Carotid Stenosis–Related Atherothrombotic Stroke: Evidence‑Based Management

Pathophysiology

Carotid‑artery stenosis‑related stroke is a classic atherothrombotic event caused by rupture of an atherosclerotic plaque, formation of a thrombus, and subsequent cerebral embolization. [1][2]

Non‑stenotic carotid plaques that display high‑risk features can serve as a source of cerebral embolism, conferring a recurrent stroke or transient ischemic attack risk of approximately 2.6–4.9 events per 100 person‑years. [1][2]3
Patients with overt cardiovascular disease or diabetes experience a markedly higher annual risk of recurrent stroke (up to 2.5 % per year), and the risk is even greater in those with prior cerebral infarction. [1][2][3][5]

In individuals with symptomatic carotid stenosis who are not candidates for immediate revascularization, dual antiplatelet therapy (low‑dose aspirin + clopidogrel 75 mg) is recommended for the first ≥21 days, followed by long‑term single‑agent antiplatelet therapy. 4

High‑intensity statin therapy (e.g., atorvastatin 80 mg daily) reduces subsequent cerebrovascular events, as demonstrated in the SPARCL trial.
Comprehensive secondary‑prevention programs should also include optimal blood‑pressure control and modification of other vascular risk factors. [2][3]5

For symptomatic carotid stenosis ≥70 % (NASCET criteria), carotid endarterectomy or stenting should be performed ideally within 2 weeks of the index event to minimize recurrence. 6