Histological composition and progression of carotid plaque (original) (raw)
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The Histologic Characteristics of Primary and Restenotic Carotid Plaque
Journal of Surgical Research, 1998
Proliferative activity was most pronounced in macrophages associated with intraplaque hemorrhage or Background. Although smooth muscle cell proliferaatheroma. The contribution of inflammatory cells to tion is a prominent feature of restenosis in experimenthe biologic behavior of restenotic lesions requires furtal models, the role of cellular proliferation in the initither investigation. ᭧ 1998 Academic Press ation and progression of carotid restenosis is not well Key Words: restenosis; carotid plaque; cellular prolifdocumented. eration. Methods. Between 1985 and 1995, 35 carotid endarterectomies (CEA) in 34 patients were performed for restenosis. Patient risk factors, cerebrovascular symptoms, and operative findings were recorded. Tissue INTRODUCTION specimens from 29 of these cases and 14 original specimens from the same patient were examined by light Restenosis due to neointimal thickening (NT) or recurmicroscopy (H&E, trichrome, elastochrome, and Alrent atherosclerosis (RA) occurring in 1 to 36% of pacian blue) and immunohistochemistry (a actin, CD 68, tients is the major factor limiting long-term patency fol-vWF, and proliferating nuclear cell antigen (PCNA)) lowing carotid endarterectomy . Although several in order to determine the morphologic characteristics etiologic factors, including age, gender, diabetes, hyperand cellular proliferative activity of the plaque.
The Symptomatic Carotid Plaque
2010
Conclusions—Infiltration of inflammatory cells to the surface of carotid plaques may be a critical step in promoting plaque rupture and resultant embolization or carotid occlusion. Further understanding of cell recruitment and behavior in carotid atherosclerosis may allow better detection of unstable plaques and therapeutic methods of plaque stabilization. (Stroke. 2000;31:774-781.)
European Journal of Vascular and Endovascular Surgery, 2001
Objectives: to investigate the inflammatory response within intact carotid plaques from carotid eversion endarterectomy (CEE) to determine the relationship between immunohistological plaque morphology and ischaemic cerebrovascular symptoms. Material and methods: intact CEE plaques from 71 patients with high-grade (>70%) stenosis undergoing CEE (group I, symptomatic, n=42; group II, asymptomatic, n=29) and 12 normal postmortem arteries (control group) were analysed with ). Both groups were matched for gender, age, risk factors, degree of carotid artery stenosis. Plaques were measured using a semiquantitative score system in a blinded fashion by two observers. Statistical analysis of the group differences were performed by using the Kruskal-Wallis test and the Multitest Procedure with Permutation-Testing. Significance was taken as a p<0.05. Results: there were significantly more inflammatory cells, an overexpression of P-selectin and the procoagulatory markers thrombomodulin and tissue factor in symptomatic compared to both asymptomatic plaques and the ones of the control group. In both groups there was no significance for ICAM-1, VCAM-1, macrophages and co-stimulatory molecule CD40. There was also no significance for any factor between the asymptomatic and the control group. However, the differences between the symptomatic and the asymptomatic group were highly significant for all factors. Conclusion: these data suggest that structural changes and inflammatory damage within the individual plaque seems to be a critical step in promoting plaque rupture with embolic sequelae.
Degree of carotid plaque calcification in relation to symptomatic outcome and plaque inflammation
Journal of Vascular Surgery, 2004
Objective: We undertook this study to quantitate differences in the degree of calcification between symptomatic and asymptomatic plaques removed at carotid endarterectomy (CEA) and to determine associated extent of plaque macrophage infiltration, a histopathologic feature of plaque instability. Methods: CEA plaques (n ؍ 48) were imaged at 1.25-mm intervals with spiral computed tomography (CT; 10-15 images per plaque). Indications for CEA were transient ischemic attack (n ؍ 16), stroke (n ؍ 5), amaurosis (n ؍ 4), and critical asymptomatic stenosis (n ؍ 23). The percent area calcification for each plaque was determined in spiral CT serial sections and averaged for each plaque. In 31 of 48 plaques macrophage infiltration was quantitated in corresponding histologic sections with immunohistochemical techniques. Results: The mean (؎ SD) age of patients with symptomatic and asymptomatic plaques was 66 ؎ 7 years vs 71 ؎ 7 years, respectively, and degree of stenosis was 76% versus 82%, respectively (P ؍ .05). Atherosclerosis risk factors were similar between groups. Percent plaque area calcification was twofold greater in asymptomatic versus symptomatic plaques (48% ؎ 19% vs 24% ؎ 20%, respectively; P < .05). At receiver operating characteristic curve analysis, 80% of symptomatic plaques were below and 87% of asymptomatic plaques were above a cutoff point of 30% plaque area calcification. Macrophage burden was greater in the symptomatic plaques than in the asymptomatic plaques (52% vs 23%; P < .03). A strong inverse relationship between the degree of plaque calcification and macrophage infiltration was found in critical carotid stenoses (r ؍ ؊0.87; P < .001). Conclusions: Symptomatic plaques are less calcified and more inflamed than asymptomatic plaques. Regardless of clinical outcome, a strong inverse correlation was found between the extent of carotid plaque calcification and the intensity of plaque fibrous cap inflammation as determined by the degree of macrophage infiltration. Carotid plaque calcification is associated with plaque stability, and is a potential spiral CT in vivo quantitative marker for cerebrovascular ischemic event risk. (J Vasc Surg 2004;40:262-9.)
Journal of Vascular Surgery, 1989
To identify microanatomic and chemical features that may mark the transition from asymptomatic to symptomatic atherosclerotic carotid lesions, we evaluated 62 carotid artery bifurcation plaques including 45 high-grade stenoses removed at endarterectomy and 17 nonstenotic plaques recovered at autopsy. Morphologic features were evaluated on multiple-interval histologic sections and were graded for the presence of hemorrhage, ulceration, thrombosis, lumen surface irregularity, and calcification. Plaque hemorrhage, recent and remote, was found in most of the specimens, and did not discriminate between symptomatic and asymptomatic stenotic plaques. High-grade carotid stenotic plaques were associated with a significantly higher incidence of ulceration (53%), thrombosis (49%), and lumen irregularity (78%) when compared to nonstenotic asymptomatic plaques (6%, 0%, and 17%, respectively; p < 0.01). Although these features were more prominent in lesions that produced symptoms, they were present in 80% of the stenotic bifurcations, and did not distinquish between symptomatic and asymptomatic endarterectomy plaques. No significant differences were found between symptomatic and asymptomatic high-grade lesions with respect to collagen, DNA, total cholesterol, fibrinogen, lipase, elastase, or collagenase content. We conclude that intraplaque hemorrhage is commonly seen in carotid plaques even without severe stenosis, and it does not appear to be a dominant determinant of symptoms. Ulceration and surface thrombi that may lead to cerebral embolization are prominent features in markedly stenotic plaques even when symptoms are absent. The disruptive processes that underlie plaque instability appear to be closely associated with plaque size and stenosis rather than plaque composition.
Cerebrovascular diseases extra, 2018
Echolucent carotid plaques have been related to an increased risk of ischemic cerebrovascular events. The aim of the present study was to evaluate whether a new objective ultrasonographic parameter, the statistical geometric feature (SGF), reflecting spottiness of carotid plaques, can be associated with cerebrovascular symptoms and with a rupture-prone plaque phenotype. The plaques of 144 patients who underwent carotid endarterectomy were included in this study. SGF and plaque area were estimated by outlining the plaque on ultrasound (US) images. The correlation coefficient for inter- and intraobserver variability was 0.69 and 0.93, respectively. The SGF values were normalized to the degree of stenosis (SGF/DS). The plaques collected at surgery 1 day after the US were analyzed histologically, and inflammatory markers and matrix metalloproteinases (MMPs) were measured. Patients with ipsilateral hemispheric symptoms had higher SGF/DS compared to patients without symptoms (0.82 [0.59-1...
Vasa, 2013
Background: Intraplaque neovascularization and vasa vasorum (VV) proliferation contribute in the progression and rupture of atherosclerotic lesions. Contrast Enhanced Ultrasonography (CEUS) has been reported to attain data regarding intraplaque neovessels and VV. However, whether the detection of microbubbles by CEUS within atherosclerotic plaques truly represents microvessels is a point of concern. We aimed to evaluate stable and unstable carotid artery plaque (CAP) VV pattern by CEUS and its correlation with histology and immunochemistry. Patients and methods: Patients with CAP scheduled for plaque endarterectomy were enrolled. CAP was initially identifi ed by conventional ultrasonography and subsequently CEUS (harmonic ultrasound imaging with simultaneous intravenous contrast agent injection) was performed. Th e recorded image loops were evaluated by a semi-automated method. Plaque specimens were excised and underwent histological and immunochemical (for CD34, Vascular Endothelial Growth Factor, CD68 and CD3 antibodies) analysis. Results: Fourteen patients (67.6 ± 10.2 years, 10 males) with a 86.9 ± 11.5 % degree of carotid artery stenosis were evaluated. Histology showed that half of the plaques were unstable. Enhancement of plaque brightness on CEUS was signifi cant for both stable and unstable plaque subgroups (p = 0.018 for both). Immunochemistry showed that microvessels, as assessed by CD34 antibody, were more dense in unstable vs. stable plaques (36.6 ± 17.4 vs. 13.0 ± 7.2 respectively, p = 0.002). However, correlation between plaque brigthness enhancement on CEUS and microvessel density was signifi cant only for stable (r = 0.800, p = 0.031) plaques. Conclusions: Th e identifi cation of brightness enhacement during CEUS in carotid atherosclerotic plaques may not always refl ect the presence of VV.