atrial septal defect wiki

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Atrial septal defect

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"PFO" redirects here. For the airport, seePaphos International Airport.

Atrial septal defect

Classification and external resources

Heart of human embryo of about thirty-five days

ICD-10 Q21.1

ICD-9 745.5-745.6

OMIM 108800

DiseasesDB 1089

eMedicine med/3519

MeSH C14.240.400.560.375
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This article's introductory sectionmay be tootechnical for most readers tounderstand. Please helpimprove this article to make it understandable to non-experts,

without removing the technical details. The talk page may contain suggestions. (January2009)

Atrial septal defect (ASD) is a form ofcongenital heart defectthat enables blood flow betweenthe left and right atria via the interatrial septum. The interatrial septum is the tissue that divides

the rightand left atria. Without this septum, or if there is a defect in this septum, it is possible forblood to travel from the left side of the heart to the right side of the heart, or vice versa.[1] This

results in the mixing of arterial and venous blood, which may or may not be clinically

significant. This mixture of blood may or may not result in what is known as a "shunt". Theamount of shunting present, if any, dictates hemodynamic significance (see Pathophysiology

below). A "right-to-left-shunt" typically poses the more dangerous scenario (see

Pathophysiology below).

The right side of the heart contains venous blood with a low oxygen content, and the left side of

the heart contains arterialblood with a high oxygen content. A normal heart has an interatrialseptum that prevents oxygen-rich blood and oxygen-deficient blood from mixing together.

During development of the fetus, the interatrial septum develops to separate the left and right

atrium. However, theforamen ovale ( /fr em n ovli /) allows blood from the

right atrium to the left atrium during fetal development. This opening allows blood to bypass thenonfunctional fetal lungs when the fetus obtains its oxygen from theplacenta. 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 pulmonary circulatory system drops, thus causing the foramen ovale toclose entirely. In approximately 25% of adults,[2] the foramen ovale does not entirely seal.[3] In

this case, elevation of pressure in the pulmonary circulatory system (i.e.:pulmonary

hypertension due to various causes, or transiently during acough) can cause the foramen ovale toremain open. This is known as a patent foramen ovale (PFO).

Contents

[hide]

1 Pathophysiology

2 Epidemiology

3 Types of atrial septal defects

o 3.1 Ostium secundum atrial septal defect

3.1.1 Natural history 3.1.2 Patent foramen ovale

o 3.2 Ostium primum atrial septal defect

o 3.3 Sinus venosus atrial septal defect

o 3.4 Common or single atrium

o 3.5 Mixed Atrial septal defect

4 Diagnosis
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o 4.1 Diagnosis in children

o 4.2 Diagnosis in adults

4.2.1 Physical exam auscultation of the heart

4.2.2 Echocardiography

4.2.3 Transcranial Doppler (TCD) Bubble

study 4.2.4 Electrocardiogram

5 Treatment

o 5.1 Evaluation prior to correction

o 5.2 Catheter Procedure

o 5.3 Surgical ASD closure

o 5.4 Percutaneous ASD closure

6 Associated conditions

o 6.1 Decompression sickness

o 6.2 Paradoxical emboli

o 6.3 Migraine

o 6.4 Viral Meningitis 7 See also

8 External links

9 References

[edit] 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 produceenough pressure to pump blood throughout the entire body, while the right ventricle only has 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-rightshunt, blood will shunt from the left atriumto 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,
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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 ventriclecan 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 theaortic valve during ventricularsystole, and coronary artery diseasewhich increases the stiffness of the left ventricle, thereby increasing the filling pressure of the

left ventricle during ventriculardiastole.

The right ventricle will have to push out more blood than the left ventricle due to the left-to-right

shunt. This constant overload of the right side of the heart will cause an overload of the entire

pulmonary vasculature. Eventuallypulmonary hypertension may develop.

The pulmonary hypertension will cause the right ventricle to face increased afterload in additionto the increasedpreloadthat the shunted blood from the left atrium to the right atrium caused.

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 systolicfunction of the right ventricle) or elevations of the right sided pressures relative to left sided

pressures.

When the pressure in the right atrium rises to the level in the left atrium, there will no longer be a

pressure gradient between these heart chambers, and the left-to-right shunt will diminish orcease.

If left uncorrected, the pressure in the right side of the heart will be greater than the left side of

the heart. This will cause the pressure in the right atrium to be higher than the pressure in the left

atrium. This will reverse the pressure gradient across the ASD, and the shunt will 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 ofcyanosis.

[edit] 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 disease that is seen in adults.[5]

The ostium secundum atrial septal defect accounts for 7% of all congenital heart lesions. Thislesion shows a female preponderance, with a male : female ratio of 1:2.[6]

[edit] Types of atrial septal defects
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Schemating drawing showing the location of different types of ASD, the view is into an opened

right atrium.HV: right ventricle; VCS: superior caval vein; VCI: inferior caval vein; 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.

[edit] Ostium secundum atrial septal defect

The ostium secundum atrial septal defect is the most common type of atrial septal defect, andcomprises 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]

[edit] Natural history

Most individuals with an uncorrected secundum ASD do not have significant symptoms through

early adulthood. About 70% develop symptoms by the time they are in their 40s. Symptoms are

typically decreased exercise tolerance, easy fatigueability,palpitations, and syncope.

Complications of an uncorrected secundum ASD includepulmonary hypertension, right-sidedheart failure,atrial fibrillationorflutter, stroke, andEisenmenger's syndrome.

While pulmonary hypertension is unusual before 20 years of age, it is seen in 50% of individuals

above the age of 40. Progression to Eisenmenger's syndrome occurs in 5 to 10% of individuals

late in the disease process.
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[edit] Patent foramen ovale

A patent foramen ovale (PFO) is a small channel that has little hemodynamic consequence; it

is a remnant of the fetalforamen ovale. Clinically it is linked to decompression sickness,paradoxical embolism andmigraine. 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 ischemiaattacks (TIAs) without any other potential cause. Some data suggested that PFOs may be

involved in the pathogenesis of some migraine headaches.[citation needed] Several clinical trials are

currently underway to investigate the role of PFO in these clinical situations. [citation needed]

[edit] 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,[8] but it ismore commonly classified as an atrioventricular septal defect.[9][10]

[edit] Sinus venosus atrial septal defect

A sinus venosus ASD is a type of atrial septum defect in which the defect in the septuminvolves 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-sidedpulmonary veins into theright atrium (instead of the normal drainage of the pulmonary veins into the left atrium).[11]

Ultrasound picture of the heart, seen in asubcostal view. The apex towards the right, atria tothe 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.

[edit] Common or single atrium
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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.[12]

[edit] 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]

[edit] Diagnosis

[edit] Diagnosis in children

Most individuals with a significant ASD are diagnosed in utero or in early childhood with

the use ofultrasonography orauscultation of theheart sounds duringphysical examination.

[edit] Diagnosis in adults

Some individuals with an ASD will have undergone surgical correction of their ASD duringchildhood. 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, orcerebrovascularaccident (stroke). They may be noted on routine testing to have an abnormalchest x-ray or

an abnormal ECG and may haveatrial fibrillation.

[edit] Physical exam auscultation of the heart

The physical findings in an adult with an ASD include those related directly to theintracardiac shunt, and those that are secondary to the right heart failure that may be present

in these individuals.

Upon auscultation of theheart sounds, there may be an ejection systolic murmurthat is

attributed to the pulmonic valve. This is due to the increased flow of blood through thepulmonic 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 causesincreased 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 ventricularsystole. This

causes a normal delay in the P2 component of S2. During expiration, the positive intrathoracic
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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 getsequalized 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 splittingof S2. Thus, S2 is split to the same degree during inspiration as expiration, and is said to be

fixed.

[edit] 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 specialcatheters 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 theechocardiogram 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.

[edit] Transcranial Doppler (TCD) Bubble study

A less invasive method for detecting a PFO or other ASDs than transesophagal ultrasound is

Transcranial Doppler with bubble contrast.[13] This method reveals the cerebral impact of the

ASD or PFO.

[edit] Electrocardiogram
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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 atriathat 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 theAV node.[14]

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 theQRS 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 RBBB (Right Bundle BranchBlock). In fact this finding is so characteristic that if it is absent, the diagnosis of ASD

should be revised.

[edit] Treatment

Once someone is found to have an atrial septal defect, a determination of whether it shouldbe 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 40mmHg.

IfEisenmenger's syndrome has occurred, there is significant risk of mortality regardless ofthe 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 hassuddenly 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-matchedpopulation). 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 andpreventing the progression of pulmonary hypertension.

Methods of closure of an ASD include surgical closure and percutaneous closure.

[edit] 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
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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 heartcatheterization. This involves placing a catheter in the venous system of the heart and

measuring pressures and oxygen saturations in theSVC, 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 (includingNYHAfunctional 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, thereshould 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.)

[edit] Catheter Procedure

Until the early 1990s, surgery was the usual method for closing all ASDs. Now, thanks tomedical 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 (athin, 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 holebetween 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 toreplace the closure device as the child grows.Doctors often use echocardiography (echo) or

transesophageal (tranz-ih-sof-uh-JEE-ul) echo (TEE) as well as angiography (an-jee-OG-ra-fee) 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 thansurgery 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 children having this

procedure is excellent. Closures are successful in more than 9 out of 10 patients, with nosignificant leakage. Rarely, a defect is too large for catheter closure and surgery is needed.

[edit] Surgical ASD closure

Surgical closure of an ASD involves opening up at least oneatrium and closing the defectwith a patch under direct visualization.

[edit] Percutaneous ASD closure
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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 theSVC, IVC, or the tricuspidormitral valves. The AmplatzerSeptalOccluder (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 0.0040.005 Nitinol

wire mesh filled with Dacron fabric. Implantation of the device is relatively easy. Theprevalence 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.[15]

[edit] Associated conditions

Due to the communication between the atria that occurs in ASDs, disease entities or

complications from the condition, are possible.

[edit] Decompression sickness

ASDs, and particularly PFOs, are a predisposing risk factor fordecompression sickness in

divers because a proportion of venous blood carrying inert gases, such as helium ornitrogendoes not pass through the lungs.[16][17] 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 ismore likely to form large bubbles in the arterial blood stream causing decompression

sickness.

[edit] Paradoxical emboli

Venous thrombi (clots in theveins) are quite common. Embolization (dislodgement of

thrombi) normally go to the lung and causepulmonary emboli. In an individual with ASD,

these emboli can potentially enter the arterial system. This can cause any phenomenon that isattributed to acute loss of blood to a portion of the body, including cerebrovascular accident

(stroke), infarction of the spleen orintestines, or even a distal extremity .......(i.e.: finger or

toe).

This is known as aparadoxicalembolus because the clot material paradoxially enters thearterial system instead of going to the lungs.

[edit] Migraine

Main article:Migraine surgery#Patent foramen ovale closure

Some recent research has suggested that a proportion of cases ofmigraine may be caused by

patent foramen ovale. While the exact mechanism remains unclear, closure of a PFO can
http://en.wikipedia.org/wiki/Superior_vena_cavahttp://en.wikipedia.org/wiki/Superior_vena_cavahttp://en.wikipedia.org/wiki/Inferior_vena_cavahttp://en.wikipedia.org/wiki/Tricuspid_valvehttp://en.wikipedia.org/wiki/Tricuspid_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Kurt_Amplatzhttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-14http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-14http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=23http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=24http://en.wikipedia.org/wiki/Decompression_sicknesshttp://en.wikipedia.org/wiki/Decompression_sicknesshttp://en.wikipedia.org/wiki/Heliumhttp://en.wikipedia.org/wiki/Nitrogenhttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-15http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-16http://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=25http://en.wikipedia.org/wiki/Thrombushttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Cerebrovascular_accidenthttp://en.wikipedia.org/wiki/Spleenhttp://en.wikipedia.org/wiki/Intestinehttp://en.wikipedia.org/wiki/Intestinehttp://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=26http://en.wikipedia.org/wiki/Migraine_surgery#Patent_foramen_ovale_closurehttp://en.wikipedia.org/wiki/Migrainehttp://en.wikipedia.org/wiki/Migrainehttp://en.wikipedia.org/wiki/Superior_vena_cavahttp://en.wikipedia.org/wiki/Inferior_vena_cavahttp://en.wikipedia.org/wiki/Tricuspid_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Kurt_Amplatzhttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-14http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=23http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=24http://en.wikipedia.org/wiki/Decompression_sicknesshttp://en.wikipedia.org/wiki/Heliumhttp://en.wikipedia.org/wiki/Nitrogenhttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-15http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-16http://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=25http://en.wikipedia.org/wiki/Thrombushttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Cerebrovascular_accidenthttp://en.wikipedia.org/wiki/Spleenhttp://en.wikipedia.org/wiki/Intestinehttp://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=26http://en.wikipedia.org/wiki/Migraine_surgery#Patent_foramen_ovale_closurehttp://en.wikipedia.org/wiki/Migraine


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reduce symptoms in certain cases.[18][19] 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, theplacebo effect in migraine typically averages around40%. 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 migrainepatients was confirmed, but migraine headache cessation was not more prevalent in the

group of migraine patients that underwent closure of their patent foramen ovale.[20]

[edit] Viral Meningitis

It's likely that a virus can pass through PFO, therefore not being filtered by the lungs, and

sent directly to the brain. This can cause a type ofsinusitis which can lead to viralmeningitis. (This claims requires supporting evidence)
http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-17http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-18http://en.wikipedia.org/wiki/Placebo_effecthttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-19http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=27http://en.wikipedia.org/wiki/Sinusitishttp://en.wikipedia.org/wiki/Sinusitishttp://en.wikipedia.org/wiki/Viral_meningitishttp://en.wikipedia.org/wiki/Viral_meningitishttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-17http://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-18http://en.wikipedia.org/wiki/Placebo_effecthttp://en.wikipedia.org/wiki/Atrial_septal_defect#cite_note-19http://en.wikipedia.org/w/index.php?title=Atrial_septal_defect&action=edit&section=27http://en.wikipedia.org/wiki/Sinusitishttp://en.wikipedia.org/wiki/Viral_meningitishttp://en.wikipedia.org/wiki/Viral_meningitis

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