Catheterization and Cardiovascular Interventions 86:1264–1270 (2015)
Transcatheter Closure of Postmyocardial Infarction, Iatrogenic, and Postoperative Ventricular Septal Defects: The Mayo Clinic Experience Alexander C. Egbe,1 MD, MPH, Joseph T. Poterucha,2 DO, Charanjit S. Rihal,1 MD, MBA, Nathaniel W. Taggart,2 MD, Frank Cetta,2 MD, Allison K. Cabalka,2 MD, Peter M. Pollak,2 MD, Guy S. Reeder,1 MD, and Donald J. Hagler,2* MD Objectives: To determine event-free survival after transcatheter closure of ventricular septal defect (VSD), and to identify predictors of adverse events (AE) in post myocardial infarction VSD (post-MI VSD) subgroup. Background: There are limited data on mid-term follow-up after transcatheter VSD closure. Methods: Retrospective review of 27 cases of transcatheter VSD closure (post-MI 5 18 and non-ischemic 5 9) performed from 1999 to 2013. We defined AE as death, device embolization, hemolysis requiring blood transfusion, heart block and reintervention. Results: In the post-MI VSD subgroup, mean age and follow-up was 69 6 11 and 7.3 6 7 years, respectively. AE occurred in 8 (44%) patients (death-3, device embolization-1, hemolysis-1, surgical VSD closure-2, reintervention-1). Event-free survival was 56% at 1 month and 5 years, and all AE occurred in the periprocedural period. Cardiogenic shock (HR: 3.21, CI: 1.82–5.41, P 5 0.002), and VSD closure in acute phase (HR: 2.14, CI: 1.12–4.31, P 5 0.004) were independent predictors of AE. In the non-ischemic VSD subgroup, mean age and follow-up was 49 6 15 and 8.7 6 8 years, respectively. AE occurred in 3 (33%) patients (late death-1, surgical VSD closure-2). For the entire cohort, freedom from death was 89% and 85% at 1 month and 5 years, and event-free survival was 70% and 61% at 1 month and 5 years. Conclusions: Transcatheter closure of post-MI VSD carries a moderate risk of periprocedural complications but low event rates afterwards. By comparison, device closure of non-ischemic VSD has lower periprocedural morbidity but some patients continued to experience AE during follow-up. VC 2015 Wiley Periodicals, Inc. Key words: transcatheter; myocardial infarction; ventricular septal defect
INTRODUCTION
Transcatheter closure of ventricular septal defect (VSD) is considered a less invasive option in the management of certain types of VSD. Since its introduction in the late 1980s, transcatheter VSD closure has been used in the treatment of post myocardial infarction VSD (post-MI VSD), postoperative and congenital VSD [1–4]. Post-MI VSD is a relatively uncommon complication of acute myocardial infarction but it is responsible for a significant proportion of early deaths following an MI [5,6]. Evolution of Post-MI VSD can be broadly categorized into 2 phases: acute and chronic phase. The acute phase occurs within the first 2 weeks after infarction. This phase is characterized by coagulation necrosis and release of lytic enzymes from neutrophils resulting in myocardial necrosis. As necrosis progress, resorption and retraction of infarcted tissue typically leads to enlargement of the defect size [7]. The chronic phase begins after 3–4 weeks and is characterized by fibrosis and scar formation around the C 2015 Wiley Periodicals, Inc. V
edges of the defect [7]. Surgical closure of post-MI VSD is associated with high mortality especially in the acute phase [8,9], and medical therapy alone yields survival rate less than 10% at 1 year [10]. Additional Supporting Information may be found in the online version of this article. 1 Division of Cardiovascular Diseases, Mayo Clinic Rochester, Minnesota 2 Division of Pediatric Cardiology, Mayo Clinic Rochester, Minnesota Conflict of interest: Nothing to report. *Correspondence to: Donald J. Hagler, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester MN 55905. E-mail: [email protected] Received 19 February 2015; Revision accepted 5 April 2015 DOI: 10.1002/ccd.25989 Published online 29 May 2015 in Wiley Online Library (wileyonlinelibrary.com)
Transcatheter Closure of VSD
Transcatheter VSD closure is a less invasive palliative measure to clinically stabilize patients. Postoperative residual VSD can occur after surgical repair of isolated VSD or complex cardiac defect due to patch dehiscence, suture disruption or incomplete closure of the defect [11]. Residual VSDs are well tolerated if they are restrictive but large defects may result in significant left-to-right shunting and left ventricular volume overload [12]. Transcatheter closure of residual postoperative and iatrogenic VSDs has emerged over the years as a less invasive approach in selected patients because of the high morbidity and mortality associated with reoperation [12–14]. The objective of this study is to review our institutional experience with transcatheter closure of VSD and to report outcome of mid-term follow up.
MATERIALS AND METHODS Data Collection
The study protocol was reviewed and approved by the Mayo Clinic Institutional Review Board. We queried our medical records for patients that underwent transcatheter VSD closure at the Mayo Clinic from January 1999 to December 2013. We divided our cohort into two groups based on VSD etiology: postMI VSD and non-ischemic VSD (postoperative and iatrogenic VSD). Our primary endpoint was event-free survival at 1 month and at last follow-up; the secondary end-point was to identify predictors of adverse events in the post-MI VSD group. Clinical and echocardiographic data were abstracted from the medical record from the time of initial presentation to last follow-up. Clinical data collected include age, gender, NYHA class, diagnosis, history of prior surgical or percutaneous interventions, time interval from myocardial infarction for patients with postMI VSD, and associated comorbid conditions such as hypertension (blood pressure >140/90 mm Hg or systolic blood pressure >140 mm Hg for patients with severe AR), hyperlipidemia (total cholesterol >200 mg dl1 or patient under lipid-lowering therapy), diabetes (fasting blood glucose > 120 mg dl1 or random blood glucose > 200 mg dl1), atrial fibrillation, renal failure and history of coronary artery disease (history of prior myocardial infarction, angioplasty, coronary artery bypass grafting, or angiographically documented coronary artery stenosis). Echocardiographic data collected include location and size of VSD, estimated Qp: Qs or qualitative assessment of shunt, left ventricular dimensions (left ventricular end-diastolic dimension [LVEDD], left ventricular end-systolic dimension [LVESD], left ventricular ejection fraction [EF], left
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atrial volume), valvular regurgitation, right ventricular systolic pressure, and right ventricular size and function. Procedural Data
The procedure was performed under fluoroscopic and echocardiographic guidance (either intracardiac or transesophageal). All patients received periinterventional antibiotic prophylaxis with a single dose of Cefazolin and unfractionated heparin to maintain activated partial thromboplastin time (APTT) > 250 sec. Standard technique of transcatheter VSD closure has been described in detail previously [15,16]. The procedure was performed via percutaneous approach (femoral or internal jugular venous access) in 26 patients. One patient underwent VSD closure via perventricular (hybrid) approach. Amplatzer occluders (St Jude Medical, St. Paul, MN) were used in all patients. Procedural success was defined as successful device deployment and patient leaving the catheterization lab with the device. Residual shunt was qualitatively categorized into trivial, mild, moderate and severe. We defined complete closure as none or trivial residual shunt; Table I. Adverse Events and Risk Factors We defined adverse events as death, device embolization, heart block, new valvular regurgitation, hemolysis requiring blood transfusion, and need for surgical or percutaneous reintervention. Only cardiac morbidities/ mortalities were included in adverse event count. Patients who required subsequent surgical VSD closure were excluded from follow-up and these patients were coded as ‘not applicable-NA’ in the Supporting Information Table. Sub-group analysis was performed for the post-MI VSD group to identify predictors of adverse events. For risk assessment, patients were divided into those with and without cardiogenic shock at the time of VSD closure. Similar to published data [17], we defined cardiogenic shock as (i) persistent systolic blood pressure < 90 mm Hg or vasopressors required to maintain blood pressure > 90 mm Hg; (ii) evidence of end organ failure (e.g. urine output 2 mmol L1); (iii) evidence of elevated left ventricular filling pressures with clinical signs of pulmonary congestion. We defined acute phase as the first 2 weeks after MI. Statistical Analysis All statistical calculations were performed with the JMP version 11.0 software (SAS Institute, Cary, NC).
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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Egbe et al. Baseline and Procedural Data of Entire VSD
n Age (years) Male (%) Follow up (years) VSD size (mm) Device size (mm) Device type (Amplatzer) -PI Muscular VSD occluder -Muscular VSD occluder -ASD occluder -Membranous VSD occluder Percutaneous/Hybrid approach Procedural time (min) Fluoroscopy time (min) Cardiogenic shock LVEF (%) Intervention in acute phasea Successful deployment Complete closure at 1 year Early mortality Late mortality Periprocedural adverse eventb Late adverse events
Entire cohort
PMI-VSD
Nonischemic
27 61 14 11(41%) 8.1 8 14 5 20 8
18 69 11 7(39%) 7.3 7 16 6 22 7
9 49 15 4(44%) 8.7 8 14 2 16 5
11 8 9 1 26/1 151 29 31 11 NA 57 9
9 1 9 0 17/1 159 33 27 9 9 (50%) 45 12
NA 26 (96%) 15/18 (83%) 3 1 8 3
10 (56%) 17 (94%) 10/12 (83%) 3 0 8 0
2 7 0 1 9/0 141 46 33 15 NA 60 (IQR: 54–65) NA 9 (100%) 5/6 (83%) 0 1 0 3
LVEF: Left ventricular ejection fraction. Acute phase: within 2 weeks of myocardial infarction. b Periprocedural adverse event: adverse events within 30-days post procedure. IQR: Interquartile range. a
Categorical variables were expressed as percentages while continuous variables were expressed as mean SD or median (IQR) for skewed data. Univariate and multivariate Cox proportional-hazard models were used to identify predictors of adverse event in the postMI VSD group. Event-free survival rate curves were generated with the Kaplan–Meier method and compared by using the log-rank test. All P values were two sided, and P values < 0.05 were considered significant.
RESULTS
Twenty-seven patients underwent transcatheter VSD closure at the Mayo Clinic between January 1999 and December 2013. Eighteen patients had post-MI VSD while nine patients had non-ischemic (iatrogenic and postoperative) VSD. Baseline characteristics of the entire cohort are summarized in Table I. Freedom from death for the entire cohort was 89, 85, and 85% at 1 month, 1 year and 5 years, and did not vary significantly between post-MI VSD and non-ischemic groups (P ¼ 0.58). Event-free survival for the entire cohort
was 70, 61, and 61% at 1 month, 1 year and 5 years, and was similar in both subgroups (P ¼ 0.34); Fig. 1. In the post-MI VSD group, the mean age was 69 11 years and mean follow-up duration was 7.3 7 years. Nine patients (50%) underwent VSD closure in the acute phase and eight of them were in cardiogenic shock at the time of the procedure, (Supporting Information Table). Three patients were on mechanical support (Extracorporeal membrane oxygenation, ECMO ¼ 1, Intra-aortic balloon pump ¼ 2). Procedure was performed via percutaneous approach in 17 patients and perventricular (hybrid) approach in one patient (patient #18). This patient was a 42-year-old female with post-MI VSD who initially underwent surgical VSD closure and required ECMO support for cardiogenic shock postoperatively. Patient had a large residual VSD patch leak, which was successfully closed with 18 mm Amplatzer ASD occluder using hybrid approach while on ECMO support. Device deployment was successful 17/18 patients yielding procedural success rate of 94%. Complete closure rate was 58% (7 out of 12) at 1 month and 83% (10 out of 12) at 1-year follow-up. The only procedural failure occurred in patient #4 who suffered device embolization immediately during the procedure. This device was successfully retrieved in the catheterization lab and patient later underwent surgical VSD closure. Adverse events occurred in 44% (8/18). These events were death from multi-organ failure (three patients), device embolization (one patient), hemolysis requiring blood transfusion (one patient), surgical VSD closure (two patients), and deployment of a second VSD occluder (one patient). All deaths were attributed to progressive to multi-organ failure at post procedure day 4 (patient #9), day 5 (patient #18), and day 7 (patient #11). Patient #1 subsequently died from chronic renal failure 9-years post procedure and we excluded his death from adverse event count based on criteria defined in our methods section. Freedom from adverse event was 56% at 1 month, 1 year and 5 years. Event-free survival was significantly lower for patients that underwent VSD closure in the acute phase (P ¼ 0.005) or had cardiogenic shock (P ¼ 0.016), Fig. 2. Cardiogenic shock (HR: 3.21, CI: 1.82–5.41, P ¼ 0.002), and VSD closure in acute phase (HR: 2.14, CI: 1.12–4.31, P ¼ 0.004) were independent predictors of adverse events, Table II. In the non-ischemic VSD group, procedure was performed via percutaneous approach all patients. The mean age was 49 15 years and mean follow-up duration was 8.7 8 years. Device deployment was successful in all patients and complete closure rate was 83% (5 out of 6) at 1-year follow-up. Patient #24 required two devices (16 mm and 14 mm post-
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Transcatheter Closure of VSD
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Fig. 1. Survival curve for the entire cohort (n 5 27). Survival stratified by VSD type (Post-MI VSD vs. non-ischemic VSD). Event-free survival stratified by VSD type. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
infarction muscular VSD occluders) to achieve complete closure. Adverse events occurred in 33% (3 out of 9) as follows: patient #21 subsequently underwent surgical VSD closure 8 months post procedure because of persistent moderate residual shunt; patient #20 also underwent surgical VSD closure 6-weeks post procedure because of persistent hemolysis, and patient #25 died 11 months post procedure from Staphylococcus aureus endocarditis, Table III. There were no independent predictors of adverse events in the non-ischemic VSD group, Table IV. DISCUSSION
Transcatheter VSD closure is a less invasive option in the management of post-MI VSDs and non-ischemic VSDs. Post-MI VSD is a relatively uncommon complica-
tion of acute MIs but it is responsible for a significant proportion of early deaths following an MI [5,6]. Medical and surgical therapy is associated with very high mortality [8–10] and as a result transcatheter VSD closure is often used a temporizing bridge to clinically stabilize patients. In post-MI VSDs, failure of transcatheter VSD closure can be classified into 3 sub-types: failure to implant the device, failure to close the shunt even after proper device implantation, and clinical deterioration irrespective of the shunt closure in a dying patient [18]. Failure to implant device occurred in 1 out of the 18 post-MI VSD patients. Most of our failures were due to failure to close the shunt and clinical deterioration irrespective of proper device implantation in five patients. Our data showed 17% (3 out of 18) inhospital mortality and 44% (8 out of 18) adverse event rates. Freedom from adverse event was 56% at 1
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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Fig. 2. Event-free survival curve for the post myocardial infarction (Post MI group, n 5 18). Event-free survival for Post MI group. Event-free survival stratified by time interval from myocardial infarction to VSD closure (device closure in acute phase vs. non-acute phase). Eventfree survival stratified by presence of cardiogenic shock at the time of VSD closure (cardiogenic shock vs. no cardiogenic shock). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
month, 1 year and 5 years. No adverse events occurred beyond 30 days post procedure. Our result compares favorably with data from Landzberg and Lock who reported their single center experience of percutaneous closure of PMIVSD using Clam-shell double umbrella and the Cardio SEAL [19]. They reported successful deployment of the device in 17 of 18 patients. Overall survival in their initial series
was 55% (10/18). Three patients out of the seven patients that were treated with primary percutaneous closure survived, and all three survivors underwent VSD closure months after myocardial infarction. Holzer et al. reported outcome of 18 patients from multicenter US registry using Amplatzer postinfarct muscular VSD device [4]. Device deployment was successful in 16 of 18 patients. Their 30-day mortality
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Transcatheter Closure of VSD
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ative residual VSD using Amplatzer perimembranous VSD occluder. Ninety-five percent of their cohort achieved complete closure at 6 months follow-up and adverse event occurred in three patients (10%) of which two of them had transient heart block [13]. Similarly, we did not have any procedural mortality, and the only death in our cohort occurred at 11 months post procedure due to Staphylococcus aureus endocarditis involving the device. None of our patients experienced heart block. Two patients subsequently underwent surgical VSD closure for persistent hemolysis and moderate residual shunt respectively. Holzer and colleagues [16] reported their experience in 75 patients with muscular VSD, and one-third of their patients had prior cardiac surgery. Amplatzer muscular VSD occluders (AGA Medical Corp, MN) were used in all cases [16]. Device implantation was successful in 87%, procedure-related major complications occurred in 10% and procedure-related deaths occurred in 2.7% of their patients. They did not perform subgroup analysis showing how many of these adverse events occurred in the postoperative VSD subset. This makes it difficult to draw a direct analogy to our study.
was 28%, and 11 of 16 (69%) patients were still alive at median follow-up of 11 months. Two patients (13%) required a second procedure to close a residual VSD. In our series, one patient required a second procedure to close residual shunt, our 30-day mortality was 17%, and 83% of post-MI VSD group were still alive at a mean follow-up of 7.3 years. Thiele et al. [17] reported their experience in the management of post-MI VSD in 29 patients using Amplatzer devices. Five patients (17%) died due to procedural related complications and overall 30-day survival was 35%. The dismal outcome noted in their study was mostly due to the fact that all their patients underwent percutaneous VSD closure in the acute phase compared to our study where only 50% of our patients underwent procedure in the acute phase. Similar to our result and other prior studies, Thiele and colleagues identified presence of cardiogenic shock as a strong predictor of early mortality [3,17,19]. For our non-ischemic VSD group, device deployment was successful in all patients, and all patients survived to hospital discharge. Eighty-eight percent of our patients achieved complete closure at 1-year follow-up and adverse events occurred in 33% (3 out of 9). A recent study by Zhang and colleagues [13] reported 100% survival in a cohort of 29 patients with postoper-
LIMITATIONS
TABLE II. Multivariate Predictors of Adverse Events for Post-MI VSD Group
Our study had some limitations. This is a retrospective study based on a cohort from a single tertiary
Variables Age > 70 years Male LVEF < 50% Cardiogenic shock Acute phase VSD size > 16 mm Device size > 22 mm
HR (95% CI)
P value
0.71 (0.31–3.43) 2.21 (0.76–3.14) 1.19 (0.73–2.42) 3.21 (1.82–5.41) 2.14 (1.12–4.31) 1.85(0.46–3.91) 1.52 (0.66–3.89)
0.09 0.71 0.55 0.002 0.004 0.16 0.42
HR: Hazard ratio. CI: Confidence interval.
TABLE III. Patient # 19 20 21 22 23 24 25 26 27
TABLE IV. Multivariate Predictors of Adverse Events for Nonischemic VSD Group Variables Age > 40 years Male LVEF 16 mm Device size > 22 mm
HR (95% CI)
P value
1.12 (0.63–2.14) 1.33 (0.28–4.08) 2.02 (0.36–4.11) 1.17(0.86–2.61) 1.26 (0.45–4.13)
0.23 0.19 0.25 0.09 0.29
HR: hazard ratio; CI: confidence interval.
Non-ischemic VSD Group Age/gender
Etiology
Diagnosis
VSD size (mm)
EF
Device (mm)
AE
Last FU (NYHA)
64/M 54/F 75/F 64/M 38/M 49/F 31/F 3/F 16/M
Iatrogenic Iatrogenic Iatrogenic Iatrogenic Iatrogenic Iatrogenic Postoperative Postoperative Postoperative
HOCM s/p septal myectomy s/p AVR and MVR HOCM s/p modified Konno HOCM s/p septal myectomy cc-TGA s/p TVR HOCM s/p septal myectomy DORV s/p Rastelli procedure DORV s/p Rastelli procedure PA-VSD s/p repair
8 12 14 9 12 12 11 8 10
55 65 67 55 40 72 65 65 55
10 14 18 14 14 16/14 16 10 12
N Y Y N N N Y N N
I NA NA I I I DEAD I I
HOCM: hypertrophic obstructive cardiomyopathy; s/p: status post; DORV: double outlet right ventricle; PA-VSD: pulmonary atresia with ventricular septal defect; AVR: aortic valve replacement; MVR: mitral valve replacement; cc-TGA: congenitally corrected transposition of great arteries; TVR: tricuspid valve replacement. Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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center, which lends itself to potential bias. We used more than one type of device in our study making it difficult to draw inference from our data. CONCLUSIONS
Our study is unique and different from prior studies because it presents a comprehensive experience of transcatheter VSD closure both for post-MI and non-ischemic VSD. Additionally, our duration of follow-up was significantly longer than most other published series [1,2,4,12,13,16–20]. In conclusion, we showed that transcatheter closure of Post-MI VSD has significant peri-procedural morbidity especially in patients with cardiogenic shock who underwent procedure in the acute phase. However, event-free survival at mid-late followup is reassuring with no adverse event occurring beyond periprocedural period. Transcatheter closure of nonischemic VSD had lower periprocedural mortality and morbidity but some patients continued to experience adverse events beyond the early post-procedural period. REFERENCES 1. Lock JE, Block PC, McKay RG, Baim DS, Keane JF. Transcatheter closure of ventricular septal defects. Circulation 1988; 78:361–368. 2. Kalra GS, Verma PK, Dhall A, Singh S, Arora R. Transcatheter device closure of ventricular septal defects: Immediate results and intermediate-term follow-up. Am Heart J 1999;138:339– 344. 3. Deja MA, Szostek J, Widenka K, Szafron B, Spyt TJ, Hickey MS, Sosnowski AW. Post infarction ventricular septal defect— Can we do better? Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 2000;18:194–201. 4. Holzer R, Balzer D, Amin Z, Ruiz CE, Feinstein J, Bass J, Vance M, Cao QL, Hijazi ZM. Transcatheter closure of postinfarction ventricular septal defects using the new amplatzer muscular vsd occluder: Results of a US registry. Catheter Cardiovasc Intervent Off J Soc Cardiac Angiogr Intervent 2004; 61:196–201. 5. Madsen JC, Daggett WM Jr. Repair of postinfarction ventricular septal defects. Semin Thorac Cardiovasc Surg 1998;10:117–127. 6. Calderon M, Ott DA. Surgical treatment of postinfarction rupture of the interventricular septum. Texas heart institute journal/ from the Texas heart institute of St. Luke’s Episcopal Hospital. Texas Children’s Hospital 1991;18:282–285. 7. 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.
8. Killen DA, Piehler JM, Borkon AM, Gorton ME, Reed WA. Early repair of postinfarction ventricular septal rupture. Ann Thorac Surg 1997;63:138–142. 9. Pretre R, Ye Q, Grunenfelder J, Lachat M, Vogt PR, Turina MI. Operative results of “repair” of ventricular septal rupture after acute myocardial infraction. Am J Cardiol 1999;84:785–788. 10. Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, Slater JN, Forman R, Monrad ES, Talley JD, Hochman JS. 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. 11. Bol-Raap G, Weerheim J, Kappetein AP, Witsenburg M, Bogers AJ. Follow-up after surgical closure of congenital ventricular septal defect. Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 2003;24:511–515. 12. Pedra CA, Pontes SC Jr, Pedra SR, Salerno L, Sousa JB, Miaira MA, Guerra AL, Santana MV, Silva MA, Fontes VF. Percutaneous closure of postoperative and post-traumatic ventricular septal defects. J Invasive Cardiol 2007;19:491–495. 13. Zhang B, Liang J, Zheng X, Jiang G, Yang Z, Zhang L, Zhang Y, Sun H. Transcatheter closure of postoperative residual ventricular septal defects using amplatzer-type perimembranous VSD occluders. J Invasive Cardiol 2013;25:402–405. 14. Chessa M, Carminati M, Cao QL, Butera G, Giusti S, Bini RM, Hijazi ZM. Transcatheter closure of congenital and acquired muscular ventricular septal defects using the amplatzer device. J Invasive Cardiol 2002;14:322–327. 15. 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. 16. Holzer R, Balzer D, Cao QL, Lock K, Hijazi ZM. Amplatzer muscular ventricular septal defect I. Device closure of muscular ventricular septal defects using the amplatzer muscular ventricular septal defect occluder: Immediate and mid-term results of a US Registry. J Am Coll Cardiol 2004;43:1257–1263. 17. Thiele H, Kaulfersch C, Daehnert I, Schoenauer M, Eitel I, Borger M, Schuler G. Immediate primary transcatheter closure of postinfarction ventricular septal defects. Eur Heart J 2009;30: 81–88. 18. Demkow M, Ruzyllo W, Kepka C, Chmielak Z, Konka M, Dzielinska Z, Wilczynski J, Juraszynski Z. Primary transcatheter closure of postinfarction ventricular septal defects with the amplatzer septal occluder- immediate results and up-to 5 years follow-up. EuroIntervention J EuroPCR Collaborat Working Group Intervent Cardiol Eur Soc Cardiol 2005;1:43–47. 19. Landzberg MJ, Lock JE. Transcatheter management of ventricular septal rupture after myocardial infarction. Semin Thoracic Cardiovasc Surg 1998;10:128–132. 20. Wollenek G, Wyse R, Sullivan I, Elliott M, de Leval M, Stark J. Closure of muscular ventricular septal defects through a left ventriculotomy. Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 1996;10:595–598.
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Transcatheter Closure of Postmyocardial Infarction, Iatrogenic, and Postoperative Ventricular Septal Defects: The Mayo Clinic Experience Alexander C. Egbe,1 MD, MPH, Joseph T. Poterucha,2 DO, Charanjit S. Rihal,1 MD, MBA, Nathaniel W. Taggart,2 MD, Frank Cetta,2 MD, Allison K. Cabalka,2 MD, Peter M. Pollak,2 MD, Guy S. Reeder,1 MD, and Donald J. Hagler,2* MD Objectives: To determine event-free survival after transcatheter closure of ventricular septal defect (VSD), and to identify predictors of adverse events (AE) in post myocardial infarction VSD (post-MI VSD) subgroup. Background: There are limited data on mid-term follow-up after transcatheter VSD closure. Methods: Retrospective review of 27 cases of transcatheter VSD closure (post-MI 5 18 and non-ischemic 5 9) performed from 1999 to 2013. We defined AE as death, device embolization, hemolysis requiring blood transfusion, heart block and reintervention. Results: In the post-MI VSD subgroup, mean age and follow-up was 69 6 11 and 7.3 6 7 years, respectively. AE occurred in 8 (44%) patients (death-3, device embolization-1, hemolysis-1, surgical VSD closure-2, reintervention-1). Event-free survival was 56% at 1 month and 5 years, and all AE occurred in the periprocedural period. Cardiogenic shock (HR: 3.21, CI: 1.82–5.41, P 5 0.002), and VSD closure in acute phase (HR: 2.14, CI: 1.12–4.31, P 5 0.004) were independent predictors of AE. In the non-ischemic VSD subgroup, mean age and follow-up was 49 6 15 and 8.7 6 8 years, respectively. AE occurred in 3 (33%) patients (late death-1, surgical VSD closure-2). For the entire cohort, freedom from death was 89% and 85% at 1 month and 5 years, and event-free survival was 70% and 61% at 1 month and 5 years. Conclusions: Transcatheter closure of post-MI VSD carries a moderate risk of periprocedural complications but low event rates afterwards. By comparison, device closure of non-ischemic VSD has lower periprocedural morbidity but some patients continued to experience AE during follow-up. VC 2015 Wiley Periodicals, Inc. Key words: transcatheter; myocardial infarction; ventricular septal defect
INTRODUCTION
Transcatheter closure of ventricular septal defect (VSD) is considered a less invasive option in the management of certain types of VSD. Since its introduction in the late 1980s, transcatheter VSD closure has been used in the treatment of post myocardial infarction VSD (post-MI VSD), postoperative and congenital VSD [1–4]. Post-MI VSD is a relatively uncommon complication of acute myocardial infarction but it is responsible for a significant proportion of early deaths following an MI [5,6]. Evolution of Post-MI VSD can be broadly categorized into 2 phases: acute and chronic phase. The acute phase occurs within the first 2 weeks after infarction. This phase is characterized by coagulation necrosis and release of lytic enzymes from neutrophils resulting in myocardial necrosis. As necrosis progress, resorption and retraction of infarcted tissue typically leads to enlargement of the defect size [7]. The chronic phase begins after 3–4 weeks and is characterized by fibrosis and scar formation around the C 2015 Wiley Periodicals, Inc. V
edges of the defect [7]. Surgical closure of post-MI VSD is associated with high mortality especially in the acute phase [8,9], and medical therapy alone yields survival rate less than 10% at 1 year [10]. Additional Supporting Information may be found in the online version of this article. 1 Division of Cardiovascular Diseases, Mayo Clinic Rochester, Minnesota 2 Division of Pediatric Cardiology, Mayo Clinic Rochester, Minnesota Conflict of interest: Nothing to report. *Correspondence to: Donald J. Hagler, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester MN 55905. E-mail: [email protected] Received 19 February 2015; Revision accepted 5 April 2015 DOI: 10.1002/ccd.25989 Published online 29 May 2015 in Wiley Online Library (wileyonlinelibrary.com)
Transcatheter Closure of VSD
Transcatheter VSD closure is a less invasive palliative measure to clinically stabilize patients. Postoperative residual VSD can occur after surgical repair of isolated VSD or complex cardiac defect due to patch dehiscence, suture disruption or incomplete closure of the defect [11]. Residual VSDs are well tolerated if they are restrictive but large defects may result in significant left-to-right shunting and left ventricular volume overload [12]. Transcatheter closure of residual postoperative and iatrogenic VSDs has emerged over the years as a less invasive approach in selected patients because of the high morbidity and mortality associated with reoperation [12–14]. The objective of this study is to review our institutional experience with transcatheter closure of VSD and to report outcome of mid-term follow up.
MATERIALS AND METHODS Data Collection
The study protocol was reviewed and approved by the Mayo Clinic Institutional Review Board. We queried our medical records for patients that underwent transcatheter VSD closure at the Mayo Clinic from January 1999 to December 2013. We divided our cohort into two groups based on VSD etiology: postMI VSD and non-ischemic VSD (postoperative and iatrogenic VSD). Our primary endpoint was event-free survival at 1 month and at last follow-up; the secondary end-point was to identify predictors of adverse events in the post-MI VSD group. Clinical and echocardiographic data were abstracted from the medical record from the time of initial presentation to last follow-up. Clinical data collected include age, gender, NYHA class, diagnosis, history of prior surgical or percutaneous interventions, time interval from myocardial infarction for patients with postMI VSD, and associated comorbid conditions such as hypertension (blood pressure >140/90 mm Hg or systolic blood pressure >140 mm Hg for patients with severe AR), hyperlipidemia (total cholesterol >200 mg dl1 or patient under lipid-lowering therapy), diabetes (fasting blood glucose > 120 mg dl1 or random blood glucose > 200 mg dl1), atrial fibrillation, renal failure and history of coronary artery disease (history of prior myocardial infarction, angioplasty, coronary artery bypass grafting, or angiographically documented coronary artery stenosis). Echocardiographic data collected include location and size of VSD, estimated Qp: Qs or qualitative assessment of shunt, left ventricular dimensions (left ventricular end-diastolic dimension [LVEDD], left ventricular end-systolic dimension [LVESD], left ventricular ejection fraction [EF], left
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atrial volume), valvular regurgitation, right ventricular systolic pressure, and right ventricular size and function. Procedural Data
The procedure was performed under fluoroscopic and echocardiographic guidance (either intracardiac or transesophageal). All patients received periinterventional antibiotic prophylaxis with a single dose of Cefazolin and unfractionated heparin to maintain activated partial thromboplastin time (APTT) > 250 sec. Standard technique of transcatheter VSD closure has been described in detail previously [15,16]. The procedure was performed via percutaneous approach (femoral or internal jugular venous access) in 26 patients. One patient underwent VSD closure via perventricular (hybrid) approach. Amplatzer occluders (St Jude Medical, St. Paul, MN) were used in all patients. Procedural success was defined as successful device deployment and patient leaving the catheterization lab with the device. Residual shunt was qualitatively categorized into trivial, mild, moderate and severe. We defined complete closure as none or trivial residual shunt; Table I. Adverse Events and Risk Factors We defined adverse events as death, device embolization, heart block, new valvular regurgitation, hemolysis requiring blood transfusion, and need for surgical or percutaneous reintervention. Only cardiac morbidities/ mortalities were included in adverse event count. Patients who required subsequent surgical VSD closure were excluded from follow-up and these patients were coded as ‘not applicable-NA’ in the Supporting Information Table. Sub-group analysis was performed for the post-MI VSD group to identify predictors of adverse events. For risk assessment, patients were divided into those with and without cardiogenic shock at the time of VSD closure. Similar to published data [17], we defined cardiogenic shock as (i) persistent systolic blood pressure < 90 mm Hg or vasopressors required to maintain blood pressure > 90 mm Hg; (ii) evidence of end organ failure (e.g. urine output 2 mmol L1); (iii) evidence of elevated left ventricular filling pressures with clinical signs of pulmonary congestion. We defined acute phase as the first 2 weeks after MI. Statistical Analysis All statistical calculations were performed with the JMP version 11.0 software (SAS Institute, Cary, NC).
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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Egbe et al. Baseline and Procedural Data of Entire VSD
n Age (years) Male (%) Follow up (years) VSD size (mm) Device size (mm) Device type (Amplatzer) -PI Muscular VSD occluder -Muscular VSD occluder -ASD occluder -Membranous VSD occluder Percutaneous/Hybrid approach Procedural time (min) Fluoroscopy time (min) Cardiogenic shock LVEF (%) Intervention in acute phasea Successful deployment Complete closure at 1 year Early mortality Late mortality Periprocedural adverse eventb Late adverse events
Entire cohort
PMI-VSD
Nonischemic
27 61 14 11(41%) 8.1 8 14 5 20 8
18 69 11 7(39%) 7.3 7 16 6 22 7
9 49 15 4(44%) 8.7 8 14 2 16 5
11 8 9 1 26/1 151 29 31 11 NA 57 9
9 1 9 0 17/1 159 33 27 9 9 (50%) 45 12
NA 26 (96%) 15/18 (83%) 3 1 8 3
10 (56%) 17 (94%) 10/12 (83%) 3 0 8 0
2 7 0 1 9/0 141 46 33 15 NA 60 (IQR: 54–65) NA 9 (100%) 5/6 (83%) 0 1 0 3
LVEF: Left ventricular ejection fraction. Acute phase: within 2 weeks of myocardial infarction. b Periprocedural adverse event: adverse events within 30-days post procedure. IQR: Interquartile range. a
Categorical variables were expressed as percentages while continuous variables were expressed as mean SD or median (IQR) for skewed data. Univariate and multivariate Cox proportional-hazard models were used to identify predictors of adverse event in the postMI VSD group. Event-free survival rate curves were generated with the Kaplan–Meier method and compared by using the log-rank test. All P values were two sided, and P values < 0.05 were considered significant.
RESULTS
Twenty-seven patients underwent transcatheter VSD closure at the Mayo Clinic between January 1999 and December 2013. Eighteen patients had post-MI VSD while nine patients had non-ischemic (iatrogenic and postoperative) VSD. Baseline characteristics of the entire cohort are summarized in Table I. Freedom from death for the entire cohort was 89, 85, and 85% at 1 month, 1 year and 5 years, and did not vary significantly between post-MI VSD and non-ischemic groups (P ¼ 0.58). Event-free survival for the entire cohort
was 70, 61, and 61% at 1 month, 1 year and 5 years, and was similar in both subgroups (P ¼ 0.34); Fig. 1. In the post-MI VSD group, the mean age was 69 11 years and mean follow-up duration was 7.3 7 years. Nine patients (50%) underwent VSD closure in the acute phase and eight of them were in cardiogenic shock at the time of the procedure, (Supporting Information Table). Three patients were on mechanical support (Extracorporeal membrane oxygenation, ECMO ¼ 1, Intra-aortic balloon pump ¼ 2). Procedure was performed via percutaneous approach in 17 patients and perventricular (hybrid) approach in one patient (patient #18). This patient was a 42-year-old female with post-MI VSD who initially underwent surgical VSD closure and required ECMO support for cardiogenic shock postoperatively. Patient had a large residual VSD patch leak, which was successfully closed with 18 mm Amplatzer ASD occluder using hybrid approach while on ECMO support. Device deployment was successful 17/18 patients yielding procedural success rate of 94%. Complete closure rate was 58% (7 out of 12) at 1 month and 83% (10 out of 12) at 1-year follow-up. The only procedural failure occurred in patient #4 who suffered device embolization immediately during the procedure. This device was successfully retrieved in the catheterization lab and patient later underwent surgical VSD closure. Adverse events occurred in 44% (8/18). These events were death from multi-organ failure (three patients), device embolization (one patient), hemolysis requiring blood transfusion (one patient), surgical VSD closure (two patients), and deployment of a second VSD occluder (one patient). All deaths were attributed to progressive to multi-organ failure at post procedure day 4 (patient #9), day 5 (patient #18), and day 7 (patient #11). Patient #1 subsequently died from chronic renal failure 9-years post procedure and we excluded his death from adverse event count based on criteria defined in our methods section. Freedom from adverse event was 56% at 1 month, 1 year and 5 years. Event-free survival was significantly lower for patients that underwent VSD closure in the acute phase (P ¼ 0.005) or had cardiogenic shock (P ¼ 0.016), Fig. 2. Cardiogenic shock (HR: 3.21, CI: 1.82–5.41, P ¼ 0.002), and VSD closure in acute phase (HR: 2.14, CI: 1.12–4.31, P ¼ 0.004) were independent predictors of adverse events, Table II. In the non-ischemic VSD group, procedure was performed via percutaneous approach all patients. The mean age was 49 15 years and mean follow-up duration was 8.7 8 years. Device deployment was successful in all patients and complete closure rate was 83% (5 out of 6) at 1-year follow-up. Patient #24 required two devices (16 mm and 14 mm post-
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Transcatheter Closure of VSD
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Fig. 1. Survival curve for the entire cohort (n 5 27). Survival stratified by VSD type (Post-MI VSD vs. non-ischemic VSD). Event-free survival stratified by VSD type. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
infarction muscular VSD occluders) to achieve complete closure. Adverse events occurred in 33% (3 out of 9) as follows: patient #21 subsequently underwent surgical VSD closure 8 months post procedure because of persistent moderate residual shunt; patient #20 also underwent surgical VSD closure 6-weeks post procedure because of persistent hemolysis, and patient #25 died 11 months post procedure from Staphylococcus aureus endocarditis, Table III. There were no independent predictors of adverse events in the non-ischemic VSD group, Table IV. DISCUSSION
Transcatheter VSD closure is a less invasive option in the management of post-MI VSDs and non-ischemic VSDs. Post-MI VSD is a relatively uncommon complica-
tion of acute MIs but it is responsible for a significant proportion of early deaths following an MI [5,6]. Medical and surgical therapy is associated with very high mortality [8–10] and as a result transcatheter VSD closure is often used a temporizing bridge to clinically stabilize patients. In post-MI VSDs, failure of transcatheter VSD closure can be classified into 3 sub-types: failure to implant the device, failure to close the shunt even after proper device implantation, and clinical deterioration irrespective of the shunt closure in a dying patient [18]. Failure to implant device occurred in 1 out of the 18 post-MI VSD patients. Most of our failures were due to failure to close the shunt and clinical deterioration irrespective of proper device implantation in five patients. Our data showed 17% (3 out of 18) inhospital mortality and 44% (8 out of 18) adverse event rates. Freedom from adverse event was 56% at 1
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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Fig. 2. Event-free survival curve for the post myocardial infarction (Post MI group, n 5 18). Event-free survival for Post MI group. Event-free survival stratified by time interval from myocardial infarction to VSD closure (device closure in acute phase vs. non-acute phase). Eventfree survival stratified by presence of cardiogenic shock at the time of VSD closure (cardiogenic shock vs. no cardiogenic shock). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
month, 1 year and 5 years. No adverse events occurred beyond 30 days post procedure. Our result compares favorably with data from Landzberg and Lock who reported their single center experience of percutaneous closure of PMIVSD using Clam-shell double umbrella and the Cardio SEAL [19]. They reported successful deployment of the device in 17 of 18 patients. Overall survival in their initial series
was 55% (10/18). Three patients out of the seven patients that were treated with primary percutaneous closure survived, and all three survivors underwent VSD closure months after myocardial infarction. Holzer et al. reported outcome of 18 patients from multicenter US registry using Amplatzer postinfarct muscular VSD device [4]. Device deployment was successful in 16 of 18 patients. Their 30-day mortality
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Transcatheter Closure of VSD
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ative residual VSD using Amplatzer perimembranous VSD occluder. Ninety-five percent of their cohort achieved complete closure at 6 months follow-up and adverse event occurred in three patients (10%) of which two of them had transient heart block [13]. Similarly, we did not have any procedural mortality, and the only death in our cohort occurred at 11 months post procedure due to Staphylococcus aureus endocarditis involving the device. None of our patients experienced heart block. Two patients subsequently underwent surgical VSD closure for persistent hemolysis and moderate residual shunt respectively. Holzer and colleagues [16] reported their experience in 75 patients with muscular VSD, and one-third of their patients had prior cardiac surgery. Amplatzer muscular VSD occluders (AGA Medical Corp, MN) were used in all cases [16]. Device implantation was successful in 87%, procedure-related major complications occurred in 10% and procedure-related deaths occurred in 2.7% of their patients. They did not perform subgroup analysis showing how many of these adverse events occurred in the postoperative VSD subset. This makes it difficult to draw a direct analogy to our study.
was 28%, and 11 of 16 (69%) patients were still alive at median follow-up of 11 months. Two patients (13%) required a second procedure to close a residual VSD. In our series, one patient required a second procedure to close residual shunt, our 30-day mortality was 17%, and 83% of post-MI VSD group were still alive at a mean follow-up of 7.3 years. Thiele et al. [17] reported their experience in the management of post-MI VSD in 29 patients using Amplatzer devices. Five patients (17%) died due to procedural related complications and overall 30-day survival was 35%. The dismal outcome noted in their study was mostly due to the fact that all their patients underwent percutaneous VSD closure in the acute phase compared to our study where only 50% of our patients underwent procedure in the acute phase. Similar to our result and other prior studies, Thiele and colleagues identified presence of cardiogenic shock as a strong predictor of early mortality [3,17,19]. For our non-ischemic VSD group, device deployment was successful in all patients, and all patients survived to hospital discharge. Eighty-eight percent of our patients achieved complete closure at 1-year follow-up and adverse events occurred in 33% (3 out of 9). A recent study by Zhang and colleagues [13] reported 100% survival in a cohort of 29 patients with postoper-
LIMITATIONS
TABLE II. Multivariate Predictors of Adverse Events for Post-MI VSD Group
Our study had some limitations. This is a retrospective study based on a cohort from a single tertiary
Variables Age > 70 years Male LVEF < 50% Cardiogenic shock Acute phase VSD size > 16 mm Device size > 22 mm
HR (95% CI)
P value
0.71 (0.31–3.43) 2.21 (0.76–3.14) 1.19 (0.73–2.42) 3.21 (1.82–5.41) 2.14 (1.12–4.31) 1.85(0.46–3.91) 1.52 (0.66–3.89)
0.09 0.71 0.55 0.002 0.004 0.16 0.42
HR: Hazard ratio. CI: Confidence interval.
TABLE III. Patient # 19 20 21 22 23 24 25 26 27
TABLE IV. Multivariate Predictors of Adverse Events for Nonischemic VSD Group Variables Age > 40 years Male LVEF 16 mm Device size > 22 mm
HR (95% CI)
P value
1.12 (0.63–2.14) 1.33 (0.28–4.08) 2.02 (0.36–4.11) 1.17(0.86–2.61) 1.26 (0.45–4.13)
0.23 0.19 0.25 0.09 0.29
HR: hazard ratio; CI: confidence interval.
Non-ischemic VSD Group Age/gender
Etiology
Diagnosis
VSD size (mm)
EF
Device (mm)
AE
Last FU (NYHA)
64/M 54/F 75/F 64/M 38/M 49/F 31/F 3/F 16/M
Iatrogenic Iatrogenic Iatrogenic Iatrogenic Iatrogenic Iatrogenic Postoperative Postoperative Postoperative
HOCM s/p septal myectomy s/p AVR and MVR HOCM s/p modified Konno HOCM s/p septal myectomy cc-TGA s/p TVR HOCM s/p septal myectomy DORV s/p Rastelli procedure DORV s/p Rastelli procedure PA-VSD s/p repair
8 12 14 9 12 12 11 8 10
55 65 67 55 40 72 65 65 55
10 14 18 14 14 16/14 16 10 12
N Y Y N N N Y N N
I NA NA I I I DEAD I I
HOCM: hypertrophic obstructive cardiomyopathy; s/p: status post; DORV: double outlet right ventricle; PA-VSD: pulmonary atresia with ventricular septal defect; AVR: aortic valve replacement; MVR: mitral valve replacement; cc-TGA: congenitally corrected transposition of great arteries; TVR: tricuspid valve replacement. Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
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center, which lends itself to potential bias. We used more than one type of device in our study making it difficult to draw inference from our data. CONCLUSIONS
Our study is unique and different from prior studies because it presents a comprehensive experience of transcatheter VSD closure both for post-MI and non-ischemic VSD. Additionally, our duration of follow-up was significantly longer than most other published series [1,2,4,12,13,16–20]. In conclusion, we showed that transcatheter closure of Post-MI VSD has significant peri-procedural morbidity especially in patients with cardiogenic shock who underwent procedure in the acute phase. However, event-free survival at mid-late followup is reassuring with no adverse event occurring beyond periprocedural period. Transcatheter closure of nonischemic VSD had lower periprocedural mortality and morbidity but some patients continued to experience adverse events beyond the early post-procedural period. REFERENCES 1. Lock JE, Block PC, McKay RG, Baim DS, Keane JF. Transcatheter closure of ventricular septal defects. Circulation 1988; 78:361–368. 2. Kalra GS, Verma PK, Dhall A, Singh S, Arora R. Transcatheter device closure of ventricular septal defects: Immediate results and intermediate-term follow-up. Am Heart J 1999;138:339– 344. 3. Deja MA, Szostek J, Widenka K, Szafron B, Spyt TJ, Hickey MS, Sosnowski AW. Post infarction ventricular septal defect— Can we do better? Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 2000;18:194–201. 4. Holzer R, Balzer D, Amin Z, Ruiz CE, Feinstein J, Bass J, Vance M, Cao QL, Hijazi ZM. Transcatheter closure of postinfarction ventricular septal defects using the new amplatzer muscular vsd occluder: Results of a US registry. Catheter Cardiovasc Intervent Off J Soc Cardiac Angiogr Intervent 2004; 61:196–201. 5. Madsen JC, Daggett WM Jr. Repair of postinfarction ventricular septal defects. Semin Thorac Cardiovasc Surg 1998;10:117–127. 6. Calderon M, Ott DA. Surgical treatment of postinfarction rupture of the interventricular septum. Texas heart institute journal/ from the Texas heart institute of St. Luke’s Episcopal Hospital. Texas Children’s Hospital 1991;18:282–285. 7. 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.
8. Killen DA, Piehler JM, Borkon AM, Gorton ME, Reed WA. Early repair of postinfarction ventricular septal rupture. Ann Thorac Surg 1997;63:138–142. 9. Pretre R, Ye Q, Grunenfelder J, Lachat M, Vogt PR, Turina MI. Operative results of “repair” of ventricular septal rupture after acute myocardial infraction. Am J Cardiol 1999;84:785–788. 10. Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, Slater JN, Forman R, Monrad ES, Talley JD, Hochman JS. 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. 11. Bol-Raap G, Weerheim J, Kappetein AP, Witsenburg M, Bogers AJ. Follow-up after surgical closure of congenital ventricular septal defect. Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 2003;24:511–515. 12. Pedra CA, Pontes SC Jr, Pedra SR, Salerno L, Sousa JB, Miaira MA, Guerra AL, Santana MV, Silva MA, Fontes VF. Percutaneous closure of postoperative and post-traumatic ventricular septal defects. J Invasive Cardiol 2007;19:491–495. 13. Zhang B, Liang J, Zheng X, Jiang G, Yang Z, Zhang L, Zhang Y, Sun H. Transcatheter closure of postoperative residual ventricular septal defects using amplatzer-type perimembranous VSD occluders. J Invasive Cardiol 2013;25:402–405. 14. Chessa M, Carminati M, Cao QL, Butera G, Giusti S, Bini RM, Hijazi ZM. Transcatheter closure of congenital and acquired muscular ventricular septal defects using the amplatzer device. J Invasive Cardiol 2002;14:322–327. 15. 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. 16. Holzer R, Balzer D, Cao QL, Lock K, Hijazi ZM. Amplatzer muscular ventricular septal defect I. Device closure of muscular ventricular septal defects using the amplatzer muscular ventricular septal defect occluder: Immediate and mid-term results of a US Registry. J Am Coll Cardiol 2004;43:1257–1263. 17. Thiele H, Kaulfersch C, Daehnert I, Schoenauer M, Eitel I, Borger M, Schuler G. Immediate primary transcatheter closure of postinfarction ventricular septal defects. Eur Heart J 2009;30: 81–88. 18. Demkow M, Ruzyllo W, Kepka C, Chmielak Z, Konka M, Dzielinska Z, Wilczynski J, Juraszynski Z. Primary transcatheter closure of postinfarction ventricular septal defects with the amplatzer septal occluder- immediate results and up-to 5 years follow-up. EuroIntervention J EuroPCR Collaborat Working Group Intervent Cardiol Eur Soc Cardiol 2005;1:43–47. 19. Landzberg MJ, Lock JE. Transcatheter management of ventricular septal rupture after myocardial infarction. Semin Thoracic Cardiovasc Surg 1998;10:128–132. 20. Wollenek G, Wyse R, Sullivan I, Elliott M, de Leval M, Stark J. Closure of muscular ventricular septal defects through a left ventriculotomy. Eur J Cardio-Thoracic Surg Off J Eur Assoc Cardio-Thoracic Surg 1996;10:595–598.
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