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1 The Development oftheCoronary Arteries
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Comment
The evidence from both developing human and
murine embryos shows that the key stages of
development of the coronary arteries take place
during the transition from the embryonic to the
foetal stages. It is at these stages, representing
CSs 19 through 23in human development, and
then continuing through the initial weeks of foetal development subsequent to 8weeks after fertilisation, that there is closure of the embryonic
interventricular communication. This is combined with the transition during which the
ventricular walls change to have predominantly
compact rather trabeculated walls. The comparable changes in murine development take place
during embryonic days 13.5 through 15.5. It is
during these stages, furthermore, that the epicardial coronary arteries achieve their connection
with the aortic root. Over the same period, the
arterial circulation is developed with compact
ventricular walls.
The manner of connection of the epicardial
coronary arteries with the aortic root has long
been controversial. The process was initially suggested to depend on the outgrowth of stems from
the arterial roots. The stems, however, were
alleged to sprout not only from the aortic sinuses,
but also from the sinuses of the pulmonary root
[25]. This notion was supplanted by the belief
that the stems grew into the aortic root from the
crown-like plexus formed within the middle part
of the outow tract [6]. The evidence is now
overwhelming that the stems do, indeed, bud out
from the aortic component of the outow tract [7,
8, 19]. Our morphological evidence, however,
reveals that the stems grow out from walls of the
intrapericardial aorta distal to the developing
sinutubular junction. They can rst be recognised
prior to any formation of the arterial valvar
sinuses. Only with the ongoing formation of the
sinuses are the arterial orices translocated to
achieve their anticipated denitive positions
proximal to the sinutubular junctions. Lack of
such translocation provides an obvious explanation for the frequent nding of distal origin of the
coronary arteries relative to the sinutubular junction in otherwise normal hearts [26]. It is unlikely
to be coincidental, furthermore, that the high origin of the left coronary artery is a frequent nding in the setting of the aortic valve with two
leaets [27]. These ndings point to an obvious
relationship between maldevelopment of the
arterial roots and abnormal origin of the coronary
arteries. Further evidence in this regard is provided by the association of origin of the left coronary artery from the pulmonary trunk with the
persistence of the aortopulmonary foramen as an
aortopulmonary window [28]. The latter nding
then points to completion of separation of the
intrapericardial trunks and arterial roots one from
the other as underscoring appropriate budding of
the coronary arterial stems. It has been suggested
that this process might be guided by “aortic cardiomyocytes” [7]. This term, however, is a contradiction in itself. The walls of the arterial valvar
sinuses contain smooth muscle cells, rather than
cardiomyocytes. The aortic root does have myocardium incorporated at the bases of the two
sinuses that give rise to the coronary arteries.
This myocardium is formed by the so-called
“myocardialisation” of the outow cushions. Its
location at the bases of the aortic sinuses that
usually give rise to the coronary arteries, nonetheless, could, be inuential in determining the
appropriate origin of the developing arterial
stems. All three sinuses of the pulmonary root,
however, are supported by comparable crescents
of myocardium. Those arguing in favour of the
role of “aortic cardiomyocytes” suggest that such
cells are lacking in the pulmonary root [7]. This
is manifestly not the case. The arterial stems, furthermore, originate distal to the myocardial border. And, when rst formed, they take an
intramural course through the adventitial linings
of the developing sinusal walls. Abnormal development of the sinuses themselves, therefore, is
more likely to be responsible for origin of one or
other of the major coronary arteries from an inappropriate valvar sinus. Further studies on the
mechanism of formation of the sinusal walls, and
the incorporation of the coronary arterial orices
within the sinuses, will be required to resolve
these issues.
The same goes for clarifying the morphogen-
esis of stulous communications between the
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R. H. Anderson et al.
ventricular cavities and the epicardial coronary
arteries. Such stulous communications can be
found as isolated lesions [3]. Much more frequently they are found as complicating malformations in the setting of hypoplasia of either the
right or left ventricle when there is atresia of the
arterial valve and an intact ventricular septum.
When found in the setting of pulmonary atresia
with an intact ventricular septum, the stulous
communications are most frequent when there is
a so-called “unipartite” arrangement of the cavity. This occurs when mural hypertrophy has
overgrown the apical trabecular and outlet ventricular components [29]. The nding implies
that the insult responsible for the pulmonary atresia occurred early in foetal development, but subsequent to closure of the embryonic
interventricular communication. When found in
the setting of hypoplastic left heart syndrome, in
contrast, the stulous communications are found
only in those phenotypes that include mitral stenosis rather than mitral atresia [30]. In both
instances, nonetheless, the arrangements are suggestive that increased ventricular pressure is
involved in creating the communications from
the ventricular cavity, via the mural arterial circulation, to the epicardial coronary arteries, with
the latter vessels then frequently becoming
ectatic. Further investigations on the timing and
mechanisms of formation of the mural arterial
channels will be required to resolve these issues.
Acknowledgements Our study would not have been possible without access to the Human Developmental Biology
Resource, housed at Newcastle University. We express
our thanks to all those who prepared the datasets and
made them available for online evaluation. We are also
indebted to the archivists of the Hamilton collection of
human embryos, initially housed at Charing Cross
Hospital Medical School, transferred to St George’s
Medical University, but now maintained, along with the
Boyd archive, at Cambridge University. Selected murine
datasets are available for study in the website of the Crick
Institute, London.
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Congenital Anomalies ofCoronary
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Arteries: Anatomy, Embryology
andRisk ofSudden Death
StefaniaRizzo, CristinaBasso, MichelaMuriago,
andGaetanoThiene
2
Anatomy ofCoronary Arteries
withHistorical Notes
Arturo Banchi, assistant in anatomy to Prof.
Chiarugi in Florence, published in 1903 the paper
entitled “Morfologia delle arteriae coronariae
cordis” (Fig.2.1), rst introducing the concept of
coronary arterial patterns [1] (Fig.2.2).
(a) Right dominant when the right coronary
artery gives origin to the posterior descending artery (“branch of the posterior longitudinal groove”) and branches to the posterior
wall of the left ventricle.
(b) Left dominant when the posterior descend-
ing coronary artery and branches to the posterior left ventricular wall take origin from
the left circumex artery (“circumex
branch”).
(c) Balanced when the posterior descending cor-
onary artery takes origin from the right
coronary artery whereas branches to the pos-
S. Rizzo · C. Basso · G. Thiene (*)
Department of Cardio-Thoraco-Vascular Sciences
and Public Health, University of Padua, Medical
School, Padua, Italy
e-mail: s.rizzo@unipd.it; cristina.basso@unipd.it;
gaetano.thiene@unipd.it
M. Muriago
Internal Medicine, Pietro Milani Ospital, Noventa
Vicentina, Vicenza, Italy
terior left ventricular wall originate from the
left circumex artery.
At that time, the cause of myocardial infarction, by sudden coronary thrombotic occlusion,
was not yet established. Nowadays, we are well
aware of how much important is the coronary
arterial pattern for the site and extension of myocardial infarction (“infarct related artery”).
Moreover, among Bianchi’s drawings, a coronary
arterial branch called “right atrial branch” is well
evident, arising from the right coronary artery in
right dominant pattern and from the left circumex artery in the left dominant pattern. We know
that it is the artery for the sino-atrial node, which
at that time had not been yet discovered as the
cardiac pacemaker.
The variability of coronary artery network
was conrmed with post-mortem casts by Giorgio
Baroldi. His book, published in 1967, is known
as the “Bible” of the anatomy and pathology of
coronary arteries [2] (Fig.2.3).
Overall, these information, deriving from
research of anatomists and pathologists, would
have become fundamental for the development of
in vivo diagnosis, invented by Mason Sones at
the Cleveland Clinic (Fig.2.4) in 1962 by coronary angiography [3] and followed by surgical
therapy of coronary artery disease, with aortocoronary by-pass with saphenous vein by Renè
Favaloro in 1967 [4] (Fig.2.5).
© Springer Nature Switzerland AG 2023
G. Butera, A. Frigiola (eds.), Congenital Anomalies of Coronary Arteries,
https://doi.org/10.1007/978-3-031-36966-7_2
19
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Fig. 2.1 Title page of
Dott. Banchi paper
S. Rizzo et al.
Fig. 2.2 The original drawings of coronary artery patterns. (a, b) Right dominance and (c, d) left dominance. From
Banchi A [1]
ab
cd
2 Congenital Anomalies ofCoronary Arteries: Anatomy, Embryology andRisk ofSudden Death
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Fig. 2.3 Postmortem casts of coronary arteries. (a) Left coronary artery anatomy, (b) dominant right pattern, (c) domi-
nant left pattern, and (d) balanced pattern. From Baroldi G etal. [2]
22
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Fig. 2.4 Mason Sones (1918–1985), the inventor of selective coronary angiography (1962)
S. Rizzo et al.
RITA ligated
Radial-artery graft from
aorta to diagonal
coronary artery
Saphenous-vein graft
from aorta to RCA
In situ graft from
LITA to LAD
Composite RITA
graft from LITA
graft to circumflex
coronary artery
Fig. 2.5 René Favaloro (1923–2000). The inventor of aorto-coronary bypass with autologous saphenous vein (1967)
Embryology ofCoronary Arteries
Earlier, the myocardial blood supply originated directly from the ventricular cavities
Both subepicardial coronary arteries (CAs) and
veins derive from epicardial cells [5, 6].
Their development begins with the formation of a plexus-like vasculature, located in
the subepicardium, which invades the myocardium and develops small vessels and
capillaries.
through the intertrabecular spaces lined by endocardium (Fig.2.6a). This source of blood to the
primitive spongy myocardium disappears with
the myocardial compaction (Fig. 2.6b). At this
point, the whole intramyocardial vascularization
consists of vessels with endothelium derived
from the subepicardium [6–8].
2 Congenital Anomalies ofCoronary Arteries: Anatomy, Embryology andRisk ofSudden Death
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ab
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Fig. 2.6 Embryology of the myocardium. (a) Spongy
myocardium with blood supply deriving directly from the
endocardium of the ventricular cavities. (b) The myocar-
Fig. 2.7 Origin of coronary arterial stems from the peritruncal epicardial ring
The origin of both CAs and veins, whether
intra- or extramural, is similar. Their denitive
identity and function depend upon the connection, arteries with the aorta, and veins with the
sinus venosus.
dium becomes compact, with blood supply deriving from
the subepicardial vasculature
A subepicardial network of cells surrounds the
orices of the great arteries (peritruncal ring) and
eventually connects with the facing aortic sinuses
[5, 9] (Fig. 2.7). The question is whether the
development of CAs origin is a matter of ingrowth
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S. Rizzo et al.
or outgrowth [10]. There are two hypotheses to
explain the connection.
The rst is the outgrowth hypothesis, namely,
the development of sprouts or buds from the aortic wall of facing sinuses, capturing the peritruncal
ring of coronary subepicardial arterial vasculature [5, 11] (Fig.2.8).
The second developmental hypothesis is supported by the observation that the prongs of the
peritruncal ring penetrate the aortic wall and
make contact with the endothelial lining of the
aorta [9, 10] (Fig.2.9).
Until the late 1980s, it was thought that CAs
entirely derived from an aortic endothelial outgrowth that would expand to form the complete
coronary system, including coronary veins. Further
research in avian models partially argued against
this, demonstrating that CA endothelial cells do not
bud from the aortic root, but instead grow into the
aortic wall from the aortic peritruncal plexus to
connect to the systemic circulation, most likely
Fig. 2.8 The hypothesis according to which sprouts or
buds arise from the facing aortic sinuses and make contact
with the subepicardial coronary vasculature
under the guidance of vascular endothelial growth
factor (VEGF) and periaortic cardiomyocytes. At
least part of the early arterial coronary vascular system forms through a process of vasculogenesis
with subsequent fusion of endothelial cell clusters
to form new blood vessels [12, 13].
Recent investigations conrmed that the proximal CAs do not grow from the aorta. In the contrary, they develop from the peritruncal ring of
the subepicardial vascular plexus [14, 15] penetrating into the aorta.
Septation of the arterial pole of the heart
(42 days in the human embryo) precedes the
appearance of coronary ostia when cells from the
peritruncal ring migrate into the aortic root.
Septation therefore cannot be responsible for the
nal position of coronary orices.
Formation of the left CA precedes the
right CA.
Moreover, unlike from the tunica media of the
ascending aorta, the tunica media of the CAs
does not derive from the neural crest.
Cellular cross-talks and signaling pathways
take place (notch and hippo signals, transcription
factors, angiogenic molecules, and apoptosis)
[16–20]. VEGF plays a crucial role in the development of coronary ostia and main stem formation [14]. Absence of VEGF was shown to inhibit
ostia formation. Epicardial inhibition, reducing
apoptotic remodelling at the ventricular-arterial
junction, alters vascular connection with the
aorta and may produce CA anomalies equal to
those observed in humans [21].
Why the primitive subepicardial coronary
arterial vasculature tends to connect with the facing aortic sinuses, instead of facing pulmonary
sinuses, is still a mystery. The explanation cannot
be the posterior position of the aorta since in
Fig. 2.9 Ingrowth
Developmental Hypothesis
with cells of the peritruncal
ring penetrating the aortic
wall. (a–e) show the
progression of the ingrowth of
epicardial cells trouth thye
aortic wall until the
endocardium
AO
CA
(LEFT POSTERIOR)
SINUTUBULAR
2 Congenital Anomalies ofCoronary Arteries: Anatomy, Embryology andRisk ofSudden Death
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JUNCTION
25
RIGHT CORONARY
AORTIC SINUS
(ANTERIOR)
Fig. 2.10 The topographical variability of coronary artery orices in normal hearts. From Muriago M. etal. [32]
transposition of the great arteries (TGA), where
the aorta is anterior, the CAs regularly arise from
NON-CORONARY
AORTIC SINUS
(RIGHT POSTERIOR)
a
LEFT CORONARY
AORTIC SINUS
the facing sinuses of the aorta. Indeed, an anomalous origin of a coronary artery from the posterior
pulmonary artery in TGA is quite rare [22, 23].
Coronary Artery Anomalies
The incidence of reported coronary artery anomalies is [15, 24–29]
• 0.17% in autopsy,
• 1.2% in coronary angiography, and
• 0.17% in echo series.
Ogden [30] distinguished major anomalies,
like coronary artery origin from the pulmonary
artery, and minor anomalies, such as high take
off, single coronary artery, and origin from a
wrong coronary sinus. However, this classication turned out to be untenable, since even some
Ogden “minor” anomalies were proven to be lifethreatening as well.
Familial clustering of coronary artery anomalies has been sporadically reported [31]. It does
not exceed the rate of recurrence in siblings and
off-springs of other congenital heart diseases
and, as such, they cannot be considered a
Mendelian disorder.
There is a large spectrum of coronary artery
anomalies, from variants of normal without functional signicance to real morbid entities at risk
of myocardial infarction and sudden death.
b
Fig. 2.11 (a) The right coronary artery orice (arrow) is
just above (2mm) the sino-tubular junction, within normal limits. (b) The right coronary orice (arrow) is well
above the sino-tubular junction (10mm), over the threshold of normal limits. From Thiene, G., Corrado, D., Basso,
C. (2016). Coronary Artery Disease. In: Sudden Cardiac
Death in the Young and Athletes. Springer, Milano. https://
doi.org/10.1007/978- 88- 470- 5776- 0_3
(a) Variants of normal
• High take off from the aortic root with
coronary ostium located less than 2.5mm
above the sino-tubular junction [32, 33]
(Figs.2.10 and 2.11).
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