Atherogenesis and inflammation, Regional accumulation of T-cells macrophages and smooth muscle cells in the human atherosclerotic plaque, Human atherosclerosis. C. Annex (B) shows a detail of the erosion underneath the thrombus. In this paper, we analyze a simplified model of plaque growth to derive physically meaningful results about the growth of plaques. Libby Glagov A.I. M. G. Libby Ongoing inflammation or a rapid progression of growth due to thrombus organization could imply a progression to unstable syndromes [18, 42]. E.L. G.T. Clarijs van der Loos Hangartner et al. J.H. Arrow to the right indicates the reparative effects of smooth muscle cells, leading to the formation of a stable fibrous plaque. Koch M. Kovanen et al. On the other hand, lipid associated inflammation introduces tissue degrading effects. A.E. 3). Still, it is presently unclear what impact the various biologically active mediators released from eroded aortic surfaces may have on the human body. Apoptosis, an intrinsically programmed mode of cell death, can be activated by inflammatory mediators, and is recognized as a mechanism of foam cell death in plaques. Wensing This situation suggests that there was active plaque formation in the past, but now the inflammation in the artery wall has settled down. vector art, clipart and stock vectors. The majority of coronary thrombi (∼75%) is caused by plaque rupture.1,2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1).3,4 Other common features include expansive remodelling, large plaque size, plaque haemorrhage, neovascularization, adventitial inflammation, and ‘spotty’ calcifications.4 Thin-cap fibroatheroma caps are usually <65 µm thick.4Figure 2 summarizes factors co… P.M. An adjacent tissue section shows accumulations of macrophages (red cells) at the rupture site. In another study which included 47 patients who died of myocardial infarction, a total of 103 ruptured plaques were identified and only 40 of these ruptures could be associated with the infarct related coronary thrombosis [69]. The T-cell cytokine IFN-γ appears to play an important role in this process, by inhibiting the proliferation of smooth muscle cells, as well as decreasing their synthesis of collagen fibrils [47]. Borst N. Stable plaque formation in the cerebral artery stock vector 86283254 from Depositphotos collection of millions of premium high-resolution stock photos, vector images and illustrations. Studies on experimental atheromas have endorsed these observations: isolated lipid laden macrophages obtained from the aortic wall of cholesterol fed rabbits spontaneously synthesize and release metalloproteinases, whereas alveolar macrophages derived from the same animals and under the same circumstances do not [58]. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. (From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. In human plaques, clusters of lymphocytes are regularly observed in close proximity of ceroid pigments [40], which are considered as an end product of lipid oxidation [61]. Zarins Therefore, although basically protective, in these advanced plaques the inflammatory process has a worse side-effect: destabilization and plaque rupture. Jr. Giddens - Acheter ce vecteur libre de droit et découvrir des vecteurs similaires sur Adobe Stock M.C. Henney Basically the leukocytes have a protective function and serve in host defense by eliminating injurous agents, but their secretory products may also augment injury by damaging surrounding tissue components. Atherosclerotic plaques are classified into 2 types, stable and vulnerable, the latter having a high risk of rupture. Libby A. The same shoulder parts of eccentric lesions represent the vulnerable sites of plaques where most ruptures take place. N.J. However, in young patients and females, plaque erosions are a more common cause of coronary thrombosis underlying myocardial infarction [32]. Save to Lightbox. Pathologic analysis of coronary atherectomy specimens allowed the further investigation of the relationship between plaque inflammation and acute plaque events, also in patients with less severe coronary artery disease. Lendon et al. Larger, but apparently clinically silent ruptures have been observed also at autopsy in coronary arteries of 9% of persons who died of non-cardiac disease, increasing to 22% in those with diabetes or hypertension. The stenotic areas tend to become more stable despite increased flow velocities at these narrowings. J. J. van der Wal Burke Anti-Inflammatory Effect of Mangiferin on an Experimental Model of Allergic Rhinitis through the Inhibition of NF-κB Signaling Pathways. On the other hand, typically vulnerable plaques are characterized by large lipid pools and have a thin or virtually absent fibrous cap. Dental Plaque is defined as a BioFiolm of Structured Resilient Yellow Greyish substance that adheres to intra oral tooth surface or other hard surface in the oral cavity including removal and fixed restoration.. J.S.T. Le gravier ou les gravillons restent compacts grâce à la structure en nid d'abeilles de la plaque pour gravillons. Deciphering the Role of Human Gastrointestinal Microbiota in the Pathogenesis of Vaginal Infection and Cervical Cancer. Becker And search more of iStock's library of royalty-free vector art that features Anatomy … Other findings of interest concern the various inflammatory products released by cells in unstable plaques: increased numbers of macrophages producing the proteolytic enzyme gelatinase B (MMP9) [34, 35], the inflammatory cytokine TNF- and tryptase-producing mast cells [28], vasoactive substances such as angiotensin I [36] and endothelin [37], larger amounts of the thrombosis initiator Tissue Factor [38, 39], and increased numbers of Interleukin-2 receptors on T cells (as marker for acute T cell activation in unstable lesions) [40]. The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. R.Y. Smooth muscle cells (blue) are in the media and focally in the fibrous cap where they cover the site of macrophage accumulation. J Am Coll Cardiol 1998;31:420. S.D. et al. Fibrous tissue provides the structural integrity of a plaque. atherosclerosis detailed illustration. Hemodynamic factors such as local disturbances in flow velocity and alterations in shear stress form another risk factor for plaque initiation and growth [81]. Corley P.K. 1, 2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1). These biologic features of the plaque determine to a large extent whether or not a plaque will be vulnerable, and set the stage for rupture triggers to induce a rupture event. Armonk, NY: Futura Publishing Company, Inc. 1996, pp. Search for other works by this author on: The pathogenesis of atherosclerosis: a perspective for the 1990s, Plaque fissuring the cause of acute myocardial infarction, sudden ischemic death and crescendo angina, Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes, Significance of plaque ulceration in symptomatic patients with high grade carotid stenosis, A macro and microview of coronary vascular insult in ischemic heart disease, Stability and instability: two faces of coronary atherosclerosis, Lipoproteins and atherogenesis: current concepts, Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma, Risk of thrombosis in human atherosclerotic plaque: role of extracellular lipid, macrophages and smooth muscle cell content, Fibrous and lipid-rich plaques atherosclerotic plaques are part of interchangeable morphologies related to inflammation B. Studies on atherectomy specimens of patients with different clinical ischemic syndromes have provided some circumstantial evidence for this concept. These observations have led to a concept of unstable atherosclerotic plaques: plaques with an unstable morphology giving rise to the onset of unstable coronary artery disease. Avec la plaque stabilisatrice EuroGravel, vous obtenez très facilement une surface de gravier stable et sans traces. But, certainly not all the plaques in patients with stable coronary artery disease fulfil these criteria for stability. J. Lathérosclérose est une atteinte fréquente, qui se développe avec lâge, a fortiori chez les personnes exposées à certains comportements liés à lhygiène de vie (sédentarité, tabagisme) et présentant des facteurs de risque cardiovasculaires (hypercholestérolémie, hypertension artérielle, ). Stemme These observations provide a link between lipids and inflammation, and furthermore could give at least one explanation why the lytic effects of inflammation are most prominent in lipid-rich plaques (Fig. 8). A.L. et al. Disruptions in these cases were either deep ruptures (60%) (see also Fig. Fishbein Pentilla Rennick Moreover, inflammation appears to be associated also with the initiation of plaque rupture, a notion derived from several clinicopathological investigations using autopsy materials and atherectomy specimens. For example, phagocytosis of lipids is basically a protective mechanism, but unlimited uptake and foam cell death may lead to expansion of the soft atheroma. M. Born Cross-section of an atherosclerotic plaque, which is heavily infiltrated with macrophages (red) and contains only scarce smooth muscle cells (blue) in the fibrous cap (anti-CD68/anti-α-actin immunodouble stain). Jonasson Stable & Unstable Plaques. Lipid plaques, therefore, are considered ‘rupture prone'. Discontinuity of the endothelium allows a contact between the blood stream and highly thrombogenic plaque materials (collagen fibrils and lipid debris insulated with Tissue Factor), which initiates activation of the coagulation system with at least some degree of thrombus formation 4. It would be more likely the plaque is hard, stable plaque. (B) Adjacent section shows abundant stromelysin-1 (MMP3) staining of foam cell macrophages around the lipid core, and to a lesser extent some smooth muscle cells in the fibrous cap (anti-MMP3 immunostain). Denning Studies using computer modeling of plaques have identified circumferential tensile stress on the fibrous cap as the most important intrinsic mechanical stress factor involved in plaque rupture [15, 21]. Isner Whether a plaque tends to stability or instability will depend on which mechanism dominates the course of plaque formation in a given period of time. Moreover, this study and several other atherectomy investigations documented fragments of thrombus in substantial numbers (up to 20%) of apparently stable plaques [16–18, 33, 41, 42]. 6. Apoptose et syndromes coronariens aigus. When compared with lesions underlying chronic stable angina, the lesions of patients with unstable coronary syndromes contain significantly larger amounts of inflammatory cells [17, 18, 33], including activated inflammatory cells, as indicated by the expression of HLA-DR molecules on cells [18]. Once activated by plasmin or mast cell products, they initiate a cascade of proteolytic activities with a very broad substrate specificity, including all the extracellular matrix components of the fibrous cap [57]. Bland Zhou Davies et al. M. G.K. Falk E. Advanced lesions and acute coronary syndromes: a pathologist's view. Differences between lipid-rich and fibrous plaques. In carotid plaques, rupture sites are also associated with plaque inflammation [31] and indeed, in 70% of the ruptured plaques that were encountered in our series, the rupture site was found in the upstream shoulder. 1). Becker Local arterial dilation is a well-known and important mechanism of compensatory enlargement of the vessel at sites where plaques grow [72]. G.C. et al. Several mediators produced by activated T-lymphocytes and macrophages in plaques promote destabilizing effects. They are found in most cases of acute transmural myocardial infarction. •destruction of the underlying vessel wall → aneurysm formation → secondary rupture and / or thrombosis. Lark We investigated coronary atherectomy specimens of 58 patients with clinically well defined coronary artery diseases, of which 28 had chronic stable angina of more than 2 months duration without progression. Hangartner Davies The image below illustrates the evolution of atherosclerotic plaques and also indicates that there are two possible forms of evolution. Schoneveld Enright J. M.W. compared morphologic plaque features with the profile of risk factors of corresponding patients [79]. However, in the advanced lipid plaque which needs the support of an intact fibrous cap the same effect appears to be dangerous. Less well known are the quantitative differences in these structural components: histopathologic examinations of a large series of plaques have revealed substantial variations in the thickness of fibrous caps, in the size of atheromas, in the extent of dystrophic calcification and, as has been shown more recently, in the relative amounts of major cell types: and inflammatory cells [12, 13]. Woolf C.E. Chait N. Recent investigations by this group give more insight in this paradoxical situation. Formation stable de plaques dans l'artère cérébrale, 86283254, parmi la collection de millions de photos stock, de dessins vectoriels et d'illustrations, de qualité supérieure et en haute définition, de Depositphotos. Plaques derived from the aorta also show a clear relationship between the size of the lipid core and rupture events. K.T. J. Davies The defining characteristics of a vulnerable plaque include but are not limited to: a thin fibrous cap, large lipid-rich necrotic core, increased plaque inflammation, positive vascular … B.H. C.K. et al. Smoking did not influence the composition of the plaques with respect to features of vulnerability, but appeared to be highly thrombogenic. P. O'Brien But they may become vulnerable, there is a risk of rupture and lead to thrombosis. However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. These studies also showed the importance of the thickness of a fibrous cap (thickness in millimetres being inversely related to the peak stress in the cap), and the stenosis rate (circumferential stresses in the plaques gradually decreased when stenosis severity increased) [21]; it gives at least one explanation for the fact that many plaques rupture at a stenosis rate of less than 50%. Fox et al. G. Lipid related inflammation in the plaque leads to degradation and weakening of the plaque tissue. Asthénosphère : Partie du globe terrestre située sous la lithosphère, moins rigide mais pas liquide, qui s’étend jusqu’à 700 km. Kaski Fig. Allen van der Wal Un article de la revue M/S : médecine sciences (Volume 20, numéro 3, mars 2004, p. 259-381) diffusée par la plateforme Érudit. A principal feature of inflammation is the accumulation of leukocytes; in longlasting chronic inflammatory processes these leukocytes are macrophages, lymphocytes and mast cells. Das T.O. Zeiher Implications for cell mediated thrombogenicity in acute coronary syndromes, Recent onset activation of the plaque immune response in coronary lesions underlying acute coronary syndromes, Histological characteristics of tissue excised during directional coronary atherectomy in stable and unstable angina pectoris, Smooth muscle cell abundance and fibroblast growth factors in coronary lesions of patients with non fatal unstable angina: a clue to the mechanism of transformation from the stable to the unstable clinical state, Rapid angiographic progression of coronary artery disease in patients with angina pectoris. 7 and Fig. F.E. Gimbrone A.E. et al. In coronary arteries most of these lesions remain clinically silent, or on the long term, may lead to stable angina pectoris [5]. (Anti-CD68/anti-α-actin immunodouble stain). et al. 7 and 8, which show examples of a plaque composed of a large lipid core with an extremely attenuated cap and infiltrated by large amounts of macrophages (extremely vulnerable, Fig. et al. A clue to the mechanism of increased vasoreactivity of the culprit lesion in unstable angina, Differential expression of tissue factor protein in directional atherectomy specimens from patients with stable and unstable coronary syndromes, Macrophages, smooth muscle cells, and tissue factorin unstable angina. Weisenberg Smooth muscle cells increase the structural strength by producing the connective tissue matrix of a plaque. Isner Falk In fact, most patients had mixtures of plaque types in varying proportions [19]. M.J. In this large diameter vessel the process of plaque disruption and thrombosis is not ended by luminal occlusion, and may lead to extensive surface ulcerations comprising large areas of the aortic wall, as can be observed in many autopsy cases at older age. C.K. R. B.L. L. A. Kearney Thickening of the intima-media complex implies occult plaque formation, but plaque may, of course, be seen directly with ultrasound when it achieves sufficient size to protrude into the carotid artery lumen. E. The continued recruitment of T-cells and macrophages at sites of ‘dysfunctional endothelium’ appears to be a constant feature of lesion initiation and progression as it accentuates the chronic inflammatory nature of atherosclerosis [23]. In: Fuster V, editor. R. Richardson Hibbs (A) Example of an intact (non-ruptured) eccentric lipid-rich plaque in a coronary artery. A.J. In the test group, 29 and 80 frames were stable and unstable plaques, respectively. The atherectomy specimens are grouped according to the type of coronary syndrome. G.V.R. P. P.K. Kaartinen A. Ambrose A concept, Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques, Comparing of histopatologic features of coronary lesions obtained from directional atherectomy in stable versus acute coronary syndromes, Comparison of coronary lesions obtained by directional atherectomy in unstable angina, stable angina and restenosis after either atherectomy or angioplasty, Clinically stable angina is not necessarily associated with histologically stable atherosclerotic plaques, Morphological characteristics of clinically significant coronary artery stenosis in stable angina, Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology, Distribution of circumferential stress in ruptured and stable atherosclerotic lesions: a structural analysis with histopathologic correlation, Atherosclerotic plaques are locally weakened when macrophage density is increased, The pathogenesis of atherosclerosis. Additional support for the influence of risk factors on plaque disruption stems from autopsies on diabetic patients with coronary thrombosis, which revealed erosion of the plaque surface as the most common type of plaque disruption (66% of diabetic infarct patients) [8]. G.R. Copyright © 2021 European Society of Cardiology. S. Expression of adhesion molecules on neovessels in atherosclerotic plaques. Certainly, external factors including systemic thrombotic factors and ‘rupture triggers’ such as vasospasms or elevated blood pressure will play a role in the ultimate thrombotic occlusion of the vessel or reduction of flow between a critical threshold [6, 65, 66]. Role of smooth muscle cell death in advanced coronary primary lesions: implications for plaque instability, Biphasic pattern of cell turnover characterizes the progression from fatty streaks to ruptured human atherosclerotic plaques, Mechanisms of plaque rupture: mechanical and biologic interactions. D. O.J. S. For this reason, large plaques may angiographically be visualized as only mildly stenotic. (Anti-CD68/anti-α-actin immunodouble stain). J.J. Microscopic foci of endothelial loss associated with platelet thrombi are present on the surface of in many advanced plaques [67]. Kume Un lien pour définir votre mot de passe a été envoyé à : Nous avons trouvé un historique des licences, des crédits ou une formule d’abonnement dans votre profil personnel. An interesting relationship between the type of remodelling of the vessel wall and the tissue composition of the local plaque was found: lipid-rich plaques with many inflammatory cells were often associated with local arterial dilation. In contrast, in downstream (distal shoulders) the smooth muscle cells densities were larger than upstream [85]. There is abundant anti HLA-DR reactivity on plaque cells indicating active inflammation. A.P. But, despite these differences an overlap in the extent of inflammation was noticed between the groups of stable and unstable patients; at least a number of stable patients had considerable amounts of inflammatory cells in their culprit lesions. Vulnerable plaques were defined as lesions with a fibrous cap of less than 65 μm and infiltrated with >25 macrophages per high power field. Das Atherosclerosis detailed illustration. M.J. Macrophage contents, visualized by immunostaining with anti-CD68, were found to be significantly higher in the upstream parts of plaques than in their downstream parts. de Boer Piek extended this view by using used entire (atherosclerotic) arteries to investigate atherosclerosis associated vascular wall remodeling. S. Coronary heart disease (CHD) and other manifestations of atherosclerosis were not among the most common causes of death until the beginning of the 20th century, but thereafter a dramatic increase was observed in industrialized countries, including Western Europe and the United States, peaking around 1960 to 1980.1 Comparable increases in the incidence of CHD have later occurred or are currently occurring in many other parts of the world mainly because of population growth and an increased avera… On the other hand, fibrous plaques coincided more often with local shrinkage of the vessel wall [75]. The result is a reparative and stabilizing effect on the plaque structure [46, 47, 51]. Atherosclerosis, the formation of life-threatening plaques in blood vessels, is a form of cardiovascular disease. Although basically expressions of the same disease, the plaques in Fig. E. (A) High grade stenosing lesion with occlusive thrombosis of a 32 year old male who died instantly of acute myocardial infarction. Escaned Price for. Streifler Intrinsic mechanical forces clearly contribute to the process of plaque rupture, but of equal importance is the tissue composition of the fibrous cap. An interesting relationship was seen between the amounts of inflammatory cells in the lesions and the severity of various unstable ischemic syndromes [18, 33, 40]. H. Chen There is focal accumulation of macrophages (red), creating a vulnerable site in the periphery of the fibrous cap. Alpers J. J. Kaartinen Pearce Richardson Passeri R. A. Kovanen Since inflammation occurs also at the base of the atheroma of lipid plaques, dilation may result from destruction and attenuation of the media underlying plaques [76, 77]. S. formation de l’ Himalaya La lithosphère océanique qui séparait l’inde et l’Asie a été absorbée par une subduction, l’océan s’est fermé ; lorsque les deux lithosphères continentales se sont affrontées , l’inde a embouti le continent asiatique l’Himalaya s’est formé . The plaque is largely fibrocellular/fibrosclerotic and contains only small deeply located atheromas (hematoxylin–eosin stain). Large mural thrombi due to large surface erosions or superficial fissures in the fibrous cap have found in many of the lesions underlying unstable angina. This was in contrast to the overall morphology of the ruptured lesions, which was heterogeneous both with respect to plaque architecture (lipid or fibrous) and presence or absence inflammation [20]. Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. Charlston Over the past years several studies have pointed out that both inflammation and repair are key events in the natural course of atherosclerosis [1, 23, 45, 46], and there is a great deal of evidence that inflammatory cells and their secretory products have profound effects on the integrity of the connective tissue meshwork of plaques [47]. Holm Loree The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. [22] tested the mechanical strength of human fibrous cap tissue and observed significantly reduced maximum stress at fracture when fibrous caps are infiltrated with macrophages. J.A. La plaque en plastique placée sous le gravier ou les gravillons stabilise le revêtement. Download this Stable Plaque Formation In The Human Artery vector illustration now. (anti-HLA-DR immunostain). However, data from both pathologic and angiographic studies on large series of patients indicate that most lesions that underlie coronary complications such as unstable angina or acute myocardial infarction, are only mildly to moderately stenotic [70, 71]. Allard C. van der Wal, Anton E. Becker, Atherosclerotic plaque rupture – pathologic basis of plaque stability and instability, Cardiovascular Research, Volume 41, Issue 2, February 1999, Pages 334–344, https://doi.org/10.1016/S0008-6363(98)00276-4. And more recently, active plaque inflammation associated with plaque rupture could be demonstrated also in carotid artery plaques obtained from stroke patients [31]. Therefore, clinical stability does not always indicate biologic stability in terms of (absence of) inflammation and thrombus formation. Hansson However, Pasterkamp et al. G. Indeed, many plaques that underlie coronary thrombus are high grade stenotic lesions. Filamentous bacteria (f) appear to be invading cocci microcolonies. The purpose of this study was to determine whether bone formation and extensive dystrophic calcification are associated with stable plaques and protective against ischemic vascular events. The recruitment appears to be specific for macrophages, T lymphocytes and mast cells [24–27], and the arterial endothelium covering the plaque surface is considered as the principal site of entrance for these cells [1]. Triposkiadis F(1), Sitafidis G, Kostoulas J, Skoularigis J, Zintzaras E, Fezoulidis I. E. T. Carr For full access to this pdf, sign in to an existing account, or purchase an annual subscription. N. Walpola M.J. Holm Ihling These lesions may also calcify and in some cases undergo osseous metaplasia (bone formation) over time. This view is illustrated in Fig. This notion may illustrate the value of a proper understanding of atherosclerotic plaque pathology for patients with acute ischemic syndromes. Related keywords. Ehsani (A) Coronary plaque of a 67 year old male, containing an eccentric mildly stenosed plaque with complete disruption of the fibrous cap (boxed area), mural thrombus and hemorrhage into the lipid core. 2- Dégagez à partir du doc b et c les caractéristiques structurales des roches métamorphiques. J.J. 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