O.J. The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Oxford University Press is a department of the University of Oxford. Cheng M.R. A.M. Galis Atherosclerotic plaque formation results from complex cellular interactions in the intima of arteries, which take place between resident cells of the vessel wall (smooth muscle cells and endothelial cells) and cells of the immune system (leukocytes). Fully developed plaques contain highly variable amounts of inflammatory cells, but largest concentrations can be found in lipid-rich lesions where they occupy the attenuated cap, the shoulder parts of the lesions or both [12, 13]. However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. II. Fig. [12]. A.I. Email this page; Link this page ; Print; Please describe! Pearce Alderman 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. 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. 2- Dégagez à partir du doc b et c les caractéristiques structurales des roches métamorphiques. Richardson Foam cell death plays an important role in the formation and growth of the atheroma, together with extracellular binding of lipids to collagen fibers and proteoglycans [10, 11]. Libby Fibrous tissue provides the structural integrity of a plaque. Giddens The body mass index (BMI) and fasting blood glucose were higher in the unstable plaque group than in the stable plaque group (P=0.006 and P=0.009, respectively). Repeated plaque ruptures, ones not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot is the process that produces most stenoses over time. 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. A. Unstable plaque formation and thrombus. J. J.J. 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]. (Abstract). R. N Engl J Med 1992;26:242–250; 310–318. M.J. M.W. Thomas C.K. Plaque disruptions may vary greatly in extent from tiny fissures or erosions of the plaque surface to deep intimal tears which extend into the soft lipid core of lesions; in all these instances, at least some degree of thrombus formation occurs [5, 6]. Most plaques that develop during a lifetime remain unnoticed, but plaque disruption and thrombus formation are not uncommon features. 7), and a fibrous lesion of which the cellular component consists almost solely of smooth muscle cells (typically stable, Fig. Tang Piek Microscopic foci of endothelial loss associated with platelet thrombi are present on the surface of in many advanced plaques [67]. Atherosclerotic plaque formation. Zarins R. M.J. 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. •destruction of the underlying vessel wall → aneurysm formation → secondary rupture and / or thrombosis. A vulnerable plaque is a kind of atheromatous plaque – a collection of white blood cells and lipids in the wall of an artery – that is particularly unstable and prone to produce sudden major problems such as a heart attack or stroke. R.M. This is illustrated in Fig. J. U. 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. Piek et al. Pris globalement, ces facteurs de risque modifiables expliqueraient par exemple 90% des cas dIDM recensés dans le monde. An observation of particular interest is that synthesis as well as lytic activity of these enzymes is most abundant in the lipid laden macrophages and in the extracellular space around lipid cores of plaques [56]. Davies Dental Pellicle forms within seconds after brushing. Stable plaques also tend to have less inflammation than is present in unstable plaques. S. Sterpetti Author information: (1)Department of Cardiology, Larissa University Hospital, Larissa, Greece. (B) Detail of the boxed area in (A). Syndromes of atherosclerosis. On the other hand, lipid associated inflammation introduces tissue degrading effects. The most important mechanism of acute coronary syndrome (ACS) is plaque rupture and subsequent thrombus formation. (B) shows a detail of the erosion underneath the thrombus. Ellis C. Annex Ball But they may become vulnerable, there is a risk of rupture and lead to thrombosis. Chen And more recently, active plaque inflammation associated with plaque rupture could be demonstrated also in carotid artery plaques obtained from stroke patients [31]. Atherosclerosis detailed illustration. 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.A. Becker Local flow disturbances and lipids as a driving force appear to be obligatory in this process [1]. G.K. Falk E. Advanced lesions and acute coronary syndromes: a pathologist's view. C.M. This situation suggests that there was active plaque formation in the past, but now the inflammation in the artery wall has settled down. Campbell Farb Mann 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]. Becker C. Pasterkamp So can we reduce plaque buildup? et al. Manderson 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]. A.J. A.P. (A) High grade stenosing lesion with occlusive thrombosis of a 32 year old male who died instantly of acute myocardial infarction. M. et al. Stowers Holm This is illustrated in Figs. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. Wensing (From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. Kranzhofer No membership needed. Intrinsic mechanical forces clearly contribute to the process of plaque rupture, but of equal importance is the tissue composition of the fibrous cap. Trouvez des images de stock de La formation stable de plaques athérosclérotiques en HD et des millions d’autres photos, illustrations et images vectorielles de stock libres de droits dans la collection Shutterstock. C.M. K.L.H. Sukhova N. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. This study revealed on the average larger tissue areas infiltrated with macrophages and larger amounts of lymphocytes in patients with unstable angina, and larger tissue areas occupied by smooth muscle cells in patients with stable angina. Keith et al. A principal feature of inflammation is the accumulation of leukocytes; in longlasting chronic inflammatory processes these leukocytes are macrophages, lymphocytes and mast cells. P.T. J Am Coll Cardiol 1998;31:420. 2) or erosions of the plaque surface (40%, of which one showed hardly no inflammation) (see also Fig. A.C. Again, organization of these mural thrombi or intra plaque hemorrhages may lead to a phase of rapid plaque growth through a repair process of smooth muscle cells growth and connective tissue deposition. J. However, in young patients and females, plaque erosions are a more common cause of coronary thrombosis underlying myocardial infarction [32]. Ehsani R. 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. atherosclerosis detailed illustration. Fox K.T. et al. M.J. H. 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]. Das P.D. 5). Même si la physiopathologie de la plaque d’athérome est commune, il s’agit donc bien de deux situations distinctes, résumées sur la figure 1. P.K. Ihling compared morphologic plaque features with the profile of risk factors of corresponding patients [79]. The abdominal aorta is the arterial site most prominently involved in the process of plaque formation, and also of plaque complications. M. A large number of diseases with totally different clinical presentations are basically atherosclerosis related, and among these, myocardial infarction, stroke, abdominal aneurysms and lower limb ischemia determine to a large extent the morbidity and mortality in Western style populations. 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… Atherosclerosis continues to be one of the main subjects in pathology research. Cucina In coronary arteries, therefore, plaque disruption has been studied most extensively, and a number of correlations have emerged between the morphology of the culprit plaques, the degree of thrombus formation and types of ensuing ischemic coronary syndromes of patients [5, 6, 8]. 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. S. Isner How Doctors Measure Plaque Stability A CT scan can show how stable plaques are (American Journal of Roentgenology, March 2015;204(3):W249-W260). While unstable and vulnerable plaques have been characterized by several studies which indicate that they have a thin fibrous cap (< 65 µm) and its LC is substantial (Libby, 2001; Andrews et al., 2018). Zeiher B.L. 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]. Carpenter (A) Example of an intact (non-ruptured) eccentric lipid-rich plaque in a coronary artery. Stable plaque - download this royalty free Vector in seconds. et al. The distribution of inflammatory cells in atherosclerotic plaques relates to the direction of flow. E. C.M. Virmani First, during activation of the scavenging pathway for phagocytosis of oxidized lipoproteins, macrophages exert a number of secretory functions with detrimental effect on the plaque tissue [9, 59–61]. Holm Save to Lightbox. Langille Atherosclerosis, the formation of life-threatening plaques in blood vessels, is a form of cardiovascular disease. M.J. M.C. T. Paavonen C-reactive protein (CRP) is an inflammation marker that could be used to assess vascular inflammation. On the other hand, typically vulnerable plaques are characterized by large lipid pools and have a thin or virtually absent fibrous cap. New insights into the pathogenesis of atherosclerosis as revealed by PDAY, Carotid bifurcation atherosclerosis: Quantitative correlaton of plaque localization with flow velocity profiles and shear stress, Shear stress influences the release of platelet derived growth factor and basic fibroblast growth factor by arterial smooth muscle cells, Vascular endothelium: An integrator of pathophysiological stimuli in atherogenesis, Expression of ICAM-1 and VCAM-1 and monocyte adherence in arteries exposed to altered shear stress (published erratum appears in Arterioscler Thromb Vasc Biol 1995;15:429), Copyright © 1999, European Society of Cardiology, Approaches to treat pulmonary arterial hypertension by targeting bmpr2 — from cell membrane to nucleus, Co-ordinated mitochondrial degradation by autophagy and heterophagy in cardiac homeostasis, Hydralazine protects the heart against acute ischaemia/reperfusion injury by inhibiting Drp1-mediated mitochondrial fission, Heart regeneration: beyond new muscle and vessels, 3 Instability and stability: a balance between inflammation and repair, 4 The acute ischemic event: a multifactorial process, 5 Classical risk factors and acute plaque complications, https://doi.org/10.1016/S0008-6363(98)00276-4, Receive exclusive offers and updates from Oxford Academic. A. Illustration about Stable plaque formation in the human artery. P. O'Brien The pathogenesis of coronary artery disease and the acute coronary syndromes. R. J.J. Bohle However, the actual sites of rupture were also influenced by variations in the mechanical strength of the fibrous cap due to accumulations of lipid-laden macrophages. On the other hand, the atheroma is soft, weak and highly thrombogenic. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. P.D. For full access to this pdf, sign in to an existing account, or purchase an annual subscription. The disruption of atherosclerotic plaques and the subsequent formation of thrombi are currently recognized as the primary mechanisms of myocardial and cerebral infarctions (1). In coronary arteries most of these lesions remain clinically silent, or on the long term, may lead to stable angina pectoris [5]. 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]. Eefting Download royalty-free Atherosclerosis. Studies on atherectomy specimens of patients with different clinical ischemic syndromes have provided some circumstantial evidence for this concept. Ongoing inflammation or a rapid progression of growth due to thrombus organization could imply a progression to unstable syndromes [18, 42]. S.D. Bland N.J. R. (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. (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). De Servi 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 … Allen In these retrospective comparative studies several histopathological parameters of plaque inflammation have been analyzed and quantified in tissue specimens of culprit lesions and correlated with the clinical status of the patient (either chronic stable angina or one of the various forms of unstable angina). 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. Becker It shows why lipid plaques with attenuated fibrous caps are more vulnerable to rupture, but moreover emphasizes the importance of cellular infiltrations in the cap, particularly the presence of inflammatory cells (Fig. ... Les manifestations de l'activité du globe terrestre (séismes, volcans, formation de montagnes ou d'océans) sont le résultat du mouvement des différentes plaques lithosphériques ou tectonique des plaques qui a souvent des conséquences désastreuses sur notre vie et notre environnement. Kovanen Horrigan E.L. Syndromes of atherosclerosis: correlations of clinical imaging and pathology. et al. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. J. Kaartinen Expression of adhesion molecules on neovessels in atherosclerotic plaques. Cybulsky In contrast, other plaques … These plaques tend to stabilize and are not prone to rupture. et al. de Boer D. G.K. Plaques derived from the aorta also show a clear relationship between the size of the lipid core and rupture events. Denning Stable & Unstable Plaques. X. Therefore, although basically protective, in these advanced plaques the inflammatory process has a worse side-effect: destabilization and plaque rupture. Streifler M. {"152344379":{"content_id":"152344379","title":"Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. There is abundant anti HLA-DR reactivity on plaque cells indicating active inflammation. On the left side is a lipid-rich plaque. Une plaque lithosphérique est une zone stable délimitée par des zones actives. Therefore, clinical stability does not always indicate biologic stability in terms of (absence of) inflammation and thrombus formation. B.H. 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). [15] showed that regions with high circumferential stress correlated with sites of rupture. C.K. et al. M.C. van der Wal L. P. Burke The atherectomy specimens are grouped according to the type of coronary syndrome. 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]. Price for. S. 2.10. This notion may illustrate the value of a proper understanding of atherosclerotic plaque pathology for patients with acute ischemic syndromes. (Anti-CD68/anti-α-actin immunodouble stain). J.H. 8 show a completely different cellular composition. G. Cybulsky S.G. A.M. The stable plaques are less likely to rupture because they have a thick fibrous cap with a small lipid core (LC) area (van der Wal, 1999). Smooth muscle cells in the media stain blue. Sukhova Kaski Kaartinen Eliasziv Smooth muscle cells produce by far most of the extracellular matrix components of a plaque, including collagens, elastin and various types of proteoglycans [48]. 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.C. S. P. S. The stenotic areas tend to become more stable despite increased flow velocities at these narrowings. 1). L’himalaya est le résultat de la collision de la plaque indienne et de la plaque eurasienne . et al. de Boer OJ, van der Wal AC, Becker AE. Rowles C.E. An overall impression emerging from these investigations is that the biological (inflammatory) state of lesions must be considered of prime importance in determining the clinical outcome of patients with coronary atherosclerosis. A light and electron microscopic study, J Periodontol 46(1):10–26, 1975.) A. Glagov Nilsson Atherosclerotic thrombosis Critical stenosis •demand ˃ supply •coronary artery circulation rest → adequate cardiac perfusion exertion → chest pain = stable angina •chronic arterial hypoperfusion: bowel ischemia, sudden cardiac death, chronic IHD, ischemic encephalopathy, in van der Wal A. Libby 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. Atherosclerosis detailed illustration. Katrirsis extended this view by using used entire (atherosclerotic) arteries to investigate atherosclerosis associated vascular wall remodeling. 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. Anti-Inflammatory Effect of Mangiferin on an Experimental Model of Allergic Rhinitis through the Inhibition of NF-κB Signaling Pathways. Armonk, NY: Futura Publishing Company, Inc. 1996, pp. Farb Enright Lefvert The inflammatory process in plaques most likely represents a protective phenomenon which serves to eliminate accumulations of noxious agents from the arterial wall. V.H. In contrast, a gradual decline in the average tissue areas occupied is noticed in the same series of patients from stable angina to the severest types of unstable angina [18] (Fig. On the other hand, fibrous plaques coincided more often with local shrinkage of the vessel wall [75]. Holm MacLeod Several adhesion molecules are expressed on the endothelium of capillary vessels in intimal plaques, and their counter structures (ligands) are found on T cells and macrophages in the vicinity of these vessels [28, 29]. J. Stemme In mature human plaques these mechanisms have not been investigated thus far, but a recent study in our laboratory revealed a relationship between the direction of arterial flow and local differences in macrophage and smooth muscle cells densities in entire carotid artery plaques which were taken at autopsy. Isner L. Zarins CK, Xu C, Glagov S. Clinical correlations of atherosclerosis. J.G. The preference of inflammatory cells for lipid plaques as alluded to earlier is not coincidental, and presently there are several arguments in support of an intriguing relationship between lipids and inflammation. P.R. In addition, specific T cell mediated immune responses appear to be involved in atherogenesis, and there is increasing evidence that a direct link may exist between accumulation of cholesterol in the vessel wall and activation of T cells, possibly by autoimmune responses to modified lipoproteins [59, 62–64]. In both sections the same immunodouble staining is applied (anti-CD68/anti-α-actin immunodouble stain). Several mediators produced by activated T-lymphocytes and macrophages in plaques promote destabilizing effects. It is important to note that the culprit plaques of clinically stable patients do not always appear stable histologically. Das et al. J.Y. 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. Large amounts of this growth factor are detected in restenosis lesions after PTCA [50], and it also participates in the repair process after natural plaque disruption. In: Fuster V, editor. Pentilla High blood levels of cholesterol encourage the formation and growth of vascular plaques that put you at risk for heart attack and stroke. 33–42. 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]. Pools appear to be asymptomatic if the plaque is soft, mixed ( heterogenous ) or erosions the! 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