Sami asd work

Atrial Septal
Defect
Dr sami Nazrul
Islam
Final Part Student
NHF&RI

An atrial septal defect is a communication between the
atria resulting from a deficiency of tissue in the septum,
as distinguished from a patent foramen ovale, where
septum primum, though preserved, is not adherent to
the superior limbic band of septum secundum.
Definition:

Prevalence:
• ASD occurs in 5% to 10% of all congenital heart defects.
• Male:Female = 1:2
• About 30% to 50% of children with CHDs have an ASD as
part of the cardiac defect.
• Excluding bicuspid aortic valve and mitral valve prolapse,
ASD is the most common form of congenital heart defect
found among adults and is the most common acyanotic
shunt lesion in adults as well.

 The primitive atrium is first
partitioned into right and
left atria by growth of the
septum primum—a thin,
crescent-shaped
membrane that grows from
the roof of the primitive
atrium toward the
endocardial cushions.
 Foramen primum,
composed of the free edge
of the septum primum and
the endocardial cushions.

 Fenestrations develop in
the septum primum that
coalesce to form the
ostium secundum.
 As the septum primum
then fuses with the
endocardial cushions, the
ostium secundum
maintains a right-to-left
atrial flow that is important
in the fetal circulation.
 Failure of this fusion results
in the development of a
primum ASD.

 A second septum, the
septum secundum,
then forms to the right
of the septum primum,
growing toward the
endocardial cushions
and usually closing the
ostium secundum.
 Failure to close the
ostium secundum
results in the
formation of a
secundum ASD.

 Ostium secundum defects
(70%-75%)
 Ostium primum defects
 (15%-20%)
 Sinoseptal defects (5%-
10%)
 SVC type
 IVC type
 Coronary sinus ASD
 (1%-2%)

Etiology
 Actual etiology of this congenital defect is unknown.
 Some factors may play role as there are some
evidences of being association with ASD.
 Factors include:
 - Genetic factor
 - Environmental factor including antenatal use
of teratogenic drugs, congenital infection

The degree of left to right shunting is dependent on:
• the size of the defect
• the relative compliance of the right ventricle and left
ventricle and
• the relative vascular resistance in the pulmonary and
systemic circulations.

Pathophysiology
In moderate-to-large defects, a considerable shunt of
oxygenated blood flows from the left to the right atrium
↓
Volume overload and dilation of the right atrium and
ventricle
↓
The tricuspid and pulmonary annuli may dilate and become
incompetent
↓
Increased flow into the lungs
↓
Pulmonary arteries, capillaries & the veins are dilated

Pulmonary arteries, capillaries & the veins are dilated
↓
Flow-related pulmonary artery hypertension
↓
Medial hypertrophy of pulmonary arteries and
muscularization of the arterioles resulting in pulmonary
vascular obstructive disease
↓
Reversal of the shunt
↓
Eisenmenger syndrome

 ASD smaller than 3 mm, diagnosed before 3 months of age,
spontaneous closure occurs in 100% of patients at 1½ years of age.
 Spontaneous closure occurs more than 80% of the time in patients
with defects between 3 and 8 mm before 1½ years of age.
 An ASD with a diameter larger than 8 mm rarely closes
spontaneously.
 Spontaneous closure is not likely to occur after 4 years of age
 Most children with an ASD remain active and asymptomatic.
Rarely, congestive heart failure (CHF) can develop in infancy.
Natural History

 If a large defect is untreated, CHF and pulmonary hypertension
begin to develop in adults who are in their 20s and 30s, and it
becomes common after 40 years of age.
 With or without surgery, atrial arrhythmias (flutter or fibrillation)
may occur in adults. The incidence of atrial arrhythmias increases
to as high as 13% in patients older than 40 years of age.
 Infective endocarditis does not occur in patients with isolated
ASDs.
 Cerebrovascular accident, resulting from paradoxical embolization
through an ASD, is a rare complication.

Ostium Secundum ASD:
Location:
• This defect is present at
the site of fossa ovalis.
• Secundum ASDs may
be single or multiple
(fenestrated atrial septum).

Associations:
• Partial anomalous pulmonary venous return
• Pulmonary valvular stenosis
• VSD
• Pulmonary artery branch stenosis
• Persistent left superior vena cava
• Mitral valve prolapse and insufficiency
• Holt-Oram syndrome

Ostium primumASD
Location:
• In the lower portion of the
atrial septum and overlies
the mitral and tricuspid
valves.

Associations:
Isolated ostium primum ASD occurs in about 15% of all
ASDs.
Other defects include-
• Ostium primum defects with clefts in the anterior
mitral and septal tricuspid valve leaflets and
• Small ventricular septal defects.

Sinus venosus ASD
Location:
• It is most commonly
located at the entry of the
SVC into the RA (superior
vena caval type) and
• rarely at the entry of the
IVC into the RA (inferior
vena caval type).

Associations:
• The superior vena caval type is very commonly
associated with anomalous drainage of the right
upper pulmonary vein (into the RA), and
• The inferior vena caval type is often associated with
anomalous drainage of the right lung into the IVC
(“scimitar syndrome”)

Coronary sinus ASD
Location:
• There is a defect in the roof of the coronary sinus,
resulting in direct communication with the left atrium.
Types:
• Complete unroofing of the CS
• Partial unroofing of the CS
Associations:
• Commonly with a persistent left SVC

The Clinical Presentation:
INITIAL PRESENTATION:
Exercise intolerance with fatigue and dyspnea.
LATE PRESENTATION:
Supraventricular arrhythmias, such as atrial fibrillation
or flutter, severe irreversible pulmonary vascular disease,
and, eventually, right heart failure.
Occasionally, a paradoxical embolus causing a stroke or
transient ischemic attack (TIA) is the first clue to an ASD.

Physical findings:
 Hyperdynamic cardiac impulse, the characteristic widely
or fixed split second heart sound, and a soft systolic
murmur at the second left intercostal space due to
increased flow across the pulmonary valve.
 If the shunt is more than a shunt fraction (Qp/Qs) of
2.5:1, there may be a diastolic murmur secondary to
increased flow across the tricuspid valve.

Auscultation:
• Wide, fixed splitting of the second heart sound (S2).
• A systolic ejection murmur best heard at the left upper sternal
border.
• A short, rumbling mid-diastolic murmur is often audible at the
lower left sternal border.

 ECG:
Secundum ASD:
 RSR’ pattern in lead V1
 QRS duration < 0.11 seconds (Incomplete right bundle branch
block)
 Right-axis deviation
 RV hypertrophy
 First-degree AV block (20%)
 RA enlargement (about 50%) with a prominent P wave in lead II
Primum ASD:
 RSR’ pattern in lead V1
 Left-axis deviation
 First-degree AV block, classically seen with right bundle branch
block and left anterior fascicular block.

CXR Findings
 Cardiomegaly
 RA enlargement
 RV enlargement
 Full pulmonary conus
 Increased pulmonary
vascular markings
 Plethoric lung fields

Echocardiography
A 2D echocardiographic study is diagnostic. The study shows
the position as well as the size of the defect, which can best be
seen in the subcostal four chamber view.
A. The SVC type of sinus venosus defect shows a defect in the
posterosuperior atrial septum.
B. In secundum ASD, a dropout can be seen in the midatrial
septum.
C. The primum type shows a defect in the lower atrial septum.

Subcostal Sagittal:
The subxiphoid sagittal TTE view is acquired by turning the
transducer 90 clockwise from the frontal view. This view can be
used to measure the rim from the defect to the SVC and IVC
and is an excellent window to image a sinus venosus type
defect.

Apical Four-Chamber :
This view is used to assess the hemodynamic consequences of
ASDs, such as RA and RV dilation, and to estimate RV
pressure using the tricuspid valve regurgitant jet velocity.

Parasternal Short-Axis
This view is ideal to identify the aortic rim of the defect. It
also highlights the posterior rim (or lack thereof) in sinus
venosus and posteroinferior secundum defects.

Left Anterior Oblique.
Ideal to identify ostium primum ASDs and for assessment
of coronary sinus dilation

Cardiac catheterization
Typically not required for diagnostic purposes except to
assess pulmonary pressures and resistance or as part of a
planned transcatheter device closure.
Oximetry measurements:
Oximetry samples obtained during catheterization
demonstrate a step-up within the right atrium due to
shunting across the defect.

Hemodynamic assessment:
 An important assessment is comparison of pulmonary artery
pressure with systemic pressure and measurement of
pulmonary vascular resistance. If pulmonary pressures are
elevated, the response to oxygen or other vasodilators
should be assessed. Alternatively, the ASD can be balloon
occluded with assessment of hemodynamics to ensure that
closure is safe.

Management Strategies:
 Patients with small shunts and normal RV size are
generally asymtomatic and require routine follow up for
assessment of symptoms specially arrythmias and
possible paradoxical embolic events.
 A repeat echocardiogram should be obtained every 2/3
year to assess RV size and function and pulmonary
pressure.
 Congestive symptoms may be improved with standard
diuretic therapy.
 Atrial arrythmias should be treated to restore and
maintain sinus rhythm.

Indication for closure of ASD:
 Small ASD’s with a diametre of less than 5mm and no
evidence of RV volume overload may not require closure
unless associated with paradoxical embolism.
 If there is hemodynamically significant shunt.
(Qp/Qs ≥ 1.5:1)
 Closure of an ASD either percutaneously or surgically is
indicated for RA & RV enlargement with or without
symptoms.(Class I )
 A sinus venosus, coronary sinus, or primum ASD should be
repaired surgically rather than by percutaneous closure.

Contraindications:
Defect is too small to be hemodynamically significant.
Pulmonary vascular resistance more than one-half of the
systemic vascular resistance or an indexed pulmonary
vascular resistance > 7 Wood units/m2.
Severe LV dysfunction, where ASD is acting as a “pop-off”
valve for the left ventricle.
In most cases where ASD is diagnosed in pregnancy,
closure can be postponed until 6 months after delivery.

Transcatheter closure.
 Any patient with an isolated secundum ASD may be
suitable for transcatheter closure.
 In the United States, currently only the Amplatzer septal
occluder and Helex septal occluder are approved for
secundum ASD closure.
 The use of the closure device may be indicated to close a
secundum ASD measuring ≥ 5 mm in diameter (but less
than 32 mm for Amplatzer device and less than 18 mm
for Helex device)

The Amplatzer Septal Occluder
 The Amplatzer device consists of two disks made of
Nitinol wire mesh filled with polyester fabric and
separated by a narrower waist, which is appropriately
fitted by balloon sizing.

The Helex Septal Occluder
The Helex device is also disk like and consists of
expanded polytetrafluoroethylene (ePTFE) patch
material supported by a single Nitinol wire frame.

 There must be enough rim (4
mm) of septal tissue around
the defect for appropriate
placement of the device.
 The defect must be located
centrally with adequate room
for the device to be
positioned, without
interference of other
intracardiac structures such as
the AV valves, coronary sinus,
or pulmonary veins.

Complications of Device Closure:
 Device mal-alignment/embolization
 Device erosion of the atrial wall or aorta
 Device impingement on adjacent structures AV valve,
Coronary sinus, SVC, Pulmonary veins, Aorta
 Infection including endocarditis
 Thromboembolic Complication
 Allergic reaction
 Valvular regurgitation
 Residual shunt

Post-device Closure Follow-up
 Aspirin and clopidogrel, is prescribed for a minimum of 6
months, after that time device will be endothelialized.
 Postprocedure echocardiographic studies to check for a
residual atrial shunt and unobstructed flow of pulmonary
veins, coronary sinus, and venae cavae, and proper
function of the mitral and tricuspid valves.
 If 1-month and 1-year follow-up echocardiographic
findings are normal then yearly follow-up will suffice.

Indications:
 When device closure is not considered appropriate.
 Treatment of choice for ostium primum and sinus
venosus type defects.
 Patients with secundum ASDs and anatomy that is not
amenable to percutaneous closure:
 ASD diameter > 35 mm
 Inadequate septal rims to permit device deployment
 Close proximity to AV valves, coronary sinus, or
venae cavae are also candidates for open surgical
closure.

Timing for Surgery:
 Surgery is usually delayed until 2 to 4 years of age
because the possibility of spontaneous closure
exists.
 If CHF does not respond to medical management,
surgery is performed during infancy (if device
closure is considered inappropriate)

Procedure:
 Secundum ASD can be closed by primary suture
or, if needed, by the use of an glutaraldehyde
treated autologous pericardial or synthetic patch.

 Ostium primum defects require patch
closure as well as repair of the cleft mitral
valve.

 Sinus venosus defects
is technically more
challenging, as the
pulmonary veins often
have anomalous
drainage and require
rerouting.

Follow Up:
 Occasionally, sick sinus syndrome, which
occurs especially after the repair of a
sinus venosus defect, may require
antiarrhythmic drugs, pacemaker therapy,
or both.

Associated malformations presents in 30% of cases:
Secundum ASD
● Pulmonic stenosis
● Mitral valve prolapse
● Partial anomalous pulmonary venous connection
Primum ASD
● Cleft mitral valve
● Discrete subaortic stenosis
Sinus Venosus septal defect
● Partial anomalous pulmonary venous return
Coronary Sinus septal defect
● Partial and total anomalous pulmonary venous return
● Persistent left superior vena cava

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