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Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence
Published on: December 23, 2022
Is stroke a paradoxical embolism in patients with patent foramen ovale?
Masahiro Yasaka1, Ryoichi Otsubo, Hiroshi Oe
1Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan.
Insights
In stroke patients with patent foramen ovale (PFO), paradoxical embolism is not the sole cause of stroke. Other stroke mechanisms frequently contribute, even in the presence of PFO.
Area of Science:
- Cardiology
- Neurology
- Vascular Medicine
Background:
- Patent foramen ovale (PFO) is a potential cause of stroke, particularly paradoxical embolism.
- Distinguishing stroke mechanisms in PFO patients is crucial for effective treatment.
Purpose of the Study:
- To investigate and compare stroke mechanisms in patients with PFO and sinus rhythm versus those with PFO and atrial fibrillation, and those with atrial fibrillation alone.
- To assess the prevalence of paradoxical embolism in stroke patients with PFO.
Main Methods:
- Retrospective review of medical records for 111 PFO with sinus rhythm (PFO-S) patients, 25 PFO with atrial fibrillation (AF) patients (PFO-AF), and 67 AF patients without PFO.
- Clinical and neuroradiological findings were compared.
- Deep vein thrombosis (DVT) was investigated to assess for paradoxical embolism criteria.
Main Results:
- PFO-S patients showed more hypercholesterolemia and posterior circulation lesions compared to PFO-AF and AF groups.
- Other embolic sources were identified in 52.9% of PFO-S and PFO-AF patients.
- Definite paradoxical embolism was rare (3.2%), while probable paradoxical embolism was found in 35.5% of PFO patients with DVT screening.
Conclusions:
- Stroke in PFO patients can result from mechanisms beyond paradoxical embolism.
- Identifying alternative stroke etiologies is essential for comprehensive stroke management in PFO patients.
Objective:
Purpose was to assess the stroke mechanism in patients with patent foramen ovale (PFO).
Methods:
We reviewed the medical records of 111 stroke patients with PFO and sinus rhythm (PFO-S group), 25 with PFO and atrial fibrillation (AF) (PFO-AF group) and 67 with AF but not PFO (AF group), who had received contrast transesophageal echocardiography. The clinical and neuroradiological findings were then compared among the three groups. Deep vein thrombosis was investigated in 93 patients with PFO. We determined the number of patients with definite paradoxical embolism who met three criteria: deep vein thrombosis, neuroradiological features indicating embolic stroke, and the absence of other sources of emboli. We also evaluated those with probable paradoxical embolism who met two of the three criteria.
Results:
The PFO-S group more frequently exhibited hypercholesterolemia (p<0.0001) and lesions limited to the posterior circulation (p<0.0004), and less frequently exhibited large or cortical lesions in the anterior circulation (p=0.0008, p<0.0001, respectively), than the PFO-AF and AF groups. In the PFO-S and PFO-AF groups, other sources of emboli such as a cardiac source of emboli, cerebral artery stenosis > or =50%, or complicated atheroma in the aortic arch were identified in 72 cases (52.9%). In the 93 patients with examination for deep vein thrombosis, the definite and probable criteria of paradoxical embolism were fulfilled only in three (3.2%) and 33 cases (35.5%), respectively.
Conclusion:
In stroke patients with PFO, not only paradoxical brain embolism through the PFO but also other causes of stroke may contribute to the development of stroke.
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