Sinus Node Function and Conduction System after Complete Repair of Tetralogy of Fallot By HANSULRICH NIEDERHAUSER, M.D., PHILIPPE SIMONIN, M.D., AND
BEAT FRIEDLI, M.D., M.Sc.
SUMMARY
Twenty-three children underwent electrophysiological studies during routine postoperative catheterization two months to five years after complete correction of tetralogy of Fallot. The aim of the study was to investigate the whole conduction system, including sinus node function, using His bundle recordings and atrial pacing. H-V intervals were normal at rest and with pacing in twenty-two patients, including four patients with evidence of bifascicular block on the surface ECG. One patient with cardiomegaly and evidence of diffuse myocardial damage had a prolonged H-V interval but did not develop a block at this level during pacing. A-H interval was slightly prolonged in four patients and normal in all others. The threshold of pacing-induced atrioventricular block ranged from 75 to 240/min and was somewhat dependent (r = -0.55). Two patients fell below the 95% confidence limit of this regression and are considered abnormal. One returned to normal after intravenous injection of atropine. Corrected sinus node recovery time ranged from 60 to 2000 msec. Three patients had values above 500 msec which are considered abnormal. These patients had other minor signs of sinus node dysfunction, i.e., episodes of sino-atrial block at rest or intermittent sinus bradyeardia. Thus, while the His Purkinje system performed satisfactorily in all patients, sinus node dysfunction and AV node dysfunction were demonstrated in a few patients after correction of tetralogy of Fallot. age
Material and Methods
OPEN HEART SURGERY in congenital heart disease carries a risk of damage to the conduction system at various sites, impairment of the His-Purkinje system being the most widely recognized hazard. While the incidence of early postoperative permanent complete heart block (CHB) has been reduced to approximately 1 %,1 late CHB has been observed increasingly in recent years.2 4 It has been suggested that an electrocardiographic pattern of right bundle branch block (RBBB) with left axis deviation (LAD), especially if associated with a history of transient CHB in the immediate postoperative period, increases the risk of late CHB.3-6 However, the HisPurkinje system is not the only part of the conduction system at risk, and clinical and electrophysiological evidence of sick sinus syndrome after intracardiac surgery has been reported.7 This study has therefore been undertaken to assess the whole conduction system as well as the sinus node function in an unselected group of children after complete repair of tetralogy of Fallot, using His bundle recordings and atrial pacing.
Patients
The study group included 23 unselected children who underwent catheterization 2 months to 5 years (mean 8 months) after complete repair of tetralogy of Fallot (21 patients) or double outlet right ventricle with pulmonary stenosis (2 patients). An atrial septal defect (ASD) was associated in seven. Their ages ranged from 2½/2 to 22 yr (mean 9.6 yr). Before operation all children were in sinus rhythm and presented no atrioventricular (A-V) conduction defect. The clinical and electrocardiographic data are summarized in table 1. A control group of eight children with tetralogy underwent electrophysiological studies preoperatively, most without pacing because of the risk of hypoxic spells. Three of these children had an associated ASD. Their ages ranged from 3'/2 to 13½/2 yr (mean 9.1 yr). The clinical and electrocardiographic data are summarized in table 2. Technique
All studies were done under light sedation with a mixture of pethidine, promethazine and chlorpromazine, and before any angiograms were taken. The technique of Scherlag et al.9 was used to obtain recordings of the A-V conduction system. Bipolar and tripolar electrode catheters (USCI) were used, and recordings were made on a standard 3-channel electrocardiographic writer (Mingograf 34, Elema-Scho5nander) equipped with a preamplifier. Paper speed was 100 mm/sec. A standard lead I electrocardiogram and a high atrial electrogram from the stimulating intracardiac electrode, were recorded simultaneously with the His bundle electrogram
From the Clinique Universitaire de P6diatrie and the Centre de
Cardiologie, University of Geneva, Medical School, Geneva, Switzerland. Address for reprints: Dr. B. Friedli, Clinque de Pediatrie, Hopital Cantonal, Geneva, Switzerland. Received February 20, 1975; accepted for publication March 11,
(HBE). Atrial pacing was performed with a second electrode
1975. 214
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CONDUCTION SYSTEM AFTER TF REPAIR
215
Table 1 Study Group: Clinical and Electrocardiographic Data Case
1 2 3 4 5 6 7 8 9 10 11 12
13 14 15 16 17 18 19 20 21 22 23
Age
Cardiovase.
diagnosis
(yr)
Sex
612
m
TF
4.2
F
TF,ASD
M M M M F F M AI M M
TF
M
DORV, PS, ASD TF TF TF TF TF TF TF, ASD TF TF TF, ASD, LSVC
12 4 6 15 5
141Y 2'V 5 10 11
8 k2
9'2 11 2 10'2 8'2 10 22 16 3 12 12
F M M M F M M F M F
Interval between surgery and study
TF,ASD TF,ASD TF TF
TF,ASD TF TF TF
DORV, PS, LSVC
5mo 4mo 3 mo 4 mo 3mo 3mo 22 mo 2mo
5mo 2 mo 2 mo 5 yr 2 mo 2mo 2mo 3mo 3 mo 2 mo
4yr 9 mo 10mo
Postoperative surface ECG
Medication
kcardiovase.)
RBBB
RBBB RBBB
Digoxin
-
Digoxin
TransCHB;RBBB
RBBB Trans CHB; RBBB RBBB + Trars LAD AV Dissociation RBBB + LAD RBBB + LAD RBBB RBBB RBBB RBBB RBBB +LAD AV Dissociation; RBBB
RIBBB
Digoxin
-Digoxin Digoxin
RBBB +LAD Trans CHB; RBBB + Trans LAD; Intermittent SA block Abbreviations: TF = tetralogy of Fallot; LSVC = left superior veisa cava; PS = pulmonary stenosis; SA = sino-atrial; ASD = atrial septal defect; DORV = double outlet right ventricle; Trans = transient.
catheter. Care was taken to place the tip at the junction of the right atrium and superior vena cava, close to the sinoatrial node (SA node), in order to avoid bias for P-A and A-H intervals'0 and to make sure of SA node depolarization, even in the presence of intraatrial conduction defects. Three modes of pacing were used in every patient: first, pacing with continuously increasing stimulus frequency until Mobitz type I second degree A-V block developed, or until an atrial rate of 240/min with 1:1 conduction was achieved. Secondly, the pacing rate was increased stepwise by increments of 10 beats/min, with short interruptions, over the same range. Finally continuous pacing was performed for 2 min at 130/min. The two latter modes were used to determine sinus node recovery time. Measurements
The following intervals were measured at rest and during atrial pacing. P-A: (intraatrial conduction time). From the earliest onset of the P wave on the standard ECG, or the A wave on the high atrial electrogram, to the onset of the A wave on the HBE. A-H: (conduction time through the A-V node). From the onset of the A wave on the HBE to the first rapid deflection of the His bundle potential. H-V: (conduction time from the HB to the ventricular septum). From the first rapid deflection of the HB potential to the earliest activation of the ventricle in either the surface or the intracardiac electrograms. The threshold of pacing-induced second degree A-V block (PAVB) was defined as the lowest atrial stimulation rate at which second degree A-V block developed, independently
2mo 3 mo
of the mode of pacing. The site and the type of second degree A-V block was observed. Sinus node recovery time, or postpacing depression of the SA node, was measured from the last paced A wave to the onset of atrial activity apparently due to SA node discharge. The corrected sinus node recovery time (CSRT) was obtained by subtracting the mean of three P-P intervals preceding pacing from the SA node recovery time;" the values given here are the longest CSRT intervals measured for each patient. Pharmacological Tests
Three patients with abnormal sinus node or A-V node function were given 0.5-1 mg of atropine intravenously and the electrophysiologic studies were repeated.
Results
Postoperative conduction defects and arrhythmias as seen on the surface ECG appear in table 1. There was no case of permanent CHB, either early or late postoperatively. Transient CHB was seen in three patients and lasted from 1 hour to 21/2 days. Six children had complete RBBB with LAD, in two of whom LAD was transient, lasting 2 weeks and 4 weeks respectively. At the time of study, 14 children showed complete RBBB and five had no conduction defect at all on surface ECG. During investigation 19 children were in sinus rhythm and one was in A-V dissociation with in-
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NIEDERHAUSER, SIMONIN, FRIEDLI
216 Table 2
Control Group Electrophysiological data Case no.
1 2 3 4 5 6 7 8
Age
(yr)
6 12
33½
13 12½ 12
131/
1012
Clinical data Cardiovasc. Sex
At rest
PA
diagnosis
M M M M F M M F
TF
Medication
Rhythm
(msec)
Propranolol
sinus
25 15
-
sinus sinus sinus sinus sinus sinus sinus
TF
TF, ASD
TF TF, ASD DORV, PS TF
Propranolol
TF, ASD
terference, due to accelerated junctional rhythm. Three other children showed episodes of A-V dissociation, due to intermittent slowing of the sinus rate in two, and to persistent sinus bradyeardia in one (P-P: 1300 msec). This last case (patient 20) showed junctional and multifocal atrial escape rhythms.
AH (msee)
145 80 85 80 75 105 75
20 20 10 30 10 30
110
(msec)
Corrected sinus node recovery time (msec)
35 40
260 320
HV
35 3535 40 40 45
175
Electrophysiological Findings (tables 2 and 3). 1. Intervals at Rest Values for the control group are shown in table 2; they do not differ from those found in normal children or patients with a variety of congenital heart lesions. 12-4 Values for the study group appear in table
Table 3
Electrophysiological Findings At rest Case no.
1 2
3 4 5 6 7 8 9 10 11 12
Atrial pacing IiP AV Block Site Threshold rate Below Above His His (beats/min)
Corrected
sinus node
time
P-A
A-H
H-V
H-V
(msec)
(msec)
(msec)
(msec)
sinus AV dissociation
30 30
130*
35 25
35 25
216
+
180
210
+
230
interference sinus sinus sinus
15 25 10
35 50* 40 40 30
100
35 50 40 40 30 30
95 70 95 100
25 35 35 45
35 35 45
210 210 230 197 220 154 200 240 218 200
160 340 260 240 110 335 190 60 210
105 65 70 75 70
25 40 40 35 30 40 35 45
25 40 40 35 30 40 35 45
200 185 240 200 240 182
160 75*
280 260 130 270 320 320 210 640*
130*t
5OOt
Rhythm
sinus sinus sinus
sinus arrhythmia sinus sinus AV dissoc, SA block
20 20 25 25 15
25 45
80
115* 70 75 100
30 25
recovery
(msec)
540*
Escape
rhythm
junctional
junctional
(acceleration
21 22
junctional rhythm) sinus sinus sinus sinus sinus sinus sinus sinus bradyeardia SA-block; PAC; (acceleration low atrial rhythm) sinus sinus
23
sinus, SA block
13 14 15 16 17 18
19 20
25 25 20 15 25 20 15 15
80
140* 140*
20 35
65 95
2St
75t
15
95
30 30 30t 35
+
30 30
230 146*
177t
280t
35
240
2000*
+
junctional, low atrial junctionalt
170 270
junctional
*Values considered abnormal.
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CONDUCTION SYSTEM AFTER TF REPAIR 3 and are plotted against the regression lines (relating intervals to age) established by Abella et al.14 P-A interval. This was somewhat shorter than previously found by Abella et al.,' possibly because a different surface ECG lead was used. There was no difference in P-A interval between children with and without an associated ASD. A-H interval (fig. 1). The conduction time through the A-V node was normal in 19 and prolonged in four subjects. Two of these (patients 4 and 20) received therapeutic doses of digoxin at the time of the study, which could explain the A-H prolongation. H-V interval (fig. 2). The H-V interval was normal for age in 22 children, including all patients with bifascicular block and the three with a history of transient postoperative heart block. Only one patient had a prolonged H-V interval. This child was in chronic congestive heart failure with a dilated right ventricle, a high left ventricular end-diastolic pressure and A-V conduction disturbance (prolonged P-R, A-H and H-V intervals). It is likely that he had widespread myocardial damage. 2. Atrial Pacing
During atrial pacing the H-V interval remained unchanged in all children, including the boy with prolonged H-V interval at rest. With increasing pacing rate, the A-H interval became prolonged, until second degree A-V block occurred. In one patient the block was localized distal to the His bundle at a very high pacing rate (240/min). In all the other children the block was situated at the A-V nodal level and was of Wenckebach type. Threshold of PAVB (fig. 3). The pacing rate at
which second degree A-V block occurred ranged from 75/min to 240/min and was age dependent (r = - 0.55). Two patients fell below the 95% confidence limits of the regression and were considered abnormal.
217 H-V (mrs)
60
-
40
-
0
a .
000 00 'D~O
1
,
20
-
0Age
0
9
1
40
80
120
' '
9
c
160
200
-
( r-nhtt,) to
r2R
1
Figure 2 Diagram of H-V intervals with average values and upper and lower limits of normal (+ 2 SD) after Abella et al.'4 Postoperative H-V intervals found in the children of our study group are entered into the diagram of normal values. Patients with the ECG pattern of RBBB with LAD are indicated by squares.
Corrected sinus node recovery time (CSRT) (fig. 4). Sufficient data about normal limits of CSRT in children are not yet available. In three patients from our study-group the CSRT exceeded 500 msec and was therefore higher than the generally accepted normal values for adults, which are 375-525 msec according to various authors;", 15, 16 they also exceed the normal values for children from our laboratory (unpublished data) and those found by Gillette et al.8 The values of CSRT in these three patients are therefore considered abnormal. Moreover, junctional and low atrial escape beats, prior to SA node recovery, could be observed in all three (fig. 5). These three patients had rhythm disturbances on the surface ECG: A-V dissociation by interference, sinoatrial block or sinus bradyeardia. One had episodes of paroxysmal atrial tachycardia. Atrial pacing ratte
( Beats / mn
250 l
*
-;
_
_.
A-H (ms)
As
0
_-- _-4
-
_,
200 -
'
-it*.
a
n-
,.D-
160 C
*
100-
0 120
0
-, e
_cl ~
-
_.@
*
.
_
50 -
.
Age
80
-
40
-
114
.
' ~ _
@SX X0 *e XX
0
0
.,
40
80
120
100
150
200
months ,
280
Figure 3 Age
0
50
160
T-_ 260
_-
(-months
300
Figure 1 Postoperative A-H intervals found in our study group, plotted against the graph for normal values according to Abella et al.'14
The threshold of pacing-induced second degree A-V block (PAVB) for each patient is plotted against age. (regression: HR = - 0.36 x age + 242.0; r = - 0.55). Symbols: circle = PAVB of Wenckebach type proximal to the His bundle; triangle = PAVB distal to His bundle; square = PAVB after administration of atropine intravenously. The figure indicates abnormally low PAVB in two cases (below the 95% confidence limit), one case returning to normal after atropine administration.
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NIEDERIIAUSER, SIMONIN, FRIEDLI
218
Discussion
I(ms
1Q00
-
800
-
;
2 000
600
400 * *
200
-
0
0.00
t
*
0
0 ,
W
0
40
lct
120
80
2 0
240
28C
`; 20
Figure 4 t ; tinw ('St 71' in ontr f)is t-ibiition cf o1pe'tt'c sinus iiocic it'od rac aisi's c,s czfulic tico cJf agu. I n t/h recc' actie t.s (ts 'S/iTlx-> p)osto1t)'Pt ctis Hit' upper limit (f whrt1icil ic/tt/i is inldicated bhy t/ic docittedi 'lit'e
Piarmi-acological. LTsts
\tropinie improved cortduction tlhrotugh the A\V niode in both p)atienits xith ablnormally lowx threshold of PA\V13, but in one case the thresholcd rate remained al)normal (fig. 3). In two children with prolonged CSRT, atropine accelerated the junctional and low atrial (case 20) escape rhythms, but hardly accelerated sinus rhythm. Furthermore CSRT was prolonged to 5000 msec in one case.
(Conduction dlisorders after irntracardiac repair of tetralogy of [allot and their relationr to imme(liate and late (:111B have b)een given incereasirg attention in recent vears.17 19 The incidence of early postoperative permanent heart 1)lock hias l)een greatlx reXduce(d;1 attenitioni has been focised more recently on the oc)ear a currence of late (113, whlich seems to relationship to R ba)anid LI), a transient (C1B in the earl> postoperative phase, or a combination of both.2 4 (;odnLan e t al. hasve (lemonstrated that in those cases, HBFE may be of help in assessing the remaininig conduIliction sxste,m, as it mav (lemonstrate a conduction dIelay in the His-Purkinje system (prolonged 11-V initerval). lloxx xesr, the hlis l)llidle and its branches are not the onlx1 part at risk cluiring open heart suirgery: the atrial inicisioin andC the, placing of cannutlas might dlaiimage the SA iio(le; closure of arn ASD and other reconstructixve procedures in the atria could irnterrupt atrial patlhwavs or injure the A-V dcle. ITllis studvs w as (lesigned to evaluate the xhole conduction system, idc lu(litng siinuis node function, of 23 Unselected children after complete repair of tetralogy of Fallot. This group included. fouir children with an EC;( patterni of R331B13 with IAXD wlio may have an increased1 risk of (CH1B.' 6 .n adiditiorial txx ) patients Figure 5 t P115sec the itc simts 11l0(1 re(cur rs promiiptlyj as imfiidateci b)1/ a short A-A tiiterual. 1 = slitjace fIC6c1d(1 1S stlus a1111,Sartfa( t. 11Ff = Its bwidle
pat iis 4z.sctiittiit' I eft\ .fP>1 atual /lfitga
1S*1 H.B
I~v\ 1
lecst togitti (1111 f \
9 I, '; K>ii
ipitpacarttt citctogratti fotmni theloigli rigl t
'ifter ttriail )0t itg at i liig/l rate S itc rc cii' 270 ns'ec: 2:1 A-\ bl1) ck rctrJ.tiiial to thli iIIs 1)/iidleSJ is cfi.sccittiiitled stimts iiocfc tto1rt i iis liti ('SiId7a = .5)W m.sec 1/hits i.s xprst'cS.t1 1)/t IJitzrkcci] dielcti; of tlcfs t pota-1)t i?ig N itae c isiblc on lIft tij roitP Ithit/i is bry' 11111 a ]itiie(tiolial et it bceat cist . T1w itricllczr ea)tire st'(coiili jiost QRp S l bIt' (ti 1fti I/it' el) a jiiic'tional t'st'cipc hcit (last (itS tomiptletx) is agtaii jo/loubI toulpie 1 atrtim. Bolf3lot
V
. H
A
5.8., BY
H
AI 250 me
E NJHB
¶4
7'
HBE.v
j.
'4 .~~~~~V p
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=A
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Aug-iiiP
/1975
219
CONDUCTION SYSTEM AFTER TF REPAIR
presented transient bifascicular block postoperatively. All of these six children showed normal His-Purkinje conduction time at rest and during atrial pacing. These findings may seem to be at variance with the report of Godman et al. who found H-V prolongation in 50% of patients with RBBB and LAD. However in Godman's report,3 all the patients with bifascicular block and H-V prolongation also had transient CHB in the postoperative period. In our series the uniformly satisfactory His-Purkinje conduction may be explained by the fact that no patient had the ominous combination of transient postoperative heart block followed by bifascicular block. H-V conduction time was normal in children with transient CHB and RBBB with a normal axis at the time of study and this is in agreement with the observations of Godman et al. Hence, His-Purkinje conduction time was normal in all children, except one boy who had a prolonged H-V interval in the presence of RBBB. This might indicate damage to the left bundle branch. However, in this child angiography showed considerable right ventricular dilatation with diminished contractility. We believe, along with Wen-Pin Lien et al.,20 that ventricular dilatation may affect A-V conduction intervals, and this may explain the observed H-V prolongation. The fact that atrial pacing did not further prolong the H-V interval, nor induce a block at that level, seems to strengthen this hypothesis. Atrial pacing represents a well known provocative stress of the conduction system, which may reveal conduction defects not apparent at rest.21-23 Pacing usually induces second degree A-V block of the Wenckebach type localized in the A-V node, whereas the His-Purkinje conduction time should remain constant.'6' 21"24 On this basis, it may be stated that all children in this study showed adequate His-Purkinje conduction during atrial pacing. The only block distal to the His bundle occurred at a very high pacing rate; we believe it was due to an extremely high permeability of the A-V node, rather than to a damaged His-Purkinje system. It has been suggested that normal 1:1 conduction up to a high rate of pacing does not necessarily exclude damage to the HisPurkinje system. Indeed, Narula25 and others23' 24 saw CHB appear within a short time of demonstration of excellent conduction by the method described above. However, their observations were made on aged patients with ischemic heart disease and do not necessarily apply to children. Certainly our results do not support the premise that prophylactic implantation of a demand pacemaker should be considered in patients with bifascicular block postoperatively.4 The A-H interval represents conduction time through the A-V node and therefore reflects a part of
A-V node function. Atrial pacing, as previously mentioned, allows further assessment of A-V node function. The threshold rate at which PAVB occurs in adults is well established;16' 24 we are not aware of any data concerning the threshold in children, and its relation to age. The findings in the study group patients (fig. 4) indicate that the threshold of pacing-induced second degree A-V block exceeds normal adult values and is age dependent. We believe that assessment of the threshold of PAVB, associated with pharmacological tests, is a more reliable indicator of A-V node dysfunction, than is the bare measurement of A-H interval at rest. Three out of four patients with prolonged A-H interval at rest, had an excellent response to pacing and a very high threshold of PAVB; only one had a low threshold which remained abnormal after administration of atropine. On the other hand, a low threshold of PAVB was found in a patient with a normal A-H interval at rest, but returned within normal limits after administration of atropine; this may be evidence against organic damage of the A-V node. Intraatrial conduction is difficult to assess with accuracy, because the P-A interval is short and the onset difficult to determine. However, it is of interest that the presence of an associated ASD had no bearing on the P-A intervals, either preoperatively or after surgery. This contrasts with the observation of Anderson et al.26 who found significantly prolonged P-A intervals in children with a large ASD. This difference may be explained by the presence of a large left-to-right shunt in Anderson's patients who thus represent a different hemodynamic situation. An unexpected yet important finding of this study is the evidence of SA node dysfunction in three out of 23 unselected patients. The evidence is based on the presence of postoperative arrhythmias similar to those seen in the sick sinus syndrome:' 6.27. 28 sinus bradycardia, sinoatrial block of second degree and supraventricular tachycardia. These three patients had an abnormal CSRT, and prolonged postpacing depression of the sinus node is now generally taken as a sign of SA node dysfunction."' 15, 16, 29 Intravenous administration of atropine produced inadequate responses in two cases, who developed enhancement of junctional and low atrial pacemakers, isorhythmic dissociation, and further prolongation of CSRT. Such a response strengthens the diagnosis of SA node dysfunction,8'1 especially as the ectopic rhythm lasted for several minutes.30 It has been known for some time that damage to the SA node may occur after correction of transposition of the great arteries by the Mustard procedure.8' 31 This is not unexpected because this operation requires extensive reconstruction at the level of the atria; during
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220
NIEDERHAUSER, SIMONIN, FRIEDLI
insertion of the baffle, damage to the SA node may be caused by direct trauma to the node, or interruption of the sinus node artery.3` Only recently has it become apparent that SA node dysfunction may be seen after correction of other heart defects. Indeed, Greenwood et al.7 found a "sick sinus syndrome" in some patients after correction of tetralogy of Fallot, atrial septal defect and ventricular septal defect; their evidence was based on clinical data and surface ECG, but electrophysiological studies were not done. In these situations, there is no extensive atrial reconstruction. We may speculate with Aberdeen and Carr32 that damage results from insertion of the superior vena cava cannula or sealing of the atrium around it. There is a possibility that the atrial incision may divide the node.33 In our series, no specimens are available, so that we cannot bring forward anatomic or histologic evidence of SA node injury. In conclusion, the majority of patients in this study, all of whom had undergone extensive intracardiac surgery, showed little or no damage to the conduction system. The serious consequences of injury to the His bundle are now well recognized, and new surgical techniques have succeeded in avoiding it. However this study has shown that other parts of the conduction system, especially the SA and A-V nodes, may be vulnerable. These structures should also be avoided if possible during open heart surgery. References 1. KIRKLIN JW, WALLACE RB: Surgical treatment of congenital heart disease. In The Heart, Arteries and Veins, ed 2, edited by HU.RST JW, LOGUE RB. New York, McGraw-Hill, 1970, p 698 2. Moss AJ, KLYMAN G, EmM1IANOUILIDEs GC: Late onset complete heart block. Am J Cardiol 30: 884, 1972 3. GODMAN. MJ, ROBERTS NK, IZUKAWx A T: Late postoperative conduction disturbances after repair of ventricular septal defect and tetralogy of Fallot. Circulation 49: 214, 1974 4. WOLFF GS, ROW LAN-D TW, ELLISON RC: Surgically induced right bundle branch block with left anterior hemiblock. Circulation 46: 587, 1972 5. ALLEN HD, ANDERSON RC, NOREN GR, MOLLER JH: Postoperative follow-up of patients with ventricular septal defect. Circulation 50: 465, 1974 6. FRIEDLI B, IZUKAWx A T, KIDD BSL: Evolution a long terme des communications interventriculaires operees. Ann Cardiol Ang6iol 23: 203, 1974 7. GREENWOOD RD, ROSENTHAL A, SLOss LJ, CASTANEDA AR, NADAS AS: Sick sinus syndrome after cardiac surgery in childhood. (abstr) Circulation 50: (suppl III): 111-176, 1974 8. GILLETTE PC, EL-SAID GM, SIVARAJAN N, MULLI.NS CE, WILLIAMS RL, MCNAMARA DG: Electrophysiological abnormalities after Mustard's operation for transposition of the great arteries. Br Heart J 36: 186, 1974 9. SCHERLAG BJ, LAL SH, HELFANT RH, BERKOWITZ WD, STEI.N E, DAMIATO AN: Catheter technique for recording His bundle activity in man. Circulation 39: 13, 1969 10. BAT.SFORD WP, AKHTAR M, CARACTA AR, JOSEPHSON ME, SEIDES
SF, DAM ATO AN: Effect of atrial stimulation site on the electrophysiological properties of the atrioventricular node in man. Circulation 50: 283, 1974 11. NARULA OS, SAMET P, JAxTIER RP: Significance of the sinusnode recovery time. Circulation 45: 140, 1972 12. ROBERTS NK, OLLEY PM: His bundle recordings in children with normal hearts and congenital heart disease. Circulation 13. 14. 15. 16.
17. 18.
19.
20.
45: 295, 1972 ROBERTS NK, OLLEY P: His bundle electrogram in children. Br Heart J 34: 1099, 1972 ABELLA JB, TEIXEIRA OHP, MISRA KP, HASTREITER AR: Changes of atrioventricular conduction with age in infants and children. Am J Cardiol 30: 876, 1972 GuPTA PK, LICHSTEIN E, CHADDA KD, BADUI E: Appraisal of sinus nodal recovery time in patients with sick sinus syndrome. Am J Cardiol 34: 265, 1974 SIMIONIN Ph, NIEDERHAUSER HU: L exploration electrique
endocavitaire dans la dysrythmie auriculaire. Schweiz Med Wschr 104: 1584, 1974 TITIUS JL, DAUGHERTY GW, KIRKLIN JW, EDWAARDS JE: Lesions of the atrioventricular conduction system after repair of ventricular septal defect. Circulation 28: 82, 1963 KlJLBEBTULS HE, COYNE JJ, HALLIDIE-SASITH KA: Conduction disturbances before and after surgical closure of ventricular septal defect. Am Heart J 77: 123, 1969 ANDERSON PAW, ROGERS MC, CANENT RV, JARMAKANI JMM, JEWETT PH, SPACH MS: Reversible complete heart block following cardiac surgery. Circulation 46: 514, 1972 LIEN W-P, LEE Y-S: Unusual atrioventricular conduction disturbances in secundum atrial septal defects. Communication at the World Congress of Cardiology, Buenos Aires,
1974 21. LISTER JW, STEIN E, KoSOWvSKY BD, LAL SH, DAMATO AN: Atrioventricular conduction in man. Am J Cardiol 16: 516, 1965
22. CHENG TO: Atrial pacing: Its diagnostic and therapeutic applications. Prog Cardiovasc Dis 14: 230, 1971 23. ROSEN- KM: Evaluation of cardiac conduction in the cardiac catheterization laboratory. Am J Cardiol 30: 701, 1972 24. DODINOT R, HU-A G, MENTRE B, FAIVRE G: Stimulation auriculaire et explorations hisiennes dans les indications de lentralnement 6lectro-systolique au long cours. Arch Mal Coeur 66: 257, 1973 25. NARULA OS: Atrioventricular conduction defects in patients with sinus bradyeardia. Circulation 44: 1096, 1971 26. ANDERSON PAW, ROGERS MC, CANENT RV, SPACH MS: Atrioventricular conduction in secundum atrial septal defects. Circulation 48: 27, 1973 27. FERRER MI: The sick sinus syndrome. Circulation 47: 635, 1973 28. Moss AJ, DAVIs RJ: Brady-tachy syndrome. Prog Cardiovasc Dis 16: 439, 1974 29. MANDEL WJ, HAYAKAWA H, ALLEN HN, DANZIG R, KERMAIER AI: Assessment of sinus node function in patients with the sick sinus syndrome. Circulation 46: 761, 1972 30. AVERILL KH, LAMB LE: Less commonly recognized actions of atropine on cardiac rhythm. Am J Med Sci 237: 304, 1959 31. EL-SAID G, ROSENBERG HS, MULLINS CE, HALLMAN GL, COOLEY DA, McNAM ABA DG: Dysrhythmias after Mustard's operation for transposition of the great arteries. Am J Cardiol 30: 526, 1972 32. ABERDEEN E, CARR I: Transposition of the great arteries. In Modern Trends in Cardiac Surgery, vol 2. London, Butterworth's, 1968, p 182 33. TUN(. KSK, JAMES TN, EFFLER DB: Injury to the sinus node in open heart surgery. J Thorac Cardiovasc Surg 53: 814, 1967 Circulation. Volume 52, August 1975
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Sinus node function and conduction system after complete repair of tetralogy of Fallot. H Niederhauser, P Simonin and B Friedli Circulation. 1975;52:214-220 doi: 10.1161/01.CIR.52.2.214 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1975 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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BEAT FRIEDLI, M.D., M.Sc.
SUMMARY
Twenty-three children underwent electrophysiological studies during routine postoperative catheterization two months to five years after complete correction of tetralogy of Fallot. The aim of the study was to investigate the whole conduction system, including sinus node function, using His bundle recordings and atrial pacing. H-V intervals were normal at rest and with pacing in twenty-two patients, including four patients with evidence of bifascicular block on the surface ECG. One patient with cardiomegaly and evidence of diffuse myocardial damage had a prolonged H-V interval but did not develop a block at this level during pacing. A-H interval was slightly prolonged in four patients and normal in all others. The threshold of pacing-induced atrioventricular block ranged from 75 to 240/min and was somewhat dependent (r = -0.55). Two patients fell below the 95% confidence limit of this regression and are considered abnormal. One returned to normal after intravenous injection of atropine. Corrected sinus node recovery time ranged from 60 to 2000 msec. Three patients had values above 500 msec which are considered abnormal. These patients had other minor signs of sinus node dysfunction, i.e., episodes of sino-atrial block at rest or intermittent sinus bradyeardia. Thus, while the His Purkinje system performed satisfactorily in all patients, sinus node dysfunction and AV node dysfunction were demonstrated in a few patients after correction of tetralogy of Fallot. age
Material and Methods
OPEN HEART SURGERY in congenital heart disease carries a risk of damage to the conduction system at various sites, impairment of the His-Purkinje system being the most widely recognized hazard. While the incidence of early postoperative permanent complete heart block (CHB) has been reduced to approximately 1 %,1 late CHB has been observed increasingly in recent years.2 4 It has been suggested that an electrocardiographic pattern of right bundle branch block (RBBB) with left axis deviation (LAD), especially if associated with a history of transient CHB in the immediate postoperative period, increases the risk of late CHB.3-6 However, the HisPurkinje system is not the only part of the conduction system at risk, and clinical and electrophysiological evidence of sick sinus syndrome after intracardiac surgery has been reported.7 This study has therefore been undertaken to assess the whole conduction system as well as the sinus node function in an unselected group of children after complete repair of tetralogy of Fallot, using His bundle recordings and atrial pacing.
Patients
The study group included 23 unselected children who underwent catheterization 2 months to 5 years (mean 8 months) after complete repair of tetralogy of Fallot (21 patients) or double outlet right ventricle with pulmonary stenosis (2 patients). An atrial septal defect (ASD) was associated in seven. Their ages ranged from 2½/2 to 22 yr (mean 9.6 yr). Before operation all children were in sinus rhythm and presented no atrioventricular (A-V) conduction defect. The clinical and electrocardiographic data are summarized in table 1. A control group of eight children with tetralogy underwent electrophysiological studies preoperatively, most without pacing because of the risk of hypoxic spells. Three of these children had an associated ASD. Their ages ranged from 3'/2 to 13½/2 yr (mean 9.1 yr). The clinical and electrocardiographic data are summarized in table 2. Technique
All studies were done under light sedation with a mixture of pethidine, promethazine and chlorpromazine, and before any angiograms were taken. The technique of Scherlag et al.9 was used to obtain recordings of the A-V conduction system. Bipolar and tripolar electrode catheters (USCI) were used, and recordings were made on a standard 3-channel electrocardiographic writer (Mingograf 34, Elema-Scho5nander) equipped with a preamplifier. Paper speed was 100 mm/sec. A standard lead I electrocardiogram and a high atrial electrogram from the stimulating intracardiac electrode, were recorded simultaneously with the His bundle electrogram
From the Clinique Universitaire de P6diatrie and the Centre de
Cardiologie, University of Geneva, Medical School, Geneva, Switzerland. Address for reprints: Dr. B. Friedli, Clinque de Pediatrie, Hopital Cantonal, Geneva, Switzerland. Received February 20, 1975; accepted for publication March 11,
(HBE). Atrial pacing was performed with a second electrode
1975. 214
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CONDUCTION SYSTEM AFTER TF REPAIR
215
Table 1 Study Group: Clinical and Electrocardiographic Data Case
1 2 3 4 5 6 7 8 9 10 11 12
13 14 15 16 17 18 19 20 21 22 23
Age
Cardiovase.
diagnosis
(yr)
Sex
612
m
TF
4.2
F
TF,ASD
M M M M F F M AI M M
TF
M
DORV, PS, ASD TF TF TF TF TF TF TF, ASD TF TF TF, ASD, LSVC
12 4 6 15 5
141Y 2'V 5 10 11
8 k2
9'2 11 2 10'2 8'2 10 22 16 3 12 12
F M M M F M M F M F
Interval between surgery and study
TF,ASD TF,ASD TF TF
TF,ASD TF TF TF
DORV, PS, LSVC
5mo 4mo 3 mo 4 mo 3mo 3mo 22 mo 2mo
5mo 2 mo 2 mo 5 yr 2 mo 2mo 2mo 3mo 3 mo 2 mo
4yr 9 mo 10mo
Postoperative surface ECG
Medication
kcardiovase.)
RBBB
RBBB RBBB
Digoxin
-
Digoxin
TransCHB;RBBB
RBBB Trans CHB; RBBB RBBB + Trars LAD AV Dissociation RBBB + LAD RBBB + LAD RBBB RBBB RBBB RBBB RBBB +LAD AV Dissociation; RBBB
RIBBB
Digoxin
-Digoxin Digoxin
RBBB +LAD Trans CHB; RBBB + Trans LAD; Intermittent SA block Abbreviations: TF = tetralogy of Fallot; LSVC = left superior veisa cava; PS = pulmonary stenosis; SA = sino-atrial; ASD = atrial septal defect; DORV = double outlet right ventricle; Trans = transient.
catheter. Care was taken to place the tip at the junction of the right atrium and superior vena cava, close to the sinoatrial node (SA node), in order to avoid bias for P-A and A-H intervals'0 and to make sure of SA node depolarization, even in the presence of intraatrial conduction defects. Three modes of pacing were used in every patient: first, pacing with continuously increasing stimulus frequency until Mobitz type I second degree A-V block developed, or until an atrial rate of 240/min with 1:1 conduction was achieved. Secondly, the pacing rate was increased stepwise by increments of 10 beats/min, with short interruptions, over the same range. Finally continuous pacing was performed for 2 min at 130/min. The two latter modes were used to determine sinus node recovery time. Measurements
The following intervals were measured at rest and during atrial pacing. P-A: (intraatrial conduction time). From the earliest onset of the P wave on the standard ECG, or the A wave on the high atrial electrogram, to the onset of the A wave on the HBE. A-H: (conduction time through the A-V node). From the onset of the A wave on the HBE to the first rapid deflection of the His bundle potential. H-V: (conduction time from the HB to the ventricular septum). From the first rapid deflection of the HB potential to the earliest activation of the ventricle in either the surface or the intracardiac electrograms. The threshold of pacing-induced second degree A-V block (PAVB) was defined as the lowest atrial stimulation rate at which second degree A-V block developed, independently
2mo 3 mo
of the mode of pacing. The site and the type of second degree A-V block was observed. Sinus node recovery time, or postpacing depression of the SA node, was measured from the last paced A wave to the onset of atrial activity apparently due to SA node discharge. The corrected sinus node recovery time (CSRT) was obtained by subtracting the mean of three P-P intervals preceding pacing from the SA node recovery time;" the values given here are the longest CSRT intervals measured for each patient. Pharmacological Tests
Three patients with abnormal sinus node or A-V node function were given 0.5-1 mg of atropine intravenously and the electrophysiologic studies were repeated.
Results
Postoperative conduction defects and arrhythmias as seen on the surface ECG appear in table 1. There was no case of permanent CHB, either early or late postoperatively. Transient CHB was seen in three patients and lasted from 1 hour to 21/2 days. Six children had complete RBBB with LAD, in two of whom LAD was transient, lasting 2 weeks and 4 weeks respectively. At the time of study, 14 children showed complete RBBB and five had no conduction defect at all on surface ECG. During investigation 19 children were in sinus rhythm and one was in A-V dissociation with in-
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NIEDERHAUSER, SIMONIN, FRIEDLI
216 Table 2
Control Group Electrophysiological data Case no.
1 2 3 4 5 6 7 8
Age
(yr)
6 12
33½
13 12½ 12
131/
1012
Clinical data Cardiovasc. Sex
At rest
PA
diagnosis
M M M M F M M F
TF
Medication
Rhythm
(msec)
Propranolol
sinus
25 15
-
sinus sinus sinus sinus sinus sinus sinus
TF
TF, ASD
TF TF, ASD DORV, PS TF
Propranolol
TF, ASD
terference, due to accelerated junctional rhythm. Three other children showed episodes of A-V dissociation, due to intermittent slowing of the sinus rate in two, and to persistent sinus bradyeardia in one (P-P: 1300 msec). This last case (patient 20) showed junctional and multifocal atrial escape rhythms.
AH (msee)
145 80 85 80 75 105 75
20 20 10 30 10 30
110
(msec)
Corrected sinus node recovery time (msec)
35 40
260 320
HV
35 3535 40 40 45
175
Electrophysiological Findings (tables 2 and 3). 1. Intervals at Rest Values for the control group are shown in table 2; they do not differ from those found in normal children or patients with a variety of congenital heart lesions. 12-4 Values for the study group appear in table
Table 3
Electrophysiological Findings At rest Case no.
1 2
3 4 5 6 7 8 9 10 11 12
Atrial pacing IiP AV Block Site Threshold rate Below Above His His (beats/min)
Corrected
sinus node
time
P-A
A-H
H-V
H-V
(msec)
(msec)
(msec)
(msec)
sinus AV dissociation
30 30
130*
35 25
35 25
216
+
180
210
+
230
interference sinus sinus sinus
15 25 10
35 50* 40 40 30
100
35 50 40 40 30 30
95 70 95 100
25 35 35 45
35 35 45
210 210 230 197 220 154 200 240 218 200
160 340 260 240 110 335 190 60 210
105 65 70 75 70
25 40 40 35 30 40 35 45
25 40 40 35 30 40 35 45
200 185 240 200 240 182
160 75*
280 260 130 270 320 320 210 640*
130*t
5OOt
Rhythm
sinus sinus sinus
sinus arrhythmia sinus sinus AV dissoc, SA block
20 20 25 25 15
25 45
80
115* 70 75 100
30 25
recovery
(msec)
540*
Escape
rhythm
junctional
junctional
(acceleration
21 22
junctional rhythm) sinus sinus sinus sinus sinus sinus sinus sinus bradyeardia SA-block; PAC; (acceleration low atrial rhythm) sinus sinus
23
sinus, SA block
13 14 15 16 17 18
19 20
25 25 20 15 25 20 15 15
80
140* 140*
20 35
65 95
2St
75t
15
95
30 30 30t 35
+
30 30
230 146*
177t
280t
35
240
2000*
+
junctional, low atrial junctionalt
170 270
junctional
*Values considered abnormal.
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CONDUCTION SYSTEM AFTER TF REPAIR 3 and are plotted against the regression lines (relating intervals to age) established by Abella et al.14 P-A interval. This was somewhat shorter than previously found by Abella et al.,' possibly because a different surface ECG lead was used. There was no difference in P-A interval between children with and without an associated ASD. A-H interval (fig. 1). The conduction time through the A-V node was normal in 19 and prolonged in four subjects. Two of these (patients 4 and 20) received therapeutic doses of digoxin at the time of the study, which could explain the A-H prolongation. H-V interval (fig. 2). The H-V interval was normal for age in 22 children, including all patients with bifascicular block and the three with a history of transient postoperative heart block. Only one patient had a prolonged H-V interval. This child was in chronic congestive heart failure with a dilated right ventricle, a high left ventricular end-diastolic pressure and A-V conduction disturbance (prolonged P-R, A-H and H-V intervals). It is likely that he had widespread myocardial damage. 2. Atrial Pacing
During atrial pacing the H-V interval remained unchanged in all children, including the boy with prolonged H-V interval at rest. With increasing pacing rate, the A-H interval became prolonged, until second degree A-V block occurred. In one patient the block was localized distal to the His bundle at a very high pacing rate (240/min). In all the other children the block was situated at the A-V nodal level and was of Wenckebach type. Threshold of PAVB (fig. 3). The pacing rate at
which second degree A-V block occurred ranged from 75/min to 240/min and was age dependent (r = - 0.55). Two patients fell below the 95% confidence limits of the regression and were considered abnormal.
217 H-V (mrs)
60
-
40
-
0
a .
000 00 'D~O
1
,
20
-
0Age
0
9
1
40
80
120
' '
9
c
160
200
-
( r-nhtt,) to
r2R
1
Figure 2 Diagram of H-V intervals with average values and upper and lower limits of normal (+ 2 SD) after Abella et al.'4 Postoperative H-V intervals found in the children of our study group are entered into the diagram of normal values. Patients with the ECG pattern of RBBB with LAD are indicated by squares.
Corrected sinus node recovery time (CSRT) (fig. 4). Sufficient data about normal limits of CSRT in children are not yet available. In three patients from our study-group the CSRT exceeded 500 msec and was therefore higher than the generally accepted normal values for adults, which are 375-525 msec according to various authors;", 15, 16 they also exceed the normal values for children from our laboratory (unpublished data) and those found by Gillette et al.8 The values of CSRT in these three patients are therefore considered abnormal. Moreover, junctional and low atrial escape beats, prior to SA node recovery, could be observed in all three (fig. 5). These three patients had rhythm disturbances on the surface ECG: A-V dissociation by interference, sinoatrial block or sinus bradyeardia. One had episodes of paroxysmal atrial tachycardia. Atrial pacing ratte
( Beats / mn
250 l
*
-;
_
_.
A-H (ms)
As
0
_-- _-4
-
_,
200 -
'
-it*.
a
n-
,.D-
160 C
*
100-
0 120
0
-, e
_cl ~
-
_.@
*
.
_
50 -
.
Age
80
-
40
-
114
.
' ~ _
@SX X0 *e XX
0
0
.,
40
80
120
100
150
200
months ,
280
Figure 3 Age
0
50
160
T-_ 260
_-
(-months
300
Figure 1 Postoperative A-H intervals found in our study group, plotted against the graph for normal values according to Abella et al.'14
The threshold of pacing-induced second degree A-V block (PAVB) for each patient is plotted against age. (regression: HR = - 0.36 x age + 242.0; r = - 0.55). Symbols: circle = PAVB of Wenckebach type proximal to the His bundle; triangle = PAVB distal to His bundle; square = PAVB after administration of atropine intravenously. The figure indicates abnormally low PAVB in two cases (below the 95% confidence limit), one case returning to normal after atropine administration.
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NIEDERIIAUSER, SIMONIN, FRIEDLI
218
Discussion
I(ms
1Q00
-
800
-
;
2 000
600
400 * *
200
-
0
0.00
t
*
0
0 ,
W
0
40
lct
120
80
2 0
240
28C
`; 20
Figure 4 t ; tinw ('St 71' in ontr f)is t-ibiition cf o1pe'tt'c sinus iiocic it'od rac aisi's c,s czfulic tico cJf agu. I n t/h recc' actie t.s (ts 'S/iTlx-> p)osto1t)'Pt ctis Hit' upper limit (f whrt1icil ic/tt/i is inldicated bhy t/ic docittedi 'lit'e
Piarmi-acological. LTsts
\tropinie improved cortduction tlhrotugh the A\V niode in both p)atienits xith ablnormally lowx threshold of PA\V13, but in one case the thresholcd rate remained al)normal (fig. 3). In two children with prolonged CSRT, atropine accelerated the junctional and low atrial (case 20) escape rhythms, but hardly accelerated sinus rhythm. Furthermore CSRT was prolonged to 5000 msec in one case.
(Conduction dlisorders after irntracardiac repair of tetralogy of [allot and their relationr to imme(liate and late (:111B have b)een given incereasirg attention in recent vears.17 19 The incidence of early postoperative permanent heart 1)lock hias l)een greatlx reXduce(d;1 attenitioni has been focised more recently on the oc)ear a currence of late (113, whlich seems to relationship to R ba)anid LI), a transient (C1B in the earl> postoperative phase, or a combination of both.2 4 (;odnLan e t al. hasve (lemonstrated that in those cases, HBFE may be of help in assessing the remaininig conduIliction sxste,m, as it mav (lemonstrate a conduction dIelay in the His-Purkinje system (prolonged 11-V initerval). lloxx xesr, the hlis l)llidle and its branches are not the onlx1 part at risk cluiring open heart suirgery: the atrial inicisioin andC the, placing of cannutlas might dlaiimage the SA iio(le; closure of arn ASD and other reconstructixve procedures in the atria could irnterrupt atrial patlhwavs or injure the A-V dcle. ITllis studvs w as (lesigned to evaluate the xhole conduction system, idc lu(litng siinuis node function, of 23 Unselected children after complete repair of tetralogy of Fallot. This group included. fouir children with an EC;( patterni of R331B13 with IAXD wlio may have an increased1 risk of (CH1B.' 6 .n adiditiorial txx ) patients Figure 5 t P115sec the itc simts 11l0(1 re(cur rs promiiptlyj as imfiidateci b)1/ a short A-A tiiterual. 1 = slitjace fIC6c1d(1 1S stlus a1111,Sartfa( t. 11Ff = Its bwidle
pat iis 4z.sctiittiit' I eft\ .fP>1 atual /lfitga
1S*1 H.B
I~v\ 1
lecst togitti (1111 f \
9 I, '; K>ii
ipitpacarttt citctogratti fotmni theloigli rigl t
'ifter ttriail )0t itg at i liig/l rate S itc rc cii' 270 ns'ec: 2:1 A-\ bl1) ck rctrJ.tiiial to thli iIIs 1)/iidleSJ is cfi.sccittiiitled stimts iiocfc tto1rt i iis liti ('SiId7a = .5)W m.sec 1/hits i.s xprst'cS.t1 1)/t IJitzrkcci] dielcti; of tlcfs t pota-1)t i?ig N itae c isiblc on lIft tij roitP Ithit/i is bry' 11111 a ]itiie(tiolial et it bceat cist . T1w itricllczr ea)tire st'(coiili jiost QRp S l bIt' (ti 1fti I/it' el) a jiiic'tional t'st'cipc hcit (last (itS tomiptletx) is agtaii jo/loubI toulpie 1 atrtim. Bolf3lot
V
. H
A
5.8., BY
H
AI 250 me
E NJHB
¶4
7'
HBE.v
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Downloaded from http://circ.ahajournals.org/ at UNIV OF CALIFORNIA LIB on March 9, 2015
Aug-iiiP
/1975
219
CONDUCTION SYSTEM AFTER TF REPAIR
presented transient bifascicular block postoperatively. All of these six children showed normal His-Purkinje conduction time at rest and during atrial pacing. These findings may seem to be at variance with the report of Godman et al. who found H-V prolongation in 50% of patients with RBBB and LAD. However in Godman's report,3 all the patients with bifascicular block and H-V prolongation also had transient CHB in the postoperative period. In our series the uniformly satisfactory His-Purkinje conduction may be explained by the fact that no patient had the ominous combination of transient postoperative heart block followed by bifascicular block. H-V conduction time was normal in children with transient CHB and RBBB with a normal axis at the time of study and this is in agreement with the observations of Godman et al. Hence, His-Purkinje conduction time was normal in all children, except one boy who had a prolonged H-V interval in the presence of RBBB. This might indicate damage to the left bundle branch. However, in this child angiography showed considerable right ventricular dilatation with diminished contractility. We believe, along with Wen-Pin Lien et al.,20 that ventricular dilatation may affect A-V conduction intervals, and this may explain the observed H-V prolongation. The fact that atrial pacing did not further prolong the H-V interval, nor induce a block at that level, seems to strengthen this hypothesis. Atrial pacing represents a well known provocative stress of the conduction system, which may reveal conduction defects not apparent at rest.21-23 Pacing usually induces second degree A-V block of the Wenckebach type localized in the A-V node, whereas the His-Purkinje conduction time should remain constant.'6' 21"24 On this basis, it may be stated that all children in this study showed adequate His-Purkinje conduction during atrial pacing. The only block distal to the His bundle occurred at a very high pacing rate; we believe it was due to an extremely high permeability of the A-V node, rather than to a damaged His-Purkinje system. It has been suggested that normal 1:1 conduction up to a high rate of pacing does not necessarily exclude damage to the HisPurkinje system. Indeed, Narula25 and others23' 24 saw CHB appear within a short time of demonstration of excellent conduction by the method described above. However, their observations were made on aged patients with ischemic heart disease and do not necessarily apply to children. Certainly our results do not support the premise that prophylactic implantation of a demand pacemaker should be considered in patients with bifascicular block postoperatively.4 The A-H interval represents conduction time through the A-V node and therefore reflects a part of
A-V node function. Atrial pacing, as previously mentioned, allows further assessment of A-V node function. The threshold rate at which PAVB occurs in adults is well established;16' 24 we are not aware of any data concerning the threshold in children, and its relation to age. The findings in the study group patients (fig. 4) indicate that the threshold of pacing-induced second degree A-V block exceeds normal adult values and is age dependent. We believe that assessment of the threshold of PAVB, associated with pharmacological tests, is a more reliable indicator of A-V node dysfunction, than is the bare measurement of A-H interval at rest. Three out of four patients with prolonged A-H interval at rest, had an excellent response to pacing and a very high threshold of PAVB; only one had a low threshold which remained abnormal after administration of atropine. On the other hand, a low threshold of PAVB was found in a patient with a normal A-H interval at rest, but returned within normal limits after administration of atropine; this may be evidence against organic damage of the A-V node. Intraatrial conduction is difficult to assess with accuracy, because the P-A interval is short and the onset difficult to determine. However, it is of interest that the presence of an associated ASD had no bearing on the P-A intervals, either preoperatively or after surgery. This contrasts with the observation of Anderson et al.26 who found significantly prolonged P-A intervals in children with a large ASD. This difference may be explained by the presence of a large left-to-right shunt in Anderson's patients who thus represent a different hemodynamic situation. An unexpected yet important finding of this study is the evidence of SA node dysfunction in three out of 23 unselected patients. The evidence is based on the presence of postoperative arrhythmias similar to those seen in the sick sinus syndrome:' 6.27. 28 sinus bradycardia, sinoatrial block of second degree and supraventricular tachycardia. These three patients had an abnormal CSRT, and prolonged postpacing depression of the sinus node is now generally taken as a sign of SA node dysfunction."' 15, 16, 29 Intravenous administration of atropine produced inadequate responses in two cases, who developed enhancement of junctional and low atrial pacemakers, isorhythmic dissociation, and further prolongation of CSRT. Such a response strengthens the diagnosis of SA node dysfunction,8'1 especially as the ectopic rhythm lasted for several minutes.30 It has been known for some time that damage to the SA node may occur after correction of transposition of the great arteries by the Mustard procedure.8' 31 This is not unexpected because this operation requires extensive reconstruction at the level of the atria; during
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insertion of the baffle, damage to the SA node may be caused by direct trauma to the node, or interruption of the sinus node artery.3` Only recently has it become apparent that SA node dysfunction may be seen after correction of other heart defects. Indeed, Greenwood et al.7 found a "sick sinus syndrome" in some patients after correction of tetralogy of Fallot, atrial septal defect and ventricular septal defect; their evidence was based on clinical data and surface ECG, but electrophysiological studies were not done. In these situations, there is no extensive atrial reconstruction. We may speculate with Aberdeen and Carr32 that damage results from insertion of the superior vena cava cannula or sealing of the atrium around it. There is a possibility that the atrial incision may divide the node.33 In our series, no specimens are available, so that we cannot bring forward anatomic or histologic evidence of SA node injury. In conclusion, the majority of patients in this study, all of whom had undergone extensive intracardiac surgery, showed little or no damage to the conduction system. The serious consequences of injury to the His bundle are now well recognized, and new surgical techniques have succeeded in avoiding it. However this study has shown that other parts of the conduction system, especially the SA and A-V nodes, may be vulnerable. These structures should also be avoided if possible during open heart surgery. References 1. KIRKLIN JW, WALLACE RB: Surgical treatment of congenital heart disease. In The Heart, Arteries and Veins, ed 2, edited by HU.RST JW, LOGUE RB. New York, McGraw-Hill, 1970, p 698 2. Moss AJ, KLYMAN G, EmM1IANOUILIDEs GC: Late onset complete heart block. Am J Cardiol 30: 884, 1972 3. GODMAN. MJ, ROBERTS NK, IZUKAWx A T: Late postoperative conduction disturbances after repair of ventricular septal defect and tetralogy of Fallot. Circulation 49: 214, 1974 4. WOLFF GS, ROW LAN-D TW, ELLISON RC: Surgically induced right bundle branch block with left anterior hemiblock. Circulation 46: 587, 1972 5. ALLEN HD, ANDERSON RC, NOREN GR, MOLLER JH: Postoperative follow-up of patients with ventricular septal defect. Circulation 50: 465, 1974 6. FRIEDLI B, IZUKAWx A T, KIDD BSL: Evolution a long terme des communications interventriculaires operees. Ann Cardiol Ang6iol 23: 203, 1974 7. GREENWOOD RD, ROSENTHAL A, SLOss LJ, CASTANEDA AR, NADAS AS: Sick sinus syndrome after cardiac surgery in childhood. (abstr) Circulation 50: (suppl III): 111-176, 1974 8. GILLETTE PC, EL-SAID GM, SIVARAJAN N, MULLI.NS CE, WILLIAMS RL, MCNAMARA DG: Electrophysiological abnormalities after Mustard's operation for transposition of the great arteries. Br Heart J 36: 186, 1974 9. SCHERLAG BJ, LAL SH, HELFANT RH, BERKOWITZ WD, STEI.N E, DAMIATO AN: Catheter technique for recording His bundle activity in man. Circulation 39: 13, 1969 10. BAT.SFORD WP, AKHTAR M, CARACTA AR, JOSEPHSON ME, SEIDES
SF, DAM ATO AN: Effect of atrial stimulation site on the electrophysiological properties of the atrioventricular node in man. Circulation 50: 283, 1974 11. NARULA OS, SAMET P, JAxTIER RP: Significance of the sinusnode recovery time. Circulation 45: 140, 1972 12. ROBERTS NK, OLLEY PM: His bundle recordings in children with normal hearts and congenital heart disease. Circulation 13. 14. 15. 16.
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45: 295, 1972 ROBERTS NK, OLLEY P: His bundle electrogram in children. Br Heart J 34: 1099, 1972 ABELLA JB, TEIXEIRA OHP, MISRA KP, HASTREITER AR: Changes of atrioventricular conduction with age in infants and children. Am J Cardiol 30: 876, 1972 GuPTA PK, LICHSTEIN E, CHADDA KD, BADUI E: Appraisal of sinus nodal recovery time in patients with sick sinus syndrome. Am J Cardiol 34: 265, 1974 SIMIONIN Ph, NIEDERHAUSER HU: L exploration electrique
endocavitaire dans la dysrythmie auriculaire. Schweiz Med Wschr 104: 1584, 1974 TITIUS JL, DAUGHERTY GW, KIRKLIN JW, EDWAARDS JE: Lesions of the atrioventricular conduction system after repair of ventricular septal defect. Circulation 28: 82, 1963 KlJLBEBTULS HE, COYNE JJ, HALLIDIE-SASITH KA: Conduction disturbances before and after surgical closure of ventricular septal defect. Am Heart J 77: 123, 1969 ANDERSON PAW, ROGERS MC, CANENT RV, JARMAKANI JMM, JEWETT PH, SPACH MS: Reversible complete heart block following cardiac surgery. Circulation 46: 514, 1972 LIEN W-P, LEE Y-S: Unusual atrioventricular conduction disturbances in secundum atrial septal defects. Communication at the World Congress of Cardiology, Buenos Aires,
1974 21. LISTER JW, STEIN E, KoSOWvSKY BD, LAL SH, DAMATO AN: Atrioventricular conduction in man. Am J Cardiol 16: 516, 1965
22. CHENG TO: Atrial pacing: Its diagnostic and therapeutic applications. Prog Cardiovasc Dis 14: 230, 1971 23. ROSEN- KM: Evaluation of cardiac conduction in the cardiac catheterization laboratory. Am J Cardiol 30: 701, 1972 24. DODINOT R, HU-A G, MENTRE B, FAIVRE G: Stimulation auriculaire et explorations hisiennes dans les indications de lentralnement 6lectro-systolique au long cours. Arch Mal Coeur 66: 257, 1973 25. NARULA OS: Atrioventricular conduction defects in patients with sinus bradyeardia. Circulation 44: 1096, 1971 26. ANDERSON PAW, ROGERS MC, CANENT RV, SPACH MS: Atrioventricular conduction in secundum atrial septal defects. Circulation 48: 27, 1973 27. FERRER MI: The sick sinus syndrome. Circulation 47: 635, 1973 28. Moss AJ, DAVIs RJ: Brady-tachy syndrome. Prog Cardiovasc Dis 16: 439, 1974 29. MANDEL WJ, HAYAKAWA H, ALLEN HN, DANZIG R, KERMAIER AI: Assessment of sinus node function in patients with the sick sinus syndrome. Circulation 46: 761, 1972 30. AVERILL KH, LAMB LE: Less commonly recognized actions of atropine on cardiac rhythm. Am J Med Sci 237: 304, 1959 31. EL-SAID G, ROSENBERG HS, MULLINS CE, HALLMAN GL, COOLEY DA, McNAM ABA DG: Dysrhythmias after Mustard's operation for transposition of the great arteries. Am J Cardiol 30: 526, 1972 32. ABERDEEN E, CARR I: Transposition of the great arteries. In Modern Trends in Cardiac Surgery, vol 2. London, Butterworth's, 1968, p 182 33. TUN(. KSK, JAMES TN, EFFLER DB: Injury to the sinus node in open heart surgery. J Thorac Cardiovasc Surg 53: 814, 1967 Circulation. Volume 52, August 1975
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Sinus node function and conduction system after complete repair of tetralogy of Fallot. H Niederhauser, P Simonin and B Friedli Circulation. 1975;52:214-220 doi: 10.1161/01.CIR.52.2.214 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1975 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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