PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis
Version 1
: Received: 6 September 2023 / Approved: 7 September 2023 / Online: 7 September 2023 (10:47:14 CEST)
How to cite:
Balmos, I.A.; Slevin, M.; Brînzaniuc, K.; Mureșan, A.V.; Suciu, H.; Molnár, G.B.; Mocian, A.; Nagy, E.E.; Horváth, E. Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis. Preprints2023, 2023090464. https://doi.org/10.20944/preprints202309.0464.v1
Balmos, I.A.; Slevin, M.; Brînzaniuc, K.; Mureșan, A.V.; Suciu, H.; Molnár, G.B.; Mocian, A.; Nagy, E.E.; Horváth, E. Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis. Preprints 2023, 2023090464. https://doi.org/10.20944/preprints202309.0464.v1
Balmos, I.A.; Slevin, M.; Brînzaniuc, K.; Mureșan, A.V.; Suciu, H.; Molnár, G.B.; Mocian, A.; Nagy, E.E.; Horváth, E. Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis. Preprints2023, 2023090464. https://doi.org/10.20944/preprints202309.0464.v1
APA Style
Balmos, I.A., Slevin, M., Brînzaniuc, K., Mureșan, A.V., Suciu, H., Molnár, G.B., Mocian, A., Nagy, E.E., & Horváth, E. (2023). Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis. Preprints. https://doi.org/10.20944/preprints202309.0464.v1
Chicago/Turabian Style
Balmos, I.A., Előd Ernő Nagy and Emőke Horváth. 2023 "Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis" Preprints. https://doi.org/10.20944/preprints202309.0464.v1
Abstract
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.
Medicine and Pharmacology, Cardiac and Cardiovascular Systems
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
,
