Microscopic foci of endothelial loss associated with platelet thrombi are present on the surface of in many advanced plaques . Becker It can be anticipated from the extensive experimental work in this field that local differences in arterial flow or shear stress over a bulging plaque surface may induce local variations in endothelial function (expression of adhesion molecules, production of growth factors) within one and the same plaque, with local differences in leukocyte recruitment and platelet adherence as a consequence [82–84]. X rays can show the difference between stable plaques that are safe and those that are unstable and … C.M. (From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. A.E. 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. A. Farb (Abstract). In a series of 20 acute myocardial infarction related thrombosed coronary arteries of patients who died acute or within 2 days after the onset of the infarct, we noticed abundant infiltration of activated T cells and macrophages at the immediate site of erosion or rupture in 19 cases. K.L.H. And more recently, active plaque inflammation associated with plaque rupture could be demonstrated also in carotid artery plaques obtained from stroke patients . Email this page; Link this page ; Print; Please describe! This notion may illustrate the value of a proper understanding of atherosclerotic plaque pathology for patients with acute ischemic syndromes. Stanunavicius In contrast, other plaques … 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. Atherosclerosis, the formation of life-threatening plaques in blood vessels, is a form of cardiovascular disease. Asthénosphère : Partie du globe terrestre située sous la lithosphère, moins rigide mais pas liquide, qui s’étend jusqu’à 700 km. R. A. 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. Franke However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. Avec la plaque stabilisatrice EuroGravel, vous obtenez très facilement une surface de gravier stable et sans traces. McEwan M. Streifler These lesions, which occur more often in younger individuals and in women, have less often or smaller foci of inflammation . van Suylen 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]. A.I. Allen Chen This is where it is important to determine if the plaque is soft, mixed (heterogenous) or hard plaque. Sixty percent of these plaques were fibrous, but 40% had a pool of extracellular lipids. Das Illustration about Stable plaque formation in the human artery. Normal CIMT and presence of plaque. Smooth muscle proliferation and matrix synthesis implies a mechanism of slowly progressive growth of plaques; it serves to encapsulate the soft atheroma and organizes episodes of thrombus formation, either spontaneously or artificially induced. However, in young patients and females, plaque erosions are a more common cause of coronary thrombosis underlying myocardial infarction . Gimbrone Indeed, many plaques that underlie coronary thrombus are high grade stenotic lesions. Another example is provided by the T-cell cytokine IFN-gamma. et al. J.G. Das Faites l’expérience d’Adobe Stock avec 10 images offertes. 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. Filamentous bacteria (f) appear to be invading cocci microcolonies. 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 , vasoactive substances such as angiotensin I  and endothelin , 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) . Jonasson A.E. Eefting A.C. Hibbs P. O'Brien 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 P. Dollery Kume Deep intimal tears which extend into the highly thrombogenic lipid core of lesions, and sometimes showing extrusion of parts of the atheroma are often associated with massive thrombus formation. There is abundant anti HLA-DR reactivity on plaque cells indicating active inflammation. Zeiher New insights have emerged on a possible role for inflammation and repair also in local arterial wall remodeling in terms of dilation and shrinkage, with consequences for the geometry of the entire vessel . P. Mitchinson Palacios Hemodynamic factors such as local disturbances in flow velocity and alterations in shear stress form another risk factor for plaque initiation and growth . Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. Differences in histological composition inside the plaque and its relation to the geometry of the arterial wall have implications for the biomechanical properties of plaques. Background and Purpose— Bone formation and dystrophic calcification are present in carotid endarterectomy plaques. Bentz van de Berg P. D. S.D. Percentages of tissue areas occupied by smooth muscle cells (SMC) and macrophages (MAC) are quantified planometrically and the number of T cells are counted per mm2 in immunostained sections. Kovanen Wensing Cybulsky M.R. et al. Pepper Rosenschein The stenotic areas tend to become more stable despite increased flow velocities at these narrowings. Asmaa ROUILLI 2 1- Décrivez la répartition des roches métamorphiques dans la région d’Uzerche. These lesions may also calcify and in some cases undergo osseous metaplasia (bone formation) over time. 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. Vulnerable plaques. J.J. Post Smooth muscle cells in the media stain blue. (B) Adjacent section stained with Picro Sirius Red (collagen red, media yellow) shows a decrease in collagen density where the macrophages have accumulated. J. Stemme Tannenbaum T. N. Souhaitez-vous les transférer vers votre profil d’entreprise ? 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].  tested the mechanical strength of human fibrous cap tissue and observed significantly reduced maximum stress at fracture when fibrous caps are infiltrated with macrophages. Collins But they may become vulnerable, there is a risk of rupture and lead to thrombosis. This view is illustrated in Fig. 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. Richardson 4). S. Alexpoulos Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and … 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). Atherogenesis: Unstable Plaque Formation Variant Image ID: 3377 Add to Lightbox. J.H. Recent investigations by this group give more insight in this paradoxical situation. Bland Brown Stable plaque formation - Buy this stock vector and explore similar vectors at Adobe Stock 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. S.M. M. Charlston R. However, in an autopsy study primarily focused on plaque erosion as the underlying cause of coronary thrombosis, this type of disruption was also identified in a proteoglycan-rich and smooth muscle-rich type of plaque. P.D. Fishbein van der Wal Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. Price for. The result is a reparative and stabilizing effect on the plaque structure [46, 47, 51]. O.J. Maximum accumulation of Plaque takes place in 21 days. A principal feature of inflammation is the accumulation of leukocytes; in longlasting chronic inflammatory processes these leukocytes are macrophages, lymphocytes and mast cells. These external factors will not be discussed, but still some other plaque features require attention. Escaned 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. J.M. Most of these are intra plaque hemorrhages, due to entrance of blood into the lipid core of the lesion and followed by healing of the rupture . Malcolm 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. 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 . Vulnerable plaques were defined as lesions with a fibrous cap of less than 65 μm and infiltrated with >25 macrophages per high power field. Kaartinen This situation suggests that there was active plaque formation in the past, but now the inflammation in the artery wall has settled down. He has been diagnosed with triple vessel disease — a condition triggered by plaque formation in the arteries — and underwent a coronary angioplasty to unclog his … Piek M.A. In only 15% of these patients, all the plaques causing >50% stenosis were fibrous, while in 13% of patients virtually all plaques had a lipid core. G.K. (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. R. Giddens During inflammation another series of events is initiated that must lead to the healing of injured tissue, either by regeneration or by scarring (fibrosis). Rowles Atherosclerosis. Local flow disturbances and lipids as a driving force appear to be obligatory in this process . 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. aortic disease. J.J. P.K. Keaney Any form of endothelial denudation leads to activation of the coagulation system due to exposition of highly thrombogenic plaque constituents (lipids, tissue factor, collagens) to the blood stream. The plaque is largely fibrocellular/fibrosclerotic and contains only small deeply located atheromas (hematoxylin–eosin stain). G.K. Falk E. Advanced lesions and acute coronary syndromes: a pathologist's view. Ehsani Mann Pentilla 3). The onset of plaque rupture is a complex process. Armonk, NY: Futura Publishing Company, Inc, 1996, pp. Ainsi, la quasi-totalité des adultes seraient touchés. L.D. Holm Unlimited phagocytosis of oxidized LDL by macrophages through scavenger receptors with a high ligand specificity for ox-LDL results in the formation of foam cells, which is another hallmark of atherosclerosis . Fibrosis related contraction (a well known phenomenon in wound healing) could explain why many highly stenotic lesions are fibrous. Dental Pellicle forms within seconds after brushing. Becker Author information: (1)Department of Cardiology, Larissa University Hospital, Larissa, Greece. Skalli Ball Smooth muscle cells (blue) are in the media and focally in the fibrous cap where they cover the site of macrophage accumulation. G.K. Burke et al. This is illustrated in Fig. They also observed dilation at sites of atherosclerotic plaques, but in other instances (plaques) shrinkage of the vessel wall leading to lumen narrowing could be objectivated [73, 74]. 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]. In early lesions and in restenosis lesions, smooth muscle cell apoptosis could have beneficial effects and promote regression, but in the fibrous cap of advanced lesions it introduces another potential of plaque destabilization through the loss of repair cells. N Engl J Med 1992;26:242–250; 310–318. A.K. Born F.D. The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Davies G.V.R. 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. J. Davies 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. Men with stable coronary artery disease fulfil these criteria for stability features require attention confer excess risk rupture... 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