Download Intraoperative Recording of Specialized Atrioventricular Conduction

CIRCULATION
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VOL 59, No 1, JANUARY 1979
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Intraoperative Recording of Specialized
Atrioventricular Conduction Tissue Electrograms
in 47 Patients
MACDONALD DICK,
II,
M.D., WILLIAM I. NORWOOD, M.D., CARL CHIPMAN, B.S.,
AND ALDO R. CASTANEDA, M.D.
SUMMARY Intraoperative mapping of the specialized atrioventricular conduction system was performed in
47 patients during cardiac surgery. Specialized conduction tissue electrograms were identified in 37, and atrioventricular conduction preserved in 92%. Specialized conduction tissue was identified in 27 patients with atrioventricular canal defect; complete heart block was avoided in 25. Conduction tissue was located in six of 12
patients with complex transpositions; atrioventricular conduction was preserved in all six. Other lesions in
which the technique was useful were Ebstein's anomaly and single atrium. Limitations to the technique are 1)
deep hypothermia and circulatory arrest; 2) interruption in atrioventricular conduction during mapping; 3) inadequate exposure and access to probable sites of conduction tissue; 4) variation of size and spatial relations of
individual malformations; and 5) limited time for identification of unusually located conduction tissue. Indications for use of this technique include patients with both forms of atrioventricular canal, complex transpositions, atrioventricular discordance, single ventricle and single atrium.
ELECTROPHYSIOLOGIC IDENTIFICATION of
the specialized cardiac conduction system was introduced in 1970 to prevent major injury to the cardiac conduction tissue during open heart surgery.'
Several reports have described mapping the conduction system in patients with selected cardiovascular
malformations, including incomplete atrioventricular
(AV) canal, complete AV canal,2 transposition of
the great arteries, atrial septal defect,3 ventricular septal defect, tetralogy of Fallot,4 corrected transposition of the great arteries with either situs solitus5-8
From the Departments of Cardiology and Cardiovascular
Surgery, Children's Hospital Medical Center, and the Departments
of Pediatrics and Surgery, Harvard Medical School, Boston,
Massachusetts.
Supported in part by Grants HI 10436 and HL05855 from the
National Institutes of Health, Bethesda, Maryland.
Address for reprints: Macdonald Dick, II, M.D., Department of
Cardiology, Children's Hospital Medical Center, 300 Longwood
Avenue, Boston, Massachusetts 02115.
Received March 10, 1978; revision accepted August 22, 1978.
Circulation 59, No. 1, 1979.
or situs inversus,9 Ebstein's anomaly,8 and single ventricle.7 8, 10, 11 In this report we review our experience
with intracardiac mapping and define the limitations
and indications of this electrophysiologic technique in
patients with congenital heart disease.
Materials and Methods
Between March 1, 1974 and August 31, 1977, intraoperative mapping of the specialized AV conduction
tissue was performed at the Children's Hospital
Medical Center, Boston, in 47 patients with complex
congenital heart disease. In all the patients the course
of the specialized conduction system was either unpredictable, unknown or particularly vulnerable and
thus at risk at surgery; identification by the electrophysiologic technique was performed in an attempt to
preserve AV conduction.
Recording of the intracardiac specialized conduction tissue potentials was performed in the manner
previously described.3'5 I After institution of cardiopulmonary bypass the area suspected of containing
INTRAOPERATIVE MAPPING/Dick et al.
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AV conduction tissue was explored with a hand-held
probe 3-5 mm in diameter, with three biopolar pairs
of electrodes (1 mm apart). The patients' esophageal
temperatures were maintained between 30-37°C.
Each bipolar pair of electrodes was connected to a
Hewlett-Packard high impedance differential
amplifier (MN8811 A) and was isolated from both
ground and the recording apparatus by an isolation
transformer. Electrograms were recorded at frequencies between 15-300 Hz. All tracings were monitored
on a Hewlett-Packard 1308A oscilloscope and
recorded simultaneously on a photographic paper
moving at 100 mm/sec. During the mapping
procedure AV conduction was maintained by either a
normal sinus rhythm or atrial pacing; in a few patients
specialized conduction tissue electrograms were
recorded in the presence of other mechanisms (atrial
fibrillation or AV dissociation). Time required for the
mapping procedure was generally no more than 3-5
minutes; in one patient unsuccessful exploration for
specialized conduction time electrograms was
prolonged to 10 minutes.
Table 1 shows patient diagnoses, ages, electrophysiologic findings and results. Twenty-seven
patients had either partial or complete AV canal. One
additional patient had ventricular septal defect of the
AV canal type. Twelve patients with complex cardiac
malformations had either complete or corrected transposition, with either situs solitus or inversus of viscera
and atria. Two patients had single ventricle with right
ventricular outflow tract chamber and corrected transposition of the great arteries;'2 13 one of these patients
had, in addition, a restricted bulbo-ventricular
foramen with a hypertensive left ventricle. One patient
had tricuspid atresia with d-transposition of the great
arteries and restrictive bulbo-ventricular foramen.
Two patients had double outlet right ventricle with
ventricular septal defect and pulmonary artery band,
and one patient each had Ebstein's anomaly and single
atrium with AV canal defect.
Results
In 39 of the 47 patients studied, specialized atrial
ventricular conduction tissue was identified by the
electrophysiologic technique (table 1).
Incomplete Atrioventricular Canal
We successfully mapped 14 patients with incomplete AV canal. The median age at surgery of this
group was 9 years. None developed complete heart
block postoperatively, although two patients
developed symptomatic tachy-bradyarrhythmia syndrome and one (patient 1 1) had intermittent junctional
mechanism. All three of these patients also had mitral
valve replacement because of significant mitral
regurgitation. Two of these three (patients 12 and 14)
received their xenograft valves at a later operation,
after initial unsuccessful valvuloplasty. Figure 1 illustrates the findings in a 3-year-old boy with an atrial
septal defect primum type; the course of the intra-
151
atrial conduction tissue began inferior to the coronary
sinus and proceeded along the intervalvar ridge
between mitral and tricuspid orifices. Approaching the
ventricular crest, the conduction tissue deviated
slightly to the left; this pattern was observed in three
additional patients. The atrial septal patch was placed
to the right of this area. In two patients the conduction
tissue was traced beneath the septal leaflet of the
tricuspid valve onto the ventricular crest. Conduction
tissue was avoided in these two cases by placing the
patch on the left side of the ventricular crest. In the
remainder of the patients the conduction tissue was
found along the intervalvar ridge in the middle of the
ventricular crest. Conduction tissue was avoided by
placing sutures to the right. One- to 4-year follow-up
revealed normal sinus rhythm in nine patients, persistent sick sinus syndrome in two, and sinus rhythm
with intermittent AV dissociation in one. One infant
(patient 1) 6 months of age and weighing 4 kg, died 3
days after surgery of pulmonary complications. Postoperatively, AV conduction was intact.
Complete Atrioventricular Canal
Thirteen patients were operated on for primary
repair of complete AV canal, with successful electrophysiologic delineation of the specialized conduction
tissue. These patients were considerably younger at
the time of surgery (median age 4 years) than those
with incomplete AV canal. Two patients (15 and 16),
both younger than 18 months and weighing less than 5
kg, developed complete heart block. One additional
patient (21) had AV dissociation after surgery.
Although hospital mortality was high in this group
(four of 13, with one additional late death), conduction disturbances could be implicated as the primary
cause of death in only two. Figure 2 illustrates the
relationship between the recorded intracardiac electrogram and the anatomic sites within the heart of
patient 26. With the probe slightly inferior and to the
right of the coronary sinus orifice, both atrial and His
bundle electrograms were recorded; the ventricular
electrogram was small. Proceeding along the His bundle toward the ventricle, the ventricular electrogram
became larger as the atrial electrogram diminished.
Upon reaching the ventricular crest, both the a wave
of the atrial electrogram and the His bundle potential
disappeared; only a ventricular electrogram was
recorded. In this manner the course of the conduction
system was outlined.
In seven of the 13 patients the specialized conduction tissue could be traced onto the middle of the ventricular crest before the signal was lost. Conduction
tissue was avoided by careful placement of the inferior
posterior margin of the patch to the right of this area.
In six of the patients the intraventricular portion of
the specialized conduction tissue was identified
beneath the tricuspid posterior leaflet. In these cases
the septal patch was placed to the left of this area. In
the two smallest infants, complete heart block
developed. Satisfactory identification of the
specialized conduction tissue had been accomplished
VOL 59, No 1, JANUARY 1979
CIRCULATION
152
TABLE 1. Clinical Data
Identification
of SAVC tissue
Pt
Age
Postop
Postop AV
conduction
rhythm
Incomplete atrioventricular canal
Follow-up
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1
6 months
Yes
2
3
4
5
6
7
8
9
10
11
212 years
3 3/12 years
4 years
6 years
7 years
9 years
9 years
12 years
14 years
15 years
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
12
13
14
15 years
18 years
18 years
Yes
Yes
Yes
Sinus intermittent
junctional
Sinus
Sinus
Sinus
Sinus
Sinus
Sinus
Sinus
Sinus
Sinus
Sinus intermittent
junctional with AV
dissociation
SSS
Sinus
SSS
15
16
17
18
19
20
21
22
23
24
25
26
27
9 months
16 months
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Complete AV canal
Pacemaker
Surgical CHB
Pacemaker
Surgical CHB
Intact
Sinus
Intact
Sinus
Intact
Sinus
Intact
Sinus
AV dissociation
Junctional
Sinus
Intact
Sinus
Intact
Intact
Sinus
Intact
Sinus
Intact
Sinus
Intact
Sinus
Dead
1 year--died
Dead
3 years
3 years
Dead
Dead
3 years
2 years
3 years
2 years
2 years
2 years
Yes
Ventricular septal defect
(AV canal type)
Sinus
Intact
3 years
28
112 years
20 months
23 months
2 years
4 years
412 years
4 years
7 years
7 years
12 years
14 years
12 years
Intact
Dead
Intact
Intact
Intact
Intact
Intact
Intact
Intact
Intact
Intact
Intact
1st degree
2 years
2 years
4 years
6 months
312 years
2 years
4 years
3 years
4 years
112 years
Other
MVR
heart block
Intact
Intact
Intact, 1st degree
heart block
A-H 250 mscc
H-V 45 mscc
at postop cath
4 years
1 year
4 years
MVR
MVR
PAB
PAB, MVR
MVR
Transposition
IVS
29
30
31
13 months
11 years
13 years
No
Sinus
Intact
3 years
Yes
Yes
Transposition
VSD, PS, (S, D, D)
Sinus
Intact
Sinus
Intact
3 years
3 years
Transposition
VSD, PS, (I, D, D), dextrocardia
32
33
34
35
36
37
38
1412 years
27 years
10 years
14 years
22 years
10 years
38 years
Yes
Yes
No
Sinus
Sinus, SSS
Sinus
No
No
Yes
Yes
Corrected transposition
VSD, PS, (S, L, L)
Pacemaker
Congenital CHB
Pacemaker
Surgical CHB
Sinus
Intact
Sinus
Intact
TCHB, Sinus
Intact
Intact
3 years
3 years
3 years
Dead
3 years
3 years
1 year
Surgical
CHB after
reoperation
39
1 1 years
No
Corrected transposition
Left-sided AV valve regurgitation (S, L, L)
Sinus
Intact
2 years
INTRAOPERATIVE MAPPING/Dick et al.
TABLEar 1. (Continuel)
Age
Pt
40
Iden-tificatioin
of SAVC tissue
Postop
Postop AV
rhythm
conidtuctioni
7 years
3 years
No
Sinlgle venitricle with I transpositioni
Puilrnon ary steniosis, restrictive VSI)
Pacemiaker
CUIB, Surgical
Dead
8 years
No
Tricuspid atresia
with d-tranisposition, restr-ictive VSI)
CUB. Surgical
Pacemaker
Dead
44
4 years
D)ouble outlet right ventricle
VSI) Subaortic, subaortic stenosis, PAB, (S, 1), I))
3 years
Intact
Siirus
No
45
12 years
Yes
Sirius
46
11
Yes
Sinus
Junction-al
43
Other
Tr ansposition
VSD, (I, L, L), purlnorrary atresia, Waterstorr shunllt, PAII
9 months->I)ied PAIL, CHF
Intact
No
Sinulls
No
42
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:
Follow-tip
Sinigle ventricle with I transposition
(S, 1), 1)), PAB, restrlictive VSI)
Pacemnaker
CHIB, Surgical
41
153
6 years
13 years
VSI), PAB, S, L L mal
Intact
3
years
Single atrium
2 years
Intermittenit
AV dissociation
Intact
MMVt
Ebstein's anomaly
1 year
Intact
Yes
Sinu-s
=
atrioventricular; CH13 - complete hear-t block;
atrial-Ilis btundle initerval; AV
Abbreviationis: A-fl
CIIF Scongestive heart failiire; Il-V
His btuindle-ventricular initerval; (1,L), I)) s;tits iniversus of viscera
situs
and atria; d-loop; aurtie valve to right of ptulmolary valve; (1,L,L)
iLrversus of viscera arid atra;
1-loop; aortic valve tIo left of pulimoriary valve; IV = initact venitricultar septumn; MVII - mitral valve
replacemnenit; PAB3 =puilrnoiiay artery banid; PAIl pulmoniary artery hypertens;iol; PS - pulmoinary
stetiosis; SAVC xspecialized atrioveitrictular comiductioni tissuie; (S, 1) ) sitU: solitis of viscera anad atria;
d-loop; aortic valve t.lo might;of pulmoniary valve; (S,TL,LT) sit-its solit is of viscera and atria; 1-loop; aortic
valve to the left, of puilmonary valve; (S,L,L inal) esitus solitis of viscera arid atria; 1-loop; aoritic valve to
the left of pulmonary valve, rnal-abriorinally placed but rnot tranisposed across the venitricuLlar septturm; SSS
sick sinus sytndrome; VSI) venitricular septal defect.
47
13
=
=
=
=
SUP
ECG P
ANT.-
POS.
HVI'
AH
HBEH
_~~~
INF
A
V
----
mmommo
FIGURE 1. The left panel is a photograph taken at repair of an atrial septal defect primum type; the right
panel is an intraoperative His bundle tracing obtained at surgery. The intervalvar ridge, between the mitral
and tricuspid orifices, was the site of intra-atrial electrogram recordings (indicated by the dotted line). The
patch was placed to the right of this ridge. A = atrial electrogram; H = His bundle electrogram; HBE = His
bundle recording; HRA high right atrial recording; P P wave; R R wave; V ventricular electrogram.
=
=
=
154
CIRCULATION
VOL 59, No 1, JANUARY 1979
ECG
AHVB
HBE
1fA
0.i .., ^
I
4 it
lS
I
interior
Posterior
ll19
AHB
f
HBE2
I
1
t
Interior
dI
RAO VIEW
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A~~~~~~~~ :
FIGURE 2. Photograph of intracardiac anatomy and intraoperative His bundle recording obtained at
vario us sites in the atria of a 12-year-old girl with complete atrioventricula r canal. With the probe high in the
right atrium, both atrial and His bundle electrograms (HBE) were recorded. The ventricular electrogram
was quite small. Proceeding along the His bundle toward the ventricle, the ventricular electrogram became
larger as the atrial electrogram diminished; upon reaching the ventricular crest the a wave of the atrial electrogram and HBE disappeared and only a ventricular electrogram persisted. In this manner, the course of
the conduction system was outlined. Abbreviations: same as in figure 1.
in both, but the atrial anatomy necessitated placement
of the inferior margin of the patch on the identified
sites. During the later part of this study (1976-1977),
three children with complete AV canal had their
defects repaired using deep hypothermia and cir-
culatory arrest without intraoperative mapping;
therefore, they were not included in this study. Two of
these children weighed 8 kg and were 1 '/2 years old;
both of these children had intact AV conduction postoperatively. The third child, 11 months of age,
I_
FIGURE 3. Diagrammatic sketch (left panel) of the relationship between ventricular septal defect (VSD),
atrioventricular canal type and the location of His bundle electrograms (HBE). The tricuspid valve has been
removed. HBEB were recorded along the superior margin of this. VSD, but in the usual inferior location in
relationship to the membraneous septum and parietal band. A bbreviations. same as figure 1.
INTRAOPERATIVE MAPPING/Dick et al.
weighed approximately 4 kg at surgery and was in
severe congestive heart failure. Transient complete
heart block persisted for 7 days after surgical repair,
before AV conduction with first degree heart block
returned.
A 12-year-old boy (patient 28) required closure of a
large ventricular septal defect and removal of a
pulmonary artery band. At surgery the defect was
located posteriorly and inferiorly behind the posterior
leaflet of the tricuspid valve, with no intervening
muscular tissue between the margin of the ventricular
septal det-ect and the insertion at the AV groove of the
posterior leaflet, indicating an AV canal type of
defect Normal intra-atrial electrograms were
recorded. When exploring the margin of the ventricular septal defect the specialized conduction tissue
electrograms were found along the anterior-superior
rim of the defect (fig. 3).
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pulmonary stenosis presented different findings. In
spite of the AV discordance, and in contrast to the
usual form of corrected (1) transposition of the great
arteries [S,L,L], the intraventricular conduction tissue
was identified along the posterior-inferior margin of
the ventricular septal defect.9 In the third similar
patient (34), specialized conduction tissue electrograms were not recorded.
In the four patients with corrected transposition of
the great arteries (1-transposition) with ventricular
septal defect and pulmonary stenosis [S,L,L],13
specialized conduction tissue electrograms were identified in two and AV conduction preserved postoperatively. In the other two, specialized conduction
tissue was not identified and surgically induced complete heart block occurred in one (patient 46),
probably due to the failure to explore the subpulmonic
area for His bundle electrograms. The other (patient
35) had complete heart block before surgery. Figure 4
(patient 38) illustrates the location of the specialized
intraventricular conduction tissue in a patient with 1transposition of the great arteries, situs solitis, ventricular septal defect and pulmonary stenosis. As
previously reported,', 8, 10, 11 specialized conduction
tissue electrograms were recorded on the anteriorsuperior margin of the ventricular septal defect rather
than the inferior margin, its usual location in transposition of the [S,D,D] configuration. However, in
this patient, specialized conduction tissue electrograms were not recorded until the probe was placed on
the far left-sided right ventricular (anterior-superior)
margin of the ventricular septal defect. Because of this
Transpositions
Five patients (30-34) with d-transposition of the
great arteries; ventricular septal defect, and
pulmonary stenosis were examined at surgery by the
electrophysiologic technique. In d-transposition of the
great arteries with situs solitis and membranous ventricular septal defect, the conduction system is located
along the posterior-inferior margin of the ventricular
septal defect;'5 early in our experience, we studied two
patients, with the expected findings. In contrast, two
patients with d-transposition of the great arteries with
situs inversus, ventricular septal defect, and
EC0-
-
~ w
I
155
::::::
--4
'I'-eF
~~~~~~ ~ ~~~~~~~~~ : ..:..
... ... ....
....
FIGURE 4. This figure shows the anatomy
of corrected transposition in situs solitus
(adapted from Kupersmith et al.5) and the
intraoperative electrograms. Specialized
conduction tissue electrograms were identified along the superior-anterior margin of
the ventricular septal defect, Hut on the right
ventricular (left side) rather than left ventricular (right side) side of the anterior ventricular septum. Abbreviations: same as
figure 1.
156
CIRCULATION
VOL 59, No 1, JANUARY 1979
SUPERIOR
R
ECG_AtaS
ECG Atrial
RIGHT
INFERIOR
2 msec.
m
200
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FIGURE 5. Intraoperative recording (right) in a patient with double outlet right ventricle, ventricular septal
defect (VSD), and pulmonary artery bank (not shown). Intraventricular conduction tissue was found in the
expected location, along the posterior-inferior margin of the VSD. Abbreviations: same as figure 1.
finding, sutures were placed on the right side, left ventricular aspect of the ventricular septal defect. AV
conduction was preserved. Follow-up catheterization
demonstrated residual severe pulmonary stenosis. At
reoperation 1 year later, attempts at resection of the
subpulmonary obstruction without the benefit of mapping resulted in complete heart block, and the patient
required a permanent pacemaker. In two patients with
1-transposition, one (patient 39) with situs solitis
[S,L,L] and left-sided AV valve regurgitation (intact
ventricular septum) and one (patient 40) with situs inversus [I,L,L], pulmonary atresia and ventricular sep-
tal defect, specialized AV conduction tissue was not
identified. AV conduction was intact postoperatively
in both patients.
Other Cardiac Malformations
Two patients with single ventricle, type A,'2 and 1transposition of the great arteries required surgery.
One (patient 41), 6 years of age, had a restrictive
bulbo-ventricular foramen and a hypertensive right
ventricle. At surgery the margin of the bulbo-ventricular foramen (ventricular septal defect) was thickened
SUPERIOR
IJEC
LEFT
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....~~~~~~~~~O
\)TV
A'
ifi
74.-.-
POSTERIOR
..._. ..&. .......
I
aI
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X
/
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ANTFRIOR
. . i.
'I
.
'f1
_.-.
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r
..-....
.. ..
..
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...................................................
........
1
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tL
FIGURE 6. The illustration (left panel) schematically outlines the atrioventricular (A V) canal anatomy
viewed from above in a 12-year-old patient with single atrium. The atria have been removed. The right panel
is the intraoperative His bundle recording (HBE). Note the location of the HBE posterior to the left-sided
A Vorifice. Also note atrialfibrillation and spontaneous His bundle rhythm. A V conduction was maintained
during placement of the inferior margin of the patch. MV = mitral valve; TV = tricuspid valve;
A. Fib. = atrial fibrillation; other abbreviations same as figure 1.
INTRAOPERATIVE MAPPING/Dick et al.
157
Superior
ECO
ECG
Lef t
Right
i
Anterior
Posterior
:X{~' Mi 4
A: H
HBE
W
'
0# /
p
9t\,
A
A
200
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IAH
91lmsec
HV
47msec.
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Inferior
FIGURE 7. Intraoperative photograph ofright atrial anatomy in a 13-year-old girl with Ebstein's anomaly,
and the simultaneous His bundle tracing (HBE). HBEs were recorded at a point (arrow) just superior and
anterior to the coronary sinus. The tricuspid valve is displaced leftward and inferiorly beyond the margins of
the photograph. The bottom tracing is an atrial electrogram recorded through high right atrial electrodes.
with fibrous tissue. Exploration of the entire margin of
the ventricular defect failed to disclose specialized
conduction tissue electrograms. Incision of the
superior-anterior margin of the ventricular septal
defect to enlarge the foramen resulted in complete
heart block, and the patient required a permanent
pacemaker. In the second patient (42) with similar
anatomic findings, ventricular septation was unsuccessful; extensive exploration (10 minutes) for
specialized conduction tissue was also unsuccessful,
resulting in complete heart block and postoperative
death (24 hours).
A 12-year-old boy (patient 43) with tricuspid
atresia, d-transposition of the great arteries, and a
restrictive bulbo-ventricular foramen (ventricular septal defect) was operated on to relieve the hypertensive
left ventricle. No specialized intraventricular conduction tissue was identified. This patient died after surgery, in part related to the surgically-induced complete heart block.
Two patients with double outlet right ventricle, subaortic ventricular septal defect [S,D,D] and
pulmonary artery banding required intracardiac
repair; at surgery, intra-atrial and intraventricular
specialized conduction tissue electrograms were
recorded in one (patient 45) (fig. 5) at the expected
atrial location adjacent to the coronary sinus, and
along the posterior-inferior margin of the ventricular
septal defect. In the other patient (44), specialized
conduction tissue electrograms were not obtained.
An 11 -year-old girl (patient 46) with single atrium
and AV canal defect was repaired using the electrophysiologic technique to identify the specialized con-
duction tissue. Intra-atrial electrograms were
recorded from the posterior margin of the mitral
orifice, and traced inferiorly onto the left side of the
ventricular crest (fig. 6). Conduction was maintained
during placement of the inferior margin of the patch.
However, the ring of the mitral valve prosthesis, by
necessity, rested on the point where the electrograms
were recorded; AV dissociation with intermittent intact AV conduction developed.
A 13-year-old girl (patient 47) received a
heterograft valve at the tricuspid position for Ebstein's
anomaly. Intra-atrial electrograms (fig. 7) were recorded for a short distance within the atrium above
the inferiorly and leftwardly-displaced posterior right
AV valve, and superior and anterior to the coronary
sinus. Sutures for the tricuspid valve prosthesis were
placed to either side of this point. After surgery, AV
dissociation was present for 24 hours. Intact AV conduction with first degree heart block then returned.
Discussion
The primary objective of intraoperative electrophysiologic identification of specialized conduction
tissue is the preservation of AV conduction after surgery.' We were successful in identifying specialized
conduction tissue in 79% of our patients (37 of 47). In
92% of these patients (34 of 37) surgically induced
complete heart block was avoided. In one other (patient 32), transient complete heart block developed, but
AV conduction resumed before discharge from the
hospital. Intermittent AV dissociation was present in
three (1, 11 and 46) and junctional rhythm in one
158
CIRCULATION
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(patient 21). In contrast, 40% (four of 10) of the
patients in whom specialized conduction tissue was
not identified developed complete heart block.
Complete heart block has been reported to develop
in 15% of patients during repair of incomplete AV
canal,16 and is known to appear as a late complication
after AV canal repair.'6 17 In all of the 27 patients
with AV canal defects in this report, specialized AV
conduction tissue potentials were identified and AV
conduction was preserved in 95%. Little or no variation in the origin of the specialized AV conduction
tissue, inferior (caudal) and anterior (ventral) to the
coronary sinus, was found, in contrast to the experience of others.2' 3 We did observe variation,
however, in the course of the His bundle as it reached
the ventricular crest. In 11 of 13 patients with incomplete AV canal defects and seven of 14 with complete AV canal defects, AV block was avoided by
placement of the inferior margin of the patch on the
right side of the crest. Thus, in the majority of patients
with incomplete AV canal defects, conduction tissue
can be avoided by adhering to the right margin of the
ventricular crest. In a few patients, however, (15% in
our series, two of 13) the conduction tissue may
precede beneath the right-sided tricuspid valve on to
the ventricular crest. This variation can only be identified by recording His bundle electrograms, and underscores the necessity of mapping patients with incomplete AV canal. In patients with the complete
form of AV canal the position of the conduction tissue
on the ventricular crest was even more variable and
thus, also required mapping to locate precisely its
course. Even with this technique anatomic limitations
such as size and spatial relations may require placement of suture at points where specialized conduction
time electrograms are recorded, as occurred in two of
our patients (15 and 16).
The course of the conduction system in membranous ventricular septal defect is along the inferior
posterior margin of the defect.14' 18 In the AV canal
type of defect, conduction tissue has been identified
along the posterior margin;" in contrast, the conduction tissue in muscular defects is often unrelated to the
defect and may thus be located anterior and superior
to it.'8 In patient 28, the anatomic features of the
defect suggested an AV canal type, but the conduction
tissue was anterior, proceeding in a more normal
course, indicating that this defect probably did not impinge upon the membranous septum,15 and resembled
in its relationships to the conduction tissue the
muscular type of defect.'8
Intraventricular specialized conduction tissue electrograms were not recorded in six of the 12 patients
with complex transpositions. In the single patient (29)
with d-transposition with intact ventricular septum
and one patient (34) with d-transposition, pulmonary
stenosis, and ventricular septal defect in situs inversus
[I,D,D], intraventricular mapping was not pursued for
technical reasons. In one patient (36) with corrected
transposition of the great arteries [S,L,L], failure to
explore the anterior margin of the pulmonary outflow
VOL 59, No 1, JANUARY 1979
tract probably led to false negative findings. Resection
of subpulmonary tissue containing conduction tissue6' 15
resulted in complete heart block. In this patient the
transatrial approach to the ventricular septal defect
was sufficient for electrophysiologic exploration of the
margin of the ventricular septal defect and its subsequent closure, but inadequate for mapping of the
anterior pulmonary valve area; this poor exposure
probably accounted for failure of identification of the
conduction tissue. Specialized conduction tissue at
risk in this location may be avoided by use of a left
ventricular (pulmonary ventricle) pulmonary artery
valve containing conduit.'9' 20 The second failure in
corrected transposition occurred in a girl (patient 35)
with an idioventricular rhythm arising distal to detectable conduction pathways; retrograde activation of
specialized conduction tissue was lost in the ventricular electrogram.
Limited exposure and access to the conduction
system may impede adequate recording of the
specialized conduction electrograms. Two additional
patients with 1-transposition were unsuccessfully explored for specialized conduction time electrograms.
One patient with 1-transposition [S,L,L], intact ventricular septum and left-sided AV valve regurgitation
received a xenograph valve in one left-sided tricuspid
position. After native valve resection and before
prosthetic valve insertion, the septal surface of the
left-sided right ventricle beneath the aortic valve was
explored with the probe; visualization of the area was
poor, and we could not locate specialized AV conduction tissue. In the patient (40) with 1-transposition
[I,L,L] with pulmonary atresia, ventricular septal
defect had previously been palliated with a Waterston
shunt. Pulmonary artery hypertension developed and
surgical repair was advised. At operation a transventricular approach through the markedly hypertrophied right-sided left ventricle (pulmonary ventricle) did not provide adequate exposure for mapping.
Similar difficulty was encountered in one (patient 44)
with double outlet right ventricle, ventricular septal
defect, subaortic stenosis, and pulmonary artery band.
In these four patients AV conduction was intact
postoperatively.
In the patient with tricuspid atresia, exposure
through the hypoplastic right ventricle may not have
been sufficient; the intraventricular His bundle lies
subendocardially on the left ventricular aspect of the
ventricular septum and posterior to the ventricular
septal defect." Although the incision to enlarge the
ventricular septal defect was made anteriorly
(leftward and superior), complete heart block resulted.
Patients with complex cardiac malformations
those with abnormally related great arteries, AV discordance and single ventricles - presented more
difficult problems, with poorer results. The variability
of the conduction system in these anatomic entities is
well described.7 8 11, 21, 22 Although intraventricular conduction tissue has been identified by the
electrophysiologic technique, complete heart block is
a major problem in this group" and a major cause of
INTRAOPERATIVE MAPPING/Dick et al.
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operative mortality. In our two patients with single
ventricles, failure to identify specialized conduction
tissue resulted in complete heart block. In one (patient
41) extensive endothelialization of the bulbo-ventricular foramen probably played a role in our inability to
identify specialized conduction tissue electrograms.
An incision in the anterior-superior margin of the ventricular septal defect, a probable site for the conduction tissue,15 resulted in complete heart block. In the
second patient (42) with single ventricle, in spite of
prolonged (10-minute) exploration during sinus
rhythm and intact AV conduction, specialized conduction tissue potentials could not be identified.
Tricuspid valve replacement for Ebstein's anomaly
has been complicated by a 30% instance of complete
heart block;8 electrophysiologic identification of the
specialized AV conduction system contributed to the
preservation of intact AV conduction, both in our
single case and that of others.8
Single atrium is accompanied by absence of a
recognizable coronary sinus orifice, an anatomic landmark of the AV node and proximal His bundle. Thus
identification of the conduction tissue by the electrophysiologic technique is especially useful. In our case
His bundle potentials were located posterior to the
mitral valve orifice (fig. 5) and continued onto the left
side of the ventricular crest. AV dissociation, however,
occurred after placement of the mitral valve
prosthesis, probably on the basis of local compression
or edema adjacent to vulnerable underlying conduction tissue.
The major limitation of intraoperative mapping is
the use of deep hypothermia and circulatory arrest.
Under these conditions, although AV conduction is
generally maintained to approximately 25°C, minor
manipulations on the endocardial surface often lead to
arrhythmias or further conduction disturbances. At
deep hypothermic temperatures, below 200C, spontaneous impulse formation and propagation cease.23
Other technical and theoretical considerations are important. Maintenance of intact AV conduction, either
by sinus mechanism or by atrial pacing during the
mapping procedure, is necessary to insure a normal
activation sequence and promote detection of the
specialized conduction tissue in question. Although
His bundle rhythms can be recorded during atrial
fibrillation during surgery (fig. 4) and specialized conduction tissue electrograms have been recorded in the
presence of AV dissociation,9 the absence of intact AV
conduction makes identification more difficult. Local
metabolic factors such as hypokalemia, ischemia,
acidosis and hypothermia also alter impulse formation
and propagation sufficient to interfere with identification of underlying conduction tissue by locally
recorded electrograms.24 The margin for error
provided by the technique is 2-3 mm to either side of
the specialized conduction tissue,25 a precision requiring careful gentle exploration.
Until rapid, nontoxic histochemical techniques
become available for visualization of viable
specialized conduction tissue, the electrophysiologic
159
technique remains useful. Based on our experience and
that of others,2 3 including those not using the technique,'6' 17 mapping should be used in all patients with
both forms of AV canal, when operating conditions
(near normothermia) permit. In addition, in patients
who are demonstrated to have abnormal atrial
anatomy, such as single atrium or Ebstein's anomaly,
and associated lesions, identification of specialized
AV conduction tissue electrograms is necessary. In
patients with complex transpositions and abnormal intersegmental relationships, where the course of the
conduction system is variable and unknown, the mapping technique is also imperative. Single ventricle,
when surgical intraventricular intervention is indicated, requires electrophysiologic delineation of the
specialized conduction tissue. Even when mapping
identifies the site of conduction tissue, individual
anatomic and spatial relations of the malformation
may necessitate suture placement (or insertion of
prosthetic devices) on vulnerable sites of conduction
tissue. Exposure and access to expected sites of special
conduction tissue may be poor, preventing adequate
mapping. In these situations, postoperative intact AV
conduction is less likely to occur.
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Circulation. 1979;59:150-160
doi: 10.1161/01.CIR.59.1.150
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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