Discussion
Two of the leading concepts of mural ventricular architecture are the
unique myocardial band and the myocardial mesh
model(1). Torrent-Guasp suggested the presence of the
ventricle walls act as a continuous myocardial bar, which runs from the
root of the pulmonary trunk to the root of the
aorta(1). The sculpted muscle fascia of the
ventricular mass was maintained to form two rings (basal and apical),
which surround the two ventricular cavities. Presumably there are split
planes or sliding surfaces between these segments, which allow parts of
the band to move over each other(1). As we know,
aortic dissection occurs when an injury to the innermost layer of the
aorta allows blood to flow between the layers of the aortic wall,
forcing the layers apart. The point of entry and return of dissection
are usually distant. If the blood-filled false lumen breaks through an
outward weakness, it creates a spill point. This mechanism occurs due to
the layered nature of the aorta. Thus, if the concept of the unique
myocardial band were true, logically in cases of a ruptured left
ventricle, the entry point and the exit point should be spaced apart.
Instead the classification of a ventricular rupture between the mitral
ring and papillary muscles during the replacement of the mitral valve
shows that the rupture is close to the initial point of trauma. In one
case report we previously presented(8), it can be
verified that the ventricle rupture entry and exit points are positioned
face to face (figura2). I think this observation could favour the
myocardial mesh model concept in which the myocardium is represented as
a continuous 3D meshwork that has no large-scale
subdivision(1).
The shape of the left ventricle approximates to that of a cone with the
right ventricle almost seeming to embrace it. Consequently, the septal
component of the ventricular wall is curved. Normally, the left
ventricular free wall is thicker at the cardiac base and it gradually
becomes thinner moving towards the apex. At the very tip of the
ventricle, the musculature is only 1–2 mm thick, even in hypertrophied
ventricles(2). On the other hand, if the concept of a
unique band were realistic, then the exit point of the rupture of the
left ventricle, following a lesion of the free wall under the mitral
valve, should appear at the level of the ventricular apex where it is
thinnest. In fact for many years the classification of left ventricular
rupture has been limited to levels above the papillary
muscles(3). It might be thought that the thickness of
the left ventricle could be a protective factor from ventricular
rupture, but in reality, the rupture of the left ventricle following MVR
has been described at the thickened part of the free wall of the left
ventricle above the papillary muscles.
However, whatever the composition of the wall of the ventricles, the
complex architecture, that connects the ventricular wall with the
fibrous skeleton of the heart through the papillary muscles, the cords
and the leaflets of the valves, support the ventricle wall during the
cardiac cycle. It has been demonstrated that the loss of
annulo-ventricular continuity still leads to progressive left
ventricular dilatation with eventual decline of left ventricular
function in the long-term(4). The role of the
secondary (strut) chordae was determined to maintain the left
ventricular geometry and function. Therefore, the secondary chordae are
placed centrally within the subvalvular apparatus to ensure the force
transmission and geometric stability of the left
ventricle(5). Hansen demonstrated that transection of
chordae to the anterior mitral leaflet (AML) reduced the left
ventricular function to a greater degree compared to the transection of
chordae to the posterior mitral leaflet (PML)(6).
In fact, as we have learned from mitral surgery, the posterior left
ventricular (LV) wall is exposed to iatrogenic trauma. Thus, during
mitral valve repair or replacement, the surgeon pays meticulous
attention to the possible occurrence of ventricular ruptures that mostly
involve the posterior left ventricular wall. Particularly, the
mechanical injury levied at the sites of papillary muscles (PM),
especially during mitral valve replacement (MVR) performed under
ischaemic arrest with a flaccid heart, can be responsible for left
ventricular rupture(7).
Nevertheless, the myomectomy of the In-S, which is itself a myocardial
trauma, has been used for 50 years with no, or few, descriptions of
surgery-induced ruptures or inter-ventricular defects.
Left ventricular rupture after MVR is classified into three types,
according to its variable location between the atrioventricular groove
and the base of the PM(3). We introduced the concept
of a fourth type of rupture (type IV), that could be located at the site
between the base of the PM and the left ventricular apex which can be
the consequence of the ventricular access required to apply new
procedures as we pointed out in one of our previous
works(8). Depending on the time of the tear appearance
post surgery, left ventricular rupture has been also categorized as
immediate, delayed, and chronic. Chronic tears occur days to years after
MVR and share clinical and morphologic aspects with left ventricular
pseudo-aneurysm(8), and this confirms that the rupture
starts as an endocardial break. Thus, the iatrogenic trauma of the left
ventricular endocardium may be the initial phase of the wall rupture
process.
From a surgical point of view, Cobbs considered the mitral valve as a
morphological and functional unit, called “the
mitral-loop”(3). It includes two arms: the inner arm,
composed of the PMs, the cords and the leaflets, which is a
longitudinally coursing loop connected at both ends to the mitral
annulus; the outer arm of this loop, consisting of longitudinal muscle
fibres and the wall of the left ventricle, superiorly fixed to the
mitral annulus. Cobbs’ “untethered ventricle” theory suggests that
spontaneous rupture of the left ventricle could occur in some patients
following excision of the posterior leaflet and the PM, creating an
”untethered loop”(3). The Cobbs theory is very
remarkable and was supported by others, for example Ross’ and Streeter’s
“Letter to the Editor”(3). It is well known that
preservation of the mitral valve posterior leaflet is the basic
requirement to avoid serious complications. Respecting this pivot of
mitral surgery has led to a dramatic reduction of left ventricular
rupture cases reported in the literature. This supports the idea that
iatrogenic trauma to the left ventricular endocardium and the
”untethered ventricle” could both contribute to the rupture of the left
ventricle free wall.
As an extension of this theory, observing the anatomy of the heart, two
other loops divided by the septum could be envisaged (fig.1). First, the
left loop: the outer arm formed by the ventricular apex, PMs, cords,
anterior leaflet and anterior annulus between the trigons. The septal
arm (central arm) of this loop consists of the mitro-aortic continuity,
the aortic valve and the inter-ventricular septum. Secondly, the apex of
the right ventricle, the septal portion of the tricuspid annulus and the
tricuspid septal leaflet form the right loop of the outer arm. The
septal arm (central arm) of this loop consists of the inter-ventricular
septum.
Therefore, it can be hypothesized that the In-S is supported
longitudinally during diastole by these two loops on both sides, right
and left, and that this support is missing in the free wall of the left
ventricle.
On the other hand, dilation in the transverse plane of the left
ventricle at the level of the In-S results from a combination of various
factors. Septal motion originates from the blood pressure applied on the
right and left sides of the In-S, as well as the active tension and the
intrinsic stiffness of the tissue itself. Thus, during the cardiac
cycle, the In-S is affected by the stress of the different pressures and
volumes in the right and left ventricles. The changes in the diastolic
curvature of the In-S, from a slight flattening to a complete inversion
towards the left ventricle, determined by the right ventricle volume
overload(9), demonstrate the presence of a direct
cross-sectional support of the right ventricle to the In-S. A similar
support to the LV free wall is lacking, particularly after opening the
pericardium. However, in the presence of hypertrophic obstructive
cardiomyopathy, the end-diastolic dimension is lower than the ‘normal’,
even at full ventricular filling which may be particularly due to In-S
and ventricular wall thickness .
Histological analysis of tissue from patients with hypertrophic
obstructive cardiomyopathy (HOCM) show muscle fibre disarray that is
absent in normal subjects. This histopathology typically involves more
than 10% of the myocardium, is widely distributed and typically
localized to the hypertrophied inter-ventricular
septum(10). The myomectomy procedure thins the In-S,
increasing its elasticity compared to the rest of the ventricular wall.
During end diastole, the dissected zone of the septum should undergo
further tension with increased diastolic stress on the ventricle. It is
possible that this stress exposes the thinner septum to the risk of a
subsequent rupture, which could lead to a ventricle septal defect, a
rare eventuality, as the majority of the reports in the field. This
might support the hypothesis that the longitudinal support, described
above, is pivotal in giving the resistance to the surgical trauma caused
by myomectomy. In cases where this longitudinal support is impaired,
right ventricular volumes become responsible for cross sectional support
of the inter-ventricular septum.
Obviously, further studies focused on for example hemodynamics and
exploiting new accurate imaging technologies are required to demonstrate
this theory.