Successful Percutaneous Closure of Patent Foramen Ovale Seven Years After Surgical Closure

Patent foramen ovale (PFO) is a common phenomenon, affecting approximately one-quarter of the normal healthy population. The prevalence of PFO in patients with ischemic stroke is significantly higher than in the normal population.¹ Many patients with PFO who have had a stroke are initially treated therapeutically with aspirin, warfarin or clopidogrel, or a combination thereof. However, a percentage of these patients either fail or wish to discontinue medical therapy. In these patients, closure of PFO is an attractive goal. With the emergence of percutaneous transcatheter closure, there are now 2 viable options for closure of PFO. We report a patient whose PFO was successfully closed with a transcatheter device 7 years after the initial surgical closure. Case Report. A 39-year-old male was transferred to our institution with a dense expressive aphasia and right hemiparesis. A head computed tomography (CT) scan was consistent with a left middle cerebral artery thrombotic stroke. He had a history of hyperlipidemia and a 14-year history of essential stage 2-stage 3 hypertension. Doppler ultrasound of the legs revealed no evidence of deep vein thrombosis (DVT) in either leg and a carotid ultrasound demonstrated no significant lesions. A transesophageal echocardiogram (TEE) showed a PFO with a contrast study that was negative at rest but showed a 1+ right to left shunt (RLS) on release of the Valsalva maneuver. Following comprehensive rehabilitation, the patient was discharged on aspirin after nearly a month and clinically followed. At time of discharge, he was able to speak in a dysfluent but clearly intelligible manner. Less than 1 year later, the patient was admitted with a painless right homonymous hemianopsia lasting approximately 15 minutes. Carotid ultrasound, transcranial Doppler and cerebral angiography were unremarkable. Head CT showed no evidence of a new stroke and magnetic resonance imaging (MRI) findings were consistent with the previous middle cerebral infarction. Another TEE was performed, which demonstrated a small RLS at rest and a 1+ RLS with Valsalva maneuver. At this time, the decision was made to proceed with surgical closure of the PFO. Later that month, the patient was brought to the operating room, where he underwent median sternotomy. He was in surgery for 80 minutes and was under cardiopulmonary bypass for 23 minutes. The defect measured 4–5 mm intraoperatively and was closed with a running suture of 4-0 Prolene (Ethicon, Inc., Somerville, New Jersey) without the use of patch material. Good closure of the defect was noted during intraoperative inspection and there were no periprocedural complications. The patient was discharged the fifth day after the operation with no complications. Seven years after the initial surgical closure, the patient presented with neurocardiogenic presyncope, fatigue and dizziness, which were exacerbated when he was dehydrated. The patient was not hypoglycemic. These symptoms had been occurring for 6 months and usually resolved when the patient ate or drank something or sat down. A TEE demonstrated a moderate-severe 3+ RLS with Valsalva release (Figure 1). Also, a trivial left to right shunt was seen by color Doppler. The patient decided to proceed with percutaneous PFO closure using the CardioSEAL septal occluder (Nitinol Medical Technologies, Inc., Boston, Massachusetts). He was brought to the cardiac catheterization laboratory and a 28 mm device was implanted using the standard technique. Good left and right atrial apposition were noted at the time of implantation. His mean left atrial pressure was 8 mmHg. Fluoroscopy time during the procedure was 17.1 minutes and the procedure took 58 minutes. There were no complications during or after the procedure and there was no evidence for interatrial shunting immediately following device implantation. He was discharged the following day on warfarin, clopidogrel and aspirin. The patient had a follow-up TEE performed 109 days after the procedure. At this time, there was no evidence for a residual shunt, either with contrast injection or color Doppler (Figure 2). The patient has had no subsequent neurological events and is no longer taking warfarin or clopidogrel. Discussion. Surgical repair has long been the standard for closure of PFO and is a safe procedure that can be performed with minimal morbidity and mortality.^2,3 Two advantages of this method of closure are that the surgeon can visually identify the defect and the PFO can be closed regardless of the anatomy.⁴ However, this method requires that patients undergo cardiopulmonary bypass and the formation of scar tissue could predispose to arrhythmias. Percutaneous closure of interatrial septal communications has been performed for over 25 years.^4–6 At this time, there are a variety of devices used to percutaneously close PFO. The CardioSEAL device has been shown to be effective in closing atrial septal defects.⁶ In a Canadian study using the CardioSEAL device for atrial septal defects (ASD), forty-nine out of 50 patients were discharged the day after the procedure. However, at a mean follow-up of 9.9 months, forty-six percent of patients had residual shunting.⁶ Ultimately, randomized, prospective studies are needed to compare the efficacy and safety of this device with medical therapy or surgical closure. In medical management of patients with recurrent stroke resulting from PFO, anticoagulation with warfarin has been considered the gold standard of care. In a recent study, a total of 630 stroke patients, including 203 with PFO, were randomized to warfarin or aspirin. In patients with PFO, there was no significant difference in rate of recurrent ischemic stroke or death between those on warfarin and those on aspirin. The recurrence rates were 16.5% for warfarin and 13.2% for aspirin at 2 years.⁷ This suggests that aspirin may be just as effective as warfarin in the prevention of recurrent neurological events. However, the effectiveness of medical management of PFO in general needs to be further evaluated. In 2 large, long-term studies of patients with presumed paradoxical embolism, the rates for neurological event-free survival were slightly higher for percutaneous closure when compared to surgical closure. Patients who underwent percutaneous closure (n = 152) with a variety of devices had an event-free rate of 95.1% at 1 year and 90.6% at 2 and 6 years.8 Patients who underwent surgical PFO closure (n = 91) had an event-free rate of 92.5% at 1 year and 83.4% at 4 years.² Surgical patients also have a significantly longer hospital stay than those undergoing percutaneous closure and have more complications.⁴ Percutaneous transcatheter closure of PFO is a promising new technique that frees patients from the risks of life-long anticoagulation therapy by permanently closing the defect. Surgical closure offers the same benefits as percutaneous closure, but carries with it the additional risks associated with open-heart surgery. Both of the intended goals of the percutaneous procedure, to discontinue anticoagulation and to completely close the PFO, were achieved in this case. In addition, the patient was in the hospital for 4 fewer days with transcatheter closure compared to his surgical stay. This case demonstrates that percutaneous closure of PFO may be a viable option for patients in whom surgical closure has not been successful. This adds to considerable previous evidence that percutaneous closure of PFO is an important procedure and will only increase in value with future advances in device technology. Additionally, as this case demonstrates, surgical closure has its own failure rate. This fact, along with the increased chance of complications from surgery, should be kept in mind when deciding on an initial therapeutic approach for each patient.

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