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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The arteries of monkeys given atherogenic diets develop marked intimal thickening and medial thinning, but luminal size apparently changes minimally. The hemodynamic significance of the atherosclerotic changes is therefore uncertain. To evaluate vascular function in atherosclerotic arteries, we studied the hind-limb vessels of adult male rhesus and cynomolgus monkeys to assess the structural and hemodynamic responses to an atherogenic diet given for about 1.5 years or for much longer periods (6.5 years for rhesus and 4.3 years for cynomolgus monkeys). The intimal cross-sectional area greatly increased after the atherogenic diet, but there was no significant luminal narrowing after either the 1.5-year diet or the longer diet periods. The media of atherosclerotic arteries showed focal atrophy and focal thinning after pressure fixation, but the total medial mass was not decreased even after the long diet periods. Hemodynamic studies indicated mild functional impairment in the atherosclerotic vessels; resting resistance increased and vasodilator responses decreased, but adrenergic responses were preserved. Thus, the marked changes that occur in the arterial wall in experimental primate atherosclerosis include adaptations to lesion formation that permit a long prestenotic phase of atherosclerosis in which vascular dysfunction is minimal.
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PMID:Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet. 401 7

Transluminal angioplasty has shown promise as a nonoperative treatment of atherosclerotic obstruction. Despite its increasing clinical use and potential importance, little is known of its mechanism and acute effects. To evaluate transluminal angioplasty, three rabbit models of experimental atherosclerosis were developed: Group 1 (n = 20) = high cholesterol diet plus balloon de-endothelialization; Group 2A (n = 12) = high cholesterol diet plus an indwelling catheter; Group 2B (n = 10) = normal diet plus an indwelling catheter. After 6 weeks or 8 weeks, distinct angiographic and pathological lesions in the iliac artery were evident in all groups. Group 1 showed predominant foam cell lesions, while Group 2 showed eccentric mixed fibrous and foam cell or only fibrous lesions. Significant angiographic stenosis was present in 78% of the animals. Angioplasty of the highest grade iliac stenosis resulted in at least a 20% reduction in luminal diameter narrowing in 26 of 37 animals (70%). Histopathological examination 1 day following angioplasty in 17 animals showed two patterns. In Group 1 animals, neointimal fracture and dissection were evident, while in Group 2 animals thinning and stretching of the nonatherosclerotic portion of the vessel walls could be demonstrated. This study demonstrates that the New Zealand rabbit can be used to produce a spectrum of morphologically distinct atherosclerotic lesions that lend themselves to the study of transluminal angioplasty. The immediate consequences of angioplasty, which appear to depend upon the underlying histopathology and widening of the narrowed lumen, are frequently concurrent with intimal fracture, dissection, or thinning of the nonatherosclerotic portion of the vessel wall.
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PMID:Acute effects of transluminal angioplasty in three experimental models of atherosclerosis. 646 20

Chronic periaortitis is a local complication of human atherosclerosis. It is defined as the triad of advanced atherosclerosis, medical thinning and aortic adventitial chronic inflammation. It is present to a variable degree in association with atherosclerotic abdominal aortic aneurysms. These aortic adventitial infiltrates differ from those described solely within the atheroma itself, in that they consist predominantly of B lymphocytes. Many of the lymphocytes are activated and proliferating, and germinal centres are common. In this study, an immunohistochemical analysis was carried out on fresh surgical aortic aneurysm tissue in order to investigate the presence and distribution of activation-inducible adhesion molecules, and to correlate this with the degree of inflammation. A consistent finding was the presence of E-selectin on endothelial cells in up to 50% of the vessels throughout the aortic wall and at the base of the atheroma, independent of the severity of inflammation. ICAM-1 expression was abundant on many cell types and increased with the severity of chronic inflammation, being strongest in the germinal centres. VCAM-1 expression was predominant on follicular dendritic cells and also increased with severity of inflammation. VCAM-1 expression was also detected on vessels within lymphoid follicles. The pattern of expression of the adhesion molecules suggests a role in the initiation and progression of chronic inflammation associated with advanced atherosclerosis.
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PMID:The distribution of adhesion molecules in chronic periaortitis. 751 59

Sclerotic involvement of abdominal aorta and lower limb arteries is related to 2 types of fundamental lesions: atherosclerosis and arteriosclerosis. Atherosclerosis is a focal intimal thickening (plaque) of large- and medium-sized arteries, which combines atheroma (lipid deposition) and fibrosis. Plaque rupture is the crucial event in the progression of atherosclerosis, directly causing most acute thrombotic events, and contributing in great part to plaque expansion. Arteriosclerosis is a diffuse fibrosis of the arterial wall with thickening of the intima, and thinning of the media. Two forms of arteriosclerosis probably exist with distinct mechanisms and consequences. Obliterating arteriosclerosis mainly involves leg arteries (causing poor distal run-off) and appears to be essentially enhanced by ageing, diabetes and chronic renal insufficiency. Dilating arteriosclerosis involves large arteries where it provokes aneurysm formation; it is related to ageing, but seems also to be dependent upon an inborn dystrophy of arterial connective tissue. These 3 components of sclerotic arterial diseases of the lower limbs are often combined in the same individual.
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PMID:[Description and mechanisms of sclerotic arterial diseases of the lower limbs]. 772 5

To clarify the mechanism of ulcer formation of atherosclerotic plaques in human carotid arteries, autopsy investigations were performed on eight patients who had died of cerebral infarction due to recent carotid thrombosis. Eleven control patients who had carotid atherosclerosis without thrombosis were also investigated. Histological changes of the arteries in serial sections were reconstructed three-dimensionally. Each artery with occlusive thrombosis was found to have an intimal ulcer at the head of the thrombus on the proximal slope near the base of the thickened atheromatous plaque at the carotid sinus. Most ulcers formed obliquely or longitudinally, were parallel to the vessel axis, had a fusiform shape, and measured 7 +/- 2 x 3 +/- 1 mm (mean +/- s.d.). The ulcers arose by marginal separation of the innermost layer from the underlying layer of the stratified intima. An underlying atheroma developed along the borders of these intimal layers reaching the subendothelium, with thinning of the intimal cap to less than 150 microns. The process of ulceration may be generated by vessel injury induced by hemodynamic forces, such as tensile forces and shear stress. The ulcer may extend along the fragile region where the wall may exhibit uneven compliance due to differences in the tissue structures of each intimal layer. Furthermore, macrophages may play a key role in ulcer formation.
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PMID:Three-dimensional analysis of human carotid atherosclerotic ulcer associated with recent thrombotic occlusion. 783 75

The morphological findings of 2 basilar artery giant fusiform aneurysms are presented. In one case (a 63-year-old man) the aneurysm was accidentally found at autopsy. Its wall was mainly formed by fibrous tissue without a smooth muscle layer and presented fragmented but still recognizable elastic lamina. In the media there were small well-formed bony spicules. In the other case (a 59-year-old man) the aneurysm had broken causing subarachnoid hemorrhage. The wall showed a marked reduction of smooth muscle cells and thinning and fragmentation of elastic lamina. A second sacciform aneurysm was present at the basilar tip. The review of the literature and the morphological findings of the 2 cases, characterized by abnormality of the portion of the basilar artery not directly involved in the aneurysm wall, consisting of a diffuse deficit of the tunica media and lamina elastica, might suggest that the fusiform aspect of the aneurysm may be the result of the degenerative effect of atherosclerosis on a cogenital, structural or dysmetabolic, or acquired, inflammatory, weakening of the arterial wall.
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PMID:Megalodolichobasilaris: the effect of atherosclerosis on a previously weakened arterial wall? 883 2

Most measures taken to prevent atherosclerosis still aim at lowering the cholesterol content of the plasma lipoproteins by dietary and pharmacological means. This approach has only proved successful to a limited extent. Diseases secondary to atherosclerosis are still the commonest cause of death in western industrialized countries. As all metabolic processes are regulated by opposing processes of equilibrium, i.e. by processes directed towards performance and recovery, we asked ourselves whether the fatty degeneration and sclerosis of the arteries could be causally related to a continuous dysregulation of these processes. We consider this to be the case, with a continuous deficiency of glycosaminoglycans (heparin, heparinoids) on the endothelial surface of the vessels. Numerous studies indicate that in the case of thinning of the anionic glycosaminoglycan film on the endothelial surface, the lipoprotein-lipase and antithrombin III activity induced by heparin is reduced, as result of which hyperlipoproteinaemia and increased tendency to thrombosis can only by compensated for to an inadequate extent. The formation of glycosaminoglycans is a characteristic of all mesenchymal cells, whereby the exogenous introduction of glycosaminoglycans into the extracellular space is of decisive importance for adequate glycosaminoglycan synthesis. Since Engelberg reported outstanding results obtained with heparin injections in the prevention and treatment of atherosclerotic disorders of the cardiac circulation, we considered it appropriate to use the well-proven dietary supplement of glycosaminoglycans in rheumatology, in the treatment of arthrosis, as well as in the prevention and treatment of atherosclerosis.
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PMID:The pathogenesis and prevention of atherosclerosis. 895 6

The integrity of the cerebral vasculature is crucial to the maintenance of cognitive functions during ageing. Prevailing evidence suggests that cerebrovascular functions decline during normal ageing, with pronounced effects in Alzheimer's disease (AD). The causes of these changes largely remain unknown. While previous studies recorded ageing-related impairments, such as atherosclerosis and loss of innervation in basal surface arteries of the brain, it only recently has been realized that a number of subtle alterations in both the intracranial resistance vessels and the smaller capillaries is apparent in both ageing animals and humans. The dominant changes include alterations in composition of connective tissues and smooth muscle of large vessel walls, thickening of the vascular basement membrane, thinning of the endothelium in some species, loss of endothelial mitochondria and increased pericytes. Some of these attributes appear more affected in AD. Other abnormalities entail profound irregularities in the course of microvessels, unexplained inclusions in the basement membrane and changes in unique proteins and membrane lipids associated with the blood-brain barrier. Brain imaging and permeability studies show no clear functional evidence to support the structural and biochemical anomalies, but it is plausible that focal and transient breach of the blood-brain barrier in ageing, and more notably in AD, occurs. Thus, circumscribed neuronal populations in certain brain regions could become vulnerable. Furthermore, the characteristic deposition of amyloid in vessels in AD may exacerbate the decline in vascular function and promote chronic hypoperfusion. Although not explicit from current studies, it is likely that the brain vasculature is continually modified by growth and repair mechanisms in attempts to maintain perfusion during ageing and disease.
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PMID:Cerebral vessels in ageing and Alzheimer's disease. 936 75

Advanced glycation end products (AGE) in tissues are important for the central pathological features of diabetic complication. Although AGE bind to several cell-surface sites, resulting in altered cellular functions, receptor for AGE (RAGE) appears to have a central role. We examined AGE accumulation and RAGE expression in the aorta and heart of rats with streptozotocin (STZ)-induced diabetes, 0, 4, 8, 12, 16 and 24 weeks after STZ administration. Early atherosclerotic findings in the intima and medial thinning were observed in the aorta after 16 weeks of STZ-Induced diabetes. Immunohistochemistry and microscope spectrophotometry showed that AGE deposition increased significantly in the aorta and vessels of the myocardium, depending on the period of hyperglycaemia. RAGE was expressed in the endothelial cells and vascular smooth muscle cells of all animals. The number of smooth muscle cells with RAGE immunoreactivity increased until 12 weeks after STZ injection, and then decreased in rats with diabetes between 16 and 24 weeks. On the other hand, total RAGE mRNA levels in the aorta and heart continued to increase with the duration of hyperglycaemia. Furthermore, AGE-BSA induced RAGE mRNA expression of human umbilical vein endothelial cells in vitro. Taken together, the AGE accumulation might initiate diabetic macroangiopathy through RAGE, and the increase of RAGE expression by endothelial cells could be a reason that diabetes mellitus accelerates atherosclerosis rapidly.
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PMID:Deposition of advanced glycation end products (AGE) and expression of the receptor for AGE in cardiovascular tissue of the diabetic rat. 979 17

Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. The risk for plaque disruption depends more on plaque vulnerability (plaque type) than on degree of stenosis (plaque size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a plaque's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap thinning, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a plaque's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.
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PMID:Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. 1038 96


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