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Objective: To assess the risk of recurrent ipsilateral ischemic stroke in patients with symptomatic near-occlusion with and without full collapse.

Methods: Included were consecutive patients eligible for revascularization, grouped into symptomatic conventional ≥ 50% carotid stenosis (n = 266), near-occlusion without full collapse (n = 57) and near-occlusion with full collapse (n = 42). The risk of preoperative recurrent ipsilateral ischemic stroke was analyzed, or, for cases not revascularized within 90 days, 90-day risk was analyzed.

Results: The risk of a preoperative recurrent ipsilateral ischemic stroke or ipsilateral retinal artery occlusion was 15% (95% CI 9–20%) for conventional ≥ 50% stenosis, 22% (95% CI 6–38%) among near-occlusion without full collapse and 30% (95% CI 16–44%) among near-occlusion with full collapse (p = 0.01, log rank test). In multivariate analysis, near-occlusion with full collapse had a higher risk of recurrent ipsilateral ischemic stroke (adjusted HR 2.6, 95% CI 1.3–5.3) and near-occlusion without full collapse tended to have a higher risk (adjusted HR 2.0, 95% CI 0.9–4.5) than conventional ≥ 50% stenosis. Only 24% of near-occlusion with full collapse underwent revascularization, common causes for abstaining were misdiagnosis as occlusion (31%), deemed surgically unfeasible (21%) and low perceived benefit (10%).

Conclusions: Symptomatic carotid near-occlusion has a high short-term risk of recurrent ipsilateral ischemic stroke, especially near-occlusion with full collapse.

Objective: Assess the sensitivity and specificity of computed tomography angiography (CTA) for carotid near-occlusion diagnosis interpreted in clinical practice against expert assessment.

Methods: CTAs were graded by two expert interpreters for near-occlusion. Findings were compared with clinical reports in 383 consecutive cases with symptomatic ≥ 50% carotid stenosis. In addition, 14 selected CTA exams (8 near-occlusions and 6 controls) were analyzed in a national effort by 13 radiologists experienced with carotid CTA.

Results: In clinical practice, imaging reports were 20% (95% CI 12–28%) sensitive for near-occlusion, ranging 0–58% between different radiologists; specificity was 99%. Among the 13 radiologists reviewing the same 8 near-occlusions, the average sensitivity was 8%, ranging 0–75%; specificity was 100%.

Conclusions: Carotid near-occlusion is systematically under-reported in clinical routine practice, caused by limited application of grading criteria when assessing CTA.

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.

Background: Carotid near-occlusion is the most severe form of carotid stenosis, where a critical stenosis leads to distal internal artery (ICA) collapse. While embolism is the primary mechanism in conventional ≥50% carotid stenosis, stroke pathophysiology in carotid near-occlusion remains uncertain. This study aimed to investigate the potential embolic mechanism in carotid near-occlusion by assessing the prevalence of ipsilateral intracranial medium- and large-vessel occlusions.

Methods: We retrospectively analyzed patients with symptomatic ≥50% carotid stenosis who underwent computed tomography angiography (CTA) on the same day following stroke onset. Carotid near-occlusion was diagnosed using a feature-based approach categorized into with or without full collapse in distal ICA, based on the extent of luminal narrowing. The primary outcome was the presence of ipsilateral intracranial medium- or large-vessel occlusion, defined as “ipsilateral presumed embolic vessel occlusion” (iPEVO) in the terminal ICA bifurcation (T-occlusion), middle cerebral artery (M1-M3), or anterior cerebral artery (ACA).

Results: Among 124 participants with symptomatic ≥50% carotid stenosis, the prevalence of iPEVO was 89% in carotid near-occlusion with full collapse, 44% in carotid near-occlusion without full collapse and 10% in conventional ≥50% carotid stenosis (p < 0.001). The crude odds ratio (OR) for iPEVO was 73 (95% CI 17-297) for carotid near-occlusion with full collapse and 7 (95% CI 2-23) for carotid near-occlusion without full collapse. After adjusting for age, the adjusted OR was 89 (95% CI 18 – 454) for carotid near-occlusion with full collapse and 4.9 (95% CI 1.4-17.4) for carotid near-occlusion without full collapse. Prevalence of iPEVO was also correlated with the lumen diameter of stenosis and distal ICA lumen diameter.

Conclusion: Our findings of a high prevalence of iPEVO among carotid near-occlusion strongly support an embolic mechanism. This study challenges the traditional assumption of hemodynamic instability in carotid near-occlusion, as greater stenosis severity and distal collapse appeared to increase embolic prevalence.