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Atrial septal defect
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Atrial septal defect

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Heart of human embryo of about thirty-five days







However.240. (see Pathophysiology below. determines the hemodynamic significance of the ASD (see Pathophysiology below). which is a type of atrial septal defect.560. allows blood from the right atrium to enter the left atrium during fetal development.400.375 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. After birth. causing the foramen ovale to close entirely. This is known as a patent foramen ovale (PFO). If this septum is defective or absent.) can cause the foramen ovale to remain open. etc. In approximately 25% of adults. This opening allows blood to bypass the nonfunctional fetal lungs while the fetus obtains its oxygen from the placenta. the right and left atria are separated by a septum called the interatrial septum. Normally. Contents [hide]    1 Pathophysiology 2 Epidemiology 3 Genetic research . the interatrial septum develops to separate the left and right atria. an ASD may not produce noticeable signs or symptoms. either from left to right or right to left. the pressure in the right side of the heart drops as the lungs open and begin working. A layer of tissue called the septum primum acts as a valve over the foramen ovale during fetal development.DiseasesDB 1089 MedlinePlus 000157 eMedicine med/3519 article/894813 MeSH C14.[2] the foramen ovale does not entirely seal. a hole in the septum called the foramen ovale /fɒˈreɪmən oʊˈvɑːliː/. especially if the defect is small.[1] This can lead to lower-than-normal oxygen levels in the arterial blood that supplies the brain. A "shunt" is the presence of a net flow of blood through the defect. However. organs.) During development of the fetus. temporarily while coughing. or vice versa. and tissues. if any. 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.[3] In these cases. any elevation of the pressure in the pulmonary circulatory system (due to pulmonary hypertension. A "right-to-left-shunt" typically poses the more dangerous scenario. The amount of shunting present.

2 Catheter procedure 6.5 Mixed atrial septal defect 5 Diagnosis o o 5.3 Paradoxical emboli 7.1 Physical exam auscultation of the heart 5.1.2 Eisenmenger's syndrome 7.1 Evaluation prior to correction 6.4 Electrocardiogram 6 Treatment o o o o  6. 4 Types of atrial septal defects o 4.4 Migraine 8 Associated conditions 9 See also 10 References o  10.2 Diagnosis in adults      5.4 Percutaneous ASD closure 7 Complications o o o o    Sinus venosus atrial septal defect 4.1 Diagnosis in children 5.1 Natural history 4.2 Echocardiography 5.1 Additional references 11 External links .4 Common or single atrium 4.3 Transcranial Doppler (TCD) bubble study 5.2.1 Ostium secundum atrial septal defect   o o o o  4.1 Decompression sickness 7.3 Surgical ASD closure Patent foramen ovale 4.2 Ostium primum atrial septal defect 4.

thereby increasing the filling pressure of the left ventricle during ventricular diastole. The pulmonary hypertension will cause the right ventricle to face increased afterload. This constant overloading of the right side of the heart will cause an overload of the entire pulmonary vasculature. This extra blood from the left atrium may cause a volume overload of both the right atrium and the right ventricle. 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. This includes hypertension. The left-to-right shunt increases the filling pressure of the right heart (preload) and forces the right ventricle to pump out more blood than the left ventricle. and the left-to-right shunt will diminish or cease. and coronary artery diseasewhich increases the stiffness of the left ventricle. blood will shunt from the left atrium to the right atrium.Pathophysiology[edit source | editbeta] Atrial septal defect with left-to-right shunt In unaffected individuals.[4] Any process that increases the pressure in the left ventricle can cause worsening of the left-to-right shunt. . In other words. This may lead to right ventricular failure (dilatation and decreased systolic function of the right ventricle). this condition can result in enlargement of the right side of the heart and ultimately heart failure. Eventually. there is no longer a pressure gradient between these heart chambers. there is no longer a net flow of blood across the ASD. the chambers of the left side of the heart are under higher pressure than the chambers of the right side of the heart. which may result in a clinically remarkable left-to-right shunt. The right ventricle will be forced to generate higher pressures to try to overcome the pulmonary hypertension. which increases the pressure that the left ventricle has to generate in order to open the aortic valve during ventricular systole. pulmonary hypertensionmay develop. In the case of a large ASD (>9mm). When the pressure in the right atrium rises to equal the pressure in the left atrium. If untreated.

[6] Genetic research[edit source | editbeta] In May 2013 team of researchers led by Professor Bernard Keavney of British Heart Foundation (BHF) discovered a new gene associated with the disease. According to them a common genetic variation near a gene called MSX1 is strongly associated with the risk of an ASD and this discovery of the particular gene is an important step forward as it will lead to better understanding of why some patients are born with ASD.[5] The ostium secundum atrial septal defect accounts for 7% of all congenital heart lesions. a right-to-left shunt will exist. Epidemiology[edit source | editbeta] As a group. This reversal of the pressure gradient across the ASD causes the shunt to reverse.[7] Types of atrial septal defects[edit source | editbeta] . the pulmonary hypertension progresses and the pressure in the right side of the heart will become greater than the left side of the heart. 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.If the ASD is left uncorrected. atrial septal defects are detected in 1 child per 1500 live births. This will cause signs of cyanosis. 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 phenomenon is known as Eisenmenger's syndrome. with a male:female ratio of 1:2. This lesion shows a female preponderance. Once right-to-left shunting occurs.

it is seen in 50 percent of individuals above the age of 40. easy fatigueability. of unknown cause) neurologic events such as strokes and transient ischemia attacks (TIAs) without any other potential cause. Symptoms are typically decreased exercise tolerance. or excessive absorption of the septum primum.Schematic drawing showing the location of different types of ASD. Progression to Eisenmenger's syndrome occurs in 5 to 10 percent of individuals late in the disease process. there may not be any shunting of blood noted except when the patient coughs. Some data suggested that PFOs may be involved in the pathogenesis of . the view is into an opened right atrium. VCI: inferior vena cava. 3: secundum defect.[9] Natural history[edit source | editbeta] Most individuals with an uncorrected secundum ASD do not have significant symptoms through early adulthood. 5. 4: defect involving coronary sinus. 1: upper sinus venosus defect. The secundum atrial septal defect usually arises from an enlarged foramen ovale. There are many types of atrial septal defects. 2: lower sinus venosus defect. paradoxical embolism and migraine.[9] Patent foramen ovale[edit source | editbeta] A patent foramen ovale (PFO) is a small channel that has some hemodynamic consequence. There is debate within the neurology and cardiology communities about the role of a PFO in cryptogenic (i. it is a remnant of the fetal foramen ovale.palpitations. On echocardiography.e. 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. stroke. primum defect. Ten to twenty percent of individuals with ostium secundum ASDs also have mitral valve prolapse. inadequate growth of the septum secundum. and Eisenmenger's syndrome. VCS: superior vena cava. atrial fibrillation orflutter. Ostium secundum atrial septal defect[edit source | editbeta] The ostium secundum atrial septal defect is the most common type of atrial septal defect. Clinically it is linked to decompression sickness. that is called Lutembacher's syndrome.[8] If the ostium secundum ASD is accompanied by an acquired mitral valve stenosis. HV: right ventricle. and syncope. More than 70 percent develop symptoms by about 40 years of age. and comprises 6– 10% of all congenital heart diseases. Complications of an uncorrected secundum ASD include pulmonary hypertension. right-sided heart failure. While pulmonary hypertension is unusual before 20 years of age.

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).[14] Ultrasound picture of the heart.[11][12] Ostium primum defects are less common than ostium secundum defects.some migraine headaches. If the defect involves 2 or more of the 5 septal zones. Enlarged right atrium below. seen in asubcostal view. Common or single atrium[edit source | editbeta] Common (or single) atrium is a failure of development of the embryologic components that contribute to the atrial septal complex.[15] Mixed atrial septal defect[edit source | editbeta] The inter atrial septum can be divided into 5 septal zones.[4] .[13] Sinus venosus atrial septal defect[edit source | editbeta] 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. It is frequently associated with heterotaxy syndrome. atria to the left. 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. then the defect is termed a mixed atrial septal defect.[citation needed][dubious – discuss] Several clinical trials are currently underway to investigate the role of PFO in these clinical situations.[citation needed] Ostium primum atrial septal defect[edit source | editbeta] Main article: Ostium primum atrial septal defect A defect in the ostium primum is occasionally classified as an atrial septal defect. ASD secundum seen as a discontinuation of the white band of the atrial septum. Enlarged pulmonary veins seen entering left atrium above. The apex towards the right.[10] but it is more commonly classified as an atrioventricular septal defect.

In unaffected individuals. there is a fixed splitting of S2. and those that are secondary to the right heart failure that may be present in these individuals. Because the atria are linked via the atrial septal defect. there are respiratory variations in the splitting of the second heart sound (S2). the pulmonary vasculature in both lungs may appear dilated on chest x-ray. Individuals with a larger shunt tend to present with symptoms at a younger age.Diagnosis[edit source | editbeta] Diagnosis in children[edit source | editbeta] 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. This causes a normal delay in the P2 component of S2. The development of signs and symptoms due to an ASD are related to the size of the intracardiac shunt. In individuals with an ASD. The right ventricle can be thought of as continuously overloaded because of the left to right shunt. Adults with an uncorrected ASD will present with symptoms of dyspnea on exertion (shortness of breath with minimal exercise).[16] Physical exam auscultation of the heart[edit source | editbeta] The physical findings in an adult with an ASD include those related directly to the intracardiac shunt. there may be a systolic ejection murmur that is attributed to the pulmonic valve. During respiratory inspiration. due to the increase in pulmonary blood flow. causing P2 to occur earlier. inspiration produces . Diagnosis in adults[edit source | editbeta] Some individuals with an ASD will have undergone surgical correction of their ASD during childhood. Upon auscultation of the heart sounds. the negative intrathoracic pressure causes increased blood return into the right side of the heart. 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 increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during ventricular systole. During expiration. or cerebrovascular accident (stroke). producing a widely split S2. congestive heart failure. the positive intrathoracic pressure causes decreased blood return to the right side of the heart. 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 reduced volume in the right ventricle allows the pulmonic valve to close earlier at the end of ventricular systole. This is due to the increased flow of blood through the pulmonic valve rather than any structural abnormality of the valve leaflets.

[18] In addition to the PR prolongation. A common finding in the ECG is the presence of incomplete right bundle branch block. If the individual has adequate echocardiographic windows. Electrocardiogram[edit source | editbeta] The ECG findings in atrial septal defect vary with the type of defect the individual has. Transcranial Doppler (TCD) bubble study[edit source | editbeta] A less invasive method for detecting a PFO or other ASDs than transesophagal ultrasound is Transcranial Doppler with bubble contrast. and has no effect on the splitting of S2. an atrial septal defect may be seen on color flow imaging as a jet of blood from the left atrium to the right atrium. Because better visualization of the atria is achieved with transesophageal echocardiography. Individuals with a sinus venosus ASD exhibit a left axis deviation of the P wave (not the QRS complex). 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. 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. (Bubbles will only flow from right atrium to left atrium if the RA pressure is greater than LA). Individuals with atrial septal defects may have a prolonged PR interval (a first degree heart block). Both of these can cause an increased distance of internodal conduction from the SA node to the AV node. .[17] This method reveals the cerebral impact of the ASD or PFO. This type of imaging is becoming more common and involves only mild sedation for the patient typically. If agitated saline is injected into a peripheral vein during echocardiography. small air bubbles can be seen on echocardiographic imaging. 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. The presence of a right bundle branch block is so characteristic that if it is absent. it is possible to estimate the shunt fraction using echocardiograpy. it is possible to use the echocardiogram to measure the cardiac output of the left ventricle and the right ventricle independently. It may be possible to see bubbles travel across an ASD either at rest or during a cough. and is said to be “fixed. the diagnosis of ASD should be reconsidered. this test may be performed in individuals with a suspected ASD which is not visualized on transthoracic net pressure change between them. Thus. S2 is split to the same degree during inspiration as expiration. In this way.” Echocardiography[edit source | editbeta] In transthoracic echocardiography.

and individuals have a normal lifespan (comparable to a healthy age-matched population). there is significant risk of mortality regardless of the method of closure of the ASD. it must be proven that the right-to-left shunt is reversible with pulmonary artery vasodilators prior to surgery. the afterload that the right ventricle has to act against has suddenly increased. the evaluation may include a right heart catheterization. Individuals with a pulmonary vascular resistance (PVR) of less than 7 wood units show regression of symptoms (including NYHA functional class). If pulmonary hypertension is present. Evaluation prior to correction[edit source | editbeta] Prior to correction of an ASD. right ventricle. Methods of closure of an ASD include surgical closure and percutaneous closure. there should be a net left-to-right shunt of at least 1. Closure of an ASD in individuals between the ages of 25 and 40 who are asymptomatic but have a clinically significant shunt is controversial. individuals with a PVR of greater than 15 wood units have increased mortality associated with closure of the ASD. Pulmonary hypertension is not always present in adults that are diagnosed with an ASD in adulthood). since it may not be able to pump the blood against the pulmonary hypertension. If the pulmonary arterial pressure is more than 2/3 the systemic systolic pressure. Closure of an ASD in individuals under age 25 has been shown to have a low risk of complications. a determination of whether it should be corrected has to be made. to avoid such a complication in the first place. On the other hand. The lowest mortality rates are achieved in individuals with a pulmonary artery systolic pressure of less than 40 mmHg. In individuals who have developed Eisenmenger's syndrome. IVC. and in the wedge position. This may cause immediate right ventricular failure. (If Eisenmenger's physiology has set in. the pressure in the right ventricle has raised high enough to reverse the shunt in the atria.Treatment[edit source | editbeta] Once someone is found to have an atrial septal defect. This involves placing a catheter in the venous system of the heart and measuring pressures and oxygen saturations in the SVC. 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.) . pulmonary artery.5:1 or evidence of reversibility of the shunt when given pulmonary artery vasodilators prior to surgery. Those that perform the procedure believe that they are preventing long-term deterioration in cardiac function and preventing the progression of pulmonary hypertension. Surgical mortality due to closure of an ASD is lowest when the procedure is performed prior to the development of significant pulmonary hypertension. If the ASD is then closed. right atrium. If Eisenmenger's syndrome has occurred.

Percutaneous closure is the method of choice in most centres. 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. a defect is too large for catheter closure and surgery is needed. IVC. The catheter has a tiny umbrella-like device folded up inside it. with no significant leakage. the patient is given medicine so he or she will sleep through it and not feel any pain.Catheter procedure[edit source | editbeta] Until the early 1990s. the device is pushed out of the catheter and positioned so that it plugs the hole between the atria. Closures are successful in more than 9 out of 10 patients. The outlook for patients having this procedure is excellent. The prevalence of residual defect is low.005´´ Nitinol wire mesh filled with Dacron fabric. the most common type of ASD. Within 6 months.[19] . Implantation of the device is relatively easy. doctors can use catheter procedures to close secundum ASDs. Rarely. The Amplatzer Septal Occluder (ASO) is commonly used to close ASDs. During the procedure. flexible tube) into a vein in the groin (upper thigh) and threads it to the heart's septum. the doctor inserts a catheter (a thin. When the catheter reaches the septum. Catheter procedures are much easier on patients than surgery because they involve only a needle puncture in the skin where the catheter is inserted. The ASO consists of two self-expandable round discs connected to each other with a 4 mm waist.004–0. For this procedure. surgery was the usual method for closing all ASDs. or the tricuspid or mitral valves. There is no need to replace the closure device throughout the patient's life. thanks to medical advances. This means that recovery is faster and easier. made up of 0. 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. Surgical ASD closure[edit source | editbeta] Surgical closure of an ASD involves opening up at least one atrium and closing the defect with a patch under direct visualization. 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). The device is secured in place and the catheter is withdrawn from the body. Now. normal tissue grows in and over the device. Percutaneous ASD closure[edit source | editbeta] 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.

as well as more frequent respiratory infections.[20][21] 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. including cerebrovascular accident (stroke). causing pulmonary hypertension. This is known as a paradoxical embolus because the clot material paradoxically enters the arterial system instead of going to the lungs. it avoids the lungs and the inert gas is more likely to form large bubbles in the arterial blood stream causing decompression sickness. (i.Complications[edit source | editbeta] Due to the communication between the atria that occurs in ASDs. that is called Eisenmenger's syndrome.. This can cause any phenomenon that is attributed to acute loss of blood to a portion of the body.e. or even a distal extremity . Embolization (dislodgement of thrombi) normally go to the lung and cause pulmonary emboli. In an individual with ASD. If some of the inert gas-laden blood passes through the PFO. called a left-to-right shunt. then there is an increase in the blood flow through the lungs. Paradoxical emboli[edit source | editbeta] Venous thrombi (clots in the veins) are quite common.. The syndrome is a rare and late complication of an ASD.[13] Decompression sickness[edit source | editbeta] ASDs. but if it persists. The pulmonary hypertension increases the pressures in the right side of the heart. these emboli can potentially enter the arterial system. the pulmonary blood vessels may stiffen. such as helium or nitrogen does not pass through the lungs. are possible. Migraine[edit source | editbeta] Main article: Migraine surgery#Patent foramen ovale closure . finger or toe). leading to the reversal of the shunt into a right-to-left shunt. and the blood begins flowing in the opposite direction through the ASD. infarction of thespleen or intestines. and particularly PFOs. this increased blood flow is asymptomatic. Eisenmenger's syndrome[edit source | editbeta] Main article: Eisenmenger's syndrome If a net flow of blood exists from the left atrium to the right atrium.. Once the reversal of the shunt occurs. disease entities or complications from the condition. Initially. are a predisposing risk factor for decompression sickness in divers because a proportion of venous blood carrying inert gases. Patients with an uncorrected atrial septal defects may be at increased risk for developing a cardiac arrhythmia.

Both the osteium secundum and osteum primum types of ASD are associated with Holt–Oram syndrome[28]  Lutembacher's syndrome .[27]  Holt–Oram syndrome .[25]   Ebstein's anomaly[26] Fetal alcohol syndrome . While the exact mechanism remains unclear.Some recent research has suggested that a proportion of cases of migraine may be caused by patent foramen ovale.patients with Down Syndrome have higher rates of ASDs. 20% of the female population have migraines. but migraine headache cessation was not more prevalent in the group of migraine patients that underwent closure of their patent foramen ovale. closure of a PFO can reduce symptoms in certain cases. 20% of the general population have a PFO. The high frequency of these facts makes statistically significant relationships between PFO and migraine difficult (i. which for the most part. especially a particular type that involves the ventricular wall.e. the relationship may just be chance or coincidence). the placebo effect in migraine typically averages around 40%.[22][23] This remains controversial.. And. ^ Atrial septal defect at Mount Sinai Hospital . In a large randomized controlled trial the higher prevalence of patent foramen ovale in migraine patients was confirmed. is asymptomatic.[9] See also[edit source | editbeta]          Atrioventricular septal defect Cardiac output Congenital heart disease Heart sounds Pulmonary hypertension Vascular resistance Pulmonary vascular resistance Ventricular septal defect Minimally Invasive Heart Surgery References[edit source | editbeta] 1.about one in four patients with fetal alcohol syndrome has either an ASD or a ventricular septal defect.[24] Associated conditions[edit source | editbeta]  Down Syndrome .[25] As many as one half of Down Syndrome patients have some type of septal defect.the presence of a congenital ASD along with acquired mitral stenosis.

7. 357. Retrieved 27 May 2013. "Transcranial doppler monitoring. O. 16. Vinay (2007). PMID 4569755. South Pacific Underwater Medicine Society Journal 25 (2).. 5. S. 9. 52. Echocardiographic diagnosis of congenital heart disease.2. J. 4. pp. Embryology. ^ Valdes-Cruz. doi:10. Cheitlin M. 1950–1969". Philadelphia: Saunders/Elsevier. ^ Fix. "Congenital heart disease in adolescents and adults. Natural and postoperative history across age groups". ^ Davia J. Abrol. 6.. doi:10. ^ Kumar. 12. R. p. ed. Retrieved 2008-0406. Titus J (1971). PMID 8252558. ^ Goldman 2011. .jacc. Am Heart J 85 (2): 177–85. "Sinus venosus atrial septal defect: analysis of fifty cases". "Mixed atrial septal defect coexisting ostium secundum and sinus venosus atrial septal defect. p. ^ a b John. Shani.. Retrieved 17 June 2012. Philadelphia. S.11. Bedynek J (1973). Oliver (26 May 2013). James D. Dudek. PMID 952260. "Incidence of congenital heart disease in children born to residents of Olmsted County.077. 14. OCLC 16986801. Cayre. ^ Rhodes. Baltimore: Williams & Wilkins. Am J Cardiol 38 (2): 167–9.1016/0002-8703(73)90458-4. ISBN 978-0-07-176137-6. pp. Yoshimasu F. ^ Leachman R.ISBN 0683-30272-8. M. ^ a b c Goldman 2011. ^ Feldt R. p. 11. A. Journal of the American College of Cardiology 58 (5): e9. Cokkinos D. doi:10.). Medscape. New York: McGraw-Hill Medical. Avasthey P. ISSN 0813-1988. Mayo Clin Proc 46 (12): 794– 9. (letter to editor)". 8. First aid for the USMLE step 2 CK (8th ed.1016/j. (1998).2 13.1016/0002-9149(76)901442. Kurland L. Retrieved 5 November 2012. PMID 21777739. Robbins Basic Pathology (8th ed. Vikas Bhushan. 270 17. Cardiol Clin 11 (4): 543–56. (1998). J. Mancunian Matters.). Sadiq. Douglas. 400–401 10. Ronald W. ed. ^ "Ostium Secundum Atrial Septal Defects". Cooley D (1976). ^ "Atrial Septal Defect Types – Mayo Clinic". ^ a b Skelley.". 384. "Association of ostium secundum atrial septal defects with mitral valve prolapse". 15. "„Hole in the heart‟ disease gene discovered by Manchester researchers could curb childhood deaths". ISBN 1416029737. L. Tao Le. J (2011 Jul 26). Nathan William. ^ Glen.2010. PMID 5128021. ^ Q21. 3. WebMD. Retrieved 2007-10-14. ^ Kaplan S (1993). Archived from the original on 28 September 2007. Minnesota. (1995).

Klug. Cardiol Young 16 (1): 3– 10. Walther. Suh W. Huisman. Chan V.". 24.65. ^ Dowson.4065/79. Hubald. "Association of interatrial shunts and migraine headaches: impact of transcatheter closure". Gray G (2001). Hering R (2004). Hildick-Smith. Wynne. doi:10. ^ Bossert. ME. sham-controlled trial to evaluate the effectiveness of patent foramen ovale closure with STARFlex septal repair implant to resolve refractory migraine headache. PMID 14708944. "Migraine Intervention With STARFlex Technology (MIST) trial: a prospective. PMID 18316488.1016/j. ^ Lier H. L. multicenter. SA.|accessdate= requires |url= (help) 27. Kostelka. "Down syndrome: a cardiovascular perspective.jacc. 19. S.1017/S1047951105002027. R. |accessdate= requires |url= (help) 28. WS. BJ (May 2009). JC. R. Hillis. "Patent foramen ovale: an underrated risk for divers?". Moustapha-Nadler.18. MM. doi:10.1055/s-2004-812652. Weijerman.doi:10. Khan. ^ Adams H (2004). DeBord. "Congenital heart defects and fetal alcohol spectrum disorders. Retrieved 7 November 2012. MG. Duffels. Mullen. SL. ^ Bjørnstad P (2006). Malik. FW (October 2002). Winter. Aviat Space Environ Med 72 (12): 1113–20. "Preoperative secundum atrial septal defect with coexisting sinus node and atrioventricular node dysfunction". ^ Clark E. Dtsch Med Wochenschr 129 (1–2): 27–30. PMID 19606562. J. The Thoracic and cardiovascular surgeon 50 (5): 312–4. PMID 16454871.PMID 12375192."Cardiac malformations associated with the Holt-Oram syndrome--report on a family and review of the literature.". N (June 2009). MG (July-Aug).075.PMID 18377476.5. Cobben. Wells. Circulation 65 (5): 976– 80. ^ Saary M. "Patent foramen ovale: paradoxical embolism and paradoxical data". C. 25.". Adickes. Muir.976. PMID 7074763. R.09. double-blind. JM. quiz 1111– 4. ^ a b Vis. Rios. WL. ^ Cherry.1161/01. Mohr. Rickards.". J Am Coll Cardiol 45 (4): 489– 92.doi:10. Deal. PMID 15708691. PMID 11763113. IS. G. Elrington. 21. "Is interventional closure the current treatment of choice for selected patients with deficient atrial septation?". 22. "Ebstein's anomaly: a complex congenital heart defect. 20. Gummert. "A review of the relationship between patent foramen ovale and type II decompression sickness". T. T. ^ Burd. A (18). D. Rees.". PMID 19228275.1. K. Gaster R (2005). Mayo Clin Proc 79 (1): 15–20.15. E. Andrew. Kugler J (1982). Congenital heart disease 2 (4): 250– 5. AA. JV. MJ. Peatfield. Schroeder S. Tobis J. J. T. |accessdate= requires |url= (help) 26. M.Circulation 117 (11): 1397– 404. Lipscombe. . Dao C.2004. Journal of intellectual disability research : JIDR 53 (5): 419–25. Mulder.CIR. PMID 14703578. ^ Azarbal B. De Giovanni. AORN journal 89 (6): 1098–110. Morrison. C. E. 23.doi:10.

Additional references[edit source | editbeta]  Goldman. 400–401. 270. physics and environment Categories:   Congenital heart disease Diving medicine . Lee (2011).). Philadelphia: Elsevier Saunders. [show]  V  T  E Congenital heart defects (Q20–Q24. pp. physiology. External links[edit source | editbeta]     Pediatric Heart Surgery The Congenital Heart Surgery Video Project Pediatric Cardiac Surgery: Atrial Septal Defect Repair Atrial septal defect information for parents. ISBN 1437727883. and Blood Institute".This article incorporates public domain material from the United States Department of Health and Human Services document "National Heart. 745–746) [show]  V  T  E Diving medicine. Goldman's Cecil Medicine (24th ed ed. Lung.

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