Pediatric Patent Foramen Ovale Atrial Septal Defects

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The foramen ovale is a normal cardiac structure found in all newborns and can be best described as a “door” between the right and left atria.

The foramen ovale is essential for proper fetal circulation, directing oxygenated, nutrient-rich blood from the placenta, preferentially to the developing fetal brain. During fetal life, the “door” is open, and blood passes from the right to left atrium. However, with separation from the placenta and with the first few breaths, the left atrium fills with blood returning from the lungs and closes the “door.”

During the first years of life, the foramen ovale seals shut and becomes a true wall that separates the right and left atria. However, in a significant proportion of people, the foramen ovale does not seal shut and remains a potential trapdoor between the 2 atria. A patent foramen ovale (PFO) is defined as a foramen ovale that does not seal. See the images below.

All newborns are expected to have a patent foramen ovale. The time frame over which most seal shut varies. However, adult autopsy studies have shown that 20-34% of adults from the third to ninth decades of life have at least a small patent foramen ovale. [1]

Although it is a normal structure, a foramen ovale has several special circumstances under which it may be implicated in disease.

The foramen ovale is an interatrial communication that permits blood from the inferior vena cava to freely enter the left atrium in utero. Anatomically, a thick muscular ridge, the limbus of the fossa ovalis, borders the foramen ovale. A thin tissue flap on the left atrial side of the septum, which represents an embryological remnant of the septum primum, forms the valve of the fossa ovalis. At birth, the left atrial pressure exceeds the right atrial pressure and forces the valve against the limbus, thus achieving physiological closure. During the first weeks of life, Doppler echocardiographic studies in healthy newborns can often demonstrate incompetence of the valve that allows some degree of left-to-right shunting. Shunting generally resolves by age 1 year as the foramen ovale seals shut. [2]

Persistent left atrial enlargement associated with specific cardiac lesions, such as mitral valve stenosis, mitral valve regurgitation, patent ductus arteriosus, or ventricular septal defect, can render the foramen ovale “incompetent.” Atrial left-to-right shunting can continue as a result.

Right-to-left shunting can occur through a patent foramen ovale, especially in conditions associated with elevated right atrial pressure such as tricuspid valve stenosis or right ventricular hypoplasia with decreased right ventricle compliance. Patients with persistent or transient elevation of right atrial pressure can experience a paradoxical embolus through a patent foramen ovale. Some congenital heart lesions depend on the foramen ovale for obligatory left-to-right (mitral atresia) or right-to-left (tricuspid atresia, total anomalous pulmonary venous return) shunting to maintain adequate cardiac output.


Several echocardiography and postmortem studies indicate that the foramen remains competent in 30% of patients with otherwise normal cardiac anatomy.

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Barry A Love, MD Assistant Professor , Department of Medicine, Division of Cardiology, Assistant Professor, Division Pediatric Cardiology, Director, Pediatric Electrophysiology Service, Department of Pediatrics, Division of Pediatric Cardiology, Mount Sinai School of Medicine

Disclosure: Nothing to disclose.

Michael A Portman, MD, MD Professor, Department of Pediatrics, University of Washington School of Medicine; Director of Research, Division of Cardiology, Seattle Children’s Hospital; Attending Physician, Seattle Children’s Heart Center; Attending Physician, Cardiology Clinic, Providence Everett Medical Center

Michael A Portman, MD, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Physiological Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Alvin J Chin, MD Emeritus Professor of Pediatrics, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Syamasundar Rao Patnana, MD Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children’s Memorial Hermann Hospital

Syamasundar Rao Patnana, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society for Pediatric Research

Disclosure: Nothing to disclose.

Paul M Seib, MD Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children’s Hospital

Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Pediatric Patent Foramen Ovale Atrial Septal Defects

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