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Transcatheter Approach toCoarctation ofAorta andIsolated Interrupted Aortic Arch inAdults
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a
d
337
ghi
Fig. 8 (a–i) Right CFA angiography showed an accept-
able diameter of the SFA, CFA, EIA, and CIA (a).
Simultaneous antegrade and retrograde aortography at the
level of the aortic isthmus and descending aorta with
Pigtail catheter and Multipurpose catheter at working
view projection depicted interrupted aorta just at the level
of left subclavian artery. The interrupted segment length
was discrete and both proximal and distal ends were
tapered (b). Antegrade wiring was performed by CTO
guidewire (Gaia 2nd) and after conrming of the position
of the wire to be in the true lumen by aortography in sev-
eral projections (c, d), the wire was snared in the CIA (e).
Through the diagnostic Multipurpose catheter, the interrupted segment was dilated by coronary balloon (2.5*15)
and by balloon swallow technique, the catheter was
advanced toward the descending aorta (f). After manual
crimping of the covered Optimus CoCor stent XL-48mm
on the table, it was passed through the sheath and by
repetitive aortography by Pigtail catheter, it’s appropriate
position was conrmed (g). Final angiography demonstrated appropriate position of the stent without any complications (h, i). The nal gradient was zero
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A. Firouzi et al.
(Fig. 8c, d), the wire was snared in the CIA
(Fig. 8e). After that, through the diagnostic
Multipurpose catheter, the interrupted segment
was dilated by coronary balloon (2.5*15) and by
balloon swallow technique, the catheter was
advanced toward the descending aorta (Fig.8f).
After insertion a super-stiff guidewire 260 cm
(Amplatzer), a long delivery sheath (Cook-14F)
was advanced with it’s tip positioned in the aortic
arch and the dilator was removed and the sheath
was de-aired. Based on the size of the transverse
aorta, BIB 20*40 was selected. After manual
crimping of the covered Optimus CoCor stent
XL-48mm on the table, it was passed through the
sheath and by repetitive aortography by Pigtail
catheter, it’s appropriate position was conrmed
(Fig. 8g). After retracting the sheath, rst, the
inner balloon was inated to stabilize the stent
and then the outer balloon was inated. Finally,
after deating the balloon, the sheath was
advanced over that, and the balloon was removed.
Final angiography demonstrated appropriate
position of the stent without any complications
(Fig.8h, i). The nal gradient was zero.
Post-procedure Aortic CT
Angiography
Aortic CTA, 1 month later illustrated: Patent
stent at the proximal and distal portion of
descending aorta, no evidence of recoarctation,
no sign of complication at the site of stenting
(Fig.9a and b).
Complications
During the procedure, major complications
occur in approximately 15% of cases: Intimal
tearing, dissection, perforation, stent migration,
CVA (<3%), tamponade, and the most important
one, vascular complications (<1%). As the
chance of delayed complications such as: aneurysm and pseudoaneurysm formation at the site
of the stenting, re-coarctation, restenosis, stent
fracture, and progressive aortic dilatation and
dissection especially in those with BAV appears
to be increased with more extended follow-up
periods, all patients need careful periodic surveillance (Fig.10).
Another issue in these patients is persistent,
recurrent, and resistant systemic hypertension
and disproportionate systolic hypertension with
exercise.
• Hypertension is more common in patients
whose repair was performed after 20years of
age compared with those who were corrected
in early childhood [17]. So, close observation
and treatment of hypertension by beta-
blockers, angiotensin converting enzyme
(ACE) inhibitors, or angiotensin receptor
blockers (ARB) is mandatory.
Fig. 9 (a and b) Follow-up aortic CTA 1month later conrmed patent stent at proximal and distal portions of descend-
ing aorta, without evidence of recoarctation or any complications at the site of stenting (a and b)
Transcatheter Approach toCoarctation ofAorta andIsolated Interrupted Aortic Arch inAdults
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of stent diameter to pre-intervention narrowest
coarctation segment should be <3.5 [13].
• There are several types of balloons and
stents (either balloon-expandable or self-
expandable, bare metal or covered types) at
marketing. Each of them has its singular
designs which have been improved during
recent years regarding their materials (from
stainless steel to platinum-iridium alloy, and
chromium- cobalt alloy), expansion diame-
ters, cell types and sizes (open or close cell
design), wall thickness, foreshortening per-
centage, exibility, prole, and the delivery
sheath sizes.
• Both balloon-expandable and self-expandable
stents have been used for the endovascular
Fig. 10 CT angiogram sagittal plane showing Coarctation
of Aorta complicated by mycotic aneurysm formation and
infective endocarditis
treatment of CoA. A randomized trial by
Sadeghipour et al. [14] revealed that both
balloon- expandable CP stents and self-
expandable nitinol stents are safe and effective
Clinical Controversies andPearls
in treating native coarctation.
• Also, Firouzi etal [15] showed that both stent
• While balloon angioplasty effectively relieves
vascular obstructions, it has some limitations,
including elastic recoil of the vessel wall and
intimal dissection.
• Stent insertion after balloon angioplasty or
surgery reduces the complications, improves
luminal diameter, results in minimal residual
gradient, and sustains hemodynamic benet
[11, 12].
• The choice of stent depends on the coarctation
anatomy, patient size and operator’s preference. The imaging ndings (the type and
location of the COA or IAAs, the residual
lumen width, the length of the stenosis or
interruption, collateral vessels, and the size of
the thoracoabdominal aorta at different levels
and nding the optimal uoroscopic angles
especially in those with IAAs), assist in select-
types were safe and effective in the treatment
of non-interrupted COA during 1-year follow up by CTA. A comparison between covered
and non-covered stents in the non-interrupted
aorta was made in a randomized controlled
trial by Sohrabi etal. [16], who conrmed no
signicant superiority for covered stents.
• Regarding the potential risk of aortic dissection or perforation during the wiring and initial ballooning, most experts have
recommended covered stents in the treatment
of IAAs. Covered stents have been used by
our group in these patients with the following
conditions: (1) critical or sub-atretic obstructions, dened by a minimum diameter at the
COA site of 2–3mm on angiography (2) COA
associated with the atresia of the aortic lumen
(interrupted) [11].
ing the appropriate trans-catheter approach
(either antegrade or retrograde approach) and
selecting the proper balloon and stent size and
type.
• Final stent diameter is based on the proximal
arch diameter (transverse or distal arch), with
the diameter not exceeding the size of the aorta
Key Points
Coarctation of aorta (COA) is a congenital
juxta ductal localized aortic narrowing
(usually post-ductal in adults) that mainly
remains undiagnosed in adulthood and
at the diaphragm level. Furthermore, the ratio
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A. Firouzi et al.
detected incidentally in a hypertensive
patient with Radial- Femoral pulse delay.
An Interrupted aortic arch (IAA) is an
anatomical and luminal disruption between
the ascending and descending aorta that
can be considered the most severe form of
CoA.
The most common causes of death are
congestive heart failure, aortic dissection,
rupture of the aorta, infective endocarditis,
premature coronary artery disease, and
intra-cranial hemorrhage. In adults, the
most common presentation is systemic
hypertension, accounting for 0.2% of all
hypertension cases in adults.
The systolic blood pressure gradient
≥20mmHg between upper (right arm) and
lower extremities suggests signicant CoA
that requires therapeutic intervention.
TTE showing suprasternal window
provides the best view for visualizing the
narrowing of the aorta and accelerated ow
proximal to the narrowing with a characteristic Doppler pattern of “Sawtooth” appearance. Abdominal aorta Doppler study
shows delayed and low velocity systolic
and diastole forward ow associated with
absent early diastolic ow reversal
Cardiac magnetic resonance (CMR)
imaging and computed tomography (CT)
angiography are recommended imaging
modalities for evaluating CoA site, entire
aorta and planing surgical vs trans-catheter
approach.
Surgery is the standard management of
native coarctation in infants and young
children and TC approach is the preferred
method in older children, adolescents, and
adults.
Both balloon-expandable and selfexpandable stents have been shown to be
safe and effective for the endovascular
treatment of CoA.
Interval surveillance by physical examination and imaging modalities
(Echocardiography, CTA, and MRA),
seems to be crucial as the chance of
delayed complications such as: aneurysm
and pseudoaneurysm formation at site of
the stenting or surgical repair, recoarctation, restenosis, stent fracture, and
progressive aortic dilatation and dissection
especially in those with BAV appears to
increase during longer follow-up periods.
Patients need close monitoring and optimal treatment for their systemic
hypertension.
CTA and preferably MRA are suggested
imaging modalities to assess the postinterventional anatomy and possible complications every 3–5years (Table1).
Transcatheter Approach toCoarctation ofAorta andIsolated Interrupted Aortic Arch inAdults
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Imaging modalities
Table 1
Imaging study Benets Disadvantages
Echocardiogram
CT The gold-standard tool to characterize the types and site of the COA or
MRI
Angiogram
– The proper initial imaging modality for detecting the COA in
suspicious cases. Also, assess biventricular function, the aortic valve
(eg, bicuspid aortic valves, aortic stenosis, and aortic insufciency), as
well as detects other concomitant anomalies.
– No radiation
IAAs, the residual lumen width, the length of the stenosis or
interruption, collateral vessels, and the size of the aorta at the level of
sinus of valsalva, ascending, proximal arch, transverse arch, descending
aorta at the level of the diaphragm by 3D volume-rendered and dene
any other anomalies. Further, assist to sort out the most appropriate
treatment options (surgical or trans-catheter approach [TC]) in the
pre-procedural planning and appropriate device selection before invasive
angiography, and nding the optimal uoroscopic views especially in
those with IAAs
– Additional information about ventricular size and function
– No radiation
– Preferred modality during follow-up
– The gold-standard tool to conrm the diagnosis and hemodynamic
assessment of CoA, to characterize the types and site of the COA or
IAAs, the residual lumen width, the length of the stenosis or
interruption, collateral vessels, and the size of the aorta dene the
suitability for the trans-catheter approach and the device type
– Limited value to
dene the detailed
thoracoabdominal
aorta anatomy in
CoA and IAA
– Radiation
exposure during
follow-up
– Risk of iodinated
contrast nephropathy
– Needs patient’s
cooperation
– Invasive
– Radiation
exposure
– Risk of iodinated
contrast nephropathy
341
Disclosures There are no conicts of interest to disclose.
Chapter Review Questions
1. Which of the following Doppler study is NOT
compatible with signicant CoA of aorta?
A. High-velocity systolic turbulent ow in
the thoracic aorta detected in the suprasternal window
B. Diastolic antegrade ow (diastolic tail) in
the thoracic aorta detected in the suprasternal window
C. The delayed and low-velocity systolic
ow of the abdominal Aorta by pulse
wave Doppler study
D. Early diastolic ow reversal of the abdom-
inal Aorta by pulse wave Doppler study
Answer: D
Explanation: In patients with signicant
CoA of aorta, abdominal pulse wave Doppler
study shows slow and low-velocity systolic
ow extending to the diastole with absent
early diastolic ow reverse. More importantly,
in post-CoA evaluation, the presence of the
early diastolic ow reverse of the abdominal
Aorta suggests no signicant stenosis.
2. In an 18-year-old man with a history of severe
hypertension and possible diagnosis of CoA,
which of the following is NOT correct:
A. Weak or absent pulses in the lower
extremities are seen in all CoA patients
B. Figure 3 conguration and rib notching
can be seen in the Chest X Ray
C. Continuous murmurs in inter-scapular
might be heard on cardiac auscultation
D. Radial-Femoral pulse delay is a common
nding
Answer: A
Explanation: Radial-Femoral pulse delay
and weak or absent pulses in the lower
extremities are common ndings except in the
presence of the signicant AR
3. A 25 years old woman with uncontrolled
hypertension was referred to the ACHD clinic
for further evaluation of coarctation (CoA) of
aorta. Which of the following ndings are
NOT consistent with signicant CoA:
A. Mean Doppler systolic gradient at CoA
site >20mmHg
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A. Firouzi et al.
B. Mean Doppler gradient at CoA site
>10mmHg associated with signicant AR
or decreased LV systolic function
C. Mean Doppler gradient at CoA site
>10mmHg with collateral ow
D. Mean Doppler gradient at CoA site
>10mmHg with less than 50% narrowing
of aorta relative to the aortic diameter at
the level of the diaphragm
Answer: D
Explanation: In the signicant CoA, more
than 50% narrowing of aorta is seen relative to
the aortic diameter at the level of the
diaphragm
4. The preferred method of management of
adults with signicant coarctation of aorta is:
A. End to end surgical repair
B. CoA balloon aortoplasty
C. CoA balloon aortoplasty with stenting
D. Medical treatment and blood pressure
controlAnswer: C
Explanation: Trans catheter approach is
the preferred method in older children, adolescents, and adults.
5. What is the recommended imaging interval
follow-up in patients without associated
anomaly after coarctation of aorta interventional treatment?
A. CMR or CTA every 1–2years
B. CMR or CTA every 2-3years
C. CMR or CTA every 3–5years
D. Usually, TTE is the recommended follow
up imaging modalityAnswer: C
Explanation: CTA and preferably MRA
are suggested imaging modalities to assess the
postinterventional anatomy and possible complications every 3–5years.
References
1. Topol EJ, Teirstein PS, editors. Textbook of interventional cardiology. 8th ed. Amsterdam, Netherlands:
Elsevier; 2019. p.959–62.
2. Rao PS.Coarctation of the aorta. Curr Cardiol Rep.
2005;7:425–32.
3. Campbell M. Natural history of coarctation of the
aorta. Br Heart J. 1970;32:633–40.
4. Backer CL, Mavroudis C. Congenital heart surgery
nomenclature and database project: patent ductus
arteriosus, coarctation of the aorta, interrupted aortic
arch. Ann Thorac Surg. 2000;69(4 Suppl):S298–307.
5. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol.
2002;39(12):1890–900.
6. Ramirez Alcantara J, Mendez MD.Interrupted aortic
arch. In: StatPearls. Treasure Island, FL: StatPearls
Publishing; 2020.
7. Celoria GC, Patton RB. Congenital absence of the
aortic arch. Am Heart J. 1959;58:407–13.
8. Sudhir Chandra Sinha. Transcatheter intervention
for Coarctation of aorta: current status. Indian J Clin
Cardiol. 2021;2(1):44–50.
9. Baumgartner H, Backer JD, Babu-Narayan SV,
et al. 2020 ESC guidelines for the management of
adult congenital heart disease: the task force for the
management of adult congenital heart disease of the
European Society of Cardiology (ESC). Eur Heart
J. 2020;42(6):563–645. https://doi.org/10.1093/
eurheartj/ehaa554.
10. Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B,
Broberg CS, Colman JM, et al. 2018 AHA/ACC
guideline for the management of adults with congenital heart disease: a report of the American College
of Cardiology/American Heart Association Task
Force on clinical practice guidelines. Circulation.
2019;139(14):e698–800.
11. Firouzi A, Hosseini Z, et al. Paradigm shift in management of interrupted aortic arch in adulthood. Curr
Probl Cardiol. 2021;46(3):100717.
12. Chessa M, Carrozza M, Butera G, Piazza L, Negura
DG, Bussadori C, et al. Results and mid-longterm follow-up of stent implantation for native
and recurrent coarctation of the aorta. Eur Heart J.
2005;26(24):2728–32.
13. Forbes TJ, Moore P, et al. Intermediate follow-up
following intravascular stenting for treatment of
coarctation of the aorta. Catheter Cardiovasc Interv.
2007;70:569–77.
14. Sadeghipour P, Mohebbi B, Firouzi A, etal. Balloonexpandable Cheatham-platinum stents versus selfexpandable nitinol stents in Coarctation of aorta.
JACC Cardiov Interv. 2022;15:308–17.
15. Firoozi A, Mohebbi B, Noohi F, Bassiri H, Mohebbi
A, Abdi S, et al. Self-expanding versus balloonexpandable stents in patients with isthmic Coarctation
of the aorta. Am J Cardiol. 2018;122(6):1062–7.
16. Sohrabi B, Jamshidi P, Yaghoubi A, Habibzadeh
A, Hashemi-Aghdam Y, Moin A, et al. Comparison
between covered and bare Cheatham-platinum
stents for endovascular treatment of patients with
native post-ductal aortic coarctation: immediate and
intermediate-term results. JACC Cardiovasc Interv.
2014;7(4):416–23.
17. Fawzy ME, Fathala A, Osman A, Badr A, Mostafa
MA, Mohamed G, etal. Twenty-two years of follow up results of balloon angioplasty for discreet native
coarctation of the aorta in adolescents and adults. Am
Heart J. 2008;156(5):910–7. Epub 2008/12/09
Percutaneous Closure ofPatent
https://t.me/med1917
Ductus Arteriosus
LourdesPrieto andDanielDuarte
Abstract
A patent ductus arteriosus (PDA) is a connection between the aorta and the pulmonary
artery typically the proximal LPA. It is
reported in 1 in 2000 full-term births, and
accounts for 10% of all congenital heart
defects. Although most of these are detected
early in life, some of them are picked up in the
adult population. Most patients are asymptomatic; however, some present with heart
failure or with pulmonary hypertension and
Eisenmenger syndrome. Percutaneous closure
is now considered the standard of care. This
section will discuss the physiology, as well as
the role of different imaging modalities in the
diagnosis of a PDA, indications for closure
and periprocedural assessment.
Keywords
Patent ductus arteriosus · Percutaneous closure
· Congenital heart disease · Transcatheter
closure · Cardiac imaging in PDA
Abbreviations
CT Computed tomography
LA Left atrial
LPA Left pulmonary artery
LV Left ventricle
MRI Magnetic resonance imaging
PA Pulmonary artery
PDA Patent ductus arteriosus
PVR Pulmonary vascular resistance
RV Right ventricle
SVR Systemic vascular resistance
TTE Transthoracic echocardiography
Test your learning and check your understanding of this book’s contents: use the
“Springer Nature Flashcards” app to access
questions using ▶ https://sn.pub/ambACS.
To use the app, please follow the instructions in the chapter “Transcatheter Aortic
Valve Replacement.”
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 50740- 3_15.
L. Prieto (*) · D. Duarte
Pediatric and Congenital Interventional Cardiology,
Heart Institute, Nicklaus Children’s Hospital,
Miami, FL, USA
e-mail: lourdes.prieto@nicklaushealth.org; daniel.
duarte-caceres@nicklaushealth.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. M. Kelsey et al. (eds.), Cardiac Imaging in Structural Heart Disease Interventions,
https://doi.org/10.1007/978-3-031-50740-3_15
Learning Objectives
1. Understand the pathophysiology and natural
history of a PDA.
2. Know the most common clinical presentations and choose the most adequate imaging
modality.
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L. Prieto and D. Duar te
3. Understand the indications and contraindications for PDA closure, as well as potential
complications.
4. Know how to evaluate the patient pre and post
procedure, and when to follow up.
Case Study
A 20-year-old patient presented for murmur evaluation noticed by the primary care
physician during an ofce visit. He had no
signicant past medical history. He recently
immigrated from Central America for college and according to him, he had no symptoms referable to the cardiovascular system
such as activity intolerance, chest pain or
palpitations.
Background andDenitions
Introduction
Pathophysiology
The diameter of the PDA, and to a lesser degree
the length, are the major determinant factors for
the ow resistance. In large PDAs, the resistance
is minimal and therefore, the ow will depend on
the difference between the systemic and the pulmonary vascular resistance. Normally the pulmonary vascular resistance is lower than the systemic
vascular resistance, and the shunt is left to right
causing pulmonary overcirculation. To maintain
adequate cardiac output, the left ventricle
increases the stroke volume by increasing the end
diastolic volume, or preload, and over time the
end diastolic pressure increases. Different than
ventricular septal defects, the shunting across the
PDA occurs throughout the cardiac cycle, and in
large PDAs the “run-off” of ow during diastole
decreases the diastolic pressure. Occasionally,
the combination of decreased diastolic pressure
and increased ventricular end diastolic pressure
can compromise the perfusion pressure of the
coronary circulation [2, 4].
The ductus arteriosus is a vascular connection of
the proximal left pulmonary artery with the aorta.
In-utero, this connection is maintained in fetal
life by prostaglandins and low oxygen levels and
diverts the blood from the pulmonary circulation
into the systemic circulation. After birth, blood
oxygen concentration increases inducing contraction of the smooth muscle resulting in physiologic closure within the rst 72 h. Then, the
endothelium necroses, and anatomical closure is
nally achieved after 2–4 weeks. However, in
some cases it can remain patent. The incidence of
a patent ductus arteriosus (PDA) is reported as
1in 2000 (0.3–0.8%) live births accounting for
5–10% of all congenital heart disease, yet this
number can be underestimated in silent cases
[1–3].
High altitudes, congenital rubella syndrome,
prematurity and some gene mutations, such as
TFAP2B, have been identied as risk factors for
PDA [2]. Although it is commonly associated
with more complex congenital heart defects the
scope of this chapter is the isolated PDA.
Clinical Assessment
The clinical presentation mostly depends on the
size of the PDA, and it varies from asymptomatic
patients with no signs of volume overload, to
patients with heart failure or Eisenmenger physiology if left untreated. Frequently, large PDAs
induce symptoms early in life that are noticed by
the parents. However, it is not unusual for some
of these patients to deny symptoms but avoid any
physical activity. When symptoms are present,
dyspnea and palpitations are the most frequent
symptoms at the time of diagnosis [3, 5]. Left
atrial dilatation can result in arrhythmias and
sometimes it is the initial presentation. Wu etal.
showed the incidence of tachyarrhythmias in
adult patients with a PDA can be as high as 30%
by age 59 [6].
Physical Examination
The typical murmur is a continuous “machinery”
murmur throughout systole and diastole heard in
the left upper parasternal border [2, 7].
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345
Occasionally, there can be a diastolic rumble at
the apex and the point of maximal impulse is
deviated to the left. In a large PDA, the diastolic
pressure is low increasing the pulse pressure
resulting in bounding peripheral pulses. It is necessary to measure upper and lower extremities
saturations to look for differential cyanosis that
could indicate Eisenmenger syndrome, in which
case the shunting is right to left. In these cases,
the lower extremities saturation is lower than the
upper, and can eventually manifest as lower
extremity clubbing. In Eisenmenger syndrome,
the typical murmur of the PDA is absent but the
S2 component can be accentuated [2].
Cardiac Imaging
Echocardiogram: Echocardiogram is crucial to
establish the diagnosis. The main objectives of
the echocardiogram are:
– Visualizing the PDA by 2D, Doppler and
Color Doppler study. Figure 1a, Movie 1
showing the typical location of PDA in parasternal short axis view by Doppler and color
Doppler study
– Dene anatomy: Dening the arch anatomy is
essential especially before transcatheter closure is pursued. In patients with a right aortic
arch the origin of the left subclavian artery
may be aberrant coursing behind the esophagus. In these cases, most of the time, the PDA
originates from the left subclavian artery constituting a vascular ring which can result in
airway compression. Percutaneous closure of
the defect can result in exacerbation of airway
compression.
– Determine the directionality and velocity of
the shunt by color and spectral Doppler. The
velocity across the PDA is an indirect way to
estimate the PA pressures (measure simultaneous systemic BP). A large, unrestrictive PDA
a
b
Fig. 1 Transthoracic echocardiogram (a) Parasternal
short axis view, color Doppler imaging shows PDA ow
(b) Continuous ow by Doppler study (c) 2D and color
images demonstrating a PDA (star) with left to right shunting. Ao aorta; PA pulmonary artery; RPA right pulmonary
artery; LPA left pulmonary artery; DAO descending aorta
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L. Prieto and D. Duar te
has laminar ow and no turbulence in color
Doppler indicating equal systolic pressure in
the PA and aorta.
– Evaluate for volume overload. Enlargement
of the left sided heart structures, left atrium
and left ventricle, indicate volume overload.
However, in patients with a large PDA who
have developed Eisenmenger physiology,
the left sided structures may be of normal
size.
– Assess for other intra and extracardiac associ-
ated lesions such as coarctation of the aorta or
LPA stenosis. As previously mentioned, a
PDA can be associated with other congenital
heart defects.
Acoustic windows in adults are generally limited,
and the best view often is obtained from the
suprasternal long axis view, angling the probe
posteriorly to visualize the aorta and parasternal
short axis view. Although 2D imaging can be useful to show the anatomy, color Doppler interrogation is very sensitive detecting even tiny PDAs,
and estimates the degree of ductal shunting
(Fig.1). In patients with Eisenmenger and unrestrictive PDA, the ductal ow can be difcult to
discern from ow in the LPA [7, 8].
Computed Tomography
andCardiacMRI
In younger patients transthoracic echocardiogram is often adequate to establish the diagnosis.
However, in adult patients echocardiography
may not be sufcient to make a denitive diagnosis, or to visualize other important anatomic features. In such cases, either cardiac CT or MRI
should be performed to delineate the anatomy
and size of the PDA.Additionally, 3D imaging
can be helpful when the arch branching is questionable such as in vascular rings or cervical
arches. It can also rule out a ductal aneurysm,
although this is a very rare nding in the adult
population. When performed, the MRI can help
provide the Qp:Qs. In cases when surgical ligation is needed, the CT can help establish the
degree of calcication [2, 7] (Figs.2 and 3).
ab
Fig. 2 (a and b) Three-dimensional render of a CT show-
ing a patient with a large PDA in the setting of a vascular
ring: right aortic arch with circumex retroesophageal
aorta, left descending aorta (DAo), aberrant left subcla-
vian artery and left-sided PDA. AAo ascending aorta; DAo
descending aorta; PA pulmonary artery; PDA patent ductus arteriosus; Cx Ao circumex aorta
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