Download Anatomy and myoarchitecture of the left ventricular wall in normal

European Journal of Echocardiography (2009) 10, iii3–iii7
doi:10.1093/ejechocard/jep159
Anatomy and myoarchitecture of the left ventricular
wall in normal and in disease
Siew Yen Ho*
Cardiac Morphology Unit, Imperial College London, Royal Brompton Hospital, London, UK
KEYWORDS
Anatomy;
Myocardium;
Myoarchitecture;
Ventricular function
The normal left ventricle comprises an inlet, apical trabecular, and an outlet portion although these
portions do not have discrete anatomical borders. The ventricular wall is thickest near the cardiac
base and thins to 1–2 mm at the apex. Characteristically, the muscle bundles at the apical portion
are thin, but there are also thicker bundles and very fine strands that may be mistaken on imaging as
pathologies. Transmurally through the ventricular wall, the myoarchitecture has a typical arrangement
of myocardial strands that change orientation from being oblique in the subepicardium to circumferential in the middle and to longitudinal in the subendocardium. The circumferential portion is the thickest
with the longitudinal portion the thinnest. In the hypertrophied ventricle the circumferential portion is
reduced. In combination with alterations in the quality and quantity of the connective tissue matrix,
myoarchitecture impacts on myocardial function.
Introduction
This review focuses on the myocardial component of the left
ventricle, leaving aside the aortic and mitral valves. First,
the muscular structures and normal variants within this
chamber are described and then the potential misinterpretation of normal structures is discussed. Secondly, the orientation of the myocardial strands in the normal and abnormal
left ventricle is reviewed together with a consideration of
the connective tissue matrix of the myocardium.
Anatomy of the left ventricle
The normal left ventricle comprises an inlet portion containing the mitral valve apparatus, an outlet portion leading to
the aortic valve, and an apical portion containing fine trabeculations (Figure 1). From a simplistic viewpoint, the shape
of the left ventricle approximates to a cone with the right
ventricle hugging it. Consequently, the septal component
of the ventricular wall is curved. Thus, when the heart is
viewed from the anterior aspect, most of the left ventricle
is hidden by the right ventricle. Furthermore, the left ventricular outlet overlaps the inlet. Normally, the left ventricular free wall is thickest at the cardiac base and it
gradually becomes thinner towards the apex. At the very
tip of the ventricle, the musculature is only 1–2 mm thick,
even in hypertrophied ventricles (Figure 2). The normal
thickness at the obtuse margin of the left ventricle for an
adult heart is 12–15 mm, excluding trabeculations, when
* Correspondending author: Tel: þ44 207 351 8751, fax: þ44 207 351 8230.
E-mail address: [email protected]
measured approximately 1.5 cm below the mitral hingeline
(annulus). The endocardial aspect of the ventricle is characterized by a criss-crossing meshwork of thin muscle bundles
(trabeculations) at the apical third of the ventricle. Not
infrequently, fine muscular strands or so-called false
tendons extend between the septum and the papillary
muscles or the parietal wall (Figure 2). Autopsy series of
normal hearts have reported an incidence of 55 and
62%.1,2 On echocardiography they may be mistaken for ruptured chords of the valve apparatus or vegetations. In contrast, the outlet portion of the septum is relatively smooth
whereas relatively thick muscle bundles line the anterosuperior, postero-inferior, and posterior walls (Figure 2).
The latter, described as numbering three or fewer, are
normal structures that when prominent may cause overdiagnosis of non-compaction of the left ventricular myocardium on echocardiography.3 The pathological entity of
non-compaction cardiomyopathy, or spongy myocardium, is
characterized by prominent and excessive trabeculations
with correspondingly deep recesses in between within the
hypertrophied wall.4,5 The left ventricular wall most frequently affected is the apical, mid-lateral, and mid-inferior
portions.6–8 On heart specimens the affected segments have
two components transmurally: a thin compact, or normal,
layer in the subepicardium and a thicker subendocardial
layer of trabeculations with deep recesses giving a
thickness ratio of approximately 1:2. It remains unclear
whether non-compaction is a distinct entity from hypertrabeculation where there are more than three prominent trabeculations and is often associated with extracardiac
disorders.9
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2009.
For permissions please email: [email protected].
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S.Y. Ho
Figure 1 (A) and (B) Two parts of the same heart sectioned longitudinally. The broken lines divide the left ventricle into three portions. Note the cross-over relationship between right and left
ventricular outflow tracts and the smooth upper part of the ventricular septum leading to the aorta. RVOT, right ventricular outflow
tract
The ventricular septum in the normal heart is curved, convexing into the right ventricular cavity. It is muscular except
for a small portion immediately beneath the aortic valve
which is a thin fibrous structure, the ventricular component
of the membranous septum. Together with the right fibrous
trigone, this thin component forms the central fibrous body
that encases the atrioventricular conduction bundle and is
an anatomical landmark for the emergence of the conduction bundle onto the crest of the muscular septum
(Figure 2). Over the age of 60 years, there is an increase
in angulation of the basal part of the muscular septum, producing a sigmoid appearance on imaging that can produce
features of hypertrophic cardiomyopathy.10,11
The papillary muscles supporting the mitral valve are an
integral component of the left ventricular wall. There are
usually two groups of papillary muscles disposed in anterolateral and postero-medial locations of the left ventricle
when the ventricle is seen in short-axis cuts. The anterolateral group is often a single pillar or base whereas there is a
more variation in the posteromedial group (Figure 2). Each
pillar may have one head or multiple heads into which the
tendinous cords insert. Occasionally, there is muscularization of cords with the muscular tip inserting into the undersurface of the leaflet.12 The belly of the papillary muscle
Figure 2 (A) The papillary muscles in the left ventricle, fine apical
trabeculations, a long false tendon (green arrows), and broad
muscle bundles (triangles). The asterisk marks the membranous
septum. Note the thin musculature at the apex (arrow). (B) Simulated ‘four-chamber’ cut through a heart with a dilated left ventricle. The bases of the papillary muscles are continuous with the
trabeculations. This heart shows multiple fine strands of false
tendons crossing the cavity, and trabeculations also on the posterior
and postero-inferior walls. AL, anterolateral papillary muscle; PM,
postero-medial papillary muscle.
may be finger-like or broad, long or short, or nearly sessile
with very short free length. There may be multiple bellies
that interlink or are arranged in two tiers.13 In between
the two groups, there may be additional papillary muscles.
Relating to the mural (posterior) leaflet of the mitral
valve, there are basal cords that arise directly from the
free wall or via small papillary muscles to insert to the
under-side of the leaflet. All in all, the bases of the papillary
Anatomy and myoarchitecture of the LV wall
muscles are attached to the middle to apical thirds of the
ventricular wall but there are wide variations. But, the
basal parts of the papillary muscles are not solid muscle
(Figure 2). Multidetector-row computed tomography
imaging in recent years has provided a novel observation
that the bases are attached to muscular trabeculations
rather than directly to the compact myocardium.14
The myocardium
The bulk of the myocardium is formed by the contractile
cardiac myocytes. The adult myocyte is usually 120 mm
long and 20–30 mm in diameter. The ends of each
myocyte branches and adjoin adjacent myocytes to
produce a complex three-dimensional network, or syncytium, of anastomosing fibres. In any attempt to relate
structure to function, however, one should not ignore the
network of interstitial connective tissue (Figure 3A). A
fine network of fibrocollagenous connective tissue, the
endomysium, surrounds each myocyte providing it with
the supportive frame work. The endomysial weave coordinate the transmission of force and prevent slippage
between cells. A network of thicker connective tissue
surrounds groups of myocytes. Known as the perimysium,
this weave bears the shearing forces between groups
of cardiomyocytes and its lateral strands prevent
malalignment between bundles.15 Abnormal accumulation
and/or change in the quality of the connective tissue
increases myocardial stiffness.16
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Ventricular myoarchitecture
Myoarchitecture has been and remains a contentious issue
right from the early days. Indeed, Keith,17 in his Harveian
lecture in 1918, commented that such meticulous work
was dismissed by Hunter in the phrase ‘Much more pains
than were necessary have been taken to dissect and
describe the course and arrangement of the muscular
fibres of the heart’. Based on investigation techniques,
some argue that there are discrete systems of myocyte
arrangements in each ventricle while others are insistent
of a single rope-like configuration that encompasses both
ventricles.18–20 Even in more recent years, using advanced
reconstruction techniques and imaging tools there is much
discussion on this subject.21–23 Despite obvious limitations
of gross dissections, the myocardial strands (previously
termed myocardial or muscle fibres) that are revealed
using this basic technique provide a guide to the general
longitudinal orientation of the myocytes and serve as an
overview of myocyte arrangement, the myoarchitecture.24–27
Normal left ventricle
On gross dissection, the left ventricular wall comprises three
‘layers’ according to the longitudinal alignment of the myocardial strands: superficial (subepicardial), middle, and
deep (subendocardial). Importantly, these ‘layers’ represent
changes in orientation of the myocardial strands transmurally. They are not separated by cleavage planes or sheets
Figure 3 (A) Diagram showing the network like arrangement of the connective tissue matrix around individual myocytes and groups of myocytes. (B) The diagrams are of the frontal aspect of a heart rotated so as to show more of the left ventricle. They depict the orientation of the
myocardial strands from subepicardium to subendocardium. The superficial strands are oblique, middle strands are circumferential, while
deep strands are longitudinal. The circumferential portion is thickest in the normal heart. LV, left ventricle; RV, right ventricle.
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of fibrous tissue since strands of one ‘layer’ interconnect
with strands of the next ‘layer’ in a continuum.
When traced from the base to the apex, the superficial
layer extends from one ventricle to the other (Figure 3B).
The myocardial strands arise from the insertions of the
cardiac valves at the cardiac base. The superficial strands
on the sternocostal aspect run obliquely crossing the interventricular groove, sweep leftward over the obtuse margin
and descend towards the cardiac apex. The strands arising
from the mitral insertions continue to the diaphragmatic
aspect rightward where they cross the inferior (posterior)
interventricular groove. At the obtuse margin, they are at
an angle of 10–208 to the long axis of the left ventricular
inlet.26 The superficial ‘layer’ occupies approximately 25%
of the wall thickness.28 At the vortex of the left ventricle,
the myocardial strands invaginate in a spiral pattern to
give rise to the subendocardial ‘layer’. There is a similar
continuity between superficial and deep ‘layers’ at the
base of the ventricle.
The middle ‘layer’ occupies approximately 53–59% of the
ventricular wall thickness. It is thicker in the elderly.29 The
myocardial strands are more circumferentially arranged,
nearly parallel to the plane of the mitral orifice (Figure 3B).
They do not insert into the mitral or aortic valves, nor to
the ventricular apex. This layer is thickest near the base, thinning out towards the cardiac apex. At the base, it encircles the
inlet together with the outlet portions.
From the apex of the left ventricle, the deep ‘layer’ of
myocardial strands radiate in longitudinal fashion in the subendocardium, to insert into the aortic and mitral valves and
the membranous septum (Figure 3B). They fuse with the trabeculations and broader muscle bundles that line the ventricular cavity, and also continue into the papillary muscles.
Consequently, the deep myocardial strands form a meshwork
determined by the trabeculations at the apical third, muscle
bundles on the middle, and the valvar insertion at the basal
third. This is the thinnest ‘layer’, accounting for ,20% of
the wall thickness.28
The myoarchitecture of the ventricular septum reflects
the parietal wall of both right and left ventricles, the
major contribution coming from the middle ‘layer’ of the
left ventricle except at the apical portion where
the middle ‘layer’ is lacking.
Abnormal left ventricle
There are only a few anatomical studies on abnormal
myoarchitecture. A study comparing hearts from normal
patients with hearts from patients with history of hypertension without clinical heart failure, and patients with both
ventricular overload and congestive failure showed the
orientation of the myocardial strands is not altered.
Instead, there was an increase in connective tissue
content with the greatest increase in the failing heart.30
Another study, an experimental study on dogs in which histological sections were sampled only at the equator of the left
ventricle revealed the myoarchitecture in the pressure,
volume, and exercise-overloaded hearts, was remarkably
similar to normals.31 However, these investigators reported
an increase in the proportion of longitudinally aligned
strands in the subepicardial and subendocardial regions of
the wall thickness, with corresponding decrease of circumferential strands in the middle.
S.Y. Ho
Figure 4 (A) Reduced left ventricular cavity in a heart with hypertrophic cardiomyopathy. (B) Histological section showing myocyte
disarray (red) and fibrosis (green). Masson’s trichrome stain.
The ‘classical’ heart with hypertrophic cardiomyopathy
presents with asymmetric thickening of the ventricular
septum, with endocardial thickening representing mitral
impact lesion in approximately a third of cases at autopsy.
Septal thickening can exceed twice that of the parietal
wall. Many hearts with hypertrophic cardiomyopathy,
however, show symmetric hypertrophy presenting with an
evenly thick-walled left ventricle and a reduced cavity
(Figure 4). Cross-sectional slices often display a macroscopic
whorl-like appearance reflecting a combination of myocyte
disarray and fibrosis. Mid-ventricular cross sections of
human heart specimens with hypertrophic cardiomyopathy
were sampled in the study by Kuribayashi and Roberts.32
They reported extensive loss of the circular orientation of
myocardial strands and deep endocardial clefts in the junctional regions of the parietal wall with the septum. The
affected regions showed marked disarray and usually, but
not always, accompanied by increased interstitial and
focal fibrosis. There is an increase in the thickness of the
longitudinal deep ‘layer’, an observation also reported in a
study carried out using cardiac diffusion and strain magnetic
resonance imaging.33
It is known that the connective tissue matrix supporting
the myocardium is altered in disease.34 In the hypertrophied
heart, there is an increase in the diameter of the perimysial
tendons and density of the weave leading to a loss of intercellular contact and conductivity.16,35 In contrast, the cross
connections are lost in dilated cardiomyopathy resulting in
slippage and realignment of adjacent bundles of myocytes
and wall thinning.
Anatomy and myoarchitecture of the LV wall
Conclusions
The normal left ventricular wall has characteristic muscle
bundles and myoarchitecture. The myoarchitecture may be
altered in ventricular hypertrophy by fibre disarray and/or
increased proportion of longitudinally orientated myocardial
strands. Myoarchitecture in combination with alterations in
the connective tissue matrix provide the structural basis
for abnormalities in myocardial function.
Conflict of interest: none declared.
Funding
The Cardiac Morphology Unit at the Royal Brompton Hospital
receives funding support from the Royal Brompton and
Harefield Hospital Charitable Fund.
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