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

Atherosclerosis is the principal cause of diabetic morbidity and mortality. Diabetic dyslipidemia, obesity, and hypertension are significant contributing factors in the acceleration of the atherosclerotic process. Regardless of the type of diabetes, increased levels of very-low-density lipoprotein triglyceride, modified levels of low-density lipoprotein cholesterol, and decreased levels of high-density lipoprotein (HDL) cholesterol are the main lipoprotein abnormalities in diabetic patients. These abnormalities can be improved in part by glycemic control, but additional intervention may be needed. Diet and exercise are important elements in the management of dyslipidemia, but lipid-lowering drugs (especially fibrates and HMG-CoA reductase inhibitors) also may be necessary for the control of diabetic dyslipidemia. Based on these findings, the American Diabetes Association Consensus Panel and the revised treatment guidelines of the National Cholesterol Education Program recommend treatment of hypertriglyceridemia/low HDL cholesterol as a risk factor of coronary heart disease in diabetic and nondiabetic individuals alike. Aggressive treatment is recommended, therefore, particularly in diabetic patients and in all patients with existing vascular disease.
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PMID:Prevention of atherosclerosis in diabetes: emphasis on treatment for the abnormal lipoprotein metabolism of diabetes. 826 43

Hypertension and diabetes appear to increase coronary heart disease risk in part by causing an abnormality in lipid metabolism. Most affected are patients with familial dyslipidemic hypertension (FDH) and noninsulin-dependent diabetes mellitus (NIDDM). The lipid disorders most often encountered in these patients are increased levels of triglycerides, very low-density lipoprotein (VLDL) cholesterol, and small, dense low-density lipoprotein (LDL) cholesterol, and low levels of high-density lipoprotein (HDL) cholesterol. These abnormalities appear to result from increased hepatic secretion of VLDL particles due to increased concentrations of free fatty acids and glucose, reduced VLDL clearance due to reduced activity of lipoprotein lipase, and reduced LDL clearance due to glycosylation of ligand proteins. Treatment of the dyslipidemia associated with FDH should follow the guidelines from the National Cholesterol Education Program. Treatment in men and women with NIDDM should be considered when LDL cholesterol levels are 130 mg/dl or above, triglyceride levels are 200 mg/dl or above, or non-HDL cholesterol levels are 160 mg/dl or greater. Aggressive lifestyle changes should be initiated first, including weight loss in obese patients, control of glucose levels in those with NIDDM, avoidance of antihypertensive drugs that may worsen lipid levels in patients with FDH, and eating a diet restricting saturated fat and cholesterol. Addition of lipid-altering drugs should be considered if such changes do not achieve effective lipid control. The agent should be tailored to the patient's lipid profile, in general by using bile acid resins, niacin, or reductase inhibitors to lower LDL cholesterol and gemfibrozil or niacin to lower triglycerides. Niacin should be avoided in patients with NIDDM.
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PMID:Understanding and treating dyslipidemia associated with noninsulin-dependent diabetes mellitus and hypertension. 836 60

The small changes in luminal narrowing observed with lowering total cholesterol are unlikely to be the principal mechanism by which lipid-lowering achieves a reduction in clinical events and revascularization rates. Endothelium dependent vasomotor function, and the cellular characteristics of plaques that seem to be intimately related to rupture and thrombosis, are factors that may explain the clinical success from correcting the dyslipidemias. Dyslipidemias cause endothelial dysfunction that predisposes to vasoconstriction of the epicardial coronary arteries and the resistance vessels relative to metabolic demand. Dysfunctional endothelium also promotes the recruitment of inflammatory cells into the vessel wall which contributes to the activation of vascular smooth muscle cells and sets up an environment within the plaque that predisposes to rupture and a prothrombotic state. Aggressive lowering of total cholesterol, and especially LDL and oxidized LDL, improves coronary endothelial function both of the epicardial and resistance vessels, and leads to a reduction in myocardial ischemia. Lipid-lowering may promote plaque stability in part by reducing the recruitment of inflammatory cells, and possibly by changing the size or consistency of the lipid-rich core of plaques. A thicker fibrous cap and stiffer plaque that is less likely to rupture may result, and in the event that rupture does occur, cholesterol lowering may reduce the formation of overlying thrombus. Testing coronary or peripheral artery endothelial vasomotor dysfunction may be a surrogate measure for assessing the effectiveness of interventions to prevent coronary heart disease. These tests are likely to be used increasingly to identify interventions that deserve greater attention in larger clinical trials, as well as providing mechanisms for any observed clinical benefits.
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PMID:Biological mechanisms for the clinical success of lipid-lowering in coronary artery disease and the use of surrogate end-points. 911 44

People with type II diabetes have a twofold to fourfold increased risk of dying from the complications of cardiovascular disease. Atherosclerosis and vascular thrombosis are major contributors. The increased risk is present before fasting hyperglycemia is seen. These individuals often have a sedentary life-style, poor physical conditioning, insulin resistance, centripetal obesity, hypertension, dyslipidemia, and a prothrombotic state. Chronic hyperglycemia is then added to these risk markers. Microalbuminuria may precede hyperglycemia in type II diabetes, occurs in 30% to 40% of these individuals after diabetes is established, and is a predictor of cardiovascular events. Early intervention in high-risk individuals may delay or prevent fasting hyperglycemia. An all-inclusive approach that focuses on early risk factor (or marker) identification and management to prevent or delay accelerated atherosclerosis and thrombosis in type II diabetes is an attractive strategy. However, the database to support this strategy is limited. In particular, large-scale prospective trial data are not available to support the concept of intensive glycemic regulation to prevent progression of macrovascular disease in type II diabetes. This is in contrast to the situation regarding microvascular disease of the eyes and kidneys. Recently, indirect data of a correlative nature have emerged, and short- and long-term prospective trials at early and late stages of type II diabetes are now being reported. These studies are analyzed and interpreted in this report. In contrast, the database to support an intensive antiplatelet regimen to prevent vascular thrombotic events in people with type II diabetes is large, and these studies are reviewed. They are of a type and magnitude to allow definite recommendations for aspirin therapy in type II diabetes. Aggressive therapy directed at hypertension, hyperlipidemia, and elevated urinary albumin in people with type II diabetes appears to be indicated. Increased attention to the multifactorial aspects of treatment of the type II diabetic patient is needed. Our present challenge is to translate these findings for patients and primary health care providers so that effective actions may be implemented.
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PMID:Multifactorial aspects of the treatment of the type II diabetic patient. 943 50

A substantial number of treated patients with or at high risk for coronary artery disease continue to have fatal and nonfatal coronary artery events in spite of significant reduction of elevated levels of low-density lipoprotein cholesterol. Other lipoprotein abnormalities besides an elevated level of low-density lipoprotein cholesterol contribute to risk of coronary artery disease and coronary artery events, and the predominant abnormalities that appear to explain much of this continued risk are an elevated serum triglyceride level and a low level of high-density lipoprotein cholesterol. Most patients with coronary artery disease have a mixed dyslipidemia with hypertriglyceridemia, which is associated and metabolically intertwined with other atherogenic risk factors, including the presence of triglyceride-rich lipoprotein remnants, low levels of high-density lipoprotein cholesterol, small, dense, low-density lipoprotein particles, postprandial hyperlipidemia, and a prothrombotic state. Aggressive treatment of these patients needs to focus on these other lipoprotein abnormalities as much as on low-density lipoprotein cholesterol. Combination drug therapy will usually be required. Reliable assessment of risk of coronary artery disease from lipoprotein measurements and response to therapy requires inclusion of all atherogenic lipoproteins in laboratory measurements and treatment protocols. At present this may be best accomplished by use of non-high-density lipoprotein cholesterol (total cholesterol minus high-density lipoprotein cholesterol) calculated from standard laboratory lipoprotein values. Ultimately, a more comprehensive assessment of coronary artery disease risk and appropriate therapy may include measurement of lipoprotein subclass distribution including determination of low-density lipoprotein particle concentration and sizes of the various lipoprotein particles.
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PMID:Preventing, stopping, or reversing coronary artery disease--triglyceride-rich lipoproteins and associated lipoprotein and metabolic abnormalities: the need for recognition and treatment. 1094 22

Type 2 diabetes is a complex metabolic disorder characterized by elevated blood glucose levels and a marked increase in the risk of cardiovascular disease (CVD). The increased CVD risk is caused by a unique cluster of metabolic abnormalities, including dyslipidemia, hypertension, insulin resistance, and hyperglycemia. To reduce the risk of cardiovascular complications in patients with type 2 diabetes, comprehensive management of risk factors is essential. Aggressive treatment of dyslipidemia and hypertension is known to benefit patients with type 2 diabetes. In addition, intensive glycemic control and targeted treatment of insulin resistance can further reduce the enormous burden of CVD in this high-risk population. Increasing evidence suggests that insulin resistance is one of the earliest markers of risk for both CVD and diabetes, and it is known that insulin resistance alone can significantly increase the risk of CVD. Type 2 diabetes and insulin resistance are both associated with disordered lipid metabolism, manifest in elevated triglyceride levels, low levels of high-density lipoprotein cholesterol, and small, dense low-density lipoprotein cholesterol particles. Patients with type 2 diabetes and insulin resistance have an increased risk of hypertension, which further contributes to their CVD risk. Each of these factors can also contribute to the risk of microvascular disease. To ensure that patients with type 2 diabetes receive comprehensive, high-quality care, specific standards have been developed. These standards can help providers establish clear treatment targets, identify specific priorities of care, and use therapies of known efficacy to reduce the risk of complications. This review summarizes the current standards of care for patients with type 2 diabetes, with an emphasis on treatments that reduce the cardiovascular risk factors. Using a case study approach, it reviews the essential components of diabetes care and proposes a rational approach to these complex cases--an approach that should result in consistent, high-quality care.
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PMID:Comprehensive management of patients with type 2 diabetes: establishing priorities of care. 1151 98

Cardiovascular complications are frequently encountered in the HIV-infected population. Cardiac care providers should implement appropriate preventive, screening, and therapeutic strategies to maximize survival and quality of life in this increasingly treatable, chronic disease. All HIV-infected individuals should undergo periodic cardiac evaluation, including echocardiography, in order to identify subclinical cardiac dysfunction. Left ventricular (LV) dysfunction can result from, or be exacerbated by, a variety of treatable infectious, endocrine, nutritional, and immunologic disorders. Aggressive diagnosis and treatment of these conditions may lead to improvement or even normalization of myocardial function. Endomyocardial biopsy should be considered to direct etiology-specific therapy. Standard measures for the prevention and treatment of congestive heart failure are recommended for HIV-infected patients. Afterload reduction with angiotensin-converting enzyme inhibitors may be indicated for patients with elevated afterload and preclinical LV dysfunction diagnosed by echocardiogram. However, judicious drug selection and titration are necessary in this cohort of patients with frequent autonomic dysfunction, at risk for a number of potentially lethal drug interactions. Carnitine, selenium, and multivitamin supplementation should be considered, especially in those with wasting or diarrhea syndromes. Monthly intravenous immunoglobulin (IVIG) infusions have been demonstrated to preserve LV parameters in HIV-infected children; ventricular recovery has been documented in some children with recalcitrant HIV-related cardiomyopathy following IVIG infusion. We support the use of immunomodulatory therapy in the pediatric population, and look forward to further study into the efficacy and broader application of this approach. Highly active antiretroviral therapy (HAART) may be associated with dyslipidemia and the metabolic syndrome. This should be treated with dietary and possibly with pharmacologic interventions. Drug interactions need to be considered when instituting pharmacologic therapies. Pericardial effusions are often seen in patients with advanced HIV infection. Asymptomatic effusions are most often nonspecific in nature, related to the proinflammatory milieu found in advanced AIDS. Nonspecific effusions are a marker of advanced disease and do not require exhaustive etiologic evaluation. In contrast, large or symptomatic effusions are often associated with infection or malignancy, and warrant thorough investigation and etiology-specific treatment.
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PMID:Myocardial and Pericardial Disease in HIV. 1240 91

Diabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetic people have cardiovascular disease (CVD) risk factors comparable to those of nondiabetics who have had a myocardial infarction or stroke. Physiologic changes in diabetic hypertensive people include endothelial dysfunction, altered platelet activity, and microalbuminuria, all of which may increase coronary heart disease risk. Hyperglycemia and dyslipidemia have been shown to effect physiologic changes in the vasculature; therefore, establishing normoglycemia, reducing cholesterol levels, and controlling blood pressure are the primary and initial goals in the management of diabetic hypertensive patients. The atherosclerotic risk is greatest in poorly controlled patients, possibly because of associated hypercholesterolemia and hypertriglyceridemia. Aggressive management of risk factors such as hypertension, dyslipidemia, and platelet dysfunction in diabetics has been shown to reduce morbidity and mortality in prospective randomized controlled clinical trials. In this article we review the impact of diabetes mellitus on cardiovascular morbidity and mortality.
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PMID:Diabetes and cardiovascular diseases. 1242 9

The use of combination lipid-altering therapy for dyslipidemia is becoming increasingly important for effective management of patients with coronary heart disease (CHD). In accordance with the Adult Treatment Panel III guidelines, the primary target of therapy is lowering low-density lipoprotein (LDL) cholesterol. Studies have demonstrated the benefit of LDL cholesterol reduction in decreasing CHD event rates and all-cause mortality. However, low high-density lipoprotein (HDL) cholesterol remains a significant predictor of CHD events. In addition, lipid-lowering therapy targeting aberrant lipoprotein subclass and triglyceride levels afford additional benefit for patients with mixed dyslipidemias. Aggressive lipid-altering therapy often requires the use of combination therapy involving statins in conjunction with niacin, fibric-acid derivatives, or bile acid resins or intestinal inhibitors of active cholesterol transport. This article reviews the rationale for the use of combination therapy in the treatment of dyslipidemia, highlighting management strategies.
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PMID:The rationale for combination therapy. 1246 35

The use of combination therapy is an effective way to manage dyslipidemia in patients with coronary artery disease (CAD). However, combination therapy is not a frequently used strategy in the treatment of CAD. Aggressive lipid-altering therapy often requires the use of combination therapy involving statins in conjunction with niacin, fibric-acid derivatives, ezetimibe, or bile acid resins. Yet, safety concerns regarding the combination of statins with other lipid-altering drugs and patient acceptance of combination therapy have influenced its application in the treatment of CAD. This article discusses several safety and regulatory considerations for the use of combination therapy for dyslipidemia.
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PMID:Combination therapy for dyslipidemia: safety and regulatory considerations. 1246 40


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