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Congenital
Anomalies
ofCoronary Arteries
GianfrancoButera
AlessandroFrigiola
Editors
123
Congenital Anomalies of Coronary
Arteries
Gianfranco Butera • Alessandro Frigiola
Editors
Congenital Anomalies
of Coronary Arteries
Editors
Gianfranco Butera
Pediatric Cardiology and Cardiac
Surgery
Bambino Gesù Hospital
Rome, Italy
Alessandro Frigiola
Cardiac Surgery Unit
Policlinico San Donato
SAN DONATO MILANESE
Milano, Italy
ISBN 978-3-031-36965-0 ISBN 978-3-031-36966-7 (eBook)
https://doi.org/10.1007/978-3-031-36966-7
© Springer Nature Switzerland AG 2023
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microlms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software,
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specic statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publisher nor
the authors or the editors give a warranty, expressed or implied, with respect to the material
contained herein or for any errors or omissions that may have been made. The publisher remains
neutral with regard to jurisdictional claims in published maps and institutional afliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Acknowledgments
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Paolo Angelini 1941–2023
Professor Paolo Angelini has been a true giant in medicine, particularly in
the eld of coronary artery anomalies, where he was a pioneer. He was always
easy to reach and available to share his knowledge and wisdom when a difcult case came to the attention of colleagues from all over the world. He has
been a true inspiration and also a strong force within this book, which he had
been waiting for a long time.
Sadly, he will not be able to hold it in his hands.
His legacy will last and his contribution to this book is the last witness of
his passion, knowledge and wisdom that will guide colleagues worldwide.
Gianfranco Butera and Alessandro Frigiola
v
Contents
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Part I From Embryology to Diseases
1 The Development of the Coronary Arteries . . . . . . . . . . . . . . . . . 3
Robert H. Anderson, Timothy J. Mohun, and Deborah
Henderson
2 Congenital Anomalies of Coronary Arteries: Anatomy,
Embryology and Risk of Sudden Death . . . . . . . . . . . . . . . . . . . . 19
Stefania Rizzo, Cristina Basso, Michela Muriago, and
Gaetano Thiene
3 Normal Coronary Flow Physiology . . . . . . . . . . . . . . . . . . . . . . . . 37
Carlo Trani, Cristina Aurigemma, and Filippo Crea
4 Myocardial Bridge(s) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
Alberto Barioli, Flavia Belloni, and Giuseppe Tarantini
5 Isolated Coronary Artery Fistulas . . . . . . . . . . . . . . . . . . . . . . . . . 57
M. Rebonato, G. Butera, S. Qureshi, and M. Carminati
6 Coronary Artery Abnormalities Associated to Congenital or
Non- congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
Roberto Formigari and Micol Rebonato
7 Anomalous Origin of the Coronary Arteries from
the Pulmonary Artery: ALCAPA and ARCAPA . . . . . . . . . . . . . 75
Alessandro Giamberti, Massimo Chessa, Martina Evangelista,
and Federica Caldaroni
8 Coronary Artery Anomalies: An Updated Discussion on
Nomenclature, Pathophysiology, and Screening . . . . . . . . . . . . . 85
Paolo Angelini and Carlo Uribe
Part II Diagnosis and Risk Stratication
9 Role of Patient History and Non- invasive Tests in the
Workflow of Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
Julie A. Brothers
vii
viii
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10 Advanced Imaging in Congenital Abnormalities of Coronary
Arteries in Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Jan Marek, Kristian Mortensen, and Claudio Capelli
11 Role of Invasive and Provocative Tests . . . . . . . . . . . . . . . . . . . . . 131
Francesco Bedogni
12 Pediatric Patients: Role of Invasive and Provocative Tests . . . . . 153
Silvana Molossi and Tam T. Doan
13 AAOCA in Young Athlete: How to Detect, What to Do,
When to Allow Coming Back to Competitive Sport? . . . . . . . . . 171
Massimiliano Bianco, Vincenzo Palmieri, and Paolo Zeppilli
14 Sudden Death: Differential Diagnosis and AOCA . . . . . . . . . . . . 187
Barbara Barra and Gherardo Finocchiaro
15 Congenital Coronary Artery Anomalies: Differential
Diagnosis of Ventricular Arrhythmias in Young Athletes . . . . . . 195
Carlo Pappone, Gabriele Negro, and Giuseppe Ciconte
Part III Modelling and Treatment(s)
16 How Computational Model May Help in Mechanism
Understanding? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
G. M. Formato, V. Ceserani, R. M. Romarowski,
M. Lo Rito, and M. Conti
Contents
17 Computational Modeling for Decision Making . . . . . . . . . . . . . . 217
Gianluca Rigatelli and Marco Zuin
18 Anomalous Aortic Origin of Coronary Arteries
Data from the Registries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Massimo A. Padalino and Matteo Ponzoni
19 Surgical Techniques for AAOCA . . . . . . . . . . . . . . . . . . . . . . . . . . 241
M. Lo Rito, O. Raisky, and A. Frigiola
20 Impact and Management of Anomalous Aortic
Origin of Coronary Arteries in Adult Patients
Undergoing Cardiac Surgery for Acquired Heart Disease . . . . . 251
Massimo Massetti, Maria Grandinetti, Federico Cammertoni,
Piero Farina, and Piergiorgio Bruno
21 Pre- and Postoperative Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265
Giuseppe Isgrò
22 Postoperative Complications and Outcomes
After AAOCA Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275
Anusha Jegatheeswaran
Part I
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From Embryology to Diseases
The Development oftheCoronary
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Arteries
RobertH.Anderson, TimothyJ.Mohun,
andDeborahHenderson
1
Introduction
Our aim with this chapter is to provide an account
of the development of the coronary arteries so as
to help in understanding the malformations that
afict them in the setting of congenital heart disease. Many, if not most, of the controversies that
continue to surround their embryological development are of limited signicance when considered relative to the understanding of the variations
found when the heart, or the coronary arteries
themselves, are congenitally malformed. This is
not to suggest that the knowledge of initial formation of the coronary vasculature is itself insignicant. On the contrary, it is vital to know how,
and when, the endothelial linings of the developing vessels can rst be identied, and whether
they form by a process of angiogenesis or vasculogenesis. Knowledge of this early development,
however, does not impact directly on understanding how the developing epicardial coronary arteries achieve their connection with the aortic root.
Nor is it directly relevant to an appreciation of
how the epicardial channels themselves extend so
R. H. Anderson (*) · D. Henderson
Biosciences Division, Newcastle University,
Newcastle-upon-Tyne, UK
e-mail: sejjran@ucl.ac.uk;
Deborah.henderson@Newcastle.ac.uk
T. J. Mohun
Francis Crick Institute, London, UK
as to percolate through the so-called compact
components of the ventricular walls. The manner
of formation of the compact component of the
ventricular walls remains controversial in itself.
Those investigating the interaction between formation of the coronary arteries and the development of the compact portions of the ventricular
walls have presumed that the compact layer is
thinned in the presence of so-called “noncompaction” [1]. This is not the case. There is
signicant evidence to show that such “noncompaction” is better described in terms of
excessive trabeculation [2]. As such, the presence
of an extensive non-trabeculated meshwork is
more likely to be an epiphenomenon rather than a
discrete cardiomyopathy [2]. Irrespective of these
potential disagreements, there can be no question
that the mural coronary arterial circulation cannot be established without the appropriate formation of the compact ventricular wall. Once the
circulation is established, the capillaries are able
to return to the arterial ow from the aortic root
into the coronary venous system, and eventually
back to the cavities of the heart itself. It is the
manner of connection of the epicardial plexus to
the aortic root that provides the understanding of
lesions such as anomalous origin of the coronary
arteries from the pulmonary trunk, or anomalous
origin from an inappropriate aortic sinus.
Understanding the abnormal arrangements found
in the setting of either the hypoplastic left heart
syndrome or pulmonary atresia with an intact
© 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_1
3
4
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R. H. Anderson et al.
ventricular septum, in contrast, is dependent on
the knowledge of how the ventricular walls are
converted from the initial pattern, which is a
meshwork of trabeculations, with minimal formation of the compact mural component, to the
situation in which it is the trabeculations which
are of minimal signicance. It is these two features, therefore, namely the connection of the
epicardial arteries to the aortic root and the
establishment of the ventricular mural circulation, on which we concentrate our attention. We
begin, nonetheless, with a brief overview of the
ongoing discussions regarding the origins of the
different components of the coronary arterial
walls.
Angiogenesis Versus
Vasculogenesis
An elegant overview of this important topic, and
its relevance to the understanding of the anatomy of both normal and abnormal coronary
arteries, is provided in the document prepared
by the Working Group on Cardiovascular
Development of the European Society of
Cardiology [3]. In that review, the authors base
their analysis on the fact that the denitive coronary arteries are formed on the basis of their
endothelial lining. This endothelial scaffold is
subsequently surrounded by the wall of vascular
smooth muscle, which itself is encased in a
brous matrix continuous with the external
adventitial layer. It is the endothelial primordiums that appear rst during embryological
development. And it is these components that
continue to be the subject of debate with regard
to angiogenesis as opposed to vasculogenesis. It
was initially accepted that the overall coronary
arterial endothelium was produced by angiogenesis [4]. This meant that new vessels were
formed from pre-existing ones by a process of
endothelial sprouting [5]. The initial “sprout”
was presumed to grow out of the aortic root [4].
This notion fell from grace when it became
accepted that the epicardial arteries, rather than
sprouting out from the aorta, grew into the valvar sinuses [6]. There is now much evidence,
both molecular [7] and morphologic [8], to
show that the initial arterial stems do, indeed,
grow out from the aortic root to join with the
developing epicardial vessels. But since the epicardial channels themselves are present prior to
the emergence of the aortic sprouts, it remains
appropriate to question the notion that the entire
vascular network, including the coronary venous
system, is generated by angiogenesis from solitary aortic primordiums. Indeed, much evidence
has accrued to show that at least part of the
endothelial network is formed by vasculogenesis [9]. In this latter process, it is presumed that
angioblasts, which are the progenitors of the
endothelial cells themselves, coalesce to form
clusters, which then transform to become new
vessels.
Irrespective of whether the endothelial linings
are generated by vasculogenesis as opposed to
angiogenesis, further debate has surrounded the
origin of the endothelial cells themselves.
Excluding the possibility that they all expand
from original aortic sprouts [5], various investigators have suggested that they derive from the
endocardial lining of the ventricular trabeculations [10], the liver sinusoids [11], or the epicardium [12]. Yet another theory has now achieved
prominence. The channels, rather than sprouting
from the aorta, are alleged to sprout initially from
the systemic venous sinus. In this concept, the
channels are then presumed to reprogram to
become arterial rather than venous [13]. That the
entirety of the coronary arterial network is derived
by sprouting from the systemic venous sinus
seems just as unlikely as that it would sprout from
the aorta. And, if the initial channels are re-programmed to become arterial, a second parallel
system will be required to form the veins.
Subsequent molecular biological evidence, furthermore, has questioned the unitary origin of the
endothelial cells. In this regard, it has been shown
that a subset of epicardial progenitors, at least in
the murine heart, make endothelial contributions
[14]. It has then been shown that parts of the network, at least for the coronary arteries, are derived
from the endocardial linings of the ventricular trabeculations [15]. Questions must now be posed
regarding yet another piece of evidence advanced
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