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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study platelet activation as a phenomenon that may precede development of angiopathy in diabetes mellitus, we compared platelet adhesion and thrombus formation in a flow system with blood from insulin-dependent (type I) diabetic subjects with and without macroangiopathy and age- and sex-matched control subjects. Adhesion and thrombus formation on matrix of cultured human endothelial cells (ECM) and adhesion on matrix of human fibroblasts (FBM) were studied after exposure to flowing blood at shear rates of 300 and 1300 s-1 and exposure times of 1, 3, 5, and 10 min (and 20 min in adhesion experiments). Blood was anticoagulated with trisodium citrate (1:10 vol/vol, 110 mM) or low-molecular-weight heparin ([LMWH] 20 U/ml). Endothelial cell cultures were either unstimulated or stimulated with 4 beta-phorbol 12-myristate 13-acetate (PMA) 16 h before isolating their matrix. Platelet adhesion on ECM and FBM in citrated and LMWH-anticoagulated blood was identical in diabetic patients and control subjects, with comparable increases of adhesion with increasing perfusion times. Platelet aggregate formation on ECM of PMA-stimulated cells with LMWH-anticoagulated blood was similar in diabetic patients, whether macroangiopathy was present, compared with control subjects. Fibrin deposition and fibrinopeptide A generation during perfusion were comparable in diabetic and control subjects. Platelet thromboxane B2 formation after stimulation with arachidonic acid was increased in diabetic patients without macroangiopathy compared with age- and sex-matched control subjects. In the perfusion system, the patterns of platelet adhesion and aggregate formation on extracellular matrix in flowing blood of diabetic patients (with or without macroangiopathy), and healthy age- and sex-matched control subjects followed a similar pattern.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet adhesion and aggregate formation in type I diabetes under flow conditions. 193 2

We report on the incidence of new macrovascular disease among the 497 members of the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics (aged 35-54 years at recruitment) over a mean 8.33 year follow-up period. Overall at the end of the follow-up period the prevalence of macrovascular disease in the cohort was 45%; 43% of the subjects showed evidence of ischaemic heart disease, 4.5% of cerebrovascular disease and 4.2% of peripheral vascular disease. The incidence rates for new disease in those subjects who were free at baseline expressed per 1000 patient years of follow-up were: ischaemic ECG abnormality 23.6 (patients with insulin-dependent diabetes 19.8, patients with non-insulin-dependent diabetes 28.1), myocardial infarction 17.6 (patients with insulin-dependent diabetes 16.5, patients with non-insulin-dependent diabetes 18.8), all ichaemic heart disease 31.7 (patients with insulin-dependent diabetes 30.3, patients with non-insulin-dependent diabetes 33.4), cerebrovascular disease 5.9 and peripheral vascular disease 5.2. Incidence rates were generally similar among men and women except for myocardial infarction in patients with non-insulin-dependent diabetes where men had a significantly higher incidence rate. Macrovascular disease is a major problem in patients with diabetes and in this age group is mainly manifested as ischaemic heart disease.
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PMID:Incidence of macrovascular disease in diabetes mellitus: the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics. 193 62

We have examined the relationship between baseline variables and the incidence of new macrovascular complications amongst the 497 members of the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics over a mean 8.33-year follow-up. In univariate logistic regression analysis the incidence of new ischaemic electrocardiographic abnormality was significantly associated with systolic and diastolic blood pressure, diabetes duration and hypertension in patients with insulin-dependent diabetes, and with smoking in patients with non-insulin-dependent diabetes. New myocardial infarction was associated with systolic blood pressure, plasma cholesterol, proteinuria and smoking in patient with non-insulin-dependent diabetes; there were no significant associations among patients with insulin-dependent diabetes. All new ischaemic heart disease was associated with hypertension in patients with insulin-dependent diabetes, and plasma cholesterol and smoking in patients with non-insulin-dependent diabetes. New cerebrovascular disease was associated with systolic and diastolic blood pressure, ECG abnormality and hypertension. New peripheral vascular disease was associated with smoking. Multivariate analysis showed the following significant associations 1) in patients with insulin-dependent diabetes: ECG abnormality; hypertension, myocardial infarction; smoking, ischaemic heart disease; hypertension, diabetes duration and smoking, 2) in patients with non-insulin-dependent diabetes: ECG abnormality; smoking, myocardial infarction; serum cholesterol, proteinuria and smoking ischaemic heart disease; smoking. For new cerebrovascular disease, proteinuria and ECG abnormality were significant predictors in multivariate analysis. Patients with diabetes share many of the established risk factors for nondiabetic subjects, in addition proteinuria may be of significance in the prediction of macrovascular disease in diabetes.
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PMID:Risk factors for macrovascular disease in diabetes mellitus: the London follow-up to the WHO Multinational Study of Vascular Disease in Diabetics. 193 63

From a large prospective study on diabetes risks, 1112 professionally active, non-menopausal, non-pregnant, healthy women were cross-sectionally analysed according to their use of oral contraception. After adjustment for age, weight and diabetes risk factors, those taking the pill, compared to those who did not, had significantly higher fasting serum insulin, triglycerides and 2-h 75 g OGTT blood glucose levels. The insulin-resistance markers which have recently been cited as ischemic vascular disease risk factors should be carefully monitored in pill users.
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PMID:Oral contraceptives, insulin resistance and ischemic vascular disease. 196 68

Patients with non-insulin-dependent diabetes mellitus (NIDDM) and hypertension were studied before and after three months of combined beta-blocker-diuretic treatment. Blood pressure fell significantly (P less than .001) from (mean +/- SEM) 167 +/- 3/99 +/- 1 to 142 +/- 3/88 +/- 1 mm Hg. However, mean (+/- SEM) fasting plasma glucose concentration increased significantly (P less than .001) from 132 +/- 11 to 153 +/- 10 mg/dL. In addition, significant increases (P less than .05) were noted in fasting concentration of plasma total triglyceride, very-low-density lipoprotein (VLDL)-triglyceride and VLDL-cholesterol, whereas fasting plasma high-density lipoprotein (HDL)-cholesterol was significantly lower (P less than .05). Thus, a common treatment program for hypertension exacerbated the abnormalities of carbohydrate and lipid metabolism commonly present in patients with NIDDM. Since the changes noted would increase risk of vascular disease, attention should be focused on selection of treatment programs for lowering blood pressure in patients with NIDDM in order to avoid this outcome.
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PMID:Metabolic effects of diuretic and beta-blocker treatment of hypertension in patients with non-insulin-dependent diabetes mellitus. 197 24

Atherosclerotic vascular disease is a major cause of morbidity and mortality in insulin-dependent diabetes mellitus. The frequent coexistence in these patients of microangiopathy and coronary artery disease was observed more than 30 years ago and later verified in large epidemiological studies. Thus, the subgroup (30-40%) of patients who develop clinical nephropathy, also are at extremely high risk of early cardiovascular death. A number of established cardiovascular risk factors are present not only in advanced clinical nephropathy but also in its earliest stages. These include elevated blood pressure, atherogenic changes in the plasma concentrations of lipids and lipoproteins, elevated plasma levels of fibrinogen and probably hyperreactivity of platelets. However, it seems unlikely that these risk factors fully explain the excess cardiovascular morbidity and mortality in insulin-dependent diabetic patients with clinical nephropathy. Patients with slightly elevated urinary albumin excretion are at increased risk of developing not only clinical nephropathy and coronary heart disease but also proliferative retinopathy and cardiomyopathy. We have, therefore, hypothesised that elevated urinary albumin excretion is a marker of generalized disease in the vascular wall of small and large blood vessels. Findings of elevated transcapillary escape rate of albumin, elevated plasma concentration of von Willebrand factor and impaired fibrinolytic capacity in early diabetic nephropathy have supported this hypothesis. However, the initial pathophysiological mechanisms involved are still hypothetical and largely unknown. During recent years the incidence of clinical nephropathy has declined and the prognosis of insulin-dependent diabetic patients has improved. Whether intervention directed against the often clustered cardiovascular risk factors will further improve the prognosis in proteinuric patients is suggested but still unknown. However, the key question is still, why is the vascular wall, in small and large blood vessels, vulnerable in some but not all diabetic patients? In the future more studies of the initial pathophysiological mechanisms involved in this vulnerability are needed.
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PMID:Albuminuria--a marker of renal and generalized vascular disease in insulin-dependent diabetes mellitus. 206 Mar 21

The initial treatment in the past of diabetes was one "of trial and error" as easily understandable. Carbohydrate restriction and their replacement by fats was followed, happily, last century already, by global caloric restriction. Around the fourties, after the introduction of insulin in 1922, the principle of the carbohydrate tolerance was introduced as an objective+ measure, followed by the proposal of "bread equivalencies" in the dietetic practice, assuring in this manner a figured evaluation. Around the seventies years the diet fiber came into its own and seemed very important for the evolution of the postprandial glycemia and insulinemia. Next to this, complex polysaccharides looked also of prime impact on this two biochemical parameters. The nature of this complex character is due to their liaison with other diet components (lectins, phytins, tannins etc.). So the concept of the glycemic index was born which explains why next to the presence of a given carbohydrate quantity the evolution of the glycemia is different from what is expected, just because the absorption is accelerated or retarded by the structure or the manipulation of these polysaccharides. This novel data are so much the more important because actually the hyperglycemia on the long run seems so important for the development of micro-angiopathy, at the base of the famous diabetic triad (nephropathy, retinopathy, neuropathy). The hyperlipemia is also beneficially influenced by the diet fiber and at the same level by the complex polysaccharides. All this statements are at the base of novel ways for the dietetic treatment of diabetes, as well on the quantitative as on the qualitative level and equally so for the diabetes of type I as of type II.
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PMID:[Diet treatment of the diabetic patient: yesterday and today. What has changed? What can be learned from it?]. 208 51

Insulin-induced hypoglycaemia in humans is associated with the rapid mobilization of leucocytes in peripheral blood. The aim of the present study was to determine whether neutrophil activation, manifested in plasma by neutrophil elastase concentration, occurs in response to insulin-induced hypoglycaemia. Acute hypoglycaemia (mean blood glucose 1.3 +/- 0.2 mmol l-1; mean +/- SD) was induced with intravenous insulin in 15 normal human subjects, and provoked an increase in the neutrophil count from 3.4 (range 1.9-6.5) to 10.7 (9.4-16.3) X 10(9) l-1 (p less than 0.001), and in the total leucocyte counts from 5.7 (4.1-8.1) to 12.8 (11.3-18.6) X 10(9) l-1 (p less than 0.001), with associated elevations in plasma neutrophil elastase concentration from 21 (12-34) to 29 (14-70) micrograms l-1 (p less than 0.05), and in total neutrophil elastase concentration from 5.90 (3.13-8.20) to 25.20 (23.00-52.00) mg l-1 (p less than 0.001). As neutrophil elastase is implicated in the development of vascular disease, this rise in response to hypoglycaemia may be of pathological importance in insulin-treated diabetic patients.
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PMID:Leucocyte mobilization and release of neutrophil elastase following acute insulin-induced hypoglycaemia in normal humans. 214 53

Diabetes mellitus is associated with fetal growth acceleration and retardation. These aberrations in fetal growth seem to be influenced by a variety of factors including vascular disease, glycemic control, hypertension and smoking. In order to characterize fetal growth under the above conditions, longitudinal sonographic evaluations were performed in 52 pregnant, insulin-dependent diabetic women with the usual monitoring of the patients' metabolic control. Regression analyses revealed that vascular disease and glycemic conditions were the most important influences for growth, with manifestation beyond the second trimester. With stringent glucose control (mean whole blood less than or equal to 100 mg/dl) in the absence of vasculopathy (white classes A, B, C), fetal growth was similar to that in normal pregnancies. In the presence of vasculopathy (white classes D and FR), growth was reduced, especially when near-normal glycemic levels were achieved. Conversely, in poorly controlled diabetic women, enhanced fetal growth were observed in patients with and without vasculopathy. No aberrations in fetal growth were observed, however, before the third trimester. The findings of our study demonstrate that vasculopathy and glycemia are dominant and independent regulators of fetal growth. However, their influences are not manifested in growth changes before the third trimester.
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PMID:A longitudinal study comparing growth in diabetic pregnancies with growth in normal gestations: I. The fetal weight. 219 Jan 30

The 5-year incidence of myocardial infarction and claudication was examined in a group of middle-aged patients (n = 133, 70 men and 63 women) with newly diagnosed non-insulin-dependent diabetes and nondiabetic control subjects (n = 144, 62 men and 82 women). The effects of general risk factors, plasma insulin level, and lipoprotein abnormalities on the incidence of myocardial infarction and claudication were also evaluated by univariate analyses in both diabetic patients and nondiabetic subjects and by multivariate analyses combining both groups. The age-adjusted incidence of myocardial infarction was higher both in diabetic men (19.4%) and diabetic women (11.0%) than in nondiabetic men (3.2%, p = 0.009) and nondiabetic women (3.0%, p = 0.047). Similarly, the age-adjusted incidence of claudication was higher among the diabetic patients (20.3% vs. 8.0% for men, p = 0.06; 21.8% vs. 4.2% for women, p = 0.003). None of the general risk factors (i.e., low density lipoprotein [LDL] cholesterol, blood pressure, smoking, and high density lipoprotein [HDL] cholesterol) showed an association with the risk of myocardial infarction either in the diabetic or nondiabetic groups of subjects, but an ischemic electrocardiographic abnormality at the baseline examination predicted myocardial infarction in diabetic men. In univariate analyses in diabetic subjects, high serum total cholesterol, low HDL cholesterol, high very low density lipoprotein (VLDL) cholesterol, and high total, LDL and VLDL triglycerides, and in nondiabetic subjects, high VLDL cholesterol and LDL triglycerides were associated with the appearance of claudication. In multivariate analyses including both diabetic and control subjects, only diabetes had an independent association with myocardial infarction, whereas smoking, high LDL triglycerides or VLDL cholesterol, and high fasting plasma insulin showed independent relations to claudication. The present results indicate that changes in lipoprotein composition characteristic of non-insulin-dependent diabetes are atherogenic and increase the risk of atherosclerotic vascular disease. Furthermore, high plasma insulin might also be involved in atherogenesis, independent of lipoprotein abnormalities.
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PMID:5-year incidence of atherosclerotic vascular disease in relation to general risk factors, insulin level, and abnormalities in lipoprotein composition in non-insulin-dependent diabetic and nondiabetic subjects. 219 96


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