DR J P SONI Professor and Head of the Department Pediatrics Division of Pediatric Cardiology DR S N Medical College Jodhpur Doc_jpsoni@yahoo.com

1. DR J P SONI
Professor and Head of the Department Pediatrics
Division of Pediatric Cardiology
DR S N Medical College
Jodhpur
Doc_jpsoni@yahoo.com

2. Acyanotic CHD’s
ACYANOTIC
CHDS
PURE
ACYANOTIC
POTENTIALLY
CYANOTIC

3. Acyanotic
CHD
Without shunt(normal
or decreased flow)
Right side of heart
PULMONARY
STENOSIS
Left side of heart
AORTIC STENOSIS
COARCTATIONOF
AORTA
L-> R SHUNT ↑ PBF
ASD
VSD
P.D.A.
Aorto-pulmonary
Window

4. Ventricular septal defect (VSD) is the most common congenital heart defect (excluding
bicuspid aortic valve [BAV]) and constitutes 20%–30% of all congenital heart defects.
The prevalence varies from 3 to 5/1000 live births. However, a much higher prevalence
(50/1000 live births) is reported due to ease of detection of small muscular VSDs by
echocardiography.
Clinical manifestations depend on the size of the defect and the pulmonary and systemic
vascular resistances. About 10% of patients with large VSDs die in 1st year, primarily due to
congestive heart failure.
Rate of spontaneous closure depends on the size and location of the defect. Spontaneous
closure is uncommon in large VSDs. Inlet and malaligned VSDs almost never close spontaneously.

5. Muscular VSDs are more likely to close spontaneously, especially if they are not large. Decrease
in size of VSD is seen in 25% of patients.
Small VSDs have a >50% chance of spontaneous closure by 5 years of age and a >80% chance by
adolescence.
Progressive right ventricular outflow tract obstruction (Gasul phenomenon) may develop in 13%
and aortic regurgitation (AR) in 6% of patients.
In the historic series of Dr. Paul Wood, 52% of patients with large VSD developed irreversible
pulmonary vascular disease with the onset in infancy in four-fifths of them.
The incidence of IE in patients with small VSD is 1.3 per 1000 patient-years.

6. VSD EMBRYOLOGY

7. Diagrammatic representation of normal development of the IVS. The IVS is formed from 3 separate septa:
muscular, outlet, and inlet septa.
Early in embryologic development, the muscular septum (MS) grows upward from the floor of the ventricles
toward the already fused endocardial cushions (EC). The gap between the edge of the muscular IVS and EC is
called the interventricular foramen (IVF).
Meanwhile, 2 spiral ridges of tissue, the conotruncal ridges or truncoconal swellings, appear on the sides of the
truncus arteriosus (TA). The conotruncal ridges grow toward each other and fuse, forming a spiral-shaped
septum termed the aortopulmonary septum (APS). The APS divides the TA into the pulmonary trunk and aorta.
The conotruncal ridges also grow downward into the ventricles, meeting with the already fused endocardial
cushions and the muscular portion of the IVS. By the seventh to eighth week of gestation, the membranous
septum is formed when the APS, endocardial cushions, and muscular septum completely fuse, closing off the
IVS.

8. Diagrammatic representation of normal common developmental anomalies of the IVS. Defects in the fusion of the
muscular septum (MS) and the endocardial cushions (EC) result in membranous VSDs. Openings in the trabecular
portion of the IVS lead to muscular VSDs. Incomplete fusion of the aortopulmonary septum (APS) with the EC-MS
septum results in supracristal VSDs (SC-VSD).

9. Perimembranous VSD (yellow),
subarterial VSD (red),
muscular VSD (blue),
inlet VSD (green). IVC indicates
inferior vena cava; SVC, superior
vena cava.

10. Ventricular Septal Defects: Embryology and Imaging Findings
Rojas, Carlos Andres MD*; Jaimes, Camilo MD†; Abbara, Suhny
MD‡Author Information
Journal of Thoracic Imaging: March 2013 - Volume 28 - Issue 2 -
p W28-W34
doi: 10.1097/RTI.0b013e31824b5b95
Smaller defects, also called restrictive defects,
provide intrinsic resistance to flow and limit the amount of
shunted blood, maintaining a gradient between the 2
ventricles.
In contrast, large defects allow for unrestricted flow through
the defect and equalization of interventricular chamber
pressures.

11. Classification of ventricular septal defect
i. Peri-membranous: 80%
ii Outlet or sub-pulmonary (doubly committed): 5%–7%
iii. Inlet: 5%–8%
iv. Muscular: 5%–20%, these could be central (mid-muscular), apical, marginal (anterior,
septal-free wall area),
or multiple, “Swiss cheese” type.

12. Classification according to the size of the defect
Small (restrictive) VSD:
Diameter of the defect is less than one-third of the size of aortic orifice.
Right ventricular and pulmonary artery pressure is normal, left-to-right shunt is <1.5:1
Left side cardiac chambers are normal size.
Moderate VSD (restrictive):
Diameter of the defect is more than one-third but less than the size of aortic orifice.
Right ventricular and pulmonary artery pressure varies from normal to two-thirds of systemic
pressure.
Left-to-right shunt is >1.5:1
Left sided cardiac chambers are dilated.
Large VSD (non-restrictive):
Diameter of the defect is equal to or more than the size of aortic orifice.
Right ventricular and pulmonary artery systolic pressures are systemic or near systemic.
Degree of left-to-right shunt depends on PVR.
The left-sided cardiac chambers are dilated when PVR is normal or mildly elevated.

14. CLINICAL FEATURES
• Race : no particular racial predilection
• Sex : no particular sex preference
• Age : of presentation -
Neonate and infants– difficult postnatal period, although ccf during first 6mths
is frequent, x ray chest cardiomegaly ECG LVH.
Children—after first year have variable clinical picture, depending upon the size
and location of the V S D.
small VSD – asymptomatic
large VSD – common symptoms, palpitation, feeding difficulties - suck & rest cycle
in neonate and infants, breathing difficulty on exertion, poor growth , frequent
cough and fever requiring hospitalization –suggestive of chest infections.

15. PHYSICAL FINDINGS
• Pulse pressure is relatively wide.
• Precordium is hyperkinetic with a systolic thrill at LSB
• S1&S2 are masked by a PSM at Lt. sternal border, max. intensity of
• the murmur is best heard at 3rd,4th&5th Lt interspace.
• Murmur well heard at the 2nd space but not conducted beyond apex

16. PHYSICAL FINDINGS
• Lt. 2nd space –widely and variable split second sound & accentuated P2
• Delayed diastolic murmur at the apex & S3
• Presence of mid-diastolic ,low pitched rumble at the apex is caused by increased
flow across the mitral valve & indicates Qp:Qs=2:1/greater
• Maladie de Roger – small VSD presenting in older children as a loud PSM without
other significant hemodynamic changes. S1 and S2 are distinct. Murmur ends well
before S2.

17. Natural History of VSD
Spontaneous diminution in size or closure : I 50-75% of restrictive perimembranous and
muscular VSD after birth
This occur in within first year, 60% before 3 years and 90% before 8 years.
Infant may develop -
Acquired RVOT or LVOT obstruction,
Develop AR due to AV prolapse
Infective endocarditis and
patient with VSD > 2/3 of aortic size and pulmonary arterial systolic pressure > 50% of
systemic arterial pressure is at risk of developing CHF initially and
pulmonary arterial obstruction later on in life if not treated appropriately.

18. VSD size & Haemodynamic
Size PA pressure PVR CHF
Restrictive <1/3 of aortic size Normal Normal NO
Moderately
restrictive
1/3-2/3 of aortic size < 50 % or systemic pressure LOW May be
large > 2/3 of aortic size >50% systemic pressure High Yes

19. INVESTIGATIONS
• CHEST RADIOGRAPHY
- Normal if VSD is small
- Cardiomegaly(Biventricular hypertrophy) & Pulmonary plethora
if VSD is moderate to large size
• ELECTROCARDIOGRAPHY
-Small VSD ~ normal tracing
- Mod.VSD ~ broad, notched P wave characteristic of Lt. Atrial overload as well as LV
overload, deep Q waves & tall R waves in leads V5 and V6 and often AF
- Large VSD ~ RVH with RAD. With further progression biventricular hypertrophy; P waves
may be notched/peaked.
- RVH with RAD and absence of left ventricular force with large VSD & increased PVR
- Suggestive of Eisenmenger syndrome
-
- ECHO CARDIOGRAPHY : It is the essential tool for finding out size and location of
V S D beside assessing size of heart and degree & direction of shunt.

20. P L A X VIEW
PERI MEMBRANOUS VSD
SUB-AORTIC VSD
SUB PUL. VSD
- ECHO CARDIOGRAPHY : It is the essential tool for finding out size and location of V S D
beside assessing size of heart, degree & direction of shunt for the management of patient.

21. Peri-membranous ventricular septal defect
AO
LA
AO
AO
LV
LA
LA
RV
RV RV
RA RA
PA PA
PM VSD
TV
PLAX
PSAX

22. Peri-membranous ventricular septal defect 80%

23. Peri-membranous V S D partially closed by
Septal leaflet of TV, making aneurysm with
fenestrated multiple small V S D

24. Sub aortic ventricular septal defect
AO
LV
LA
AO
AO
AO
LA
LA
LA
SUB. AO VSD
RA
RV
LV
RV
RV
RV
RA
TV
TV
PSAX
PLAX

25. Sub aortic ventricular septal defect
PSAX

26. Sub pulmonary ventricular septal defect
PSAX
PLAX

27. PSAX

29. VSD PERIMEMBRANOUS SUBAORTIC SUBPULMONARY
PSAX

30. Inlet ventricular septal defect
iii. Inlet: 5%–8%

31. Mid Muscular ventricular septal defect

32. Apical muscular ventricular septal defect
iv. Muscular: 5%–20%
Apical

33. Swiss cheese ventricular septal defect

35. Gerbode ventricular septal defect
iii. Inlet: 5%–8%
RV RV
LV LV
LA
LA
RA
RA
TV
TV
MV
MV

37. Mid Muscular VSD with TR

38. The Tricuspid regurgitation with membranous VSD mainly occurred because of
1. short tricuspid valve septa – Dysplastic TV
2. Interminable anterior tricuspid valve septa – Richoceting TR
High velocity jet by impinging on anterior tricuspid leaflet and richoceting as TR.The TR is produced by the VSD jet (
Venturi effect) pushing the tricuspid anterior leaflet forward to open the tricuspid valve orifice and richoceting jet enter
right atrium as TR. In these patients, a moderate paramembranous VSD extended slightly below the septal tricuspid leaflet
with only partial obstruction of the VSD jet. We believe that when this mechanism for TR is found in association with a
moderate VSD, surgical VSD closure is warranted
3. Abnormal attachment point of the chordae tendineae to muscular VSD
4. Irregular adhesion of STL to right ventricular septal defect - Sometimes tricuspid septal aneurysm (which is closing large
VSD) can distort the tricuspid valve and cause tricuspid regurgitation.
If pulmonary arterial pressure is estimated by the tricuspid regurgitation method, the pulmonary artery systolic pressure
would be overestimated. Due to this the differential pressure of the tricuspid valve was not the same as that of the right
ventricle and right atrium, but instead the same as the left ventricle and right atrium.
Investigation of membranous ventricular septal defect complicated with tricuspid regurgitation in ventricular septal defect
occlusion
shu-ping liu, li li, ke-chun yao, na wang and jian-chang wang experimental and therapeutic medicine 5: 865-869, 2013

44. 5. Gerbode VSD
6. Cleft in Tricuspid valve with inlet VSD - TR
7. Large VSD with Pulmonary arterial hypertension I Eisenmenger syndrome

45. Cardiac catheterization
It is required in patients with pulmonary hypertension and suspected pulmonary vascular
disease.
Cardiac catheterization is performed for interventional purpose - device closure

46. 74
78
74
95
90
90
95
95
Where is shunt ?
What is the direction of shunt ?
What is diagnosis?

47. Where is shunt ?
74
78
74
95
90
90
95
95
Answer : At ventricular level
Left to right from LV to RV
V S D
Qp = 1/PAO2- PVO2 X 100= 1/90-95 X 100 =20
Qs= 1/SAO2- MVO2 X 100 = 1/95-74 X 100= 5
Qp/Qs=
𝟐𝟏
𝟓
= 4.2 :1
QeS = 1/ PAO2-MVO2 X 100 = 1/90-74 X 100 = 6.6
LEFT TO RIGHT SHUNT = Qp-QeS = 20-6.6 = 14.6

48. Qp= 1/PAO2-PVO2 X 100 = 1/87-94 X 100 = 1/7 X 100 = 14.2L
Qs = 1/SAO2-MVO2 X 100 = 1/95-68 X100= 1/27 X 100 = 3.8
QeS =1/ PVO2- MVO2 X 100 = 1/ 94-68 = 1/26 X 100 = 3.8
Qp/QS = 14.21/3.8 = 3.7
LT TO RT = QP – QeS = 14.2 -3.8 = 10. 4 L
RT TO LEFT = Qs- QeS = 3.8 – 3.8 = 0
NET SHUNTING 10.41 FROM LEFT TO RIGHT AT VSD

49. 74
78
74
90
74
74
100
90
Where is shunt ?
What is the direction of shunt ?
What is diagnosis?

50. 74
78
74
90
74
74
100
90
Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
Ventricular
Right to left
VSD
Qp=1/PAO2-PVO2 X 100= 1/74-100 X 100 = 1/26 X 100 = 4 L
Qs = 1/SAO2-MVO2X 100 = 1/90-74 X 100 = 1/16 X 100 = 6.6L
QeS = 1/PVO2-MVO2 X 100 = 1/100-74 X 100 = 1/26 X100 = 4
Qp /Qs = 4/6 = 0.6.6
RT to LT shunt = Qs –QeS = 6-4 = 2
LT to Rtshunt = Qp-QeS = 4-4 = 0

51. Fetus with VSD

52. What is spectrum of VSD ?
VSD – Peri-memberanous, Subaortic, Sub-pulmonary, Inlet, Muscular
Fetal echo revealed
1st Step : – 4 CV lateral and basal view will revealed echo dropout with bidirectional color on color
doppler.

53. V S D
Peri-membranous Sub- aortic
Muscular Inlet
Sub -
pulmonary
Pul. Stenosis
Pul. Atresia
Absent Pul valve
PS
MR,TR ( AV Regurgitation
Associated cardiac abnormality - Fetus with VSD

54. What are the Associated extra cardiac abnormality
in Fetus with VSD ?
V S D
Peri-membranous Sub- aortic
Muscular Inlet
Sub -
pulmonary
21 trisomy with AVSD 40%
Sub aortic VSD one out let
Vessel - 22q11.1 deletion
Pul stenosis with absent radius
And thumb – Holt Oram syn
13T - Omphalocele,
Holo-procencephaly
cleft lip & palate
Polydactyly cutis aplasia
Micro-ophthalmia
18 T- Abnormal
fisting of hand
Low birth weight, under developed finger nail
Microcephaly, Ptosis, blephrophymosis

55. What is the possibility of genetic Etiology ?
Fetus VSD without extra cardiac abnormality – no genetic cause
Fetus with VSD and Extra-cardiac abnormality –
AVSD - 21 trisomy
VSD with Omphalocele and holoprocencephaly – 13T
Fisting of hand 18 T
Sub aortic VSD & PS and absent radius and thumb - Holt Oram syn
Sub aortic VSD & single outlet vessel - truncus arteriosus – 22q11.1

56. Which genetic test you will offer to couple ?
Karyotyping as first test if we suspect aneuploidy in fetus with DNA preservation.
FISH – For 22q11.1 deletion if fetus have CoA/absent thymus/TOF with pul atresia
CGH array is the second line test to detect aneuploidy, micro deletion and duplication
NGS – is third line investigation to diagnose single gene disorders – Holt Oram syn etc

57. How to counsel couple regarding risk of recurrence ?
(TGA)
•The general population CHD risk is ~1%
•For parents with one affected child the recurrence risk of CHD is between 2-5%
•For parents of two affected children the recurrence risk of CHD is 10-15%
• If father have VSD risk is 2% and if mother had VSD recurrence risk is 6%
•It depends upon cause – aneuploidy, syndrome

58. Does fetus need regular follow up after diagnosis ?
VSD
isolated With VSD&/or PS Extra cardiac anomalies
Follow regularly by echo
Patient with extra cardiac anomaly – omphalocele need regular follow up
Patient with AVSD need follow up

59. How to counsel couple regarding pregnancy management ?
SITE OF DELIVERY : Hospitral
TIMING OF DILERY : AT TERM IF PFO & / OR PDA IS NORMAL; NO CONSTRICTION IN-UTERO
MODE OF DELIVERY : NORMAL, IF NO OBSTETRIC COMPLICATION
PLANNING OF POSTNATAL CARE: POST NATAL ECHO TO CONFIRM DIAGNOSIS AND NATURE OF CARDIAC LESION

60. How to counsel couple regarding post natal management ?
(AVSD)
VSD
isolated VSD &/or PS Extra cardiac anomalies
Rx depends up on the size of VSD Rx depends up on severity of PS and SPO2

61. Medical management of ASD
Drug therapy is recommendation for patients with CHDs- ASD,VSD and PDA, who have
abnormal cardiac morphology or function like –
Cardiac volume over load that is dilated cardiac chamber despite preserved systolic function,
Valvular regurgitation
Pulmonary hypertension because of volume overload, but no symptoms of heart failure.

62. Digoxin is indicated in heart failure associated with reduced systolic function of heart.
Utility of Digoxin in heart failure secondary to volume overload of the ventricle, as seen
in left to right shunt lesions, is less clear, since the myocardial contractility is normal in
such cases.
Rapid digitalization is usually not indicated when using digoxin for heart failure.
Rapid digitalization may be indicated for treatment of acute tachyarrhythmias.
The maintenance dose is given in twice daily doses for children under 10 years and once daily
for children above 10 years.
Digoxin “holiday” is generally not needed in children.
The half life of digoxin is markedly prolonged in preterm babies and in those with renal
dysfunction.
Dose of digoxin should he halved when using amiadarone.

63. Diuretics
are widely used in heart failure because of the symptomatic relief from fluid overload with in
minutes of administration - Furosemide, torsemide.
Dosages and Pharmacodynamics: Oral: 1-2 mg/kg every 12 hours, maximum of 4 mg/kg/day;
intravenous: 1 mg/kg/dose up to 3-4 times a day;
Continuous IV infusion: 1-4 mg/kg/day. Continuous infusion may be better and safer in acute
heart failure and in postoperative setting.
The onset of action starts in 10-20 minutes after an IV dose and 20-30 minutes after oral
administration. The duration of action is six hours.
The dose does not need to be adjusted in renal or hepatic impairment.
Furosemide may increase chances of digoxin toxicity by producing hypokalemia.
It activates the renin angiotensin aldosterone axis (RAAS), producing vasoconstriction, which
is detrimental in heart failure. Concomitant use of ACEi (vasodilator) is recommended,
whenever possible.

64. Vasodilators:
Angiotensin Converting Enzyme Inhibitors (ACEi)
ACEi decrease the adrenergic drive and block the heart failure induced activation of renin
angiotensin aldosterone axis (RAAS).
Increased levels of aldosterone and angiotension II have been associated with poor outcome in
heart failure.
ACEi also increase bradykinin which has natrinuretic properties.
Currently ACEi therapy is recommended as the first line treatment for heart failure, when it
is not secondary to an obstructive lesion.
Enalapril. Enalapril is useful for older children. It is longer acting and given twice daily. The
dose is 0.1- 0.5 mg/kg/dose twice a day. The initial dose may be smaller.
BP and renal parameters should be monitored when up titrating the dose

65. Beta blockers
Heart failure results in activation of sympathetic nervous system and increased levels of
circulating catecholamines. Chronic activation of sympathetic nervous system leads to worsening
of heart failure by inducing myocardial apoptosis and fibrosis. Circulating catecholamines also
induce peripheral vasoconstriction along with renal retention of salt and water. Betablockers
antagonize these deleterious effects. In addition, betablockers also have antiarrhythmic
effect.
Carvedilol is a non selective beta blocker which also has an anti-oxidant property. Due to its
alpha blocking effect, carvedilol exerts a vasodilatory effect. It improves functional class and
fractional shortening in children with ventricular dysfunction
Carvedilol: 0.1 mg/kg/day in two divided doses, increase at 1-2 weekly interval to 1 mg/kg/day
with a maximum of 2 mg/kg/day.
Metoprolol: 0.2-0.4 mg/kg/day initially, gradually increase to a maximum of 1 mg/kg/day in two
divided doses.

66. Do
• Treat the underlying cause of heart failure.
• Digoxin has a narrow safety window in
children.
• Continuous infusion of furosemide may be
better in acutely ill cases .
• A persistent tachycardia (>180) may indicate
“tachycardio-myopathy” as the cause of heart
failure.
• Rapid digitalization is not required for
majority.
drug therapy of cardiac diseases in children working group on management of congenital heart diseases in india correspondence to: dr anita saxena,
professor of cardiology, all india institute of medical sciences, new delhi 110029, india indian pediatrics 2009
Do Not
• Combine angiotensin converting enzyme
inhibitors
(ACEi) with Angiotensin receptor blockers (ARB)
(Class III).
• Avoid combining ACEi and spironolactone, if
necessary, monitor potassium levels (Class II b)
• Do not give ACEi in heart failure secondary to
pressure overload (Class III)
• Avoid using ACEi in acute decompensated heart
failure (Class II b)
• Betablockers should not be initiated in acute
decompensated stage of heart failure (Class III)
• Potassium supplements are not required in early
infancy

67. 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. b. Closure indicated if the patient has had an episode of
1. Endocarditis
2. Develops cusp prolapse with AR or any VSD if have aortic cusp prolapse of any degree at
the time of diagnosis, should be operated as early as possible to prevent AV damage.
3. Develops progressive significant right ventricular outflow tract obstruction.

68. Sub-aortic VSD with RCC prolapse & AR
C C

69. Indications and timing of closure (all Class I recommendations)
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.

70. Indications and timing of closure (all Class I recommendations)
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

71. Contra - indications of closure
Severe pulmonary arterial hypertension with irreversible pulmonary vascular occlusive disease
(Class III). Patients with borderline operability due to pulmonary vascular disease should be
referred or subjected to for cardiac catheterization evaluation for operability.
The decision to operate or not should be made on an individual basis taking into account the
total picture of the case including results of the investigations.

72. Method of closure
Surgery
i. Patch closure is the standard therapy in most patients. Route of closure depends on the
location of the defect, but left ventri-culotomy is best avoided.
ii. Temporary pulmonary artery banding: Palliative option in patients with-
a. Multiple VSDs (Swiss cheese VSDs), inaccessible VSDs (Class I)
b. Patients with contraindications for cardiopulmonary bypass, e.g., sepsis (Class IIa). iii.
Surgical options for patients with borderline operability: Fenestrated VSD patch closure,
fenestrated flap valve VSD patch closure, or leaving (or creating) a 5 mm ASD. Such
procedures should only be done after discussion with the family as in some cases, pulmonary
hypertension may not regress or may regress and later worsen following surgery (Class IIb).

73. Large Apical VSD
Bidirectional flow
PAH
Controlled by
Oral diuretic & enalapril

74. large mid muscular VSD PA banding

75. 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.
iii. 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, subpulmonic VSD.

76. Device closure
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.

77. Recommendations for follow-up
i. Follow-up after surgery:
Clinical, ECG, and echo in the 1st year only. No further follow-up is required if no residual defect
or pulmonary hypertension. Patient/guardians should be explained about reporting to hospital in
case of any cardiac symptoms or symptoms suggestive of arrhythmias.
ii. Follow-up protocol for device closure:
a. Antiplatelet agents: Aspirin (3–5 mg/kg/day) is given a day before or immediately after
procedure and continued for total duration of 6 months.
b. b. Follow-up visits: At 1 month, 6 months, 1 year, then annually till 5 years, and then every 3–5
years. Echocardiogram and ECG are to be done at each visit in addition to clinical evaluation. c.
iii. IE prophylaxis is recommended for 6 months after device or surgical closure. However, all
patients are advised to maintain good oro-dental hygiene after this period also.