Key words
heart CT - myocardium - ventricular stucture - myocardial function - heart anatomy
& histology - animal models
Introduction
It is perhaps surprising that after four centuries of investigation [1] there is still no consensus as to how cardiomyocytes are aggregated together within
the ventricular walls. As well as demonstrating their clinical utility [2], computed tomography and magnetic resonance imaging have proven valuable in the
experimental setting for imaging the ventricular mural architecture. Diffusion tensor
magnetic resonance imaging, for example, is able to reveal the tracks formed by the
long chains of cardiomyocytes [3]
[4]
[5]. Previous histological studies had shown marked changes in so-called helical angulation
when the chains of cardiomyocytes were traced through the depths of the ventricular
walls [6]. It has been assumed, however, that the cardiomyocytes themselves are aggregated
together to form so-called “sheets”, with the alleged sheets, as viewed relative to
the long axis of the ventricular cone, shown as extending in full transmural fashion,
and said to uniformly contain four to six cardiomyocytes in their thickness [7]. These assumptions are in conflict with older histological studies of Feneis [8] and Hort [9]. These investigators showed that, when assessed in the short axis of the ventricular
cone, an obvious feathered pattern could be seen in the ventricular walls. The widely
held notion that all cardiomyocytes are aligned in tangential fashion within the cone,
as proposed by Frank [10], is incompatible with studies revealing populations of cardiomyocytes that intrude
or extrude in a transmural fashion [11]
[12]
[13]. Despite these potential disagreements, there is little doubt that the cardiomyocytes
are aggregated together to form units separated by planes of cleavage. This is the
consequence of the packing together of the individual cardiomyocytes within the endomysial
component of the fibrous matrix to form the units, with looser perimysial tissues
occupying the spaces between the aggregated cardiomyocytes [14]. In an earlier study, these spaces between the units were exaggerated by pneumatic
distension, thus providing better evidence of the extent and alignment of the myocardial
components formed from the aggregated cardiomyocytes [15]. In this current study, we carried out further analysis of the angulation of the
aggregated units of the myocardium visualized subsequent to pneumatic distension,
which reveals the marked regional heterogeneity of the mural architecture within the
ventricular cone. Our findings call into question whether the long chains of cardiomyocytes
are aggregated together to form sheets that extend in a fully transmural fashion.
Materials and methods
We pneumatically distended 10 excised porcine hearts, following all procedures for
animal care and experimentation as summarized in the guidelines of the American Physiological
Society and the German Law of Animal Protection. Our protocols were approved by the
University of Muenster Institutional Animal Care and Use Committee and adhered to
the guidelines for the use of laboratory animals of the National Institutes of Health
and Prevention.
All hearts were excised at the end of the experiments of different nature, with the
procedures themselves in some instances lasting for several hours. The pigs remained
under general anesthesia while the hearts were quickly excised, excision beginning
when the main investigator had indicated that the primary experiment was finalized.
In four instances, after the excision, cannulas were inserted into the right coronary,
circumflex, and anterior interventricular arteries while the hearts were still beating.
The arteries were then perfused with crystalline cardioplegic solution (Custodiol,
Köhler Chemie) until contractile activity had ceased, thus inducing arrest in a state
of diastole. In an additional 4 hearts, we perfused the cannulated coronary arteries
with barium chloride, thus inducing systolic cardiac arrest. We excised a further
2 hearts for histological examination. In all instances, having excised the hearts,
we inflated the coronary arteries with compressed air. For this purpose, cannulas
were sewn into the coronary arteries to produce an airtight seal. The pressure of
perfusion was measured using a manometer at the entrance of the tubing through which
we delivered compressed air. The hearts arrested in either systole or diastole were
then imaged using computed tomography, first in the control state, and then while
the coronary arteries were gently inflated by delivering compressed air at rising
pressures of 100, 150, 200 and 300 kilopascals. The insufflation of air continued
throughout the period of computed tomographic interrogation. For computed tomographic
imaging, we used a dual-source system (Somatom Definition, Siemens Healthcare, Forchheim,
Germany) with the following scan parameters: 120 kV, 100 mAs, collimation 16 × 0.3 mm,
matrix 512 × 512, FOV 12 cm, rotation time 1 s, pitch factor 0.8. We used an ultra-high
resolution reconstruction kernel U75 u for image reconstruction. After denoising,
we gained a 3 D dataset with a nominal spatial resolution of 0.23 mm × 0.23 mm × 0.4 mm.
To establish any dimensional changes produced by the pneumatic distension, we measured
the changes in cross-sectional thickness of the walls at the left ventricular base
and equator before and during pneumatic distension. We also measured the changes in
length of the posterior, superior, septal and inferior walls. We then assessed the
transverse transmural distribution of the aggregated units of cardiomyocytes in the
superior, inferior, and posterior walls in the hearts prepared for computed tomographic
analysis. To describe the visualized anatomic arrangements, we made multiplanar reconstructions
of the superior, inferior and posterior walls with a slice thickness of 0.5 mm using
OsiriX software (Pixmeo SARL, Bernex, Switzerland). This was achieved by aligning
the selected mural segments along the long axis of the left ventricle, defined by
the apex and the middle of the mitral valve, and along its short axis, which is defined
by the tangential axis of the respective wall. While scrolling through the walls from
the epicardium to the endocardium in the radial direction ([Video 1]), the local helical angles were measured in 20 equidistant steps through the regionally
normalized depths ([Fig. 2b]). The points of measurement, therefore, refer to the relative thicknesses in the
selected mural segments. Using an automatic, investigator-independent, computer-assisted
technique depending on customized software based on algorithms described recently
by Brune et al. [16], we measured the angulations of the chains of cardiomyocytes in one single heart,
assessing the changes in terms of both the helical and transmural directions. In the
2 hearts prepared for histological validation, we rinsed the coronary arteries with
saline, inflated them for several minutes with compressed air, and perfused them with
4 % formaldehyde for 2 days, using a pressure of perfusion comparable to distension
at 300 kilopascals. We then sampled the walls at the regional sites identified for
the purpose of echocardiographic analysis [17]. We sectioned the blocks taken from the first heart in the short axis ([Fig. 4], [6]), with those from the second heart cut parallel to the ventricular long axis ([Fig. 5]), ensuring that all sections extended in a fully transmural fashion. The sections
were stained with Azan, rendering the cardiomyocytes red, and the supporting connective
tissue blue.
Fig. 1 The panels show the measured mean changes in ventricular dimensions of the 8 porcine
hearts subjected to pneumatic distension followed by computed tomographic assessment.
The rows show the changes for ventricular length and internal and external diameters
of the ventricular cone as a proportion of the control measurements. The columns show
the changes in the various quadrants of the ventricular walls with increasing pressure
of distension shown in kilopascals (kp).
Abb. 1 Die Grafiken zeigen die mittleren Änderungen in den Kammerdimensionen der 8 Schweineherzen
nach Blähung mit nachfolgender Computertomographie. Zunächst ist die Änderung der
Kammerlänge, dann die Änderung des inneren und äußeren Durchmessers im Vergleich zur
Ausgangsgröße dargestellt. Die Säulen stellen die Änderungen in den verschiedenen
Quadranten der Wand bei wachsendem Blähdruck gemessen in kilopascal (kp) dar.
Fig. 2 a The panels show the measurement of the transmural change in helical angulation of
the chains of aggregated cardiomyocytes in the hearts arrested in diastole (fine lines)
compared to those arrested in systole (bold lines). The measurements were made in
segments from the superior (upper), inferior (middle) and posterior (lower) quadrants
of the ventricular cone. The differences did not reach statistical significance in
any segment, although there is a trend to higher mean helical angles in the inner
two thirds of the walls of hearts arrested in systole, as shown in the insets. b Measurement of a helical angle of 28° in a dataset aligned perpendicular through
the posterior wall.
Abb. 2 a Die Grafik zeigt die transmurale Drehung der Helix-Winkel von Aggregaten langer Myozyten-Ketten
in Herzen, die einerseits in Diastole (feine Linien) oder in Systole (dicke Linien)
stillgestellt wurden und dies in der superioren (oben), inferioren (mitte) und posterioren
(unten) Wand der linken Kammer. In keiner Position wurde statistische Signifikanz
erreicht. In systolisch stillgelegten Herzen zeigt sich ein Trend zu höheren mittleren
Winkeländerungen (Einschub).
b Messung eines Helixwinkels von 28° in einem Datensatz, der rechtwinklig durch die
posteriore Wand ausgerichtet ist.
Fig. 3 The upper three rows of the figures show the distribution of helical angles (left
hand panels) and transversely intruding angles (middle panels) as assessed using the
computed tomographic images from the basal, middle, and apical thirds of the ventricular
cone as measured using the computer-derived system [16]. The right-hand panels show the location of the site of measurement relative to
the long axis of the posterior ventricular wall (right panel). On the x-axes of the
plots, we have shown the angles between plus and minus 90 degrees of the chains of
aggregated cardiomyocytes. The y-axes show the mural depth between the epicardium
and endocardium as a proportion of the mural thickness. On the z-axes, we show the
density of aggregated cardiomyocytes with comparable angulations. The lower panel
depicts in cartoon fashion our interpretation of the three-dimensional aggregation
of the chains of cardiomyocytes, with negative intruding chains shown in red and positive
intruding chains shown in green. A positive sign is denoting an epi- to endocardial
spiral in clockwise direction seen from the apex, while a negative sign denotes a
counterclockwise spiral from the epicardium to the endocardium. Tangentially aligned
chains of cardiomyocyes are shown in pink.
Abb. 3 Die oberen drei Reihen der Grafik zeigen die Verteilung der Helix-Winkel (links)
und der queren Eindring-Winkel (mittlere Spalte) abgeleitet aus den computertomographischen
Bildern nach Blähen der Herzen und unter Verwendung eines computerassistierten automatischen
Auswertverfahrens. Die rechten Graphiken zeigen die Messorte in der freien Wand der
linken Kammer. Auf der x-Achse sind die Winkel zwischen plus und minus 90 Grad aufgetragen,
die y-Achse zeigt die Wandtiefe des Messortes in % der Wanddicke, die z-Achse zeigt
die Dichte der Messwerte am Messort an. Die untere Darstellung zeigt im Model grob
vereinfacht die Anordnung von langen Myozytenketten mit der Angabe der positiven (grün)
oder negativen (rot) Eindringrichtung der Vernetzung in die Wandtiefe – von der Kammerspitze
aus betrachtet –, wobei das positive Vorzeichen einen Schrägverlauf im Uhrzeigersinn,
das negative einen solchen im Gegenuhrzeigersinn anzeigen.
Fig. 4 The images show longitudinal sections through the walls of the ventricular mass as
obtained from ventricular segments 5 (upper panels) and 12 (lower panels), comparing
the findings obtained using computed tomography (left-hand panels) and histology (right-hand
panels). The areas shown by computed tomography and histology are not identical, although
taken from the same ventricular segments hence single sheet-like formations in the
one image cannot be identified in the other. Nonetheless, the main striation prevailing
in each segment is documented in both images. Note that, although many components
of myocardium are aggregated in sheet-like formation, none of the sheets extend in
a fully transmural fashion. Note also the marked difference in architecture between
the patterns of the aggregates in the basal (upper) and middle (lower) thirds of the
ventricular cone.
Abb. 4 Die Darstellung zeigt histologische Längsschnitte (links) durch die linke Kammerwand
in den Segmenten 5 (oben) und 12 (unten) und die entsprechenden Segmente im CT (rechts).
Der Herzmuskel ist zu Lamellen aufgefächert. Kein Fächer durchbricht die gesamte Wanddicke.
Beachte die hohe strukturelle Variabilität innerhalb der Kammerwand.
Fig. 5 The images show the comparisons between the findings revealed by computed tomography
(upper panels) and histology (lower panels) following analysis of short axis sections
of the ventricular walls obtained from segments 6 (left hand panels), 12 (middle panels)
and 16 (right hand panels). The colouring to the left hand side of the histological
sections show the compartments of the wall deemed to be formed by the aggregated cardiomyocytes.
The blue layer showing the transitional blocks extending from epicardium towards the
middle layer, shown in orange. The green layer then depicts the transition towards
the endocardial blocks. The drawings at the bottom of the figure show the alignment
of the chains of cardiomyocytes within the designated layers. Note the markedly variable
thickness of the different layers, and the variation of the depth of the circular
aggregates relative to the thickness of the ventricular walls. Note also the lack
of any fully transmural aggregates.
Abb. 5 Gegenüberstellung histologischer Querschnitte durch die Segmente 6, 12 und 16 und
ihrer Darstellung im CT: Die Farbmarkierung begrenzt Kompartimente in der Wand in
ein subepikardiales äußeres Fan (blau), eine Mittellage (orange) und ein inneres subendokardiales
Fan (grün). Darunter ist die typische Lamellenanordnung in den drei Kompartimenten
skizziert. Beachte, dass die Kompartimente in den drei Wandsegmenten deutlich unterschiedlich
dick sind und dass insbesondere die Mittellage unterschiedlich tief in der Wand liegt.
Auch hier sind keine Lamellen erkennbar, die die gesamte Wanddicke durchbrechen.
Fig. 6 The upper panel of the figure shows a cross-section through the middle third of the
ventricular cone as obtained using computed tomographic visualization of the distended
ventricular mass. The three lower panels show the corresponding long axial images
along planes A–C through the cross-sectional image. Note the marked discrepancy between the patterns
of the blocks of the myocardium as seen on the short axial and long axial images.
To date, it has not proved possible to assess the full extent of an individual block
of the myocardium.
Abb. 6 Das obere Bild zeigt einen Querschnitt durch das Herz in der mittleren Äquatorialzone
im CT-Bild nach pneumatischer Entfaltung des Myokards. Die drei unteren Bilder zeigen
Längsschnitte durch dasselbe Herz in den Positionen A, B, und C. Beide Darstellungen
lassen die hohe regionale Variabilität der Struktur erkennen. Bisher ist eine Darstellung
von Lamellen in ihrer ganzen Ausdehnung nicht gelungen.
Results
Irrespective of arrest in systole or diastole, the ventricular length increased with
pressure, albeit variably at the different sites of measurement ([Fig. 1]). The changes in mural thickness were similarly variable, but small. Small differences
were noted in the turn of helical angles in the hearts arrested in systole as opposed
to diastole, with helical angles being minimally increased when arrest was achieved
in diastole ([Fig. 2a]).
Computed tomography
Assessment of the ventricular cone in its short and long axes revealed that the cardiomyocytes
were aggregated together into units separated by exaggerated spaces due to the cleavage
induced by the pneumatic distension. The dimensions of the units produced by the aggregation
of the individual cardiomyocytes varied within the different depths of the ventricular
walls. With visual assessment, we were able to describe broad layers within the thickness
of the walls but in the absence of any discrete anatomical boundaries. The extent
and alignment of the units produced by the aggregation of the individual cardiomyocytes
also varied markedly within the different ventricular regions. When seeking to provide
a meaningful account for our observations, we therefore considered that assessment
of the findings as seen in the short axis of the ventricular cone permitted recognition
of endocardial and epicardial layers of aggregated cardiomyocytes, along with a central
zone, in which the individual cardiomyocytes were aggregated together in circumferential
fashion. Units of aggregated cardiomyocytes could then be seen transitioning between
the central and peripheral layers. This produced an obvious feathered appearance within
individual short-axis sections, with the central layer of aggregated cardiomyocytes
forming the spine of the observed feather. When the findings were assessed in the
long axis of the ventricular cones, however, the aggregated cardiomyocytes were seen
to be inter-related in a complex three-dimensional fashion. Scrolling through the
overall sequence of cross-sectioned slices from base to apex and from apex to base
([Video 2]), revealed a virtual rotation of the inner and outer fans of the feather, with the
spine of the feather seeming to remain motionless. The direction of rotation was reversed
when traced from base to apex, as opposed to apex to base. Comparable scrolling through
the long axis series ([Fig. 6], lower panel and [Video 3]) again showed the cardiomyocytes to be aggregated into units with complex relationship
to each other. Those originating in the lower half of the left ventricle ascended
towards the ventricular base, seemingly also moving from epicardial to endocardial
locations within the thicknesses of the ventricular walls. The spaces between the
aggregated units, however, as assessed anatomically were less obvious in the upper
half of the septum. The observations described above take account of our interpretations
as based on gross anatomical observation and were comparable in all distended hearts.
To provide some quantification of the anatomic observations, we used computer-assisted
rendering to qualitatively assess the angulation of the chains of aggregated cardiomyocytes
in helical and transmural directions. This analysis revealed marked variations between
the basal, middle, and apical thirds of the ventricular cone ([Fig. 3]). An obvious S-like distribution of the helical angles was seen in the basal region
of the cone (upper left panel of [Fig. 3]), but was less obvious in the middle third of the cone, and absent from the apical
third. Analysis of the intruding or extruding transmural populations revealed a low
distribution in the outer half of the wall in the basal and middle thirds of the ventricular
cone, with intrusion being greatest in the lower third.
Video 1: The stack of computed tomographic tangential sections is scanned through the posterior
wall of the left ventricle from the epicardium to the endocardium.
Video 1: Sequenz von CT-Bildern der posterioren linken Kammerwand in transmuraler Richtung
vom Epikard zum Endokard.
Video 2: The stack of computed tomographic images as obtained in cross-section of the ventricular
cone are scanned from apex to base.
Video 2: Sequenz von CT-Bildern von Querschnitten durch das Herz in apiko-basaler Abfolge.
Video 3: The stack of computed tomogaphic images is scanned in long axial fashion.
Video 3: Sequenz von CT-Bildern im Längsschnitt des Herzens unter Drehung um eine Achse im
Zentrum des linken Kammerlumens.
Histological findings
Analysis of the sections taken in both short and long axis planes confirmed our gross
anatomical evaluations of the computed tomographic images. The histological sections
showed that the individual cardiomyocytes were aggregated together into units separated
by spaces, presumably induced by the pneumatic distension ([Fig. 4]). However, the units of aggregated cardiomyocytes separated by the spaces showed
marked variation in both their shape and orientation within the different ventricular
regions. As assessed in the short axis ([Fig. 4]), a layer of cardiomyocytes aggregated in circumferential fashion was seen in all
regions. In a gross assessment, the extent of this central layer was seen to vary
markedly, not only in terms of thickness but also with respect to its depth between
the epicardium and the endocardium. Examination of the segments taken from the middle
third of the ventricular cone confirmed the feathered appearance as revealed by the
tomographic analysis, with aggregated units of the myocardium extending away from
the circumferential cardiomyocytes towards the endocardial and epicardial layers.
Densely aggregated layers of cardiomyocytes were seen in some, but not all, of the
subendocardial parts of the wall in the different ventricular regions, with similar
variation noted in the pattern of the sub-epicardial layers. Throughout the segments
it nonetheless proved possible to recognize an overall mural architecture based on
division of the wall into central, endocardial, and epicardial components, with transitional
zones then extending between the central and border zones. Although the cardiomyocytes
aggregated together to form, these units were separated from one another by spaces,
with additional spaces within each layer as defined for the purpose of description.
There were no discrete anatomical boundaries between any of the observed components.
The five-layered appearance observed in the middle third of the ventricular cone,
however, was lacking at the apex, where thick strands of parallel units spiraled in
a centripetal direction. The five-layered arrangement was similarly lacking at the
ventricular base, where the spaces between the aggregated cardiomyocytes were aligned
more or less at right angles to one another. In the middle third of the ventricular
cone, when assessed in the long axis, the spaces between the units of the myocardium
extended across the wall in an almost radial fashion. These series of spaces between
units of the myocardium descended towards the apex in the subepicardial third of the
walls, but ascended towards the base in the subendocardial third, with the lengths
of the spaces between the units, as assessed in terms of gross anatomy, varying markedly
within the different ventricular regions.
Discussion
By using passive pneumatic distension of the ventricular cone, injecting compressed
air through the coronary arteries, we succeeded in exaggerating the mural architecture
produced by the binding together of chains of cardiomyocytes within the endomysial
components of the fibrous matrix to produce aggregated units [14]. We have described these units simply as “aggregated cardiomyocytes”, since we found
no structures that could be interpreted as representing discrete anatomical “fascicles”
or “fibers”. Our interpretation of our current findings regarding the gross anatomical
arrangement of these aggregated units nonetheless differ from presumptions made previously
by some investigators subsequent to analysis of ventricular mural architecture using
diffusion tensor magnetic resonance imaging [3]
[4]
[5]. We should emphasize, however, that our own findings are not necessarily incompatible
with the findings produced by diffusion tensor imaging. The angulations of the tracts
revealed by such analysis reflect the alignment of the long chains of aggregated cardiomyocytes.
It is presumed, however, that the secondary or the tertiary eigenvector of the diffusion
tensor then provides a surrogate of the alignment of the sheets into which the cardiomyocytes
themselves are believed to be aggregated. Although it is now possible to obtain high
resolution when using diffusion tensor imaging, the resolution available to earlier
investigators [3]
[4]
[5] was insufficient to make such conclusions regarding the extent of the “sheets” inferred
to be present on the basis of the measurement of the primary and tertiary eigenvectors.
Our own analysis confirms that there is an obvious organization of cardiomyocytes
to produce aggregated units within the ventricular walls. The specific mural architecture,
however, varies markedly within the different ventricular regions now recognized echocardiographically
[17]. The arrangement of the units into which the cardiomyocytes are aggregated, the
spaces between the units being accentuated by the pneumatic distension, is then seen
to vary markedly when assessed in the short axis as opposed to the long axis of the
ventricular cone. Even within our images, as produced by computed tomography, it is
still not possible to recognize individual cardiomyocytes or to assess the full extent
of the units into which the cardiomyocytes are aggregated. Therefore, we do not consider
it justified to maintain that the alignment of the presumed sheets into which the
cardiomyocytes are aggregated is normal to the alignment of the long chains of cardiomyocytes
within them as has been the case to date. Our overall findings, as interpreted on
the basis of the three-dimensional gross anatomic analysis permitted by the computed
tomographic reconstruction, must call into question the generally accepted notion
that the sheets of cardiomyocytes extend in a fully transmural fashion, and that,
in terms of thickness, they are composed of four to six cardiomyocytes [7].
Our images, in fact, support the descriptions provided quite some time ago by Feneis
[8] and Hort [9]. They also endorse the observation made over a century ago, namely that at various
depths within the central component of the ventricular wall, when assessed in the
short axis, the cardiomyocytes positioned centrally within the thickness of the ventricular
walls are aligned in a circumferential fashion. These are the cardiomyocytes believed
by Krehl [18] to provide the driving force for ventricular emptying. Perhaps more importantly,
the quantitative, as opposed to qualitative, observations we were able to make using
an automated system that avoids the need for subjective interpretation [16] confirm that a significant proportion of cardiomyocytes are aligned in a transmural
fashion across the ventricular walls [11]. These measurements provided no support for the notion that all cardiomyocytes are
aligned in a virtually tangential fashion. It is the latter dogma, put forward initially
by Frank [10], that has prevailed to date, with support for this notion provided by the histological
measurements made by Streeter and colleagues [6].
From a mechanistic point of view, the myocardium represents a highly structured continuum.
Our current observations show that a notable characteristic of this continuum is the
marked heterogeneity of the mural architecture in the different ventricular regions.
In particular, our qualitative observations, supported by our quantitative measurements,
reveal a variable mixture of populations of cardiomyocytes aligned in surface-parallel
or transmural directions. It is the presence of the spaces between the aggregated
cardiomyocytes occupied by loose perimysial tissue that permits their gliding relative
to one another during systolic ventricular contraction, thus explaining the paradox
of systolic mural thickening [19]. The dense packing of the cardiomyocytes produced by the endomysial component of
the fibrous matrix, however, limits the diastolic extension of the myocardium, yet
transmits forces and stores energy during systole [19]. When considered on the basis of continuum mechanics, because of the numerous branchings
between the individual cardiomyocytes, the principal stresses occurring during systolic
contraction do not coincide with the striation of the myocytes. It is the linkage
within the fibrous matrix that permits action as a power train. Taken together, the
slippage between the myocardial units accounts for the large changes in shape and
dimension of the ventricular mass over the cardiac cycle, underscoring the major transmural
gradients of three-dimensional strain, with predominant dimensional changes observed
in the inner wall [19].
The marked heterogeneity in the extent of aggregation of the individual cardiomyocytes,
furthermore, indicates a local “fingerprint” for each ventricular region, these regions
representing the “segments” as identified echocardiographically [17], thus pointing to the well-recognized regional variability in antagonistic function
of the wall [11]
[12]
[20]
[21]
[22]. The simultaneous coexistence of dilating and constrictive activity in the ventricular
myocardium was measured previously, a feature which prevails throughout the cardiac
cycle [11]. We suggest that this mechanism, which was described as antagonism, is designed
to control the mean ventricular shape and size. It also controls the speed and amount
of regional systolic inward motion, hence molding intra-cavitary flow, and accounting
for the known spiraling shape and speed of flow through the aortic outflow tract [23]. By intermittently storing elastic forces, the antagonistic mechanism operates the
early diastolic outward motion, and hence the shape and velocity of early diastolic
inflow [24]. We should emphasize that our focus on regionally confined mural dynamics contrasts
with the notion of a band-like myocardial continuum, as was postulated initially by
Torrent-Guasp [25]. This latter concept, while still accepted by some [26], is incompatible with the demonstrated anatomic arrangement of the individual cardiomyocytes
being aggregated together into a three-dimensional array of units separated by spaces
occupied by loose perimysial tissues. Our account of continuum mechanics serves to
correlate local with global ventricular dynamics in the normal heart, but particularly
in the setting of heart failure. Global function is the joint effect of the highly
variable patterns of local wall motion, which also means that an almost deliberate
pattern of even partially disturbed local functions may fail to disrupt global function
[27]. An essential component of this global function is the antagonism provided between
the tangential and intruding populations of cardiomyocytes, thus underscoring the
co-existence of unloading and auxotonic systolic forces [11]
[28]. It is axiomatic that knowledge of ventricular mural architecture is essential when
assessing the clinical findings now revealed using computed tomography or magnetic
resonance imaging [2]. Our current findings should also provide the means of interpreting new imaging
modalities currently in development, such as the integration of positron emission
tomography and magnetic resonance imaging [29]. It is our hope that they will provide a deeper understanding of the processes underscoring
the different disease entities.
We nonetheless recognize the obvious limitation of our study, i. e., that we investigated
pig hearts, not human hearts. However, our current study is methodological and should
serve to optimize the details of processing before making it potentially applicable
to autopsied human hearts.
-
Pneumographic distension of the autopsied heart, coupled with computed imaging, reveals
the structure of the myocardium of the whole heart within minutes.
-
The myocardium is a highly structured continuum with local segmental differentiation.
-
The ventricular walls are arranged neither in the form of transmural sheets, nor a
unique band, but rather in the form of blocks of aggregated cardiomyocytes separated
by planes of cleavage.
