Atrial septal defect ostium secundum overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
For a full discussion on atrial septal defects click here.
Overview
Atrial septal defect ostium secundum are ASDs at the fossa ovalis. It accounts for 75% of all atrial septal defects.
Anatomy
During fetal development, the septal wall may fail to fuse causing an atrial septal defect to arise. An ostium secundum atrial septal defect is one such type of malformation arising from the irregular development of the foramen ovale, septum secundum or septum primum. It is the most common type of atrial septal defect.
Epidemiology and Demographics
Ostium secundum atrial septal defects are the most common form of atrial septal defect. They constitute approximately 60%-75% of all the atrial septal defects and account for 6%-10% of all congenital heart defects.
Natural History, Complications and Prognosis
Most individuals with an uncorrected secundum ASD are asymptomic or experience minimal symptoms through early adulthood. About 70% of all ostium secundum ASD patients' develop symptoms by the time they are in their 40s. Symptom onset and severity is largely dependent upon the size of the defect. Without intervention prior to the development of Eisenmenger's syndrome, the mortality rate for symptomatic adults is greater than 50%. Possible complications include atrial fibrillation, pulmonary hypertension and stroke.
Diagnosis
Echocardiography
Echocardiography may be used as a diagnostic tool in the evaluation of an atrial septal defect. Common malformations of the septal wall include: ostium primum, ostium secundum, sinus venosus, and patent foramen ovale. Uncommonly, a defect may occur in the coronary sinus. Specific characteristics exist in echocardiography to identify these various classifications of atrial septal defects.
Treatment
Medical Therapy
Definitive treatment of atrial septal defect involves surgical closure of the defect. Medical therapy has a limited role in the management of ASD, and is often used to manage complications like arrhythmia, congestive heart failure and other comorbidities associated with atrial septal defects such as stroke and migraine.
Indications for Surgical Repair in Adults
The decision to surgically close an atrial septal defect depends upon many contributing factors including the type of defect, the size of defect, the amount of left-to-right shunting, the development or worsening of symptoms, the presence of pulmonary hypertension and the presence of any associated anomalies.
Surgical Closure
Surgical closure is the commonest treatment method for atrial septal defect and has been the gold standard for many years. Many surgeons prefer more minimally invasive techniques over the conventional sternotomy to avoid potentials for additional complications. Special consideration must be taken into account for the age of the patient and the size of the defect involved. Surgical closure is indicated for patients with primum, sinus venosus and coronary sinus type of atrial septal defects. However, ostium secundum atrial septal defects are commonly treated by percutaneous closure. With uncomplicated atrial septal defect, (without pulmonary hypertension and other comorbidities) the post-surgical mortality is as low as 1%
Percutanous Closure
Percutaneous device closure is commonly performed to close an ostium secundum type of atrial septal defect and patent foramen ovales. It is still not FDA approved for closure of other forms of atrial septal defects such asprimum, sinus venosus and coronary sinus. With proper patient selection at experienced centers, it has been found to be as successful, safe and effective as surgical closure. Additionally, it has been associated with fewer complications and a reduced length of stay compared to surgical closure [1].
References
- ↑ Du ZD, Hijazi ZM, Kleinman CS, Silverman NH, Larntz K, Amplatzer Investigators (2002). "Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults: results of a multicenter nonrandomized trial". J Am Coll Cardiol. 39 (11): 1836–44. PMID 12039500.