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

Between 120 and 140 million people suffer from diabetes mellitus (type 1 and type 2) worldwide, and this number may well double by the year 2025. Patients with diabetes are at increased risk of atherosclerosis and its clinical sequelae: coronary, peripheral vascular, and cerebrovascular diseases. Concurrently, the most common cause of death in persons with diabetes is myocardial infarction. The pathogenesis, progression, and epidemiology of atherosclerotic disease are distinct in patients with diabetes. Atherosclerosis can develop much earlier in life, and at an accelerated rate, compared with non-diabetic individuals. One of the factors responsible for increased atherosclerosis is related to the atherogenic lipid profile in diabetes. The pathobiological processes that are responsible for transforming dormant atherosclerotic plaques into active rupture-prone plaques may be enhanced in diabetes as well. It follows that a major challenge in the treatment of patients with diabetes is to reduce the risk of atherosclerotic disease. The third National Cholesterol Education Program (NCEP) report recently recommended that the management of dyslipidaemia in patients with diabetes should be as aggressive as in those with established coronary heart disease (CHD). The NCEP Adult Treatment Panel III guidelines recommend statins for patients at elevated risk for CHD.
Acta Diabetol 2002 Jun
PMID:Impact of the atherosclerotic process in patients with diabetes. 1222 24

Metabolic syndrome, insulin resistance, prediabetes, and overt type 2 diabetes mellitus are associated with an accelerated atherosclerosis (atheroscleropathy). This quartet is also associated with multiple metabolic toxicities resulting in the production of reactive oxygen species. The redox stress associated with these reactive oxygen species contribute to the development, progression, and the final fate of the arterial vessel wall in prediabetic and diabetic atheroscleropathy. The prevention of morbidity and mortality of these intersecting metabolic diseases can be approached through comprehensive global risk reduction.
Cardiovasc Diabetol 2002 Sep 27
PMID:Intimal redox stress: accelerated atherosclerosis in metabolic syndrome and type 2 diabetes mellitus. Atheroscleropathy. 1239

Our aim is to summarize and discuss the recent literature linking diabetes mellitus with heart failure, and to address the issue of the optimal treatment for diabetic patients with heart failure. THE STUDIES LINKING DIABETES MELLITUS (DM) WITH HEART FAILURE (HF) : The prevalence of diabetes mellitus in heart failure populations is close to 20% compared with 4 to 6% in control populations. Epidemiological studies have demonstrated an increased risk of heart failure in diabetics; moreover, in diabetic populations, poor glycemic control has been associated with an increased risk of heart failure. Various mechanisms may link diabetes mellitus to heart failure: firstly, associated comorbidities such as hypertension may play a role; secondly, diabetes accelerates the development of coronary atherosclerosis; thirdly, experimental and clinical studies support the existence of a specific diabetic cardiomyopathy related to microangiopathy, metabolic factors or myocardial fibrosis. Subgroup analyses of randomized trials demonstrate that diabetes is also an important prognostic factor in heart failure. In addition, it has been suggested that the deleterious impact of diabetes may be especially marked in patients with ischemic cardiomyopathy. TREATMENT OF HEART FAILURE IN DIABETIC PATIENTS : The knowledge of the diabetic status may help to define the optimal therapeutic strategy for heart failure patients. Cornerstone treatments such as ACE inhibitors or beta-blockers appear to be uniformly beneficial in diabetic and non diabetic populations. However, in ischemic cardiomyopathy, the choice of the revascularization technique may differ according to diabetic status. Finally, clinical studies are needed to determine whether improved metabolic control might favorably influence the outcome of diabetic heart failure patients.
Cardiovasc Diabetol 2003 Jan 08
PMID:Influence of diabetes mellitus on heart failure risk and outcome. 1255 46

Several general population studies and those carried out in diabetic patients with complications have pointed to serum sialic acid as a marker of inflammation in atherosclerosis. In this study we examined whether total sialic acid (TSA) was changed in the sera of 28 newly diagnosed subjects with type 2 diabetes (type 2 DM), 47 subjects with impaired glucose tolerance (IGT) and 72 subjects with normal glucose tolerance (NGT). The associations between sialic acid and other atherosclerotic risk factors such as lipid profile, baseline diene conjugates in low-density lipoproteins (LDL-BDC) and fasting insulin were also investigated. We found a trend to TSA increase in subjects with impaired glucose tolerance and a significant increase in TSA in newly diagnosed patients with type 2 DM (2.2+/-0.3 vs. 1.9+/-0.3 mmol/l; p<0.03) when compared to subjects with NGT. Lipid profile and LDL-BDC, as a marker of circulating oxidized LDL, did not differ among glucose tolerance categories. Significant associations between total sialic acid and 2-h post-load glucose level, fasting insulin, insulin sensitivity, HDL-cholesterol and log of triglycerides were found in the examined subjects. Multiple regression analysis showed significant correlations between serum sialic acid and 2-h post-load glucose levels and insulin sensitivity. This study indicates that measurement of TSA as a marker of subclinical inflammation may be valuable as an independent parameter in identifying subjects at higher risk of developing type 2 diabetes and those who might benefit from anti-inflammatory treatment.
Acta Diabetol 2003 Jun
PMID:Serum sialic acid in subjects with impaired glucose tolerance and in newly diagnosed type 2 diabetic patients. 1286 8

Hyperglycaemia as a common feature of diabetes mellitus is a cause of different pathogenic mechanisms influencing endothelial function. Oxidative stress is one of the main causative factors inducing endothelial dysfunction and changes in plasma protein or platelet function. In type 2 diabetes mellitus, a combination of hyperglycaemia together with dyslipidaemia, obesity and other factors may accelerate the process of glycoxidation and lipid oxidation, causing an early impairment of the vessel wall or properties of circulating blood. This induces hypercoagulability characterised by impaired fibrinolysis and hyperaggregability. The initial functional changes are later substituted by morphologically impaired structure of the blood capillaries (microangiopathy) or arteries (macroangiopathy). The latter represent advanced atherosclerosis when typical plaques are formed. Failure of protective scavenger mechanisms is one possible explanation of vessel wall pathology in diabetes.
Acta Diabetol 2003 Dec
PMID:Pathogenesis of angiopathy in diabetes. 1470 62

Macroangiopathy is the most frequent complication in type 2 diabetic patients. Coexistence of atherosclerosis and diabetes may cause diagnostic difficulties resulting from an asymptomatic course. Alternatively, patients may overexpress their symptoms as the result of awareness the consequences of the disease. Careful assessment of clinical symptoms followed by preventive diagnosis of high-risk patients as well as proper patient education allow for significant reductions of hazard of the consequences of macrovascular complications in diabetic patients
Acta Diabetol 2003 Dec
PMID:Features of macrovascular complications in type 2 diabetic patients. 1470 64

Prevention of atherosclerosis in type 2 diabetes ideally should start a long time before the diagnosis of diabetes since type 2 diabetes and atherosclerosis have a common background of metabolic syndrome. Identifying subjects with metabolic syndrome and beginning with lifestyle and drug interventions in such subjects would most probably delay the development of both diabetes and atherosclerosis. After the clinical diagnosis of diabetes, it is necessary to continue with multifactorial interventions targeted on risk factors, such as hyperglycaemia, dyslipidaemia and hypertension. Some interventions appear to have a benefit beyond the effect on risk factors. Effects of these interventions can be explained by their influence on some pathogenic mechanisms, such as insulin resistance and endothelial dysfunction. Multifactorial interventions decrease the incidence of macrovascular disease in diabetes at least by one-half and should be routinely used in the majority of patients with type 2 diabetes.
Acta Diabetol 2003 Dec
PMID:Pharmacological treatment of diabetic patients with respect to prevention of macrovascular disease. 1470 65

We investigated the age-, gender- and race-specific 1-year case fatality rates of diabetic and non-diabetic individuals with a myocardial infarction. Data were obtained from the Atherosclerosis Risk in Communities (ARIC) Surveillance Study, which monitors both hospitalized myocardial infarction and coronary heart disease (CHD) deaths in residents aged 35-74 years in four communities in the USA. The study population comprised 3242 hospitalized myocardial infarctions (HMIs) in diabetic subjects and 9826 HMIs in non-diabetic individuals between 1987 and 1997. Age-adjusted and gender- and race-specific odds ratios (OR) for 1-year case fatality comparing diabetic to non-diabetic patients were 2.0 (95% CI, 1.6-2.4) for white men and 1.4 (95% CI, 1.1-1.8) for white women. Further adjustment for severity of HMI, history of previous MI, stroke and hypertension, and therapy variables showed significantly higher case fatality in white diabetic men than in non-diabetic white men (OR=1.5; 95% CI, 1.2-1.9), but no significant association in the other race-gender groups. The age-adjusted odds of out of hospital death was significantly higher among white diabetic men (OR=1.7; 95% CI, 1.2-2.3), white women (OR=2.3; 95% CI, 1.4-3.8), and African-American women (OR=2.9; 95% CI, 1.5-5.9) as compared to their non-diabetic counterparts. In conclusion, diabetes is an independent factor for mortality within one year following a myocardial infarction among white men, and following out-of hospital coronary death in white men and women and in African-American women. It is possible that these differences could be explained, at least in part, by a less than optimal medical management of the high cardiovascular risk profile of these patients after hospital discharge.
Acta Diabetol 2004 Jun
PMID:Is diabetes an independent risk factor for mortality after myocardial infarction? The ARIC (Atherosclerosis Risk in Communities) Surveillance Study. 1522 9

Cardiovascular complications, characterized by endothelial dysfunction and accelerated atherosclerosis, are the leading cause of morbidity and mortality associated with diabetes. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Overproduction and/or insufficient removal of these free radicals result in vascular dysfunction, damage to cellular proteins, membrane lipids and nucleic acids. Despite overwhelming evidence on the damaging consequences of oxidative stress and its role in experimental diabetes, large scale clinical trials with classic antioxidants failed to demonstrate any benefit for diabetic patients. As our understanding of the mechanisms of free radical generation evolves, it is becoming clear that rather than merely scavenging reactive radicals, a more comprehensive approach aimed at preventing the generation of these reactive species as well as scavenging may prove more beneficial. Therefore, new strategies with classic as well as new antioxidants should be implemented in the treatment of diabetes.
Cardiovasc Diabetol 2005 Apr 29
PMID:Oxidative stress and the use of antioxidants in diabetes: linking basic science to clinical practice. 1586 33

Hypertension commonly occurs as part of a genetically complex disorder of carbohydrate and lipid metabolism known as the metabolic syndrome. Most current antihypertensive drugs appear ineffective against the metabolic syndrome, which is a strong predictor of cardiovascular disease and death in affected patients. Angiotensin II can influence the activity of certain genes and cellular and biochemical pathways that may contribute to the pathogenesis of the metabolic syndrome. However, as a class, angiotensin II receptor blockers (ARBs) have proven only minimally to modestly effective in ameliorating the disturbances in carbohydrate and lipid metabolism that characterise the metabolic syndrome. Recent preclinical studies indicate that the ARB telmisartan acts as a selective peroxisome proliferators-activated receptor-gamma (PPARgamma) modulator when tested at concentrations that might be achievable with oral doses recommended for treatment of hypertension; this property does not appear to be shared by other ARBs. PPARgamma is a nuclear receptor that influences the expression of multiple genes involved in carbohydrate and lipid metabolism and is an attractive therapeutic target for the prevention and control of insulin resistance, type 2 diabetes and atherosclerosis. In cellular transactivation assays, telmisartan functioned as a partial agonist of PPARgamma and achieved 25-30% of maximal receptor activation attained with conventional PPARgamma ligands. Preclinical and clinical studies indicate that administration of telmisartan can improve carbohydrate and lipid metabolism without causing the side effects that accompany full PPARgamma activators. If the preliminary data are supported by the results of ongoing large-scale clinical studies, telmisartan could have a central role in the prevention and treatment of metabolic syndrome, diabetes and atherosclerosis.
Acta Diabetol 2005 Apr
PMID:Treating the metabolic syndrome: telmisartan as a peroxisome proliferator-activated receptor-gamma activator. 1586 21


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