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Atrial Septal Defect

  • Author: David H Adler, MD, FACC; Chief Editor: Park W Willis IV, MD  more...
 
Updated: Dec 06, 2015
 

Background

Atrial septal defect (ASD) is one of the more commonly recognized congenital cardiac anomalies presenting in adulthood. Atrial septal defect is characterized by a defect in the interatrial septum allowing pulmonary venous return from the left atrium to pass directly to the right atrium. Depending on the size of the defect, size of the shunt, and associated anomalies, this can result in a spectrum of disease from no significant cardiac sequelae to right-sided volume overload, pulmonary arterial hypertension, and even atrial arrhythmias.

With the routine use of echocardiography, the incidence of atrial septal defect is increased compared to earlier incidence studies using catheterization, surgery, or autopsy for diagnosis.[1]  The subtle physical examination findings and often minimal symptoms during the first 2-3 decades contribute to a delay in diagnosis until adulthood, the majority (more than 70%) of which is detected by the fifth decade. However, earlier intervention of most types of atrial septal defect is recommended.

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Pathophysiology

The magnitude of the left-to-right shunt across the ASD depends on the defect size, the relative compliance of the ventricles, and the relative resistance in both the pulmonary and systemic circulation. With small ASD, left atrial pressure may exceed right atrial pressure by several millimeters of mercury, whereas with large ASD, mean atrial pressures are nearly identical. Shunting across the interatrial septum is usually left-to-right and occurs predominantly in late ventricular systole and early diastole. Likely some augmentation occurs during atrial contraction. Note, however, that a transient and small right-to-left shunt can occur, especially during respiratory periods of decreasing intrathoracic pressure, even in the absence of pulmonary arterial hypertension.

The chronic left-to-right shunt results in increased pulmonary blood flow and diastolic overload of the right ventricle. Resistance in the pulmonary vascular bed is commonly normal in children with ASD, and the volume load is usually well tolerated even though pulmonary blood flow may be more than 2 times systemic blood flow. Altered ventricular compliance with age can result in an increased left-to-right shunt contributing to symptoms. The chronic significant left-to-right shunt can alter the pulmonary vascular resistance leading to pulmonary arterial hypertension, even reversal of shunt and Eisenmenger syndrome.

Because of an increase in plasma volume during pregnancy, shunt volume can increase, leading to symptoms. Pulmonary artery pressure usually remains normal.

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Etiology

Atrial septal defect (ASD) is a congenital cardiac disorder caused by the spontaneous malformation of the interatrial septum. Note the following:

  • Ostium secundum ASD: This type of ASD results from incomplete adhesion between the flap valve associated with the foramen ovale and the septum secundum after birth. The patent foramen ovale usually results from abnormal resorption of the septum primum during the formation of the foramen secundum. Resorption in abnormal locations causes a fenestrated or netlike septum primum. Excessive resorption of the septum primum results in a short septum primum that does not close the foramen ovale. An abnormally large foramen ovale can occur as a result of defective development of the septum secundum. The normal septum primum does not close this type of abnormal foramen ovale at birth. A combination of excessive resorption of the septum primum and a large foramen ovale produces a large ostium secundum ASD.
  • Ostium primum ASD: These defects are caused by incomplete fusion of septum primum with the endocardial cushion. The defect lies immediately adjacent to the atrioventricular (AV) valves, either of which may be deformed and incompetent. In most cases, only the anterior or septal leaflet of the mitral valve is displaced, and it is commonly cleft. The tricuspid valve is usually not involved.
  • Sinus venosus ASD: Abnormal fusion between the embryologic sinus venosus and the atrium causes these defects. In most cases, the defect lies superior in the atrial septum near the entry of superior vena cava. Often there is associated anomalous drainage of the right superior pulmonary vein. The relatively uncommon inferior type is associated with partial anomalous drainage of the right inferior pulmonary vein. Anomalous drainage can be into the right atrium, the superior vena cava, or the inferior vena cava.
  • Coronary sinus ASD: Coronary sinus defect is characterized by unroofed coronary sinus and persistent left superior vena cava that drains into the left atrium. A dilated coronary sinus often suggests this defect. This can result is desaturation due to right-to-left shunt into the left atrium. The diagnosis can be made by injecting contrast agent into left upper extremity; coronary sinus opacification precedes right atrial opacification.

Genetics

Atrial septal defect (ASD) may occur on a familial basis. Holt-Oram syndrome characterized by an autosomal dominant pattern of inheritance and deformities of the upper limbs (most often, absent or hypoplastic radii) has been attributed to a single gene defect in TBX5.[2] The penetrance is nearly 100% for Holt-Oram syndrome. Approximately 40% of Holt-Oram cases are due to new mutations.

Ellis van Creveld syndrome is an autosomal recessive disorder associated with skeletal dysplasia characterized by short limbs, short ribs, postaxial polydactyly, dysplastic nails and teeth, and a common atrium, occurring in 60% of affected individuals.[3]

Mutations in the cardiac transcription factor NKX2.5 have been attributed to the syndrome familial ASD associated with progressive atrioventricular block.[4, 5, 6]  This syndrome is an autosomal dominant trait with a high degree of penetrance but no associated skeletal abnormalities.

Variants in the GATA4 gene have also been implicated in ASD.[5, 7] More recently, a novel mutation at the methylation position of GATA4 (c.A899C, p.K300T) has been reported in association with ASD.[7]

Wang et al reported that downregulation of the following genes in ASD may affect heart atrial septum formation, cardiomyocyte proliferation, and cardiac muscle development[5] :

  • Cardiac specific transcriptional factors GATA4 and NKX2-5
  • Extracellular signal molecules VEGFA and BMP10
  • Cardiac sarcomeric proteins MYL2, MYL3, MYH7, TNNT1, and TNNT3

The investigators noted that dysregulation of these genes during heart septum morphogenesis may lead to cell cycle as the dominant pathway among downregulated genes, with the potential for the decreased expression of the proteins included in the cell cycle then disturbing cardiomyocyte growth and differentiation during atrial septum formation.[5]

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Epidemiology

The 3 major types of atrial septal defect (ASD) account for 10% of all congenital heart disease and as much as 20-40% of congenital heart disease presenting in adulthood. The most common types of ASD include the following:

  • Ostium secundum: The most common type of ASD accounting for 75% of all ASD cases, representing approximately 7% of all congenital cardiac defects and 30-40% of all congenital heart disease in patients older than 40 years.
  • Ostium primum: The second most common type of ASD accounts for 15-20% of all ASDs. Primum ASD is a form of atrioventricular septal defect and is commonly associated with mitral valve abnormalities.
  • Sinus venosus: The least common of the three, sinus venosus (SV) ASD is seen in 5-10% of all ASDs. The defect is located along the superior aspect of the atrial septum. Anomalous connection of the right-sided pulmonary veins is common and should be expected. Alternate imaging is generally required.

Sex- and age-related demographics

ASD occurs with a female-to-male ratio of approximately 2:1.

Patients with ASD can be asymptomatic through infancy and childhood, though the timing of clinical presentation depends on the degree of left-to-right shunt. Symptoms become more common with advancing age. By age 40 years, 90% of untreated patients have symptoms of exertional dyspnea, fatigue, palpitation, sustained arrhythmia, or even evidence of heart failure.

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Contributor Information and Disclosures
Author

David H Adler, MD, FACC Assistant Professor of Medicine, Eastern Virginia Medical School; Cardiologist, Cardiovascular Associates, Ltd

David H Adler, MD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Alexander R Ellis, MD, MSc, FAAP, FACC Assistant Professor of Internal Medicine and Pediatrics, Eastern Virginia Medical School; Co-Director, Pediatric Echocardiography Laboratory, Division of Pediatric Cardiology, Director, Adult Congenital Heart Disease Program, Children’s Hospital of the King’s Daughters; Director of Resident and Medical Student Education, Division of Cardiology, Children’s Hospital of the King’s Daughters and Eastern Virginia Medical School

Alexander R Ellis, MD, MSc, FAAP, FACC is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Park W Willis IV, MD Sarah Graham Distinguished Professor of Medicine and Pediatrics, University of North Carolina at Chapel Hill School of Medicine

Park W Willis IV, MD is a member of the following medical societies: American Society of Echocardiography

Disclosure: Nothing to disclose.

Additional Contributors

Park W Willis IV, MD Sarah Graham Distinguished Professor of Medicine and Pediatrics, University of North Carolina at Chapel Hill School of Medicine

Park W Willis IV, MD is a member of the following medical societies: American Society of Echocardiography

Disclosure: Nothing to disclose.

Acknowledgements

Marc G Cribbs, MD Fellow, Department of Pediatric Cardiology, Vanderbilt University Medical Center

Marc G Cribbs, MD is a member of the following medical societies: American Heart Association, American Medical Association, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Larry W Markham, MD Assistant Professor of Pediatrics and Medicine, Vanderbilt University School of Medicine

Larry W Markham, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Bekir Hasan Melek, MD Assistant Professor of Clinical Medicine, Department of Medicine, Section of Cardiology, Tulane University School of Medicine

Bekir Hasan Melek is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Echocardiography, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Jeffrey C Milliken, MD Chief, Division of Cardiothoracic Surgery, University of California at Irvine Medical Center; Clinical Professor, Department of Surgery, University of California, Irvine, School of Medicine

Jeffrey C Milliken, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, California Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Thoracic Surgeons, Southwest Oncology Group, and Western Surgical Association

Disclosure: Nothing to disclose.

Peter B Smulowitz University of California, Irvine, School of Medicine

Disclosure: Nothing to disclose.

James V Talano, MD, MBA, MM, FACC, FAHA Director of Cardiovascular Medicine, SWICFT Institute

James V Talano, MD, MBA, MM, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, and Society of Geriatric Cardiology

Disclosure: Nothing to disclose.

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Parasternal short axis: RV dilation with RV pressure overload as evidenced by flattening of the interventricular septum in systole.
Transesophageal echocardiogram: Moderate-large ASD with left-to-right shunt across the interatrial septum.
Apical 4-chamber view.
 
 
 
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