Background and purpose: Carotid atherosclerotic stroke arises through overlapping hemodynamic and embolic mechanisms, yet management remains anchored to stenosis severity. Although stenosis reflects structural plaque burden, it incompletely captures plaque biology. We compared calcification features of symptomatic carotid plaques with ≥70% versus <50% stenosis and examined whether calcification attenuation is associated with intraplaque hemorrhage (IPH), a surrogate of plaque vulnerability. Materials and methods: A single-center retrospective cross-sectional study of ipsilateral symptomatic carotid plaques from two registries were compared: patients undergoing revascularization (≥70% stenosis) and patients with embolic stroke of undetermined source (<50% stenosis). Plaque calcifications were segmented to quantify total calcification volume (TCV), surface area (SA), maximum diameter, and attenuation (Hounsfield Units [HU]). Using semi-automated CTA segmentation software, IPH ≥10 mm³ defined an IPH-positive phenotype. Calcification features between stenosis categories (≥70% vs <50%) and IPH status were compared using the Mann-Whitney U test. Associations were evaluated using ridge logistic regressions. Results: Eighty-five patients were included (N=25, ≥70% stenosis and N=60, <50% stenosis). ≥70% stenotic plaques demonstrated greater TCV (297 vs 68mm³), SA (372 vs 113mm2), and maximum diameter (15.0 vs 7.1mm), yet lower median attenuation (392 vs 504 HU) compared with <50% stenotic plaques (all P<.001). Adjusting for demographics, clinical covariates and TCV, lower attenuation remained associated with ≥70% stenosis (OR: 0.89 per 100 HU increase, 95% CI: 0.86-0.93, P<.001). In secondary analyses, IPH-positive plaques (N=47) exhibited greater TCV and lower attenuation than IPH-negative plaques (all P<.001). In adjusted models, lower calcification attenuation (OR 0.92 per 100 HU increase, 95% CI 0.87-0.96; P<.001) and greater TCV (OR 1.05 per 100 mm³ increase, 95% CI 1.01-1.10; P=.01) were associated with IPH-positive plaques. Conclusions: CTA-derived calcification attenuation, independent of stenosis severity and calcification burden, may provide insight into carotid plaque vulnerability and stroke mechanism beyond luminal narrowing.
Low Plaque Calcification Attenuation on CTA Marks Vulnerable Cervical Carotid Plaque Independent of Stenosis Severity
Saba, Luca;
2026-01-01
Abstract
Background and purpose: Carotid atherosclerotic stroke arises through overlapping hemodynamic and embolic mechanisms, yet management remains anchored to stenosis severity. Although stenosis reflects structural plaque burden, it incompletely captures plaque biology. We compared calcification features of symptomatic carotid plaques with ≥70% versus <50% stenosis and examined whether calcification attenuation is associated with intraplaque hemorrhage (IPH), a surrogate of plaque vulnerability. Materials and methods: A single-center retrospective cross-sectional study of ipsilateral symptomatic carotid plaques from two registries were compared: patients undergoing revascularization (≥70% stenosis) and patients with embolic stroke of undetermined source (<50% stenosis). Plaque calcifications were segmented to quantify total calcification volume (TCV), surface area (SA), maximum diameter, and attenuation (Hounsfield Units [HU]). Using semi-automated CTA segmentation software, IPH ≥10 mm³ defined an IPH-positive phenotype. Calcification features between stenosis categories (≥70% vs <50%) and IPH status were compared using the Mann-Whitney U test. Associations were evaluated using ridge logistic regressions. Results: Eighty-five patients were included (N=25, ≥70% stenosis and N=60, <50% stenosis). ≥70% stenotic plaques demonstrated greater TCV (297 vs 68mm³), SA (372 vs 113mm2), and maximum diameter (15.0 vs 7.1mm), yet lower median attenuation (392 vs 504 HU) compared with <50% stenotic plaques (all P<.001). Adjusting for demographics, clinical covariates and TCV, lower attenuation remained associated with ≥70% stenosis (OR: 0.89 per 100 HU increase, 95% CI: 0.86-0.93, P<.001). In secondary analyses, IPH-positive plaques (N=47) exhibited greater TCV and lower attenuation than IPH-negative plaques (all P<.001). In adjusted models, lower calcification attenuation (OR 0.92 per 100 HU increase, 95% CI 0.87-0.96; P<.001) and greater TCV (OR 1.05 per 100 mm³ increase, 95% CI 1.01-1.10; P=.01) were associated with IPH-positive plaques. Conclusions: CTA-derived calcification attenuation, independent of stenosis severity and calcification burden, may provide insight into carotid plaque vulnerability and stroke mechanism beyond luminal narrowing.
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