Download Device Closure for Ventricular Septal Defect After Myocardial Infarction

COVER STORY
Device Closure for
Ventricular Septal
Defect After
Myocardial Infarction
An overview of the potential use of transcatheter options to treat anatomically
suitable patients with postmyocardial infarction VSD.
BY NIKOLAOS KAKOUROS, BSC, MBBS, MRCP, AND STEPHEN J.D. BRECKER, MD, FRCP, FESC, FACC
A
(LAD) coronary artery that supplies both the anterior and
inferior apical septum, with extensive myocardial damage
and poor septal collateral blood supply are at increased risk
of developing septal rupture.9-12 There is a higher incidence
of triple-vessel disease in autopsy series, but this may reflect
bias due to these patients being less likely to survive the septal rupture event.13
(Courtesy of AGA Medical Corporation.)
cquired ventricular septal defect (VSD) is one of
the three major mechanical complications of
acute myocardial infarction (AMI), the other two
being acute mitral regurgitation and rupture of
the ventricular free wall. Although ventricular septal rupture
was described on autopsy as early as 1847, its clinical correlation with AMI was not established until almost 100 years
later.1 In the era before thrombolysis, VSD was not an infrequent complication of AMI, occurring in as many as 1% to
3% of patients.2-5 With the advent of early reperfusion
strategies and adjunct medical therapy, the incidence of this
complication has significantly decreased to < 1% of cases
(0.2% in the Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Coronary Arteries-I
[GUSTO-I] trial)6 but remains associated with a high morbidity and mortality. Data on the impact of primary percutaneous coronary intervention (PPCI) on the incidence of
VSD are limited, but a study of 1,321 patients by Yip et al
suggested a significant impact on the incidence of this complication (0.23% with PPCI vs 3% with no acute reperfusion
therapy; P = .0001).7
Development of a VSD correlates with delayed hospital
admission after the infarction (> 24 hours) and may be triggered by undue physical activity in the early postinfarction
(PI) period, as well as recurrent ischemia.8 Risk factors
include age > 60 years, female gender, no history of previous
MI, and hypertension. Patients with single-vessel disease,
particularly of a wrap-around left anterior descending
Figure 1. The Amplatzer PI muscular VSD occluder (AGA
Medical Corporation, Plymouth, MN). Note the longer waist
(10 mm) compared to the muscular VSD Amplatzer device.
NOVEMBER 2009 I CARDIAC INTERVENTIONS TODAY I 43
COVER STORY
VSDs tend to occur 3 to 8 days after the index AMI but
may also occur within the first 24 hours, or as late as 2
weeks.2,5,13 Fibrinolysis may promote the breakdown of the
necrosing septum, and reperfusion injury can result in hemorrhagic infarct leading to earlier VSD development. The
median time from AMI symptoms to VSD diagnosis was
just 1 day in the GUSTO-I thrombolysis trial6 and 16 hours
in the Should We Emergently Revascularize Occluded
Coronaries in Cardiogenic Shock (SHOCK) trial,14 with a
tendency for earlier timing of rupture also noted in the
more recent PPCI study.7
Transmural tissue necrosis causes loss of structural integrity with a dynamic perforation of the interventricular septum at the interface of necrotic and nonnecrotic myocardium. The defect is most often at the apical septum in anterior AMIs and the base of the heart after inferior AMIs, with
the orifice varying from 1 to several centimeters in
diameter.13 The architecture may be complex with serpiginous tunnels traversing the interventricular septum, particularly in ruptures involving the inferobasal septum, and multiple orifices can, less commonly, occur. Intramural extension
with dissection of the interventricular septum or, rarely, the
right ventricular free wall may occur.15-17
DIAGNOSIS AND IMAGING
Diagnosis traditionally involved the passage of pulmonary
artery balloon catheters to document the left-to-right shunt
but is now achieved reliably and less invasively with Doppler
transthoracic echocardiography (TTE). On TTE, VSD is suggested by a new regional wall motion abnormality suggestive of AMI and protrusion of the interventricular septum at
this site toward the right ventricle. Doppler interrogation
reveals a high-velocity, left-to-right ventricular shunt in
almost all cases. Transesophageal echocardiography (TEE)
may be occasionally necessary to establish the extent of the
defect, particularly in the case of inferior infarction.18,19
Severity of the intraventricular shunt varies depending on
the size of the defect, but most patients are clinically gravely
ill with incipient or established cardiogenic shock. Even the
minority of patients who are initially stable tend to develop
rapid, progressive, or unexpected hemodynamic compromise. In addition to hypotension, patients have clinical evidence of biventricular (although predominantly right heart)
failure and a loud, harsh, holosystolic parasternal murmur
associated with a thrill in as many as 50% of cases.
MANAGEMENT
The prognosis of post-AMI VSD is very poor, with mortality rates as high as 50% at 1 week and 90% at 2 months with
conservative medical treatment.13 Acute surgery is technically complicated by the myocardial tissue being soft and
friable. Retrospective studies have suggested that better sur44 I CARDIAC INTERVENTIONS TODAY I NOVEMBER 2009
Figure 2. Transcatheter closure of PI VSD. Fluoroscopy shows
the Amplatzer PI muscular VSD occluder device fully
deployed and released.
gical results were obtained in patients in whom surgery was
delayed by 6 weeks until some myocardial fibrosis had
occurred compared to operating during the acute
phase.5,20,21 Although scarring at the tissue edges certainly
permits better hold of the sutures and a more secure and
long-lasting closure, the apparent favorable outcome of
delayed surgery more likely reflects a selection bias, with
hemodynamically stable patients with small defects selfselecting by surviving to a relatively lower-risk interim operation. Delaying surgery in hemodynamically stable patients
engenders the risk of unpredictable and catastrophic deterioration, and multiple studies support rapid intervention.22-26
Coronary artery bypass grafting for underlying coronary disease at the time of VSD repair significantly improves longterm survival compared to VSD repair alone;27,28 consequently, evaluation of the coronary anatomy by cardiac
catheterization is indicated before undertaking surgical
repair of post-AMI VSD. The joint American Heart
Association/American College of Cardiology (AHA/ACC)
2004 Guidelines recommend emergent repair of the VSD
with concurrent coronary artery bypass grafting, as indicated, irrespective of hemodynamic status,29,30 with no change
in this class I recommendation on the 2007 ACC/AHA
focused guideline update.31 In-hospital mortality after surgery is significantly lower than with conservative management but remained as high as 47% in the GUSTO-I trial.6,32-34
A residual shunt persists in 10% to 37% of patients after surgery due to an overlooked additional defect or development of a new VSD such that up to 11% of patients may
require a further surgical procedure.35 Patch dehiscence may
COVER STORY
Figure 3. Postmortem photograph of the heart showing an
Amplatzer device in situ across an interventricular septal
defect from a patient who died despite successful device
implantation.
also occur because the sutures may tear out of the friable,
recently infracted myocardium. The long-term prognosis of
patients who survive the acute 30-day postoperative period
is, however, good.6
TR ANSCATHETER POST-AMI VSD CLOSURE
Early surgery is considered the gold standard for postinfarction VSD, with the high surgical risk being acceptable
in the face of the even higher risk of death without surgery.
More recently, however, an additional option of percutaneous closure of the rupture has become available.
Transcatheter closure of the VSD was initially reported in
patients deemed to be at too high risk for surgical repair
due to their recent post-AMI status, advanced age, severe
coronary artery disease, hemodynamic instability, and
added comorbidity (such as renal failure and diabetes mellitus). Transcatheter closure was also used in patients with
residual leak after VSD repair surgery at excessive risk of a
repeat surgical operation that ranges from 13% to 31%.35-37
Lately, the use of transcatheter VSD closure as primary therapy for post-AMI VSD has emerged.
After the initial report by Lock et al in 1988 using the
Rashkind double umbrella,38 various devices have been
used, including the Clamshell occluder (USCI Angiographics,
Tewksbury, MA),39 the CardioSeal (NMT Medical, Boston,
MA),40 and the Amplatzer septal occluder (AGA Medical
Corporation).37 Previous experience with congenital VSDs
has found the Amplatzer system to have a higher success
rate than other devices,41,42 and extrapolation of this experience has led to the tendency to also use this family of
devices for the closure of acquired post-AMI ventricular septal ruptures. The Amplatzer muscular VSD occluder is a self-
expanding, single-unit nitinol device with incorporated
polyester fabric that comprises two discs connected by a 7mm-long waist portion, compared with a 4-mm waist in the
atrial septal defect (ASD) device. The device is sized
between 4 and 18 mm by the diameter of the central waist,
with the discs being 8 mm larger than this segment. The
device is secured onto a delivery cable and implanted via a
5- to 9-F diameter sheath. It is self-centering and permits
several positioning attempts because it is retrievable before
release.
Specially designed devices for the closure of post-AMI
VSDs have also become available. The Amplatzer PI muscular VSD device has larger disks and a longer waist (10 mm)
than the muscular VSD Amplatzer device to accommodate
the thicker adult interventricular septum. It is available in
sizes of 16 to 24 mm in 2-mm increments, as determined by
the diameter of the waist section (Figure 1). It requires a
minimum 9- to 10-F sheath for delivery. The newer sheaths
include wire braiding that obviates the previously troublesome risk of kinking.
In some cases, the Amplatzer cribriform septal occluder
and the CardioSeal septal occluder have been used to
address multifenestrated defects.15,19
TECHNIQUES
Antibiotic prophylaxis is administered periprocedure, and
full heparinization is maintained for up to 24 hours.
Antiplatelet therapy is administered for at least 6 months to
protect the device but should probably be given to the
patient lifelong in view of the AMI. Endocarditis prophylaxis
is commonly recommended for 6 months or indefinitely for
patients with residual shunts based on congenital ASD/VSD
closure practice.
The procedure is usually performed with fluoroscopic
control under general anesthesia to permit intraoperative
TEE. The use of real-time three-dimensional TEE to provide
detailed assessment of the defect orifice and to guide the
closure procedure has been recently reported.43 Procedure
under conscious sedation is also possible for apical defects
adequately visualized by TTE.19 Intracardiac echocardiography may prove a suitable alternative, but reports on its use
in this setting are lacking.
The defect anatomy and size are carefully evaluated using
axial projection left ventriculography and multiple echocardiographic views. The orifice size measured on echocardiography forms the basis for the decision of what size of device
to use. Intraoperative echocardiography also helps guide
catheter manipulations, positioning, and deployment of the
occluder device. Echocardiographic dropout due to the
catheter may occasionally appear as a residual tissue defect,
but careful assessment by color Doppler duplex echocardiography can help differentiate the two.
NOVEMBER 2009 I CARDIAC INTERVENTIONS TODAY I 45
COVER STORY
TABLE 1. TRANSCATHETER CLOSURE OF POSTMYOCARDIAL INFARCTION VSD
WITH AMPLATZER OCCLUDER DEVICESa
Total N
Acute
S/C
Success
of Patients (N Patients) (N Patients) Rate
Chessa44
2002
12
Szkutnik45 7
2003
Goldstein46 4
2003
Holzer47, 48 18
2004
Demkow49 11
2005
Martinez50 5
2007
Bialkowski51 19
2007
Marinakis52 8
2007
Ahmed53 5
2008
Maltais24 12
2009
29
Thiele54
2009
Total N
130
Survival at 30 Days
Residual Shunts
Acute
S/C
Small/
Trivial
Moderate/
Severe
3
9
11/12
0/3
8/9
0
0
0
7
5/7
-
4/5
3
1
0
4
3/4
-
3/3
2
2
5
13
16/18
2/5
9/13
8
2
3
8
10/11
0/2
8/8
4
0
3
2
5/5
2/3
2/2
3
1
1
18
14/19
0/1
9/13
9
3
6
2
7/8
0/6
1/2
0
0
2
3
4/5
0/1
3/3
3
1
12
0
11/12
7/11
-
10
1
29
0
25/29
10/29
-
6
4
64
66
111/130
21/61
47/58
48/111
15/111
85
34
81
43
14
Total %
Abbreviations: N, number; S/C, subacute/chronic.
aLiterature review for published series. Acute phase is considered the period within 14 days from the index infarction event, and the
subacute/chronic phase is if closure was performed beyond this time period.
The standard technique for muscular septum device
implantation has been described in the literature.44,47,55-60 In
brief, a Judkins right catheter is advanced retrogradely via
the aortic valve to the left ventricle from a peripheral arterial access point. Access to the left ventricle via an atrial
transseptal puncture has also been described when peripheral arterial access is not possible.61 The defect is then
crossed from left to right using a soft wire that is advanced
to the pulmonary artery or superior vena cava. The catheter
may then be advanced to the right ventricle and the wire
46 I CARDIAC INTERVENTIONS TODAY I NOVEMBER 2009
exchanged for a more supportive 260-cm or 400-cm wire.
Venous access is established via the right internal jugular
vein, where a snare (such as an Amplatz Gooseneck, ev3
Inc., Plymouth, MN) is introduced to capture and exteriorize
the transseptal wire creating an arteriovenous guidewire circuit.
Balloon sizing of the defect may be performed by three
principal methods. First, an OBW balloon may be placed
in the left ventricle and expanded with dilute contrast to
a volume that produces VSD occlusion on TEE when
COVER STORY
pulled gently against the defect and such that it can just
be pulled through the defect. The diameter at this volume is then measured ex vivo and used to guide device
size selection. Alternatively, the stop-flow technique may
be used when a longer compliant balloon is placed across
the defect and measured at the volume at which shunting is eliminated on Doppler echocardiography (not to
the point of waist formation). Finally, an Amplatzer sizing
balloon (AGA Medical Corporation) may be inflated
across the defect and the stretched defect diameter
measured as the balloon waist size. An occluder with a
waist sized 1 to 7 mm larger than the maximal measured
defect diameter is then selected.19,48 There are concerns
regarding the use of these techniques in the setting of
post-AMI VSD, because the tissue at the edges of the
defect can be very friable, and application of pressure
may easily lead to VSD enlargement, particularly with the
last method. Some interventionists have, therefore, abandoned balloon sizing altogether (even in the non-AMI
setting) and use two-dimensional TEE or even TTE measurements, oversizing the device by 2 to 8 mm and up to
50% above this reading to reduce the incidence of device
embolization or residual shunt.44,49,54
The delivery sheath is then advanced from the venous
side to the left ventricular cavity over the wire, and the
dilator and wire are gently removed. The selected
occluder device is then delivered to the left ventricle.
The device is extruded from the sheath until the left
ventricular disc is opened and then withdrawn toward
the interventricular septum. After further satisfactory
left ventriculography and echocardiographic evaluation
of septal alignment, the proximal right ventricular disc is
also deployed, and the device is released from the delivery cable (Figure 2).
RESULTS AND COMPLICATIONS
Outcomes using Amplatzer devices have been reported in
multiple single-case reports but also in a number of case
series studies, which are summarized in Table 1.
Percutaneous device implantation was either the primary
therapy or was used to treat a residual shunt after primary
surgical VSD closure. The results of these series must be cautiously evaluated against surgical outcomes because the
numbers in each series are small, and patients were not randomized, leading inevitably to a degree of patient selection
bias. This bias may favor the percutaneous option—because
larger, more complex defects are excluded due to lack of
anatomical suitability—or favor surgery as higher-risk surgical
candidates are referred for transcatheter device therapy. The
largest series to date, including 29 consecutive unselected
patients with VSD who underwent primary transcatheter
closure, was reported earlier this year by Thiele et al.54
In total, 130 patients are reported in these 11 series, 64 of
whom were treated in the acute phase after AMI. In the
remaining 66 patients, the procedure was performed at
least 14 days after the index infarction event.
The overall device implantation success rate was 85%
(95% confidence interval [CI] for mean, 81%–90%), with no
significant difference between the acute and
subacute/chronic phase patients. Despite successful device
implantation, the morbidity and mortality remain very high
when the procedure is performed in the acute phase, especially for patients in cardiogenic shock (Figure 3). The 30-day
survival was 34% (95% CI, 10%–58%) in the acute phase
patients, compared to an encouraging 81% (95% CI,
71%–91%) in the subacute/chronic group.
In the recent large series, five of 29 patients died in the
catheterization laboratory from procedure-related complications.54 Subsequent in-hospital death is attributed in the
series to ventricular failure secondary to extensive infarction
or associated comorbidity, such as renal failure, multiorgan
failure, and sepsis.15,52 As for surgical repair, if a transcatheter
procedure is technically feasible, it is prudent not to delay it,
because secondary complications may ensue and impair
subsequent prognosis even if the VSD is subsequently adequately corrected. Transient complete atrioventricular block
is reported,15,49,51,54 but the long-term need for permanent
pacing system implantation is unclear. Ventricular tachycardia or fibrillation, or atrial fibrillation requiring cardioversion
may also arise.40,45 Contrast medium nephropathy may
develop secondary to the implantation procedure, although
the relative contribution of this to subsequent morbidity
and mortality is difficult to dissect from preexisting renal
impairment or nephropathy due to low cardiac output.
Iatrogenic right or left ventricular free wall perforation and
tamponade has also been reported.24,51,54,62
Device migration, although of primary concern in transcatheter device closure, is rare and associated with treatment of larger defects; it tends to be associated with incorrect device sizing, inaccurate deployment, and operator
inexperience. Treatment of basal defects may lead to trapping of mitral or tricuspid chordae and interference with
the aortic valve leading to valvular regurgitation. Although
this is a concern stemming from treatment of perimembranous congenital VSDs, it does not appear to be a significant
reported problem in the VSD literature.
The rate of complete closure with no or small-volume
residual shunting is reduced in the acute setting because the
peri-VSD tissue may subsequently necrose and scar, resulting
in retraction from the device causing an increasing
shunt.47,52
Residual shunting after device implantation may need to
be addressed by interval surgery or deployment of additional devices.44,45,48,63 On pooling the literature series data
NOVEMBER 2009 I CARDIAC INTERVENTIONS TODAY I 47
COVER STORY
(Table 1), small or trivial shunts remain in approximately
43% (95% CI, 27%–59%) of patients, and moderate-tosevere shunts remain in 15% (95% CI, 0%–34%), rates similar
to surgical data.
PATIENT SELECTION
Not all patients are anatomically suitable for transcatheter closure. The exact position of the defect, its
anatomy (simple vs complex), and its size affect the likelihood of successful deployment and subsequent stability
of a percutaneously implanted device. Consequently,
careful assessment by two-dimensional/three-dimensional TTE or TEE and (when hemodynamic stability permits)
cardiac magnetic resonance imaging is important in
patient selection.64 Maltais et al recently reported their
single-center experience in which small or medium VSDs
were preferentially treated with a transcatheter device,
and defects larger than 15 mm (< 10 mm smaller than
the largest available Amplatzer occluder) were considered for surgery, with no significant in-hospital or 30-day
mortality outcome between the two groups. In the
Amplatzer muscular VSD occluder US registry, exclusion
criteria were more lenient, with defects up to 24 mm
(maximum available device size) treated successfully with
no reports of device embolization.48 In the more recent
study by Thiele et al, patients with defects up to 35 mm
were accepted, but the incidence of device dislocation
was a relatively high 17% (five of 29 patients).54
Nonetheless, the paradigm may prove useful as the basis
of a patient selection algorithm, with patients who have
defects anatomically suitable for percutaneous closure
being referred for primary transcatheter therapy and
patients with larger, more complex or multiple defects
preferentially referred for surgery.
CONCLUSION
Transcatheter device closure is an accepted alternative to
medical therapy or surgery for congenital VSDs, and the
application of the technology to the post-AMI VSD is
expanding. Although cardiac surgery with concurrent coronary artery bypass grafting, as indicated, remains the gold
standard, a significant proportion of patients are at too high
risk for surgery due to their post-AMI status, cardiogenic
shock, and comorbidities. Transcatheter device placement
may provide a stabilization bridge to urgent surgery or even
permit deferral of surgery until the peri-VSD tissue has
strengthened.65 There is increasing evidence supporting the
use of transcatheter device placement as a definitive primary treatment for anatomically suitable patients, and the
procedure may also provide an alternative to repeat surgery
for patients with residual shunts and patch dehiscence.37-39,66
Patients with large or multiple defects are best treated surgi48 I CARDIAC INTERVENTIONS TODAY I NOVEMBER 2009
cally when possible because the risk of transcatheter device
embolization in this group may be greater.24 A multidisciplinary team, including interventional cardiologists and cardiac
surgeons, should evaluate these high-risk patients to determine the optimal management strategy. Large series are
needed in the future to further compare percutaneous with
surgical options, as well as different occlusion devices,
although the feasibility of randomized trials is likely to prove
limited given the rarity, anatomic variability, and hemodynamic instability of these patients.
Finally, the currently available devices do have significant
shortcomings. They have been criticized for the rigid sheath
that may traumatize and enlarge the VSD and for the
requirement to remove the guidewire before device deployment such that the arteriovenous circuit is lost should the
chosen device dislocate into the right ventricle.
Furthermore, devices come in a limited range of sizes, and
closure of the shunt in the acute period may be suboptimal
because the polyester fabric requires time to thrombose
and endothelialize before being efficient in preventing shunt
across the high transventricular pressure gradient.54 Some of
these shortcomings are being addressed,67 and newer
devices are eagerly awaited. ■
Nikolaos Kakouros, BSc, MBBS, MRCP, is an interventional
cardiology postdoctoral research fellow at the Johns Hopkins
University in Baltimore, Maryland. He has disclosed that he
holds no financial interest in any product or manufacturer
mentioned herein. Dr. Kakouros may be reached at (410) 5026133; [email protected].
Stephen J.D. Brecker, MD, FRCP, FESC, FACC, is a consultant
cardiologist at St George’s Hospital in London, United Kingdom.
He has disclosed that he holds no financial interest in any
product or manufacturer mentioned herein. Dr. Brecker may
be reached at +44-(0)20-8725-3556; [email protected].
1. Sager RV. Coronary thrombosis: perforation of the infarcted interventricular septum. Arch
Intern Med. 1934;53:140-152.
2. Topaz O, Taylor AL. Interventricular septal rupture complicating acute myocardial infarction:
from pathophysiologic features to the role of invasive and noninvasive diagnostic modalities in
current management. Am J Med. 1992;93:683-688.
3. Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture. Ann Thorac Surg. 1986;41:683-691.
4. Pohjola-Sintonen S, Muller JE, Stone PH, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of
Infarct Size. Am Heart J. 1989;117:809-818.
5. Moore CA, Nygaard TW, Kaiser DL, et al. Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival. Circulation.
1986;74:45-55.
6. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I
(Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators.
Circulation. 2000;101:27-32.
7. Yip HK, Fang CY, Tsai KT, et al. The potential impact of primary percutaneous coronary intervention on ventricular septal rupture complicating acute myocardial infarction. Chest.
2004;125:1622-1628.
8. Figueras J, Cortadellas J, Calvo F, et al. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: study in 225 patients with free wall,
septal or papillary muscle rupture. J Am Coll Cardiol. 1998;32:135-139.
COVER STORY
9. Radford MJ, Johnson RA, Daggett WM Jr, et al. Ventricular septal rupture: a review of clinical
and physiologic features and an analysis of survival. Circulation. 1981;64:545-553.
10. Skehan JD, Carey C, Norrell MS, et al. Patterns of coronary artery disease in post-infarction
ventricular septal rupture. Br Heart J. 1989;62:268-272.
11. Pretre R, Rickli H, Ye Q, et al. Frequency of collateral blood flow in the infarct-related coronary
artery in rupture of the ventricular septum after acute myocardial infarction. Am J Cardiol.
2000;85:497-499, A10.
12. Birnbaum Y, Wagner GS, Gates KB, et al. Clinical and electrocardiographic variables associated with increased risk of ventricular septal defect in acute anterior myocardial infarction. Am J
Cardiol. 2000;86:830-834.
13. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute
myocardial infarction: identification of simple and complex types in 53 autopsied hearts. Am J
Cardiol. 1984;54:1201-1205.
14. Menon V, Webb JG, Hillis LD, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. Should we
emergently revascularize Occluded Coronaries in cardiogenic shock? J Am Coll Cardiol.
2000;36:1110-1116.
15. Giombolini C, Notaristefano S, Santucci S, et al. Transcatheter closure of postinfarction ventricular septal defect using the Amplatzer atrial septal defect occluder. J Cardiovasc Med.
2008;9:941-945.
16. Paul S, Mihaljevic T, Leacche M, et al. Postinfarction ventricular septal defect with pseudoaneurysm repair after failed percutaneous closure. Ann Thorac Surg. 2005;79:701-703.
17. Tighe DA, Paul JJ, Maniet AR, et al. Survival in infarct related intramyocardial dissection:
importance of early echocardiography and prompt surgery. Echocardiography. 1997;14:403-408.
18. St John Sutton MG, Maniet AR. Atlas of multiplane transesophageal echocardiography.
Evaluation of the cardiac chambers, and pericardium: structure and function. Vol. 2. London,
England: Martin Dunitz; 2003: 487.
19. Szkutnik M, Kusa J, Bialkowski J. The use of two Amplatzer “cribriform” septal occluders to
close multiple postinfarction ventricular septal defects. Tex Heart Inst J. 2008;35:362-364.
20. Deville C, Fontan F, Chevalier JM, et al. Surgery of post-infarction ventricular septal defect:
risk factors for hospital death and long-term results. Eur J Cardiothorac Surg. 1991;5:167-174;
discussion 75.
21. Held AC, Cole PL, Lipton B, et al. Rupture of the interventricular septum complicating acute
myocardial infarction: a multicenter analysis of clinical findings and outcome. Am Heart J.
1988;116:1330-1336.
22. Pretre R, Ye Q, Grunenfelder J, et al. Operative results of “repair” of ventricular septal rupture
after acute myocardial infraction. Am J Cardiol. 1999;84:785-788.
23. Scanlon PJ, Montoya A, Johnson SA, et al. Urgent surgery for ventricular septal rupture complicating acute myocardial infarction. Circulation. 1985;72:II185-II190.
24. Maltais S, Ibrahim R, Basmadjian AJ, et al. Postinfarction ventricular septal defects: towards a
new treatment algorithm? Ann Thorac Surg. 2009;87:687-692.
25. David TE. Operative management of postinfarction ventricular septal defect. Semin Thorac
Cardiovasc Surg. 1995;7:208-213.
26. Daggett WM. Postinfarction ventricular septal defect repair: retrospective thoughts and historical perspectives. Ann Thorac Surg. 1990;50:1006-1009.
27. Muehrcke DD, Daggett WM Jr, Buckley MJ, et al. Postinfarct ventricular septal defect repair:
effect of coronary artery bypass grafting. Ann Thorac Surg. 1992;54:876-882; discussion 82-83.
28. Cox FF, Plokker HW, Morshuis WJ, et al. Importance of coronary revascularization for late
survival after postinfarction ventricular septal rupture. A reason to perform coronary angiography
prior to surgery. Eur Heart J. 1996;17:1841-1845.
29. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of
patients with ST-elevation myocardial infarction—executive summary: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing
Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial
Infarction). Circulation. 2004;110:588-636.
30. Eagle KA, Guyton RA, Davidoff R, et al. ACC/AHA 2004 guideline update for coronary artery
bypass graft surgery: a report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery
Bypass Graft Surgery). Circulation. 2004;110:e340-3437.
31. Antman EM, Hand M, Armstrong PW, et al. 2007 Focused Update of the ACC/AHA 2004
Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines:
developed in collaboration With the Canadian Cardiovascular Society endorsed by the American
Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the
ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial
Infarction, Writing on Behalf of the 2004 Writing Committee. Circulation. 2008;117:296-329.
32. Bolooki H. Emergency cardiac procedures in patients in cardiogenic shock due to complications of coronary artery disease. Circulation. 1989;79:I137-I148.
33. Davies RH, Dawkins KD, Skillington PD, et al. Late functional results after surgical closure of
acquired ventricular septal defect. J Thorac Cardiovasc Surg. 1993;106:592-598.
34. Jones MT, Schofield PM, Dark JF, et al. Surgical repair of acquired ventricular septal defect.
Determinants of early and late outcome. J Thorac Cardiovasc Surg. 1987;93:680-686.
35. Deja MA, Szostek J, Widenka K, et al. Post infarction ventricular septal defect - can we do better? Eur J Cardiothorac Surg. 2000;18:194-201.
36. Skillington PD, Davies RH, Luff AJ, et al. Surgical treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac
Cardiovasc Surg. 1990;99:798-808.
37. Lee EM, Roberts DH, Walsh KP. Transcatheter closure of a residual postmyocardial infarction
ventricular septal defect with the Amplatzer septal occluder. Heart. 1998;80:522-524.
38. Lock JE, Block PC, McKay RG, et al. Transcatheter closure of ventricular septal defects.
Circulation. 1988;78:361-368.
39. Landzberg MJ, Lock JE. Interventional catheter procedures used in congenital heart disease.
Cardiol Clin. 1993;11:569-587.
40. Pienvichit P, Piemonte TC. Percutaneous closure of postmyocardial infarction ventricular septal defect with the CardioSeal septal occluder implant. Catheter Cardiovasc Interv. 2001;54:490494.
41. Arora R, Trehan V, Kumar A, et al. Transcatheter closure of congenital ventricular septal
defects: experience with various devices. J Interv Cardiol. 2003;16:83-91.
42. Michel-Behnke I, Le TP, Waldecker B, et al. Percutaneous closure of congenital and acquired
ventricular septal defects—considerations on selection of the occlusion device. J Interv Cardiol.
2005;18:89-99.
43. Halpern DG, Perk G, Ruiz C, et al. Percutaneous closure of a post-myocardial infarction ventricular septal defect guided by real-time three-dimensional echocardiography. Eur J Echocardiogr.
2009;10:569-571.
44. Chessa M, Carminati M, Cao QL, et al. Transcatheter closure of congenital and acquired muscular ventricular septal defects using the Amplatzer device. J Invasive Cardiol. 2002;14:322-327.
45. Szkutnik M, Bialkowski J, Kusa J, et al. Postinfarction ventricular septal defect closure with
Amplatzer occluders. Eur J Cardiothorac Surg. 2003;23:323-327.
46. Goldstein JA, Casserly IP, Balzer DT, et al. Transcatheter closure of recurrent postmyocardial
infarction ventricular septal defects utilizing the Amplatzer postinfarction VSD device: a case
series. Catheter Cardiovasc Interv. 2003;59:238-243.
47. Holzer R, Balzer D, Cao QL, et al. Device closure of muscular ventricular septal defects using
the Amplatzer muscular ventricular septal defect occluder: immediate and mid-term results of a
U.S. registry. J Am Coll Cardiol. 2004;43:1257-1263.
48. Holzer R, Balzer D, Amin Z, et al. Transcatheter closure of postinfarction ventricular septal
defects using the new Amplatzer muscular VSD occluder: results of a U.S. Registry. Catheter
Cardiovasc Interv. 2004;61:196-201.
49. Demkow M, Ruzyllo W, Kepka C, et al. Primary transcatheter closure of postinfarction ventricular septal defects with the Amplatzer septal occluder- immediate results and up-to 5 years followup. EuroIntervention. 2005;1:43-47.
50. Martinez MW, Mookadam F, Sun Y, et al. Transcatheter closure of ischemic and post-traumatic ventricular septal ruptures. Catheter Cardiovasc Interv. 2007;69:403-407.
51. Bialkowski J, Szkutnik M, Kusa J, et al. Transcatheter closure of postinfarction ventricular
septal defects using Amplatzer devices. Rev Esp Cardiol. 2007;60:548-551.
52. Marinakis A, Vydt T, Dens J, et al. Percutaneous transcatheter ventricular septal defect closure
in adults with Amplatzer septal occluders. Acta Cardiol. 2007;62:391-395.
53. Ahmed J, Ruygrok PN, Wilson NJ, et al. Percutaneous closure of post-myocardial infarction
ventricular septal defects: a single centre experience. Heart Lung Circ. 2008;17:119-123.
54. Thiele H, Kaulfersch C, Daehnert I, et al. Immediate primary transcatheter closure of postinfarction ventricular septal defects. Eur Heart J. 2009;30:81-88.
55. Amin Z, Gu X, Berry JM, et al. New device for closure of muscular ventricular septal defects in
a canine model. Circulation. 1999;100:320-328.
56. Thanopoulos BD, Rigby ML. Outcome of transcatheter closure of muscular ventricular septal
defects with the Amplatzer ventricular septal defect occluder. Heart. 2005;91:513-516.
57. Hijazi ZM, Hakim F, Al-Fadley F, et al. Transcatheter closure of single muscular ventricular
septal defects using the Amplatzer muscular VSD occluder: initial results and technical considerations. Catheter Cardiovasc Interv. 2000;49:167-172.
58. Arora R, Trehan V, Thakur AK, et al. Transcatheter closure of congenital muscular ventricular
septal defect. J Interv Cardiol. 2004;17:109-115.
59. Carminati M, Butera G, Chessa M, et al. Transcatheter closure of congenital ventricular septal
defects: results of the European Registry. Eur Heart J. 2007;28:2361-2368.
60. Carminati M, Butera G, Chessa M, et al. Transcatheter closure of congenital ventricular septal
defect with Amplatzer septal occluders. Am J Cardiol. 2005;96:52L-58L.
61. Perez-David E, Garcia Fernandez MA, Garcia E, et al. Successful transcatheter closure of a
postmyocardial infarction ventricular septal rupture in a patient rejected for cardiac surgery: usefulness of transesophageal echocardiography. J Am Soc Echocardiogr. 2007;20:1417.e9-12.
62. Eshtehardi P, Garachemani A, Meier B. Percutaneous closure of a postinfarction ventricular
septal defect and an iatrogenic left ventricular free-wall perforation using two Amplatzer muscular
VSD occluders. Catheter Cardiovasc Interv. 2009;74:243-246.
63. Webb I, De Giovanni J, Hildick-Smith D. Multiple percutaneous VSD closures post-myocardial infarct. Eur Heart J. 2006;27:552.
64. Kaulfersch C, Daehnert I, Schuler G, et al. Transcatheter closure of postinfarction ventricular
septal defects. Minerva Cardioangiol. 2007;55:693-701.
65. Costache VS, Chavanon O, Bouvaist H, et al. Early Amplatzer occluder closure of a postinfarct
ventricular septal defect as a bridge to surgical procedure. Interact Cardiovasc Thorac Surg.
2007;6:503-504.
66. Hachida M, Nakano H, Hirai M, et al. Percutaneous transaortic closure of postinfarctional
ventricular septal rupture. Ann Thorac Surg. 1991;51:655-657.
67. Majunke N, Sievert H. ASD/PFO devices: what is in the pipeline? J Interv Cardiol.
2007;20:517-523.
NOVEMBER 2009 I CARDIAC INTERVENTIONS TODAY I 49