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Objective: It is unclear whether ischaemic stroke among patients with symptomatic carotid near occlusion is caused by an embolic or haemodynamic mechanism. An embolic mechanism can be reflected by the occurrence of microembolic signals (MES) on transcranial Doppler. This study aimed to compare the incidence of MES between patients with symptomatic near occlusion, symptomatic conventional ≥ 50% stenosis, and asymptomatic ≥ 50% stenosis.

Methods: This cross sectional study included patients with ≥ 50% symptomatic or asymptomatic carotid stenosis. The degree of stenosis was assessed with computed tomography angiography, where near occlusion was diagnosed by feature interpretation. Symptomatic was defined as ipsilateral events within six months. Occurrence of MES was recorded bilaterally in the middle cerebral artery for 30 minutes with transcranial Doppler.

Results: A total of 109 participants with ≥ 50% carotid stenosis were included, comprising 52 with symptomatic ≥ 50% conventional stenosis, 41 symptomatic near occlusion, and 16 asymptomatic ≥ 50% stenosis. The incidence of MES was 46% (19/41; 95% confidence interval [CI] 30 – 62%) among symptomatic near occlusion, 27% (14/52; 95% CI 14 – 39%) among symptomatic ≥ 50% conventional stenosis, and 6% (1/16; 95% CI 0 – 20%) among asymptomatic ≥ 50% carotid stenosis. The incidence of MES tended to be higher among symptomatic near occlusions compared with symptomatic ≥ 50% conventional stenoses (unadjusted odds ratio [OR] 2.3, 95% CI 1.0 – 5.6; p = .054), but was statistically significantly higher after adjustments (adjusted OR 3.9, 95% CI 1.4 – 10.7; p = .009). The MES incidence was higher among symptomatic near occlusions than asymptomatic ≥ 50% stenoses (p = .005).

Conclusion: Microembolic signals appear to be more prevalent in symptomatic near occlusions compared with both symptomatic conventional ≥ 50% carotid stenoses and asymptomatic conventional ≥ 50% carotid stenoses. These findings could reflect a possible embolic mechanism behind ischaemic stroke in symptomatic carotid near occlusion patients, but do not rule out concurrent haemodynamic mechanisms. Additional studies using various markers of both embolic and haemodynamic mechanisms are warranted.