How does a Patent Foramen Ovale (PFO) cause cardioembolic events?

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Last updated: February 27, 2025View editorial policy

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From the Guidelines

Patent foramen ovale (PFO) causes cardioembolic stroke through a mechanism called paradoxical embolism, where a venous blood clot bypasses the lungs and enters the arterial circulation, potentially traveling to the brain and causing an ischemic stroke. Normally, the foramen ovale closes after birth, but in about 25% of people, it remains partially open [ 1 ]. A PFO creates a potential right-to-left shunt between the atria of the heart. When a person has a venous blood clot (typically from deep vein thrombosis in the legs), these clots usually travel to the lungs where they're filtered out. However, with a PFO, the clot can pass directly from the right atrium to the left atrium, bypassing the lungs, and enter the arterial circulation. From there, the clot can travel to the brain, causing an ischemic stroke. This risk increases during activities that raise right atrial pressure (like straining, coughing, or Valsalva maneuver), which can temporarily open the PFO flap wider.

Key Factors Increasing Stroke Risk with PFO

  • Having an atrial septal aneurysm
  • A large shunt size
  • Hypercoagulable states
  • Recent studies, such as the CLOSE trial [ 1 ], have demonstrated that PFO closure can be superior to medical therapy for prevention of stroke recurrence in carefully-selected patients.
  • The REDUCE trial [ 1 ] also showed that PFO closure can reduce the rate of ischemic stroke in patients with a PFO and a right-to-left shunt.

Treatment Options

  • Antiplatelet therapy (typically aspirin 81-325mg daily)
  • Anticoagulation (such as warfarin or direct oral anticoagulants)
  • PFO closure via a percutaneous procedure, depending on individual risk factors and stroke recurrence risk, as recommended by the Canadian stroke best practice recommendations [ 1 ]. PFO closure is recommended for very carefully-selected patients aged 60 years or younger with an unexplained embolic stroke event who are found to have a PFO and who do not require chronic anticoagulant therapy for another reason. Patient counseling and shared decision-making, taking into account patient values and preferences, are important considerations [ 1 ].

From the Research

Mechanism of Cardioembolic Events

A Patent Foramen Ovale (PFO) can cause cardioembolic events through the following mechanisms:

  • Paradoxical embolism, where venous thrombi enter the arterial circulation through the PFO, avoiding filtration by the lungs, and causing ischemic stroke 2, 3, 4, 5
  • Right-to-left shunting through the PFO, which can exacerbate hypoxia in the setting of severe pulmonary embolism 6

Pathophysiology

The PFO serves as a conduit for harmful circulatory factors to travel directly from the venous to the arterial circulation, contributing to neurovascular disease 2 The anatomy of the PFO allows for the passage of thrombi and other harmful factors, making it a potential cause of cardioembolic events 4

Clinical Implications

PFO-related strokes affect a significant number of people, with PFO present in up to 60% of migraine patients with aura and in one out of four normal individuals 2 The presence of a PFO is associated with an increased risk of ischemic stroke, and the best treatment modality to prevent recurrent stroke remains undefined 5 PFO closure, either surgical or percutaneous, may reduce event rates, but further research is needed to demonstrate its effectiveness 3, 5

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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