What is the treatment for vertebral artery dissection?

Treatment of Vertebral Artery Dissection

Initiate antithrombotic therapy for 3-6 months immediately upon diagnosis, using either anticoagulation (heparin followed by warfarin with target INR 2.0-3.0) or antiplatelet therapy (aspirin 81-325 mg daily or clopidogrel 75 mg daily), then transition to long-term antiplatelet therapy. 1, 2

Initial Antithrombotic Management

The American Heart Association/American Stroke Association provides a Class IIa recommendation for antithrombotic therapy in symptomatic vertebral artery dissection. 1, 2 The choice between anticoagulation and antiplatelet therapy depends on specific clinical features:

Anticoagulation Preferred:

• Patients with angiographic evidence of thrombus in the extracranial vertebral artery 3
• Acute ischemic syndromes involving the vertebral artery territory with visible thrombus 3
• Treatment regimen: IV heparin initially, followed by warfarin targeting INR 2.0-3.0 for 3-6 months 1, 2

Antiplatelet Therapy as Alternative:

• Patients without evidence of thrombus 3
• Options include aspirin 81-325 mg daily, clopidogrel 75 mg daily, or combination aspirin plus extended-release dipyridamole 1, 2, 3
• The combination of aspirin plus extended-release dipyridamole has shown benefit in reducing vertebrobasilar territory stroke or TIA with moderate strength of evidence 3

Comparative Outcomes:

Observational data shows annual rates of recurrent stroke, TIA, or death of 8.3% with anticoagulation versus 12.4% with aspirin alone, though this difference is not definitive. 1, 2

Critical Contraindication: Intracranial Extension

Anticoagulation is absolutely contraindicated if subarachnoid hemorrhage occurs from intracranial extension of the dissection. 1 Intracranial vertebrobasilar dissections carry higher rupture risk, and anticoagulation may adversely influence outcomes in this scenario. 1 This is why concurrent brain imaging (MRI or CT) should be performed with vascular imaging to assess for hemorrhagic complications. 2

Duration and Transition

• Initial antithrombotic therapy: 3-6 months 1, 2
• After initial period: transition to antiplatelet therapy for long-term management 1
• The risk of hemorrhagic transformation with anticoagulation appears low (<5%) in appropriately selected patients 1

Invasive Treatment Indications

Surgical or endovascular revascularization is reserved exclusively for specific failure scenarios:

• Persistent or recurrent ischemic symptoms despite optimal antithrombotic therapy 1, 2
• Endovascular options include angioplasty and stenting (Class IIb recommendation) 1
• Surgical options include direct vertebral artery repair or resection with vein graft replacement 1
• Endovascular risks include death (0.3%), periprocedural neurological complications (5.5%), and posterior stroke (0.7%) 3
• Restenosis occurs in approximately 26% of proximal vertebral artery interventions 3

Blood Pressure Management

The role of pharmacological blood pressure reduction with beta-blockers, angiotensin inhibitors, or non-dihydropyridine calcium channel blockers to reduce arterial wall stress is not well established (Class IIb recommendation). 1 This should not be a primary focus of management.

Prognosis and Follow-up Considerations

• With appropriate antithrombotic treatment, prognosis is usually favorable 1, 2
• Anatomic healing occurs in 72-100% of patients with medical management alone 1
• Dissections that do not fully heal anatomically are not associated with increased recurrent stroke risk, so further intervention for asymptomatic residual lesions is not warranted 1
• Vertebral artery dissection accounts for 10-15% of ischemic strokes in patients under 45 years, making it a critical diagnosis in younger stroke patients 1

Common Pitfalls to Avoid

• Do not delay antithrombotic therapy while awaiting complete diagnostic workup – treatment should begin immediately after diagnosis confirmation 2
• Do not assume elevated CRP indicates vasculitis – dissection itself causes inflammatory marker elevation 2
• Do not anticoagulate without excluding intracranial extension or subarachnoid hemorrhage 1
• Do not pursue invasive revascularization for asymptomatic lesions or as first-line therapy 1, 2