ISCHEMIC STROKE / PREVENTION

Patent foramen ovale (PFO)

Created 25/01/2023, last revision 21/04/2023

before birth, the atrial septum is formed by two leaves. After birth, the pressure rises in the left atrium and the two leaves fuse together
in 1/3 of people, the leaves do not fuse, and a different-sized opening called a patent foramen ovale (PFO) or foramen ovale apertum (FOA) persist
PFO causes a right-to-left shunt – blood can flow from the right atrium directly into the left atrium, bypassing the pulmonary circulation
various particles in the blood can bypass the pulmonary circulation together with the blood and enter the systemic circulation (paradoxical embolism)
- small blood clots released from the veins of the lower limbs and pelvis
- gas bubbles (formed during rapid decompression in scuba divers or administered by IV injections)
- certain hormones (serotonin in migraine with aura?)
PFO alone does not cause hemodynamic problems
PFO is not the only cause of right-to-left shunting:
- intracardiac shunts (90%) – patent foramen ovale (PFO), atrial septal defects
- extracardiac shunts (10%) – mostly pulmonary AV shunts
- combination of extra- and intracardiac shunts is possible

PFO and cryptogenic stroke

patent foramen ovale (PFO) is associated with cryptogenic stroke (CS), though the pathogenicity of discovered PFO in the setting of CS is typically unclear
- the prevalence of PFO is approx. 25% in the general population and up to 46% in patients with CS
PFO is occasionally associated with the following conditions:
- atrial septal aneurysm (ASA) / hypermobile atrial septum – defined as excursion ≥ 10-15 mm from the midline
- atrial septal defect
PFO-related stroke mechanisms:
- paradoxical embolization from peripheral veins
- embolization of a thrombus formed directly within the PFO canal

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2D or 3D + bubble test – sensitivity and specificity between 89-95%
information on PFO shape and size and associated pathologies (ASA, septal hypermobility, LAA thrombus, etc.)
disadvantages:
- invasive nature of the procedure; some patients may not tolerate it
- lower sensitivity for small PFOs

primary prevention: PFO closure not indicated
secondary prevention: consider antiplatelet or anticoagulant therapy and PFO closure

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a higher prevalence of PFO has been reported in patients with migraine with aura than in patients with migraine without aura or patients without migraine (48% vs. 23% and 20%, respectively).
the causal association remains unclear
some small non-randomized trials have reported a reduced incidence of migraine after PFO closure
randomized trials MIST (Starfix, 2016) and PREMIUM (Amplatzer, 2017) did not show a preventive effect
- MIST – primary outcome: migraine regression in 3 of 74 (occlusion) vs. 3 of 74 (control), significant complications (SAEs) in 16 of 74 patients
- PREMIUM – primary outcome: 45/117 (Amplatzer) vs. 33/103 (control)
in conclusion, it is less likely that PFO plays a role in the development migraine headache
the role of PFO in the development of ischemic stroke in migraineurs has not been determined yet
- patients with both migraine and stroke had larger shunts than patients with migraine without stroke, patients without migraine with stroke, and controls
- with respect to the white matter hyperintensities (WMH), overall WMH did not differ by PFO presence; however, juxtacortical WMH are more frequently found in patients with migraine and right-to-left shunting
- these findings suggest that incidental PFO may increase the risk of ischemic stroke in migraineurs