Background:
Although surgical correction is the gold standard for ASD closure, transcatheter approach to correct this congenital defect has increased in popularity since the first successful use of a percutaneous closure device in the 1970s.
Percutaneous ASD closure is known to be safe and adds the benefit of avoiding open heart surgery, shorter hospital stay, and lower rates of mortality/morbidity. However, several potential complications are known, including device embolization.
Case Description:
A 40-yr-old asymptomatic male was noted to have a significant murmur on physical exam. TEE and cardiac MRI revealed a large secundum ASD measuring 2.7 cm x 1.1 cm, with flow through the defect of 8 L/min, a Qp/Qs 3:1, moderate/severe RV dysfunction, and moderate TR. The MRI also demonstrated a poor inferior/caudal rim tissue with the defect relatively close to the coronary sinus/RA junction. Using TEE and fluoroscopic guidance, 34 mm Amplatzer septal occluder was placed through the ASD. Following deployment, there was some concern for prolapse of the left atrial disc of the device. The device was removed from the ASD using a gooseneck snare and while attempting to pull the device into a 14F sheath, the device broke free from the snare and embolized to the RVOT. Several attempts were then made to retrieve the device using a snares and bioptomes, but this was unsuccessful. The device was removed from the RVOT and stabilized in the right atrium using a bioptome.
The patient was transferred to the operating room and underwent removal of the embolized ASD occluder, closure of the large ASD with bovine pericardial patch, and tricuspid valve repair via a minimally invasive right thoracotomy approach. After this successful operation, the patient was transferred to the ICU and ultimately discharged from the hospital on post op day 5.
Discussion:
As percutaneous closure of ASDs has increased, several device related safety issues have been described in the literature including embolization, atrial perforation, thrombus formation, and erosion with hemopericardium. The incidence of device embolization is rare, with a recent study describing a 0.55% rate of embolization (3). Device embolizations usually occurs during the procedure or in the periprocedural period, as in this case. Several mechanisms for device embolization have been proposed in the literature, include limited operator experience (learning curve), inadequate defect rim to hold the device, and inaccurate deployment (4). Damage to the tricuspid valve due to embolized occlusion devices has also been described in the literature. In this case, the patient had existing tricuspid insufficiency due to a dilated RV, and this pathology necessitated the surgical repair of the tricuspid valve.
Fortunately during this case we did not see any hemodynamically significant arrhythmias, severe RVOT obstruction or tamponade secondary to hemoparicardium. Having a cardiothoracic surgery team available on standby was of benefit in this particular situation. Addtionally, heparinization of the patient following device embolization and TEE guidance to track the position of the device as the patient is transitioned from a percutaneous to open surgical procedure was essential for proper management of this rare complication.
