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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic macroangiopathy is often viewed as an accelerated and aggravated form of atherosclerosis. Several biological disturbances that are associated with diabetes partially account for a possible aggravation of atherosclerosis. Such are disorders of blood lipids (increased triglyceride concentration, modifications of low density lipoproteins) of haemostatis (increased platelet activity, decreased fibrinolytic activity) or of arterial vasomotility. Yet, many uncertainties and inconsistencies still obfuscate the links between diabetes and atherosclerosis, which remain hypothetical, and debatable. Clinical experience and all clinical epidemiological studies show that the incidence and severity of ischaemic arterial diseases (coronary heart disease, lower limb ischaemia, cerebral ischaemic events) are increased in diabetic individuals. However, intermediates other than worsened atherosclerosis may account for these associations. For instance, several anatomical epidemiological studies, based on routine autopsies, have note consistently found that atherosclerotic lesions (plaques) are larger and more extensive in diabetic than in non-diabetic individuals. The basic mechanisms of diabetic macroangiopathy could therefore be not as closely related to atherosclerosis as is usually thought. Among the non-atherosclerotic lesions that could explain the increased arterial risk in diabetic patients, the best documented and most plausible is arteriosclerosis--a pure sclerosis of the arterial wall (without lipid deposition) which, in its advanced forms, can compromise tissue vascularization. Arteriosclerosis is considered as a normal consequence of arterial ageing which would be accelerated in diabetes. Chronic hyperglycaemia is and independent and influent marker of arterial risk in diabetic patients. It could stimulate arterial sclerosis by enhancing non-enzymatic glycation of various components of the arterial matrix, through formation of advanced glycation end-products (AGEs).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanisms of macrovascular involvement in diabetic subjects]. 782 80

Diabetic macroangiopathy comprises: on one hand, atherosclerosis which seems to appear earlier and to progress more rapidly than in non-diabetic individuals; and, on the other hand, a less well characterised involvement of arteries affecting their structure (diffuse fibrosis) and function (vasomotility). Hyperinsulinaemia is suspected to enhance macroangiopathy, yet the biological and epidemiological facts to support this hypothesis are weak and somewhat discrepant. By contrast, a role for hyperglycaemia, in terms of intensity and duration, is supported by growing evidence. In addition to the correction of classical risk factors for arterial disease, the strict control of hyperglycaemia is likely to become an essential intervention in the prevention of macroangiopathy.
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PMID:[Atherosclerosis and cardio-vascular complications of diabetes]. 894 10

Diabetic macroangiopathy is a major cause of morbidity and mortality of patients with non-insulindependent diabetes mellitus. Bad metabolic control of diabetes increases the risk of developing atherosclerotic complications. Hyperglycemia aids to increase the process of non-enzymatic protein glycosylation. Advanced glycation end products (AGEs) created in Maillard reaction play multidirectional role in creation of atherosclerosis in NIDDM. AGEs form in LDL, HDL and VLDL particles and increase their oxidative modification. They aid deposition of cholesterol and its esters in macrophages as well as creation of foam cells. Reaction of LDL-AGE particles with proteoglycans of blood vessel intima results in its thickening. LDL-AGE and ox-LDL take part in formation of late atherosclerotic changes influencing the expression of genes for cytokines and growth factors. AGEs promote prothrombotic changes. They block formation of nitric oxide which results in impaired vessel relaxation. They also take part in progressive vessel narrowing up to complete vessel occlusion by atheroslerotic plaque.
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PMID:[The importance of advanced glycosylation end products in the creation and progression of atherosclerosis in non-insulin-dependent diabetes mellitus]. 1105 18

Diabetic macroangiopathy has already developed before diagnosis of diabetes mellitus. Postprandial hyperglycemia has been known as a risk factor for diabetic macroangiopathy and may be more powerful than fasting hyperglycemia. To intervene in hyperglycemia, insulin secretagogues, glinides which selectively stimulate early meal-induced insulin secretion and improve postprandial hyperglycemia, and sulfonylureas which enhance total daily insulin secretion and improve fasting hyperglycemia, have been prescribed as major oral antidiabetic agents. Few evidences that amelioration of glycemic control with insulin secretagogues lower the risk of cardiovascular diseases have been reported. But current studies have shown that intervention in postprandial hyperglycemia with drugs including glinides decreased thickness of carotid IMT as a surrogate marker of atherosclerosis. Results from on-going large scale intervention study with glinides may clarify whether amelioration of hyperglycemia lower the risk of atherosclerotic events.
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PMID:[Glinide(s), sulfonylurea(s)]. 1708 4

Diabetic macroangiopathy is severe complication for diabetes mellitus, and inflammatory cytokines induces various reactions for the formation of atherosclerosis in diabetes. In addition, recent reports indicate the accumulation of macrophages in the adipose tissue occurs in diabetes and these macrophages secret an inflammatory cytokines. It is also known macrophages produce most of circulating TNF-alpha. Accordingly, inflammatory cytokines, produced in adipose tissue, influence systemic inflammation possibly. Leukocyte-endothelial interactions are critical in the progression of inflammation and atherosclerosis. Recruitment of leukocytes to the sites of inflammation or atherosclerosis prone vasculature involves multistep complex cascades of adhesion events, which inflammatory cytokines induce. Inflammatory cytokines are not the only factor in diabetic macroangiopathy, however, it is certain that inflammation plays important role in diabetes and diabetic vascular complication.
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PMID:[Inflammatory cytokines]. 2044 75

Diabetic macroangiopathy, atherosclerosis secondary to diabetes mellitus (DM), causes cerebro-cardiovascular diseases, which are major causes of death in patients with DM and significantly reduce their quality of life. The alterations in vascular homeostasis due to endothelial and vascular smooth muscle cell dysfunction are the main features of diabetic macroangiopathy. Although multiple metabolic abnormalities that characterize diabetes are involved in the progression of atherosclerosis in patients with DM, it may be said that prolonged exposure to hyperglycemia and insulin resistance clustering with other risk factors such as obesity, arterial hypertension, and dyslipidemia play crucial roles. Laboratory and clinical researches in the past decades have revealed that major biochemical pathways involved in the development of diabetic macroangiopathy are as follows: overproduction of reactive oxygen species, increased formation of advanced glycation end-products (AGEs) and activation of the AGEs-receptor for AGE axis, polyol and hexosamine flux, protein kinase C activation, and chronic vascular inflammation. Among them, oxidative stress is considered to be a key factor.
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PMID:Mechanism of Development of Atherosclerosis and Cardiovascular Disease in Diabetes Mellitus. 2896 36

Diabetic macroangiopathy - a specific form of accelerated atherosclerosis - is characterized by intra-plaque new vessel formation due to excessive/abnormal neovasculogenesis and angiogenesis, increased vascular permeability of the capillary vessels, and tissue edema, resulting in frequent atherosclerotic plaque hemorrhage and plaque rupture. Mechanisms that may explain the premature and rapidly progressive nature of atherosclerosis in diabetes are multiple, and to a large extent still unclear. However, mechanisms related to hyperglycemia certainly play an important role. These include a dysregulated vascular regeneration. In addition, oxidative and hyperosmolar stresses, as well as the activation of inflammatory pathways triggered by a dysregulated activation of membrane channel proteins aquaporins, have been recognized as key events. Here, we review recent knowledge of cellular and molecular pathways of macrovascular disease related to hyperglycemia in diabetes. We also here highlight how new insights into pathogenic mechanisms of vascular damage in diabetes may indicate new targets for prevention and treatment.
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PMID:Diabetic macroangiopathy: Pathogenetic insights and novel therapeutic approaches with focus on high glucose-mediated vascular damage. 2942 94