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Invited article
 (0.6M)
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McCarthy KP*, Ho
SY**, Anderson RH***. Ventricular Septal Defects: Morphology of the Doubly
Committed Juxtaarterial and Muscular Variants. Images Paediatr
Cardiol 2000;4:5-23 |
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*
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Senior Research Technician, Institute of Child
Health, University College London, Cardiac Unit, 30 Guilford Street, London
WC1N 1EH |
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**
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Reader in Cardiac Morphology, National Heart
& Lung Institute, Imperial College, Paediatric Cardiac Morphology,
Dovehouse Street, London SW3 6LY |
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***
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Joseph Levy Professor of Paediatric Cardiac Morphology, Institute
of Child Health, University College London, Cardiac Unit, 30 Guilford Street,
London WC1 1EH |
| MeSH |
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|
| Heart septal defects,
ventricular |
Heart defects, congenital |
Heart ventricle/pathology |
| Heart ventricles/abnormalities |
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Abstract
In our previous review of the phenotypic features of ventricular septal
defects, we concentrated on the perimembranous variant, showing how its
distinguishing feature, as viewed from the right ventricle, was fibrous
continuity in its postero-inferior rim between the leaflets of the aortic
and tricuspid valves. In this second review, we focus on the morphology
of those defects which have exclusively muscular rims when viewed from
their right side, and the variant with the phenotypic feature of fibrous
continuity between the leaflets of the two arterial valves. As with the
defects described as being perimembranous, once they have been characterised,
it is the position of the defect relative to the components of the morphologically
right ventricle that is the primary determinant of the options and strategies
for treatment. Therefore, clarification of the morphology is the key to
establishing the related risks for each particular defect.
Article
Introduction
In our first review,1 we emphasised the
phenotypic feature of the type of ventricular septal defect which is defined
as being perimembranous within the classification now established by the
Association for European Paediatric Cardiology.2-3 At the same
time, we highlighted the potential anatomic discrepancies that exist between
this classification and the one promoted by The Society of Thoracic Surgeons.4
The defect characterised by fibrous continuity between the leaflets of
the arterial and atrioventricular valves, however, although the type most
frequently encountered during surgical repair, is just one of the anatomical
variants of the holes which can be found between the ventricles. In this
review, we describe the phenotypic features of the other two anatomic possibilities.
These are defects which have an exclusively muscular rim when viewed from
their right ventricular aspect, and those defects which have fibrous continuity
between the leaflets of the aortic and pulmonary valves. As with the perimembranous
defect, understanding the system of classification is greatly facilitated
by knowledge of the structure of the normal ventricular septum. Our review
will commence, therefore, by revisiting the normal morphology, paying particular
reference to the features that are of importance in appreciating defects
with exclusively muscular rims, and those roofed by fibrous continuity
between the leaflets of the arterial valves.
The normal ventricular septum
The ventricular septum in the normal heart is mostly muscular. Only
a small part, which is integrated into the aortic root, is made of fibrous
tissue. This fibrous component is the so-called membranous septum.5
It is located inferiorly to the inter-leaflet triangle that fills the space
between the ascending hinges of the non-coronary and right coronary leaflets
of the aortic valve (Fig.1).
Figure 1: The membranous septum is found at the base of the
inter-leaflet triangle which interposes between the right coronary and
non-coronary leaflets of the aortic valve
| When transilluminated from the right atrioventricular aspect, it can
be seen, in most cases, to be crossed by the hinge of the tricuspid valve,
thus dividing it into atrioventricular and interventricular components.
It is then the position of the hinge which determines the proportions which
are atrioventricular as opposed to interventricular6 (Fig.2). |
Figure 2: Trans-illumination from the left ventricle shows how
the right atrioventricular aspect of the membranous septum is crossed by
the hinge of the tricuspid valve. This divides it into an atrial and ventricular
components. The conduction axis penetrates through the atrioventricular
part of the septum.
|
| The atrioventricular component of the septum is itself pierced by the
atrioventricular conduction axis as it passes from the apex of the triangle
of Koch to reach the crest of the muscular septum.5. Our first
review emphasised that the normal ventricular septum “came apart” between
its muscular and fibrous components in the presence of a defect which had
fibrous continuity between the leaflets of the arterial and atrioventricular
valves. With the exception of hearts with straddling and overriding of
the tricuspid valve, this feature explains why the conduction axis is always
found in postero-inferior position when these perimembranous defects are
found in the setting of concordant atrioventricular connections (Fig.3). |
Figure 3: A perimembranous septal defect, showing the fibrous
postero-inferior rim of the defect penetrated by the conduction axis
|
In terms of the variants seen with this particular lesion, the arrangement
of the muscular septum, and particularly its relationship with the free-standing
muscular subpulmonary infundibulum, are of crucial importance, as deficiencies
of the muscular septum can be found opening to different parts of the right
ventricle. To differentiate between these various defects, therefore, we
find it helpful to relate their location relative to the components of
the right ventricle, namely its inlet, outlet, and apical trabecular parts.
As we will see, defects with exclusively muscular rims can also open into
any of these components. In the normal heart, however, it is incorrect
to imagine that the subpulmonary outlet component is separated from the
subaortic outlet of the left ventricle by a discrete muscular septum, albeit
that this is the impression given in some earlier works.7 In
reality, in the normal heart, the leaflets of the pulmonary valve are supported
by a sleeve of free-standing muscular infundibulum (Fig.4).
Figure 4: A normal heart showing the relationship of the great
arteries. The pulmonary trunk is lifted away from the base of the heart
by a free-standing muscular infundibulum
| This sleeve lifts the leaflets of the pulmonary valve away from the
base of the ventricular mass. A discrete extracardiac tissue plane is to
be found between the offset hinges of the two arterial valves which contains
fibroadipose tissue, and which separates the posterior aspect of the subpulmonary
infundibulum from the aortic valvar sinuses. This arrangement continues
to be seen in anomalies such as tetralogy of Fallot (Fig.5). |
Figure 5: The attachment of the hinge points ( blue dots) of
the aortic (Ao), and the pulmonary valves (PV), are off-set, with
an extracardiac tissue plane separating the two arterial trunks. The situation
is illustrated here in the setting of tetralogy of Fallot
|
Appreciation of this arrangement is particularly important for those seeking
to understand the structure of the defect which is roofed by fibrous continuity
between the leaflets of the two arterial valves. In fact, this defect,
which we describe as being doubly committed and juxtaarterial, cannot exist
in the setting of the normal heart. It has far more in common with hearts
possessing a common arterial trunk than it does with those having normal
outflow components.8
Overall classification of ventricular
septal deficiencies
|
The key feature when distinguishing between defects,
as we emphasised in our first review,1 is to identify the right
ventricular borders of the septal deficiency.9 We choose this
viewpoint since this is now the most frequent approach taken by the surgeon
during surgical correction, albeit often seen through the tricuspid valve.
On this basis, any hole between the ventricles can be placed into one of
three categories. The majority possess, as their hallmark, fibrous continuity
between the leaflets of the aortic and tricuspid valves in the postero-inferior
rim of the defect (Fig.6).
|
Figure 6: It is continuity between the leaflet of the aortic
and tricuspid valves in the postero-inferior margin which is the hallmark
of a perimembranous ventricular septal defect
|
These are the defects we describe as being perimembranous.
The second group has in common the fact that the defects within it have
entirely muscular borders, regardless of their position relative to the
components of the right ventricle. The third group of defects is characterised
by fibrous continuity between the leaflets of the two arterial valves,
or else the presence of a common truncal valve. With such defects, which
we call doubly committed and juxtaarterial, there is usually a muscular
bar postero-inferiorly that separates the hinges of the leaflets of the
aortic and tricuspid valves, or else interposes between the truncal and
tricuspid valves. An important variation seen with these doubly committed
defects, however, is for the septal deficiency to extend postero-inferiorly
to abut on the area of fibrous continuity between the arterial and atrioventricular
valves, thus making the defect also perimembranous.
Characteristics of muscular ventricular
septal defects
Muscular defects can exist at any location within
the septum (Fig.7). They can be multiple, or can co-exist with perimembranous
or doubly committed defects, and their size can vary considerably. Their
phenotypic feature, nonetheless, is the presence of exclusive muscular
boundaries as seen from the right ventricle, even when there is overriding
of the leaflets of an arterial valve (Fig.8).
Figure 7. This diagrammatic representation shows the possible
locations of muscular ventricular septal defects, and their relationship
to the conduction axis.(TV= tricuspid valve, PV= pulmonary valve)
|
Figure 8: When viewed from the right ventricle, this ventricular
septal defect has a complete muscular rim, despite the overriding of the
aortic valve
|
Defects that open to the inlet of the ventricle
are closely related to the septal leaflet of the tricuspid valve (Fig.9-10).
Figure 9: Both of these ventricular septal defects are closely
related to the tricuspid valve. This shows the right ventricular aspect.
( PV= pulmonary valve, P-VSD= perimembranous ventricular septal defect)
|
Figure 10: From the left ventricular aspect, the defect under
the mitral valve (MV) is seen to have a muscular rim. This other defect
is perimembranous ventricular septal defect (P-VSD) being roofed by fibrous
continuity between the aortic valve (Ao) and the atrioventricular valves
|
Those opening between the apical trabecular components
of the ventricles can take various forms and guises. The apical muscular
septum itself is covered on its right ventricular aspect by a coarse meshwork
of apical trabeculations. These include the moderator band, which arises
as one of a series of septoparietal trabeculations from the prominent septomarginal
trabeculation (Fig.11).
Figure 11: This view of the right ventricular aspect of the
normal heart shows
the septomarginal trabeculation, which gives rise to the moderator
band
The presence of these trabeculations influences markedly
the nature of deficiencies within the apical muscular septum. Those defects
which are large and solitary are usually seen in mid-ventricular position,
located either immediately posterior to (Fig.12) or anterior (Fig.13) to
the body of the septomarginal trabeculation.
Figure 12: This muscular ventricular septal defect is posterior
to the septomarginal trabeculation
Figure 13: This muscular ventricular septal defect is anterior
to the septomarginal trabeculation
Defects opening to the right ventricle anterior to
the septomarginal trabeculation, but located closer towards the ventricular
apex, however, are often crossed by the septoparietal trabeculations. In
other instances, an apical defect can be crossed by the septomarginal trabeculation
itself. Because of this, the obviously solitary defect as seen from the
left ventricle (Fig.14) can have multiple openings as viewed from the right
ventricle (Fig.15).
This is the structure that is removed by the surgeon
when preparing the pulmonary autograft for use in the Ross procedure. The
very fact that the pulmonary valve can be removed in this manner (Fig.17)
shows clearly that the infundibulum has no relationship with the apical
component of the septum. Although we differ with regard to the definition
of the “infundibulum”, the points of clinical significance made with relation
to these defects are of considerable importance. Thus, unless the presence
of multiple right-sided orifices, but with a solitary left-sided opening,
is appreciated, then complete surgical repair can be difficult, with the
potential for leaving residual defects.11
Figure 17. The pulmonary trunk has been resected in this normal
heart, along with the free-standing muscular infundibulum. The dissection
has not encroached upon the cavity of the left ventricle
|
Although in this case the defect is strictly a solitary
hole, other variants, particularly towards the apex can exist. The apical
muscular septum can be sponge-like, and truly multiple defects produce
the so-called “swiss-cheese” septum. This represents failure of compaction
of the apical septum, such that multiple tracks now persist between the
ventricles. As a result these defects can also pose significant problems
for complete surgical repair. The final type of muscular defect is the
one that opens to the right ventricular outlet. This can take the form
of a defect, usually small, which opens immediately beneath the free-standing
muscular subpulmonary infundibulum (Fig.18). Alternatively, muscular outlet
defects can be associated with overriding of the leaflets of the aortic
valve, either in the setting of tetralogy of Fallot (Fig.19), or with an
unobstructed subpulmonary outlet (Fig.20).
|
Figure 18: An outlet muscular defect, showing its relationship
to the pulmonary valve (PV)
|
Figure 19: A heart with tetralogy of Fallot, with overriding
of the aortic valve (Ao), which is connected to both ventricles, and separated
from the tricuspid valve (TV) by a muscle bar of the septomarginal trabeculation
(SMT)
|
Figure 20: This specimen has deviation of the of the muscular
outlet septum, but with an unobstructed pulmonary outflow tract
|
|
When categorising these defects, it is important
to appreciate that, although the direct extension of the plane of the muscular
ventricular septum transects the leaflets of the overriding arterial valve,
with part of the aortic valve unequivocally supported by right ventricular
structures, (Fig.21) the septal defect still has exclusively muscular borders
when viewed from its right ventricular aspect (Fig.22). Significantly,
a well-formed muscular bar interposes between the leaflets of the aortic
and tricuspid valves, thus providing protection for the branching components
of the atrioventricular conduction axis (Fig.23).
|
Figure 21: Sectioning the heart shown in Fig.20 reveals that
the aortic valve overrides the crest of the ventricular septum
|
Figure 22: Viewed from the right ventricular aspect, the defect,
seen in Figs. 20 & 21, has a complete muscular border
|
Figure 23: The section shows the muscular bar which separates
the aorta (Ao) from the tricuspid valve (TV), thus protecting the conduction
bundle
|
It is proper recognition of the location of the
muscular defects relative to the septomarginal trabeculation that provides
the information necessary to predict their relationship relative to the
ventricular conduction tissues. Inlet defects are posterior and inferior
to the conduction axis, but can be closely related to the conducting bundles
if positioned adjacent to the medial papillary muscle. Apical defects posterior
to the septomarginal trabeculation are also behind the right bundle branch,
which descends within the substance of the septomarginal trabeculation.
Those anterior to the trabeculation, and those opening to the right ventricular
outlet, are in front of the bundle. Although such defects are well distant
from the branching bundle, it is important to respect the integrity of
the septomarginal trabeculation. This is because trauma to the right ventricular
aspect can produce haemorrhage that can track along the insulating sheath
surrounding the right bundle branch.12 Such haemorrhage and
oedema can then infiltrate the more proximal segments of the conduction
axis, with the potential to produce complete atrioventricular block. With
defects that open to the ventricular outlet, it is the size of the muscular
bar interposing between the leaflets of the aortic and tricuspid valves
that is the key feature relative to the vulnerability of the conduction
tissues. When substantial, sutures can be inserted within the musculature
without fear of damaging the conducting bundles. If flimsy, however, then
sutures could pass directly into the conduction axis and induce iatrogenic
heart block.
Characteristics of doubly committed
and juxtaarterial ventricular septal defects
|
As we have emphasised, in the right ventricle of
the normal heart, the leaflets of the pulmonary valve are supported by
the sleeve of free-standing subpulmonary infundibulum (Figs.4,17). This
raises the valve away from the body of the right ventricle, and also separates
it from the leaflets of the aortic valve (Fig.24). The essence of the doubly
committed defect, however, is fibrous continuity between the leaflets of
the aortic and pulmonary arterial valves, which are now at the same level
in the roof of the defect (Figs.25). Due to the semilunar nature of their
hinges, the leaflets can be offset to some degree if one of the aortic
sinuses is wedged between two of the leaflets of the pulmonary valve (Fig.26).
|
Figure 24: In the normal setting, and seen here in tetralogy
of Fallot, the arterial valves are separated by a free standing muscular
infundibulum, so the hinge-point attachment of the pulmonary valve (PV)
is raised away from the aortic root.(Ao)
|
Figure 25: With doubly committed defects, the arterial valves
are at the same level, with fibrous continuity between the leaflets of
the aortic and pulmonary valves
|
Figure 26: Although this defect is doubly committed, the arterial
valves are still off-set
|
So the doubly committed defect, therefore, exists
where there is absence of formation of a completely muscular infundibulum
within the right ventricle. Because of this lack of infundibulum, the orifice
of one (Fig.25), or sometimes both (Fig.26), of the arterial valves can
override the crest of the ventricular septum.
| This is the arrangement seen with common arterial trunk, in which the
septal defect is again doubly committed and juxtaarterial (Fig.27). |
Figure 27: By its very nature, the defects seen with common
arterial trunk, is doubly committed and juxtaarterial, and is seen here
arising overriding the venticular septum
|
|
Typically, the common trunk arises astride the ventricular
septum, with the septal defect having exclusively muscular rims as seen
from its right ventricular aspect (Fig.28). With all these defects, the
key to the vulnerability of the conduction axis is once more the nature
of the postero-inferior rim. Usually this is muscular, and providing the
muscle bundle is substantial (Figs. 28,29), it will protect the conduction
axis. Should the muscular tissue become attenuated, or disappear, so that
the doubly committed defect extends to become perimembranous, (Fig.30)
then the conduction axis is at risk in the postero-inferior margin.
|
Figure 28: In this heart with common trunk, there is a muscular
postero-inferior rim (yellow dots), separating the truncal valve from the
tricuspid valve
|
Figure 29: The postero-inferior rim of the defect is usually
muscular in doubly committed defects
|
Figure 30: In contrast, the doubly committed defect in this
heart extends to become perimembranous, with fibrous contunity between
the leaflets of the aortic and tricuspid valves, as well as between the
aortic and pulmonary valves
|
The doubly committed defect is frequently encountered
in Asian countries.13 The crucial phenotypic feature of this
defect is the altered morphology of the arterial trunks with respect to
the normally structured heart. This defect can only exist in absence of
the “septal” component of the free-standing infundibular sleeve which normally
supports the pulmonary trunk, a trait seen in hearts with common arterial
trunk. It is no coincidence, therefore, that both these lesions are found
in the setting of 22q11 deletion, pointing to their similar genetic background
which itself is more prevalent in far-Eastern populations. 8, 14,15
Associated features
The likelihood of spontaneous closure of any ventricular septal defect
depends largely on its location. It is usually thought that the majority
of defects that close are perimembranous, followed by muscular defects.
It is also likely that many small muscular defects do not come to the attention
of the cardiologist, the defects being present during fetal life, yet closing
during the neonatal period 16 and first year of life.
Similarly, the classical murmur of the “maladie du Roger” is probably
due to small, isolated, muscular defects that close with time. In contrast,
defects sufficiently large enough to warrant referral to a tertiary centre,
show no correlation between the probability of closure and the size of
the defect. Thus, Du et al 17 found solitary muscular defects
were larger than multiple ones, yet the former were more likely to close
spontaneously. Large defects found in the apical region of the septum are
most likely to remain open. Conversely, spontaneous closure of doubly committed
defects is not at all common.18 When it does occur, it is due
to prolapse of the aortic valve leaflets, so it is not necessarily a good
thing.
In this respect, the timing of surgical or interventional
repair to prevent prolapse of the relatively unsupported leaflets of the
arterial valves is of the essence. The intense mechanical stresses due
to a high-pressure environment at the ventriculoarterial junction greatly
increase the risk of prolapse of the leaflets of the aortic valve. The
valvar tissues become exposed to increased velocities, and are then subject
to progressive mechanical weakness. The uncertain integrity of the arterial
valves, leads many centres to recommend early surgical treatment of the
doubly committed defect.(19-21 ) In the extensive study
by Tohyama and colleagues,(22) it was noted that seven-tenths
of patients aged up to 35 years developed prolapse of the aortic valve,
all involving the right coronary leaflet, and a third of the total developed
overt aortic regurgitation. Early diagnosis and repair of the doubly committed
defect has been suggested to prevent the onset of aortic regurgitation.
Offsetting of the arterial valves has also been thought to be a factor
in the formation of aneurysm of the right coronary sinus of Valsalva.
Conclusion
The most common congenital cardiac lesions are holes
between the ventricles. These can exist at any location within the muscular
septum, and can be viewed as opening into any part of the right ventricle.
When attention is paid to the borders of the hole as viewed from the right
ventricle, then all defects can be placed in one of three phenotypic groups.
Early diagnosis for such defect using echocardiography is now routine,
even in early fetal life.23 The phenotypic features we have
suggested for diagnosis are just as valid in this setting as in postnatal
life. With exact fetal diagnosis, it will almost certainly prove possible
to identify those defects that are the most likely to close, as opposed
to those which will require interventional or surgical treatment. For those
requiring treatment, use of this information for anatomic categorisation
permits an accurate assessment of any individual defect relative to the
atrioventricular conduction axis, knowledge that is essential to the surgeon
in order to achieve successful closure without fear of inducing atrioventricular
block. Thus, proper diagnosis, particularly of the doubly committed defect,
should now be the prelude to timely successful management, and hopefully
a normal post-interventional or post-operative outcome.
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