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

The association between low-density lipoprotein cholesterol (LDL-C) levels and risk of coronary heart disease (CHD) is well established and LDL-C-lowering is currently the primary target for the treatment of dyslipidemia. However, low levels of high-density lipoprotein cholesterol (HDL-C), and high levels of triglycerides (TG) are also risk factors for CHD and modifying levels of these lipid subfractions, in addition to LDL-C lowering, may have clinical benefits in many patients. Statins are the first-line drug therapy for the treatment of dyslipidemia because of their efficacy in lowering LDL-C and good tolerability. Statins also have beneficial effects on TG and HDL-C levels although they differ in the degree to which they modify the levels of these lipoproteins. Improvements across the atherogenic components of the lipid profile may be optimized by the co-administration of a statin with a fibrate, niacin or omega-3 fatty acids; however, particular combination therapies have been associated with side effects and may be poorly tolerated. Newer combinations with better tolerability, or new statins with improved efficacy on non-LDL-C lipid subfractions, would be welcome additions to the currently available therapies for the treatment of dyslipidemia.
Cardiovasc Drugs Ther 2003 Jan
PMID:HDL-C and triglyceride levels: relationship to coronary heart disease and treatment with statins. 1284 87

We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5- to 6-fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose-dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express "fetospecific" genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up-regulation of the adrenergic renin-angiotensin-aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel-active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing-induced remodeling decreases left ventricular mass remains uncertain.
J Cardiovasc Electrophysiol 2003 Jul
PMID:Structural pathways and prevention of heart failure and sudden death. 1293 Feb 59

Cardiovascular complications in the course of human immunodeficiency virus (HIV) infection are multifactorial and may be caused by the virus itself or by the related opportunistic infections and neoplasms. Highly active antiretroviral therapy (HAART) has prolonged many patients' lives, but many cardiac sequelae of HIV are not affected by HAART and continue to develop even with treatment. In addition, HAART itself causes in a high proportion of patients a metabolic syndrome, characterized by lipodystrophy/lipoatrophy, dyslipidemia and insulin resistance that may be associated with an increase in peripheral artery and coronary artery diseases. Careful cardiovascular evaluation in the course of HIV disease can identify cardiac complications early enough to treat. All HIV-infected patients candidate to antiretroviral therapy and patients already under treatment should undergo an assessment that includes the evaluation of the cardiovascular risk with the available guidelines.
Cardiovasc Res 2003 Oct 15
PMID:HIV infection, highly active antiretroviral therapy and the cardiovascular system. 1452 10

There are many metabolic consequences of insulin resistance and multiple conditions associated with insulin resistant states. The most obvious pathology associated with insulin resistance is type 2 diabetes mellitus, but other manifestations include hypertension, central obesity, a hypercoagulable state, and dyslipidemia. The atherogenic dyslipidemia associated with insulin resistant states is characterized by hypertriglyceridemia; an increase in very-low-density lipoprotein secretion from the liver; an increase in atherogenic small, dense low-density lipoprotein; and a decrease in high-density lipoprotein cholesterol. Each of these lipid abnormalities is an independent risk factor for coronary artery disease, and in concert, the cardiovascular risk is magnified. Therefore, insulin resistant states should be identified as early as possible in patients, and these lipid abnormalities should be assessed and treated.
Rev Cardiovasc Med 2003
PMID:Lipid abnormalities in insulin resistant states. 1466 90

Diabetes, a leading cause of morbidity and mortality in the United States, is associated with a 2- to 4-fold increase in the risk of coronary artery disease. As the population in the United States has aged, the incidence of obesity, hypertension, glucose intolerance, and dyslipidemia has increased significantly, culminating in the current epidemic of type 2 diabetes mellitus. Strict glycemic control must, therefore, be accompanied with proven therapies (such as antihypertensives and lipid-lowering agents) to reduce cardiovascular events. Patients with type 2 diabetes have average low-density lipoprotein (LDL) levels but have an increased number of small, dense LDL particles, which are associated with a 3-fold increase in cardiovascular disease. Type 2 diabetes mellitus is also associated with increased triglyceride rich atherogenic particles, which trigger inflammation. In addition to glycemic control and drug therapy, lifestyle modifications (eg, diet, weight loss, and exercise) also play an important role in managing diabetes. Therefore, strict glycemic control, pharmacologic therapy, and lifestyle modifications are parts of a comprehensive strategy to prevent both microvascular and macrovascular events in patients with type 2 diabetes.
Rev Cardiovasc Med 2003
PMID:Treating the diabetic patient: appropriate care for glycemic control and cardiovascular disease risk factors. 1466

Patients with diabetes are at high risk for cardiovascular (CV) events and heart failure. Approximately 2-3 million diabetics in the U.S. have had a history of prior CV events. The prevalence of diabetes in patients with heart failure ranges from 24% reported in clinical trials to 47% among hospitalized patients, and an estimated 1-2 million persons in the U.S. have diabetes and heart failure. Diabetes substantially increases the risk of mortality after acute coronary syndromes and also increases the risk of hospitalizations and mortality in patients with heart failure. It is now recognized that activation of multiple neurohormonal systems is central in the pathophysiology of diabetes, CV events, and heart failure. Pharmacologic intervention in these systems (eg, angiotensin-converting enzyme (ACE) inhibition, aldosterone-receptor antagonism, and beta-blockade) has been shown to decrease morbidity and mortality in diabetics with prior CV events and/or heart failure. Despite this awareness, ACE inhibitors, aldosterone antagonists, and beta-blockers are underutilized, and deaths and hospitalizations caused by CV events and heart failure in diabetic patients have steadily increased. Concerns about an increased incidence of hypoglycemia, worsening dyslipidemia, and decreased insulin sensitivity resulting from the use of beta-blockers may be preventing physicians from prescribing these agents for diabetic patients. Beta-blockade in conjunction with ACE inhibition should be standard therapy for all diabetic patients. Optimal glycemic control therapy for patients with heart failure has not been well-defined, and there is an urgent need for randomized clinical trials to determine optimal treatment.
Rev Cardiovasc Med 2003
PMID:The management of the diabetic patient with prior cardiovascular events. 1466 2

Plasma levels of high-density lipoprotein-cholesterol (HDL-C) are a powerful independent cardiovascular risk factor, bearing an inverse relationship with atherosclerotic cardiovascular disease (with risk rising sharply when levels are <1.04 mmol/L). Apart from its protective role in atherosclerosis, HDL-C increases fibrinolysis, is an antioxidant to low density lipoprotein-cholesterol (LDL-C), and decreases platelet aggregability. Up to a third of patients with atherosclerotic cardiovascular disease have 'desirable' plasma levels of total cholesterol but low HDL-C levels. Benefits of treating low plasma HDL-C levels were clearly demonstrated in the Veterans Affairs HDL Intervention Trial (VA-HIT) where gemfibrozil reduced nonfatal infarcts and coronary deaths by 22%. This was achieved by a 6% increase in plasma HDL-C levels, and a 24.5% decrease in plasma levels of triglycerides, without any significant decrease in LDL-C levels. Multivariate analyses revealed the rise in plasma HDL-C levels after treatment, but not decreases in plasma levels of triglycerides or LDL-C, predicted coronary artery disease events. The typical patient under consideration in this article is one with plasma levels of HDL-C <1 mmol/L, LDL-C <3.37 mmol/L [either receiving therapeutic lifestyle changes or or LDL-C-lowering therapy comprising a hydroxymethylglutaryl coenzyme-A (HMG-CoA) reductase inhibitor or bile acid sequestrant] and fasting triglycerides <2.26 mmol/L. We propose this dyslipidemia be classified as Type VI phenotype following the Frederickson and Lees classification. High-risk patients (with >/=2 risk factors for atherosclerotic cardiovascular disease, or 10-year cardiovascular risk >20%), patients with established atherosclerotic cardiovascular disease, or type 2 diabetes mellitus, or metabolic syndrome should receive pharmacotherapy. Plasma HDL-C levels >1.16 mmol/L may be considered optimal and between 1 and 1.16 mmol/L as desirable. Fibric acid derivatives, nicotinic acid, HMG-CoA reductase inhibitors, estrogens, and ethanol (not recommended as therapy) increase plasma HDL-C levels. Nicotinic acid is the most potent agent and recent reports indicate that, in contrast to gemfibrozil, it selectively increases antiatherogenic HDL subfraction, lipoprotein (Lp) AI (without apolipoprotein AII), in patients with low plasma HDL-C levels. An extended-release formulation, administered once daily, has improved the tolerability of nicotinic acid. Recent evidence also indicates that nicotinic acid may effectively correct dyslipidemia in patients with diabetes mellitus without significantly compromising glycemic control. Fibric acid derivatives and estrogen raise plasma HDL-C levels by different mechanisms of action, and these agents may be used with nicotinic acid. Combination therapy (especially HMG-CoA reductase inhibitor and nicotinic acid) should be considered in patients with atherosclerotic cardiovascular disease and low plasma HDL-C levels.
Am J Cardiovasc Drugs 2003
PMID:Optimal therapy of low levels of high density lipoprotein-cholesterol. 1472 46

In many industrialized nations, obesity is now considered an epidemic, resulting in accelerated morbidity and mortality. Obesity is associated with an increased risk of coronary artery disease as well as the metabolic syndrome comprising abdominal obesity, increased fasting blood glucose levels, dyslipidemia and hypertension, which are all recognized cardiovascular risk factors. Diet, exercise, and lifestyle changes constitute important recommendations for treatment. Unfortunately, although effective in some individuals, these recommendations have proven to be ineffective in adequately addressing the broad, enlarging scope of this public health problem. Drug treatment is often indicated but is somewhat limited by the minimal number of well tolerated drugs that have proven to have long-term efficacy in maintaining bodyweight loss. For example, phentermine may result in modest bodyweight loss through suppression of appetite, but potential cardiovascular adverse effects exist and the efficacy is mainly short-term. Sibutramine, an inhibitor of serotonin and norepinephrine (noradrenaline) reuptake, may increase satiety and result in modest bodyweight loss. However, cardiovascular adverse effects may occur in susceptible patients. Nonetheless, sibutramine is one of the few drugs that has been approved by the US Food and Drug Administration (FDA) for bodyweight loss. Orlistat, a lipase inhibitor, is also approved by the FDA for bodyweight loss but may have bothersome gastrointestinal adverse effects, especially among patients who do not adhere to the recommended low-fat diet. Ongoing studies continue to evaluate other drug treatments that may result in bodyweight reduction through a number of different mechanisms. It is anticipated that the development of effective and well tolerated antiobesity drugs will elevate the pharmacologic treatment of obesity to the status of other cardiovascular risk factors and metabolic disorders. This may be especially important given that dyslipidemia, hypertension and type 2 diabetes mellitus are often secondary to, or exacerbated by, obesity.
Am J Cardiovasc Drugs 2002
PMID:Pharmacotherapy of obesity: currently marketed and upcoming agents. 1472 70

Rosiglitazone and pioglitazone are medications from the thiazolidinedione class of compounds currently available for the treatment of type 2 diabetes mellitus. Traditionally used to enhance insulin sensitivity and decrease plasma insulin levels, added applications have emerged beyond those involving glycemic control. Cardiovascular risk factors associated with insulin resistance such as elevated blood pressure, dyslipidemia, abnormal fibrinolysis, and endothelial and vascular dysfunction have been shown to improve after thiazolidinedione treatment. Therapy with rosiglitazone or pioglitazone has been found to modify vascular reactivity and other processes involved in atherosclerosis. There may be differences between the agents in their effects on plasma lipid characteristics and particle size. These agents serve as excellent adjuncts to oral and insulin therapy for patients with type 2 diabetes mellitus and hold promise for the prevention of cardiovascular disease associated with the insulin resistance syndrome. Clinical trials are in progress to determine whether such therapy will lead to a reduction in cardiovascular events.
Am J Cardiovasc Drugs 2002
PMID:Effects of the thiazolidinediones on cardiovascular risk factors. 1472 77

Dyslipidemia, characterized by elevated serum levels of triglycerides and reduced levels of total cholesterol, low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol, has been recognized in patients with human immunodeficiency virus (HIV) infection. It is thought that elevated levels of circulating cytokines, such as tumor necrosis factor-alpha and interferon-alpha, may alter lipid metabolism in patients with HIV infection. Protease inhibitors, such as saquinavir, indinavir and ritonavir, have been found to decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with a syndrome of fat redistribution, insulin resistance, and hyperlipidemia. Elevations in serum total cholesterol and triglyceride levels, along with dyslipidemia that typically occurs in patients with HIV infection, may predispose patients to complications such as premature atherosclerosis and pancreatitis. It has been estimated that hypercholesterolemia and hypertriglyceridemia occur in greater than 50% of protease inhibitor recipients after 2 years of therapy, and that the risk of developing hyperlipidemia increases with the duration of treatment with protease inhibitors. In general, treatment of hyperlipidemia should follow National Cholesterol Education Program guidelines; efforts should be made to modify/control coronary heart disease risk factors (i.e. smoking; hypertension; diabetes mellitus) and maximize lifestyle modifications, primarily dietary intervention and exercise, in these patients. Where indicated, treatment usually consists of either pravastatin or atorvastatin for patients with elevated serum levels of LDL-C and/or total cholesterol. Atorvastatin is more potent in lowering serum total cholesterol and triglycerides compared with other hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, but it is also associated with more drug interactions compared with pravastatin. Simvastatin and lovastatin are significantly metabolized by cytochrome P450 enzymes (CYP3A4) and are therefore not recommended for coadministration with protease inhibitors. A fibric acid derivative (gemfibrozil or fenofibrate) should be used in patients with primary hypertriglyceridemia. However, it must be kept in mind that protease inhibitors, such as nelfinavir and ritonavir, induce enzymes involved in the metabolism of the fibric acid derivatives and may, therefore, reduce the lipid-lowering activity of coadministered gemfibrozil or fenofibrate. In certain patients HMG-CoA reductase inhibitors may be used in combination with fibric acid derivatives but patients should be carefully monitored for liver and skeletal muscle toxicity. Select patients may experience improvements in serum lipid levels when their offending protease inhibitor(s) is/are exchanged for efavirenz, nevirapine, or abacavir; however each patient's virologic and immunologic status must be taken closely into consideration.
Am J Cardiovasc Drugs 2002
PMID:Management of protease inhibitor-associated hyperlipidemia. 1472 85


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