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Diagnóstico histopatológico e inmunohistoquímico (IHQ) de linfoma no Hodgkin (LNH) en un canino hembra
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      Critical mechanical conditions around neovessels in carotid atherosclerotic plaque may promote intraplaque hemorrhage

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          Abstract

          Objective

          Intraplaque hemorrhage is an increasingly recognized contributor to plaque instability. Neovascularization of plaque is believed to facilitate the entry of inflammatory and red blood cells (RBC). Under physiological conditions, neovessels are subject to mechanical loading from the deformation of atherosclerotic plaque by blood pressure and flow. Local mechanical environments around neovessels and their relevant pathophysiologic significance have not yet been examined.

          Methods and results

          Four carotid plaque samples removed at endarcterectomy were collected for histopathological examination. Neovessels and other components were manually segmented to build numerical models for mechanical analysis. Each component was assumed to be non-linear isotropic, piecewise homogeneous and incompressible. The results indicated that local maximum principal stress and stretch and their variations during one cardiac cycle were greatest around neovessels. Neovessels surrounded by RBC underwent a much larger stretch during systole than those without RBCs present nearby (median [inter quartile range]; 1.089 [1.056, 1.131] vs. 1.034 [1.020, 1.067]; p < 0.0001) and much larger stress (5.3 kPa [3.4, 8.3] vs. 3.1 kPa [1.6, 5.5]; p < 0.0001) and stretch (0.0282 [0.0190, 0.0427] vs. 0.0087 [0.0045, 0.0185]; p < 0.0001) variations during the cardiac cycle.

          Conclusions

          Local critical mechanical conditions may lead to the rupture of neovessels resulting in the formation and expansion of intraplaque hemorrhage.

          Highlights

          ► High mechanical stress and stretch around the neovessles within the carotid atherosclerotic plaque were discovered. ► Neovessels surrounded by red blood cells (presumably evidence of fresh hemorrhage) underwent a much larger stress and stretch than those without red blood cells present nearby. ► These critical mechanical condition may damage the neovessles' wall promoting the formation of intraplaque hemorrhage.

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          Most cited references37

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          Association between carotid plaque characteristics and subsequent ischemic cerebrovascular events: a prospective assessment with MRI--initial results.

          Norihide Takaya, Chun Yuan, Baocheng Chu … (2006)
          MRI is able to quantify carotid plaque size and composition with good accuracy and reproducibility and provides an opportunity to prospectively examine the relationship between plaque features and subsequent cerebrovascular events. We tested the hypothesis that the characteristics of carotid plaque, as assessed by MRI, are possible predictors of future ipsilateral cerebrovascular events. A total of 154 consecutive subjects who initially had an asymptomatic 50% to 79% carotid stenosis by ultrasound with > or =12 months of follow-up were included in this study. Multicontrast-weighted carotid MRIs were performed at baseline, and participants were followed clinically every 3 months to identify symptoms of cerebrovascular events. Over a mean follow-up period of 38.2 months, 12 carotid cerebrovascular events occurred ipsilateral to the index carotid artery. Cox regression analysis demonstrated a significant association between baseline MRI identification of the following plaque characteristics and subsequent symptoms during follow-up: presence of a thin or ruptured fibrous cap (hazard ratio, 17.0; P< or =0.001), intraplaque hemorrhage (hazard ratio, 5.2; P=0.005), larger mean intraplaque hemorrhage area (hazard ratio for 10 mm2 increase, 2.6; P=0.006), larger maximum %lipid-rich/necrotic core (hazard ratio for 10% increase, 1.6; P=0.004), and larger maximum wall thickness (hazard ratio for a 1-mm increase, 1.6; P=0.008). Among patients who initially had an asymptomatic 50% to 79% carotid stenosis, arteries with thinned or ruptured fibrous caps, intraplaque hemorrhage, larger maximum %lipid-rich/necrotic cores, and larger maximum wall thickness by MRI were associated with the occurrence of subsequent cerebrovascular events. Findings from this prospective study provide a basis for larger multicenter studies to assess the risk of plaque features for subsequent ischemic events.
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            The causes and risk of stroke in patients with asymptomatic internal-carotid-artery stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators.

            D Inzitari, M Eliasziw, P Gates … (2000)
            The causes of stroke in patients with asymptomatic carotid-artery stenosis have not been carefully studied. Information about causes might influence decisions about the use of carotid endarterectomy in such patients. We studied patients with unilateral symptomatic carotid-artery stenosis and asymptomatic contralateral stenosis from 1988 to 1997. The causes, severity, risk, and predictors of stroke in the territory of the asymptomatic artery were examined and quantified. The risk of stroke at five years after study entry in a total of 1820 patients increased with the severity of stenosis. Among 1604 patients with stenosis of less than 60 percent of the luminal diameter, the risk of a first stroke was 8.0 percent (1.6 percent annually), as compared with 16.2 percent (3.2 percent annually) among 216 patients with 60 to 99 percent stenosis. In the group with 60 to 99 percent stenosis, the five-year risk of stroke in the territory of a large artery was 9.9 percent, that of lacunar stroke was 6.0 percent, and that of cardioembolic stroke 2.1 percent. Some patients had more than one stroke of more than one cause. In the territory of an asymptomatic occluded artery (as was identified in 86 patients), the annualized risk of stroke was 1.9 percent. Strokes with different causes had different risk factors. The risk factors for large-artery stroke were silent brain infarction, a history of diabetes, and a higher degree of stenosis; for cardioembolic stroke, a history of myocardial infarction or angina and hypertension; for lacunar stroke, age of 75 years or older, hypertension, diabetes, and a higher degree of stenosis. The risk of stroke among patients with asymptomatic carotid-artery stenosis is relatively low. Forty-five percent of strokes in patients with asymptomatic stenosis of 60 to 99 percent are attributable to lacunes or cardioembolism. These observations have implications for the use of endarterectomy in asymptomatic patients. Without analysis of the risk of stroke according to cause, the absolute benefit associated with endarterectomy may be overestimated.
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              Presence of intraplaque hemorrhage stimulates progression of carotid atherosclerotic plaques: a high-resolution magnetic resonance imaging study.

              Baocheng Chu, Judy Chia-Chun Yuan, Thomas S Hatsukami … (2005)
              Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression. Twenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus -0.15%; P=0.009) and lipid-rich necrotic core volume (28.4% versus -5.2%; P=0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%; P=0.006). Hemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Atherosclerosis
                Journal ID (iso-abbrev): Atherosclerosis
                Title: Atherosclerosis
                Publisher: Elsevier
                ISSN (Print): 0021-9150
                ISSN (Electronic): 1879-1484
                Publication date PMC-release: August 2012
                Publication date (Print): August 2012
                Volume: 223
                Issue: 2
                Pages: 321-326
                Affiliations
                [a ]University Department of Radiology, University of Cambridge, UK
                [b ]Department of Engineering, University of Cambridge, UK
                [c ]School of Medicine, The George Washington University, USA
                [d ]College of Computer Science and Technology, Zhejiang University of Technology, Hangzhou, China
                [e ]Department of Surgery, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
                [f ]Division of Cardiovascular Medicine, University of Cambridge, UK
                Author notes
                [∗ ]Corresponding author. Department of Engineering, Level 5, Box 218, University of Cambridge, Addenbrooke's Hospital Hills Road, Cambridge CB2 0QQ, UK. Tel.: +44 01223 746447; fax: +44 01223 330915. zt215@ 123456cam.ac.uk
                Article
                Publisher ID: ATH12614
                DOI: 10.1016/j.atherosclerosis.2012.06.015
                PMC ID: 3437553
                PubMed ID: 22762729
                SO-VID: 6300e6f0-9aba-42cf-82b6-388e71ea0fc6
                Copyright © © 2012 Elsevier Ireland Ltd.
                License:

                This document may be redistributed and reused, subject to certain conditions.

                History
                Date received : 5 April 2012
                Date revision received : 1 June 2012
                Date accepted : 11 June 2012
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: neovascularization,deformation,mechanics,carotid atherosclerosis,intraplaque hemorrhage
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: neovascularization, deformation, mechanics, carotid atherosclerosis, intraplaque hemorrhage

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