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
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
• 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.

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 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”.

10. 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.

11. 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%

13. Deaths in VSD

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. 1965

16. 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

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 to close
• 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
– Poor weight gain(Failure to thrive)
– Feeding Diaphoresis(Suck-rest-suck cycle)
– Recurrent LRTI
– No Cyanosis

21. 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

22. 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

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. RV Pressure
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. Those associated 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 step up in RV (exception :
subpulmonic VSD)

31. Qp / QS
(C SAO2 – C MVO2 ) / (C PVO2 – C PAO2 )

32. Reversibility study
• If PVRI 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 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 . 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
<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)
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 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

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. PM VSD

56. PM VSD WITH INLET EXTENSION

57. MUSCULAR INLET VSD

58. PM VSD AND INLET VSD

60. 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

61. 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

62. 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

63. 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

64. 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

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

66. 72

67. video

68. Patch Closure with interrupted sutures
74

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

77. Subpulmonic VSD closure
85

78. video

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 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

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 Trabecular VSD
Sandwich Technique

83. 92

84. 93

85. 94

86. 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.

87. 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

88. 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

89. 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)

91. 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

92. 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.

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 for band
• 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 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

97. 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

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
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

104. TRUSLER’S REPAIR

105. YACOUB’S REPAIR

108. Surgical Cure
• Survival with 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 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.

111. 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.

112. • 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.

113. 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.

114. 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

116. 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.

117. 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.

118. 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

121. 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

122. THANK YOU
132