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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

56 cerebral ischemia patients up to the age of 40 were investigated using a strict clinical and instrumental protocol in order to elicit the relative importance of the various iatrogenic factors involved. In addition to atherosclerosis risk factors (smoking, hypertension, ischemic heart disease, diabetes, dyslipidemia) other possible causes of cerebral ischemia were sought (arteritis, migraine, head injury, oral contraceptives, coagulation disorders, cardiogenic embolism, etc.). 50% of the patients examined had at least two atherosclerosis risk factors and 55% had other causes singly or in association with atherosclerosis.
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PMID:Cerebral ischemia in young adults. 733 59

The Felodipine Atherosclerosis Prevention Study is designed to evaluate the efficacy of the calcium antagonist felodipine ER and combined felodipine/simvastatin therapy on retarding the progression of atherosclerosis, estimated by serial changes in coronary calcium evaluated by noninvasive electron beam computed tomography. Subjects include 180 men and women aged 40 to 69 and 50 to 69 years, respectively, with moderate type IIa dyslipidemia, with either cardiovascular disease or risk factors. All subjects receive simvastatin lipid-lowering therapy, and are randomized either to felodipine or placebo for a treatment period of 2 years. Monitoring of blood chemistry, measures of lipids and apolipoproteins, blood pressure, evaluation of symptoms, and interim clinical event monitoring are done at routine follow-up visits. Baseline and 2-year follow-up electron beam computed tomography, measuring changes in total calcium score, area, and mass, evaluate the effects of intervention on the progression of calcified atherosclerosis. The results from the Felodipine Atherosclerosis Prevention Study will provide valuable information about the effect of felodipine alone and in combination with simvastatin on progression of calcified atherosclerosis evaluated noninvasively.
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PMID:Noninvasive tracking of coronary atherosclerosis by electron beam computed tomography: rationale and design of the Felodipine Atherosclerosis Prevention Study (FAPS). 750 3

So-called insulin resistance is a frequent phenomenon and a marker of increased risk for both type II diabetes mellitus and atherosclerosis. Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Additional defects of insulin-stimulated muscle blood flow and cellular kation balance are presently attracting increasing awareness. Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. This improvement of insulin sensitivity could mean not only improvement of glucose metabolism, but also reduction of chronically elevated serum insulin and the ensuing atherogenic consequences (hyper- and dyslipidemia, sympathetic overactivity, growth of vascular smooth-muscle cells, hypertension, etc.). Ca(2+)-channel blockers that do not increase heart rate appear to exert direct antiatherogenic effects while being metabolically neutral. Thus, the combination of Ca(2+)-channel blockade by sustained release verapamil and ACE inhibition by trandolapril in insulin-resistant type II diabetic patients with essential hypertension appears to be promising in terms of possible synergistic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible synergistic effect of ACE inhibition and calcium-channel blockade on insulin sensitivity in insulin-resistant type II diabetic hypertensive patients. 751 94

Arterial hypertension is a chronic condition regarded as one of the main risk factors for development of coronary atherosclerosis. As dyslipidemia and reduced glucose tolerance are also risk factors for coronary disease, it is considered important to use antihypertensive drugs having no negative effects on lipid and glucose metabolism when diabetic patients are treated for hypertension. Lacidipine, a new dihydropyridine-like calcium antagonist, has been shown in in vivo and in vitro preclinical studies to possess potent, long-lasting antihypertensive activity. The present study compared the efficacy and safety of once-daily treatment with lacidipine versus nifedipine SR given twice-daily in non-insulin-dependent diabetic patients. Results have shown a similar efficacy of the two treatments: 6 months later, both drugs had reduced blood pressure values [lacidipine from 184.8/105.2 mm Hg to 144.4/87.1 mm Hg; nifedipine slow-release (SR) from 182.3/106.8 mm Hg to 143.6/89.4 mmHg]. However, lacidipine exhibited a lower incidence of adverse events (particularly ankle edema and tachycardia) than nifedipine SR. Finally, both treatments showed no negative effect on metabolic parameters (total cholesterol, high-density lipoprotein cholesterol, triglycerides, and blood glucose).
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PMID:Calcium antagonist antihypertensive treatment of non-insulin-dependent diabetics: efficacy and safety of lacidipine versus nifedipine SR. 760 94

Many models of diabetes dyslipidemia are available. Animals with chemically-induced diabetes have been used to study insulin-dependent diabetes. Hypercholesterolemia in streptozotocin-induced diabetes in rats results from increased intestinal absorption and synthesis of cholesterol. Lipoproteins from diabetic rats are oxidized and demonstrate cytotoxicity, a feature which can be prevented by insulin or antioxidant treatment. Diabetic rabbits fed a cholesterol-rich diet do not develop atherosclerotic lesions because accumulated VLDL are apo E-depleted, too large and do not enter into the arterial wall. Models for non-insulin-dependent diabetes (NIDDM) are obtained through selective breeding or dietary conditions. The obese Zucker rat (fa/fa) is characterized by hyperphagy, hyperglycaemia, hyperinsulinemia, insulin-resistance, hypertriglyceridemia and hypercholesteolemia. It responds to dietary, hormonal and drug treatments, but does not develop atherosclerosis spontaneously. It is used as a model for obesity, NIDDM and type IV hyperlipidemia. The JCR:LA cp rat bears the corpulent gene and develops similar characteristics to those of the Zucker rat. However, insulin-resistance is more severe in homozygous males (cp/cp), and cardiovascular lesions are observed. Their appearance is reduced by treatments which decrease hyperinsulinemia and insulin resistance but not by lowering lipid levels alone. The sand rats (Psammomys obesus) develop obesity and NIDDM when fed a laboratory diet. When cholesterol and anti-thyroid drug are added to the diet, they develop cardiovascular lesions. This species constitutes a new model for studying atherosclerosis-related diabetes.
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PMID:Dyslipidemia and diabetes: animal models. 762 69

Atherosclerosis susceptibility associated with elevations in specific populations of apolipoprotein-B-containing particles may involve increased oxidation of lipoproteins and associated changes in their biological properties. Lipoprotein oxidation may be potentiated by the greater mass of oxidizable lipoprotein substrates, as well as by a greater intrinsic susceptibility of the specific forms of lipoproteins that arise in these disorders. The atherogenic consequences of increased lipoprotein oxidation may be further enhanced by a greater relative potency or toxicity of the oxidized products of these lipoprotein subpopulations. This review addresses these facets of lipoprotein oxidation in several forms of dyslipidemia, and in view of both differences between and commonalities among these disorders, proposes that lipoprotein oxidative behavior is determined by a complex array of physical, chemical, and metabolic factors.
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PMID:Lipoprotein oxidation in dyslipidemia: insights into general mechanisms affecting lipoprotein oxidative behavior. 767 Jul 48

The development of advanced coronary atherosclerosis was studied in the FHC swine. This model exhibits spontaneous elevations in plasma cholesterol, LDL, and apo B while fed a low-cholesterol, low-fat diet. Hypercholesterolemic animals bearing the apo B genotypes Lpb2/3, 3/3, 3/5, 5/5 and 3/8 developed stenotic coronary lesions containing necrotic cores, fibrous caps, calcification, neovascularization, hemorrhage, and fissuring. Myocardial infarction and myocardial ischemia were also observed. The complicated atherosclerotic plaques observed in this swine model closely resemble advanced coronary artery disease (CAD) found in humans. While coronary atherosclerosis was not observed in the absence of hypercholesterolemia, neither the apo B genotype nor the level of hypercholesterolemia was found to predict the extent of lesion formation. Similar to the case in humans, the familial dyslipidemia associated with the development of CAD in the FHC swine appears to be polygenic.
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PMID:Familial hypercholesterolemia associated with coronary atherosclerosis in swine bearing different alleles for apolipoprotein B. 769 72

The early lesions of atherosclerosis in youth are strongly related to antemortem levels of total and low-density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglyceride to ponderal index and to blood pressure. The major apolipoproteins of LDL and high-density lipoprotein (HDL), apoB and apoA1 respectively, and levels of Lp(a) lipoprotein are often abnormal in children born in a family with premature coronary artery disease (CAD). Other risk factors for CAD include obesity, high blood pressure, cigarette smoking, diabetes mellitus, positive family history of CAD, and physical inactivity. Children from families with premature CAD, dyslipidemia, or hypertension, and/or two other risk factors should have a lipoprotein profile determined. Treatment begins with a diet low in total fat, saturated fat, and cholesterol, combined with treatment of overnutrition and obesity, if necessary, and regular habits of aerobic physical activity. Children with inherited disorders of LDL metabolism may require the addition of lipid-lowering therapy. The early detection and treatment of youth at risk for premature CAD offer the greatest promise to decrease morbidity and mortality.
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PMID:Detection and treatment of elevated blood lipids and other risk factors for coronary artery disease in youth. 769 75

Unlike classical microvascular complications, large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions have common genetic and environmental antecedents, i.e., they spring from a "common soil." It is now known that adverse environmental conditions, perhaps related to less-than-optimal nutrition, in fetal and early life are associated with an enhanced risk of both diabetes and cardiovascular disease many decades later. These same adverse environmental conditions are also associated with the development in adult life of abdominal obesity and the insulin-resistance syndrome (IRS). The IRS consists of glucose intolerance, hyperinsulinemia, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol levels), and hypertension. Although the mechanism underlying this cluster is controversial, the statistical association is well established. All of the elements of the IRS have been documented as risk factors for type II diabetes. Some, but not all, of these elements are also cardiovascular disease risk factors, in particular, hypertension and low HDL cholesterol. Other factors associated with the IRS that may enhance cardiovascular disease risk are plasminogen activator inhibitor 1 and small, dense low-density lipoprotein particles. Whether insulin itself is a risk factor remains controversial, but recent epidemiological evidence has been mostly negative. This question has marked clinical relevance because if the IRS enhances cardiovascular disease risk by virtue of its concomitant factors and not the hyperinsulinemia per se, this would tend to alleviate concerns that intensive insulin management of type II diabetic subjects could enhance the risk of large-vessel atherosclerosis. Clinical trials are urgently needed to settle this point.
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PMID:Diabetes and cardiovascular disease. The "common soil" hypothesis. 769 2

Epidemiologic studies have demonstrated hypertension is one of the risk factors of atherosclerosis, but the underlying mechanism is complex and still controversial. Salt-sensitivity is an important characteristic demonstrated in a subgroup of hypertension, since the factors relating to salt-sensitivity also influence smooth muscle hypertrophy and proliferation which are essential processes of atherosclerosis. Insulin resistance is also involved in the causal relationship between hypertension and atherosclerosis, because accumulating data indicate a central role of insulin resistance in patients with hypertension, glucose-intolerance and dyslipidemia. Vasoacting substances give direct effects on not only the tension but also the growth of smooth muscle cells, namely vasodilators, such as nitric oxide and atrial natriuretic peptides inhibit the proliferation of smooth muscle cells. On the other hand, vasoconstrictors such as angiotensin II, vasopressin and endothelin promote the proliferation of smooth muscle cells. The factors which influence both tension and proliferation of smooth muscle cells may play a central role in the relationship between hypertension and atherosclerosis.
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PMID:[The role of hypertension as a risk factor of atherosclerosis]. 769 22


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