(1)
David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA 90095, USA
24.1 Introduction
Patent foramen ovale (PFO) affects up to 20 % of the adult population and has been linked with several clinical conditions including migraines, obstructive sleep apnea, and recurrent transient neurologic deficits [1]. PFOs have been observed in up to 40 % of patients presenting with cryptogenic stroke, which represents a particular clinical challenge [2]. To date, three randomized clinical trials have been published evaluating the efficacy of percutaneous PFO closure [3–5]. As ongoing trials continue to define the role of percutaneous PFO closure, an estimated 8000 closure procedures are performed annually in the United States. The overall safety of PFO closure has been demonstrated in several observational studies; however, complications do arise. A retrospective analysis involving 13,736 device implantations over 18 institutions showed a 0.28 % rate of device explantation [6]. While the overall rate of explantation is low, the necessity for open heart surgery makes this a particularly worrisome outcome.
The following case example illustrates a scenario that led to device explantation.
24.2 Case Example
A 54-year-old woman presented with a history of migraine headaches with aura since age 12 and subsequently was found to have a patent foramen ovale. Due to the frequency of her migraine headaches, the patient underwent PFO closure with an 18-mm cribriform Amplatzer ASD device 9 years prior to the current admission. Within days after implantation, the patient experienced an increase in the number of migraines with aura, chest pain, and episodic atrial fibrillation. She was treated with steroids and antiplatelet therapy with minimal symptom improvement. A TRUE skin patch test for nickel allergy was negative. She was referred to a tertiary medical center where surgical device explantation was recommended; however she chose continued observation and medical therapy. Nine years later, the patient experienced sudden onset of ataxia, weakness, and left hemianopsia and was found to have an embolic stroke on MRI in the absence of atrial fibrillation (Fig. 24.1). The patient underwent a transesophageal echocardiogram that revealed an atrial septal aneurysm without residual shunt or thrombus on the device on the left atrial appendage (Fig. 24.2). The patient underwent robotic-assisted surgery to remove the device. The explanted device showed severe fibrosis and scarring predominantly over the left atrial disk (Fig. 24.3). The patient underwent robotic-assisted surgery to remove the device. The explanted device showed severe fibrosis and scarring predominantly over the left atrial disk. After explantation, the patient had resolution of her chest pain, migraines, and palpitations but continued to experience a visual field defect and left-sided weakness from the prior stroke.
