Key result
Stronger macrophage CD68+ infiltration was associated with intraplaque hemorrhage (p=0.003), while dominant iNOS2+ macrophages and CD31+ neovascularization correlated with atherothrombosis.
Why the study?
Carotid stenosis causes 10-20% of strokes and transient ischemic attacks, and low-grade intraplaque inflammation is known to interfere with lesion stability and progression.
Cohort (n=119)
p-value: p=0.003
In patients with severe carotid atherosclerosis, macrophage infiltration intensity and pro-inflammatory iNOS2+ macrophages are associated with intraplaque hemorrhage and atherothrombosis.
May aid carotid plaque risk stratification; leaves open causal roles and targeted interventions.
Background: Atherosclerosis is a progressive disease that results from a combination of endothelial dysfunction and inflammatory arterial wall disorder. Stenosis of the carotid artery caused by atherosclerotic plaques is responsible for approximately 10-20% of strokes and transient ischemic attacks, and the low-grade intraplaque inflammation interferes with lesion stability and progression. Methods: In this cohort study, initially, 119 patients were enrolled who underwent carotid endarterectomy. Of these, 67 cases with active perilesional inflammatory infiltrate were chosen for further immunohistochemical examination. The CD68+ infiltrate, iNOS2+, Arg1, and CD31 expressions were quantified around the lipid core by digital morphometry. These results were correlated with the presence of morphological changes leading to plaque instability: ulceration, thrombosis, intraplaque hemorrhage, the presence of the lipid core, calcification, and neovascularization. Results: Patients with a stronger macrophage CD68+ infiltrate were associated with intraplaque hemorrhage (p=0.003). In 12 cases with dominant iNOS2 positivity, the occurrence of atherothrombosis was significantly more frequent (p=0.046). Plaque neovascularization, characterized by CD31+, was correlated with atherothrombosis (p=0.02). Conclusion: The intensity of macrophage infiltration correlates with intraplaque hemorrhage, and the presence of pro-inflammatory iNOS2+ macrophages is associated with atherothrombosis in endarterectomized carotid plaques. Neovascularization also has potential thrombotic capacity.
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Slevin et al. (2023) conducted a cohort in Severe Carotid Atherosclerosis (n=119). Intraplaque macrophage infiltration (CD68+, iNOS2+) and neovascularization (CD31+) was evaluated on Morphological changes leading to plaque instability (ulceration, thrombosis, intraplaque hemorrhage, lipid core, calcification, and neovascularization) (p=0.003). Stronger macrophage CD68+ infiltration was associated with intraplaque hemorrhage (p=0.003), while dominant iNOS2+ macrophages and CD31+ neovascularization correlated with atherothrombosis.
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