Studies in fetal sheep show that in intrauterine life the IVC carries 65–70 % of blood returning to the heart (from the lower half of the body and the placenta) [1, pp 8–9]. The location of the right atrial opening, the Eustachian valve, and the large inferior venal caval flow keep the valve of the foramen ovale open, and between 36 and 43 % of this blood crosses the foramen ovale into left atrium where it joins the 5–10 % of venous return to the heart that comes from the lungs [1, pp 8–9]. This volume of blood flow is necessary for normal development of the left ventricle.

At birth, loss of the placenta decreases inferior vena caval return and increases systemic resistance [1, pp 19–20]. Pulmonary resistance falls and pulmonary venous return increases as all systemic venous return passes through the right ventricle. Increased pulmonary venous return causes an increase in left atrial pressure and functionally closes the valve of the foramen ovale.

Once the valve of the foramen ovale is in apposition to the former septum secundum, the valve becomes adherent over several months resulting in permanent closure. Patency may, however, persist into adult life. This was described over 400 years ago. In a review of the literature, Patten noted in 1938 [2] that the foramen ovale was not completely closed in 21.2 % of adults. The process of closure is gradual, and the percentage of persistent patency falls gradually from 34 % between 1 and 9 years of life to 20 % in adults over age 80 (Fig. 2.2) [3].

As long as the foramen ovale remains patent after birth, shunting of blood may occur through the potential opening. A small amount of blood flowing from the left atrium around the valve of the foramen ovale into the right atrium is often seen in newborn infants. Lesions that elevate left atrial pressure and enlarge the left atrium (e.g. ventricular septal defect or patent ductus arteriosus) may make the valve incompetent resulting in left to right flow. Conditions that elevate right atrial pressure above that of the left may cause loss of apposition of the valve to the atrial septum and right to left flow across the atrial septum. Some congenital heart defects (tricuspid atresia, total anomalous pulmonary venous connection) require the foramen ovale to allow blood from the right atrium to enter the left side of the heart. Non-cardiac problems such as severe pulmonary disease or pulmonary hypertension can elevate right atrial pressure resulting in a right to left shunt through a patent foramen ovale. Right atrial pressure can be transiently elevated above left atrial pressure in normal individuals. Crying, breath holding, or straining will elevate intrathoracic pressure decreasing systemic venous return. With release, the transiently detained systemic venous return rushes back to the right atrium elevating right atrial pressure. When the foramen ovale is still patent, there may be a transient right to left shunt. The Eustachian valve and location of the right atrial opening encourage channeling of inferior vena caval return through the foramen ovale as they did in intrauterine life. In rare conditions such as orthodeoxia/platypnea there may be flow of desaturated right atrial blood into the left atrium across the foramen ovale under baseline conditions with no obvious cause of elevated right atrial pressure.

Normally all systemic venous blood returns to the lungs where any thrombi are filtered out. When the foramen ovale remains patent, a passing thrombus may be caught in any right to left atrial shunt bypassing the lungs (paradoxical embolus). If this thrombus arrives in a critical area (the coronary or cerebral circulation), there may be disastrous consequences. There are a significant number of adults who have a stroke and no definitive cause can be found (cryptogenic stroke). When a patent foramen ovale is identified in these patients, it may be assumed that an inducible right to left shunt is a smoking gun, with the possibility of a paradoxical embolus. Since there are a large number of these patients, there has been significant interest in developing a transcatheter mechanism of eliminating persistent patency and avoiding a lifetime of anticoagulation.

Transcatheter closure of atrial septal defects, patent ductus arteriosus and ventricular septal defects have taught us that failure to consider the human anatomy of these forms of congenital heart disease can result in unexpected complications, from erosion through the walls of the heart to protrusion of the device into the circulation. To develop a device that will safely close a patent foramen ovale, it is important to consider the anatomy of the defect. For the foramen ovale, this can be complex. Understanding the anatomy of the foramen ovale in utero helps to understand the anatomy of the persistently patent foramen. In the fetus, the valve of the foramen is attached posteriorly and inferiorly [2]. This allows blood to enter the left atrium through the residual anterior/superior communication. Persistent patency of the foramen ovale results from failure of fusion across this superior/anterior margin (Fig. 2.3).

Four primary variations of a persistently patent foramen ovale result from differences in the extent of fusion, and the character of the valve of the foramen ovale. These include lack of fusion only at the most anterior superior margin (the classic “probe patent” foramen ovale), failure of fusion across the entire anterior superior margin, fenestrations of the flap of the foramen ovale, and excessive mobility of the flap (aneurysm of the atrial septum).

The probe patent foramen ovale (Fig. 2.4) occurs superiorly and anteriorly above the aortic valve and may be short or create a tunnel of variable length depending on the length of the flap. The particularities of the length of the connection have major implications for selection of a device to occlude the defect. Since the communication has a small diameter, it is ideal for a center post device. If the tunnel has a great length, a device that can accommodate extending over that length is ideal. A “self-centering” device with a waist that expands to fill a defect may not seat appropriately in this type of opening. The inability of a self centering device to shorten and fully expand will distort the device. This type of defect can be recognized by the response to a guidewire or sheath passing across the defect, or to an inflated balloon sizing catheter across the defect (Fig. 2.5b). An inflated sizing balloon in particular will reveal the diameter of the communication, and the length of any tunnel.