It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. van der Wal
extended this view by using used entire (atherosclerotic) arteries to investigate atherosclerosis associated vascular wall remodeling.
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]. 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. Clark
As the lesion grows in size, the vascular lumen narrows, leading to reduced downstream tissue perfusion. 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 . 7 and Fig. Skalli
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. van der Loos
van der Wal
These were compared with atherectomy tissues of patients with either ‘stabilized’ unstable angina or the more severe type of ‘acute onset’ unstable angina. 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. Image 38564558. Sukhova
Most major blood-flow-stopping events occur at large plaques, which, prior to their … Les phénomènes géologiques accompagnant la formation des chaines de montagnes et leur relation avec la tectonique des plaques Pr. Schoneveld
Many research efforts have been devoted to the identification of such unstable plaques; this article tends to emphasize the central role of intrinsic plaque features in the process of plaque rupture and thrombosis.
J Am Coll Cardiol 1998;31:420. P.J.W. Das
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. Horrigan
P.K. 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.
4). Ischemic stroke in the cerebral artery. In situ immunophenotypic analysis suggesting an immune mediated response, Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture, Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content, Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction, Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis, Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death, Macrophage infiltration in acute coronary syndromes: implications for plaque rupture, Identification of 92 Kd gelatinase in human coronary atherosclerotic lesions; association of active enzyme synthesis with unstable angina, Mast cell infiltration in acute coronary syndromes: implications for plaque rupture, The expression of angiotensin-1 converting enzyme in human atherosclerotic plaques is not related to the deletion/inserton polymorphism but to the risk of restenosis after coronary interventions, Tissue endothelin-1 immunoreactivity in the active coronary atherosclerotic plaque. M.J.
Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions, Atherosclerotic lesions in humans. H.
3). This view is illustrated in Fig. Despite the pivotal role of lipids, inflammation and repair in determining the vulnerability of a plaque to rupture, the onset of an acute ischemic event depends on a complex interplay of variables in and outside the plaque. Jr.
An adjacent tissue section shows accumulations of macrophages (red cells) at the rupture site. Hansson
B.L. Studies on atherectomy specimens of patients with different clinical ischemic syndromes have provided some circumstantial evidence for this concept. This situation suggests that there was active plaque formation in the past, but now the inflammation in the artery wall has settled down. 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 is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and … P.K. G.C. R.
Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. M.R. Denning
Télécharger l'image vectorielle libre de droits Athérosclérose. L.
A.E. Lendon et al. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification. The most important mechanism of acute coronary syndrome (ACS) is plaque rupture and subsequent thrombus formation. Email this page; Link this page ; Print; Please describe! Vulnerable plaques were defined as lesions with a fibrous cap of less than 65 μm and infiltrated with >25 macrophages per high power field. 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 . 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.
Accordingly, in extreme cases that occur at both ends of the spectrum, plaques may arise with a totally different cellular composition. et al. D. van der Wal
These external factors will not be discussed, but still some other plaque features require attention. K.L.H. Faites l’expérience d’Adobe Stock avec 10 images offertes.
At autopsy, lipid-rich plaques are frequently found underlying coronary thrombosis [3, 14, 15]. Still, it is presently unclear what impact the various biologically active mediators released from eroded aortic surfaces may have on the human body. On the other hand, typically vulnerable plaques are characterized by large lipid pools and have a thin or virtually absent fibrous cap. This is illustrated in Figs. Moreover, the association between inflamed lipid lesions and local vessel dilation provides another clue why many mildly stenotic lesions do rupture.
Smooth muscle cells in the media stain blue. R.
V.H. (Anti-CD68/anti-α-actin immunodouble stain). ... intermittent claudication) may develop when stable plaques grow and reduce the arterial lumen by > 70%. Plaques derived from the aorta also show a clear relationship between the size of the lipid core and rupture events. No membership needed. A.
Identification of carotid plaques which confer excess risk of neurologic events is fundamental in the selection of patients for vascular intervention. van der Loos
Pricing . The role of complex stenosis morphology, Immune and inflammatory mechanisms in the development of atherosclerosis, Inflammation in atherosclerotic plaques: a clinically crucial event, Molecular bases of acute coronary syndromes, Arterial smooth muscle: a multifunctional mesenchymal cell, Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells, Transforming growth factor B is increased in human vascular restenosis lesons, Molecular and cell biology of native coronary and vein graft atherosclerosis: regulation of plaque stability and vessel remodelling by growth factors and cell-extracellular matrix interactions, Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability, Evidence for apoptosis in advanced human atheroma: co-localization with interleukin-beta converting enzyme, Apoptosis in human atherosclerosis and restenosis, Localization of stromelysin gene expression in atherosclerotic plaques by in situ hybridization, Increased expression of matrix metalloproteinases and matrix degrading activities in vulnerable regions of human atherosclerotic plaques, Matrix metalloproteinases and cardiovascular disease, Macrophage foam cells from experimental atheroma constitutively produce matrix degrading proteinases, Macrophages and ceroid in human atherosclerosis, Cell mediated immunity in atherosclerosis, Induction of T cell activation by oxidized low density lipoprotein, T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein, Evidence of a local immune response in atherosclerosis CD4, Haemostatic risk factors for cardiovascular diseases, Morphology of the endothelium over atherosclerotic plaques in human coronary arteries, Factors influencing the presence or absence of acute thrombi insudden ischemic death, Plaque rupture with wevere preexisting stenosis precipitating coronary thrombosis: characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi, Angiographic progression of coronary artery disease and the development of myocardial infarction, Five year follow up factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study, Compensatory enlargment of human atherosclerotic coronary arteries, Paradoxical arterial wall shrinkage may contribute to luminal narrowing of human atherosclerotic femoral arteries, Remodelling of the atherosclerotic arterial wall: a determinant of luminal narrowing in human coronary arteries, The relation of arterial geometry with luminal narrowing and histological markers for plaque vulnerability: the remodeling paradox, Medial thinning and atherosclerosis B evidence for a local inflammatory effect, An overview of the quantitative influence of several risk factors on progression of atherosclerosis in young people in the United States, Coronary risk factors and plaque morphology in men with coronary disease who died suddenly, The PDAY Collaborating Investigators. Most plaques that develop during a lifetime remain unnoticed, but plaque disruption and thrombus formation are not uncommon features. S.D. 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). (From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. 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). L.D. P. O'Brien
La sélection d’une zone géographique peut modifier la langue et le contenu promotionnel affiché sur le site web Adobe Stock.
Apoptose et syndromes coronariens aigus. G.V.R.
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 . 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. Plaque lithosphérique : zone stable faisant partie de la lithosphère à la surface de la Terre.
Role of Tilianin against Acute Lung Injury in In Vitro LPS-Induced Alveolar Macrophage Cells and an In Vivo C57BL/6 Mice Model. Atherosclerosis detailed illustration. Becker
The same shoulder parts of eccentric lesions represent the vulnerable sites of plaques where most ruptures take place. Clarijs
 tested the mechanical strength of human fibrous cap tissue and observed significantly reduced maximum stress at fracture when fibrous caps are infiltrated with macrophages. Stable plaque - download this royalty free Vector in seconds.
The result is a reparative and stabilizing effect on the plaque structure [46, 47, 51]. Vulnerable plaques. T.
La plaque en plastique placée sous le gravier ou les gravillons stabilise le revêtement. A.J. Illustration of angina, diagram, health - 51781417 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 . R.Y. M.
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). 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.L. In: Fuster V, editor.
Molecular processes such as inflammation, lipid accumulation, apoptosis, proteolysis, thrombosis and angiogenesis have shown to be highly related with plaque vulnerability. Libby
Nevertheless, it appears that the various risk factors may influence the balance between stabilizing and destabilizing mechanisms in the plaque each in their own way. It is important to note that the culprit plaques of clinically stable patients do not always appear stable histologically. J.
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
Copyright © 2021 European Society of Cardiology. G.T. Corren
Smooth muscle cells increase the structural strength by producing the connective tissue matrix of a plaque. 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). Stanunavicius
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. The pathogenesis of coronary artery disease and the acute coronary syndromes.
van der Loos
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]. Virmani
Essentially clinically stable are fibrous plaques, composed of solid fibrous or fibrocellular tissue, and only small amounts of extracellular lipid or no lipid at all. 4. Kearney
A gradual increase in macrophage and T cell content can be noticed from the lesions of patients with chronic stable angina to the severest types of unstable angina.
Transforming growth factor beta (TGF-β) is one of the most potent stimulators of connective tissue production by smooth muscle cells . 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. Fox
Lipid plaques, therefore, are considered ‘rupture prone'.
Sur le plan épidémiologique, la recherche sint… A.C.
van der Wal
This is illustrated in Fig. Interesting clinicopathological correlations, demonstrating that inflammation can be seen as a marker for plaque instability. E.
C-reactive protein (CRP) is an inflammation marker that could be used to assess vascular inflammation. Although basically expressions of the same disease, the plaques in Fig. K.T. 7), and a fibrous lesion of which the cellular component consists almost solely of smooth muscle cells (typically stable, Fig. Giddens
Download royalty-free Atherosclerosis. 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. 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. Most plaques rupture at sites of high calculated circumferential stress, which is often at the periphery of eccentric plaques. S.G.
So can we reduce plaque buildup? A.C.
Asthénosphère : Partie du globe terrestre située sous la lithosphère, moins rigide mais pas liquide, qui s’étend jusqu’à 700 km. G.
But, certainly not all the plaques in patients with stable coronary artery disease fulfil these criteria for stability. Généralités : plaque stable/plaque instable Alors que les bénéfices de la revascularisation dans le SCA sont bien établis, il a, jusqu’à présent, toujours été difficile de démontrer un tel bénéfice dans la maladie coronaire stable.  showed that regions with high circumferential stress correlated with sites of rupture. Fuster V, Badimon L, Badimon JJ, Chesebro JH. Stable plaques also tend to have less inflammation than is present in unstable plaques. Bentz van de Berg
In human plaques, clusters of lymphocytes are regularly observed in close proximity of ceroid pigments , which are considered as an end product of lipid oxidation . Local flow disturbances and lipids as a driving force appear to be obligatory in this process .
(Pico Sirius red stain: collagen red). Davies
how you will use this image and then you will be able to add this image to your shopping basket. How Doctors Measure Plaque Stability A CT scan can show how stable plaques are (American Journal of Roentgenology, March 2015;204(3):W249-W260). 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
(B) Detail of the boxed area in (A). 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. 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. C.E. Thomas
Atherosclerosis, the formation of life-threatening plaques in blood vessels, is a form of cardiovascular disease. O.J. 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 . 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. Zhou
This notion is of importance, since only specific types of lesions in this spectrum of morphologic variants appear to be associated with acute manifestations of atherosclerotic disease.
But they may become vulnerable, there is a risk of rupture and lead to thrombosis. 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 .
Atherosclerotic plaque formation.
In the atherosclerotic plaque these growth factors are produced by ‘injured’ endothelial cells and macrophages or released from thrombus [1, 51]. Born
(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.J.
Indeed, many plaques that underlie coronary thrombus are high grade stenotic lesions. The plaque is largely fibrocellular/fibrosclerotic and contains only small deeply located atheromas (hematoxylin–eosin stain). J.J.
Author information: (1)Department of Cardiology, Larissa University Hospital, Larissa, Greece.
C.M. Smoking did not influence the composition of the plaques with respect to features of vulnerability, but appeared to be highly thrombogenic. J.
In coronary arteries most of these lesions remain clinically silent, or on the long term, may lead to stable angina pectoris . 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]. 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 . S.
Apart from the undisputable role of atherosclerosis in abdominal aneurysm formation , mural thrombosis leads to a surprisingly low rate of clinically significant complications in these patients, although cholesterol emboli can be regularly found in their kidneys and skin at autopsy. •destruction of the underlying vessel wall → aneurysm formation → secondary rupture and / or thrombosis.
Recent investigations by this group give more insight in this paradoxical situation. The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Davies
Hemodynamic factors such as local disturbances in flow velocity and alterations in shear stress form another risk factor for plaque initiation and growth . Asterisk is in the lipid core of the plaque. Inflammation is involved in the formation and growth of a stable plaque but also plays an important role in the transformation into the unstable plaque by stimulating metalloproteinase, macrophages and thrombotic activity.
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).
M.Y. The stenotic areas tend to become more stable despite increased flow velocities at these narrowings. et al.
et al. Kovanen et al. N.
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. However, in the PDAY investigations smokers had more lipids in their plaques, particularly oxidized lipoproteins, than non-smokers . A.I. Campbell
Carotid plaque composition in stable and unstable coronary artery disease. "Making plaque disappear is not possible, but we can shrink and stabilize it," says cardiologist Dr. Christopher Cannon, a Harvard Medical School professor. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. P. Nikol
On the other hand, lipid associated inflammation introduces tissue degrading effects. Ross
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N Engl J Med 1992;26:242–250; 310–318. Glagov
(B) Adjacent section stained with Picro Sirius Red (collagen red, media yellow) shows a decrease in collagen density where the macrophages have accumulated. In carotid plaques, rupture sites are also associated with plaque inflammation  and indeed, in 70% of the ruptured plaques that were encountered in our series, the rupture site was found in the upstream shoulder. However, Pasterkamp et al. 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) ; it gives at least one explanation for the fact that many plaques rupture at a stenosis rate of less than 50%. Carpenter
C.C. 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. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. G.
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. Chester
In: Fuster V, editor. van der Wal
Schematic view of the two major tissue remodeling forces in atherosclerotic plaques.
Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. et al. J.H.
G.K. 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]. The onset of plaque rupture is a complex process. Ihling
Maximum accumulation of Plaque takes place in 21 days. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. et al. 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. 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.
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  (Fig. Mann
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. 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