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Query: UMLS:C0011860 (
type 2 diabetes
)
57,723
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Many clinical studies have demonstrated that lipid-altering drug treatments, including the use of statin and niacin monotherapy, can be effective in the primary and secondary prevention of coronary heart disease, but only in a minority of patients relative to placebo. Since statins and niacin have entirely different mechanisms of action and predominantly different effects on blood lipid levels, the combined use of both a statin and niacin may confer complementary benefits on multiple lipid parameters, produce a more global improvement in lipid blood levels and result in greater reductions in coronary heart disease risk factors than the administration of either agent alone. This may be of particular importance in patients with complex dyslipidemias, such as those with
Type 2 diabetes mellitus
and metabolic syndrome. This review summarizes the efficacy and safety of extended-release niacin/lovastatin (Advicor, Kos Pharmaceuticals Inc.), the first combination product approved for the management of dyslipidemia.
Expert Rev
Cardiovasc
Ther 2004 Jul
PMID:Extended-release niacin/lovastatin: the first combination product for dyslipidemia. 1522 9
Potentially important new findings have recently been reported concerning the so-called metabolic syndrome in relation to the renin-angiotensin system, ie, that treatment with inhibitors of the angiotensin-converting enzyme (ACE) not only decreases blood pressure levels but prevents the development of diabetes mellitus. The new findings described in this article highlight the potential role of the ACE system in the regulation of insulin sensitivity, thus contributing to the development of
type 2 diabetes
and metabolic syndrome. In addition to the well known selective effects of ACE inhibitors and angiotensin II receptor blockers in reducing microalbuminuria in diabetic patients, the potential ability of these drugs to reduce the risk of diabetes and the metabolic syndrome would support their use as first line agents not only in diabetic patients but also in selected groups of hypertensive patients, who are particularly at risk of developing metabolic complications. This information supports the Joint Guidelines for the Management of Arterial Hypertension by the European Society of Hypertension and the European Society of Cardiology, which highlight the crucial role of ACE inhibitors and the angiotensin II receptor blockers in preventing the development of diabetes in hypertensive patients.
Nutr Metab
Cardiovasc
Dis 2004 Apr
PMID:The role of the renin angiotensin hormonal system in the metabolic syndrome and type 2 diabetes. 1524 41
The incidence of obesity and
type 2 diabetes
mellitus (DM2) in the United States has been increasing dramatically over the past 15 years, and is now at epidemic proportions. DM2 is the clinical manifestation of a long-term metabolic process that is initiated by cells' decreased sensitivity to the actions of insulin. Many outcome studies have identified DM2 as a strong and independent risk factor for the development of cardiovascular complications such as hypertension, arteriosclerosis, and heart failure. The goals of therapy in treating DM2 are to improve the long-term outlook for these patients. However, in selecting a therapeutic regimen for patients, clinicians should be aware that potentially severe adverse events may occur at a rate not previously identified in phase 3 studies. Certain therapies used to treat DM2, by effectively increasing the sensitivity of insulin, have also been reported to cause adverse effects, which can precipitate symptomatic heart failure. The purpose of this column is to discuss the therapeutic options available for treating patients with DM2, the potential pathophysiology of the adverse events of symptomatic heart failure, encouragement of use of the US Food and Drug Administration MedWatch program for reporting adverse events associated with medication therapy, and review of newer treatment guidelines for use of insulin-sensitizing agents in patients with chronic heart failure.
Prog
Cardiovasc
Nurs 2004
PMID:Cardiovascular implications of thiazolidinedione therapy. 1524 73
This study aimed to assess the distribution of cardiovascular risk factors among subjects with type 2 clinical diabetic nephropathy, since in diabetic subjects, the excess mortality in cardiovascular events is primarily related to nephropathy. The study group consisted of 162 subjects with
type 2 diabetes
mellitus and persistent proteinuria, and the control group was 80 type 2 diabetic subjects without nephropathy. In the study group there were 81 male and 81 female subjects whose mean age was 53.4 +/- 6.3 years. There was no significant consumption of alcohol and cigarette use in the population. The mean waist-hip ratio (WHR) was 0.97 and 0.96 in male and female subjects, respectively. The mean body mass index (BMI) of the subjects was 25.5 +/- 5.2 (males: 24.4 +/- 4.3, females: 27.2 +/- 5.5). A total of 106 subjects, made up of 45 male (27.8%) and 61 female (37.7%) subjects, were hypertensive as compared with 16 controls (20%). There was a significant difference in systolic blood pressure (p < 0.05) between the obese and non-obese subjects. One hundred and thirty three subjects (82.1%) had serum total cholesterol below 200 mg% as compared with 74 (92.5% ) in the control. Seventy-eight subjects (48.1%) had left ventricular hypertrophy. Males had a higher tendency of developing left ventricular hypertrophy (p = 0.04). Stroke and peripheral vascular disease respectively occurred more commonly in
type 2 diabetes
mellitus subjects with nephropathy [7 (4%) and 44 (27.2%)] compared to type 2 diabetic subjects without nephropathy [0 (0% ) and 9 (11.3% )] (p < 0.05). We found that there is a high prevalence of cardiovascular risk factors among Nigerian subjects with clinical diabetic nephropathy.
Cardiovasc
J S Afr
PMID:Cardiovascular risk factors in type 2 diabetic Nigerians with clinical diabetic nephropathy. 1525 22
Visceral obesity is frequently associated with high plasma triglycerides and low plasma high density lipoprotein-cholesterol (HDL-C), and with high plasma concentrations of apolipoprotein B (apoB)-containing lipoproteins. Atherogenic dyslipidemia in these patients may be caused by a combination of overproduction of very low density lipoprotein (VLDL) apoB-100, decreased catabolism of apoB-containing particles, and increased catabolism of HDL-apoA-I particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance. Weight reduction, increased physical activity, and moderate alcohol intake are first-line therapies to improve lipid abnormalities in visceral obesity. These lifestyle changes can effectively reduce plasma triglycerides and low density lipoprotein-cholesterol (LDL-C), and raise HDL-C. Kinetic studies show that in visceral obesity, weight loss reduces VLDL-apoB secretion and reciprocally upregulates LDL-apoB catabolism, probably owing to reduced visceral fat mass, enhanced insulin sensitivity and decreased hepatic lipogenesis. Adjunctive pharmacologic treatments, such as HMG-CoA reductase inhibitors, fibric acid derivatives, niacin (nicotinic acid), or fish oils, may often be required to further correct the dyslipidemia. Therapeutic improvements in lipid and lipoprotein profiles in visceral obesity can be achieved by several mechanisms of action, including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. Clinical trials have provided evidence supporting the use of HMG-CoA reductase inhibitors and fibric acid derivatives to treat dyslipidemia in patients with visceral obesity, insulin resistance and
type 2 diabetes
mellitus. Since drug monotherapy may not adequately optimize dyslipoproteinemia, dual pharmacotherapy may be required, such as HMG-CoA reductase inhibitor/fibric acid derivative, HMG-CoA reductase inhibitor/niacin and HMG-CoA reductase inhibitor/fish oils combinations. Newer therapies, such as cholesterol absorption inhibitors, cholesteryl ester transfer protein antagonists and insulin sensitizers, could also be employed alone or in combination with other agents to optimize treatment. The basis for a multiple approach to correcting dyslipoproteinemia in visceral obesity and the metabolic syndrome relies on understanding the mechanisms of action of the individual therapeutic components.
Am J
Cardiovasc
Drugs 2004
PMID:Dyslipidemia in visceral obesity: mechanisms, implications, and therapy. 1528 98
The metabolic syndrome and
type 2 diabetes
mellitus are increasingly associated with cardiovascular disease morbidity and mortality in African Americans. African Americans are specifically prone to the negative effects of hypertension and risk factor clustering associated with the metabolic syndrome and diabetes. Data demonstrate a decrease in cardiovascular events in diabetic patients with secondary prevention and, most recently, primary prevention with lipid-lowering therapy. African Americans should benefit from intense risk factor control, including antihypertensive therapy and lipid lowering, to prevent cardiovascular disease. Appropriate lifestyle modification programs, glucose control, and cardiovascular risk reduction therapy will reduce the excessive morbidity and mortality in this population.
Rev
Cardiovasc
Med 2004
PMID:The epidemic of diabetes mellitus and the metabolic syndrome in African Americans. 1530 83
Type 2 diabetes mellitus
affects nearly 17 million people in the United States, and prevalence rates are expected to double within 2 decades. Although there has been a downward trend in cardiovascular morbidity and mortality in recent years, cardiovascular disease remains the leading cause of death among patients with diabetes. This observation had led many to reevaluate current treatment goals and pharmacologic regimens for at-risk patients with
type 2 diabetes
mellitus. This review focuses on the current adjunctive pharmacologic treatment regimen that is well-suited for these patients.
Rev
Cardiovasc
Med 2004
PMID:Improving the pharmacological regimen for patients with diabetes mellitus. 1534 97
Hearts from animal models of
type 2 diabetes
present with abnormal contractility patterns. The role of altered alpha(1)-adrenergic signalling in this is not understood. In this study we report overexpression and altered regulation of alpha(1)-adrenergic receptors in two models of type 2 diabetic rat hearts. In combination with reduced contractile performance, papillary muscles from these hearts presented with an enhanced ability to react to alpha(1)-adrenergic stimulation. Concurrently, these muscles were protected against anoxia/reoxygenation induced damage. This protection could be abolished by pretreatment with the alpha(1)-adrenergic antagonist, prazosin. Overexpression of alpha(1)-adrenergic receptors may therefore be a two-edged sword: supplying a contractile reserve that can protect against anoxia/reoxygenation induced effects on inotropic ability on the one hand but also predisposing the hearts to elevated induction of intracellular Ca(2+) release and possible arrhythmic effects on the other hand.
Cardiovasc
Drugs Ther 2004 Jul
PMID:A role for the alpha1-adrenergic signalling pathway in the response of papillary muscles from type 2 diabetic hearts to anoxia-reoxygenation. 1536 22
Recently, clinical trials evaluating cardiovascular outcomes with antihypertensive drugs that target the renin-angiotensin-aldosterone system have been dramatically increasing in size. The CONSENSUS trial in 1987 enrolled 253 patients, while Val-HeFT in 1999 enrolled 5,010 patients; indeed, the Val-HeFT subgroup of patients not receiving angiotensin-converting enzyme inhibitors was bigger than the whole CONSENSUS trial even though the 366 patients were only 7% of the total trial population. More recent and ongoing cardiovascular trials have even greater patient numbers with 14,703 patients enrolled in VALIANT, 15,314 in VALUE, 23,400 in ONTARGET and 33,357 in ALLHAT. Part of the reason is that in modern trials, patients in the control group are already receiving optimal therapy. Therefore, in order to be adequately powered to detect any benefit of new drugs, trials must recruit thousands of patients. This expanding trend cannot continue forever because of time and economic constraints and as a result, trials are shifting their design to include composite and surrogate endpoints. In addition, more predefined substudies are being carried out to analyze possible benefits in specific patient populations such as those with
type 2 diabetes
or renal impairment. Modern trials are also placing more emphasis on protection as a long-term strategy to control cardiovascular risks. Examples of these points, particularly regarding the size of modern cardiovascular trials to have the power to show protective effects, are illustrated by Val-HeFT, LIFE, ELITE II, VALIANT, VALUE, CHARM and NAVIGATOR.
Cardiovasc
Drugs Ther 2004 Jul
PMID:RAAS inhibitors in the cardiovascular continuum: what is still missing? 1536 29
The firm association of diabetes mellitus with congestive heart failure (CHF) has been undoubtedly established. Recent reports support the presence of the reciprocal interrelationships between CHF and glucose abnormalities. The present review provides an overview of some aspects of the multifactorial interrelationships between heart failure and diabetes mellitus. Patients with heart failure are generally at higher risk of developing
type 2 diabetes
mellitus. Several factors may be involved, such as a lack of physical activity, hypermetabolic state, intracellular metabolic defects, poor muscle perfusion, and poor nutrition. Serum levels of inflammatory cytokines and leptin are elevated in patients with heart failure. Activation of the sympathetic system in CHF not only increases insulin resistance but also decreases the release of insulin from the pancreatic beta cells, increases hepatic glucose production by stimulating both gluconeogenesis and glycogenolysis, and increases glucagon production and lipolysis. People who develop
type 2 diabetes
mellitus usually pass through the phases of nuclear peroxisome proliferator-activated receptor modulation, insulin resistance, hyperinsulinemia, pancreatic beta-cell stress and damage leading to progressively decreasing insulin secretion, and impaired fasting and postprandial blood glucose levels. Once hyperglycemia ensues, the risk of metabolic and cardiovascular complications also increases. It is possible that the cornerstone of diabetes mellitus prevention in patients with CHF could be controlled by increased physical activity in a cardiac rehabilitation framework. Pharmacologic interventions by some medications (metformin, orlistat, ramipril and acarbose) can also effectively delay progression to
type 2 diabetes
mellitus in general high risk populations, but the magnitude of the benefit in patients with CHF is unknown. In patients with CHF and overt diabetes mellitus, ACE inhibitors may provide a special advantage and should be the first-line agent. Recent reports have suggested that angiotensin receptor antagonists (angiotensin receptor blockers), similar to ACE inhibitors, provide beneficial effects in patients with diabetes mellitus and should be the second-line agent if ACE inhibitors are contraindicated. Treatment with HMG-CoA reductase inhibitors should probably now be considered routinely for all diabetic patients with CHF, irrespective of their initial serum cholesterol levels, unless there is a contraindication.
Am J
Cardiovasc
Drugs 2004
PMID:Impaired glucose metabolism in patients with heart failure: pathophysiology and possible treatment strategies. 1544 70
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