After decades of debate, patent foramen ovale (PFO) closure is now a well-established strategy to reduce recurrent stroke in patients aged 18–60 years who have had a PFO-associated stroke.1 Patients who underwent PFO closure continue to have a higher stroke risk than the general population. A recent study demonstrated a 2.1% higher stroke rate in the patients who underwent PFO closure compared with age-matched controls at 4 years.2 The reasons for this elevated post-closure risk are multifactorial. These factors would include incomplete re-endothelialization of the device placed, altered left atrial hemodynamics, residual shunt and possibly that the PFO was not causative of the stroke at all.
Kim et al. investigated patients who underwent device PFO closure by computed tomography (CT), looking at re-endothelialization.3 Incomplete re-endothelialization was present for far longer than previously suspected. Larger devices, males and older patients were more prone to incomplete re-endothelialization.
Gaspardone et al. compared atrial function post-closure with devices and with suture-based closure.4 This demonstrated that only device closure altered atrial hemodynamics.
There are no randomized studies that show elevated stroke rate with residual shunt. The literature that does exist citing elevated neurologic event rates following closure lumps true stroke and transient ischemic attack (TIA).5 TIA is less of a hard endpoint compared with stroke. TIA symptoms are often subtle and, in the post-stroke patient (a significant majority of closure patients), easily confused with residual stroke symptoms. Differentiating these is purely clinical, as TIA has no permanent imaging signal. Thus, the only legitimate comparator would be stroke alone. Gaspardone et al. followed over 700 patients with suture-mediated closure for over 4 years.6 There were no recurrent neurologic events. Beyond that, a sizeable fraction of patients with residual shunt chose not to have further PFO closure of any sort. In this cohort, there were no recurrent strokes.
Thus, a reasoned and less invasive approach should be taken in the post-closure patient as a residual shunt may, in fact, not be the cause of recurrent ischemic events. With the passage of time, residual shunts reduce and often close, irrespective of the device or procedure selected.7 Prolonged antithrombotic therapy may well be a better approach and one that should be clinically evaluated. Beyond that, the placement of additional devices or plugs to seal a residual shunt would certainly seem to unfavorably affect both re-endothelialization and atrial hemodynamics.
As the contemplated role of PFO closure broadens, the development of lower profile devices, a suture-mediated closure strategy and the role of ongoing medical therapy all need consideration.
