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Endarterectomy Specimens (endarterectomy + specimen)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Endarterectomy Specimens

  • carotid endarterectomy specimen
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    Selected Abstracts

    Association between plaque instability, angiogenesis and symptomatic carotid occlusive disease,

    BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2001
    R. Mofidi
    Background: Angiogenesis is a recognized feature of the atherosclerotic process and has been described in the context of unstable coronary atherosclerotic lesions. The aim of this study was to assess the association between angiogenesis in atherosclerotic carotid plaques and microscopic features of plaque instability, in particular intraplaque haemorrhage. Methods: Consecutive patients undergoing carotid endarterectomy were included. Endarterectomy specimens were divided into their constituent atherosclerotic lesions. Histological sections were prepared and stained with haematoxylin and eosin, and immunohistochemically with an endothelial cell marker (CD34). The quantity of intraplaque haemorrhage was measured in transverse histological sections using computerized image analysis. Microvessel counts were performed in CD34-stained sections and were verified through computerized image analysis. Results: Some 239 atherosclerotic lesions from 73 patients were available for analysis; 73 were early lesions, 74 were raised fibroatheromas and 92 were unstable atherosclerotic plaques. One hundred and fifty lesions were not haemorrhagic; 89 exhibited intraplaque haemorrhage, of which 28 involved less than 50 per cent of the plaque sectional area. There were higher microvessel counts in plaques containing over 50 per cent haemorrhage (P < 0·0001), unstable atherosclerotic lesions (P < 0·0001) and atherosclerotic lesions obtained from symptomatic patients (P < 0·001). Conclusion: There are strong associations between plaque vascularity, quantity of intraplaque haemorrhage and presence of symptomatic carotid occlusive disease. © 2001 British Journal of Surgery Society Ltd [source]

    Reactive oxygen species induce RNA damage in human atherosclerosis

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2004
    W. Martinet
    Abstract Background, Reactive oxygen species (ROS)-induced DNA damage has recently been identified in both human and experimental atherosclerosis. This study was undertaken to investigate whether RNA damage occurs in human atherosclerotic plaques and whether this could be related to oxidative stress. Materials and methods, The integrity of total RNA isolated from carotid endarterectomy specimens (n = 20) and nonatherosclerotic mammary arteries (n = 20) was analyzed using an Agilent 2100 Bioanalyser (Agilent Technologies, Palo Alto, CA). Oxidative modifications of RNA were detected by immunohistochemistry. Results, Eleven out of 20 atherosclerotic plaques showed a significant reduction of the 18S/28S rRNA peaks and a shift in the RNA electropherogram to shorter fragment sizes. In contrast, all mammary arteries showed good-quality RNA with clear 18S and 28S rRNA peaks. Strong nuclear and cytoplasmic immunoreactivity for oxidative damage marker 7,8-dihydro-8-oxo-2,-guanosine (8-oxoG) could be detected in the entire plaque in smooth muscle cells (SMCs), macrophages and endothelial cells, but not in SMCs of adjacent normal media or in mammary arteries. Cytoplasmic 8-oxoG staining in the plaque clearly diminished when tissue sections were pretreated with RNase A, suggesting oxidative base damage of RNA. In vitro treatment of total RNA with ROS-releasing compounds induced RNA degradation. Conclusion, Both loss of RNA integrity and 8-oxoG oxidative modifications were found in human atherosclerotic plaques. Because RNA damage may affect in vitro transcript quantification, RT-PCR results must be interpreted cautiously if independent experimental validation (e.g. evaluation of RNA integrity) is lacking. [source]

    Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study

    MOLECULAR ORAL MICROBIOLOGY, Issue 4 2006
    P. J. Ford
    Background:, Inflammation is a significant component of atherosclerosis lesions. Bacteria, including periodontopathogens, have been demonstrated in atherosclerotic plaques and cross-reactivity of the immune response to bacterial GroEL with human heat shock protein 60 has been suggested as a link between infections and atherosclerosis. Methods:, In this study, the nature of the inflammatory infiltrate and the presence of human heat shock protein 60 and GroEL were examined in 31 carotid endarterectomy specimens. Additionally, monoclonal antibodies were used to detect the presence of six bacteria, including those implicated in periodontal disease. Results:, The inflammatory cell infiltrate of the lesions was dominated by CD14+ macrophages and CD4+ T cells. Most cells of the infiltrate as well as the endothelium were HLA-DR+, indicating activation; however, there was an absence of CD25 expression, demonstrating that the activated T cells were not proliferating. Few CD1a+ and CD83+ cells were noted. Human heat shock protein 60 expression was evident on endothelial cells and cells with the appearance of smooth muscle cells and lymphocytes. GroEL and bacteria were detected within intimal cells. Chlamydia pneumoniae, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia, Prevotella intermedia, and Actinobacillus actinomycetemcomitans were found in 21%, 52%, 34%, 34%, 41%, and 17% of arteries, respectively. Conclusion:, These results give evidence for a specific immune response associated with atherosclerosis. Whether bacteria initiate the observed inflammation in atherosclerotic lesions is not clear; however, the present study shows that maintenance of inflammation may be enhanced by the presence of periodontopathic bacteria. [source]

    Vascular endothelial growth factor is associated with histological instability of carotid plaques,

    BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 5 2008
    D. A. Russell
    Background: Vascular endothelial growth factor (VEGF) promotes events favouring carotid plaque instability: inflammatory chemoattraction, thrombogenesis, and upregulation of matrix metalloproteinases and cell adhesion molecules. The aim of this study was to assess neovascularization, VEGF and its receptors in high-grade stable and unstable carotid plaques. Methods: Immunohistochemical staining for CD34, VEGF, VEGF receptor (VEGFR) 1 and VEGFR2 was performed in 34 intact carotid endarterectomy specimens, and compared in sections demonstrating maximal histological instability (cap rupture/thinning) or, if stable, maximal stenosis. Results: VEGF staining was increased in 12 unstable compared with 22 stable plaques (median (interquartile range, i.q.r.) plaque score 4·0 (4·0,4·0) versus 3·0 (2·0,3·0); P = 0·002) with upregulation of VEGFR1 (plaque score 4·0 (2·0,4·0) versus 2·0 (1·0,3·0); P = 0·016). In unstable plaques this was associated with increased microvessel density in the cap (median (i.q.r.) 12·1 (4·0,30·0) versus 1·1 (0·0,7·3) microvessels/mm2; P = 0·017) and shoulder regions (7·7 (3·4,21·4) versus 3·1 (0·4,10·8) microvessels/mm2; P = 0·176). Conclusion: Increased VEGF and receptor staining were seen in histologically unstable carotid plaques. Although these differences could reflect cytokine-driven inflammatory events accompanying plaque instability, VEGF and VEGFR1 could be key mediators. Copyright © 2008 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]

    Association between intraplaque haemorrhage in the carotid atherosclerotic lesion, the degree of internal carotid artery stenosis and timing of ischaemic neurological events

    BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2001
    R. Mofidi
    Background: Expansion of carotid atherosclerotic plaques as a result of intraplaque haemorrhage has been implicated in the development of ischaemic neurological events. The relationship between the quantity of haemorrhage in the dominant atherosclerotic lesion, the degree of internal carotid artery (ICA) stenosis and the chronology of patients' symptoms was examined. Methods: Consecutive patients undergoing carotid endarterectomy were included. The nature and timing of symptoms were recorded. Aortic arch injection digital subtraction angiography was performed before operation. Carotid endarterectomy specimens were serially sectioned and examined histologically. The amount of intraplaque haemorrhage was measured with digital image analysis. The influence of timing of symptoms on the quantity of intraplaque haemorrhage was compared with Kaplan,Meier analysis. Correlation between degree of ICA stenosis and quantity of intraplaque haemorrhage was assessed by means of regression analysis. Results: Seventy-four patients (20 asymptomatic, 54 symptomatic) were included. The median latency of symptoms was 28 (1,600) days. Intraplaque haemorrhage was common: 54 (73 per cent) of 74 patients. Mean(s.e.m.) cumulative symptom-free survival before operation for patients with no intraplaque haemorrhage was 0·71(0·11), compared with 0·58(0·11) in those exhibiting haemorrhage in less than 50 per cent of the plaque area, and 0·20(0·07) in lesions with over 50 per cent (P = 0·002). A close correlation was observed between the degree of ICA stenosis and haemorrhagic content of the dominant atherosclerotic lesion (r2 = 0·433, P < 0·001). Conclusion: These results confirm the association between intraplaque haemorrhage and the degree of ICA stenosis. They further demonstrate an association between the size of haemorrhage and timing of neurological events, suggesting a causative role for intraplaque haemorrhage in the development of ischaemic neurological events. © 2001 British Journal of Surgery Society Ltd [source]

    Serum interleukin-6 is elevated in symptomatic carotid bifurcation disease

    ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2009
    M. Koutouzis
    Introduction,,, The levels of circulating proinflammatory cytokines may express the extent of the inflammatory response and their participation in plaque progression and rupture needs to be evaluated. We aimed to investigate differences in circulating levels of proinflammatory cytokines and in plaque infiltration by macrophages between patients undergoing carotid endarterectomy for symptomatic and asymptomatic carotid atherosclerotic disease. Methods,,, One hundred nineteen patients (91 men and 28 women; mean age 66 ± 8 years; range 42,83 years) who underwent carotid endarterectomy for significant (>70%) carotid bifurcation stenosis were enrolled in this study. Patients were characterized as symptomatic (n = 62) or asymptomatic (n = 57) after neurological examination. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-, (TNF-,), IL-1,, serum amyloid A (SAA), and high-sensitivity C-reactive protein (hs-CRP) were evaluated. Macrophage infiltration of the plaque was assessed quantitatively from endarterectomy specimens using the monoclonal antibody CD68. Results,,, Serum IL-6 levels were significantly higher in patients with symptomatic compared with those with asymptomatic carotid disease (3.3 [2.0,6.5] pg/ml vs 2.5 [1.9,4.1] pg/ml, P = 0.02). TNF-,, IL-1,, SAA, and hs-CRP levels did not differ significantly between the two groups. Symptomatic patients had also more intense macrophage accumulation in the carotid plaque compared with asymptomatic patients (0.6 ± 0.1% vs 0.4 ± 0.1%, P < 0.001). Although there were correlations between the levels of the different inflammatory markers, there were no correlation between any of them and the extent of plaque macrophage infiltration. Conclusion,,, Patients with symptomatic carotid atherosclerotic disease have elevated serum IL-6 levels compared with asymptomatic patients. Symptomatic patients have also more intense macrophage infiltration of the atherosclerotic plaque suggesting that inflammatory process may contribute to the destabilization of the carotid plaque. [source]