Discussion
Risk Factors
Predisposing factors for device embolization may be: device too small,
atrial septal aneurysm (ASA), thick septum secundum (> 10
mm), long tunnel5 (≥ 8 mm)6,
deficient rims of surrounding tissue and device
malpositioning3. In this case, we believe that the
choice of a device too small, the presence of an ASA and a long tunnel
could have favoured the device leaving from its site. The PFO tunnel was
longer than measured at the TEE during the intervention (24 mm vs. 13-14
mm, respectively): the possible tunnel length underestimation could have
led to the choice of an unsuitable device for the PFO characteristics
and, therefore, to its displacement. The patient denied having performed
manoeuvres potentially able to facilitate the device displacement, such
as having coughed heavily or repeatedly7,8. A
peculiarity of this case is the finding of this complication in presence
of other congenital defects (BAV and previous AC). The presence of other
congenital defects may have predisposed the device displacement (e.g.
precluding an adequate device fixation). Furthermore, the surgical
repair of the aortic coarctation may have favoured a more distal drop of
the device. The device embolization in presence of multiple congenital
defects represents a unique event in the literature, which gives thought
to other possible mechanisms of the PFO occluder device displacement in
patients with multiple congenital defects.
Symptoms
The mechanisms underlying the symptoms remain unclear. We assume that
the onset of dyspnoea after the intervention was caused by the worsening
of the right-left shunt (provoked by exercise) due to the PFO
enlargement following the device displacement; this may be supported by
the detection of a significant oxygen desaturation on the 6-Minutes
Walking Test (98% to 92% after 2 minutes), an event already observed
in other patients with PFO, defined as Provoked Exercise
Desaturation (PED) 9. We excludedPlatypnea Orthodeoxia Syndrome (POS) , as the patient had a normal
arterial oxygen saturation in standing position. We also presume that
the chest pain radiated to the limbs, after having excluded
statin-induced myopathy (normal creatine kinase), was the expression of
an aortic syndrome with atypical features, due to the presence of the
foreign body into the abdominal aorta. This may be confirmed by its
disappearance after the device retrieval.
Follow-up
Lastly, we believe that if a TTE before discharge or a TTE with bubble
study within 1 month from discharge had been performed, the problem
would certainly have been identified earlier and with lower risk for the
patient. Indeed, the current guidelines recommend TTE before discharge,
TTE with bubble study after 1, 6, 12 months and, then, every 1-2
years3. However, a correct follow-up probably was
hindered by the COVID-19 pandemic.
Conclusion
As shown, the embolization of a PFO occluder device is a very rare but
possible complication (in this case reported for the first time in a
patient with multiple congenital defects). For this reason, we strongly
recommend paying attention to 1) risk factors before the intervention
(PFO characteristics and multiple congenital defects) to correctly
choose the device to be placed, and to 2) the clinical-echocardiographic
follow-up to recognize and treat this severe complication as soon as
possible.