Early Systemic Device Embolization after
Transcatheter Patent Foramen Ovale Closure

Percutaneous patent foramen ovale (PFO) closure is a treatment option for secondary prevention in patients with paradoxical embolism. Several procedural and postprocedural complications have been reported with the use of transcatheter techniques. Early device embolization after initial satisfactory implantation for PFO occlusion has been collected in the literature, but often with little detail concerning site, delay, clinical impact and potential causes of this complication.^1,2 We report a case of asymptomatic PFO occluder device embolization into the descending aorta observed 24 hours after implantation. Case Report An 80-year-old male smoker was referred to our institution due to recurrent pulmonary and systemic embolic events. The patient had a history of systemic hypertension and multivessel coronary disease and underwent percutaneous angioplasty in 1998. He had suffered a splenic infarction in 2002. Transesophageal echocardiography (TEE) had shown a PFO associated with an atrial septal aneurysm (ASA). The patient was discharged on antiplatelet therapy (aspirin 100 mg/day). One year later, he was admitted to another institution for sudden aphasia due to a brain infarction on CT-scan. Concomitant pulmonary embolism was suspected by arterial oxygen desaturation with shunt effect and abnormal ventilation-perfusion lung scintigraphy. The lower extremity Doppler ultrasound was normal. The patient was treated with intravenous anticoagulation (unfractionated heparin). The initial hospital stay was marked by a worsening of neurological conditions in relation to hemorrhagic transformation of the brain infarction. The intravenous anticoagulation was replaced by a low-molecular-weight heparin (enoxaparin 40 mg/day) and aspirin was continued. A progressive improvement in neurological status was noticed. Thereafter, the patient was transferred to our institution for discussion about percutaneous closure of his PFO. Etiologic evaluation did not show other potential embolic causes except for atrial septal abnormality. No pulmonary hypertension was present. Echocardiography also revealed a root aortic dilatation (43 mm) with enlargement of the Valsalva’s sinuses (46 mm). The thromboembolic pulmonary disease could not explain the magnitude of hypoxemia that was probably due to a permanent right-to-left shunt. An associated orthodeoxia-platypnea syndrome was not found. Despite the age of the patient, a decision was taken with neurologists to close the PFO in order to reduce the risk of stroke and avoid the need for prolonged anticoagulation therapy. The procedure was performed under general anesthesia which allowed for comfortable TEE guidance. Echocardiographic evaluation (Figure 1) was similar to the previous examination with a large PFO (6 mm diameter), with spontaneous right-to-left shunting during the contrast test and a significant ASA (20 mm base diameter with 11 mm excursion). The septum primum had an eccentric position bending into the left atrium and was not hypermobile. The length of the PFO conduit was 9 mm and the secundum septum thickness was 5 mm. After sheath placement into the right femoral vein, a 6 Fr multipurpose catheter was used to cross the PFO. A sizing balloon (NMT Medical, Boston, Massachusetts) was advanced over an exchange wire, showing a large (16 mm) indentation (Figure 2). Thereafter, a PFO-Star occluder 5 mm x 30 mm (Cardia, Inc., Burnsville, Minnesota) was implanted without difficulty through a 12 Fr transseptal sheath. The stable positioning of the device was verified by fluoroscopy and TEE (Figure 3). Surprisingly, routine transthoracic echocardiography failed to identify the interatrial device on the following day. An abdominal X-ray showed device into the descending aorta just above the renal arteries embolization without apparent damage (Figure 4). No evidence of heavy physical exertion or Valsalva’s maneuver was found shortly after the procedure. One day later, transcatheter device retrieval was attempted via left femoral arterial access using a 12 Fr sheath. The PFO-Star occluder was successfully pulled down to the iliac artery with a 7 Fr bioptome (Figure 5). We were then able to retract a great part of the device into the orifice of the sheath and pull the entire ensemble through the femoral artery (Figure 6). In order to avoid vessel injury, vascular surgery was required under general anesthesia to extract the device. The patient’s clinical evolution was uneventful. He was discharged 2 weeks later on oral anticoagulation and aspirin. A second percutaneous intervention was not attempted to close the PFO, particularly due to the patient’s advanced age. One year after the initial procedure, the patient was doing well without recurrent thromboembolic events under an antithrombotic regimen. Discussion Transcatheter closure of PFOs is supposed to reduce the incidence of embolic cerebrovascular events in at-risk patients. However, several complications have been reported, including device embolization. Malpositioning of the device is generally detected by echocardiography during the procedure. A large and mobile ASA is often involved. The choice of diameter and design of a device is generally related directly to the ASA characteristics, but the size of the PFO must be also considered. Assessment of the length of the PFO conduit and dehiscence between the septum primum and septum secundum are achieved successfully using echocardiography. Nevertheless, the true anatomical diameter of the PFO remains difficult to estimate.3 Balloon sizing is not recommended in most cases. Contrast echocardiographic studies are generally performed with semi-quantitative graduation to estimate the size of a PFO. Pending the results of ongoing randomized controlled trials, we usually close PFOs only after a consensus between neurologists and cardiologists is reached based on the following indications: (1) age 4 Our patient was much older, however our consensus was that we should close the PFO as an exception to our rules, given the hemorrhagic transformation of the brain infarct which we believed precluded continued safe anticoagulation in this patient. The true size of the PFO was clearly underestimated in our patient. The PFO stretched diameter was particularly large (16 mm). The average PFO maximal diameter previously reported in an autopsy study⁵ was 4.9 mm (ranging from 1–19 mm). Martin et al.⁶ reported the results of PFO balloon sizing in 110 patients, with a mean diameter of 11 ± 4 mm. Sievert et al.⁷ reported the diameter of PFOs measured with a balloon catheter in 281 patients, with a mean of 10 ± 3.5 mm (ranging from 3 to 24 mm). Large devices are recommended to stabilize the interatrial septum in cases of significant ASA, but the atrial septal membrane was not hypermobile in our patient. Eccentric positioning of the septum primum may be related to root aortic dilatation and regarded as a risk factor for secondary mobilization of the closure device. Studies of malpositioning and/or embolization of PFO closure devices have already been published.^6,8–11 Cardiac surgical repair is generally required in cases of a malpositioned device. Following systemic embolization, partial withdrawal by catheter to the femoral vessel is sometimes feasible,^8,10 as illustrated in our case. A groin incision is generally recommended to remove the device in order to avoid local injury.¹² This case report demonstrates that substantial complications may occur following an initial successful procedure. Due to the low risk of recurrence in cases of stroke of unknown cause associated with PFO, a low periprocedural risk is an absolute prerequisite to demonstrate any benefit in future randomized controlled studies. The shape and dimensions of PFOs are not uniform, and there are no clear guidelines to size PFOs. Large PFOs with eccentric positioning of the septum primum means the procedure will be more complex. It is imperative to optimize the methods for assessing morphological PFO and ASA characteristics and the anatomy of the atrial abnormality in order to ensure device suitability. Acknowledgements. We wish to thank Pierre Amarenco, MD, Philippe Niclot, MD, Ivan Philip, MD and Alec Vahanian, MD, for their help in the preparation of this case report.

1. Khairy P, O’Donnell CP, Landzberg MJ, et al. Transcatheter closure versus medical therapy of patent foramen ovale and presumed paradoxical thromboembolic. A systematic review. Ann Intern Med 2003;139:753–760. 2. Windecker S, Wahl A, Nedeltchev K, et al. Comparison of medical treatment with percutaneous closure of patent foramen ovale in patients with cryptogenic stroke. J Am Coll Cardiol 2004;44;750–758. 3. Marshall AC, Lock JE. Structural and compliant anatomy of the patent foramen ovale in patients undergoing transcatheter closure. Am Heart J 2000;140:303–307. 4. Amarenco P. Patent foramen and the risk of stroke. Smoking gun or guilty by association? Heart 2005;91:441–443. 5. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: An autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20. 6. Martin F, Sanchez PL, Doherty E, et al. Percutaneous transcatheter closure of patent foramen ovale in patients with paradoxical embolism. Circulation 2002;106:1121–1126. 7. Sievert H, Horvath K, Zadan E, et al. Patent foramen ovale closure in patients with transient ischemia attack/stroke. J Intervent Cardiol 2001;14:261–266. 8. Beitzke A, Schuchlenz H, Gamillscheg A, et al. Catheter closure of the persistent foramen ovale: Mid-results in 162 patients. J Intervent Cardiol 2001;14:223–230. 9. Alameddine F, Block PC. Transcatheter patent foramen ovale closure for secondary prevention of paradoxical embolic events: acute results from the FORECAST registry. Catheter Cardiovasc Interv 2004;62:512–516. 10. Braun M, Gliech V, Boscheri A, et al. Transcatheter closure of patent foramen ovale (PFO) in patients with paradoxical embolism. Periprocedural safety and mid-term follow-up results of three different device occluder systems. Eur Heart J 2004;25:424–430. 11. Schwerzmann M, Windecker S, Wahl A, et al. Percutaneous closure of patent foramen ovale: Impact of device design on safety and efficacy. Heart 2004;90:186–190. 12. Berdat PA, Chaterjee T, Pfammatter J-P, et al. Surgical management of complications after transcatheter closure of an atrial septal defect or patent foramen ovale. J Thorac Cardiovasc Surg 2000;120:1034–1039.