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Query: UMLS:C0948265 (
metabolic syndrome
)
24,271
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In myocardial damage due to ischemia-reperfusion, the administration of insulin together with glucose and potassium may be protective, although in some patients and animal models, it is ineffective. In a rat model (HTG) with characteristics of the
metabolic syndrome
, induced by sucrose feeding, ischemia-reperfusion of the isolated heart evidences a less favorable outcome than in control animals, particularly males. We investigated the effect of insulin infusion during the reperfusion period in isolated hearts from control and HTG male and female rats. Weanling Wistar rats were given commercial rat chow and tap water (C rats) or 30% sucrose solution (HTG rats) for 8 months. They developed moderate hypertension and hyperinsulinemia, central adiposity, nephropathy, and hypertriglyceridemia. Cardiac function was recorded in a Langendorff preparation subjected to 25 min ischemia and 15 min reperfusion. The handicapped functionality of HTG hearts is more apparent under conditions of stress. Insulin administration improved particularly mechanical work and +dp/dt max variables. The effect of sex was observed on the type of arrhythmias developed during reperfusion: Only the males showed lethal ventricular fibrillation, which disappeared after insulin administration. Females had lower levels of cardiac enzymes creatine kinase (CKMB) and lactic dehydrogenase (LDH), but their performance was not hindered, probably on account of protective factors such as estrogens. Summing up, the pathological features of the HTG model did not prevent insulin from exerting some of its beneficial effects in HTG hearts. Sex differences in the outcome were more apparent in the type of arrhythmias after reperfusion; they were lethal in HTG males only, but insulin prevented their onset.
Cardiovasc
Pathol
PMID:Isolated heart function during ischemia and reperfusion in sucrose-fed rats: effect of insulin infusion. 1616 99
The
metabolic syndrome
(syndrome X) is a cluster of risk factors and a common cause of cardiovascular disease in humans. Although the underlying mechanism for
metabolic syndrome
is still poorly understood, recent clinical data and studies with transgenic animals implicate elevated intracellular glucocorticoid tone in the etiology of
metabolic syndrome
. Development of selective inhibitors of 11beta-hydroxysteroid dehydrogenase (11beta-HSD)-1 and their use in rodent animal disease models encompassing several aspects of
metabolic syndrome
indicate the possibility of therapeutic intervention. This review will focus on recent advances in our understanding of the role of 11beta-HSD1 in metabolic disorders and other disease processes.
Expert Rev
Cardiovasc
Ther 2005 Sep
PMID:Inhibition of 11beta-HSD1 as a novel treatment for the metabolic syndrome: do glucocorticoids play a role? 1618 Oct 35
A growing amount of evidence suggests that regional fat distribution plays an important part in the development of an unfavorable metabolic and cardiovascular risk profile. Epicardial fat is a metabolically active organ that generates various bioactive molecules, which might significantly affect cardiac function. This small, visceral fat depot is now recognized as a rich source of free fatty acids and a number of bioactive molecules, such as adiponectin, resistin and inflammatory cytokines, which could affect the coronary artery response. The observed increases in concentrations of inflammatory factors in patients who have undergone coronary artery bypass grafting remain to be confirmed in healthy individuals. Furthermore, epicardial adipose mass might reflect intra-abdominal visceral fat. Therefore, we propose that echocardiographic assessment of this tissue could serve as a reliable marker of visceral adiposity. Epicardial adipose tissue is also clinically related to left ventricular mass and other features of the
metabolic syndrome
, such as concentrations of LDL cholesterol, fasting insulin and adiponectin, and arterial blood pressure. Echocardiographic assessment of epicardial fat could be a simple and practical tool for cardiovascular risk stratification in clinical practice and research. In this paper, we briefly review the rapidly emerging evidence pointing to a specific role of epicardial adipose tissue both as a cardiac risk marker and as a potentially active player in the development of cardiac pathology.
Nat Clin Pract
Cardiovasc
Med 2005 Oct
PMID:Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. 1618 52
Statins are a remarkably safe and efficacious class of medications that have proved to be invaluable in the fight against heart disease. Statins have been prescribed to millions of patients for nearly 20 years; thus there have been hundreds of millions of patient-years of use, with relatively few adverse effects and incalculable benefits. Results from large-scale clinical trials have shown that statins are associated with dramatic decreases in cardiovascular risk. It seems certain that statins will remain a valuable and essential part of the lipid-lowering landscape, but combinations of statins with other lipid-lowering agents are increasingly important. Even with the most potent statins, the desired low-density lipoprotein cholesterol goal might not be attained with statin monotherapy. Furthermore, because of the increasing prevalence of diabetes and the
metabolic syndrome
, along with their attendant multiple lipid abnormalities, combinations of statins with medications targeted toward multiple lipoprotein particles will emerge.
Rev
Cardiovasc
Med 2005
PMID:The past, present, and future of statin therapy. 1619 86
The severity of
metabolic syndrome
depends on the degree of insulin resistance. However, currently there is no adequate clinical marker for quantitative analysis of insulin resistance. A small quantity of lipoprotein lipase (LPL) protein, which is an inactive form and commonly called 'preheparin LPL mass', exists in serum and is detected by a sensitive immunoassay system. Recent studies have reported the clinical significance of serum preheparin LPL mass levels in various aspects. For example, preheparin LPL mass is negatively related to serum triglyceride and positively related to HDL-cholesterol, is low in type 2 diabetes mellitus, is increased by administration of insulin sensitizer, and shows an inverse relationship with visceral adiposity. Furthermore, preheparin LPL mass level is significantly lower in patients with coronary atherosclerosis compared to patients with no lesion, and correlates negatively with the severity of these lesions. From these reports, preheparin LPL mass may be considered to be the most important quantitative indicator of insulin resistance of the whole body.
Curr Med Chem
Cardiovasc
Hematol Agents 2005 Oct
PMID:Clinical determination of the severity of metabolic syndrome: preheparin lipoprotein lipase mass as a new marker of metabolic syndrome. 1625 Aug 68
The
metabolic syndrome
and type 2 diabetes mellitus are both becoming more prevalent, and both increase the risk of cardiovascular disease. Many patients are not receiving appropriate treatment for the type of dyslipidemia that commonly occurs in these disorders--the so-called 'atherogenic lipid triad' of high serum triglyceride levels, low serum high-density lipoprotein cholesterol (HDL-C) levels, and a preponderance of small, dense, low-density lipoprotein cholesterol (LDL-C) particles. All of the processes involved in atherogenesis can be exacerbated by insulin resistance and/or the
metabolic syndrome
. Hypertriglyceridemia is a strong predictor of coronary heart disease. There is also an inverse relationship between serum levels of HDL-C and triglycerides in diabetic patients, with low serum HDL-C levels possibly representing an independent risk factor for cardiovascular disease. Small, dense, LDL-C particles are also highly atherogenic as they are more likely to form oxidized LDL and are less readily cleared. Insulin resistance, which is central to the
metabolic syndrome
and type 2 diabetes mellitus, leads to high levels of very low-density lipoprotein (VLDL), which contain a high concentration of triglycerides, resulting in high serum triglyceride levels and low serum HDL-C levels. Even though modification of the atherogenic lipid triad is probably one of the most effective methods of reducing cardiovascular risk, therapy for diabetic dyslipidemia is often directed to first lowering serum LDL-C levels with a HMG-CoA reductase inhibitor. This may leave substantial excess risk for cardiovascular disease in patients with these types of dyslipidemia. The results of recent trials evaluating HMG-CoA reductase inhibitors have been mixed, with two showing no significant effect on cardiovascular outcomes in subgroups of diabetic patients. The recent CARDS (Collaborative Atorvastatin Diabetes Study) showed that atorvastatin can reduce cardiovascular events in a trial specifically designed for a diabetic population, though the population had to have at least one other risk factor in addition to diabetes mellitus. Fibric acid derivatives, such as fenofibrate, bezafibrate and gemfibrozil, are potentially well suited to the treatment of dyslipidemia that is generally associated with type 2 diabetes mellitus and the
metabolic syndrome
, as they are usually more effective than HMG-CoA reductase inhibitors for normalizing serum levels of HDL-C and triglycerides. Promising results have been obtained from several trials of fibric acid derivatives including the BIP (Bezafibrate Infarction Prevention) study and the VA-HIT (Veterans Affairs Cooperative Studies Program HDL-C Intervention Trial; gemfibrozil). The FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) trial, a clinical outcomes trial specifically designed to evaluate fenofibrate in a large population of patients with type 2 diabetes mellitus, many of whom have the
metabolic syndrome
, is underway. The FIELD trial results should shed light on the efficacy and safety of fenofibrate in reducing cardiovascular morbidity in diabetic and
metabolic syndrome
patients and on the safety profile of combination therapy with fenofibrate and a HMG-CoA reductase inhibitor.
Am J
Cardiovasc
Drugs 2005
PMID:Beyond low-density lipoprotein: addressing the atherogenic lipid triad in type 2 diabetes mellitus and the metabolic syndrome. 1625 26
Cardiovascular disease remains a leading cause of death throughout the world despite advances in its detection and treatment. Commonly used risk algorithms, such as the Framingham Risk Score fail to identify all affected individuals. Novel cardiovascular risk factors that identify these missed individuals would greatly improve overall care of patients. C-reactive protein (CRP), an inflammatory biomarker, has emerged as a leading candidate to fulfill this role. Based on the results of several prospective epidemiologic studies, CRP has emerged as one of the most powerful predictors of cardiovascular disease. This marker provides valuable information to clinicians in various clinical settings, ranging from overt cardiovascular disease, stable angina, presenting acute coronary syndromes and peripheral vascular disease, to the
metabolic syndrome
. Furthermore, CRP has been demonstrated to actively contribute to all stages of atherogenesis, participating in endothelial dysfunction, atherosclerotic-plaque formation, plaque maturation, plaque destabilization and eventual rupture. Thus, it might also serve as a therapeutic target. It is our contention that the future will see much wider use of CRP and CRP-driven therapies in clinical medicine, improving our ability to identify and manage cardiovascular disease.
Nat Clin Pract
Cardiovasc
Med 2005 Jan
PMID:C-reactive protein comes of age. 1626 40
Insulin-resistance syndromes are of pandemic proportions; 150 million people worldwide and an estimated 43 million people in the US are currently affected by type 2 diabetes mellitus or
metabolic syndrome
respectively. Treatment of heart disease in the context of type 2 diabetes requires multifactorial risk-factor management, including lifestyle modification and drug treatment for comorbidities. Management of coronary risk extends beyond simple cholesterol lowering. Early use of cardiac imaging and, where appropriate, revascularization should be considered in high-risk or symptomatic patients. Traditionally, patients with type 2 diabetes and coronary arterial disease have been treated surgically, but percutaneous revascularization of these patients is increasingly common. Indeed, revascularization by use of drug-eluting coronary stents combined with administration of novel antiplatelet agents has revolutionized percutaneous coronary intervention in patients with type 2 diabetes. Despite these advances, there is no consensus of opinion regarding revascularization strategies or risk-factor management in insulin-resistant patients with symptomatic or prognostically important coronary arterial disease. Furthermore, specific therapies and preventative strategies for diabetic cardiomyopathy and heart failure in patients with type 2 diabetes remain elusive. The identification of optimized approaches for the prevention and treatment of the
metabolic syndrome
and heart disease in insulin-resistant, nondiabetic patients remains a major global challenge.
Nat Clin Pract
Cardiovasc
Med 2005 May
PMID:Therapy insight: heart disease and the insulin-resistant patient. 1626 9
Metabolic syndrome
(MS) is associated with excess cardiovascular risk above and beyond the contribution of traditional risk factors. It is a proinflammatory and prothrombotic condition associated with underlying insulin resistance. Hypertension and hyperlipidemia in the setting of MS are also associated with excess cardiovascular risk, as is the development of new onset diabetes during the course of therapy. Although impaired fasting glucose and impaired glucose tolerance (IGT) both predict the development of diabetes mellitus, IGT more strongly predicts CV events because it is associated with a greater degree of insulin resistance. Early recognition and aggressive lifestyle interventions are the cornerstones of treatment, with aggressive pharmacologic therapy introduced when appropriate. It is expected that future studies will more clearly define the early use of insulin-sensitizing agents in MS.
Rev
Cardiovasc
Med 2005
PMID:Cardiovascular risk factors in the metabolic syndrome: impact of insulin resistance on lipids, hypertension, and the development of diabetes and cardiac events. 1637 15
Abdominal fat accumulation has been shown to play crucial roles in the development of
metabolic syndrome
. Visceral fat accumulation particularly is closely correlated to the development of cardiovascular disease and obesity-related disorders such as diabetes mellitus, hyperlipidemia and hypertension. Given these clinical findings, the functions of adipocytes have been intensively investigated in the past 10 years, and have been revealed to act as endocrine cells that secrete various bioactive substances termed adipocytokines. Among adipocytokines, tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and contribute to the development of vascular diseases. Visfatin has been identified as a visceral-fat-specific protein that might be involved in the development of obesity-related diseases, such as diabetes mellitus and cardiovascular disease. In contrast to these adipocytokines, adiponectin, which is an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. The functions of adipocytokine secretion might be regulated dynamically by nutritional state. Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor, and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. In this review, the importance of adipocytokines, particularly adiponectin, is discussed with respect to cardiovascular diseases.
Nat Clin Pract
Cardiovasc
Med 2006 Jan
PMID:Therapy Insight: adipocytokines in metabolic syndrome and related cardiovascular disease. 1639 16
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