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PATENT FORAMEN OVALE
CLOSURE FOR STROKE,
MYOCARDIAL
INFARCTION,
PERIPHERAL EMBOLISM,
MIGRAINE, AND
HYPOXEMIA
Edited by
M. KHALID MOJADIDI
Virginia Commonwealth University, Richmond, VA, United States
BERNHARD MEIER
University Hospital Bern, Bern, Switzerland
JONATHAN M. TOBIS
University of California, Los Angeles, CA, United States
Academic Press is an imprint of Elsevier
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Copyright © 2020 Elsevier Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including
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This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be
noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding,
changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information,
methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own
safety and the safety of others, including parties for whom they have a professional responsibility.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury
and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
A catalog record for this book is available from the Library of Congress
British Library Cataloguing-in-Publication Data
A catalogue record for this book is available from the British Library
ISBN: 978-0-12-816966-7
For information on all Academic Press publications visit our website at
https://www.elsevier.com/books-and-journals
Publisher: Stacy Masucci
Acquisition Editor: Katie Chan
Editorial Project Manager: Anna Dubnow
Production Project Manager: Stalin Viswanathan
Cover Designer: Christian J. Bilbow
Typeset by TNQ Technologies
Contributors
Islam Abudayyeh Loma Linda University Health, Loma
Linda, CA, United States
Nayan Agarwal Cardiovascular Institute of the South,
Zachary, LA, United States
Shikhar Agarwal Geisinger Commonwealth School of
Medicine, Danville, PA, United States
Ricardo Avendano Albert Einstein College of Medicine,
Bronx, NY, United States
Imran Baig Geisinger Medical Center, Danville, PA, United
States
Stefan Bertog Cardiovascular Center, Frankfurt, Germany
Islam Y. Elgendy Massachusetts General Hospital and
Harvard Medical School, Boston, MA, United States
Sammy Elmariah Massachusetts General Hospital and
Harvard Medical School, Boston, MA, United States
Robert T. Faillace Albert Einstein College of Medicine,
Bronx, NY, Unites States
Mohamed M. Gad Cleveland Clinic Foundation, Cleveland,
OH, United States
Adam Gershon Albert Einstein College of Medicine, Bronx,
NY, Unites States
Harsh Golwala Brigham and Women’s Hospital and
Harvard Medical School, Boston, MA, United States
Jonathan S. Gordin University of California, Los Angeles,
Los Angeles, CA, United States
Jonas Dominik Ha
¨
ner University Hospital Bern, Bern,
Switzerland
Ignacio Inglessis Massachusetts General Hospital and
Harvard Medical School, Boston, MA, United States
Simon Jung University Hospital Bern, Bern, Switzerland
Damianos G. Kokkinidis Albert Einstein College of
Medicine, Bronx, NY, United States
Dhaval Kolte Massachusetts General Hospital and Harvard
Medical School, Boston, MA, United States
Preetham Kumar University of California, Los Angeles, Los
Angeles, CA, United States
Poonam Mahato Albert Einstein College of Medicine, Bronx,
NY, Unites States
Ahmed N. Mahmoud University of Florida, Gainesville, FL,
United States
Dhruv Mahtta Baylor College of Medicine, Houston, TX,
United States
Heinrich P. Mattle University Hospital Bern, Bern,
Switzerland
Bernhard Meier University Hospital Bern, Bern,
Switzerland
M. Khalid Mojadidi Virginia Commonwealth University,
Richmond, VA, United States
Krassen Nedeltchev Cantonal Hospital Aarau, Aarau,
Switzerland
Fabian Nietlispach Cardiovascular Center Zurich,
Hirslanden Klinik im Park, Zurich, Switzerland
Leonidas Palaiodimos Albert Einstein College of Medicine,
Bronx, NY, United States
Saul A. Rios Albert Einstein College of Medicine, Bronx, NY,
United States
Christoph Schankin University Hospital Bern, Bern,
Switzerland
Erik J. Schneibel University of Florida, Gainesville, FL,
United States
Horst Sievert Cardiovascular Center, Frankfurt, Germany
Barbara E. Sta
¨
hli University Heart Center, University
Hospital Zurich, Zurich, Switzerland
Anwar Tandar
University of Utah, Salt Lake City, UT, United
States
Felix C. Tanner University Heart Center, University Hospital
Zurich, Zurich, Switzerland
David Thaler Tufts University School of Medicine, Boston,
MA, United States
Jonathan M. Tobis University of California, Los Angeles,
Los Angeles, CA, United States
Lina Ya’qoub Ochsner-Louisiana State University,
Shreveport, LA, United States
Ali Zaidi The Zena and Michael A. Wiener Cardiovascular
Institute, The Icahn School of Medicine at Mount Sinai,
New York, NY, United States
ix
Preface
A patent foramen ovale (PFO) is a congenital vestige of the fetal circulation that persists in one-fourth of adults.
Once considered benign, the presence of PFO-mediated right-to-left shunt has been associated with a multitude of
pathological conditions including ischemic stroke, migraine headache, myocardial infarction, peripheral embolism,
hypoxemia, decompression sickness, Raynaud syndrome, and coronary spasm. A unifying pathophysiologic hy-
pothesis is that a chemical substance, particulate matter, or deoxygenated blood from the venous circulation crosses
the PFO canal from the right to the left atrium to produce these clinical conditions.
The failure to significantly prove an advantage of PFO closure in three randomized cryptogenic stroke trials
(CLOSURE I, PC, early RESPECT) and three migraine trials (MIST, PRIMA, PREMIUM), with relatively wide
enrollment criteria and short follow-up duration, temporarily put transcatheter PFO closure out of the limelight, with
dwindling interest from the neurology and cardiology communities. After release of the long-term follow-up data
from the RESPECT trial, and meta-analyses of the early three cryptogenic stroke trials, that showed superiority of PFO
closure over medical therapy for secondary prevention of stroke, the United States Food and Drug Administration
approved the Amplatzer PFO Occluder (Abbott; Chicago, IL) in October 2017 for percutaneous PFO closure to reduce
risk of recurrent stroke from paradoxical embolism. Prior to this, percutaneous PFO closures were performed off-label
with the use of similar atrial septal defect closure devices. The off-label availability of PFO closure devices in the
United States and free availability in most other countries proved to be a dilemma for researchers recruiting patients
for clinical trials, resulting in slow patient enrollment and, likely, clinician-biased preference for off-label PFO closure
for the higher-risk patients, as opposed to a 50% chance of their randomization to a medical therapy arm. More recent
results retrospectively condone this attitude based on intuition.
Between late 2017 and early 2018, four positive cryptogenic stroke trials (long-term RESPECT, CLOSE, Gore
REDUCE, and DEFENSE-PFO) placed PFO closure back into the spotlight with renewed interest among clinicians.
These studies showed that with good patient selection and longer follow-up, it can be demonstrated that PFO closure
significantly reduces the risk of recurrent stroke compared to standard of care medical therapy in patients with
imaging-confirmed ischemic stroke of no other apparent etiology.
In addition to closure of PFO for cryptogenic stroke (more accurately termed a “PFO-associated stroke”), this book
also advocates for consideration of PFO closure in other symptomatic, and often debilitating, conditions. Unlike the
situation for PFO-associated stroke, there are no current randomized clinical trials that document the benefit of PFO
closure over medical therapy for any of these other pathologies. It is probable that a new randomized clinical trial for
PFO and migraine will be carried out over the next few years. The other conditions, however, are relatively infrequent
and will likely never be subjected to the rigors of a randomized trial. The data presented in these chapters will aid in
the guidance of physicians who care for these patients.
When treating patients with a PFO-mediated pathology, clinicians will encounter a multitude of questions,
including appropriateimaging assessment of the PFO anatomy and shunt physiology, ischemic stroke risk assessment
and workup, suitable patient selection, device choice and implantation technique, and consideration of percutaneous
closure for a variety of pathologies mentioned above. This book will serve cardiologists, neurologists, pulmonologists,
internists, general practitioners, and researchers with an interest in PFO-related conditions; it embodies the most
current and comprehensive review of the clinical manifestations, diagnosis, and management of PFO pathologies as
described by some of the leading experts in the field. What was once considered an innocent bystander remnant of the
fetal circulation has now been shown to be a potential pathway of death, stroke, migraine, and unexplained hypox-
emia, all preventable by transcatheter closure on an outpatient basis. Since it is present in 25% of the world’s popu-
lation, a PFO should be classified as the most common congenital heart defect and should be treated with concern for
the problems that it can generate.
M. Khalid Mojadidi, MD FACP FACC
Virginia Commonwealth University, Richmond, Virginia
Bernhard Meier, MD FACC FESC
University Hospital Bern, Bern, Switzerland
Jonathan M. Tobis, MD FACC MSCAI
University of California, Los Angeles, Los Angeles, California
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Acknowledgments
The Editors and Authors would like to express their appreciation for the support they received throughout their
careers from their families, mentors, and colleagues.
xiii
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CHAPTER
1
Embryology, Anatomy, and Physiology:
Anatomical Variations, Lipomatous
Hypertrophy, Atrial Septal Aneurysm,
Eustachian Valve, Chiari Network,
Combination With Other Atrial Septal Defects
Damianos G. Kokkinidis
1
, Saul A. Rios
1
, Ricardo Avendano
1
,
Ali Zaidi
2
, Robert T. Faillace
1
1
Albert Einstein College of Medicine, Bronx, NY, United States;
2
The Zena and Michael A. Wiener Cardiovascular Institute, The Icahn School of Medicine at Mount Sinai,
New York, NY, United States
OUTLINE
Introduction 3
PFO Embryology 3
PFO Anatomy 4
Prenatal CirculationdRole of the Foramen Ovale 4
Postnatal Circulation 5
Persistence of PFO and Its Consequences 6
Anatomic Variations and Clinical Importance 6
Lipomatous Hypertrophy and Clinical Implications
7
Atrial Septal Aneurysm (ASA)
8
Eustachian Valve and Chiari Network
8
Combination with Other Atrial Septal Defects
9
Conclusion
10
References
10
INTRODUCTION
PFO Embryology
The foramen ovale is necessary for blood flow across the fetal atrial septum. During early embryonic stages, the
atrium is composed of a single cavity. The development of the atrial septum begins 4 to 5 weeks after conception,
usually between day 27 and day 37 postconception. At this stage, the primordial single atrium divides into right
and left sides by formation and fusion of two septa: the septum primum and septum secundum. The first structure
to develop is the primary atrial septum. This originates from the craniodorsal wall of the atrium and grows toward
the endocardial cushions. The septum primum is at first crescent-shaped, creating a large window connecting the
3
PFO Closure for Stroke, Myocardial Infarction, Peripheral Embolism, Migraine, and Hypoxemia
Copyright © 2020 Elsevier Inc. All rights reserved.https://doi.org/10.1016/B978-0-12-816966-7.00001-4
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left and right atrium. It grows from the primordial atrial roof toward the endocardial cushions, partially dividing the
common atrium into right and left halves. The endocardial cushions are formed on the dorsal and ventral walls of
the atrioventricular canal, approach each other, and fuse, dividing the atrioventricular canal into right and left sides.
The foramen primum results, allowing oxygenated blood flow from the right to the left atrium. As the septum pri-
mum grows toward the endocardial cushions, perforations develop. These perforations form a large central window,
through programmed cell death, before the septum primum and endo cardial cushions fuse [1].
The window made as these perforations fuse is the ostium secundum, which also allows blood flow from the right
to the left atrium. On the right side of the septum primum, another crescent-shaped membrane grows from the ven-
trocranial atrial wall: the septum secundum. It gradually grows and overlaps part of the ostium secundum, forming
an incomplete septal partition as an oval-shaped window. The septum secundum develops by an infolding of the
atrial walls, growing downward around the right atrial aspect of the septum primum, and forming a thick arc
over the ostium secundum. A hole remains inferiorly in the septum secundum where the septum primum is exposed
on the right atrial side. This region is called the fossa ovalis and is composed only of the septum primum. The two
septa eventually fuse together in the areas where they overlap, including around the edges of the fossa ovalis. How-
ever, at the anterosuperior edge of the fossa ovalis (adjacent to the aortic root) they remain unfused. This tunnel, or
“flap valve,” permits the right-to-left shunting of blood that is necessary for normal fetal circulation. It is this win-
dow that becomes the foramen ovale. The remaining septum primum forms a flap-like valve over the foramen ovale,
which typically closes by fusing with the growing septum secundum after birth. The ostium secundum leads to
continuous blood flow from the right to left side of the heart, allowing blood to bypass the fetal pulmonary circu-
lation during fetal development [2,3].
In utero, oxygenated blood from the placenta enters the inferior vena cava and the right atrium; it then crosses the
foramen ovale to enter the systemic circulation. Most blood flow from the superior vena cava is routed through the
tricuspid valve and enters the right ventricle. At birth, right heart pressures and pulmonary vascular resistance
drop as pulmonary arterioles open in reaction to oxygen filling the alveoli. Left atrial pressure may also rise as the
amount of blood returning from the lungs increases. Either or both of these mechanisms cause flap closure against
the septum secundum. The septum primum and septum secundum begin to fuse after birth and this fusion is com-
plete by age 2 in about 75% of individuals, but patency persists in the other 25%. The patent foramen ovale (PFO) is a
residual, oblique, slit-shaped defect resembling a tunnel. The reasons why the septa fail to close and produce a PFO are
unknown but are likely related to multifactorial inheritance [4].
PFO Anatomy
The prevalence of probe-patent PFO is about 27%, with decreasing prevalence at each decade of life [4]. The mean
diameter in the 1st decade is 3.4 mm and in the 10th decade is 5.8 mm, perhaps reflecting size-based selection over
time where larger PFOs remain patent and smaller defects close [1]. An alternative explanation could be that the PFO
is small in the pediatric age group but enlarges as the heart grows. There are no studies with a serial reliable method
of quantitating the size of a PFO such as with balloon dilation. An autopsy only catches a single snapshot of a PFO
size, and echocardiograms, including transesophogeal echocardiography (TEE), are not as accurate for sizing a PFO
compared with balloon sizing (unpublished data). Greater PFO size increases the risk of paradoxical embolism, and
the heterogeneity of size and morphology are pertinent to interventional device closure selection [5,6]. The anatomy
of a PFO can be highly variable, which has important implications when considering an appropriate closure device.
The dimensions and position of the tunnel can vary and must be carefully defined before PFO closure. Some PFOs
consist of a tunnel that is long, with the septa tightly opposed, whereas others open widely. In some PFO tunnels, the
septum primum is held away from the septum secundum by a fold of tissue on the left atrial side, a so-called PFO
with fixed opening. The authors speculate that these ridges can result in a continuous baseline left-to-right shunt and
could prevent a closure device from correctly opposing the tissues of the primum and secundum septa, thus pre-
venting an adequate seal.
PRENATAL CIRCULATIONdROLE OF THE FORAMEN OVALE
The fetal circulation has unique characteristics as gas exchange occurs in the placenta instead of the fetal lungs. In
the fetus, the placenta has the lowest vascular resistance and receives 40% of the fetal cardiac output, which results in
a low systemic pressure. In contrast, the fetal lungs are filled with fluid, resulting in a high vascular resistance and
less than 10% of the cardiac output goes to the fetal lungs.
1. EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY4
I. INTRODUCTION
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The fetal circulation can be understood as two interconnected pathways; blood with high oxygen content enters
through the umbilical vein into the umbilical recess. From the placenta, oxygenated blood with a saturation of 67%
flows through the umbilical vein and splits upon entering the abdomen of the fetus. The majority flows through the
ductus venosus into the inferior vena cava, the right atrium, and then through the foramen ovale [7]; the remaining
blood supplies the liver. Blood originating from the ductus venosus enters the right atrium and, because of a stream-
ing effect by the Eustachian valve, is largely shunted through the foramen ovale into the left side of the heart and
aorta to feed the coronary, cerebral, and systemic circuits with oxygenated blood.
The second pathway directs less oxygenated blood from the superior vena cava and the inferior vena cava
distal to the ductus venous, from the right atrium into the right ventricle, with minimal mixing with the
oxygenated blood originating from the ductus venosus. Almost all of the right ventricular output (90%) bypasses
the lung and is shunted through the patent ductus arteriosus to the descending aorta, distal to the origin of the
carotid arteries. This deoxygenated blood is transported through the aorta and the umbilical arteries to the
placenta f or gas exchange, where it releases carbon dioxide and waste products and collects oxygen and
nutrients [4,5].
In the fetus, the blood flow is structured so that vital organs (e.g., liver, heart, and brain) receive blood with a
relatively high degree of oxygen saturation. The liver receives blood directly from the umbilical vein without
mixing with deoxygenated fetal blood. Blood flowing through the coronary and carotid arteries has a relatively
high degree of oxygen saturation because oxygenated blood from the umbilical vein flows to the right atrium
(via the ductus venosus and inferior vena cava) and is shunted through the foramen ovale to the left side of
the heart and aorta. This shunting is achieved through differential velocities of incoming venous bloodstreams
and directing of oxygenated blood to the foramen ovale. This reduces mixing of oxygenated blood with deoxy-
genated blood entering the right atrium from the superior vena cav a. The deoxygenated blood is directed toward
the right ventricle and shunted through the ductus arteriosus to the aorta, but distal to the origin of the carotid
and coronary arteries. The low fetal oxygen content maintains the architecture of the fetal circulation by causing
pulmonary vascular constriction, which maintains pulmonary vascular resistance at a high level, thereby pro-
moting right-to-left shunting through the foramen ovale and ductus arteriosus.
POSTNATAL CIRCULATION
During fetal life, the placental circulation is a low resistance system and receives about 40% of the fetal cardiac
output. Exchange of gas and nutrients occurs between the fetal and maternal circulation. Only 10% of the fetal car-
diac output passes through the lungs. The transition from fetal to newborn circulation begins even before the onset
of labor. At the end of the third trimester, increased levels of cortisol promote fetal lung maturation and production
of surfactant, which decreases intraalveolar surface tension, leading to a gradual decrease in pulmonary vascular
resistance.
At the moment of birth, the umbilical vessels constrict in response to increased blood PO
2
. This constriction, along
with umbilical cord clamping, decreases the blood flow through the ductus venosus which closes 3 to 10 days after
birth. Due to the elimination of blood flow through the placenta, the systemic vascular resistance at birth doubles. As
resistance rises, aortic pressure increases. There is further increase in the left atrial and left ventricular pressures. Due
to expansion of the lungs as the infant breathes, the pulmonary vascular resistance greatly decreases as the pulmo-
nary vessels dilate in response to lung expansion and higher PO
2
, and there is almost a 10-fold increase in blood flow
through the pulmonary circulation. The pulmonary arterial pressure is reduced along with the right atrial and right
ventricular pressures. Therefore, blood flow changes from the high left atrial pressure to the low right atrial pressure
through the foramen ovale. With the higher pressure in the left atrium, the septum primum part of the foramen ovale
valve is pushed against the septum secundum and physiologically closes the fossa ovalis within minutes to hours of
birth [6]. The foramen ovale now becomes the “fossa ovalis.”
At the moment of birth, the umbilical vessels constrict in response to increased blood PO
2
with closure of the duc-
tus arteriosus and ductus venosus. Closure of the ductus arteriosus is by smooth muscle contraction with complete
closure achieved in 1e8 days. It is further replaced by fibrous tissue, called the ligamentum arteriosum. This contrac-
tion of smooth muscles occurs because of the increase in availability of oxygen. At birth, the opposite direction of
blood flow from the aorta to the pulmonary artery supplies more oxygenated blood than before. The degree of
I. INTRODUCTION
POSTNATAL CIRCULATION 5
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