MANAGEMENT OF VSD

SURGICAL AND INTERVENTIONAL MANAGEMENT OF VENTRICULAR SEPTAL DEFECT

1. MANAGEMENT OF VSD

2. 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?

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 of VSD Spontaneous closure Premature death ( 10%) 1 Pulmonary vascular disease Development of aortic incompetence (6%) 2 Bacterial endocarditis ( 1.3%) 3 Development of Infundibular PS (13%) 2

5. 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 . 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 .  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  

6. 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 .

7. 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.

8. 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”.

9. Some excerpts 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.

10. Pulmonary vascular Disease Age in years Probability of developing pulmonary vascular resistance 8 units . m 2 or greater 10 10 % 20 50% 30 80% 40 100%

11. Deaths in VSD

12. Premature death 10% dead in infancy due to CHF, RTI Second phase : Second decade onwards due to Eisenmenger Hemoptysis Polycythemia Cerebral abscess Cerebral infarction RV failure

13. 1965

14. Spontaneous Closure of VSD About 80% of VSD at 1 month eventually narrow or close About 60% of VSD at 3 months eventually narrow or close About 50% of VSD at 6 months eventually narrow or close About 25% of VSD at 12 months eventually narrow or close Becomes rare after 12 ~ 18 months of age

15. Mechanisms of closure Adherence of tricuspid leaflet , or chordal tissue to the edges of VSD. Growth & hypertrophy of septum around the defect Negative pressure effect exerted by a high velocity stream flowing through the defect Ventricular septal (membranous septum) aneurysm Prolapse of aortic cusp Intrusion of a sinus of Valsalva aneurysm

16. 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

17. Evaluation Clinical features X ray ,ECG and Echo Cardiac catheterization data

18. History Poor weight gain(Failure to thrive) Feeding Diaphoresis(Suck-rest-suck cycle) Recurrent LRTI No Cyanosis

19. 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

20. 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

21. ECG findings Small : Normal Moderate : LVH Large : 3 stages LVH BVH RVH

22. Echocardiography General VSD Valves Chambers Associated anomalies

23. Echocardiography VSD Number Location Size Margins Direction of flow Gradients/Jet velocity

24. Echocardiography VSD RV Pressure a. P RV = TR gradients + P RA b. P RV = Arm pressure – VSD gradients 8. Q P – Q S a. Continuity Equation b. PISA

25. 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

26. Echocardiography Associated anomalies Those associated with MV AS, AR PS Arch Hypolasia , Coarctation PDA

27. Cardiac catheterization Indication : Doubtful operability. For Assessment of PVRI PVR :(Mean PA pressure-Mean LA pressure)/ Q p TPR: Mean PA pressure/ Q p PVRI: PVR x BSA TPRI: TPR x BSA Unit of PVRI/TPRI : unit . m 2

28. Q p Q p = V O2 / (C PVO2 – C PAO2 ) V O2 = Oxygen consumption (Calculated from charts) in L/min Oxygen content : Hb concentration x 1.34 x % saturation

29. Q s Q s = V O2 / (C SAO2 – C MVO2 ) V O2 = Oxygen consumption (Calculated from charts) in L/min Oxygen content : Hb concentration x 1.34 x % saturation

30. Oximetry Oxygen step up in RV (exception : subpulmonic VSD)

31. Q p / Q S (C SAO2 – C MVO2 ) / (C PVO2 – C PAO2 )

32. Reversibility study If PVRI is >8 Woods unit . m 2 : Pulmonary vasodilator is given. If PVRI falls below 7 unit . m 2 : Operable

33. Pulmonary vasodilators 100 % Oxygen NO Isoprenaline Milrinone Phenoxybenzamine Tolazoline

34. 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.

35. 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

36. 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 . m 2 >20 units . m 2 >> 20 units . m 2 RV/ LV Systolic Pressure 2/3 - 1 1/3 - 2/3 < 1/3 Q p / Q s Very high. Depends upon PVRI > 2 < 1.7

37. 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

38. Timing of surgery Any time , if: Very large VSD with Intractable CHF Failure to thrive Life threatening Pneumonia PVRI more than 4 AR Endocarditis

39. 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

40. 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

41. Timing of surgery Very small VSD (Shunt < 1.5:1) Normal PA Pressure No Cusp prolapse No Endocarditis

42. 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.

43. Indications and timing of closure (all Class I recommendations) 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 : Asymptomatic (normal pulmonary artery pressure with left heart dilation): Closure of VSD by 2–5 years of age Symptomatic : If controlled with medications, VSD closure by 1–2 years of age.

45. III. Large VSD: Poor growth/congestive heart failure not controlled with medications (furosemide/ spironolactone/ enalapril ± digoxin): As soon as possible 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 VSD Recommendation Small VSD – Asymptomatic Normal PA pressure Normal left heart chambers 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 : 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

48. 51 Class I Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Class IIa Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Class IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Class III Risk ≥ Benefit No additional studies needed Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL should is recommended is indicated is useful/effective/ beneficial is reasonable can be useful/effective/ beneficial is probably recommended or indicated may/might be considered may/might be reasonable usefulness/effectiveness is unknown /unclear/uncertain or not well established is not recommended is not indicated should not is not useful/effective/beneficial may be harmful Applying Classification of Recommendations and Level of Evidence Alternative Phrasing:

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

52. PM VSD

53. PM VSD WITH INLET EXTENSION

54. MUSCULAR INLET VSD

55. PM VSD AND INLET VSD

56. To summarise The conduction pathway is Always in postero -inferior border of all PM defects Always in postero -inferior border of all Juxta arterial defects It is remote from inferior borders of rest of the defects It is remote but in superior border of central muscular defect

57. Approach for VSD closure Trans RA : Perimembranous, Inlet, Trabecular Trans pulmonary : Sub-pulmonary Trans aortic : Sub-aortic Trans RV Infundibulum: Outlet Body : Perimembranous , Inlet, Trabecular Apex : Apical 5. Trans LV

58. 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

59. 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

60. 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

61. Some see things as they are and ask “why Change ” Others dream of changes that never were and ask “why not”

62. Perimembranous VSD Closure 72

63. video

64. Patch Closure with interrupted sutures 74

65. Patch Closure with continuous sutures

66. Trans pulmonary arterial approach Indications Subpulmonic VSD Doubly committed Juxta -arterial defects ( conal VSDs) Muscular defects opening in the subpulmonary area

67. Subpulmonic VSD closure 85

68. video

69. 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

70. 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 Scar in the RV Possible damage to the epicardial vessels Higher prevalence of complete RBBB than with an atrial approach abd possibly more ventricular arrhythmias in late postoperative period Ventricular aneurysm and possible RV dysfunction 88

71. Left ventricular approach

72. 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 -  

73. Closure of Trabecular VSD Sandwich Technique

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77. MANAGEMENT OF MULTIPLE VSD S 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.

78. Complications Intra-operatively Damage to Structures Bundle : CHB, RBB Aortic valve Tricuspid valve 2. Residual VSD 3. Myocardial injury 4. Air embolism

79. Immediate Post-op complications Related to VSD: Continuation of Intra-op problems: CHB, AR, TR, Residual VSD Hyperthermia / Fever Acute myocardial dysfunction/ failure Pulmonary hypertensive crisis Ventricular arrhythmias Patch dehiscence Related to open heart : Bleeding

80. Late complications after VSD closure Progression of PAH Patch endocarditis Sudden cardiac death (in patients with transient CHB in post op period)

81. 100 Muller Damman the small infants with Swiss cheese type of multiple ventricular septal defects Postponing the choice between biventricular and univentricular repair in atrioventricular or ventricular septal defects (VSD) with ventricular imbalance. 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

82. 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.

83. Newer indications that have joined the above list, aim at the following: Left ventricular preparation for an involuted subpulmonary left ventricle of late-presenting simple D-transposition of the great arteries (TGA), in preparation for an arterial switch operation. Left ventricular preparation and/or reduction of tricuspid regurgitation (TR) in congenitally corrected transposition of the great arteries (CCTGA) with tricuspid incompetence without sizeable VSD. PAB as an adjunct to another procedure, eg ., 1. bidirectional Glenn shunt to maintain antegrade flow with acceptable superior caval pressures, 2. as part of a palliative arterial switch operation.

84. 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

85. Trusler’s formula for band Two ventricle: 20 +Weight in Kg mm Complex Cyanotic : 24 +Weight in Kg mm

86. 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.

87. 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

88. 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

89. 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%

90. 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

91. 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

92. TRUSLER’S REPAIR

93. YACOUB’S REPAIR

94. RESULTS

95. Surgical Cure Survival with mean PA pressure less than 25 mm Hg after 5 years Depends upon age and PVRI at surgery

96. 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/m 2 . 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/m 2 with infusion of isoproterenol. 119

97. 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.

98. 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 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.

99. Improved physical development and increase in weight. ( Lillehei , 1955) Increase in height and head circumference. 1 Weintraub 2 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 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. 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.

100. 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.

101. 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

102. Device closure i . Eligibility criteria : Weight >8 kg (5 kg for muscular VSD) Left‑to‑right shunt >1.5:1 ii. Indications Class I – Midmuscular VSD, anterior muscular VSD, postoperative residual VSD Class IIb – Perimembranous VSD with at least 4 mm distance from the aortic valve.

103. 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.

104. 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

105. HYBRID TECHINIQUE Combination of surgery and device closure when the is a contraindication to CPB difficult to reach the defect surgically or by percutaneous technique

106. THANK YOU 132