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

Subtle abnormalities of carbohydrate metabolism and overt diabetes mellitus are both associated with a substantial increase in the prevalence of hypertension and the accelerated development of atherosclerosis. Hypertension is also a presumed independent risk factor for atherosclerosis, although some of the atherogenic properties of hypertension may be related to the recently recognized subtle metabolic abnormalities commonly found in persons with essential hypertension. The results of epidemiologic studies suggest that the elevated fasting and postprandial insulin levels that often occur in patients with essential hypertension, as well as in patients with type II diabetes mellitus, are an independent risk factor for atherosclerotic cardiovascular disease. Elevated glucose levels in patients with diabetes and hypertension appear to contribute to the acceleration of atherosclerosis, perhaps through toxic effects on the vascular endothelium. Other cardiovascular risk factors that are accentuated in persons with carbohydrate intolerance and hypertension include abnormalities in platelet function, clotting factors, the fibrinolytic system, and dyslipidemia. The goals of both nonpharmacologic and pharmacologic therapy for patients with abnormal carbohydrate metabolism and hypertension are to decrease cardiovascular risk as well as lower blood pressure.
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PMID:Hyperinsulinemia, insulin resistance, and hyperglycemia: contributing factors in the pathogenesis of hypertension and atherosclerosis. 839 10

Insulin resistance has been proposed as the metabolic basis of atherogenesis. This hypothesis is based on the concept of the "insulin resistance syndrome," according to which insulin resistance is viewed as the primary abnormality that gives rise to dyslipidemia, essential hypertension, impaired glucose tolerance, and NIDDM. However, this hypothesis takes no account of the well-established and central role of vascular endothelium in the atherogenic process. Although endothelial injury is an early and prominent feature of atherogenesis, relatively little attention has been given to its metabolic consequences. In subjects with NIDDM, we have shown that endothelial dysfunction is associated with insulin resistance, raising the question of whether this relationship could be causal. In this article, we review the factors that are considered to be responsible for the development of endothelial dysfunction during atherogenesis, together with the metabolic consequences of endothelial dysfunction. While dysfunction of the endothelium in large and medium-sized arteries plays a central role in atherogenesis, we argue that dysfunction of peripheral vascular endothelium, at arteriolar and capillary level, plays the primary role in the pathogenesis of both insulin resistance and the associated features of the insulin resistance syndrome. We propose that the insulin resistance syndrome, together with many aspects of atherogenesis, can be viewed as the diverse consequences of endothelial dysfunction in different vascular beds. This new and testable hypothesis accounts for both the endothelial and metabolic abnormalities associated with atherogenesis.
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PMID:Endothelial dysfunction: cause of the insulin resistance syndrome. 928 92

The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is evidence that oxidative stress (am imbalance between oxidant and antioxidant forces in favor of oxidants) occurs in preeclampsia, and it has been hypothesized that reactive oxygen species or their metabolites ultimately comprise the "defensive" vasodilatory, antiaggregatory, and barrier functioning of the vascular endothelium. Oxidative stress may be point at which feto-placental and maternal factors converge, resulting in the protean manifestations of preeclampsia. This review highlights the evidence for maternal dyslipidemia and altered iron kinetics in preeclampsia and gives a critical assessment of their potential impact on disease progression. The theme is developed that interaction of maternal components, particularly neutrophils and oxidation-susceptible lipids, with placental cells and placental-derived factors engenders feed-forward cycles of oxidative stress that ultimately cause widespread endothelial cell dysfunction and its clinical manifestations.
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PMID:Dyslipidemia, iron, and oxidative stress in preeclampsia: assessment of maternal and feto-placental interactions. 965 10

The progression of atherosclerosis is currently believed to involve the interaction of monocytes with the vascular endothelium. Within the last decade, the cell-surface proteins thought to control these interactions have been investigated. This review seeks to describe the nature of these interactions through what are known as adhesion molecules and their role in atherogenesis. It begins with the stages of atherogenesis from the movement of the monocyte to the endothelium, followed by the migration of smooth muscle cells from the media to the intima, and subsequently to the later stages of fibrofatty plaque formation and potential complications due to thrombosis and/or plaque fissure and embolism. The different structural classifications of the adhesion molecules, such as integrins, cadherins, selectins, and members of the immunoglobulin gene superfamily, are outlined, and interaction of binding domains are highlighted. The vascular endothelium and the basic role of adhesion molecules in dysfunction are considered. Discussion of the role of adhesion molecules in atherogenesis focuses on interactions of the endothelium, monocytes, and leukocytes, as well as the influences of cytokines, oxidized low-density lipoproteins, and genetic determinants. Finally, epidemiological risk factors associated with atherosclerosis such as hypertension and dyslipidemia are considered in light of their effects on adhesion molecule expression.
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PMID:The role of adhesion molecules in atherosclerosis. 988 76

The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is substantial evidence to suggest that the diverse manifestations of preeclampsia, including altered vascular reactivity, vasospasm, and discrete pathology in many organ systems, are derived from pathologic changes within the maternal vascular endothelium. With the theme of endothelial cell dysfunction emphasized, this review focuses on the role of oxidative stress (an imbalance favoring oxidant over antioxidant forces) in the pathogenesis of preeclampsia. Data are summarized regarding 1) the role of the placenta in preeclampsia; 2) evidence and mechanisms of oxidative stress in the preeclampsia placenta; 3) markers of oxidative stress in the maternal circulation; and 4) the potential role of maternal dyslipidemia in generation of oxidative stress. A recurrent theme is that free radical reactions, promoted by "cross-talk" between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.
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PMID:Oxidative stress in the pathogenesis of preeclampsia. 1060 81

We describe the case of a young HIV-positive patient undergoing three-drug antiretroviral therapy that included a protease inhibitor for 9 months, who was admitted to the hospital with an acute myocardial infarction. A coronary angiogram revealed occlusion caused by a thrombus in the proximal third of the anterior descending artery. Complete recanalization was obtained after an angioplasty was performed. At the time of the infarction, only the triglyceride levels were found to be high. Metabolic alterations associated with the prolonged use of protease inhibitors have been described such as an increase in the triglyceride and cholesterol serum levels, diabetes, resistance to insulin, lipodystrophy, and pancreatitis. The consequences of chronic hyperlipidemia are well known in the medical literature, especially premature coronary artery disease. No family history of coronary artery disease was identified in this patient. Whether the genesis of this localized coronary thrombosis was due to a change in the metabolism of the vascular endothelium caused by the protease inhibitors, or by related dyslipidemia, is still to be determined. In this case, the data suggest a strong link between coronary insufficiency and prolonged use of the protease inhibitor.
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PMID:Acute Myocardial Infarction in a 34-Year-Old HIV-Positive Female Patient While Undergoing Active Antiretroviral Therapy Containing a Protease Inhibitor. 1108 68

The cardiovascular metabolic syndrome is a family of risk factors that predispose patients to develop diabetes and cardiovascular disease. Indeed, macrovascular, not microvascular, disease is the leading cause of death in these patients. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) exert both direct and indirect (cholesterol-lowering) effects on the vasculature. Clinical trials have shown that these agents reduce cardiovascular disease and cerebrovascular disease in persons with diabetes. However, their beneficial effects on diabetic dyslipidemia do not account for all of the observed risk reduction. Positive effects on nitric oxide metabolism, inflammation, coagulability, and adhesion of cells to the vascular endothelium likely contribute to the mechanism of action of these agents. These pleiotropic effects of statins on the vasculature will be discussed in this review.
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PMID:Effects of statins on the vasculature: Implications for aggressive lipid management in the cardiovascular metabolic syndrome. 1261 94

The insulin resistance syndrome is composed of risk factors for cardiovascular disease, including insulin resistance with hyperinsulinemia, atherogenic dyslipidemia, hypertension, abdominal obesity, and impaired hemostasis. Patients with type 2 diabetes frequently manifest multiple risk factors for cardiovascular morbidity and mortality. Management of the insulin resistance syndrome often includes antihypertensive, lipid-lowering, and antihyperglycemic agents. Because thiazolidinediones (TZDs) directly improve insulin resistance, early use may provide substantial benefits to patients with type 2 diabetes. TZDs reduce plasma glucose and insulin concentrations, promote relocation of body fat, and have anti-inflammatory effects on the vascular endothelium. Combination oral hypoglycemic therapy may be ideal for maintaining adequate glycemic control in patients with type 2 diabetes. The combination of a TZD and a biguanide, which improves insulin sensitivity and lowers blood glucose through different pathways, offers significant benefits and may help prevent or delay prevent complications associated with type 2 diabetes.
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PMID:Insulin resistance syndrome. Description, pathogenesis, and management. 1278 29

After the acute phase, a patient who is diagnosed with cardiac or vascular disease becomes "chronically ill". This patient will then still spend many years without symptoms or impairments. One day, a percentage of such patients will be confronted with the problem of erectile dysfunction. Various studies have demonstrated that this problem occurs with a higher frequency in patients with cardiovascular diseases, in particular when they have to be treated for hypertension, diabetes mellitus or dyslipidemia. Very rarely are stenoses or occlusions found in the arteries responsible for penile circulation. More recent data indicates that a diffuse anomaly of the vascular endothelium is present, for which erectile dysfunction is a marker. Nowadays, medical care has achieved a better degree of standardization, not only thanks to knowledge about the effects of cardiovascular medication, but also because the physician can now prescribe drugs that treat erectile dysfunction.
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PMID:[Erectile dysfunction in cardiovascular diseases]. 1279 21

The optimal drug for the prevention of venous thromboembolism is one that is efficacious, associated with minimal bleeding risk, and easy to administer. Statins fulfill the latter two criteria, but their efficacy remains unproved. By examining the association between dyslipidemia and venous thromboembolism, as well as the evidence that statins might prevent venous thromboembolism, there may be a new rationale for the use of this class of drugs. There may be a common link between arterial and venous thrombosis. Dyslipidemia may be one of the many systemic factors associated not only with arterial thrombosis, but with venous thromboembolism as well. This may occur through the effects of circulating lipid molecules on the vascular endothelium, platelet function, and coagulation factors. By impeding these mechanisms, statins may be protective against venous thrombosis, but epidemiologic studies are few in number, and no randomized clinical trials have been conducted. Better epidemiologic evidence is required to establish whether dyslipidemia is a risk factor for venous thromboembolism. If future observational studies can demonstrate that statins are associated with a lower risk of venous thromboembolism, then consideration should be given to conducting a randomized clinical trial comparing statins with placebo for the prevention of venous thromboembolism. Until then, the efficacy of statins for the prevention or treatment of venous thromboembolism remains uncertain.
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PMID:Dyslipidemia, statins, and venous thromboembolism: a potential risk factor and a potential treatment. 1290 7


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