Key result
Carotid occlusive disease was associated with a non-significant reduction in semi-oval center perforating artery flow velocity compared to controls (mean difference 0.08 cm/s).
Why the study?
It was unknown whether cerebral perforating artery flow measures are altered and related to cerebral small vessel disease lesion burden in patients with carotid occlusive disease.
Does carotid occlusive disease alter cerebral perforating artery flow velocity and pulsatility compared to healthy controls?
Case-Control (n=40)
Yes
Does carotid occlusive disease alter cerebral perforating artery flow velocity and pulsatility compared to healthy controls?
Mean Difference: 0.08 (95% CI 0–0.16)
Absolute Event Rate: 0.66% vs 0.74%
p-value: p=0.053
Carotid occlusive disease may be associated with reduced cerebral perforating artery flow velocity in the semi-oval center, which tends to correlate with white matter hyperintensity volume, suggesting a hemodynamic mechanism for small vessel disease in these patients.
Non-significant trend in small observational study; leaves open hemodynamic contribution of carotid disease to small vessel disease.
Patients with carotid occlusive disease express altered hemodynamics in the post-occlusive vasculature and lesions commonly attributed to cerebral small vessel disease (SVD). We addressed the question if cerebral perforating artery flow measures, using a novel 7T MRI technique, are altered and related to SVD lesion burden in patients with carotid occlusive disease. 21 patients were included with a uni- (18) or bilateral (3) carotid occlusion (64±7 years) and 19 controls (65±10 years). Mean flow velocity and pulsatility in the perforating arteries in the semi-oval center (CSO) and basal ganglia (BG), measured with a 2D phase contrast 7T MRI sequence, were compared between patients and controls, and between hemispheres in patients with unilateral carotid occlusive disease. In patients, relations were assessed between perforating artery flow measures and SVD burden score and white matter hyperintensity (WMH) volume. CSO perforating artery flow velocity was lower in patients than controls, albeit non-significant (mean difference [95% confidence interval] 0.08 cm/s [0.00–0.16]; p = 0.053), but pulsatility was similar (0.07 [-0.04–0.18]; p = 0.23). BG flow velocity and pulsatility did not differ between patients and controls (velocity = 0.28 cm/s [-0.32–0.88]; p = 0.34; pulsatility = 0.00 [-0.10–0.11]; p = 0.97). Patients with unilateral carotid occlusive disease showed no significant interhemispheric flow differences. Though non-significant, within patients lower CSO (p = 0.06) and BG (p = 0.11) flow velocity related to larger WMH volume. Our findings suggest that carotid occlusive disease may be associated with abnormal cerebral perforating artery flow and that this relates to SVD lesion burden in these patients, although our observations need corroboration in larger study populations.
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Onkenhout et al. (2022) conducted a case-control in Carotid occlusive disease (n=40). Carotid occlusive disease vs. Matched controls without history of carotid occlusive disease was evaluated on Semi-oval center (CSO) perforating artery flow velocity (MD 0.08 cm/s, 95% CI 0.00-0.16, p=0.053). Carotid occlusive disease was associated with a non-significant reduction in semi-oval center perforating artery flow velocity compared to controls (mean difference 0.08 cm/s).
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