Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

Introduction

An artery-to-artery embolic stroke occurs when a thrombus (blood clot) or atheromatous debris dislodges from one arterial location and embolizes to occlude a downstream cerebral artery, leading to ischaemia and infarction of brain tissue. This mechanism is distinct from cardioembolic stroke, where the embolus originates from the heart. Artery-to-artery embolism is a significant cause of ischemic stroke, particularly in patients with atherosclerotic disease.

Etiologies include

• Atherosclerotic Plaque Rupture: Thrombus formation on atherosclerotic plaques can embolize to cerebral arteries.
• Arterial Dissection: Thrombus formation on exposed intima or media due to dissection can lead to embolism.
• Embolization from Proximal Arteries: Emboli can originate from the aortic arch, common carotid arteries, internal carotid arteries, vertebral arteries, or the basilar artery.

Anatomical Sources: Several arterial sites are common sources of emboli:

• Extracranial Carotid Artery Atherosclerosis:
  • Atherosclerotic plaques commonly develop at the carotid bifurcation and proximal internal carotid artery.
  • Risk factors include age, male sex, hypertension, smoking, diabetes mellitus, and hyperlipidemia.
  • The degree of stenosis correlates with stroke risk; significant stenosis can cause turbulent flow and promote thrombus formation.
• Intracranial Atherosclerosis:
  • Atherosclerosis can affect intracranial vessels such as the carotid siphon and middle cerebral artery.
  • More prevalent in Asian, African, and Hispanic populations.
  • Can lead to in situ thrombosis or embolization downstream.
• Arterial Dissection:
  • Dissection of the carotid or vertebral arteries can create a false lumen and expose subendothelial layers, promoting thrombus formation.
  • Dissections may be spontaneous or result from trauma, including minor injuries or cervical manipulations.
  • Connective tissue disorders like Ehlers-Danlos syndrome type IV, Marfan syndrome, cystic medial necrosis, and fibromuscular dysplasia increase susceptibility.
  • Intracranial dissections may lead to subarachnoid hemorrhage due to vessel fragility.
• Aortic Arch Atherosclerosis:
  • Complex plaques in the aortic arch can be a source of emboli to the cerebral circulation.
  • Plaques greater than 4 mm in thickness are associated with a higher risk of stroke.

Clinical Presentation

• The clinical features of artery-to-artery embolic stroke are similar to other ischemic strokes but may have some distinguishing characteristics:
• Sudden Onset: Neurological deficits develop abruptly and are maximal at onset.
• Territory-Specific Symptoms: Deficits correspond to the vascular territory of the affected artery (e.g., unilateral weakness, speech disturbances).
• Transient Ischemic Attacks (TIAs): May precede stroke due to intermittent embolization or fluctuating stenosis.
• Associated Symptoms:
  • In carotid artery disease: Amaurosis fugax (transient monocular blindness), carotid bruits.
  • In vertebral artery dissection: Neck pain, occipital headache, Horner's syndrome.

Investigations: comprehensive evaluation is necessary

• Laboratory Tests: Complete blood count (CBC), electrolytes, glucose, lipid profile, coagulation studies.
• Electrocardiogram (ECG): To rule out cardiac arrhythmias; however, cardioembolic sources are less likely in this context.
• Neuroimaging:
  • Non-Contrast CT Scan: Initial imaging to exclude hemorrhage and assess for early ischemic changes.
  • Magnetic Resonance Imaging (MRI): Diffusion-weighted imaging (DWI) is sensitive for detecting acute infarcts.
• Vascular Imaging:
  • Carotid Doppler Ultrasound: Non-invasive assessment of extracranial carotid stenosis.
  • Computed Tomography Angiography (CTA): Provides detailed images of both extracranial and intracranial vessels.
  • Magnetic Resonance Angiography (MRA): Alternative to CTA, useful for patients with contraindications to contrast agents.
  • Cerebral Angiography: Gold standard but invasive; used when precise vascular anatomy is required.
• Transcranial Doppler Ultrasound: Assesses intracranial blood flow velocities and detects embolic signals.
• Echocardiography: Typically to rule out cardiac sources if clinical suspicion exists.

Management

Acute Treatment and secondary prevention:

• Thrombolytic Therapy: Intravenous alteplase within the therapeutic window (generally within 4.5 hours of symptom onset) if no contraindications exist.
• Mechanical Thrombectomy: Endovascular intervention may be indicated for large vessel occlusions, particularly within 6 hours of onset (extended in select cases).
• Antiplatelet Therapy: Aspirin is initiated for patients not receiving thrombolysis or after thrombolysis if hemorrhage is excluded.

Secondary Prevention

• Antiplatelet Agents: Long-term therapy with aspirin, clopidogrel, or combination therapy in certain cases.
• Statin Therapy: Initiated to reduce LDL cholesterol levels and stabilize atherosclerotic plaques.
• Lifestyle Modifications: Smoking cessation, dietary changes, regular exercise, weight management.
• Blood Pressure Control: Antihypertensive medications to achieve target blood pressure levels.
• Diabetes Management: Tight glycemic control in diabetic patients.
• Carotid Endarterectomy (CEA):
  • Indicated for symptomatic patients with 70-99% stenosis of the internal carotid artery.
  • May be considered in patients with 50-69% stenosis based on individual risk factors.
  • Benefits must outweigh surgical risks; timing is crucial, ideally within two weeks of the index event.
• Carotid Artery Stenting (CAS): An alternative to CEA, especially in patients with high surgical risk or anatomical considerations.
• Treatment of Arterial Dissection:
  • Antithrombotic therapy with either antiplatelets or anticoagulation is recommended.
  • Duration typically 3-6 months, with ongoing assessment.
  • Endovascular interventions are reserved for patients with worsening symptoms or contraindications to medical therapy.

Prognosis depends on several factors:

• Size and Location of Infarct: Larger strokes and those affecting critical brain areas may have worse outcomes.
• Timeliness of Reperfusion Therapy: Early treatment improves outcomes and reduces disability.
• Control of Risk Factors: Effective management of hypertension, diabetes, hyperlipidemia, and smoking cessation improves long-term prognosis.
• Adherence to Secondary Prevention Measures: Reduces the risk of recurrent stroke.

References

• Caplan LR. Artery-to-artery embolism. The neglected cerebral embolism. Arch Neurol. 1989;46(6): 777-780.
• Chimowitz MI, Lynn MJ, Howlett-Smith H, et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. 2005;352(13):1305-1316.
• Brott TG, Halperin JL, Abbara S, et al. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease. Stroke. 2011;42(8):e464-e540.
• Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of stroke for the 21st century. Stroke. 2013;44(7):2064-2089.
• Messé SR, Kizer JR, Ay H, et al. Associations between aortic plaque and ischemic stroke: the APRIS study. Stroke. 2005;36(8): 1752-1756.