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Percutaneous Closure ofPatent Ductus Arteriosus
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347
a
Cardiac Catheterization
Cardiac catheterization affords the opportunity to
evaluate the anatomy by angiography, measure
hemodynamics, and provide treatment during the
same intervention. It is important to obtain hemodynamics prior to angiography as contrast can
falsely increase the lling pressures. If PVR is
elevated, pulmonary vasodilation testing should
be performed with oxygen and nitric oxide to
assess reversibility and determine whether the
PDA can be closed [1, 9]. In patients with
Eisenmenger syndrome the systemic saturation
in the descending aorta will be lower than normal, thus the saturation must be obtained in the
b
ascending aorta, and should be equal to the left
atrial saturation.
Angiography is performed in the descending
aorta just above the ductal ampulla to evaluate
the ductal anatomy. A straight lateral projection
shows the PDA anatomy best, including the narrowest diameter, length, and size of the ampulla.
The anterior projection can be in straight AP or
RAO [10]. Morphologic classication was
established by Krichenko etal. based on the location of the narrowest diameter and the shape of
the PDA (Fig.4) (Table1).
Fig. 3 (a and b) Sagital and transverse MRI “black
blood” images of a PDA (star). Ao aorta; PA pulmonary
artery
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Fig. 4 PDA Krichenko classication
Table 1
PDA classication by size
PDA size Physiology Clinical ndings Management
Silent Highly pressure restrictive and not
Small but
audible
Moderate Hemodynamically signicant.
Large No or little pressure restriction
hemodynamically signicant
Highly pressure restrictive and not
hemodynamically signicant—no
volume overload
Pulmonary overcirculation.
Pressure restriction between Ao and
PA
between Ao and PA.
+/− pulmonary vascular disease
+/− Eisenmenger physiology
Silent on auscultation.
Usually, an incidental nding
No symptoms.
Systolic grade I-II/VI in the
left parasternal border.
Normal LV and LA size.
Possible risk of infectious
endocarditis (see later
discussion)
Symptomatic:
– Dyspnea on exertion
– Chest pain
– Palpitations
– Dizziness
Continuous “machinery” on
left upper parasternal border.
Echocardiogram with
enlargement of LA and LV
Symptomatic:
– Possible arrhythmias
due to chronic LA
dilation
– Differential cyanosis
suggests Eisenmenger
physiology
Observation
Percutaneous closure vs.
observation (see
controversies)
Cardiac catheterization and
percutaneous closure
indicated
Cardiac catheterization for
hemodynamic assessment.
Percutaneous closure
contraindicated in
Eisenmenger physiology
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Diagnosis andPre-procedural
Assessment
This patient had recently emigrated from Central
America. Neither he nor his parents had ever
been told he had a murmur before. Although he
denied physical activity intolerance, he preferred
more “quiet” activities and had voluntarily
avoided physical education at school for the last
15years because according to him, he “was not
as fast as the other students”. He denied
palpitations.
His physical examination showed a PMI displaced to the left. There was a thrill on palpation
over his chest. Auscultation revealed a grade III/
VI continuous “machinery type” murmur in the
left parasternal border. Pulses were 3+ in all
a
extremities with no radiofemoral delay. The saturation in the upper and lower extremities was
96%.
Based on this, a PDA was suspected. A TTE
was obtained demonstrating a moderate-size
PDA with left-to-right shunting with LA and LV
enlargement. Diastolic ow reversal in the
descending aorta was seen. Spectral Doppler
showed a peak velocity close to 4m/s (Fig.5).
The arch was left-sided and the branching pattern
was normal.
Since transthoracic echocardiography dened
the arch branching pattern and ruled out other
structural abnormalities no further imaging was
obtained, and he underwent catheterization for
hemodynamic assessment and possible device
closure (Table2).
b
c
Fig. 5 (a–c) Transthoracic echocardiography shows a moderate sized PDA (white arrow) with continuous restrictive
left to right shunting. The LV is dilated
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L. Prieto and D. Duar te
Patient hemodynamics
Table 2
Saturation Pressure
SVC 74% –
RA 74% a=10, v=9, m=9
RV 74% 44/10
PA 86% 44/25, mean=35
LPA 82% 44/25, mean=35
LPCWp 18
RPA 89% 44/25, mean=35
RPCWp 18
LA – –
LV – 98/18
AAo 96% 98/52, mean=71
Dao 96% 98/52, mean=71
Hemoglobin 14.5g/dL
VO2 130mL/kg/min
Qs 5.1L/min (3.3L/min/m
Qp 11.35L/min (7.3L/min/m
PVR 1.5 Wu (2.3 Wu * m
SVR 12 Wu (18.8 Wu * m
Qp/Qs 2.2
PVR/SVR 0.1
SVC superior vena cava; RA right atrium; RV right ventricle; PA pulmonary artery; LPA left pulmonary artery;
LPCWp left pulmonary capillary wedge pressure; RPA
right pulmonary artery; RPCWp right pulmonary capillary
wedge pressure; LA left atrium; LV left ventricle; AAo
ascending aorta; Dao descending aorta; VO2 peak oxygen
uptake; Qs systemic ow indexed to body surface area;
Qp pulmonary ow indexed to body surface area; PVR
pulmonary vascular resistance; SVR systemic vascular
resistance
2
)
2
)
2
)
2
)
Table 3
Guideline recommendations
AHA/ACC 2019
Recommendation Class LOE
PDA closure in adults recommended if
LA or LV enlargement is present with
net left to right shunt, PA systolic
pressure <50% systemic and PVR <1/3
systemic
PDA closure in adults may be
considered in the presence of a net left to
right shunt if PA systolic pressure is
>50% systemic and the PVR >1/3
systemic
PDA closure should not be performed in
adults with a net right to left shunt and
PA systolic pressure >2/3 systemic or
PVR >2/3 systemic
Obtained with permission from: Stout KK, Daniels CJ,
Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, etal.
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–e800
I C-LD
IIb B-NR
III C-LD
enlargement. In patients with pulmonary hypertension without Eisenmenger physiology, PDA
closure may be considered depending on careful
hemodynamic evaluation. Table 3 summarizes
the guideline recommendations of the American
Heart Association/American College of
Cardiology (AHA/ACC) for PDA closure in
adults.
Heart Team Approach
andDiscussion
Although his mean pulmonary arterial pressures are
elevated, the calculated pulmonary vascular resistance was within normal limits and thus, no pulmonary vasodilation testing was needed. Leaving the
PDA open for a longer time would likely result in
pulmonary vascular disease and possibly
Eisenmenger. Therefore, closure was indicated.
Indications forPDA Closure
Closure of the PDA is indicated when there are
symptoms of congestive heart failure, and/or
signs of volume overload such as LA or LV
Heart Team Decision
Surgery
In contrast to the pediatric population, surgical
ligation of the ductus in the adult carries a signicant degree of morbidity. Calcication, ductal
aneurysm or coexisting coronary artery disease
require anterior sternotomy approach on cardiopulmonary bypass. Nowadays, surgery is
reserved only for cases where transcatheter
device closure is not possible or is contraindicated, as is the case in right aortic arch with aberrant left subclavian artery and left-sided PDA
with airway compression, very large PDAs, or
large ductal aneurysms [7, 11].
Percutaneous Closure ofPatent Ductus Arteriosus
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Percutaneous Closure
Percutaneous closure is currently the method of
choice to address a PDA. The success rate is
close to 100% and the rate of complications is
minimal [1–3, 7, 9, 10, 12]. The largest reported
series in 141 adults showed a success rate of 99%
with no major complications [3]. The procedure
can be performed under local anesthesia, and for
most cases, it requires less than 24 h of
observation.
Once the anatomy is dened, the ductus can
be closed either by a prograde approach advancing a catheter from the venous side into the pulmonary artery and crossing the ductus to the
descending aorta; or for symmetric devices retrograde from the aortic side crossing to the pulmonary artery. Nowadays, coils are rarely used as
they have been replaced by newer occluding
devices (i.e.: Amplatzer Duct Occluder I) (Fig.6).
If crossing from the PA is not possible, as sometimes happens in adult patients, a wire can be
snared after the crossing from the aortic side to
form an arterio-venous rail, allowing closure
with an Amplatzer Duct Occluder I.
Intraprocedural Imaging Modalities
andMeasurements
Angiography was obtained in the descending
aorta just above the ductal ampulla in RAO/caudal and straight lateral projections showing a
moderate sized PDA. It is important to obtain
adequate measurements with especial attention to
the narrowest diameter. These will determine the
size and type of device. In contrast to the pediatric population, it is rare for the devices to result in
compression of the LPA or the descending aorta.
Once the device is placed, angiography should be
obtained in the aorta to evaluate for device position and residual shunting (Fig.7).
Fig. 6 Amplatzer Duct Occluder attached to the delivery
wire. (Photo by the author)
352
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Fig. 7 (a and b) Angiogram in the descending aorta in the lateral projection demonstrating a moderate size PDA
(Krichenko type A) pre and post-device closure
L. Prieto and D. Duar te
Post Procedural Assessment
Immediate postoperative evaluation should
include transthoracic echocardiogram and
CXR. Occasionally, left ventricular dysfunction
can be seen following PDA closure especially
when the PDA is large and pulmonary vascular
resistance is still low. This is secondary to a sudden increase in afterload when the PDA is closed.
In this case, transthoracic echocardiogram
performed after the procedure showed no residual ow through the ductus, no obstruction of the
LPA or descending aortic ow, and normal LV
function.
Follow Up
– First 24h: Transthoracic echocardiogram and
CXR to verify stable position of the device
and evaluate residual shunting.
– Six months: outpatient visit with echocardio-
gram. If no residual shunting, normal PA pres-
sures, and normal LV size and function,
Multimodality imaging comparison
Imaging study Benets Disadvantages
Echocardiogram – More
CT
accessible.
– Provides
physiological
data such as
directionality
of shunting,
signs of
volume
overload, RV
and PA
pressures, LV
function.
– Rules out
other
anatomical
lesions.
– No radiation
– Detailed
anatomic
evaluation.
– Evaluates
degree of
calcication.
– Can help
evaluate the
ventricular
function
– Acoustic
– No
– Radiation
patient can be discharged.
– If elevated PVR or abnormal LV function—
follow up every 1–3years [9].
windows in
adults are
limited and
may not
offer
adequate
anatomic
information
physiological
information.
exposure
Percutaneous Closure ofPatent Ductus Arteriosus
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Imaging study Benets Disadvantages
MRI
Cath and
angiogram
– Provides ow
evaluation
(Qp:Qs) as
well as
detailed
anatomic
evaluation
and
ventricular
function.
– No radiation
– Anatomic
and detailed
physiologic
information.
– Opportunity
to treat
– Not adequate
to evaluate
for
calcication
– Invasive
Clinical Controversies andClinical
Pearls
• Bacterial endocarditis in small PDAs has been
reported in a few cases, and closing a small,
hemodynamically insignicant PDA for pre-
vention is a matter of controversy [12].
• The rate of signicant complications of trans-
catheter closure is quite low and thus, some
argue the lifetime risk of endarteritis is higher
than the procedural risks.
• PDA closure is indicated in patients with con-
gestive heart failure symptoms and/or with
evidence of LV volume overload and most
agree to the closure a small, hemodynami-
cally insignicant PDA as long as it is
audible.
• PDA diagnosis is established by transthoracic
echocardiogram in most cases, but 3D
imaging, or other cardiac imaging may be
necessary in adult patients.
Key Points
– A patent ductus arteriosus (PDA) is a
vascular connection between the LPA
and the aorta, and it comprises 10% of
congenital heart disease cases.
– Moderate and large PDAs result in vol-
ume overload and eventually pulmonary
arterial hypertension with vascular
353
changes, and if uncorrected can result in
Eisenmenger physiology.
– Transthoracic echocardiogram is the
imaging modality of choice for diagnosis and evaluation of the anatomy, ow
directionality and pressure restriction
across the PDA.
– CT or MRI should be obtained when
echocardiographic windows are not
adequate and further anatomical detail
is necessary, and/or if a ductal aneurysm
is suspected by echocardiography.
– When indicated, transcatheter PDA
device closure is the method of choice
with high success rates and minimal
complications.
Chapter Review Questions
1. What is the main determinant of the shunt
direction in a PDA?
A. Length and diameter of the PDA
B. Difference between SVR and PVR
C. Left ventricular end diastolic pressure
D. A and C
Answer: B
Explanation: Although the restriction of
the ow is mostly determined by the narrowest segment of the PDA, the direction of the
shunt (right to left or left to right) is determined by the difference between the SVR and
PVR. Normally the SVR is higher than the
PVR, and thus the shunt is left to right.
However, for untreated large, unrestrictive
PDAs, once the PVR is greater than the SVR
the shunt ow reverses, and patients develop
Eisenmenger physiology.
2. Which of the following is NOT an indication
for PDA closure?
A. Signs of volume overload by
echocardiography.
B. Signs and symptoms of heart failure.
C. Small non-audible “silent” PDA.
D. Moderate PDA with mildly elevated PA
pressures.
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L. Prieto and D. Duar te
Answer: C
Explanation: Small non-audible PDA is
frequently an incidental nding. They are
hemodynamically insignicant and the risk of
endocarditis is felt to be negligible to nonexistent. Therefore, closure is not indicated.
3. A 20-year-old male patient presents for evaluation of a murmur. The echocardiogram
showed moderate sized PDA with left to right
shunt. The spectral Doppler showed restrictive PDA with peak gradient of 3.8m/s and a
simultaneous blood pressure of 100/70. The
LV and LA are dilated. The arch is left-sided,
and the branching pattern is normal. What is
the best next step?
A. Start diuretics and re-evaluate in 3months.
B. Computed tomography of the chest with
contrast.
C. Cardiac magnetic resonance.
D. Transcatheter closure.
Answer: D
Explanation: The echocardiogram pro-
vided all the necessary information, and transcatheter closure is indicated. There is no need
for further imaging.
4. (Questions 4 and 5) A 55-year-old female
presents with lower extremity clubbing.
Echocardiographic windows are very limited
but shows a large PDA with possible bidirectional shunting. Spectral Doppler showed no
signicant restriction. What is the next step in
evaluation of this patient?
A. Cardiac catheterization.
B. Cardiac MRI.
C. Transesophageal echocardiogram.
D. Surgical closure.
5. After evaluation, the patient undergoes car-
diac catheterization for hemodynamic evalua-
tion. Hemodynamics showed severe
pulmonary hypertension with calculated PVR
of 15 WU and Qp:Qs of 0.7. Pulmonary vaso-
dilatory testing shows partial response to oxy-
gen and nitric oxide with improvement of the
PVR to 12. Angiography shows a large PDA
with signicant calcication. Based on the
above:
A. PDA should be closed in the catheteriza-
tion laboratory.
B. Surgical closure is indicated.
C. Closure is contraindicated.
D. None of the above
Answer to Question 4: A
Answer to Question 5: C
Explanation: The patient has clubbing of
the lower extremities, and this is caused by
chronic lower oxygen saturation in the
descending aorta due to right to left shunting
at the ductal level. It is necessary to obtain
hemodynamics in the catheterization laboratory and test for reversibility. In this case
hemodynamics showed the PVR is greater
than the SVR and the Qp:Qs is lower than 1,
indicating she has Eisenmenger physiology.
Therefore, closure is contraindicated. Surgery
is reserved for cases where device closure is
contraindicated by the anatomy such as vascular rings with compression of the airway, or
large ductal aneurysms.
References
1. 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.
2. Taggart NW, Mohammed YQ. Patent ductus arteriosus and aortopulmonary window. In: Allen HD,
Shaddy RE, Penny DJ, Feltes TF, Cetta F, editors.
Moss and Adams’ heart disease in infants, children,
and adolescents: including the fetus and young adults,
vol. 1. 9th ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2016.
3. Wilson WM, Shah A, Osten MD, Benson LN, Abraha
N, Breitner D, etal. Clinical outcomes after percutaneous patent ductus arteriosus closure in adults. Can J
Cardiol. 2020;36(6):837–43.
4. Sommer RJ, Hijazi ZM, Rhodes JF Jr. Pathophysiology
of congenital heart disease in the adult: part I: shunt
lesions. Circulation. 2008;117(8):1090–9.
5. Sudhakar P, Jose J, George OK. Contemporary outcomes of percutaneous closure of patent ductus
arteriosus in adolescents and adults. Indian Heart J.
2018;70(2):308–15.
6. Wu MH, Lu CW, Chen HC, Kao FY, Huang SK.Adult
congenital heart disease in a nationwide population
2000–2014: epidemiological trends, arrhythmia,
Percutaneous Closure ofPatent Ductus Arteriosus
https://t.me/med1917
355
and standardized mortality ratio. J Am Heart Assoc.
2018;7(4):e007907.
7. Schneider DJ, Moore JW. Patent ductus arteriosus.
Circulation. 2006;114(17):1873–82.
8. Arya B, Sable CA.Abnormalities of the ductus arteriosus and pulmonary arteries. In: Lai WW, Mertens
LL, Cohen MS, Geva T, editors. Echocardiography
in pediatric and congenital heart disease. 2nd ed.
Chichester, UK: Wiley; 2016. p.317–35.
9. Baumgartner H, De Backer J, Babu-Narayan SV,
Budts W, Chessa M, Diller GP, etal. 2020 ESC guidelines for the management of adult congenital heart
disease. Eur Heart J. 2021;42(6):563–645.
10. Bentham J, Wilson N. Patent ductus arteriosus
(PDA): background and indications for closure. In:
Interventions in structural, valvular, and congenital heart disease. 2nd ed. Boca Raton, FL: Taylor &
Francis Group; 2015. p.611–6.
11. Kouchoukos NT, Blackstone EH, Hanley FL,
Kirklin JK.Congenital heart disease in the adult. In:
Kouchoukos NT, Blackstone EH, Hanley FL, Kirklin
JK, editors. Kirklin/Barratt-Boyes cardiac surgery:
morphology, diagnostic criteria, natural history, techniques, results, and indications. 4th ed. Philadelphia,
PA: Elsevier; 2013. p.1061–147.
12. Fortescue EB, Lock JE, Galvin T, McElhinney DB.To
close or not to close: the very small patent ductus arteriosus. Congenit Heart Dis. 2010;5(4):354–65.
Index
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A
Alcohol septal ablation (ASA), 107, 108, 115, 195–205,
209, 212–217, 222–224
Amulet, 179, 181, 184–186, 188
Aortic regurgitation, 10, 20, 21, 34, 36–43, 46, 50, 54,
57, 61, 63, 156, 167, 170, 206, 288, 290, 292,
310, 311, 314, 316–318, 320, 321, 330
Aortic stenosis, 4–26, 28, 31, 38, 51, 52, 63, 139, 152,
167, 199, 329, 341
Atrial brillation (AF), 26, 58, 74, 88, 120, 121, 126,
127, 130, 135, 138, 156, 169, 178, 230, 246,
256–257, 265, 267, 270, 272, 311
Atrial septal defect (ASD), 113, 181, 189, 247, 264–266,
268–273, 275, 276, 280, 281, 297
B
Balloon valvuloplasty, 47, 51–54, 56, 57, 61–64
Bicuspid aortic valve, 28–37, 54, 63, 264, 288, 310, 329,
330, 334, 341
C
Cardiac computer tomography angiography (CCTA),
179, 189
Cardiac imaging, 37, 77, 122, 140, 284–294,
345–349, 353
Coarctation of aorta (COA), 328–334, 338–342
Complications of myocardial infarction, 233
Congenital heart disease, 138, 141, 144, 153, 168, 298,
328, 344, 346, 350, 353
Continuous murmur, 296, 297, 307, 310, 311, 322, 329, 341
Coronary artery stulas (CAFs), 296, 306, 307
Coronary-cameral stulas (CCFs), 296, 304, 306
Coronary obstruction, 13, 16, 19, 20, 28, 31, 33, 36, 38,
45–49, 51, 52, 54, 162
E
Echocardiography, 5–10, 20, 21, 24–26, 28, 34, 35, 40, 44,
47, 49, 59, 76, 97, 115, 122, 124, 126, 128, 133,
140, 144, 152, 158, 160–162, 164, 165, 168,
180, 197, 200, 201, 203, 205–209, 213, 216,
223, 224, 231, 233, 240, 269, 284, 297, 299,
306, 319, 320, 322, 330, 340, 346, 349, 353
Elevated gradients, 22–26, 47, 49–51, 112
H
Heart failure with mild range ejection fraction (HFmrEF)
treatment, 246, 247
Heart failure with preserved ejection fraction (HFpEF)
treatment, 120, 246, 247, 250, 252–254, 257
Hypertension, 28, 52, 71, 77, 87, 88, 98, 99, 104, 135,
178, 196, 246, 313, 321, 328, 329, 331, 333,
338, 340, 341, 350, 354
Hypertrophic cardiomyopathy (HCM), 196, 197, 203,
204, 212–214
Hypoattenuating leaet thickening (HALT), 22
I
Interatrial shunt device, 246–248, 250, 254, 255, 257,
259
Inter-atrial shunting, 264, 280, 281
Intra-procedural guidance, 87, 94, 97, 115, 134, 191, 268
Interrupted aortic arch (IAA), 328–342
L
Left atrial appendage closure (LAAC), 177–181,
183–186, 188, 189, 191, 192
Left atrial hypertension, 246, 250
Luminal disruption, 340
D
Device closure, 165, 178, 186, 233, 265, 266,
270–273, 285, 286, 289, 294, 298, 304, 320,
349, 350, 354
Diastolic dysfunction, 4, 121, 147, 250, 298
© The Editor(s) (if applicable) and 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
M
Mitral balloon valvuloplasty, 88
Mitral regurgitation, 5, 20, 26, 28, 33, 57, 70, 73, 86, 91,
97, 102, 103, 116, 170, 197, 204, 206, 223,
231, 268, 312
357
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