Patent Foramen Ovale and Secondary Stroke Prevention

Publication Date: April 29, 2020
Last Updated: April 5, 2023

Summary of Recommendations

Recommendation 1


Ischemic stroke may be caused by a variety of heterogeneous mechanisms, and secondary stroke prevention is optimized by targeting the most likely etiology of the preceding event. An appropriately thorough workup depends on the individual patient and whether a compelling stroke etiology has already been identified. The randomized patent foramen ovale (PFO) closure trials all mandated thorough evaluations for participants before enrollment, including CT angiography (CTA) or MR angiography (MRA) of the head and neck vessels in all studies and hypercoagulable screening in many to rule out other stroke mechanisms; moreover, all studies required transesophageal echocardiography (TEE) to characterize the PFO and ensure that it was the most likely etiology for the initial event. There is accumulating evidence that occult atrial fibrillation accounts for a meaningful portion of cryptogenic stroke. Given that they were designed and initiated before atrial fibrillation monitoring became routine, none of the PFO closure trials required prolonged monitoring before enrollment, although it is important to note that the incidence of atrial fibrillation is strongly correlated with increasing age and is unlikely to occur in patients <50 years. Other risk factors and biomarkers have been associated with atrial fibrillation and may increase clinical suspicion, including systemic hypertension, obesity, sleep apnea, enlarged left atrium, hyperthyroidism, diabetes, alcohol abuse, cigarette smoking, elevated serum N-terminal pro b-type natriuretic peptide (NT-proBNP), frequent premature atrial contractions, and increased P wave dispersion on ECG.

PFO is highly prevalent, found in approximately 25% of the general adult population on agitated-saline TEE and cadaveric studies. Transcranial Doppler ultrasonography (TCD) has been demonstrated to have similar sensitivity and specificity to TEE to detect right-to-left shunting, although TCD does not rule out other cardioembolic sources seen on TEE and cannot confirm that shunting is intracardiac or assess PFO morphology, including anatomic size, location, and length of the tunnel. Multiple studies have identified an association between PFO and otherwise cryptogenic stroke, with increasing PFO prevalence in younger patients with stroke and those lacking traditional vascular risk factors such as hypertension, hypercholesterolemia, and diabetes.

The risk of stroke recurrence in patients with PFO and no other etiology identified is low, approximately 1% per year while individuals are treated with medication alone. This stroke risk is generally lower than the stroke risk caused by other possible common stroke mechanisms. Thus, if an alternative plausible higher risk mechanism of stroke is identified, it is likely that the PFO was an “innocent bystander.”



Patent Foramen Ovale and Secondary Stroke Prevention

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