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MANAGEMENT OF VSD

1. The document discusses the management of ventricular septal defects (VSD), including their natural history, evaluation, indications for surgical intervention, surgical approaches, and outcomes. 2. Key points include that smaller VSDs often close spontaneously while larger defects have risks of pulmonary hypertension, heart failure, and death if left unrepaired. Evaluation involves assessing defect size and location by echocardiogram and measuring pulmonary pressures. 3. Surgical closure is generally indicated for moderate to large VSDs, those with pulmonary hypertension, aortic valve prolapse, or those not closing on their own in infancy. The timing of closure depends on defect size and symptoms.

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MANAGEMENT OF VSD
INTRODUCTION Defect/ Hole in the interventricular septum Closing the defect • Do we need to close it? • When do we need to close it? • Where is it? How many ? How big? • What should be our approach to it? • What material? • What all shall we expect in the outcome?
Outline • Natural History • Evaluation • Indications and Time for surgical intervention • Surgical approaches and techniques • Special cases • Post OP Complications • Results • Outcomes
Natural History of VSD 1. Spontaneous closure 2. Premature death ( 10%)1 3. Pulmonary vascular disease 4. Development of aortic incompetence (6%)2 5. Bacterial endocarditis ( 1.3%)3 6. Development of Infundibular PS (13%)2
1. Keith JD, Rose V, Collins G, Kidd BS. Ventricular septal defect. Incidence, morbidity, and mortality in various age groups. Br Heart J 1971;33Suppl:81-7. 2. Corone P, Doyon F, Gaudeau S, Guérin F, Vernant P, Ducam H, et al. Natural history of ventricular septal defect. A study involving 790 cases. Circulation 1977;55:908-15. 3. Kidd L, Driscoll DJ, Gersony WM, Hayes CJ, Keane JF, O'Fallon WM, et al. Second natural history study of congenital heart defects. Results of treatment of patients with ventricular septal defects. Circulation 1993;87:I38-51
Some excerpts • Of the I90 infants with ventricular septal defects, 83 had small defects that had closed; and 61 (58) had small defects and 46 (5o) had larger defects that were still open, the figures in brackets showing the average for the two 10-year periods I94I-50 and I95I-60. • This means that 58 per cent of small, and over 43 per cent of all, ventricular septal defects have closed within a few years.
Some excerpts • Bloomfield (I964) related the ages and causes of death of 115 patients of all ages with the age- standardized size of the defect (his Fig. 6). He concluded that smaller ventricular septal defects, less than 11mm in diameter, never led to the pulmonary hypertensive complications that cause many deaths. • These patients are, of course, unduly prone to bacterial endocarditis.
• The mean age of death with large VSD is only 23 to 27 year!! PDA ( 43), COA ( 34), CONG AS (35) , PS (30) • “Those with the larger ventricular septal defects have a worse outlook than the whole range of those with other common cardiac malformations”.
Some excerpts 1. When the PASP is normal, it remains so till the 20's. There is not much evidence after this, but what there is suggests that patients continue well. • When the PASP is about 40 to 65 mm. patients are almost equally likely to remain the same or improve, but most of the evidence is limited to the first decade. • When the PASP is approaching systemic levels, about equal numbers remain the same or deteriorate during the time (mean of 6 years) they are under observation.
Pulmonary vascular Disease Age in years Probability of developing pulmonary vascular resistance 8 units . m2 or greater 10 10 % 20 50% 30 80% 40 100%
Deaths in VSD
Premature death 1. 10% dead in infancy due to CHF, RTI 2. Second phase : Second decade onwards due to Eisenmenger 1. Hemoptysis 2. Polycythemia 3. Cerebral abscess 4. Cerebral infarction 5. RV failure
1965
Spontaneous Closure of VSD 1. About 80% of VSD at 1 month eventually narrow or close 2. About 60% of VSD at 3 months eventually narrow or close 3. About 50% of VSD at 6 months eventually narrow or close 4. About 25% of VSD at 12 months eventually narrow or close Becomes rare after 12 ~ 18 months of age
Mechanisms of closure 1. Adherence of tricuspid leaflet , or chordal tissue to the edges of VSD. 2. Growth & hypertrophy of septum around the defect 3. Negative pressure effect exerted by a high velocity stream flowing through the defect 4. Ventricular septal (membranous septum) aneurysm 5. Prolapse of aortic cusp 6. Intrusion of a sinus of Valsalva aneurysm
VSDs unlikely to close • Very large • Sub-pulmonary • Juxta-arterial • Inlet type • Gerbode defect Presence of any of this type of defect indication for surgical intervention
Evaluation • Clinical features • X ray ,ECG and Echo • Cardiac catheterization data
• History – Poor weight gain(Failure to thrive) – Feeding Diaphoresis(Suck-rest-suck cycle) – Recurrent LRTI – No Cyanosis
Examination Stunted growth Tachypnea Tachycardia Hyper dynamic precordium Apex displaced Down and Out Loud P2 component of S2 S3 in Large VSD Pansystolic murmur Mid diastolic murmur at apex
Clinical Picture of Significant PAH • Symptoms improve • Cardiomegaly disappears • Precordium is not Hyperdynamic • Parasternal heave + • Palpable P2 / Loud P2 • Systolic murmur : Small, ESM • TR murmur, PR murmur
ECG findings • Small : Normal • Moderate : LVH • Large : 3 stages – LVH – BVH – RVH
Echocardiography A. General B. VSD C. Valves D. Chambers E. Associated anomalies
Echocardiography A. VSD 1. Number 2. Location 3. Size 4. Margins 5. Direction of flow 6. Gradients/Jet velocity
Echocardiography A. VSD 7. RV Pressure a. PRV = TR gradients + PRA b. PRV = Arm pressure – VSD gradients 8. QP – QS a. Continuity Equation b. PISA
Echocardiography Valves 1.TV : Morphology, Size, TR, straddling 2. MV : Morphology ( Cleft, parachute), Size, MS, MR, Supra-mitral membrane Aorto-mitral continuity 3. AoV: BAV (AS), AR due to cusp prolapse 4. PV : Morphology, PS, RVOTO
Echocardiography Associated anomalies 1. Those associated with MV 2. AS, AR 3. PS 4. Arch Hypolasia, Coarctation 5. PDA
Cardiac catheterization • Indication : Doubtful operability. For Assessment of PVRI PVR :(Mean PA pressure-Mean LA pressure)/Qp TPR: Mean PA pressure/Qp PVRI: PVR x BSA TPRI: TPR x BSA Unit of PVRI/TPRI : unit . m2
Oximetry • Oxygen step up in RV (exception : subpulmonic VSD)
Qp / QS (C SAO2 – C MVO2 ) / (C PVO2 – C PAO2 )
Reversibility study • If PVRI is >8 Woods unit . m2 : Pulmonary vasodilator is given. • If PVRI falls below 7 unit . m2 : Operable
Pulmonary vasodilators • 100 % Oxygen • NO • Isoprenaline • Milrinone • Phenoxybenzamine • Tolazoline
Other way to assess reversibility • Admit • Do a base line echo. Measure transmitral flow velocity. • Give Oxygen by mask for 3-5 days. • Measure transmitral flow velocity again. A 50 % increase is a sign of reversibility.
Criteria of operability in patients with L R shunts A. Wood’s criteria PVRI <10 Woods unit/m2 with Qp/Qs ratio of at least 2:1 B. Lopes and O’Leary • Baseline PVRI <6 Wood units/m2 associated + PVR:SVR ratio < 0.3 : a vasoreactivity test: not needed • Baseline PVRI 6–9 Wood units/m2 associated +PVR : SVR ratio < 0.3–0.5: a vasoreactivity test: needed • i. PVRI drops by 20%: operable • ii. PVR:SVR ratio drops by 20%: operable • iii. Final PVRI <6 Wood units: operable • iv. PVR:SVR ratio <0.3: operable C. More than 20 mm Hg difference between aortic and PA diastolic/mean pressure on oxygen with Qp/Qs >1.5:1 and basal saturations not <95%. Talwar S, et al. Heart Asia 2015;7:31–37. doi:10.1136/heartasia-2015-010645
Classification of VSD Large Moderate Small Size in relation to aortic annulus 75% or more 33%-75% < 33% Flow Velocity < 1m/s 1-4 m/s >4m/s VSD Resistance Index < 20 units . m2 >20 units . m2 >> 20 units . m2 RV/ LV Systolic Pressure 2/3 - 1 1/3 - 2/3 < 1/3 Qp / Qs Very high. Depends upon PVRI > 2 < 1.7
PVRI PVR/SVR OPERABILITY <8 WOODS UNIT ≤0.4 OPERABLE 8-12 WOODS UNIT 0.5-0.7 REVERSIBILITY STUDY >12 WOODS UNIT >0.7 INOPERABLE
Timing of surgery Any time , if: • Very large VSD • with Intractable CHF • Failure to thrive • Life threatening Pneumonia • PVRI more than 4 • AR • Endocarditis
Timing of surgery 3-6 months • If VSD is unlikely to close with significant shunt: Very large VSD, Inlet VSD, Sub- pulmonary VSD, Juxta-arterial VSD • Rising PA pressure • Increasing Aortic cusp prolapse
12 months or later • Any VSD with significant shunt (>1.5 : 1) • Any VSD with Increasing Aortic cusp prolapse • Any VSD with Increasing PA pressure
Timing of surgery • Very small VSD (Shunt < 1.5:1) • Normal PA Pressure • No Cusp prolapse • No Endocarditis
Saxena A, Relan J, Agarwal R, Awasthy N, Azad S, Chakrabarty M, et al. Indian guidelines for indications and timing of intervention for common congenital heart diseases: Revised and updated consensus statement of the Working group on management of congenital heart diseases. Ann Pediatr Card 2019;12:254‐86.
Indications and timing of closure (all Class I recommendations) I. Small VSD (no symptoms, normal PA pressure, normal left heart chambers, no cusp prolapse): a. Annual follow-up till 10 years of age, then every 2–3 years b. Closure indicated if the patient has had an episode of endocarditis or develops cusp prolapse with AR or develops progressive significant right ventricular outflow tract obstruction. II.
Moderate VSD: a. Asymptomatic (normal pulmonary artery pressure with left heart dilation): Closure of VSD by 2–5 years of age b. Symptomatic: If controlled with medications, VSD closure by 1–2 years of age.
III. Large VSD: a. Poor growth/congestive heart failure not controlled with medications (furosemide/ spironolactone/enalapril ± digoxin): As soon as possible b. Controlled heart failure: By 6 months of age. IV. VSD with aortic cusp prolapse: Any VSD with cusp prolapse and directly related AR that is more than trivial: Surgery whenever AR is detected. All patients with VSD must be advised
48 Size of VSD Recommendation Small VSD – 1. Asymptomatic 2. Normal PA pressure 3. Normal left heart chambers 4. No cusp prolapse However, if – • Endocarditis episode • Development of AR • Development of RVOTO Annual Follow up till 10 years and then every 2-3 years Prompt Closure Moderate VSD: Asymptomatic (normal pulmonary artery pressure with left heart dilation) Symptomatic: (Controlled with medications) Closure of VSD by 2–5 years of age Closure by 1–2 years of age Large VSD: a. Poor growth/congestive heart failure (NOT controlled with medications (Diuretics and Digoxin) b. Controlled heart failure: Closure as soon as possible Closure by 6 months of age
Modes of closure • Surgical closure • PA banding • Device closure • Hybrid technique
Knowing the Anatomy • To know the constituents of the boundary of the VSD • To know exactly the location of the AV node, bundle of His and the branches • To avoid injury to aortic valve cusps or tricuspid valve leaflet
Various classifications • Becu (1956) • Lev (1970) • Sotto (1980) • Sotto and kirklin (1989) • Van Prague • ISNPCHD ( 11 iteration of internal classification of diseases, Barcelona , Spain jul 2017)
• Geographical location • Constituents of borders • Location of conduction bundle
PM VSD
PM VSD WITH INLET EXTENSION
MUSCULAR INLET VSD
PM VSD AND INLET VSD
To summarise • The conduction pathway is a) Always in postero-inferior border of all PM defects b) Always in postero-inferior border of all Juxta arterial defects c) It is remote from inferior borders of rest of the defects d) It is remote but in superior border of central muscular defect
Approach for VSD closure 1. Trans RA : Perimembranous, Inlet, Trabecular 2. Trans pulmonary : Sub-pulmonary 3. Trans aortic : Sub-aortic 4. Trans RV Infundibulum: Outlet Body : Perimembranous, Inlet, Trabecular Apex : Apical 5. Trans LV
68 APPROACH ADVANTAGES DISADVANTAGES SUITABLE FOR TYPE OF VSD TRANS RA 1. AVOIDANCE OF VENTRICULOTOMY SCAR- • DECREASED RISK OF POST OP RV DYSFUNCTION • DECREASED RISK OF LATE POSTOP VENTRICULAR ARRYTHMIAS 2. DECREASED RISK OF INJURY TO BUNDLE->RBBB 1. DIFFICULT TO CLOSE - • OUTLET EXTENSION / OUTLET VSD • APICAL VSD 2. DAMAGE TO TRICUSPID VALVE(CHORDAE/LEAFLETS)- >TR • PM VSD • INLET VSD • UPPER MUSCULAR (TRABECULAR) VSD • Gerbode defects TRANS RV 1. ACCURATE VISUALISATION OF AREA OF BUNDLE AND RIGHT TRIGONE 2.EASE OF CLOSURE RV SCAR -> DYSFUNCTION RBBB VENTRICULAR ARRHYTHMIAS HIGH TRANS RV • OUTLET VSD LOW TRANS RV • APICAL VSD TRANS PA SUBPULMONARY VSD TRANS AORTIC S/A VSD OR PM VSD WITH AR TRANS LV 1.VENTRICULAR DYSFUNCTION 2.LATE VENTRICULAR ARRYTHMIAS 1.SWISS CHEESE SEPTUM 2.POST MI VSD COMBINED TRANS RA-RV/PA PM VSD WITH OUTLET EXTENSION
Patch material Choice between three materials Knitted Dacron (poly ethylene terephthalate) Used for the majority of VSDs less elastic. Aggressive inflammatory process peri-patch VSD closures Autologous pericardium ± treated with glutaraldehyde Where fibrosis is not desirable Stretch PTFE ( Gore-Tex) Type of teflon Lattice n nodes Less fibrosis
History Lillehei, Varco (1954): Repaired using controlled cross circulation DuShane et al in Mayo Clinic(1955-1956): Intracardiac repair with pump oxygenator Lillehei(1957): Atrial approach to VSD closure Eisenmenger : Autopsy finding in 1897
Some see things as they are and ask “why Change” Others dream of changes that never were and ask “why not”
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video
Patch Closure with interrupted sutures 74
Trans pulmonary arterial approach Indications Subpulmonic VSD • Doubly committed • Juxta-arterial defects (conal VSDs) • Muscular defects opening in the subpulmonary area
Subpulmonic VSD closure 85
video
Right Ventricular Approach Indications: • Inaccessibility from the right atrium or pulmonary trunk • Defect opening directly into the infundibular area • Obstructive infundibular muscle bundles • Difficulty exposing the inferior margin of an outlet defect
Advantage The nadir of the NCC of the aortic valve, which is the area of the right trigone and bundle of His, can be accurately visualized Disadvantages (1) Scar in the RV (2) Possible damage to the epicardial vessels (3) Higher prevalence of complete RBBB than with an atrial approach abd possibly more ventricular arrhythmias in late postoperative period (4) Ventricular aneurysm and possible RV dysfunction 88
90 IDENTIFYING ADDL VSD - • Using blunt right angled forceps through the VSD explore on the LV side of septum(smooth LV septum) -> tip engages the VSD easily. • Switch off vent • Light test - via IAS place a paediatric bronchoscope into LV-> Illuminate LV-> see the site on IVS from where light is coming. • RV Incision-
Closure of Trabecular VSD Sandwich Technique
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93
94
MANAGEMENT OF MULTIPLE VSDS • Fibrin glue Leca F, Karam J, Vouhe PR et al. Surgical treatment of multiple ventricular septal defects using a biologic glue. J Thorac Cardiovasc Surg 1994; 107:96–102 • Intraoperative use of double umbrella devices Murzi B, Bonanomi GL, Giusti S et al. Surgical closure of muscular ventricular septal defects using double umbrella devices (intraoperative VSD device closure). Eur J Cardiothorac Surg 1997; 12:450–454.
Complications Intra-operatively 1. Damage to Structures a) Bundle : CHB, RBB b) Aortic valve c) Tricuspid valve 2. Residual VSD 3. Myocardial injury 4. Air embolism
Immediate Post-op complications Related to VSD: 1. Continuation of Intra-op problems: CHB, AR, TR, Residual VSD 2. Hyperthermia / Fever 3. Acute myocardial dysfunction/ failure 4. Pulmonary hypertensive crisis 5. Ventricular arrhythmias 6. Patch dehiscence Related to open heart : Bleeding
Late complications after VSD closure 1. Progression of PAH 2. Patch endocarditis 3. Sudden cardiac death (in patients with transient CHB in post op period)
100 Muller Damman 1. the small infants with Swiss cheese type of multiple ventricular septal defects 2. Postponing the choice between biventricular and univentricular repair in atrioventricular or ventricular septal defects (VSD) with ventricular imbalance. 3. Defects with complex anatomy, often associated with a common atrioventricular connection or a criss-cross heart, where a biventricular repair of better quality may be possible later in life when the cardiac structures are bigger. PA BANDING
1. Univentricular physiology with unrestricted pulmonary blood flow to drop PAP and pulmonary vascular resistance to levels suitable for future univentricular palliation 2. The extremely marasmic, septic infant, or in one who presents with a contraindication for CPB, eg., recent intracranial bleed.
Pulmonary artery banding • Fixed PA Band (CPAB) – Problems of band tightening in sedated, ventilated patient – Sudden increase in afterload – Acute adverse events – Multiple re-operations – High morbidity & mortality • Adjustable PA Band (APAB) – Adjustments in extubated, breathing patient on room air – Gradual tightening – Better tolerated by sicker patients
Trusler’s formula for band • Two ventricle: 20 +Weight in Kg mm • Complex Cyanotic: 24 +Weight in Kg mm
Pulmonary Artery Banding • Placed in mid MPA • Subtraction method • A 3- to 4-mm-wide tape is used. • Preferred material is silicone or silicone-impregnated polyester • Minimizes erosion into the pulmonary trunk and allows easy removal.
• Intraop pressure and saturation monitoring; aim is to lower the PAP to normal or half of systemic pressure without desaturation and bradycardia. • These depend on many variables: – GA – Mechanical ventilation – Open chest 106
Complications of PA Banding • Too tight • Inadequate banding- increased PBF/ CCF • Migration of band- impingement and stenosis of branch PA • Too proximal placement leading to distortion • Erosion of PA • Distortion of PA 107
APAB: band tightening • Pulse oxymetry, Echo guidance • By placing additional clips • Room Air • Add no more than 20 mm gradient at one sitting • 2 Ventricle: Gradient 50% of systemic pressure (max 50), Sat > 85% • 1 Ventricle: As much tight as possible, Sat > 75%
VSD with PAH • Pt with PVRI between 8-12 • Pt who shows reversibility on testing. • Use of unidirectional valved patch for repair • First proposed by Zhou and colleagues • Modified by Novick et all • Own publications
112 VSD WITH AR Laubry Pezzi 1921 • Lack of support to aortic annulus : Diastolic prolapse of unsupported cusp. • 2/3 cases RCC and 1/3 NCC • Venturi effect : Cusp is sucked during systole • Related to congenital sinus of valsalva Aneurysm
TRUSLER’S REPAIR
YACOUB’S REPAIR
Surgical Cure • Survival with mean PA pressure less than 25 mm Hg after 5 years • Depends upon age and PVRI at surgery
Rabinovitch et al: – Surgical cure likely in if VSD repaired before 6-9 months of age, irrespective of degree of pulmonary vascular disease. – At 2 years, chances of cure if preoperative Rp <5 units/m2. – At 4 years, surgical cure if Rp is normal preoperatively • Repair of a large VSD iat 6 months of age, 95% chance of surgical cure (unless preoperative Rp >8 units/m2 and does not fall to <7 units/m2 with infusion of isoproterenol. 119
Probability of overall surgical cure (survival at least 5 years postoperatively with a mean pulmonary artery pressure of <25 mm Hg) according to age (months) at repair for all patients with single large ventricular septal defects (VSD). Dashed lines enclose 70% confidence limits. 120 DuShane JW, Kirklin JW. Late results of the repair of ventricular septal defect in pulmonary vascular disease.
Outcome • Low hospital mortality. In experienced centers, hospital mortality for isolated VSD closure is 1% or less. 1 • The most common mode of death after repair of a primary VSD is acute cardiac failure – Young age and presence of multiple VSDs are no more risk factors attributing to early death – Major associated cardiac anomalies contribute • Late mortality may be attributed to arrhythmias,. Patients with a high Rp preoperatively often die from progression of pulmonary vascular disease. • 121 1. Scully BB, Morales DL, Zafar F, McKenzie ED, Fraser CD Jr, Heinle JS. Current expectations for surgical repair of isolated ventricular septal defects. Ann Thorac Surg 2010;89:544-51.
• Improved physical development and increase in weight. (Lillehei, 1955) • Increase in height and head circumference.1 • Weintraub2 et al confirmed that repair of a large VSD in the first 6 months of life results in near- normal long-term growth in most patients, so that by age 5 years, weight, length, and head circumference are normal. 122 1. Clarkson PM. Growth following corrective cardiac operation in early infancy. In: Barratt-Boyes BG, Neutze JM, Harris EA, eds. Heart disease in infancy: diagnosis and surgical treatment. London: Churchill Livingstone, 1973, p. 75. 2. Weintraub RG, Menahem S. Early surgical closure of a large ventricular septal defect: influence on long-term growth. J Am Coll Cardiol 1991;18:552.
Changes in weight after repair of ventricular septal defect in 96 patients aged 10 years or less, with ratio of pulmonary and systemic pressures greater than 0.45 and ratio of pulmonary and systemic resistances less than 0.75 preoperatively. 123 Cartmill TB, DuShane JW, McGoon DC, Kirklin JW. Results of repair of ventricular septal defect. J Thorac Cardiovasc Surg 1966; 52:486.
124 J Am Coll Cardio 1994;24;1348-54 Follow up of 109 infants and children from 1968 to 1980. Mean interval after operation was 14.5±2.6 years. 84% assessed their health as good or very good and 89% had been free from any surgical and medical interventions. 84% patients had normal exercise capacity No patients had no signs of pulmonary hypertension or symptomatic arrhythmias
Device closure i. Eligibility criteria: a. Weight >8 kg (5 kg for muscular VSD) b. Left-to-right shunt >1.5:1 ii. Indications a. Class I – Midmuscular VSD, anterior muscular VSD, postoperative residual VSD b. Class IIb – Perimembranous VSD with at least 4 mm distance from the aortic valve.
Contraindications a. VSD with irreversible pulmonary vascular disease b. Pre-existing left bundle branch block or conduction abnormalities c. Any AR d. Associated lesions requiring surgery e. Inlet, sub-pulmonic VSD. iv. Device should not be deployed if any of the following findings develop at the time of procedure: a. Any degree of AR b. Conduction defect: complete heart block (CHB)/ left bundle branch block c. Mitral or tricuspid regurgitation.
Interventional Options • Percutaneous Device Closure – Muscular VSDs can typically be closed percutaneously • Class IIb recommendation in Guidelines (i.e. surgery still preferred) – No FDA approved devices for perimembranous VSDs, although there are specific devices for this purpose • Concern re proximity of defect to AV node and high risk of complete AV block requiring pacemaker
HYBRID TECHINIQUE Combination of surgery and device closure 1. when the is a contraindication to CPB 2. difficult to reach the defect surgically or by percutaneous technique
THANK YOU 132

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In this document
Powered by AI

This section introduces the management of VSD and outlines topics including natural history, evaluation, indications, surgical approaches, special cases, complications, and outcomes.

It discusses spontaneous closure rates, complications like premature death (10%), pulmonary vascular disease, and risks associated with VSD sizes, emphasizing observation and timing.

This slide shows the age-related probability of developing pulmonary vascular resistance, increasing from 10% at age 10 to 100% by age 40.

Overviews pivotal data on mortality rates due to VSD, with 10% infant mortality due to CHF and subsequent risks such as hemoptysis and RV failure.

Discusses rates of spontaneous closure of VSD, noting that 80% close by one month, and outlines types of defects likely needing surgical intervention.

Evaluates clinical features, diagnostics using X-ray, ECG, echocardiography parameters, emphasizing how to diagnose and assess VSD accurately.

Focuses on cardiac catheterization indications, oximetry, and reversibility studies to assess operability in patients with VSD.

Defines criteria for surgical intervention in VSD patients, including Wood's criteria and associated parameters like PA pressure and symptom severity.

Summarizes timing for VSD surgery based on size and symptoms, reinforcing the recommendations for various classifications.

This discusses closure techniques including surgical, PA banding, device closure, and hybrid techniques for managing VSD.

Highlights critical anatomical knowledge and categorization of VSDs necessary for effective surgical intervention.

Explores various surgical approaches and their advantages/disadvantages, including right atrial and trans-pulmonary methods.

Details intra-operative and post-operative complications that may arise during and after VSD repair.

Addresses survival rates and long-term growth expectations after VSD repair, citing various authors and studies.

Discusses eligibility criteria and contraindications for percutaneous device closure, stressing the importance of careful selection.

Describes the combination of surgical and device approaches when traditional methods are contraindicated or challenging.

MANAGEMENT OF VSD

  • 1.
  • 2.
    INTRODUCTION Defect/ Hole inthe interventricular septum Closing the defect • Do we need to close it? • When do we need to close it? • Where is it? How many ? How big? • What should be our approach to it? • What material? • What all shall we expect in the outcome?
  • 3.
    Outline • Natural History •Evaluation • Indications and Time for surgical intervention • Surgical approaches and techniques • Special cases • Post OP Complications • Results • Outcomes
  • 4.
    Natural History ofVSD 1. Spontaneous closure 2. Premature death ( 10%)1 3. Pulmonary vascular disease 4. Development of aortic incompetence (6%)2 5. Bacterial endocarditis ( 1.3%)3 6. Development of Infundibular PS (13%)2
  • 5.
    1. Keith JD,Rose V, Collins G, Kidd BS. Ventricular septal defect. Incidence, morbidity, and mortality in various age groups. Br Heart J 1971;33Suppl:81-7. 2. Corone P, Doyon F, Gaudeau S, Guérin F, Vernant P, Ducam H, et al. Natural history of ventricular septal defect. A study involving 790 cases. Circulation 1977;55:908-15. 3. Kidd L, Driscoll DJ, Gersony WM, Hayes CJ, Keane JF, O'Fallon WM, et al. Second natural history study of congenital heart defects. Results of treatment of patients with ventricular septal defects. Circulation 1993;87:I38-51
  • 7.
    Some excerpts • Ofthe I90 infants with ventricular septal defects, 83 had small defects that had closed; and 61 (58) had small defects and 46 (5o) had larger defects that were still open, the figures in brackets showing the average for the two 10-year periods I94I-50 and I95I-60. • This means that 58 per cent of small, and over 43 per cent of all, ventricular septal defects have closed within a few years.
  • 8.
    Some excerpts • Bloomfield(I964) related the ages and causes of death of 115 patients of all ages with the age- standardized size of the defect (his Fig. 6). He concluded that smaller ventricular septal defects, less than 11mm in diameter, never led to the pulmonary hypertensive complications that cause many deaths. • These patients are, of course, unduly prone to bacterial endocarditis.
  • 9.
    • The meanage of death with large VSD is only 23 to 27 year!! PDA ( 43), COA ( 34), CONG AS (35) , PS (30) • “Those with the larger ventricular septal defects have a worse outlook than the whole range of those with other common cardiac malformations”.
  • 10.
    Some excerpts 1. Whenthe PASP is normal, it remains so till the 20's. There is not much evidence after this, but what there is suggests that patients continue well. • When the PASP is about 40 to 65 mm. patients are almost equally likely to remain the same or improve, but most of the evidence is limited to the first decade. • When the PASP is approaching systemic levels, about equal numbers remain the same or deteriorate during the time (mean of 6 years) they are under observation.
  • 11.
    Pulmonary vascular Disease Agein years Probability of developing pulmonary vascular resistance 8 units . m2 or greater 10 10 % 20 50% 30 80% 40 100%
  • 13.
  • 14.
    Premature death 1. 10%dead in infancy due to CHF, RTI 2. Second phase : Second decade onwards due to Eisenmenger 1. Hemoptysis 2. Polycythemia 3. Cerebral abscess 4. Cerebral infarction 5. RV failure
  • 15.
  • 16.
    Spontaneous Closure ofVSD 1. About 80% of VSD at 1 month eventually narrow or close 2. About 60% of VSD at 3 months eventually narrow or close 3. About 50% of VSD at 6 months eventually narrow or close 4. About 25% of VSD at 12 months eventually narrow or close Becomes rare after 12 ~ 18 months of age
  • 17.
    Mechanisms of closure 1.Adherence of tricuspid leaflet , or chordal tissue to the edges of VSD. 2. Growth & hypertrophy of septum around the defect 3. Negative pressure effect exerted by a high velocity stream flowing through the defect 4. Ventricular septal (membranous septum) aneurysm 5. Prolapse of aortic cusp 6. Intrusion of a sinus of Valsalva aneurysm
  • 18.
    VSDs unlikely toclose • Very large • Sub-pulmonary • Juxta-arterial • Inlet type • Gerbode defect Presence of any of this type of defect indication for surgical intervention
  • 19.
    Evaluation • Clinical features •X ray ,ECG and Echo • Cardiac catheterization data
  • 20.
    • History – Poorweight gain(Failure to thrive) – Feeding Diaphoresis(Suck-rest-suck cycle) – Recurrent LRTI – No Cyanosis
  • 21.
    Examination Stunted growth Tachypnea Tachycardia Hyper dynamicprecordium Apex displaced Down and Out Loud P2 component of S2 S3 in Large VSD Pansystolic murmur Mid diastolic murmur at apex
  • 22.
    Clinical Picture ofSignificant PAH • Symptoms improve • Cardiomegaly disappears • Precordium is not Hyperdynamic • Parasternal heave + • Palpable P2 / Loud P2 • Systolic murmur : Small, ESM • TR murmur, PR murmur
  • 23.
    ECG findings • Small: Normal • Moderate : LVH • Large : 3 stages – LVH – BVH – RVH
  • 24.
    Echocardiography A. General B. VSD C.Valves D. Chambers E. Associated anomalies
  • 25.
    Echocardiography A. VSD 1. Number 2.Location 3. Size 4. Margins 5. Direction of flow 6. Gradients/Jet velocity
  • 26.
    Echocardiography A. VSD 7. RVPressure a. PRV = TR gradients + PRA b. PRV = Arm pressure – VSD gradients 8. QP – QS a. Continuity Equation b. PISA
  • 27.
    Echocardiography Valves 1.TV : Morphology,Size, TR, straddling 2. MV : Morphology ( Cleft, parachute), Size, MS, MR, Supra-mitral membrane Aorto-mitral continuity 3. AoV: BAV (AS), AR due to cusp prolapse 4. PV : Morphology, PS, RVOTO
  • 28.
    Echocardiography Associated anomalies 1. Thoseassociated with MV 2. AS, AR 3. PS 4. Arch Hypolasia, Coarctation 5. PDA
  • 29.
    Cardiac catheterization • Indication: Doubtful operability. For Assessment of PVRI PVR :(Mean PA pressure-Mean LA pressure)/Qp TPR: Mean PA pressure/Qp PVRI: PVR x BSA TPRI: TPR x BSA Unit of PVRI/TPRI : unit . m2
  • 30.
    Oximetry • Oxygen stepup in RV (exception : subpulmonic VSD)
  • 31.
    Qp / QS (CSAO2 – C MVO2 ) / (C PVO2 – C PAO2 )
  • 32.
    Reversibility study • IfPVRI is >8 Woods unit . m2 : Pulmonary vasodilator is given. • If PVRI falls below 7 unit . m2 : Operable
  • 33.
    Pulmonary vasodilators • 100% Oxygen • NO • Isoprenaline • Milrinone • Phenoxybenzamine • Tolazoline
  • 34.
    Other way toassess reversibility • Admit • Do a base line echo. Measure transmitral flow velocity. • Give Oxygen by mask for 3-5 days. • Measure transmitral flow velocity again. A 50 % increase is a sign of reversibility.
  • 35.
    Criteria of operabilityin patients with L R shunts A. Wood’s criteria PVRI <10 Woods unit/m2 with Qp/Qs ratio of at least 2:1 B. Lopes and O’Leary • Baseline PVRI <6 Wood units/m2 associated + PVR:SVR ratio < 0.3 : a vasoreactivity test: not needed • Baseline PVRI 6–9 Wood units/m2 associated +PVR : SVR ratio < 0.3–0.5: a vasoreactivity test: needed • i. PVRI drops by 20%: operable • ii. PVR:SVR ratio drops by 20%: operable • iii. Final PVRI <6 Wood units: operable • iv. PVR:SVR ratio <0.3: operable C. More than 20 mm Hg difference between aortic and PA diastolic/mean pressure on oxygen with Qp/Qs >1.5:1 and basal saturations not <95%. Talwar S, et al. Heart Asia 2015;7:31–37. doi:10.1136/heartasia-2015-010645
  • 36.
    Classification of VSD LargeModerate Small Size in relation to aortic annulus 75% or more 33%-75% < 33% Flow Velocity < 1m/s 1-4 m/s >4m/s VSD Resistance Index < 20 units . m2 >20 units . m2 >> 20 units . m2 RV/ LV Systolic Pressure 2/3 - 1 1/3 - 2/3 < 1/3 Qp / Qs Very high. Depends upon PVRI > 2 < 1.7
  • 37.
    PVRI PVR/SVR OPERABILITY <8WOODS UNIT ≤0.4 OPERABLE 8-12 WOODS UNIT 0.5-0.7 REVERSIBILITY STUDY >12 WOODS UNIT >0.7 INOPERABLE
  • 38.
    Timing of surgery Anytime , if: • Very large VSD • with Intractable CHF • Failure to thrive • Life threatening Pneumonia • PVRI more than 4 • AR • Endocarditis
  • 39.
    Timing of surgery 3-6months • If VSD is unlikely to close with significant shunt: Very large VSD, Inlet VSD, Sub- pulmonary VSD, Juxta-arterial VSD • Rising PA pressure • Increasing Aortic cusp prolapse
  • 40.
    12 months orlater • Any VSD with significant shunt (>1.5 : 1) • Any VSD with Increasing Aortic cusp prolapse • Any VSD with Increasing PA pressure
  • 41.
    Timing of surgery •Very small VSD (Shunt < 1.5:1) • Normal PA Pressure • No Cusp prolapse • No Endocarditis
  • 42.
    Saxena A, RelanJ, Agarwal R, Awasthy N, Azad S, Chakrabarty M, et al. Indian guidelines for indications and timing of intervention for common congenital heart diseases: Revised and updated consensus statement of the Working group on management of congenital heart diseases. Ann Pediatr Card 2019;12:254‐86.
  • 43.
    Indications and timingof closure (all Class I recommendations) I. Small VSD (no symptoms, normal PA pressure, normal left heart chambers, no cusp prolapse): a. Annual follow-up till 10 years of age, then every 2–3 years b. Closure indicated if the patient has had an episode of endocarditis or develops cusp prolapse with AR or develops progressive significant right ventricular outflow tract obstruction. II.
  • 44.
    Moderate VSD: a. Asymptomatic(normal pulmonary artery pressure with left heart dilation): Closure of VSD by 2–5 years of age b. Symptomatic: If controlled with medications, VSD closure by 1–2 years of age.
  • 45.
    III. Large VSD: a.Poor growth/congestive heart failure not controlled with medications (furosemide/ spironolactone/enalapril ± digoxin): As soon as possible b. Controlled heart failure: By 6 months of age. IV. VSD with aortic cusp prolapse: Any VSD with cusp prolapse and directly related AR that is more than trivial: Surgery whenever AR is detected. All patients with VSD must be advised
  • 46.
    48 Size of VSDRecommendation Small VSD – 1. Asymptomatic 2. Normal PA pressure 3. Normal left heart chambers 4. No cusp prolapse However, if – • Endocarditis episode • Development of AR • Development of RVOTO Annual Follow up till 10 years and then every 2-3 years Prompt Closure Moderate VSD: Asymptomatic (normal pulmonary artery pressure with left heart dilation) Symptomatic: (Controlled with medications) Closure of VSD by 2–5 years of age Closure by 1–2 years of age Large VSD: a. Poor growth/congestive heart failure (NOT controlled with medications (Diuretics and Digoxin) b. Controlled heart failure: Closure as soon as possible Closure by 6 months of age
  • 47.
    Modes of closure •Surgical closure • PA banding • Device closure • Hybrid technique
  • 49.
    Knowing the Anatomy •To know the constituents of the boundary of the VSD • To know exactly the location of the AV node, bundle of His and the branches • To avoid injury to aortic valve cusps or tricuspid valve leaflet
  • 50.
    Various classifications • Becu(1956) • Lev (1970) • Sotto (1980) • Sotto and kirklin (1989) • Van Prague • ISNPCHD ( 11 iteration of internal classification of diseases, Barcelona , Spain jul 2017)
  • 51.
    • Geographical location •Constituents of borders • Location of conduction bundle
  • 55.
  • 56.
    PM VSD WITHINLET EXTENSION
  • 57.
  • 58.
    PM VSD ANDINLET VSD
  • 60.
    To summarise • Theconduction pathway is a) Always in postero-inferior border of all PM defects b) Always in postero-inferior border of all Juxta arterial defects c) It is remote from inferior borders of rest of the defects d) It is remote but in superior border of central muscular defect
  • 61.
    Approach for VSDclosure 1. Trans RA : Perimembranous, Inlet, Trabecular 2. Trans pulmonary : Sub-pulmonary 3. Trans aortic : Sub-aortic 4. Trans RV Infundibulum: Outlet Body : Perimembranous, Inlet, Trabecular Apex : Apical 5. Trans LV
  • 62.
    68 APPROACH ADVANTAGES DISADVANTAGESSUITABLE FOR TYPE OF VSD TRANS RA 1. AVOIDANCE OF VENTRICULOTOMY SCAR- • DECREASED RISK OF POST OP RV DYSFUNCTION • DECREASED RISK OF LATE POSTOP VENTRICULAR ARRYTHMIAS 2. DECREASED RISK OF INJURY TO BUNDLE->RBBB 1. DIFFICULT TO CLOSE - • OUTLET EXTENSION / OUTLET VSD • APICAL VSD 2. DAMAGE TO TRICUSPID VALVE(CHORDAE/LEAFLETS)- >TR • PM VSD • INLET VSD • UPPER MUSCULAR (TRABECULAR) VSD • Gerbode defects TRANS RV 1. ACCURATE VISUALISATION OF AREA OF BUNDLE AND RIGHT TRIGONE 2.EASE OF CLOSURE RV SCAR -> DYSFUNCTION RBBB VENTRICULAR ARRHYTHMIAS HIGH TRANS RV • OUTLET VSD LOW TRANS RV • APICAL VSD TRANS PA SUBPULMONARY VSD TRANS AORTIC S/A VSD OR PM VSD WITH AR TRANS LV 1.VENTRICULAR DYSFUNCTION 2.LATE VENTRICULAR ARRYTHMIAS 1.SWISS CHEESE SEPTUM 2.POST MI VSD COMBINED TRANS RA-RV/PA PM VSD WITH OUTLET EXTENSION
  • 63.
    Patch material Choice betweenthree materials Knitted Dacron (poly ethylene terephthalate) Used for the majority of VSDs less elastic. Aggressive inflammatory process peri-patch VSD closures Autologous pericardium ± treated with glutaraldehyde Where fibrosis is not desirable Stretch PTFE ( Gore-Tex) Type of teflon Lattice n nodes Less fibrosis
  • 64.
    History Lillehei, Varco (1954): Repairedusing controlled cross circulation DuShane et al in Mayo Clinic(1955-1956): Intracardiac repair with pump oxygenator Lillehei(1957): Atrial approach to VSD closure Eisenmenger : Autopsy finding in 1897
  • 65.
    Some see thingsas they are and ask “why Change” Others dream of changes that never were and ask “why not”
  • 66.
  • 67.
  • 68.
    Patch Closure withinterrupted sutures 74
  • 74.
    Trans pulmonary arterialapproach Indications Subpulmonic VSD • Doubly committed • Juxta-arterial defects (conal VSDs) • Muscular defects opening in the subpulmonary area
  • 77.
  • 78.
  • 79.
    Right Ventricular Approach Indications: •Inaccessibility from the right atrium or pulmonary trunk • Defect opening directly into the infundibular area • Obstructive infundibular muscle bundles • Difficulty exposing the inferior margin of an outlet defect
  • 80.
    Advantage The nadir ofthe NCC of the aortic valve, which is the area of the right trigone and bundle of His, can be accurately visualized Disadvantages (1) Scar in the RV (2) Possible damage to the epicardial vessels (3) Higher prevalence of complete RBBB than with an atrial approach abd possibly more ventricular arrhythmias in late postoperative period (4) Ventricular aneurysm and possible RV dysfunction 88
  • 81.
    90 IDENTIFYING ADDL VSD- • Using blunt right angled forceps through the VSD explore on the LV side of septum(smooth LV septum) -> tip engages the VSD easily. • Switch off vent • Light test - via IAS place a paediatric bronchoscope into LV-> Illuminate LV-> see the site on IVS from where light is coming. • RV Incision-
  • 82.
    Closure of TrabecularVSD Sandwich Technique
  • 83.
  • 84.
  • 85.
  • 86.
    MANAGEMENT OF MULTIPLEVSDS • Fibrin glue Leca F, Karam J, Vouhe PR et al. Surgical treatment of multiple ventricular septal defects using a biologic glue. J Thorac Cardiovasc Surg 1994; 107:96–102 • Intraoperative use of double umbrella devices Murzi B, Bonanomi GL, Giusti S et al. Surgical closure of muscular ventricular septal defects using double umbrella devices (intraoperative VSD device closure). Eur J Cardiothorac Surg 1997; 12:450–454.
  • 87.
    Complications Intra-operatively 1. Damage toStructures a) Bundle : CHB, RBB b) Aortic valve c) Tricuspid valve 2. Residual VSD 3. Myocardial injury 4. Air embolism
  • 88.
    Immediate Post-op complications Relatedto VSD: 1. Continuation of Intra-op problems: CHB, AR, TR, Residual VSD 2. Hyperthermia / Fever 3. Acute myocardial dysfunction/ failure 4. Pulmonary hypertensive crisis 5. Ventricular arrhythmias 6. Patch dehiscence Related to open heart : Bleeding
  • 89.
    Late complications afterVSD closure 1. Progression of PAH 2. Patch endocarditis 3. Sudden cardiac death (in patients with transient CHB in post op period)
  • 91.
    100 Muller Damman 1. thesmall infants with Swiss cheese type of multiple ventricular septal defects 2. Postponing the choice between biventricular and univentricular repair in atrioventricular or ventricular septal defects (VSD) with ventricular imbalance. 3. Defects with complex anatomy, often associated with a common atrioventricular connection or a criss-cross heart, where a biventricular repair of better quality may be possible later in life when the cardiac structures are bigger. PA BANDING
  • 92.
    1. Univentricular physiologywith unrestricted pulmonary blood flow to drop PAP and pulmonary vascular resistance to levels suitable for future univentricular palliation 2. The extremely marasmic, septic infant, or in one who presents with a contraindication for CPB, eg., recent intracranial bleed.
  • 93.
    Pulmonary artery banding •Fixed PA Band (CPAB) – Problems of band tightening in sedated, ventilated patient – Sudden increase in afterload – Acute adverse events – Multiple re-operations – High morbidity & mortality • Adjustable PA Band (APAB) – Adjustments in extubated, breathing patient on room air – Gradual tightening – Better tolerated by sicker patients
  • 94.
    Trusler’s formula forband • Two ventricle: 20 +Weight in Kg mm • Complex Cyanotic: 24 +Weight in Kg mm
  • 95.
    Pulmonary Artery Banding •Placed in mid MPA • Subtraction method • A 3- to 4-mm-wide tape is used. • Preferred material is silicone or silicone-impregnated polyester • Minimizes erosion into the pulmonary trunk and allows easy removal.
  • 96.
    • Intraop pressureand saturation monitoring; aim is to lower the PAP to normal or half of systemic pressure without desaturation and bradycardia. • These depend on many variables: – GA – Mechanical ventilation – Open chest 106
  • 97.
    Complications of PABanding • Too tight • Inadequate banding- increased PBF/ CCF • Migration of band- impingement and stenosis of branch PA • Too proximal placement leading to distortion • Erosion of PA • Distortion of PA 107
  • 99.
    APAB: band tightening •Pulse oxymetry, Echo guidance • By placing additional clips • Room Air • Add no more than 20 mm gradient at one sitting • 2 Ventricle: Gradient 50% of systemic pressure (max 50), Sat > 85% • 1 Ventricle: As much tight as possible, Sat > 75%
  • 100.
    VSD with PAH •Pt with PVRI between 8-12 • Pt who shows reversibility on testing. • Use of unidirectional valved patch for repair • First proposed by Zhou and colleagues • Modified by Novick et all • Own publications
  • 102.
    112 VSD WITH AR LaubryPezzi 1921 • Lack of support to aortic annulus : Diastolic prolapse of unsupported cusp. • 2/3 cases RCC and 1/3 NCC • Venturi effect : Cusp is sucked during systole • Related to congenital sinus of valsalva Aneurysm
  • 104.
  • 105.
  • 108.
    Surgical Cure • Survivalwith mean PA pressure less than 25 mm Hg after 5 years • Depends upon age and PVRI at surgery
  • 109.
    Rabinovitch et al: –Surgical cure likely in if VSD repaired before 6-9 months of age, irrespective of degree of pulmonary vascular disease. – At 2 years, chances of cure if preoperative Rp <5 units/m2. – At 4 years, surgical cure if Rp is normal preoperatively • Repair of a large VSD iat 6 months of age, 95% chance of surgical cure (unless preoperative Rp >8 units/m2 and does not fall to <7 units/m2 with infusion of isoproterenol. 119
  • 110.
    Probability of overallsurgical cure (survival at least 5 years postoperatively with a mean pulmonary artery pressure of <25 mm Hg) according to age (months) at repair for all patients with single large ventricular septal defects (VSD). Dashed lines enclose 70% confidence limits. 120 DuShane JW, Kirklin JW. Late results of the repair of ventricular septal defect in pulmonary vascular disease.
  • 111.
    Outcome • Low hospitalmortality. In experienced centers, hospital mortality for isolated VSD closure is 1% or less. 1 • The most common mode of death after repair of a primary VSD is acute cardiac failure – Young age and presence of multiple VSDs are no more risk factors attributing to early death – Major associated cardiac anomalies contribute • Late mortality may be attributed to arrhythmias,. Patients with a high Rp preoperatively often die from progression of pulmonary vascular disease. • 121 1. Scully BB, Morales DL, Zafar F, McKenzie ED, Fraser CD Jr, Heinle JS. Current expectations for surgical repair of isolated ventricular septal defects. Ann Thorac Surg 2010;89:544-51.
  • 112.
    • Improved physicaldevelopment and increase in weight. (Lillehei, 1955) • Increase in height and head circumference.1 • Weintraub2 et al confirmed that repair of a large VSD in the first 6 months of life results in near- normal long-term growth in most patients, so that by age 5 years, weight, length, and head circumference are normal. 122 1. Clarkson PM. Growth following corrective cardiac operation in early infancy. In: Barratt-Boyes BG, Neutze JM, Harris EA, eds. Heart disease in infancy: diagnosis and surgical treatment. London: Churchill Livingstone, 1973, p. 75. 2. Weintraub RG, Menahem S. Early surgical closure of a large ventricular septal defect: influence on long-term growth. J Am Coll Cardiol 1991;18:552.
  • 113.
    Changes in weightafter repair of ventricular septal defect in 96 patients aged 10 years or less, with ratio of pulmonary and systemic pressures greater than 0.45 and ratio of pulmonary and systemic resistances less than 0.75 preoperatively. 123 Cartmill TB, DuShane JW, McGoon DC, Kirklin JW. Results of repair of ventricular septal defect. J Thorac Cardiovasc Surg 1966; 52:486.
  • 114.
    124 J Am CollCardio 1994;24;1348-54 Follow up of 109 infants and children from 1968 to 1980. Mean interval after operation was 14.5±2.6 years. 84% assessed their health as good or very good and 89% had been free from any surgical and medical interventions. 84% patients had normal exercise capacity No patients had no signs of pulmonary hypertension or symptomatic arrhythmias
  • 116.
    Device closure i. Eligibilitycriteria: a. Weight >8 kg (5 kg for muscular VSD) b. Left-to-right shunt >1.5:1 ii. Indications a. Class I – Midmuscular VSD, anterior muscular VSD, postoperative residual VSD b. Class IIb – Perimembranous VSD with at least 4 mm distance from the aortic valve.
  • 117.
    Contraindications a. VSD withirreversible pulmonary vascular disease b. Pre-existing left bundle branch block or conduction abnormalities c. Any AR d. Associated lesions requiring surgery e. Inlet, sub-pulmonic VSD. iv. Device should not be deployed if any of the following findings develop at the time of procedure: a. Any degree of AR b. Conduction defect: complete heart block (CHB)/ left bundle branch block c. Mitral or tricuspid regurgitation.
  • 118.
    Interventional Options • PercutaneousDevice Closure – Muscular VSDs can typically be closed percutaneously • Class IIb recommendation in Guidelines (i.e. surgery still preferred) – No FDA approved devices for perimembranous VSDs, although there are specific devices for this purpose • Concern re proximity of defect to AV node and high risk of complete AV block requiring pacemaker
  • 121.
    HYBRID TECHINIQUE Combination ofsurgery and device closure 1. when the is a contraindication to CPB 2. difficult to reach the defect surgically or by percutaneous technique
  • 122.