatal development. Am J Cardiol 1970;25:213-26. James TN. Crder and disorder in ths rhythm of the heart. Circulation 1973;47:362-66. Saplre D, Black I, Mongkolsmal C, Casta A. Changes in cycle length, conduction times, and refractory periods induced by sedation with meperidine, promethazine and chlorpromazine (abstr). Am J Cardiol 1979;43:425.
Volume 46
ALFONSO CASTA, MD GRACE S. WOLFF, MD, FACC ASHOK V. MEHTA, MD DOLORES TAMER, MD, FACC OTTO L. GARCIA, MD, FACC ARTHUR S. PICKOFF, MD PEDRO L. FERRER, MD, FACC RUEY J. SUNG, MD, FACC HENRY GELBAND, MD, FACC Miami, Florida
The incidence and significance of dual atrioventricular (A-V) nodal pathways are described in 78 children with associated congenital or acquired heart disease. None of these patients had clinlcal or electrocardiographlc evidence of arrhythmia. Dual A-V nodal pathways were observed in 35 percent of the preoperative group and in 33 percent of the postoperative group. Desplte this substrate for A-V nodal reentry, supraventrtcular tachycardla was neither induced durlng electrophysiologlc evaluation nor did it develop clinically over a follow-up period of 1 month to 15 years. It is concluded that dual A-V nodal pathways are common and may be a benign finding in arrhythmia-free children with heart disease.
Moe et a1.l provided evidence in animals of dual atrioventricular (A-V) nodal conduction pathways when they demonstrated an abrupt increase in the A-V conduction time when the atria1 coupling interval was reduced. This resulted in discontinuous A-V conduction curves and implied the presence of parallel A-V conduction pathways with different electrophysiologic properties. Discontinuous A-V nodal conduction curves (Al-As and Hi-Hz) suggestive of the presence of dual A-V nodal pathways have been found in patients without supraventricular tachycardia213 and have been demonstrated as a common mechanism for supraventricular tachycardia in adults and children.2-10 Denes et a1.2 reported a 10 percent incidence rate of dual A-V nodal pathways in a mixed group of adults, most of whom had disease of the conduction system, whereas Thapar and Gillette3 reported an overall incidence rate of 46 percent in a group of children, most of whom were evaluated because of arrhythmias. This report describes the incidence of dual A-V nodal pathways in 78 preoperative and postoperative children with cardiac defects in whom there was no clinical or electrocardiographic evidence of arrhythmias; they were found in 35 percent of the preoperative group and 33 percent of the postoperative group. Our observations indicate that dual A-V nodal pathways are common in arrhythmia-free children with heart disease and probably represent functional properties of the human A-V node. Methods From the University of Miami School of Medicine, Departments of Pediatrics and Medicine, Miami, Fkxida. This study was supported in part by Grant 07436 from the National institutes of Health, Bethesda, Maryland, and the American Heart Association, Fiwida Afffliate, Miami. Florida. Manuscript received April 21, 1980; revised manuscript received June 24, 1980, accepted June 27, 1980. Address for reprints: Alfonso Casta, MD, Pediatric Cardiology, Department of Pediatrics, University of Miami, School of Medicine, P.O. Box 016820, Miami, Florida 33101.
Patients: Diagnostic cardiac catheterization and electrophysiologic studies were performed in 78 consecutive patients. The patients were classified into two groups. Group I consisted of 51 preoperative patients with the following heart
defects: secundum atria1 septal defect (lo), ventricular septal defect (ll), coarctation of the aorta (3), rheumatic heart disease (2), endocardial cushion defect (6), pulmonary valve stenosis (lo), aortic valve stenosis (2), tetralogy of
FaIlot (Z), corrected transposition of the great vessels (l), primary pulmonary hypertension (l), congenital mitral insufficiency (1) and myocarditis (1). One patient had a normal heart. The patients’ ages ranged between 10 months and
18 years. Group II consisted of 27 patients with repaired cardiac defects: tetralogy of Fallot (17), ventricular septal defect (3), endocardial cushion defect (3), transposition of the great vessels (l), subvalvular aortic stenosis (2) and double
December1990
The American Journal of CARDIOLOGY
Volume 46
1013
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
outlet right ventricle (1). The patients’ ages ranged between 2 and 18 years. The electrocardiograms in both groups revealed normal P-R intervals and no arrhythmias. Electrophysiologio studies: The 78 patients were premedicated with combinations of Demerole, Phenergane, Thorazine@ and Nembutale (49); Demerol, Phenergan and
Thorazine (26); Demerol and Nembutal(2); and general anesthesia (1). The electrophysiologic studies were conducted after completion of cardiac catheterization. A tripolar catheter was introduced percutaneously through the right femoral vein and positioned across the tricuspid valve for recording of the low septal right atrial and His bundle electrograms.ll A second
TABLE I Electrocardiographic and Electrophyslologic Data on 27 Children With Heart Defects and Dual A-V Nodal Pathways
Case
Sex & Age (yr)
Clinical Diagnosis
P-R
QRS
QRS Axis
Fast Pathway ERPiFRP
Slow Pathway ERPIFRP
Group I (preoperative) 1
F13
Rheumatic Ml
136
75
+50
2
M5
151
70
+45
3
F6
PS, rubella syndrome +PDA ASD(2”)
113
65
+75
4
Ml4
ASD(2”)
160
75
+120
5
M5%*
AS
156
60
+90
6
F3
VSD
159
70
+60
7
FlO
Syncope, normal heart
169
65
+60
6
Ml6
Coarctation of aorta
125
65
+60
9
Ml
VSD
70
135
+a0
10
F5
VSD
60
120
+60
11
F5
PS
95
140
+100
12
M4% 2
ASD(2’)
60
141
+60
13
F5%
Corrected TGV. VSD
65
166
+30
60
163
+90
100
136
+135
60
146
+75
100
173
+110
75
139
+60
14
M7%
15
M4%2
16
F17
17
Ml7
16
M4
PS, PPS Primary pulmonary hypertension Congenital mitral insufficiency PS VSD
S = ARl<275; P = 2401270 S = 26Oi360; P = 27OK360 S =*. P =‘240/<330 s = 3301565; P = 3iol460 s = 3ooi405; P = 3101395 S = 2201365; p =* S = 2601430; P = NR/NR S = NR/NR; P = 3201425 S = 2601315; P = NRINR s = 3401440; P = 3401415 S = AR/AR; P = 2701360 S = 2501400; P = 2501400 S = AR/AR; P = 2201340 s = 2601450; P = 300/440 s = 3401410; P = 2601410 S = ARIAR; P = 3601410 s = 3301340; P = 3501425 S = 2601355; P = 2601340
SP = ARIAR sPyARIAR; S =‘; P = ARIAR Sp=_2601660; S = 2501470; P = 2401465 S = NRINR; p=* S = NRINR; sps P L ARIAR S = <215/350; sp_T P L 3001430 S-; P = AR/AR S = AR/AR; P = ARIAR S-; P = AR/AR S = ARIAR; P = 2aol4io S = <270/>410; Sp_T P L 2701420 S = ARIAR; P = 3101555 s = 2401395; P = <260/365
Group II (postoperative) 19
F9
To F (4)+
134
120
+90
20
F5
To F (3)f
190
190
+120
21
F6
To F (2)+
149
100
+60
22
F5
To F (2)+
137
140
Indet.
23
M6
To F (2)+
160
120
Indet.
24
M6% 2
ECD
157
75
-45
25
FWW
Subaortic stenosis
26
M5%
(5)+ VSD (2%2)+
27
Ml7
(4)+
Subaortic stenosis (12)+
136
105
+75
142
100
+90
175
160
+10
s = 2951350; P = 3101370 sp==3 10/400; S = ;5/520. P = 3601446 s = 410/500; P = 4501510 S = 5701610; P = 5201590 S = 2601330; D = ?60lWU1 .S = 2’9013;;: P = 2901355 s = 3301445; P = 3301425 s = 3501490; P = 3501490
S = AR/AR; P = AR/AR S = AR/AR; p =* S = 3001665; P = 3501520 S = 4001525; Sp=4501600; PS = <260/<440; P = 2501420 S = AR/AR; P = AR/AR S = AR/AR; P = AR/AR s = 3401560; P = 3401550
Refractory periods were not determined. + Numbers in parentheses indicate number of years after operation. AR = limited by atrial refractoriness; AS = aortic stenosis; ASD(2’) = atrial septal defect (secundum); ECD = endocardial cushion defect; ERP = effective refractory period; FRP = functional refractory period; Indet. = indeterminate; Ml = mitral insufficiency; NR = not reached; P = atrial PPS = peripheral pulmonic stenosis; PS = vafvular pulrnoni~ paced cycle; P- = no dual pathways on paced rftythm; PDA = patent ductus artertt; stenosis; S = sinus cycle; S- = no dual pathways on sinus rhythm; TGV = transposition of the great vessels; To F = tetralogy of Fallot: VSD = ventricular septal defect. l
1614
December 1980
The American Journal of CARDIOLOGY
Volume 46
DUAL A-V NODAL PATHWAYS IN CHILDREN-CASTA
tripolar or tetrapolar catheter was introduced through the same femoral vein and positioned in the high right atrium for stimulation and for recording the high right atria1 electrogram. Surface electrocardiographic leads I, II, III or I, II and VI and intracardiac electrograms were recorded simultaneously on a multichannel photograpl$c recorder (Electronics for Medicine DR-12, White Plains, New York) with a pap& speed of 100 mm/s and filter settings of 40 to 500 hertz. Stimuli were delivered by a programmable digital stimulator (Medtronics model 5325 programmable stimulator) with a strength of twice diastolic threshold and a duration of 2 ms. Rapid atria1 pacing and programmed atria1 extrastimulation were performed in all patients. The atria1 and atrio-
ventricular (A-V) nodal refractory periods were determined utilizing the atrial extrastimulus technique.12 Coupling of an atria1 extrastimulus to both sinus and atria1 paced cycle lengths was performed in 61 of the 78 patients; coupling of the extrastimulus to sinus cycle length only or to an atria1 paced cycle length only was performed in 14 and 3 patients, respectively. Ventricular extrastimulation studies were performed in 54 patients and in the majority the extrastimulus was coupled to the sinus rhythm. The atria1 or ventricular test stimulus (Sp) was introduced after every eighth spontaneous or driven beat (Sl). The coupling interval was decreased by 10 to 20 ms decrements during both atria1 and ventricular extrastimulation. Definitions:HRA1, Al, HI and VI refer, respectively, to the high right atrial, low septal right atrial, His bundle and ventricular electrograms of spontaneous sinus or driven beats. HRA2, AZ, HS and VZ refer to the respective responses to the extrastimulus (SQ). Refractory periods and A-V conduction intervals were defined and measured as described by Denes et al l3 and Castellanos et al l4 respectively. The diagnosis of dual A-$ nodal pathways was based on the induction of discontinuous A-V nodal conduction curves (Al-A2 and HI-HZ) with programmed atria1 extrastimulation.2*6 The curve to the right of the discontinuity reflected fast A-V nodal pathway conduction, and to the left slow A-V nodal pathway conduction. The effective refractory period of the fast A-V nodal pathway was the longest AI-AZ interval that failed to conduct through the fast A-V nodal pathway, and its functional refractory period was the shortest HI-HZ interval on the fast A-V nodal pathway curve. The effective refractory period of the slow A-V nodal pathway was the longest Al-A2 interval that was not conducted through the slow A-V nodal pathway, and its functional refractory period was the shortest HI-HZ interval on the slow A-V nodal pathway curve. A-V nodal reentry was diagnosed by the occurrence of atrial echoes with a low to high atria1 activation sequence. The echo zone was defined as the zone within which atria1 extrastimuli induced atria1 echoes.15-l7 The critical A-H interval was the shortest AZ-HZ interval inducing an atria1 echo.‘8
Results Dual A-V nodal pathways were demonstrated in 27 (35 percent) of the 78 patients-18 (35 percent) of the 51 in the preoperative group and 9 (33 percent) of the 27 in the postoperative group. Of 27 patients who had dual atrioventricular (A-V) nodal pathways 24 were studied with the atria1 extrastimulus coupled to both sinus and paced rhythms. In 11 of these 24 patients dual A-V nodal pathways were documented during coupling
ET AL.
of the atrial extrastimulus to both sinus and paced atrial rhythms: in 7 during sinus rhythm only and in 6 during paced rhythm only. In 20 of the 27 patients with dual A-V nodal pathways, ventricular extrastimulation was performed. Ventriculoatrial (V-A) conduction was present in 10 patients, an incidence rate of 50 percent. The incidence rate of V-A conduction in patients without dual A-V nodal pathways was 49 percent. The effective and functional refractory periods of the fast A-V nodal pathway ranged between 220 and
570 and 270 and 610 ms, respectively, whereas the effective and functional refractory periods of the slow A-V nodal pathway ranged between 240 and 450 and 350 and 665 ms, respectively (Table I). Accurate measurement of the refractory periods of the slow A-V nodal pathway was limited by atria1 refractoriness in 12 patients. The effective and functional refractory periods of the fast A-V nodal pathway in the preoperative group were 287 f 42 and 398 f 61 ms, respectively. The effective and functional refractory periods of the fast A-V nodal pathway in the postoperative group was 345 f 80 and
.
1
SllUSCl430
460
.
=
. .
=: 420 t
.
.
.
330
.
02 . O. DZIB 2111.
225-215
.
.
l
,
OL,
250 c
. l
0
280
250
.
300 350 A$2 [mcc]
100
450
500
FIGURE 1. Patient 19. A-V conduction curves (AlA and HIHe; AlA;! and A2H2) during atrial extrastimulation coupled to sinus rhythm. The average sinus cycle length (CL) is 530 ms. Note discontinuity due to a sudden increase in atrioventricular (A-V) nodal conduction time (A2H2) at a coupling interval of 295 ms. In this and subsequent figures closed circler represent responses wlthout atrial echoes; open clrcfes represent responses with atrial echoes. The effective and functional refractuy pe&ds of the fast pathway were 295 and 350 ms, respectively. The effective and functiil refractory periods of the slow pathway were limited by atrial refractoriness. The echo zoned ranged between 225 and 215 ms. Sustained supraventricular tachycardia was not induced.
December 1980
The American Journal of CARDK)LOGY
Volume 46
1015
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
fractory periods of the fast A-V nodal pathway were 310 and 370 ms, respectively. The measurement of the refractory periods of the slow A-V nodal pathway was also limited by atrial refractoriness.This was the only patient in whom atrial echoes were elicited. Sustained A-V nodal reentrant tachycardia could not be elicited in any patient. Figure 3 demonstrates the electrophysiologic tracings from Patient 3 (Table I) during atria1extrastimulus coupled to a paced cycle length of 490 ms. Electrocardiographic leads I, II, III and His bundle electrograms are shown. In panel A, an atrial premature beat at a coupling interval (Ai-Az) of 250 ms results in an Az-Hz of 160 ms. In panel B, an atrial premature beat at a coupling interval (AI-AZ) of 240 ms prolongs the A-H interval to 230 ms, resulting in discontinuous A-V nodal conduction curves.
. . . .
.
The sudden increase or jump in A-V conduction time (As-Hz) resulting when conduction failed in the fast A-V nodal pathway and shifted to the slow A-V nodal pathway ranged between 40 and 185 ms in the entire group.
.
100 t
l*
Discussion
00. .
L, II
200
250
300 350 A,A2[msec]
I
400
450
508
FIGURE 2. Patient 19. A-V conduction curves (AtAs and HtHs; AlA and AsH2) during atrial extrastimulation coupled to a high right atrial pacing cycle length of 500 ms. Note discontinuity due to a sudden increase in A-V nodal conduction time (AsH2) at a coupling interval (A1A2) of 310 ms. The effective and functional refractory periods of the fast pathway were 310 and 370 ms, respectively. The effective and functional refractory periods of the slow pathway were limited by atrial refractoriness. The echo zone ranged between 250 and 2 10 ms. Sustained supraventricular tachycardia was not induced.
427 f 83 ms, respectively. Slow A-V nodal pathway refractory periods were limited by atrial refractoriness in the majority of patients. Representative cases: Figure 1 demonstrates the induction of discontinuous A-V nodal conduction curves (Ai-Az and Hi-Hz; Ai-A2 and AZ-Hz) in Patient 19 (Table I) during atrial extrastimulation coupled to sinus rhythm. The average sinus cycle length was 530 ms. At a coupling interval (Ai-Az) of 295 ms there was a sudden prolongation in the Az-Hs interval of 55 ms resultingin discontinuous A-V nodal conduction curves. The echo zone could be defined between coupling intervals (Ai-Az) of 225 and 215 ms. Sustained A-V nodal reentry was not induced. The effective and functional refractory periods of the fast A-V nodal pathway were 295 and 350 ms, respectively. The measurement of the refractory periods of the slow A-V nodal pathway was limited by atria1refractoriness. The echo zone was narrowerduring atrial extrastimulationcoupled to sinus rhythm than during that coupled to paced rhythm (Fig. 2). Figure 2 demonstrates the induction of discontinuous A-V nodal conduction curves (Ai-Az and Hi-Hz; Ai-Az and Az-Hz) in this patient during atrial pacing. The paced atrial cycle length (Si-Sz) is 500 ms. At a coupling interval (Al-As) of 310 ms there was sudden prolongation in the As-Hz interval of 50 ms resulting in discontinuous A-V nodal conduction curves. The echo zone could be defined between coupling intervals (AI-AZ) of 250 and 210 ms. The effective and functional re-
1016
December 1960
The American Journal of CARDIOLOGY
Mechanism of supraventricular tachycardia: Atrioventricular nodal reentry is a common cause of supraventricular tachycardia in adultseJa*2o and chil-
drens~8J0and electrophysiologic studies have confirmed that dual atrioventricular (A-V) nodal pathways are a frequent underlying mechanism for supraventricular tachycardia.2,3s-10 The slow-fast form of A-V nodal reentrant tachycardia involves a slow A-V nodal pathway for anterograde conduction and a fast A-V nodal pathway for retrograde conduction.lgJO However, the fast-slow form utilizes a fast A-V nodal pathway for anterograde conduction whereas retrograde conduction occurs through a slow A-V nodal pathway.7Jgp20 Both forms of A-V nodal reentry have been demonstrated in children.317,8Studies in adults have primarily involved patients with conduction disease. Denes et a1.g found a 10 percent incidence rate (41 of 397 patients) of dual A-V nodal pathways in a group of such patients, but 16 (39 percent) of the 41 patients had no history of palpitations or supraventricular tachycardia. This benignity appears to apply to pediatric patients aa well. Therefore, dual A-V nodal pathways are common in both adults and children. Incidence of dual A-V nodal pathways: Both DuBrow et allo and Thapar and Gillette3 have reported the presence of dual A-V nodal pathways in arrhythmia-free children. Of 61 children studied by Thapar and Gillette3 the majority had some rhythm disorder, but 17 children with a cardiac defect without arrhythmia demonstrated a 29 percent incidence of dual A-V nodal pathway conduction before surgery. This is in agreement with our findings of a 35 percent incidence rate in an unselected group of preoperative and postoperative patients (35 percent in the former group alone and 33 percent in the latter group alone). This high incidence rate of dual A-V nodal pathways may be related to the significantly shorter atria1 and A-V nodal refractory has been sugperiods in children.21*22 It gested3p2a,24that these electrophysiologic changes cor-
Volume 46
DUAL A-V NODAL PATHWAYS
IN CHILDREN-CASTA
ET AL.
PACED CL490
I
-
-500 mfec-
I
-556
me-
FIGURE 3. Patient 3. His bundle electrogram during atrial extrastimulation coupled to a paced cycle length (CL) of 490 ms. Electrocardiographic leads I, II and Ill and His bundle electrogram (HBE) are shown. Sf and Sp represent atrial pacing and premature stimuli, respectively. A,, HI and VI represent the low right atrium, His bundle and ventricular electrogram during pacing. As, H2 and V2 represent the responses to a premature atrial extrastimulus (Ss). A, at a coupling interval (AtAs) of 250 ms the A&f2 interval is 160 ms. 6, at a coupling interval (AtA*) of 240 ms the A2H2 interval prolongs to 230 ms resulting in discontinuous A-V nodal conduction curves.
with maturational histologic changes. In addition, Sapire et a1.25 have demonstrated that meperidine (Demerol), promethazine (Phenergan) and chlorpromazine (Thorazine) shorten A-V nodal refractory periods. These medications, by their shortening effect on refractory periods, may unmask the presence of dual A-V nodal pathways by allowing conduction at shorter coupling intervals when the slow A-V nodal pathway is utilized for conduction after the fast A-V nodal pathway refractory period has been reached. In general, atria1 paced rhythm decreases atria1 refractoriness and prolongs the refractory periods of the fast A-V pathway by shortening the atiial cycle length.13 Therefore, dual A-V nodal pathway conduction is expected to be observed more frequently during atria1 paced rhythm than during sinus rhythm. The finding that such conduction occurred during sinus rhythm but not during atria1 paced rhythm in seven of our patients was unusual. In four patients (Cases 2,4,15 and 23) we could attribute this finding to paradoxical shortening of the effective refractory period of the fast A-V nodal pathway induced by atria1 pacing. This would prevent exposure of dual A-V nodal pathways because the fast A-V nodal pathway is used at both long and short coupling intervals. This shortening of the refractory period of the fast A-V nodal pathway with atria1 pacing is the expected response of atrial and His-Purkinje tissue and is unusual in A-V nodal tissue.13
relate
Incidence of supraventricular tachycardk of
cidence of echoes is probably a reliable finding because more than half of our patients had high right atria1 recordings, and the atria1 electrograms were clearly discernible. The failure to induce sustained supraventricular tachycardia may be explained by this absence of atria1 echoes.g Supraventricular tachycardia has not been observed clinically in any of our patients during a follow-up period of 1 month to 15 years. Whether dual A-V nodal pathways will persist with maturation in an individual patient cannot be predicted from our data because only two children have had sequential electrophysiologic studies; both children demonstrated dual pathways before and 2 years after surgery. Although the substrate exists for A-V nodal reentry, the initiation of sustained supraventricular tachycardia depends on an interplay of many factors. These include the presence or absence of atria1 or ventricular extrasystoles and alterations in the functional properties of each A-V nodal pathway in relation to age, cycle length, autonomic tone and medications. In our patients the interplay of these factors was not synchronized for reentrant tachycardia. Therefore, dual A-V nodal pathways are a common and frequently a benign electrophysiologic phenomenon in children and may represent normal functional characteristics of the human A-V node. Acknowledgment
None
our patients had sustained A-V nodal reentrant tachycardia during electrophysiologic studies and only one patient (Case 19) had atria1 echoes. This small in-
We gratefully acknowledge the technical assistance of Ralph Portuondo and Francisco Garcia-Montes and the secretarial assistance of Diane McMullen.
December 1980
The American Journal of CARDIOLDDV
Volume 48
1017
DUAL A-V NODAL PATHWAYS IN CHILDREN-CASTA
ET AL.
References 1. 2.
3.
4.
5. 6.
7.
6. 9.
10.
11.
12.
13.
Mx GK,Preston JB, Burlington H. Physiologic evidence for a dual A-V transmission system. Circ Res 19564357-75. Denes P, Wu D, Dhlngra R, Amat-y-Leon F, Wyndham C, Rosen KM. Dual atrioventricular nodal pathways. A common electrophysiological response. Br Heart J 1975;37: 1069-76. Thapar MK, Glllette PC. Dual atrioventricular nodal pathways: a common electrophysiologic response in children. Circulation 1979;60:1369-74. Wu D, Denes P, Dhlngra R, Pletras RJ, Rosen KM. New manifestations of dual A-V nodal pathways. Eur J Cardiol 1975;2: 459-66. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol 1974;33:291-4. Denes P, Wu D, Dhlngra RC, Chuqulmla R, Rosen KM. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 1973;46:549-55. Wolff GS, Sung RJ, Plckoff A, et al. The fast-slow form of atrioventricular nodal reentrant tachycardia in children. Am J Cardiol 1979;43:1161-6. Gillette PC. The mechanisms of supraventricular tachycardia in children. Circulation 197&54:133-g. Denes P, Wu D, Amat-y-Leon F, Dhtngra R, Wyndmn CR, Rosen KM. The determinants of atrioventricular nodal reentrance with premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 1977;58:253-9. DuBrow IW, Fisher EA, Hastrelter AR. Dual A-V node pathways (D) with and without paroxysmal supraventricular tachycardia (PSVT) in pediatric cardiology (abstr). American Academy of Pediatrics 46th Annual Meeting, October 13-16, 1979. Scharlag BJ, Lau SH, Helfanf RH, Berkowitz WD, Stein E, Damato AN. Catheter technique for recording His bundle activity in man. Circulation 1969;39:13-16. Sung RJ, Castellanos A, Mallon SM, Gelband H, Mendoza I, Myerberg RJ. Mode of initiation of reciprocating tachycardla during programmed ventricular stimulation in the Wolff-Parkinson-White syndrome. With reference to various patterns of ventriculoatrial conduction. Am J Cardiol 1977;40:24-31. Denes P,Wu D, Dhlngra R, Pletras RJ, Rosen KM. The effects of
1016
December 1960
The American Journal of CARDIOLOGY
14.
15. 16. 17. 16.
19.
20.
21.
22.
23. 24. 25.
cycle length on cardiac refractory periods in man. Circulation 1974;49:32-41. Castellanos A Jr, Castlllo CA, Agha AS, Tessler M. His bundle electrograms in patients with short PR intervals, narrow QRS complexes, and paroxysmal tachycardias. Circulation 1971;43: 667-76. Msndez C, Moe GK. Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 1968;19:376-93. Bigger JT Jr, Goldreyer BN. The mechanism of supraventricular tachycardia. Circulation 1970;42:673-66. Goldreyer BN, Bigger JT Jr. Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 1971;43: 15-26. Goldreyer BN, Damato AN. The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 1971;43:679-67. Wu D, Denes P, Amat-y-Leon F, Wyndham CRC, Dhlngra R, Rosen KM. An unusual variety of atrioventricular nodal reentry due to retrograde dual atrioventricular nodal pathways. Circulation 1977:56:50-g. Sung RJ, Styperek JL, Myerburg RJ, Castellanos A. Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man. Am J Cardiol 1976;42:404-15. DuBrow IW, Fisher EA, Amat-y-Leon F, et al. Comparison of cardiac refractory periods in children and adults. Circulation 1975;51:465-91. DuBrow IW, Fisher EA, Denes P, Hasbelter AR. The influence of age on cardiac refractory periods in man. Pedlatr Res 197610: 135-g. James TN. Cardiac conduction system: fetal and postnatal development. Am J Cardiol 1970;25:213-26. James TN. Crder and disorder in ths rhythm of the heart. Circulation 1973;47:362-66. Saplre D, Black I, Mongkolsmal C, Casta A. Changes in cycle length, conduction times, and refractory periods induced by sedation with meperidine, promethazine and chlorpromazine (abstr). Am J Cardiol 1979;43:425.
Volume 46