Posterior Extensions of the Human Compact Atrioventricular Node

Posterior Extensions of the Human Compact
Atrioventricular Node
A Neglected Anatomic Feature of Potential Clinical Significance
Shin Inoue, MD; Anton E. Becker, MD
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Background—Catheter ablation procedures have revived interest in the detailed anatomy of the specialized atrioventricular
(AV) septal junctional area. The compact AV node usually is considered to have a blunt posterior end. The objective of
this study was to reconstruct the human compact AV node in relation to the landmarks of Koch’s triangle, with emphasis
on its posterior extension.
Methods and Results—In 21 hearts obtained from autopsies, the AV nodal septal junctional area was removed en bloc, serially
sectioned, and reconstructed. None of the hearts showed a blunt posterior ending of the compact AV node; 13 showed
posterior extensions on both the right and left sides; 7 had a rightward posterior extension only; and 1 heart showed a single
leftward extension. Hence, a rightward posterior extension was present in 20 of 21 hearts. Furthermore, in 16 of these 20
hearts, the rightward extension continued to the level of the coronary sinus ostium; in 7, the bundle extended beyond this
anatomic landmark. The mean length of the right posterior extension was 4.462.0 mm; that of the leftward posterior
extension was 1.860.9 mm. Superimposed onto the slope of the muscular AV septum, viewed from the right atrium, the
rightward extension ran close to the tricuspid annulus with the leftward extension positioned superiorly.
Conclusions—The human compact AV node contains rightward and leftward posterior extensions, with the right extension
close to the tricuspid annulus. It is tempting to speculate that these extensions are involved in “slow pathway” conduction.
(Circulation. 1998;97:188-193.)
Key Words: atrioventricular node n arrhythmia n electrophysiology n reentry n tachycardia n ablation
C
atheter ablation procedures, particularly those for AV nodal
reentrant tachycardia, have led to a renewed interest in the
detailed morphology of the AV node and its atrial inputs.1 In
this context, the precise positioning of the AV node is
increasingly important. It is generally acknowledged that the
human AV node is located in the triangle of Koch,2 delineated
by the eustachian ridge or sinus septum (which harbors the
tendon of Todaro), the membranous septum (as part of the
central fibrous body), and the line of attachment of the septal
leaflet of the tricuspid valve. The dimensions of Koch’s
triangle, however, vary considerably from one individual to
another,3 which is clinically relevant in the case of catheter
ablation procedures in this area that are guided largely by
anatomic landmarks. In this context, it is of considerable
interest that most clinical investigators are accustomed to
consider the compact part of the AV node as a structure with
a blunt posterior end. This ignores the fact that as early as 1906,
Tawara described posterior extensions of the node,4 an observation endorsed by our own studies in 1975.5,6 These posterior
extensions have not received much attention since that time,
and it seems almost as if they have been forgotten completely.
In light of the revived interest in the electrophysiological
characteristics of the AV septal junctional area, this could turn
out to be a critical omission. For instance, in patients with AV
nodal reentrant tachycardia, a “slow pathway” is considered
part of the reentrant circuit, and catheter ablation near the
coronary sinus (CS) orifice is the most favored and highly
successful approach.7–9 Thus far, however, no one has shown
such a pathway electrophysiologically, and a morphological
substrate for a slow pathway has not been traced either. Hence,
the question arises whether posterior extensions of the compact AV node could serve as potential candidates.
The present study is based on serial histological sectioning
and subsequent reconstruction of the AV septal junctional area
in human hearts, obtained from individuals without a history
of AV nodal reentrant tachycardia or paroxysmal atrial fibrillation, and has been designed to investigate in detail the
posterior extensions of the compact node.
Methods
The present study is based on 21 hearts obtained at autopsy; none of
the patients had a history of persistent supraventricular arrhythmia. All
hearts were fixed in 4% formalin. Before the microscopic investigations of the AV node, we measured the length of Koch’s triangle by
taking the distance between the membranous septum and the widest
part of the mouth of the CS. Thereafter, the AV septal junctional area
was removed en bloc, which included the anterior part of the os of the
Received July 7, 1997; revision received September 18, 1997; accepted September 25, 1997.
From the Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, The Netherlands.
Correspondence to Anton E. Becker, MD, Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, PO Box
22700, 1100 DE Amsterdam, Netherlands.
© 1998 American Heart Association, Inc.
188
Inoue and Becker
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Figure 1. Opened right side of the heart with the membranous
septum transilluminated. The block of tissue removed for histological serial sectioning is shown. It contains Koch’s triangle
and, for the purpose of this diagram, has been divided into
three parallel slices. The area posterior to the os of the coronary
sinus (CS), which is the subeustachian pouch (✽) and represents
AV free wall junction, has been removed en bloc, also if considered necessary. The dotted line represents the annular attachments of the septal tricuspid valve leaflet. ER indicates eustachian ridge.
CS. When considered necessary, the adjoining posterior tissue blocks
were also taken. The block of tissue containing the full length of
Koch’s triangle was then carefully cut into parallel slices of 5-mm
thickness each (Fig 1). All slices were embedded and serially sectioned
at 10 mm thickness. Initially, every 20th section was stained with
either hematoxylin-eosin or a trichrome stain. This allowed the
recognition of the compact AV node and posterior extensions as a first
step. Thereafter, the sections in between were mounted and stained to
achieve a full reconstruction related to the anatomic landmarks of
Koch’s triangle. The actual length of AV nodal tissues was calculated
from the microscopic sections, which also allowed a reconstruction of
the AV nodal tissues in relation to the length of Koch’s triangle. For
each heart, the results are expressed as the mean6SD. Correlations
between two parameters were assessed by the method of Spearman.
Results
There were 15 male and 6 female hearts, taken from patients
ranging in age from 31 to 84 years (mean age, 56.2 years).
Heart weights ranged from 380 to 640 g, with a mean weight
of 471 g. The mean length of Koch’s triangle was
24.664.6 mm. Structural heart disease was found in 5 hearts;
old or recurrent myocardial infarction in 3; and aortic stenosis
in 2. The major cause of death was lung disease in 9 patients,
189
Figure 2. Composite showing the histology of the AV node and
its posterior extensions. A, The compact AV node (arrows) resting on the slope of the muscular AV septum. B, A section close
to the mouth of the os of the coronary sinus, showing the leftward (L) and rightward extensions (R), both of which are encircled. C and D, Higher magnifications of the leftward and rightward extensions (arrows), respectively. Hematoxylin-eosin
stains. Bar51 mm.
malignant disease in 5, acquired immunodeficiency syndrome
in 3, heart failure in 3, and sepsis in 2.
In each of the 21 hearts, a distinct, compact AV node was
found (Fig 2A). As anticipated, the compact node was positioned on the right side of the septal slope of the muscular
component of the AV septum. Anteriorly, the compact node
could be traced into the penetrating (His) bundle before it ran
out of the block of tissue. The compact node was characterized
by a complex architecture of interweaving cells. In most
instances, a deep stratum was identified, immediately resting on
and partially buried into the connective tissue of the central
fibrous body, composed of small interlacing cells. In such
instances, a superficial stratum was present, although without a
distinct delineation from the deep stratum, composed of
latticelike bundles of cells. However, the distinction between
deep and superficial layers was not always readily identifiable.
The compact node was covered on its right atrial aspect by a
transitional cell zone. The posterior extensions described
herein were direct continuations of the compact node, whereas
a further subdivision into deep and superficial strata was no
longer present. In fact, posterior extensions were composed of
tightly packed, small cells, occasionally with a marked nodelike
190
Posterior AV Nodal Extensions in Humans
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Figure 3. Micrographs of a heart specimen with a rightward
(tricuspid) posterior extension from the compact node only. A,
Cross section immediately anterior to the mouth of the coronary
sinus; the rightward posterior extension is encircled. Note its
close proximity to the tricuspid valve (TV) attachment. The central fibrous body (CFB) and mitral valve (MV) are indicated. B,
The posterior extension at higher magnification (between
arrows). Beyond this level, the nodal axis gradually merged with
ordinary working myocardium and eventually could no longer be
distinguished. RA indicates right atrium. Hematoxylin-eosin
stains. Bar51 mm.
arrangement, and were identified as discrete posterior continuations of the compact AV node. In case of a leftward and
rightward extension, the site of origin was readily recognized.
In case of a sole leftward or rightward extension, the site of
origin was identified as the site where the posterior continuation of the compact AV node veered away from the middle
part, either to the left or the right. Each of these 21 hearts
contained a posterior extension, which originated from the
compact AV node (Fig 2B to 2D); none of the hearts had a
compact AV node with a blunt posterior ending. The cellular
component makeup was like that of the compact node.
Of these 21 hearts, 13 showed a posterior extension that was
both right and left sided; 7 hearts had a rightward posterior
extension only (Fig 3), whereas only 1 heart showed a sole
leftward extension (Fig 4). A diagrammatic survey is provided
in Fig 5.
Once the compact node and both rightward and leftward
extensions were superimposed on the slope of the muscular AV
septum, it immediately became obvious that when viewed
from the right atrial aspect, the leftward extension was positioned superior to the rightward extension (Fig 6). The latter,
moreover, took a course parallel to and closely related to the
tricuspid annulus. Except for the case with a leftward extension
only, the rightward posterior extension was by far the most
prominent in each instance. In fact, in 16 hearts, this extension
could be traced all the way underneath the anterior margin of
the CS ostium. The maximum length of the right posterior
extension was 9 mm, with a mean of 4.462.0 mm. In contrast,
the maximum length of the leftward extension was 4.0 mm,
with a mean of 1.860.9 mm. It appeared that the mean length
of the rightward posterior extension exceeded that of the
length of the compact AV node (4.462.0 versus
3.760.9 mm). Moreover, in 7 of these 16 hearts, the posterior
bundle extended even beyond the anterior margin of the os of
Figure 4. Micrographs of the heart with a leftward posterior
extension only. A, Cross section through the compact part of
the node (arrows), positioned on the slope of the muscular AV
septum (asterisk). B, At a level more posterior and closer to the
os of the coronary sinus, the leftward extension (arrow) is seen
in close proximity to the central fibrous body. In follow-up sections, the posterior extension gradually faded within the fibrous
tissue. At the site of the anticipated rightward extension, there is
fatty tissue only. TV indicates tricuspid valve. Hematoxylin-eosin
stains. Bar51 mm.
the CS and continued for some distance in the subeustachian
pouch, which represents the posteroinferior right atrial free
wall (Fig 7). In these 21 hearts, the length of the compact AV
node varied between 2 and 5 mm, with a mean of
3.760.9 mm. In the same hearts, the length of Koch’s triangle
varied between 15 and 32 mm, with a mean of 24.664.6 mm.
The length of the compact AV node and posterior extensions
showed no relation to the dimensions of Koch’s triangle.
Discussion
The human AV node is not characterized by a blunt posterior
end as depicted in most electrophysiology texts. In fact, in this
series of 21 randomly selected and basically normal hearts, not
a single specimen had such a blunt-ended AV node. On the
contrary, 20 of the 21 AV nodes had a rightward posterior
extension from the compact part of the AV node, 13 of which
had an additional leftward extension. The remaining heart
showed an AV node with only a leftward posterior extension.
These extensions showed similar cellular and architectural
characteristics as those of the compact AV node. The latter has
been described as a layered structure with superficial and deep
strata6; others have described an additional intermediate layer.10
In the posterior extensions, such an additional subdivision was
no longer apparent. The cells were small and closely packed,
with an interweaving architecture (Fig 2C and 2D) and,
occasionally, a distinct nodelike cellular arrangement (Fig 7).
The latter situation is very much reminiscent of the nodelike
structures described by Anderson et al.11 Eventually, these
extensions faded out; the leftward extension eventually disappeared within the central fibrous body at the site of the mitral
valve annulus, whereas the rightward extension gradually
disappeared amid atrial myocardium.
It is of considerable interest, moreover, that the AV nodalbundle axis reached the level of the anterior margin of the os
of the CS in 16 of 20 hearts. In addition, in 7 of these hearts,
Inoue and Becker
191
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Figure 6. The compact part of the AV node, together with the
rightward and leftward posterior extensions, are superimposed
on the right-sided view of the AV septal junction of the same
heart. The rightward posterior extension runs in close proximity
to the annular attachment of the septal tricuspid valve leaflet
and extends to the level of the os of the coronary sinus.
Figure 5. Schematic representation of posterior extensions of
the compact AV node as encountered in this series of 21 randomly selected hearts. Note that none had a blunt-ending posterior end of the compact node. One case showed a leftward
extension only; 7 showed a rightward extension only; and 13
showed both rightward and leftward extensions. The dotted
lines indicate the site of transition between compact node and
His bundle.
the axis continued even further into the subeustachian pouch,
which basically no longer reflected AV septal junction but
rather inferior free wall junction.
Recent reviews of the anatomy of the AV conduction tissues
in electrophysiology textbooks fail to mention these extensions,12 other than a rather vague statement that “nodelike cells
are often seen at or near the anulus of the tricuspid, mitral and
aortic valves. Some of these . . . may join the regular AV
node.”10 It is only in a chapter produced by Anderson and
colleagues,13 referring to previous studies in the 1970s,5,6 that
posterior extensions are clearly mentioned and shown, albeit
without further emphasis on their potential significance. We
are unaware, moreover, of any recent original works that
encompass the posterior extensions of the compact AV node in
humans. Hence, it appears as if these structures have almost
been forgotten.
Nevertheless, Tawara’s 1906 epic work “Das Reitzleitungssystem des Säugetierherzens” clearly states that a small, paralleloriented bundle of fibers originates from the node to run
posteriorly approximately to the anterior region of the CS,
where it connects with the usual atrial fibers.4 Tawara’s famous
plates, composed of meticulously reconstructed drawings of
microscopic sections, beautifully illustrate these extensions and
actually show that Tawara himself had already noticed that
these bundles of fibers diverted rightward and leftward (see his
Tafel I Menschenherz No. 136 and No. 143).
In our studies in 1975,5,6 we confirmed the existence of two
distinct contributing segments to the compact node. Both
approached the compact node from beneath the mouth of the
CS, closely adherent to the fibrous annulus (see Becker and
Anderson,6 Fig 8, page 272), being divergent posteriorly, but
Figure 7. Micrographs showing extension of the rightward posterior extension beyond the os of the coronary sinus, into the
area of the subeustachian pouch. A, The posterior continuation
of the nodal bundle axis, at the base of the tricuspid valve (TV)
leaflet (arrow), shows a nodelike configuration, as described for
Kent nodes.19 It is obvious from this micrograph that the area
involved is no longer AV septal junctional but rather posteroinferior free wall. B, The higher magnification of this posterior extension shows the nodelike arrangement of the fibers within this
tract. Hematoxylin-eosin stains. Bar51 mm.
192
Posterior AV Nodal Extensions in Humans
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anteriorly both merged with the half oval of compact nodal
cells. They probably represent the deep and superficial nodal
segments described by Truex and Smythe.14 –16 The observation
of a posterior tract in close proximity to the tricuspid annulus
raised discussions concerning whether those extensions represented a tract of cells described by James17 and considered to
run from the posterior “internodal tract” to the His bundle,
thus bypassing the compact AV node. We refuted this concept
at the time, and our present extended observations endorse this
viewpoint. The extensions always originated from the posterior aspect of the compact AV node and never from the
anterior part or from the His bundle.
It is a bit embarrassing that the discussions concerning the
possibility of AV nodal bypass tracts at the time took away
further interest in the potential significance of these peculiar
extensions. It is because of more recent electrophysiological
studies in humans, particularly those related to AV nodal
reentrant tachycardias, that interest has been revived. It has
been shown that part of the reentrant circuit is likely to be a
slow pathway. In addition, the area to ablate this slow pathway
is considered to be underneath or slightly anterior to and below
the anterior margin of the mouth of the CS.7–9 Thus far,
however, a true pathway has not been shown, either electrophysiologically or morphologically.
In an experimental study performed in isolated, blood-perfused
porcine and canine hearts, designed to identify the origin of
double potentials in Koch’s triangle, McGuire and colleagues18
provided evidence that the low-frequency component that followed a large-amplitude, high-frequency component was caused
by depolarization of nodal or conduction-type tissue. They
suggested that this tissue could represent the anatomic substrate of
the slow AV nodal pathway. This concept was endorsed by the
fact that the site of their recordings coincided with the site of the
slow pathway, as demonstrated by mapping and ablation studies in
humans.7–9,19–21 It is of considerable interest, therefore, that the
compact AV node and its posterior extensions, once superimposed onto the slope of the muscular AV septum within the
confines of Koch’s triangle, colocalize with the sites of double
potential recordings and with the area of slow pathway ablation.
Our anatomic observations suggest, therefore, that the posterior
extensions could take part in the reentrant circuit in patients with
AV nodal reentrant tachycardia. If so, and if the posterior
extensions do represent the anatomic substrate for a slow pathway
defined electrophysiologically, the implication is that the slow AV
nodal pathway basically fits within the natural variability of an
anatomically normal compact AV node.
Developmental Considerations
The observation that posterior extensions of the compact part
of the AV node are a regular feature of AV nodal anatomy is
also of considerable interest once put into the perspective of
AV nodal development. It is presently acknowledged that the
AV conduction tissues develop from a “specialized” myocardial ring that, in the early human embryo, encircles the
interventricular foramen.22 At this stage (5 weeks’ development), the AV canal is still positioned over the presumptive left
ventricle. At subsequent stages (6 to 7 weeks’ development),
the AV canal expands toward the right, thus enabling the right
atrium to directly contact the developing right ventricle.
During this process, the ring of “specialized” myocardium
moves with the rightward expansion of the AV canal and, once
fully developed, encircles the right AV junction along the
lower rim of the right atrium. The larger part of this right AV
ring is considered to disappear, with only the compact part of
the AV node and the AV (His) bundle remaining in the normal
heart. At the same time, the concept of a single interventricular
ring could explain why hearts with abnormal septation or
abnormal expansion of the right AV orifice, such as hearts with
a straddling tricuspid valve, contain an AV node and bundle in
an unusual position. Similarly, the “atriofascicular” tracts that
connect the right atrium to the right ventricle, exhibiting
Mahaim physiology, may well find their origin in so-called
Kent nodes that are considered to represent the remnants of the
ring tissue. Indeed, Kent nodes confined within the atrial
tissues, which have been shown to be a regular finding in
normal hearts,23 may fit the same concept. Along the same lines
of thought, one may anticipate that the posterior extensions of
the compact part of the AV node, as described in the present
study, reflect the remains of the ring tissue alluded to above.
Indeed, the nodelike structure found in one of our hearts (see
Fig 7) closely resembles a Kent node, as previously discussed.11
Our present observations thus appear to be endorsed by the
current concepts of AV conduction development.
Study Limitations
An obvious limitation of the present study is that we have not
been able to study hearts with documented AV nodal reentrant
tachycardias. As far as we are aware, two case reports exist24,25
that provide a histological description of the site of slow
pathway ablation, each in a patient with clinically successful
ablation. In both instances, the site of ablation was readily
identified and localized posterior to the AV node. These
observations have been claimed to refute the concept that the
AV nodal reentrant circuit is entirely intranodal. This may well
be correct, but because the posterior extensions of the AV
node are not mentioned, one should not therefore deny the
possibility that such extensions could have been part of the
slow pathway. Indeed, one may envision that part of the
reentrant circuit is formed by the posterior AV nodal approaches and that the “burn” has destroyed the approach rather
than the “slow pathway” in the strict sense. In this context, it
may be of interest to refer to an electrophysiological study
performed in patients enrolled for cardiac transplantation.26
None of the patients reported in that study had AV nodal
reentrant tachycardia, but dual AV nodal pathways could be
documented in all patients before transplantation. Histological
evaluation of these hearts did not reveal any departure from
normal, although no further specifications are provided with
respect to the posterior extensions as discussed in the present
study.
It is our opinion, therefore, that the posterior extensions of
the compact AV node in humans could provide part of the
reentrant circuit of AV nodal reentrant tachycardia, although
we readily admit that we have no definitive proof for such a
statement. Nevertheless, it is a tempting concept, particularly
because it could take further research into mechanisms underlying AV nodal reentrant tachycardia away from attempts to
identify an “abnormal pathway.”
Inoue and Becker
Acknowledgment
During the course of this study, Dr Inoue was a research fellow from
the Showa University Hospital, Showa University School of Medicine, Tokyo, Japan.
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Posterior Extensions of the Human Compact Atrioventricular Node: A Neglected
Anatomic Feature of Potential Clinical Significance
Shin Inoue and Anton E. Becker
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Circulation. 1998;97:188-193
doi: 10.1161/01.CIR.97.2.188
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