Skoglund K, Eriksson P, Svensson G, Dellborg M.
Interact Cardiovasc Thorac Surg. 2015 Sep 27. pii: ivv264. [Epub ahead of print]
PMID: 26415536 Free Article
Select item 26408070
Comment from Dr. Hafil B. Abdulgani (Indonesia), section editor of Congenital Heart Surgery Journal Watch: The aim of this study is to report outcomes after surgical RVOT reconstruction with a homograft in adult patients with congenital heart disease. It is to make qualified and accurate decisions, event-free survival, perioperative mortality and morbidity and risk factors for homograft dysfunction in adult patients. The PubMed database was search with the terms ‘homograft AND pulmonary valve’, generating 665 hits. It included only studies involving more than 50 patients with a mean or median age >18 years. Six studies with a cumulative total of 560 patients were included. The study population included adult patients with congenital heart disease undergoing RVOT reconstruction with a homograft. The outcome measure was event-free survival, defined as freedom from mortality, reoperations and percutaneous interventions, as stated in each study. Perioperative or short-term mortality (<30 days) and long-term mortality were recorded. Morbidity, length of hospital stay, functional status and health-related quality of life were also included in the analysis, as well as data from echocardiography and magnetic resonance imaging (MRI). All systematic reviews and observational studies with over 50 patients and a mean or median age of at least 18 years at surgical procedure (either first homograft or reoperation) were considered eligible. No limitation regarding publication year was set, and only studies published in English or the Scandinavian languages were included. The long-term mortality rate was 2–8.8% at 8.1–10 years. Reintervention was common during patients’ life spans, with a 10-year event-free survival rate of 78–80%. Early postoperative echocardiographic or magnetic resonance imaging defects appear to predict rapid homograft degeneration. Further studies on various malformations and risk markers for degeneration are needed to make qualified and accurate decisions regarding lifetime management.
Identification of studies included in the systematic review.
Overview of included articles
|Publication author, year||Diagnosis (n)||Mean/median follow-up||Mean age at operation|
|Hazekamp, 2001a||TOF (51)||Mean 1.7 ± 1.4 years||25.7 ± 11.9 years|
|Oosterhof, 2006||TOF (158)||Median 4.2 years||‘Adult’|
|Troost, 2007||TOF (68)||Median 8.4 years||24 years|
|Nordmeyer, 2009||Mixed (60)||Mean 40 ± 10 months||21 ± 10 years|
|Scherptong, 2010a||TOF (90)||Mean 5.5 ± 3.5 years||31.4 ± 10.3 years|
|van de Woestijne, 2011||TOF (133)||Mean 8.1 ± 5.6 years||28.1 ± 12.2 years|
Mixed refers to various malformations involving the right ventricular outflow tract.
TOF: tetralogy of Fallot.
aHazekamp and Scherptong studied patients with pulmonary regurgitation only.
Type of homograft, diameter and method of preservation in the included articles
|Publication author, year||Type of homograft||Mean diameter (mm)||Method of preservation|
|Hazekamp, 2001||49 Pulm, 2 Ao||25 ± 1.8||Cryopreserved|
|Oosterhof, 2006||167 Pulm, 8 Ao||25 ± 2.1|
|Troost, 2007||65 Pulm, 3 Ao||24, range 18–29||Cryopreserved|
|Nordmeyer, 2009||22 ± 2||Cryopreserved|
|Scherptong, 2010||Pulm||25.6 ± 1.6||Cryopreserved|
|van de Woestijne, 2011||24 ± 2, range 14–28||Cryopreserved 130/133|
Method of preservation was not stated in Oosterhof’s study.
Pulm: pulmonary homograft; Ao: aortic homograft.
Outcome data from the included studies
|Publication author, year (n)||Early mortality||Late mortality||Event-free survival|
|Hazekamp, 2001 (51)||2%||4% at 1.7 years|
|Oosterhof, 2006 (158)||2% at 5.1 years||88% at 5 years, 78% at 10 years, 68% at 15 years|
|Troost, 2007 (68)||2.9%||8.8% at 8.4 years||92% at 5 years, 79% at 10 years, 69% at 15 years|
|Nordmeyer, 2009 (60)||0%||0% at 3.3 years||95% at 3.3 years|
|Scherptong, 2010 (90)||0%||2% at 5.5 years||89% at 5 years, 78% at 10 years|
|van de Woestijne, 2011 (133)||1.5%||8% at 8.1 years||80% at 10 years, 67% at 15 years|
- Early mortality is defined as in-hospital or 30-day mortality. Event-free survival is defined as survival with freedom from reoperation or reintervention, as stated in the articles.
Take home points:
- Pregnancy after surgery was found to have no increased risk of homograft failure.
- Postoperative severe QRS prolongation (>180 ms) and absence of reduction in QRS after pulmonary valve replacement (PVR) were found to be a major determinant of adverse outcome up to 9 years after homograft surgery.
- Early mortality1.5-2.9%, late mortality 2% at 5 years; and, 9% at 8 years. Event free survival 90% at 5 years, 80% at 10 years, 69% at 15 years.
- Early postoperative high peak systolic gradient or PR in the homograft, demonstrated by echocardiography, could predict adverse events and accelerated degeneration. Asymmetrical geometry measured by MRI was associated with the development of valve incompetence.
Sandrio S, Rüffer A, Purbojo A, Glöckler M, Dittrich S, Cesnjevar R.
Interact Cardiovasc Thorac Surg. 2015 Sep 10. pii: ivv261. [Epub ahead of print]
PMID: 26362626 Free Article
Select item 26358473
Comment from Dr. Hafil B. Abdulgani (Indonesia), section editor of Congenital Heart Surgery Journal Watch: This is a retrospective analysis of a non-randomized uncontrolled patient population with a varying duration and intensity of follow-up. Only patients with common arterial trunk (CAT) were analysed in this series; patients presenting with hemitruncus, in which one PA branch arises from the aorta whereas the main PA with the other PA branch arises from the RV, were excluded. Although complete primary repair (PR) at 1–3 months postnatally represents the preferred strategy in straightforward CAT, a staged CAT repair was chosen in complex cases with poor preoperative status or coexisting interrupted aortic arch (IAA) that require surgery during neonatal period (within the first 28 days postnatally). Thus, two groups were formed according to the chosen treatment strategy: group PR and group SR. Staged CAT repair includes an initial aortic arch repair (AAR) and right ventricular-to-pulmonary artery (RV-PA) valveless conduit, followed by an intracardiac repair later in infancy (Fig. 1A–C).
Figure 1. Staged CAT repair.
(A) CAT type A4 with IAA type A. (B) First-stage surgery: aortic arch repair AAR and RV-PA shunt (6 mm GoreTex valveless conduit). (C) Second-stage surgery: VSD closure and RV-PA valved conduit (12 mm Hancock® pulmonary conduit). CAT: common arterial trunk; IAA: interrupted aortic arch; AAR: aortic arch repair; RV-PA: right ventricular-to-pulmonary artery; VSD: ventricular septal defect.
Table 1. Patient demographics, procedural data and outcome
|Case no.||Sex||Age (days)||Weight (kg)||Cardiac diagnosis||Extracardiac abnormalities||Surgery||Postoperative hospital stay (days)||Reoperation|
|1||M||14||2.9||CAT-A1, dysplastic quadricuspid truncal valve with mild stenosis and regurgitation, PFO, right aortic arch, aberrant left subclavian artery||DiGeorge syndrome, primary hypoparathyroidism, s/p ICH II°, bilateral intracranial ventriculomegaly||Primary CAT repair with 14 mm Contegra valved RV-PA conduit||33||None|
|2||M||30||4.1||CAT-A2, dysplastic quadricuspid truncal valve with mild stenosis and regurgitation, moderate mitral valve regurgitation||None||Primary CAT repair with 12 mm Contegra valved RV-PA conduit||18||Truncal valve replacement (21 mm mechanical valved conduit)|
|3||M||30||3.8||CAT-A1, right aortic arch, multiple ASD II||Epilepsy||Primary CAT repair with 12 mm Contegra valved RV-PA conduit; delayed sternal closure||42||Pacemaker implantation, PA plasty, RV-PA conduit replacement|
|4||M||54||3.3||CAT-A1, right aortic arch, mild tricuspid valve regurgitation, PA hypertension||None||Primary CAT repair with 12 mm Contegra valved RV-PA conduit||14||None|
|5||F||39||3.3||CAT-A1, anteriorly malaligned outlet septum, ASD II, PDA||None||Primary CAT repair with 12 mm Contegra valved RV-PA conduit, septal myectomy; delayed sternal closure||18||RV-PA conduit replacement|
|6||M||34||3.7||CAT-A2, VSD, ASD II, right aortic arch, PA hypertension||DiGeorge syndrome||Primary CAT repair with 12 mm Contegra valved RV-PA conduit; delayed sternal closure||19||None|
|7||F||50||3.6||CAT-A1, bicuspid truncal valve, VSD, single coronary artery||None||Primary CAT repair with 12 mm Contegra valved RV-PA conduit||10||None|
|8||F||50||3.4||CAT-A1, moderate truncal valve regurgitation, VSD, PFO, mild TR, hypoplastic PA system||None||Primary CAT repair with 12 mm Contegra valved RV-PA conduit; delayed sternal closure||21||Truncal valve repair, PA plasty, RV-PA conduit replacement|
|9||M||19||3.6||CAT-A2, bicuspid truncal valve, VSD, ASD II, flow induced PA hypertension||Sickle cell anaemia||Primary CAT repair with 11 mm Labcor valved RV-PA conduit||11||None|
|10||F||46||3.9||CAT-A3, dysplastic quadricuspid truncal valve with moderate stenosis, VSD, right aortic arch, hypoplastic LPA arising from PDA, s/p LPA angioplasty||Left lung hypoplasia||Primary CAT repair with 10 mm Dacron valveless RV-PA conduit||20||Truncal valve replacement (16 mm aortic homograft), LPA plasty|
|11||F||91||4.3||CAT-A1, mesocardia, bicuspid truncal valve, VSD, ASD II, LPA hypoplasia, small MPA, supravalvar mitral ring, PA sling with tracheal stenosis, L-SVC||Psychomotor retardation, muscular hypotonia, plagiocephalus, post-pyloric feeding due to recurrent aspiration and severe gastrooesophageal reflux||Primary CAT repair with direct RV-PA anastomosis||167||Trachea slide plasty; redo trachea repair, RV-PA conduit placement, LPA plasty|
|12||F||34||2.9||CAT-A1, VSD||None||Primary CAT repair with 12 mm Hancock valved RV-PA conduit||16||None|
|13||M||30||4.0||CAT-A1, mild truncal valve regurgitation, right aortic arch, VSD, PFO||Cleft palate, athymia||Primary CAT repair with 10 mm Dacron valveless RV-PA conduit||17||Closure of residual VSD, RV-PA conduit replacement (12 mm Hancock)|
|1||M||8||3.2||CAT-A4, IAA-A, dysplastic truncal valve, VSD, PFO, preoperative cardiogenic shock||CHARGE syndrome, severe choanal stenosis, s/p omphalocele repair||AAR, 6 mm Gore-Tex RV-PA shunt; delayed sternal closure||16||VSD closure, RV-PA conduit replacement (13 mm Matrix-P-Plus), LPA plasty|
|2||M||21||3.3||CAT-A1, bicuspid truncal valve, VSD, PFO, single coronary artery, aberrant right sub-clavian artery, truncus bicaroticus||CHARGE syndrome, bilateral cleft lip and palate, bilateral hearing impairment, hydrocephalus, multiple cerebral dysgenesis, epilepsy, renal pelvis dilatation||ARSA reimplantation, 6 mm Gore-Tex RV-PA shunt||38||Closure of VSD and PFO, RV-PA conduit replacement|
|3||M||7||2.8||CAT-A4, IAA-B, bicuspid truncal valve, mild truncal valve regurgitation, VSD, ASD II||Premature birth||AAR, 6 mm Gore-Tex RV-PA shunt; delayed sternal closure||23||Closure of VSD and ASD, truncal valve repair, RV-PA conduit replacement (12 mm Hancock)|
Group PR: complete repair group; Group SR: staged repair group; M: male; F: female; CAT: common arterial trunk; IAA-A: interrupted aortic arch Type A; IAA-B: interrupted aortic arch Type B; VSD: ventricular septal defect; ASD: atrial septal defect; PFO: patent foramen ovale; PA: pulmonary artery; MPA: main pulmonary artery; LPA: left pulmonary artery; TR: tricuspid valve regurgitation; L-SVC: left superior vena cava; ICH: intracranial haemorrhage, RV-PA: right ventricle-to-pulmonary artery; AAR: aortic arch repair; ARSA: aberrant right subclavian artery; PDA: patent ductus arteriosus.
All neonates in group SR underwent initial surgery within the first 3 weeks of life. An SR strategy was chosen due to poor preoperative condition, the presence of IAA, where prolonged CPB time is expected for complete repair or both. Median age at initial surgery was 8 days (range: 7–21 days) in group SR and 34 days (range: 14–91 days) in group PR; the difference was statistically significant (P = 0.03). Mean Aristotle Comprehensive Complexity (ACC) score was 11 ± 0.6 (range: 11–13) in group PR and 18 ± 3.1 (range: 15–21) in group SR (P < 0.01).
In group PR, the RVOT was reconstructed with bovine jugular valve conduit (Contegra®, unsupported type; Medtronic, Inc., Minneapolis, MN, USA), stentless porcine valved pulmonary conduit (T07®, Labcor, Belo Horizonte, Brazil), and valveless Dacron tube, Hancock® porcine valved pulmonary conduit (Medtronic, Inc.). In 1 case, a direct RV-PA anastomosis was performed. In contrast, a GoreTex valveless conduit (W. L. Gore & Associates) was used for all cases in group SR. The sternum was electively left open after common arterial trunk (CAT) repair in both group. Subsequent delayed sternal closure was performed in the ICU at 1–11 postoperative days. In both groups, no postoperative extracorporeal life support was required. No postoperative pulmonary hypertensive crisis was observed in group SR. In group PR, postoperative pulmonary hypertensive crises requiring inhaled nitric oxide were observed in 23% cases. Follow-up was completed with a median duration of 3.6 years (range: 8 months to 11 years). There was neither early nor late mortality in both groups. 54% patients in group PR required reoperation for RV-PA conduit failure, truncal valve repair/replacement or both. Median interval to second surgery was 1 year (range: 5 months–8 years). RV-PA conduit replacement was necessary due to conduit stenosis, conduit regurgitation and RV dilatation after previous implantation of a valveless conduit. One valved conduit was secondarily implanted in a patient with free pulmonary regurgitation after direct RV-PA anastomosis at initial repair. Kaplan–Meier freedom from reoperation after 1, 2 and 8 years was 77 ± 12, 68 ± 13 and 20 ± 17% in group PR. Correspond to the staged strategy, all patients in group SR required reoperation to complete the anatomical correction (log-rank P < 0.01, Fig. 2A). In group SR however, there was no surgical reintervention of truncal valve, aortic arch or RV-PA conduit after the second stage procedure (Fig. 2B).
Figure 2. Kaplan–Meier analysis of time-related freedom from reoperation over follow-up period.
(A) Freedom from reoperation after initial surgery; P < 0.01. (B) Freedom from reoperation after anatomical correction of CAT (after second stage surgery in group SR); P = 0.5. The numbers of patients still at risk of requiring reoperation as primary end-point are indicated. PR: primary repair; SR: staged repair; CAT: common arterial trunk.
Take home points
- In 23% of patients, a postoperative pulmonary hypertensive crisis occurred; it can be managed effectively with inhaled nitric oxide.
- Ventilation arrangement that kept arterial PaCO2 at about 30 mmHg, arterial PaO2 above 120 mmHg and arterial pH at 7.50 as well as controlled use of sedatives and muscle relaxants help to reduce the tendency for pulmonary vascular resistance to rise.
- Preventing pulmonary hypertensive episodes along with the availability of inhaled nitric oxide and iloprost has effectively reduced perioperative morbidity.
- A preoperative high pressure gradient across the truncal valve does not necessarily translate into significant stenosis
- Some degree of obstruction due to high blood flow across the truncal valve comprises both systemic and pulmonary flow. This increased amount of blood flow could be further exaggerated if truncal valve regurgitation is present.
Prifti E, Ademaj F, Baboci A, Demiraj A.
J Cardiothorac Surg. 2015 Sep 9;10(1):115. doi: 10.1186/s13019-015-0320-z.
PMID: 26353810 Free PMC Article
Select item 26363941
Comment from Dr. Hafil B. Abdulgani (Indonesia), section editor of Congenital Heart Surgery Journal Watch: The Gerbode defect is a communication between the left ventricle and right atrium. It is usually congenital, but rarely is acquired, as a complication of endocarditis, myocardial infarction, trauma, or after previous cardiac surgery. This is a rare case of young woman, with endocarditis of the tricuspid valve and acquired Gerbode defect without previous cardiac surgery. She underwent successful surgical closure of the Gerbode defect and reconstruction of the septal leaflet of the tricuspid valve using an autologous pericardial patch.
Figure 1. A. Transesophageal echocardiography demonstrating the shunt between the left ventricle and right atrium. B. Transthoracic echocardiography demonstrating the vegetation inserted above the septal leaflet of the tricuspid valve. C. Cardiac magnetic resonance.
Figure 2. A. Intraoperative view demonstrating the acquired Gerbode defect after removing the septal leaflet and part of the anterior leaflet of the tricuspid valve. B. A diagram representing the extension of the destructed valvular tissue. C. Hydraulic maneuver.
Table 1. Patients with acquired Gerbode defect without prior cardiac surgery
|2. Saiki||1994||Male/42||MV,AV||Streptococcus hemolyticus||TTE,||Surgery||Survived|
|4. Elian||1995||Male/64||TV||Staphylococcus aureus||TTE, TEE, CC||Surgery||Survived|
|5. Velebit||1995||Male/ 30||BAV||Staphylococcus aureus||TEE, CC||Surgery||Survived(AVB)|
|6. Winslow||1995||Male/ 30||AV||Staphylococcus aureus||TTE, TEE||Surgery||Survived|
|7. Michel||1996||Male/52||AV||Streptococcus viridans||TTE, TEE||Conservative||Survived|
|8. Alphonso||2003||Male/ 63||AV||Culture negative||TTE||Surgery||Survived|
|9. Raja||2006||Male/47||RA||Staphylococcus aureus||TTE, TEE||Surgery||Survived(RF)|
|10. Fukui||2007||Male/57||TV, AV, MV||na||TEE||Surgery||Survived|
|11. Tatewaki||2008||Female/7||TV, AV, MV||Staphylococcus aureus||TEE, CT||Surgery||Survived|
|12. Inouel||2009||Female/21||AV||Culture negative||TTE, TEE||Surgery||Survived|
|13. Cortez-Dias||2009||Male/59||MV||Staphylococcus aureus||TTE, TEE||Conservative||Died(AVB, RF)|
|14. Mendoza||2009||Female/52||AV||Streptococcus mutans||TTE, CT||Surgery||Survived|
|16. Matt||2010||Male/35||AV||Hemophilus aphrophilus||TTE,TEE||Surgery||Survived(AVB)|
|17. Ota||2011||Male/71||AV||Streptococcus pneumonia||TTE,TEE||Surgery||Survived|
|18. Pillai||2011||Male/12||TV||Culture negative||TEE||Surgery||Survived|
|19. Carpenter||2012||Male/22||TV||Staphylococcus lugdunensis||TEE, CT||Surgery||Survived|
|20. Hsu||2014||Male/40||BAV||Cardiobacterium hominis||TEE,||Surgery||Died(RF)|
|21. Prifti et al.||2015||Female/40||TV||Staphylococcus aureus||TTE, TEE||Surgery||Survived|
|Area of myocardial infarction|
|22. Hole||1995||Male/63||Inferior myocardial infarction||TTE||Surgery||Survived|
|23. Jobic||1997||Female/72||Inferior myocardial infarction||TTE, TEE||Surgery||Died (RF)|
|24. Newman||1996||Male/72||Inferior myocardial infarction Trauma||TTE, TEE||Surgery||Died|
|25.Venkatesh||1996||Male/16||Blunt trauma||TTE, TEE||Surgery||Survived|
|26. Selinger||1998||Male/70||Bullet, trauma||TTE,TEE,CC||Surgery||Survived|
Legend: TTE Transthoracic echocardiography, TEE Transesophageal echocardiography, CC Cardiac catheterization, CT Cardiac tomography, na not available, AV Aortic valve, BAV Bicuspid Aortic Valve, MV Mitral valve, TV Tricuspid valve, RF Renal Failure, AVB Complete atrioventricular block
Table 2. Patients with acquired Gerbode defect undergoing previous cardiac surgery
|Author||Year||Gender||Age||Diagnostic tool||Previous procedure||Treatment||Outcome|
|1. Katta et al.||1994||Male||54||TTE,TEE||Endomyocardial biopsy||Conservative||Survived|
|2. Dzwonczyk et al.||1995||Male||25||TTE||ASD repair||na||na|
|3. Dzwonczyk et al.||1995||Female||72||TTE||AVR, VSD repair||na||na|
|4. Fukui et al.||2000||Male||53||TEE||MVR x 2||Surgery||Survived|
|5. Benisty et al.||2000||Male||72||TTE, TEE||MVR||Surgery||n.a.|
|6. Benisty et al.||2000||Male||73||TTE, TEE||MVR x 3, AVR||Surgery||n.a.|
|7. Weinrich et al.||2001||Female||58||TEE, CC||MVRx 2||Surgery||Survived|
|8. Wasserman et al.||2002||Male||78||TTE, TEE,||AVR||Surgery||Survived|
|9. Cabalka et al.||2005||Female||70||TTE, TEE||MVR x 2||Percutaneous||Survived|
|10. Lorber et al.||2006||Female||78||TTE, CC||MVR||Percutaneous||Survived|
|11. Ramasubbu et al.||2006||Male||41||TEE||Aortic root reconstruction||Surgery||Survived|
|12. Ramasubbu et al.||2006||Female||44||TEE||Aortic root reconstruction||Conservative||Survived|
|13. Trehan et al.||2006||Male||22||TTE, MRI, CC||VSD + sinus Valsalva repair||Percutaneous||Survived|
|14. Martinez et al.||2007||Female||70||TTE||MVR||Percutaneous||Survived|
|15. Martinez et al.||2007||Male||67||TTE||AVR||Percutaneous||Survived|
|16. Uslu et al.||2007||Male||54||TTE||MVR||Surgery||Survived|
|17. Hilberath et al.||2007||Male||68||TEE||AVR + endocarditis||Surgery||Survived|
|18. Frigg et al.||2008||Female||77||TEE, CC||AVR||Surgery||Survived|
|19. Moaref et al.||2008||Female||51||TEE||MVR||Surgery||na|
|20. Aoyagi et al.||2008||Female||71||TTE, CC||MVR, TV repair||Surgery||Survived|
|21. Rothman et al.||2008||Male||86||TTE, CC||MVR||Percutaneous||Survived|
|22. Hansalia et al.||2009||Female||46||TTE||AVR||Surgery||Survived|
|23. Yared et al.||2009||Male||60||TTE, TTE||AVR+ endocarditis||na||na|
|24. Gorki et al.||2009||Female||69||na||AVR + endocarditis||na||na|
|25. Subramanian et al.||2009||Male||60||TEE, CT||AVR||Surgery||Survived|
|26. Amirghofran et al.||2009||Female||51||TEE||MVR||Surgery||Survived|
|27. Silbiger et al.||2009||Female||30||TTE, CC||VSD repair||Conservative||Survived|
|28. Cheema et al.||2009||Female||31||MRI||VSD repair||Conservative||Survived|
|29. Can et al.||2009||Male||72||TTE||AV nod ablation||Conservative||Survived|
|30. Can et al.||2009||Male||68||Autopsy||AV nod ablation||na||Died|
|31. Dadkhah et al.||2009||Female||73||TEE||TV repair||Conservative||Survived|
|32. Mohapatra et al||2009||Female||22||TEE||MVR (RF)||Surgery||Survived|
|33. Sun et al.||2010||na||na||na||MVR||Surgery||na|
|34. Sun et al.||2010||na||na||na||MVR||na||na|
|35. Pursnani et al.||2010||Male||78||TTE, TEE||AVR||Surgery||Survived|
|36. Sharma et al.||2011||Male||80||TTE||AV nod ablation||Conservative||Survived|
|37. Kumar et al.||2011||Female||59||TEE||AVRx2 + endocarditis||Surgery||Survived|
|38. Zhu et al.||2012||Baby||6 months||TTE, TEE||ASD, VSD repair||Percutaneous||Survived|
|39. Bochard-Villanueva||2012||Male||63||TEE, CT||AVR+ endocarditis||Surgery||Survived|
|40. Vallakati et al.||2012||Female||53||TTE||AVR||Conservative||Survived|
|41. Elmistekawy et al.||2012||Male||59||TEE||AVR||Surgery||Survived|
|42. Dores et al.||2012||Male||50||TTE, TEE||AVR, MVR||Surgery||Survived|
|43. Yurdakul et al.||2012||Male||68||TEE||AVR||Surgery||Survived|
|44. Mousavi et al.||2012||Female||76||TEE, MRI||AVR||Conservative||Survived|
|45. Ozdogan et al.||2012||Female||31||TTE, TEE||MVRx2 + endocarditis||Surgery||Died|
|46. Anderson et al.||2012||na||na||na||AVR||na||na|
|47. Toprak et al.||2013||Male||32||TTE, TEE||AVR||Conservative||Survived|
|48. Notarangelo et al.||2013||n.a.||69||TTE, TEE||MVR||Percutaneous||Survived|
|49. Sinisalo et al.||2013||Male||75||TTE, TEE, CC||AVR||Percutaneous||Survived|
|50. Sinisalo et al.||2013||Female||23||TEE, CC||VSD repair||Percutaneous||Survived|
|51. Sinisalo et al.||2013||Male||10||TEE, CC||ASD, VSD repair||Percutaneous||Survived|
|52. Sinisalo et al.||2013||Male||8||TEE, CC||VSD repair||Percutaneous||Survived|
|53. Dangol et al.||2013||Male||6 months||TTE,TEE,CC||ToF repair||Percutaneous||Survived|
|54. Lee et al.||2013||Male||3 months||TTE, CC||ASD, PDA, VSD repair||Percutaneous||Survived|
|55. Poulin et al.||2013||Female||75||TTE,TEE||MVR||Percutaneous||Survived|
|56. Primus et al.||2013||Female||76||TTE,TEE||AVR||Conservative||Survived|
|57. Chaturvedi et al.||2013||Male||62||TTE, MRI||AVR||Percutaneous||Survived|
|58. Tayama et al.||2014||Male||75||TTE, CC||MV and TV repair||Surgery||Survived|
|59. Hussain et al.||2014||Male||45||TTE, TEE||AVRx2||Surgery||Survived|
|60. Chamsi-Pasha et al||2014||Male||67||TTE, TEE||MVR, TVR||Surgery||Survived|
|61. Taskesen et al.||2014||Male||74||TTE, TEE||AVRx2||Percutaneous||Survived|
|62. Fanari et al||2015||Female||50||TTE, CT||AVR||Percutaneous||Survived|
Legend: TTE Transthoracic echocardiography, TEE Transesophageal echocardiography, CC Cardiac catheterization, CT Cardiac tomography, MRI Magnetic resonance, na-not available, AVR Aortic valve replacement, MVR Mitral valve replacement, TV Tricuspid valve, ASD Atrial septal defect, VSD Ventricular septal defect, ToF Tetralogy of Fallot, PDA Patent ductus arteriosum
Take home notes:
- The Gerbode defect is a communication between the left ventricle and right atrium.
- It is usually congenital, but rarely is acquired, as a complication of endocarditis, myocardial infarction, trauma, or after previous cardiac surgery.
- Percutaneous transcatheter closure techniques have been employed mostly in high risk surgical candidates due to previous valve replacement, advanced age, anticoagulation, and multiple comorbidities.
- Surgical treatment is always feasible, usually with excellent outcome.
- The percutaneous transcatheter closure remains an excellent option especially in high risk patients.