What is the recommended management for a patient with a patent foramen ovale (PFO) who has experienced a stroke and also has superficial venous thrombosis?

Management of Stroke in Patient with Patent Foramen Ovale and Superficial Venous Thrombosis

For patients with patent foramen ovale (PFO) who have experienced a stroke and also have superficial venous thrombosis, PFO closure plus antiplatelet therapy is strongly recommended over antiplatelet therapy alone to reduce recurrent stroke risk. 1, 2

Assessment and Risk Stratification

• Determine if the stroke is cryptogenic (no other identified cause) through:

  • Prolonged rhythm monitoring to exclude atrial fibrillation
  • Transoesophageal echocardiography or alternative imaging of the aorta and left atrial appendage
  • Carotid ultrasonography, CT, or MRI to rule out cerebrovascular disease

• Evaluate PFO characteristics using echocardiography:

  • Size of shunt (large shunts carry higher risk)
  • Presence of atrial septal aneurysm (increases risk)
  • Right-to-left shunt direction

• Consider using the PASCAL classification system to determine if PFO is the "probable," "possible," or "unlikely" cause of stroke 3

  • Combines RoPE score (age, history of stroke/TIA, diabetes, hypertension, smoking, cortical infarct) with anatomical criteria
  • Patients with "probable" PFO-related stroke benefit most from closure

Treatment Algorithm

1. For patients with PFO, stroke, and superficial venous thrombosis:

• First-line approach: PFO closure followed by antiplatelet therapy 1, 2

  • Strongest benefit in younger patients (<50 years) with large PFO
  • Reduces recurrent stroke risk by 8.7% over 5 years compared to antiplatelet therapy alone
  • Procedure typically takes under 2 hours with hospital stay of one day

• If anticoagulation is contraindicated or declined:

  • PFO closure plus antiplatelet therapy is strongly recommended over antiplatelet therapy alone 1, 2

• If PFO closure is contraindicated or declined:

  • Anticoagulation is preferred over antiplatelet therapy alone 2, 4
  • This is particularly important with concurrent superficial venous thrombosis, which represents a potential source for paradoxical embolism

2. Special considerations for superficial venous thrombosis:

• The presence of superficial venous thrombosis represents a venous source of embolism
• According to guidelines, anticoagulation is indicated when both PFO and a venous source of embolism are present 1
• When anticoagulation is contraindicated in this scenario, an inferior vena cava filter may be reasonable 1

Post-Procedure Management

• After PFO closure:

  • Continue antiplatelet therapy (typically aspirin)
  • Monitor for device-related complications (3.6% absolute risk) 2
  • Watch for new-onset atrial fibrillation (increased risk of 1.8% absolute risk) 2
  • Most atrial fibrillation occurs within the first year after the procedure

• For patients on anticoagulation:

  • Regular monitoring of anticoagulation levels if using warfarin
  • Direct oral anticoagulants are an alternative option

Potential Complications and Monitoring

• PFO closure complications:

  • Device-related adverse events (3.6% absolute risk) 2
  • Persistent atrial fibrillation (1.8% absolute risk increase) 2
  • Transient atrial fibrillation (1.2% absolute risk increase) 2
  • Pericardial effusion and pseudoaneurysm (rare) 2

• Anticoagulation complications:

  • Bleeding risk (non-significantly higher than with antiplatelet therapy) 4
  • Regular monitoring required for warfarin

Evidence Quality and Limitations

• The strongest evidence supports PFO closure in patients under 60 years with cryptogenic stroke 1, 2, 3
• Benefits of PFO closure are less certain in patients over 60 years and those with traditional cerebrovascular risk factors 2
• The CLOSE trial showed no stroke recurrence in patients who underwent PFO closure, compared to 14 strokes in the antiplatelet-only group 5
• The presence of superficial venous thrombosis strengthens the case for either PFO closure or anticoagulation, as it represents a potential source for paradoxical embolism 1