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236 4—ATRIAL SEPTAL INTERVENTIONS
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Kijima Y, Akagi T, Takaya Y, et al. Deficient surrounding rims in patients undergoing transcatheter atrial
septal defect closure. J Am Soc Echocardiogr. 2016;29:768-776.
Kuijpers, T. Patent foramen ovale closure, antiplatelet therapy or anticoagulation therapy alone for management
of cryptogenic stroke? BMJ. 2018;362:k2515.
Mas JL, Derumeaux G, Guillon B, et al.; CLOSE Investigators. Patent foramen ovale closure or anticoagulation
vs. antiplatelets after stroke. N Engl J Med. 2017;377:1011-1021. doi: 10.1056/NEJMoal705915.
Medford BA, Taggart NW, Cabalka AK, et al. Intracardiac echocardiography during atrial septal defect and
patent foramen ovale device closure in pediatric and adolescent patients. J Am Soc Echocardiogr.
2014;27:984-990.
Murphy JG, Gersh BJ, McGoon MD, et al. Long-term outcome after surgical repair of isolated atrial septal
defect: follow-up at 27 to 32 years. N Engl J Med. 1990;323:1645-1650.
Saver JL, Carroll JD, Thaler DE, et al.; RESPECT Investigators. Long-term outcomes of patent foramen
ovale closure or medical therapy after stroke. N Engl J Med. 2017;377:1022-1032. doi: 10.1056/NEJ-
Moa1610057.
Shah AH, Osten M, Leventhal A, et al. Percutaneous intervention to treat platypnea-orthodeoxia syndrome.
J Am Coll Cardiol Intv. 2016;9:1928-1938.
Silvestry FE, Cohen MS, Armsby LB, et al. Guidelines for the echocardiographic assessment of atrial septal
defect and patent foramen ovale: from the American Society of Echocardiography and Society for
Cardiac Angiography and Interventions. J Am Soc Echocardiogr. 2015;28(8):910-958.
Søndergaard L, Kasner SE, Rhodes JF, et al.; Gore REDUCE Clinical Study Investigators. Patent foramen
ovale closure or antiplatelet therapy for cryptogenic stroke. N Engl J Med. 2017;377:1033-1042. doi:
10.1056/NEJMoal707404.
Wiktor DM, Carroll JD. The case for selective patent foramen ovale closure after cryptogenic stroke. Circ
Cardiovasc Interv. 2018;11:e004152. doi: 10.1161/CIRCINTERVENTIONS.117.004152.
e1
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Abstract: Secundum atrial septal defects presenting in adult patients can often be closed percutaneously. Most present with a murmur, abnormal second heart sound, or an echocardiogram
showing right ventricular enlargement. Hemodynamic catheterization is usually unnecessary
unless there are complicating features such as pulmonary hypertension or valvular regurgitation.
Approved devices in the United States include the Amplatzer Septal Occluder, Amplatzer Cribriform Occluder, the Gore Cardioform Septal Occluder, and the Gore Cardioform ASD
Occluder. The procedure is performed with echocardiographic guidance—either transesophageal
echo or intracardiac echo. The latter is preferred for patient comfort. A transfemoral venous
approach allows easy passage of the catheter, guidewire, and closure device into the left atrium,
and subsequently deployment across the atrial septum. Closure of the patent foramen ovale
(PFO) may be considered in patients with cryptogenic stroke. A thorough search for common
stroke causes, including atrial fibrillation, is mandatory. Techniques for device closure are similar
to those for atrial septal defect. Approved devices in the United States include the Amplatzer
PFO Occluder and the Gore Cardioform Septal Occluder. PFO closure is also indicated for individuals with orthodeoxia due to atrial shunting. An emerging indication includes selected
patients with right heart pacemaker/defibrillator leads, lead-associated thrombus, and atrial
right-to-left shunting. Atrial septostomy utilizing atrial septal puncture and balloon dilation of
the atrial septum is occasionally useful for palliation of low cardiac output in patients with severe
pulmonary hypertension or palliation of left atrial hypertension in individuals with stiff left atrial
syndrome or heart failure with preserved ejection fraction. Consultation with a pulmonary hypertension specialist or heart failure specialist is desirable in these circumstances.
Keywords: Atrial septal defect, patent foramen ovale, intracardiac shunt, atrial septostomy
Ventricular Septal
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Interventions
SECTION 5
237
CHAPTER 20
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Transcatheter Closure of Post
Myocardial Infarction, Iatrogenic,
and Congenital Ventricular
Septal Defects
Alexander C. Egbe Nathaniel W. Taggart
Introduction
Transcatheter closure of ventricular septal defects (VSDs) is a less invasive treatment option for
patients with suitable anatomy for device closure and those who are considered to be high-risk
candidates for surgical therapy.
outcomes of transcatheter VSD closure.
AHA Guidelines
1,2
This chapter provides an overview, procedural techniques, and
Device closure of a muscular VSD may be considered, especially if the VSD is remote from the
tricuspid valve and the aorta, if the VSD is associated with severe left-sided heart chamber
enlargement, or if there is pulmonary arterial hypertension (PAH) (Level of Evidence: C).
Additional Indications
Four types of VSD may be amenable to transcatheter closure. This first category includes patients
with post–myocardial infarction VSD (PMI-VSD). Medical and surgical therapy is associated
with very high mortality in the acute phase of PMI-VSD, and as a result, transcatheter therapy
is often used as a temporizing bridge to clinically stabilize patients.
cludes patients with iatrogenic or postoperative residual VSD. Iatrogenic VSD can occur after
procedures such as septal myectomy, and postoperative residual VSD can be due to patch dehiscence, suture disruption, or incomplete closure of the defect.
postoperative and iatrogenic VSD is increasingly being used in this population because of the
high morbidity and mortality associated with reoperation.
Other VSD types that may be amenable to transcatheter closure are congenital muscular
VSDs (mVSD) and certain perimembranous VSDs (pmVSD). Surgery remains the standard of
care for the treatment of congenital VSD, but transcatheter therapy may be considered in patients
with mVSDs that are not easily accessible for surgical closure, especially in the setting of refractory heart failure despite optimal medical therapy.
have developed a deep aneurysm of the membranous septum but who have a persistent significant
shunt may be candidates for device closure.
238
IIb C
2-4
The second category in-
1,5
Transcatheter closure of residual
1,5
6
In addition, some patients with pmVSD who
20—TRANSCATHETER CLOSURE OF PMI, IATROGENIC, AND VSDs 239
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General Technique and Approach
Transcatheter VSD closure is generally performed under fluoroscopic and echocardiographic
guidance (either intracardiac or transesophageal). All patients should receive peri-interventional
antibiotic prophylaxis with a single dose of cefazolin or other antibiotic with similar coverage and
unfractionated heparin to maintain activated clotting time (ACT) .250 seconds.
The standard technique for transcatheter closure of mVSD has been described, although
there are many potential modifications of the technique.
namic catheterization, a high-quality left ventriculogram should define the location of the
defect. Positioning a camera at 60 degrees left anterior oblique (LAO) with cranial angulation
should provide a suitable view of the membranous and upper-to-mid muscular ventricular
septum (Fig. 20.1).
In most cases, many of the difficulties associated with catheter and wire exchange, as
well as device positioning and deployment, can be avoided by first establishing an arterialvenous (A-V) “rail” from the femoral artery to internal jugular vein (Fig. 20.2) or femoral
vein (Fig. 20.3).
A balloon wedge catheter should be used to cross the tricuspid valve to minimize the risk
of the A-V rail becoming entangled in the valve chordae. Once the catheter is in a branch
pulmonary artery (PA), it can be exchanged over a wire for a snare catheter. We typically use
a gooseneck snare. The VSD is then crossed from the left ventricle (LV ) to the right using
a soft hydrophilic wire through a sharp-angled directional catheter, such as a Judkins right
coronary catheter. The wire is directed anteriorly through the right ventricular outflow tract
to the pulmonary artery and snared. The wire course across the VSD and out to the PA
should be smooth, free of any loops or unusual turns. An unusual or difficult wire course
suggests that tricuspid valve chord may be entangled, in which case the wire should be retracted into the LV and the VSD should be recrossed. Real-time echocardiography can be
helpful, too, in identifying new or increased tricuspid regurgitation, another indicator of
chord disruption.
7,8
After vascular access and hemody-
Fig. 20.1 (A) En face view of a mid-muscular ventricular septal defect (VSD) in a 12-year-old female from a
right anterior oblique (RAO) view. (B) Left anterior oblique and cranial angulation of the lateral camera profiles
the ventricular septum in the same patient and shows the mid-muscular VSD.
240 5—VENTRICULAR SEPTAL INTERVENTIONS
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Fig. 20.2 (A) Right anterior oblique (RAO) projection of an arterial-venous wire “rail” in a patient with a midmuscular ventricular septal defect (VSD). The wire passes retrograde up the descending aorta, around the
aortic arch, into the left ventricle, crosses the VSD, passes retrograde across the tricuspid valve, and is
externalized from the right internal jugular vein. (B) Left anterior oblique (LAO)/cranial projection of the same
wire course.
With the wire snared, the directional catheter can be advanced into the pulmonary artery,
where the wire can then be exchanged for a long interventional wire. We typically use a 0.0350
Amplatzer Extra-Stiff wire. The interventional wire is then snared and exteriorized through the
right internal jugular vein or, less commonly, the femoral vein, by gently pulling the snared end
of the wire retrograde across the pulmonary and tricuspid valves. Any resistance should be investigated to ensure that there is no damage to valve function. Once the tip of the wire is externalized
from the venous sheath, it is secured with a small surgical clamp. Enough wire length should be
exposed from the venous sheath to accommodate the delivery system of the closure device.
With the rail now in place, device delivery is straightforward. A delivery sheath of appropriate
caliber for the selected closure device and the sheath dilator are advanced from the venous access
point over the wire rail. When the dilator is well into the LV or across the aortic valve, the dilator is withdrawn and the sheath advanced. When the tip of the delivery sheath is positioned well
into the LV, the support wire can be removed through the arterial sheath.
If there is difficulty advancing the sheath over the wire, this is likely due to impingement of
the wire/catheter within the tricuspid subvalvular apparatus. This problem can be addressed by
removing all catheter and wire systems and beginning the process over again—recrossing the
VSD and reestablishing the A-V rail until smooth advancement of the delivery system is
achieved.
7
If there is concern about losing position of the device or delivery system and having to recross
the defect, a “buddy wire” parallel to the closure device and delivery cable can be kept in place
during device deployment (Fig. 20.4). Should that approach be taken, the delivery sheath will
need to be sized appropriately to accommodate both the device and the buddy wire, typically 3
French sizes larger for a 0.0350 wire.
Based on the combination of angiographic and echocardiographic data, a muscular or PMI-
VSD occluder (as appropriate) that is 2 or 3 mm larger than the maximum diameter of the
defect should be attached to the delivery cable and advanced through the sheath.
7
The left disk
is deployed in the left ventricular cavity, making sure it does not impinge on the mitral valve
20—TRANSCATHETER CLOSURE OF PMI, IATROGENIC, AND VSDs 241
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Fig. 20.3 Conventional retrograde x-ray technique. 1: Retrograde, transaortic access to the left ventricle. 2: A guidewire crosses retrograde from the left to right ventricle across the ventricular septal defect
(VSD). 3: A transfemoral venous snare retrieves the transaortic guidewire from the pulmonary artery.
4: An arteriovenous loop is exteriorized to provide a rail to deliver the rigid VSD delivery sheath. 5: The
delivery sheath is positioned antegrade across the VSD. 6: The VSD occlusion device is positioned and
released. (Reproduced from Ratnayaka K, Raman VK, Faranesh Z, et al. Antegrade percutaneous closure of membranous ventricular septal defect using x-ray fused with magnetic resonance imaging.
JACC-Cardiovasc Interv. 2009;2[3]:14-17).
apparatus; then the entire system is withdrawn toward the septum. Resistance to gentle tension
on the delivery cable suggests that the left disk of the device is abutting the ventricular septum.
At that point the central waist and the proximal disk are deployed, not by pushing on the cable,
but by retracting the delivery sheath. Deployment should be performed under combined fluoroscopic and echocardiographic guidance to confirm the correct position of the two disks on the
left and right sides of the septum, respectively, and the central waist within the ventricular septum. The device can then be released and a final angiogram performed to document appropriate
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Fig. 20.4 Use of a “buddy” wire during difficult device closure of an apical postinfarction ventricular septal
defect (VSD). The wire passes parallel to the delivery cable and closure device, across the VSD, and into the
descending aorta.
Fig. 20.5 (Left) Long-axis view of a left ventricular angiography showing a mid-muscular ventricular septal
defect (VSD). (Middle) An Amplatzer muscular VSD occluder is positioned within the defect. The device is still
attached to the delivery system that had been advanced through the right internal jugular vein. (Right) Left
ventricular angiography post–device deployment showing perfectly positioned device without residual shunting. (Adapted from Carminati M, Butera G, Chessa M, Drago M, Negura D, Piazza L. Transcatheter closure
of congenital ventricular septal defect with Amplatzer septal occluders. Am J Cardiol. 2005;96:52L-58L.)
the device position (Figs. 20.5 and 20.6). Although the left disk should appear symmetric and
flat when completely deployed, trabeculations within the right ventricular myocardium may
prevent full expansion of the right disk (Fig. 20.7). In such a situation, as long as there is not
involvement of tricuspid valve chordae and no significant residual shunt, the device does not
need to be recaptured or repositioned. Fig. 20.8 is a transthoracic image (apical four-chamber
view) showing an Amplatzer occluder postclosure of mid-mVSD.
20—TRANSCATHETER CLOSURE OF PMI, IATROGENIC, AND VSDs 243
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Fig. 20.6 (Left) Long-axis view of a left ventricular angiography showing a perimembranous ventricular septal
defect (VSD). (Right) Left ventricular angiography post–device deployment showing perfectly positioned
device without residual shunting.
Fig. 20.7 (A) Abnormal but clinically irrelevant configuration of the right ventricular disk of an Amplatzer Muscular VSD Occluder device used to close a mid-muscular ventricular septal defect (VSD). Before device release, there is a small residual shunt. (B) After device release, the right ventricular disk conformation is still
abnormal, but there is only a trivial residual shunt that is likely to resolve with time.
Other Defect-Specific Considerations
POST-MI VSD
Transcatheter closure of PMI-VSD is often done in an urgent manner in medically fragile patients. It is understandable, then, that these procedures carry greater risk than closing a midmVSD in an otherwise healthy individual. Although the general technique is the same, anatomic
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Fig. 20.8 Transthoracic image (apical four-chamber view) showing Amplatzer occluder post-closure of
mid-muscular VSD.
considerations, such as an apical position of the VSD or the likelihood of ongoing myocardial
necrosis, raise the risk of device instability or embolization. Devices used for PMI-VSD include
the Amplatzer Post-MI VSD Occluder and, on occasion, the Amplatzer (atrial) Septal Occluder
device.
POSTSURGICAL VSD
Postsurgical VSDs are often located at the basal muscular septum. As a result, transcatheter
device closure of these defects carries a risk of heart block (particularly in a patient with a preexisting bundle branch block) and interference with aortic or mitral valve function. Close
echocardiographic monitoring is vital in these situations.
PERIMEMBRANOUS VSD WITH ANEURYSM
Due to the risk of heart block, there is no device specifically approved in the United States for
closure of pmVSD; several reports have been published attesting to the safety of transcatheter
closure for pmVSD with a membranous septal aneurysm. The presence of an aneurysmal “pocket”
provides for the closure device away from the crest of the muscular septum where the conduction
tissue lies. Several techniques and devices have been proposed for closing these defects. Our
preference is to use the Amplatzer Vascular Plug-II from a retrograde approach only (no A-V
rail). A device approximately the same size as the diameter of the aneurysm is used. With the
delivery catheter (usually a multipurpose guiding catheter or a long sheath) across the defect into
the apex of the right ventricle (RV), the distal disk of the device is deployed. The entire system
is then withdrawn under echocardiography and fluoroscopic guidance. Once the disk abuts the
right ventricular side of the membranous septal aneurysm, the remaining central and proximal
disks are deployed within the pocket.
Outcomes
The failure of transcatheter VSD closure can be classified into three subtypes: failure to implant
the device, failure to adequately close the shunt even after proper device implantation, and clinical
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