The foramen ovale usually closes in the first year of life. If the foramen ovale does not close in children older than 3 years of age, the foramen ovale is said to be incomplete, and in 20% to 25% of adults the foramen ovale does not close completely. The foramen ovale is by far the most common congenital heart anomaly in adults, and it can be detected in about 1 in 4 people in the normal population. For a long time, it was considered “irrelevant” because it did not cause shunting between the two chambers and had no effect on the hemodynamics of the heart. In recent years, many studies have shown a close association between patent foramen ovale and patients with unexplained stroke because the following emboli can enter the left heart system through the patent foramen ovale and cause clinical symptoms: (1) thrombus in the deep veins of the lower extremities or pelvic veins; (2) air emboli due to diving or decompression sickness; and (3) fat emboli after surgery or trauma. Moreover, the risk of recurrence remains high in patients with unclosed foramen ovale who have had thrombotic events. Therefore, treatment for the etiology and closure of the open foramen ovale in high-risk groups is expected to reduce the incidence of patients. In addition, it has also been found that patent foramen ovale is associated with the development of decompression sickness and migraine, and closing the foramen ovale may be beneficial for these patients. Etiology The formation of foramen ovale occurs during the sixth and seventh weeks of embryonic development, when two septum septum septae are formed, the septum that appears first is the primary septum or first septum, and the septum that appears later is the secondary septum or second septum. Before the primary foramen is closed, a hole is formed in the proximal cephalic portion of the primary septum, called the secondary foramen, which is the normal channel for blood during fetal life. At the same time, a sickle-shaped septum grows on the right side of the first septum from the atrial wall, called the secondary septum or the second septum, which does not continue to grow to separate the atrium midway to stop, the sickle-shaped depression is oval-shaped called the oval fossa, the primary septum and secondary septum at the oval fossa fail to adhere and fuse leaving a small cleft called the oval foramen. At birth, with the first cry, the pressure in the left atrium rises, causing the primary septum on the left to partially adhere to the secondary septum on the right, resulting in functional closure, which is achieved anatomically within 1 year. If the foramen ovale remains unclosed in children >3 years of age, it is called foramen ovale non-closure. Clinical manifestations Ovular foramen insufficiency is mostly asymptomatic, murmurs are difficult to hear, and electrocardiograms and chest X-rays are normal. Therefore, it is not easy to detect and is not taken seriously. Examination 1. Right heart catheterization Right heart catheterization can directly enter the left atrium from the right atrium through the unclosed foramen ovale, confirming the existence of unclosed foramen ovale. Currently, color Doppler ultrasonography is used to improve the accuracy of diagnosis. 2.Echocardiographic examination Transthoracic ultrasound and transesophageal ultrasound can detect unclosed foramen ovale with left-to-right shunt or right-to-left shunt, and ultrasound acoustic imaging can detect potential unclosed foramen ovale, and Valsalva maneuver or cough test can make the detection rate of unclosed foramen ovale as high as 60%-78%. In contrast, the detection rate of oval foramen ovale noncompaction can be improved. Transesophageal ultrasound is three times more likely to detect patent foramen ovale than transthoracic ultrasound. The diagnosis of patent foramen ovale is mainly made by cardiac ultrasound. The presence of a small left-to-right or right-to-left shunt in the left and right atrial septum on color Doppler imaging of the fossa ovalis is demonstrated by transthoracic ultrasound or transesophageal ultrasound. Differential diagnosis Ovular fossa nonclosure should be differentiated from small atrial septal defects, primarily by cardiac ultrasound. A small atrial defect is demonstrated on transthoracic ultrasound or transesophageal ultrasound with small contiguous interruptions in the atrial septum, with most contiguous interruptions in the septum >4 mm. Treatment Previously, closure of patent foramen ovale relied on surgical procedures. Surgical treatment has a high success rate and a very low morbidity and mortality rate, but it is highly invasive and may result in complications such as atrial fibrillation, pericardial effusion, postoperative bleeding and wound infection, and therefore has been rarely used in recent years. With the advancement of technology, especially the development of cardiac catheterization technology, a considerable proportion of left-to-right shunt congenital heart diseases (such as patent ductus arteriosus and atrial septal defect) can be radically cured by interventional treatment. Clinical practice in recent years has demonstrated that this technique is also safe, effective, and feasible for permanent closure of open patent foramen ovale.