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
Artery-to-Artery Embolic Stroke
π§ Introduction
An artery-to-artery embolic stroke occurs when thrombus or atheromatous debris from one arterial site dislodges β occludes a downstream cerebral artery, causing ischaemia & infarction.
β‘ Unlike cardioembolic stroke, the embolus here originates from diseased arteries, most often in the neck or intracranial circulation.
It accounts for a significant proportion of ischaemic strokes, particularly in patients with atherosclerosis or arterial dissection.
π Etiology
- π’ Atherosclerotic plaque rupture: Most common; plaques at carotid bifurcation prone to thrombus & embolization.
- π’ Arterial dissection: Carotid/vertebral dissections expose intima β thrombus forms β emboli.
- π’ Aortic arch plaques: Complex plaques (>4 mm) highly emboligenic.
- π’ Other: Intracranial atherosclerosis, procedural vessel injury, inflammatory arteriopathies.
π Common Sources
- Extracranial carotid bifurcation: Classic site; bruit + amaurosis fugax clue π¨
- Intracranial vessels (MCA, siphon): Common in Asian & Black populations.
- Arterial dissection: Neck pain, occipital headache, Hornerβs syndrome.
- Aortic arch: High-risk plaques seen on TEE.
π©Ί Clinical Features
- β‘ Sudden onset: Maximal deficit at onset (similar to embolic pattern).
- π§© Territory-specific symptoms: MCA = hemiparesis/aphasia; PCA = hemianopia; vertebrobasilar = ataxia, diplopia.
- β³ TIAs: Preceding stroke due to intermittent embolization (warning sign).
- π Amaurosis fugax: βCurtain coming downβ over one eye (carotid emboli).
- 𦡠Vertebral dissection: Neck pain + lateral medullary features.
π§ͺ Investigations
- π©Έ Bloods: FBC, glucose, lipids, coagulation profile.
- π ECG: Rule out AF (to distinguish from cardioembolic).
- πΌ Brain imaging: CT (exclude bleed); MRI-DWI most sensitive for acute infarcts.
- π« Vascular imaging:
- Carotid Doppler (non-invasive, for stenosis).
- CTA/MRA (visualise extracranial & intracranial vessels, dissections).
- Cerebral angiography (gold standard, reserved for intervention).
- π Transcranial Doppler: Detects embolic signals in intracranial arteries.
- π« Echocardiography: Rule out cardiac embolic sources if uncertain.
βοΈ Acute Management
- π IV Thrombolysis (tPA): Within 4.5h of onset (if eligible).
- π§© Mechanical thrombectomy: Large vessel occlusions; effective up to 6h (sometimes extended with perfusion imaging).
- π Antiplatelets: Aspirin 300 mg (unless thrombolysed β then post-24h).
π‘ Secondary Prevention
- π Antiplatelets: Aspirin, clopidogrel, or dual therapy short-term in some cases.
- π Statins: High-dose statin to stabilise plaques (LDL < 1.8 mmol/L target).
- β€οΈ Risk factor control: BP, diabetes, smoking cessation, diet & exercise.
- πͺ Carotid Endarterectomy (CEA):
- Indicated if symptomatic & 70β99% stenosis.
- Benefit greatest if performed within 2 weeks of TIA/stroke.
- πͺ‘ Carotid Stenting: Alternative in high surgical risk patients.
- π©Έ Arterial Dissection: Antithrombotic therapy (antiplatelet or anticoagulation) for 3β6 months; endovascular therapy if worsening.
π Prognosis
- π’ Better if treated early with thrombolysis or thrombectomy.
- π‘ Risk of recurrence if stenosis untreated or risk factors uncontrolled.
- π΄ Poor outcomes with large MCA/PCA occlusions or delayed recanalization.
π References
- Caplan LR. Artery-to-artery embolism: the neglected cerebral embolism. Arch Neurol. 1989.
- Brott TG et al. ASA/AHA Guidelines for extracranial carotid & vertebral artery disease. Stroke. 2011.
- Chimowitz MI et al. Warfarin vs aspirin for intracranial stenosis. NEJM. 2005.