Atrial septal defect
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Atrial
septal defect
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Classification
and external resources
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 Heart of human embryo of about thirty-five days |
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Atrial septal defect (ASD) is a form of congenital heart defect that enables blood flow between two compartments of the
heart called the left and right atria. Normally, the right and left atria
are separated by a septum called the interatrial septum. If this septum is defective or absent, then oxygen-rich blood can flow directly from the left side of the
heart to mix with the oxygen-poor blood in the right side of the heart, or vice
versa.[1]
This can lead to lower-than-normal oxygen levels in the arterial blood that
supplies the brain, organs, and tissues. However, an ASD may not produce
noticeable signs or symptoms, especially if the defect is small.
A "shunt" is the presence
of a net flow of blood through the defect, either from left to right or right
to left. The amount of shunting present, if any, determines the hemodynamic
significance of the ASD (see Pathophysiology below). A
"right-to-left-shunt" typically poses the more dangerous scenario.
(see Pathophysiology below.)
During development of the fetus, the interatrial septum develops to separate the left and right atria.
However, a hole in the septum called the foramen
ovale (
/fɒˈreɪmən
oʊˈvɑːliː/),
allows blood from the right atrium to enter the left atrium during fetal
development. This opening allows blood to bypass the nonfunctional fetal lungs
while the fetus obtains its oxygen from the placenta. A layer
of tissue called the septum primum acts as a valve over the foramen ovale
during fetal development. After birth, the pressure in the right side of the
heart drops as the lungs open and begin working, causing the foramen ovale to
close entirely. In approximately 25% of adults,[2]
the foramen ovale does not entirely seal.[3]
In these cases, any elevation of the pressure in the pulmonary circulatory
system (due to pulmonary hypertension, temporarily while coughing, etc.) can cause the foramen ovale to remain open. This is
known as a patent foramen ovale (PFO), which is a type of atrial septal
defect.
/fɒˈreɪmən
oʊˈvɑːliː/),
allows blood from the right atrium to enter the left atrium during fetal
development. This opening allows blood to bypass the nonfunctional fetal lungs
while the fetus obtains its oxygen from the placenta. A layer
of tissue called the septum primum acts as a valve over the foramen ovale
during fetal development. After birth, the pressure in the right side of the
heart drops as the lungs open and begin working, causing the foramen ovale to
close entirely. In approximately 25% of adults,[2]
the foramen ovale does not entirely seal.[3]
In these cases, any elevation of the pressure in the pulmonary circulatory
system (due to pulmonary hypertension, temporarily while coughing, etc.) can cause the foramen ovale to remain open. This is
known as a patent foramen ovale (PFO), which is a type of atrial septal
defect.
Pathophysiology
Atrial septal defect with
left-to-right shunt
In unaffected individuals, the
chambers of the left side of the heart are under higher pressure than the
chambers of the right side of the heart. This is because the left ventricle
has to produce enough pressure to pump blood throughout the entire body, while
the right ventricle needs only to produce enough pressure to pump blood to the lungs.
In the case of a large ASD
(>9mm), which may result in a clinically remarkable left-to-right shunt,
blood will shunt from the left atrium
to the right atrium. This extra blood from the left atrium may cause a volume
overload of both the right atrium and the right ventricle.
If untreated, this condition can result in enlargement of the right side of the
heart and ultimately heart failure.[4]
Any process that increases the
pressure in the left ventricle can cause worsening of the left-to-right shunt. This
includes hypertension, which increases the pressure that the left ventricle has
to generate in order to open the aortic valve
during ventricular systole, and coronary artery disease which increases the stiffness of the left ventricle,
thereby increasing the filling pressure of the left ventricle during
ventricular diastole. The left-to-right shunt increases the filling pressure of
the right heart (preload) and forces the the right ventricle to pump out more blood
than the left ventricle. This constant overloading of the right side of the
heart will cause an overload of the entire pulmonary vasculature. Eventually, pulmonary hypertension may develop.
The pulmonary hypertension will
cause the right ventricle to face increased afterload.
The right ventricle will be forced to generate higher pressures to try to
overcome the pulmonary hypertension. This may lead to right
ventricular failure (dilatation and decreased systolic function of the right ventricle).
When the pressure in the right
atrium rises to equal the pressure in the left atrium, there is no longer a
pressure gradient between these heart chambers, and the left-to-right shunt
will diminish or cease. In other words, there is no longer a net flow of blood
across the ASD.
If the ASD is left uncorrected, the
pulmonary hypertension progresses and the pressure in the right side of the
heart will become greater than the left side of the heart. This reversal of the
pressure gradient across the ASD causes the shunt to reverse; a right-to-left
shunt will exist. This phenomenon is known as Eisenmenger's syndrome. Once right-to-left shunting occurs, a portion of the
oxygen-poor blood will get shunted to the left side of the heart and ejected to
the peripheral vascular system. This will cause signs of cyanosis.
Epidemiology
As a group, atrial septal defects
are detected in 1 child per 1500 live births. PFO are quite common (appearing
in 10–20% of adults) but asymptomatic and therefore undiagnosed. ASDs make up
30 to 40% of all congenital heart diseases that are seen in adults.[5]
The ostium secundum atrial septal
defect accounts for 7% of all congenital heart lesions. This lesion shows a
female preponderance, with a male:female ratio of 1:2.[6]
Types
of atrial septal defects
Schematic drawing showing the
location of different types of ASD, the view is into an opened right atrium. HV:
right ventricle; VCS: superior vena cava; VCI: inferior vena
cava; 1: upper sinus venosus defect; 2: lower sinus venosus
defect; 3: secundum defect; 4: defect involving coronary sinus; 5;
primum defect.
There are many types of atrial
septal defects. They are differentiated from each other by whether they involve
other structures of the heart and how they are formed during the developmental
process during early fetal development.
Ostium
secundum atrial septal defect
The ostium secundum atrial septal
defect is the most common type of atrial septal defect, and comprises 6–10%
of all congenital heart diseases.
The secundum atrial septal defect
usually arises from an enlarged foramen ovale, inadequate growth of the septum secundum,
or excessive absorption of the septum primum.
Ten to twenty percent of individuals with ostium secundum ASDs also have mitral valve prolapse.[7]
If the ostium secundum ASD is
accompanied by an acquired mitral valve stenosis, that is called Lutembacher's syndrome.[8]
Natural
history
Most individuals with an uncorrected
secundum ASD do not have significant symptoms through early adulthood. More
than 70 percent develop symptoms by about 40 years of age. Symptoms are
typically decreased exercise tolerance, easy fatigueability, palpitations,
and syncope.
Complications of an uncorrected
secundum ASD include pulmonary hypertension, right-sided heart
failure, atrial fibrillation or flutter, stroke, and Eisenmenger's syndrome.
While pulmonary hypertension is
unusual before 20 years of age, it is seen in 50 percent of individuals above
the age of 40. Progression to Eisenmenger's syndrome occurs in 5 to 10 percent of individuals late in the
disease process.[8]
Patent
foramen ovale
A patent foramen ovale (PFO)
is a small channel that has some hemodynamic consequence; it is a remnant of
the fetal foramen ovale. Clinically it is linked to decompression sickness, paradoxical embolism and migraine. On
echocardiography, there may not be any shunting of blood noted except when the
patient coughs.
There is debate within the neurology
and cardiology communities about the role of a PFO in cryptogenic (i.e. of
unknown cause) neurologic events such as strokes and transient ischemia attacks
(TIAs) without any other potential cause. Data suggests that PFOs are involved
in the pathogenesis of some migraine
headaches. Several clinical trials are currently underway to investigate the
role of PFO in these clinical situations.
Ostium
primum atrial septal defect
Main article: Ostium
primum atrial septal defect
A defect in the ostium primum
is occasionally classified as an atrial septal defect,[9]
but it is more commonly classified as an atrioventricular
septal defect.[10][11]
Ostium primum defects are less common than ostium secundum defects.[12]
Sinus
venosus atrial septal defect
A sinus venosus ASD is a type of
atrial septum defect in which the defect in the septum involves the venous
inflow of either the superior vena cava or the inferior vena cava.
A sinus venosus ASD that involves
the superior vena cava makes up 2 to 3% of all interatrial communication. It is
located at the junction of the superior vena cava and the right atrium. It is
frequently associated with anomalous drainage of the right-sided pulmonary veins
into the right atrium (instead of the normal drainage of the pulmonary veins
into the left atrium).[13]
.jpg)
Ultrasound picture of the heart, seen in a subcostal
view. The apex towards the right, atria to the left. ASD secundum seen as a
discontinuation of the white band of the atrial septum. Enlarged right atrium
below. Enlarged pulmonary veins seen entering left atrium above.
Common
or single atrium
Common (or single) atrium is a
failure of development of the embryologic components that contribute to the
atrial septal complex. It is frequently associated with heterotaxy syndrome.[14]
Mixed
atrial septal defect
The inter atrial septum can be
divided in to 5 septal zones. If the defect involves 2 or more of the 5 septal
zones, then the defect is termed a mixed atrial septal defect.[4]
Diagnosis
Diagnosis
in children
Most individuals with a significant
ASD are diagnosed in utero or in early childhood with the use of ultrasonography
or auscultation of the heart sounds
during physical examination.
Diagnosis
in adults
Some individuals with an ASD will
have undergone surgical correction of their ASD during childhood. The
development of signs and symptoms due to an ASD are related to the size of the
intracardiac shunt. Individuals with a larger shunt tend to present with
symptoms at a younger age.
Adults with an uncorrected ASD will
present with symptoms of dyspnea on exertion (shortness of breath with minimal
exercise), congestive
heart failure, or cerebrovascular
accident (stroke). They may be noted on
routine testing to have an abnormal chest x-ray
or an abnormal ECG and may
have atrial fibrillation. If the ASD causes a left-to-right shunt, the pulmonary
vasculature in both lungs may appear dilated on chest x-ray, due to the
increase in pulmonary blood flow.[15]
Physical
exam auscultation of the heart
The physical findings in an adult
with an ASD include those related directly to the intracardiac shunt, and those
that are secondary to the right
heart failure that may be present in these
individuals.
Upon auscultation
of the heart sounds, there may be a systolic ejection murmur that is
attributed to the pulmonic valve. This is due to the increased flow of blood
through the pulmonic valve rather than any structural abnormality of the valve
leaflets.
In unaffected individuals, there are
respiratory variations in the splitting of the second heart sound (S2). During respiratory inspiration, the
negative intrathoracic pressure causes increased blood return into the right
side of the heart. The increased blood volume in the right ventricle causes the
pulmonic valve to stay open longer during ventricular systole. This causes a normal delay in the P2 component
of S2. During expiration, the positive intrathoracic pressure causes
decreased blood return to the right side of the heart. The reduced volume in
the right ventricle allows the pulmonic valve to close earlier at the end of
ventricular systole, causing P2 to occur earlier.
In individuals with an ASD, there is
a fixed splitting of S2. The reason that there is a fixed
splitting of the second heart sound is that the extra blood return during
inspiration gets equalized between the left and right atrium due to the
communication that exists between the atria in individuals with ASD.
The right ventricle can be thought
of as continuously overloaded because of the left to right shunt, producing a
widely split S2. Because the atria are linked via the atrial septal defect,
inspiration produces no net pressure change between them, and has no effect on
the splitting of S2. Thus, S2 is split to the same degree during inspiration as
expiration, and is said to be “fixed.”
Echocardiography
In transthoracic echocardiography,
an atrial septal defect may be seen on color flow imaging as a jet of blood
from the left atrium to the right atrium.
If agitated saline is injected into
a peripheral vein during
echocardiography, small air bubbles can be seen on echocardiographic imaging.
It may be possible to see bubbles travel across an ASD either at rest or during
a cough. (Bubbles will only flow from right atrium to left atrium if the RA
pressure is greater than LA).
Because better visualization of the
atria is achieved with transesophageal echocardiography, this test may be
performed in individuals with a suspected ASD which is not visualized on
transthoracic imaging.
Newer techniques to visualize these
defects involve intracardiac imaging with special catheters that are typically
placed in the venous system and advanced to the level of the heart. This type
of imaging is becoming more common and involves only mild sedation for the
patient typically.
If the individual has adequate
echocardiographic windows, it is possible to use the echocardiogram to measure
the cardiac output of the left ventricle and the right ventricle independently.
In this way, it is possible to estimate the shunt fraction using
echocardiograpy.
Transesophageal
Doppler (TCD) bubble study
A less invasive method for detecting
a PFO or other ASDs than transesophagal ultrasound is Transcranial Doppler with
bubble contrast.[16]
This method reveals the cerebral impact of the ASD or PFO.
Electrocardiogram
The ECG findings in atrial septal defect vary with the type of
defect the individual has. Individuals with atrial septal defects may have a
prolonged PR interval (a first
degree heart block). The prolongation of the PR
interval is probably due to the enlargement of the atria that is common in ASDs
and the increased distance due to the defect itself. Both of these can cause an
increased distance of internodal conduction from the SA node to the AV node.[17]
In addition to the PR prolongation,
individuals with a primum ASD have a left axis deviation of the QRS complex
while those with a secundum ASD have a right axis deviation of the QRS complex.
Individuals with a sinus venosus ASD exhibit a left axis deviation of the P
wave (not the QRS complex).
A common finding in the ECG is the
presence of incomplete right
bundle branch block. The presence of a right bundle
branch block is is so characteristic that if it is absent, the diagnosis of ASD
should be reconsidered.
Treatment
Once someone is found to have an
atrial septal defect, a determination of whether it should be corrected has to
be made.
Surgical mortality due to closure of
an ASD is lowest when the procedure is performed prior to the development of
significant pulmonary hypertension. The lowest mortality rates are achieved in
individuals with a pulmonary artery systolic pressure of less than 40 mmHg.
If Eisenmenger's syndrome has occurred, there is significant risk of mortality
regardless of the method of closure of the ASD. In individuals who have
developed Eisenmenger's syndrome, the pressure in the right ventricle has
raised high enough to reverse the shunt in the atria. If the ASD is then
closed, the afterload that the right ventricle has to act against has suddenly
increased. This may cause immediate right ventricular failure, since it may not
be able to pump the blood against the pulmonary hypertension.
Closure of an ASD in individuals
under age 25 has been shown to have a low risk of complications, and
individuals have a normal lifespan (comparable to a healthy age-matched
population). Closure of an ASD in individuals between the ages of 25 and 40 who
are asymptomatic but have a clinically significant shunt is controversial.
Those that perform the procedure believe that they are preventing long-term
deterioration in cardiac function and preventing the progression of pulmonary
hypertension.
Methods of closure of an ASD include
surgical closure and percutaneous closure.
Evaluation
prior to correction
Prior to correction of an ASD, an
evaluation is made of the severity of the individual's pulmonary hypertension
(If present at all) and whether it is reversible (Closure of an ASD may be
recommended for prevention purposes, to avoid such a complication in the first
place. Pulmomary hypertension is not always present in adults that are
diagnosed with an ASD in adulthood).
If pulmonary hypertension is
present, the evaluation may include a right heart catheterization. This
involves placing a catheter in the venous system of the heart and measuring
pressures and oxygen saturations in the SVC, IVC, right atrium, right ventricle,
pulmonary artery, and in the wedge position. Individuals with a pulmonary
vascular resistance (PVR) of less than 7 wood units show regression of symptoms
(including NYHA functional class).
On the other hand, individuals with a PVR of greater than 15 wood units have
increased mortality associated with closure of the ASD.
If the pulmonary arterial pressure
is more than 2/3 the systemic systolic pressure, there should be a net
left-to-right shunt of at least 1.5:1 or evidence of reversibility of the shunt
when given pulmonary artery vasodilators prior to surgery. (If Eisenmenger's
physiology has set in, it must be proven that the right-to-left shunt is
reversible with pulmonary artery vasodilators prior to surgery.)
Catheter
procedure
Until the early 1990s, surgery was
the usual method for closing all ASDs. Now, thanks to medical advances, doctors
can use catheter procedures to close secundum ASDs, the most common type of
ASD. For this procedure, the patient is given medicine so he or she will sleep
through it and not feel any pain. During the procedure, the doctor inserts a
catheter (a thin, flexible tube) into a vein in the groin (upper thigh) and
threads it to the heart's septum. The catheter has a tiny umbrella-like device
folded up inside it. When the catheter reaches the septum, the device is pushed
out of the catheter and positioned so that it plugs the hole between the atria.
The device is secured in place and the catheter is withdrawn from the body.
Within 6 months, normal tissue grows in and over the device. There is no need
to replace the closure device throughout the patient's life. Doctors often use
echocardiography (echo) or transesophageal echo (TEE) as well as angiography to
guide them in threading the catheter to the heart and closing the defect. TEE
is a special type of echo that takes pictures of the heart through the
esophagus (the passage leading from the mouth to the stomach). Catheter
procedures are much easier on patients than surgery because they involve only a
needle puncture in the skin where the catheter is inserted. This means that
recovery is faster and easier. The outlook for patients having this procedure
is excellent. Closures are successful in more than 9 out of 10 patients, with
no significant leakage. Rarely, a defect is too large for catheter closure and
surgery is needed.
Surgical
ASD closure
Surgical closure of an ASD involves
opening up at least one atrium and closing the defect with a patch under direct
visualization.
Percutaneous
ASD closure
Percutaneous closure of an ASD is
currently only indicated for the closure of secundum ASDs with a sufficient rim
of tissue around the septal defect so that the closure device does not impinge
upon the SVC, IVC, or the tricuspid
or mitral valves. The Amplatzer
Septal Occluder (ASO) is commonly used to close ASDs. The ASO consists of two
self-expandable round discs connected to each other with a 4 mm waist,
made up of 0.004–0.005´´ Nitinol wire mesh filled with Dacron fabric.
Implantation of the device is relatively easy. The prevalence of residual
defect is low. The disadvantages are a thick profile of the device and concern
related to a large amount of nitinol (a nickel-titanium compound) in the device
and consequent potential for nickel toxicity.
Percutaneous closure is the method
of choice in most centres.[18]
Complications
Due to the communication between the
atria that occurs in ASDs, disease entities or complications from the
condition, are possible. Patients with an uncorrected atrial septal defects may
be at increased risk for developing a cardiac arrhythmia, as well as more
frequent respiratory infections.[12]
Decompression
sickness
ASDs, and particularly PFOs, are a
predisposing risk factor for decompression sickness in divers because a proportion of venous blood carrying
inert gases, such as helium or nitrogen does not pass through the lungs.[19][20]
The only way to release the excess inert gases from the body is to pass the
blood carrying the inert gases through the lungs to be exhaled. If some of the inert gas-laden blood passes
through the PFO, it avoids the lungs and the inert gas is more likely to form
large bubbles in the arterial blood stream causing decompression sickness.
Eisenmenger's
syndrome
Main article: Eisenmenger's syndrome
If a net flow of blood exists from
the left atrium to the right atrium, called a left-to-right shunt, then there
is an increase in the blood flow through the lungs. Initially, this increased
blood flow is asymptomatic, but if it persists, the pulmonary blood vessels may
stiffen, causing pulmonary hypertension. The pulmonary hypertension increases
the pressures in the right side of the heart, leading to the reversal of the
shunt into a right-to-left shunt. Once the reversal of the shunt occurs, and
the blood begins flowing in the opposite direction through the ASD, that is
called Eisenmenger's syndrome. The syndrome is a rare and late complication of
an ASD.
Paradoxical
emboli
Venous thrombi (clots in
the veins) are
quite common. Embolization (dislodgement of thrombi) normally go to the lung
and cause pulmonary emboli. In an individual with ASD, these emboli can potentially
enter the arterial system. This can cause any phenomenon that is attributed to
acute loss of blood to a portion of the body, including cerebrovascular
accident (stroke), infarction of the spleen or intestines, or even a distal extremity ... (i.e., finger or toe).
This is known as a paradoxical
embolus because the clot material paradoxially enters the arterial system
instead of going to the lungs.
Migraine
Main article: Migraine surgery#Patent foramen
ovale closure
Some recent research has suggested
that a proportion of cases of migraine may be
caused by patent foramen ovale. While the exact mechanism remains unclear,
closure of a PFO can reduce symptoms in certain cases.[21][22]
This remains controversial. 20% of the general population have a PFO, which for
the most part, is asymptomatic. 20% of the female population have migraines.
And, the placebo effect in migraine typically averages around 40%. The high
frequency of these facts makes statistically significant relationships between
PFO and migraine difficult (i.e., the relationship may just be chance or
coincidence). In a large randomized controlled trial the higher prevalence of
patent foramen ovale in migraine patients was confirmed, but migraine headache
cessation was not more prevalent in the group of migraine patients that
underwent closure of their patent foramen ovale.[23]
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