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smooth muscle contraction is highly dependent on the availability of oxygen. Closure of the ductus venosus is also
caused by strong contraction of the muscular wall of the ductus venosus. This structure is changed into the fibrous
ligamentum venosum and can sometimes be continuous with the round ligament of the liver.
PERSISTENCE OF PFO AND ITS CONSEQUENCES
Immediately after birth, the systemic vascular resistance increases, while the pulmonary resistance and the right-
sided cardiac pressures decrease. The increase in the pulmonary venous return to the left atrium will increase the left
atrial pressure and there will be a reversal of the interatrial pressure gradient. Complete fusion of the septum pri-
mum and septum secundum typically happens within the first 20 months of life. This process starts with functional
closure of the foramen ovale valve at birth. However, in up to one-third of patients initially and up to one-fifth later
in life, there will remain patency (possibility to open) of the foramen ovale and intermittent or persistent right-to-left
interatrial shunting of blood at rest may occur through the PFO [7,8].
The most feared complication of a PFO is paradoxical embolism via an interatrial right-to-left shunt. This phe-
nomenon occurs when thrombi from the venous circulation reach the right atrium and pass through the PFO,
bypassing the filter of the pulmonary circulation and entering the left atrium. Thrombi from the left side of the heart
may cause embolic phenomena to the brain (stroke or transient ischemic attack) (Chapters 4e7), heart (embolic
myocardial infarction) (Chapter 8), or per ipheral circulation (limb or other organ embolism) (Chapter 9). Approxi-
mately 30% of the estimated 12 million ischemic strokes annually will not be attributed to a specifi c cause after the
standard diagnostic workup, and are commonly described as cryptogenic [9]. Undiagnosed paroxysmal atrial fibril-
lation and paradoxical embolism through a PFO are considered to be the most common causes of cryptogenic strokes
and the latter is the typical reason for embolic strokes of undetermined source.
Stroke and other systemic embolism of unclear origin are not the only conse quence of a PFO. According to some
studies, the incidence of PFO in patients with migraine headache with aura can be as high as among patients with
cryptogenic stroke (Chapters 10 and 11). Moreover, the incidence of right-to-left shunt among cryptogenic stroke pa-
tients who have migraine with frequent aura has been reported to be as high as 93% [10]. However, no clear path-
ophysiological relationship has been established thus far [9,11e13]. PFO has also been associated with upright
positional hypoxia and dyspnea, a syndrome described as platypnea-orthodeoxia (Chapter 12). This rare condition
can be dif ficult to diagnose and is almost always associated with an intracardiac or intrapulmonary shunt. Another
association that has been described is the relationship between decompression illness and PFO (Chapter 13). Divers
who develop the cutaneous or neurological forms of decompression illness have been found to have a 4-times higher
prevalence of PFO [14e17].
Earlier in life, a PFO usually remains clinically silent. However, hemodynamic abnormalities including a right-to-
left shunt may occur when there is a coexisting condition that can increase the right atrial pressure (i.e., patent
ductus arteriosus, ventricular septal defect, pulmonary hypertension). Right-to-left shunting may be induced by
conditions that elevate the right atrial pressure such as pulmonary diseases, an anomalous pulmonary venous
return, tricuspid atresia, crying, breath-holding, coughing, and straining (Valsalva maneuver).
ANATOMIC VARIATIONS AND CLINICAL IMPORTANCE
With the increasing frequency of percutaneous closure of PFO, it is important to have a clear understanding of the
anatomy that will be closed with the procedure [18,19]. The common goal of all closure devices is to successfully stop
interatrial shunting through the PFO. However, anatomic variations can be challenging for the operator and,
depending on the device, it is possible to have clinically relevant residual shunting after device placement. The
increasing use of 3D TEE has allowed more accurate preoperative assessment and characterization of PFO-
associated anatomical variations that previously remained undetected. There are many different proposed classifi-
cations of PFO defects. One classification proposed the description of PFOs as either simple or complex [19]. For a
PFO to be classified as simple, it should not have any of the following characteristics: atrial septal aneurysm (ASA);
large Eustachian valve or ridge, thickened septum secundum, or other defects of the fossa ovalis. Standard closure
devices can close the majority of simple PFOs. The subgroups of complex PFOs can be found in Table 1.1. A tunnel
length >8 mm is a challenge for devices with short nonstretchable waists, because of difficulties in their deployment.
Narrow tunnels increase this problem further. Another anatomic variation can be a PFO with multiple openings on
the left atrial side, which also requires special attention by the operator before device closure. Coexistence of
I. INTRODUCTION
1. EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY6
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additional fossa ovalis defects, apart from the PFO, is described as a hybrid defect in the literature. Hybrid defects
include either 1 or multiple (cribriform) small or larger fossa ovalis defects. When percutaneous closure is pursued,
all of these defects should be closed. Septum secundum thickness more than 10 mm, usually because of ex cessive
adipose tissue, may make the PFO harder to close with a percutaneous approach and larger or softer devices should
be utilized.
Two other anatomic characteristics that are associated with complex PFOs include a Eustachian valve or ridge and
Chiari network. It has been reported that a Eustachian valve can act as an obstacle for placement of PFO-occluding
devices by limiting the space close to the fossa ovalis on the right atrial side [19]. As a result, a residual shunt may
persist. However, this may be device dependent and is unlikely to be an important issue with current closure de-
vices. Both 2D and 3D TEE can help to better visualize the anatomy. A Chiari network is redundant tissue attached
to the Eustachian valve and may also interfere with device placement leading to catheter entrapment or device
entanglement [21,22].
LIPOMATOUS HYPERTROPHY AND CLINICAL IMPLICATIONS
Lipomatous atrial septal hypertrophy (LASH) was first described in 1964 and is defined as the deposition of fat in
the area of the interatrial septum but not in the fossa ovalis [20,23]. Depending on the imaging modality used, the
rate of LASH reported in the literature varies from 2.2% with computed tomography (CT) to 8% with TEE [24]. Au-
topsy studies suggest an incidence as low as 1%. There are studies that show an association between LASH and
obesity, while the prevalence of LASH reportedly increases with age [25e27]. LASH is created by the infiltration
of the septum secundum, also known as the limbus, by adipose cells which leads to fat accumulation during the
embryologic development of the interatrial septum [28,29]. The fossa ovalis valve is spared by the fat associated
with the lipomatous hypertrophy, which is extended both cephalad and caudad to the fossa itself [27,29]. The ceph-
alad thickening is usually more extensive than the caudad extension, projecting into the atrial cavity. LASH can be
detected with echocardiography, CT, and magnetic resonance imaging [27,29]. The pathognomonic sign is the
“dumbbell appearance” of the interatrial septum with parallel sparing of the fossa ovalis valve. With CT, LASH
has the attenuation coefficient of adipose tissue, which can be useful to differentiate it from tumors, while magnetic
resonance imaging can provide even more det ails [30]. Although LASH is usually considered a benign entity, there
are reports associating LASH with atrial arrhythmias and sudden cardiac death [29e33]. These arrhythmias may be
related to myocardial infiltration from fat, which disrupts the regular atrial depolarization. The presence of LASH is
considered to be a challenge for transseptal puncture, since the hypertrophy may interfere and require more force
than normally used to pass the needle through the septum and into the left atrium if the thin fossa ovalis is not found
[28,33]. However, successful percutaneous interventions that need transseptal punctures can still be performed,
despite the presence of LASH [35]. Biplane, 3D TEE, and intracardiac echocardiography have been shown to be
extremely useful for the guidance of the transseptal puncture needle.
The main practical concern with LASH, when performing PFO closure, is that the thickened septum secundum
causes the closure device to splay, making it stick out perpendicular to the plane of the atrial septum. If the right
atrial disk does not cover the edge of the septum secundum, then it could slip off the ridge and fall into the PFO
tunnel with a high potential of incomplete closure and also a small potential for embolization.
TABLE 1.1 Complex PFO Characteristics [20]
Complex PFO
Concomitant atrial septal aneurysm
Tunnel more than or equal to 8 mm
Multiple atrial septum fenestrations
Eustachian valve or Chiari network
Hybrid defect
Septum secundum thickness >1cm
Altered anatomy because of enlargement of the aortic root
With permission from Ref. [19].
I. INTRODUCTION
LIPOMATOUS HYPERTROPHY AND CLINICAL IMPLICATIONS 7
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ATRIAL SEPTAL ANEURYSM (ASA)
An atrial septal aneurysm (ASA) is defined as the region of the septum primum that bulges into either atrium. An
ASA can protrude into the left or the right atrium according to the pressure variation during the cardiac cycle [36].
An ASA is found in combination with other structural abnormalities, accompanied almost always by a PFO or atrial
septal defect [37e39]. There are previous descriptions of strokes caused by an ASA without concomitant PFO, but it
is suspected they were misguided by early ultrasound imaging that was able to visualize the ASA but not the PFO. A
PFO is associated with an ASA in most cases because the continuous motion of the ASA presumably precluded
septal fusion after birth. The limitations and advantages of ultrasound imaging (echocardiography and transcranial
Doppler) for PFO imaging are discussed in Chapter 2.
In stroke studies, an ASA has been found in as high as 10% of patients with a PFO, but the prevalence in the gen-
eral population is likely to be lower [40e42]. In studies investigating outpatient cohorts, the prevalence of ASA was
estimated to be 2.5% [43]. A predominance of female gender has been reported in the majority of these series [43e45].
The size of the ASA is calculated as a proportion of surfac e occupied by the aneurysmal tissue compared with the
entire atrial septum. Individuals with a PFO who also have a concomitant ASA have been found to have a higher risk
of recurrent stroke [46e48]. Recent randomized trials and their meta-analyses demonstrated a lower number needed
to treat when PFO closure was performed for strokes with high risk echocardiographic features (Chapters 7 and 18)
[49e52]. The mechanism by which an ASA increases embolic risk is not clear, but it is hypothesized to be related to
the occurrence of higher volume right-to-left shunting of blood with virtually every heartbeat. An alternative but
unproven hypothesis is that an ASA could lead to formation of platelet-fibrin aggregates on the left atrial side of
the aneurysm. The echocardiographic definition of an ASA in adults is an excursion of the septal tissue (usually
the fossa ovalis) of more than 10 mm from the midline plane of the atrial septum into either the right or left atrium,
or a combined total right and left excursion of more than 15 mm [53,54]. Recognizing the ASA before device place-
ment facilitates optimal device selection. An association between ASA and mitral valve prolapse has been reported
in both echocardiographic and autopsy studies [38,53,55] . Additionally, previous reports demonstrated an associa-
tion between ASA and cardiac arrhythmias and electrocardiographic abnormalities [43]. Transthoracic echocardiog-
raphy (TTE) can miss up to 50% of ASAs. In contrast to TTE, TEE and intracardiac echocardiography are superior for
detecting an ASA since the interatrial septum is in the near field of the imaging probe (Chapters 2 and 3).
EUSTACHIAN VALVE AND CHIARI NETWORK
The Eustachian valve, also known as the valvula venae cavae inferioris, is a vestige of the superior portion of the
right sinus valve and the sinus septum [56]. The valve is formed by a lower muscular ridge and an upper membra-
nous part (Fig. 1.1). It arises from the anterior border of the inferior vena cava orifice and typically presents as a cres-
centic fold of endocardium [57]. Prenatally, the Eustachian valve directs the oxygenated blood from the inferior vena
FIGURE 1.1 Panels A and B show a transverse and sagittal view of cadaveric hearts, respectively. Note the close proximity of the Eustachian
valve (EusV) and the inferior vena cava ostium (IVCO). CSO, coronary sinus ostium. IS, interatrial septum. With permission from Ref. [58].
I. INTRODUCTION
1. EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY8
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cava toward the PFO. Postnatally, the Eustachian valve is expected to regress. Despite the lack of data due to its low
prevalence, observational studies report a prevalence of 30%, measuring on average 5 mm in length and covering
22.914.6% of the inferior vena cava surface [58,59].
In rare cases, a prominent Eustachian valve may obstruct the right ventricular inflow due to persistence of the
right valve of the systemic venous sinus [60]. If present, it usually manifests as cyanosis during the immediate post-
natal period [61]. Presence of a prominent Eustachian valve has been well described as a risk factor for cryptogenic
stroke in patients with a PFO [56,62,63]. A large bulky Eustachian valve may rarely interfere with device deploy-
ment. This ridge limits the space available over the fossa ovalis on the right atrial side of the interatrial septum,
and may cause a PFO occluder device to be positioned away from the fossa ovalis. The disk may rest on the Eusta-
chian ridge and result in the PFO tunnel being held open, leaving a residual shunt [64].
The Chiari network is an embryonic remnant of the sinus venosus valve, which is more commonly located in
proximity to the inferior vena cava orifice and the ostium of the coronary sinus (Fig. 1.2), although it can be observed
in several locations in the right atrium. The incidence ranges from 2% to 4%, and it is usually considered a normal
anatomic variant [65].
A Chiari network has been associated with a wide array of clinical presentations that may warrant special atten-
tion, such as obstruction of cardiac blood flow and infective endocarditis, and occasionally may mimic an intracar-
diac tumor [66e68]. Due to its fenestrated nature, cardiac catheters may become entrapped by the Chiari network
fibers when performing percutaneous closure of a PFO or atrial septal def ect [69e71]. Similar to a Eustachian valve, a
Chiari network may be a risk factor for PFO-associated stroke, where these anatomical variants can guide thrombi
from the inferior vena cava straight to the PFO opening.
COMBINATION WITH OTHER ATRIAL SEPTAL DEFECTS
Before proceeding with percutaneous device closure, interventionalists shou ld be aware of the exact anatomy of
the interatrial opening. In some cases, there may be another opening (such as a coexisting atrial septal defect) in
addition to the PFO. The classification by Ewert et al. has been used to classify the multifenestrated aneurysmal
septum into 4 different subtypes (Fig. 1.3): Type A: atrial septal aneurysm with PFO, Type B: atrial septal aneurysm
with a single atrial septal defect, Type C: atrial septal aneurysm with 2 perforations located in not more than
FIGURE 1.2 Classic configuration of the mesh-like network composition of the Chiari network. Observe that it lines the septal and posterior
leaflets of the tricuspid valve. The septum spurium is a fold that eventually fuses with the atrial septum during embryonic development of the
heart. With permission from Ref. [68].
I. INTRODUCTION
COMBINATION WITH OTHER ATRIAL SEPTAL DEFECTS 9
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2 clusters, and Type D: atrial septal aneurysm with multiple perforations located in more than 2 clusters [72]. The
authors discouraged device closure of Type D, but central placement of a large Amplatzer Cribriform Occluder
has provided successful treatment in many reported cases.
CONCLUSION
Understanding the embryology and anatomical variances of the atrial septum is useful to appreciate the mecha-
nisms involved in PFO-related clinical conditions. Changes in the pulmonary circulation and left and right heart
pressures after birth contribute to physiologic PFO closure. Anatomic variations, such as the presence of an ASA
or Eustachian valve, can have important implications in terms of the likelihood of a recurrent embolic event later
in life; understanding the reasons for this increased risk may help the patients comprehend why PFO closure
may be preferable in their case.
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I. INTRODUCTION
1. EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY12
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CHAPTER
2
Echocardiography, Transcranial Doppler, and
Oximetry for Imaging and Quantification of
PFO-Mediated Shunts
Mohamed M. Gad
1
, Lina Ya’qoub
2
, Ahmed N. Mahmoud
3
,
Jonathan M. Tobis
4
, M. Khalid Mojadidi
5
1
Cleveland Clinic Foundation, Cleveland, OH, United States;
2
Ochsner-Louisiana State University, Shreveport, LA,
United States;
3
University of Florida, Gainesville, FL, United States;
4
University of California, Los Angele s, Los Angeles,
CA, United States;
5
Virginia Commonwealth University, Richmond, VA, United States
OUTLINE
Introduction 16
Ultrasound Detection of a PFO 16
Contrast Agent During a Bubble Study 16
Injection Site for a Bubble Study (Antecubital vs.
Femoral) 17
Provocation Maneuvers During a Bubble Study 17
Diagnostic Criteria for Intracardiac Right-To-Left
Shunt 17
Transthoracic Echocardiography for the Diagnosis
of PFO 17
Protocol for a Transthoracic Echocardiography
Bubble Study 18
Diagnostic Accuracy of Transthoracic
Echocardiography Bubble Study 18
Advantages and Limitations of Transthoracic
Echocardiography for Detecting a PFO 19
Transesophageal Echocardiography for the Diagnos is
of PFO 20
Protocol for a Transesophageal Echocardiography
Bubble Study 20
Diagnostic Accuracy of Transesophageal
Echocardiography Bubble Study 21
Advantages and Limitations of Transesophageal
Echocardiography for Detecting a PFO
22
Transcranial Doppler for the Diagnosis of PFO
22
Protocol for a Transcranial Doppler Bubble Study
23
Diagnostic Accuracy of Transcranial Doppler Bubble
Study
23
Advantages and Limitations of Transcranial Doppler
for Detecting a PFO
24
Intracardiac Echocardiography for the Diagnosis
of PFO
24
Angiographic Assessment of PFO and Its
Characteristics
24
Ear Oximetry for the Diagnosis of PFO
25
Cardiac Computed Tomography for the Diagnosis
of PFO
25
Magnetic Resonance Imaging for the Diagnosis
of PFO
26
Conclusions and Recommendations
26
Supplementary Materials
26
References
26
15
PFO Closure for Stroke, Myocardial Infarction, Peripheral Embolism, Migraine, and Hypoxemia
Copyright © 2020 Elsevier Inc. All rights reserved.https://doi.org/10.1016/B978-0-12-816966-7.00002-6
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INTRODUCTION
Patent foramen ovale (PFO) is characterized by a transient intracardiac right-to-left shunt that is found in one-
quarter of the general population [1]. Although most people with a PFO will remain asymptomatic, a wide range
of pathologies and clinical syndromes may arise mediated by the PFO including stroke (Chapters 4e7), myocardial
infarction (Chapter 8), peripheral embolism (Chapter 9), migraine headache (Chapters 10 and 11), hypoxemia
(Chapter 12), and decompression sickness in divers (Chapter 13) [2e7].
A number of diagnostic imaging modalities can be utilized to directly or indirectly detect and quantify a PFO, all
with different advantages and limitations [8e11]. Direct visualization of the interatrial septum, most commonly by
ultrasonography, and less frequently by cardiac computed tomography (CT) or magnetic resonance imaging (MRI),
can help identify the defect and its anat omic characteristics. Transthoracic echocardiography (TTE) with agitated sa-
line bubble study remains the most commonly used modality to screen for a PFO. Transesophageal echocardiogra-
phy (TEE) with bubble study allows the clinician to diagnose a PFO with direct visualization of the atrial septal
anatomy [11]. Transcranial Doppler (TCD) bubble study has emerged as an acceptable alternative to TTE for PFO
screening; it carries a higher sensitivity than TTE and TEE, with a negative test virtually excluding a PFO [12].
Catheter probing and angiography are used to document and categorize a PFO ad hoc or complement prior imaging.
Imaging assessment of a PFO, for diagnostic and interventional purposes, is crucial to aid clinicians in making man-
agement decisions and planning potential percutaneous closure of an offending right-to-left shunt. PFO imaging for
interventional purposes is discussed in Chapter 3. Percutaneous PFO device closure has recently re-emerged into the
spotlight, after the results were published of several randomized trials of PFO closure for stroke and migraine
[13,14]. This chapter will discuss the different imaging modalities used to detect and quantitate a PFO, and describe
the advantages and limitations of each method.
ULTRASOUND DETECTION OF A PFO
In most cases, imaging of a PFO involves direct visualization of the anatomical defect or functional detection of a
right-to-left shunt. Ultrasound assessment of right-to-left shunts, either directly utilizing echocardiography (TTE,
TEE, or intracardiac echocardiography [ICE]), or indirectly using TCD, remains the most common diagnostic
approach. Ultrasonography allows the clinician to use color flow Doppler to detect blood flow between the 2 atria
as a colored signal [3]. The advent of three-dimensional (3D) echocardiography has also enabled clinicians to visu-
alize the atrial septum anatomy in real time and view surrounding structures [15,16]. For larger PFOs, color flow
Doppler may be all that is needed to detect the defect. However, injection of a contrast agent (such as agitated saline)
with a provocation maneuver (Valsalva or cough) is usually needed to reverse the interatrial pressure gradient,
induce the right-to-left shunt, and detect crossing of bubbles with ultrasonography [11] (Video 2.1).
CONTRAST AGENT DURING A BUBBLE STUDY
During echocardiography with a bubble study, the sonographer first gets the optimal view of the interatrial septum,
and then injects contrast into the venous circulation to detect the right-to-left shunt. Agitated saline remains the most
commonly used contrast agent; it is formed by mixing about 9 mL of saline and 0.5e1 mL of air in 2 syringes. The
mixture is rapidly agitated by 5e6 alternating injections from the 2 syringes using a 3-way stopcock; this bolus is
then infused into the patient’s venous circulation while watching for the appearance of microbubbles in the left atrium
(TTE, TEE, or ICE) or the middle cerebral arteries (TCD) [17,18]. Studies have demonstrated that addition of a small
amount (1e2 mL) of the patient’s blood to the agitated saline mixture can increase the sensitivity of a bubble study
without compromising specificity. The addition of plasma protein coats the air bubbles and stabilizes their surface ten-
sion, allowing more microbubbles to be contained within the same volume, thus increasing the test’s sensitivity and
lowering the small risk of air embolism from large bubbles of air coalescing during the injection [12,18e20].Although
other contrast agents have been developed for use during bubble studies, agitated saline remains the most commonly
used mixture in many countries due to its low cost, ease of use, and high efficacy [18].
2. ECHOCARDIOGRAPHY, TRANSCRANIAL DOPPLER, AND OXIMETRY FOR IMAGING AND QUANTIFICATION OF PFO-MEDIATED SHUNTS16
II. DIAGNOSIS AND IMAGING ASSESSMENT OF PFO
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