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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of a diabetic cardiomyopathy, independent of hypertension and coronary artery disease, is still controversial. This systematic review seeks to evaluate the evidence for the existence of this condition, to clarify the possible mechanisms responsible, and to consider possible therapeutic implications. The existence of a diabetic cardiomyopathy is supported by epidemiological findings showing the association of diabetes with heart failure; clinical studies confirming the association of diabetes with left ventricular dysfunction independent of hypertension, coronary artery disease, and other heart disease; and experimental evidence of myocardial structural and functional changes. The most important mechanisms of diabetic cardiomyopathy are metabolic disturbances (depletion of glucose transporter 4, increased free fatty acids, carnitine deficiency, changes in calcium homeostasis), myocardial fibrosis (association with increases in angiotensin II, IGF-I, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, and endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels), and insulin resistance (hyperinsulinemia and reduced insulin sensitivity). This review presents evidence that diabetes is associated with a cardiomyopathy, independent of comorbid conditions, and that metabolic disturbances, myocardial fibrosis, small vessel disease, cardiac autonomic neuropathy, and insulin resistance may all contribute to the development of diabetic heart disease.
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PMID:Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. 1529 81

Cardiovascular disease has a high prevalence in diabetic patients. Diabetes mellitus is an important risk factor for atherosclerosis and coronary disease mainly through obesity, hyperlipidemia, insulin-resistance, hyperinsulinemia, hyperglycemia and altered homeostasis. The correlation between diabetes and chronic heart failure is not widely documented in the literature. According to the Framingham study, the incidence of cardiovascular morbidity per year is 39.1% in diabetic males and 17.2% in diabetic females; chronic heart failure afflicts 7.6% of diabetic males and 11.4% of diabetic females. Actual knowledge about pathophysiology suggests that cardiac involvement in diabetes is not only related to macrovascular injury but also to other factors, such as alterations of autonomic nervous system, that can contribute to diabetic cardiopathy. The present study evaluated the prevalence of chronic heart failure in an Italian diabetic population in order to discuss the rationale of the therapeutic strategies.
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PMID:Diabetes mellitus and chronic heart failure. 1537 47

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.
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PMID:Impaired glucose metabolism in patients with heart failure: pathophysiology and possible treatment strategies. 1544 70

Obesity alone is the cause of 11% of cases of cardiac failure in men and 14% of cases in women in the United States. The frequency of obesity continues to rise in our country, 41% of our compatriots being obese or overweight. It is expected that obesity will become an important cause of cardiac failure in the coming years. The Framingham study showed that, after correction for other risk factors, for every point increase in body mass index, the increase in risk of developing cardiac failure was 5% in men and 7% in women. There are three physiopathological mechanisms to explain the adverse effects of obesity on left ventricular function: an increase in ventricular preload secondary to increased plasma volume induced by the high fatty mass; an increase in left ventricular afterload due to the common association of hypertension generated by activation of the sympathetic nervous system by hyperinsulinism; and systolic and diastolic dysfunction due to changes in the myocardial genome and coronary artery disease induced by risk factors of atherosclerosis aggravated by obesity. The adipocyte also secretes a number of hormones which act directly or indirectly on the myocardium: angiotensin II, leptin, resistin, adrenomedulin, cytokines. These haemodynamic and hormonal changes profoundly modify the genetic expression of the myocardium in obesity, favourising hypertrophy of the myocyte and the development of interstitial fibrosis. Whether it be eccentric in the absence of hypertension or concentric when hypertension is associated with obesity, left ventricular hypertrophy, although normalising left ventricular wall stress, has adverse consequences causing abnormal relaxation and decreased left ventricular compliance. Therefore, in obese patients, two forms of cardiac failure may be observed. The more common is due to diastolic dysfunction, obesity being one of the principal causes of cardiac failure with preserved systolic function. Cardiac failure due to systolic dysfunction is less common and may be observed in cases with inappropriate left ventricular hypertrophy which does not normalise abnormal left ventricular wall stress leading to cardiomyopathy, and in cases with associated coronary artery disease. Whatever the underlying mechanism, the diagnosis of cardiac failure is made more difficult by obesity. From the prognostic point of view, in the global population of patients with cardiac failure, obesity improves survival because it counteracts the adverse effect of cachexia; however, obesity increases the risk of sudden death. In fact, obesity is associated with dynamic change in QT interval. In cases of cardiac failure secondary to obesity-related cardiomyopathy, loss of weight leads to an improved functional status and a reduction of left ventricular remodelling and an increase of the ejection fraction.
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PMID:[Obesity and cardiac failure]. 1572 18

We report beneficial effects of pioglitazone on insulin resistance in diabetes mellitus accompanied with myotonic dystrophy (DM1). We studied eight DM1 patients with diabetes mellitus aged 32 to 60 (mean age 52.1 +/- 8.6 years). Three of them were under glibenclamide treatment, but their plasma glucose control was poor because of occasional hypoglycemia; others had not been treated with any hypoglycemic drugs. We administered a daily dose of 15 mg pioglitazone for 6-36 months (mean period 14.8 +/- 9.1 months). Plasma glucose control improved in all patients. In a 75 g oral glucose tolerance test, plasma glucose level at 120 min dropped from 203.3 +/- 41.7 mg/dl to 153.9 +/- 39.5 mg/dl (p = 0.04); the area under the insulin curve up to 120 min (sigma IRI) dropped from 236.9 +/- 170.2 microU x hr/ml to 169.6 +/- 81.3 microU x hr/ml (p = 0.12). Sigma IRI decreased in four patients with pretreatment sigma IRI > or = 250 microU x hr/ml; it slightly increased in other patients with pretreatment sigma IRI < or = 150 microU x hr/ml. The homeostasis model assessment-insulin resistance (HOMA-IR) improved from 2.1 +/- 1.0 to 1.1 +/- 0.4 (p = 0.04). Impairment of liver functions, cardiac failure, or hypoglycemia was not observed. Pioglitazone treatment is useful to improve insulin resistance and glucose control in DM1 patients with diabetes mellitus, especially patients with reactive hyperinsulinemia to glucose loading.
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PMID:[Long-term treatment of diabetes mellitus in myotonic dystrophy with pioglitazone]. 1591 96

Recent studies suggest that adipose tissue hormones ("adipokines") are involved in the pathogenesis of various complications of obesity, including hyperlipidemia, diabetes mellitus, arterial hypertension, atherosclerosis, and heart failure. Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue. Apelin exists in at least three forms, consisting of 13, 17, or 36 amino acids, all originating from a common 77-amino-acid precursor. In the cardiovascular system, apelin elicits endothelium-dependent, nitric oxide-mediated vasorelaxation and reduces arterial blood pressure. In addition, apelin demonstrates potent and long-lasting positive inotropic activity which is preserved even in injured myocardium and is not accompanied by myocardial hypertrophy. Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia. In addition to regulating cardiovascular function, apelin inhibits water intake and vasopressin production. Visfatin, previously recognized as a pre-B cell colony-enhancing factor (PBEF), is abundantly expressed in visceral adipose tissue and is upregulated in some, but not all, animal models of obesity. Preliminary studies suggest that plasma visfatin concentration is also increased in humans with abdominal obesity and/or type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
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PMID:Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity? 1694 Sep 39

Changes of blood insulin content were studied in patients with ischemic heart disease with various functional classes of acute and chronic heart failure and at different disease stages. It was established that latent hyperinsulinemia which became evident at induced myocardial ischemia was present on all stages of development of ischemic heart disease. In acute heart failure due to developed myocardial infarction hyperinsulinemia manifested in 58.3% of patients. Amount of insulin in blood increased almost 3 times. During progression of chronic heart failure insulin content significantly decreased, probably because of exhaustion of insulin producing function and development of its relative or absolute deficit. At terminal stage of congestive heart failure insulin level was < or = 1 microU/ml. The authors believe that severity of clinical signs of acute and chronic heart failure are determined by sensitivity of myocardium to insulin, content of insulin in blood, and also depends on compensatory possibilities of insulin producing function at each stage of development of the disease.
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PMID:[Possible role of hyperinsulinemia in pathogenesis of acute and chronic cardiac failure in patients with ischemic heart disease (data of clinical studies)]. 1688 22

Diabetic cardiomyopathy is a myocardial disease caused by diabetes mellitus unrelated to vascular and valvular pathology or systemic arterial hypertension. Clinical and experimental studies have shown that diabetes mellitus causes myocardial hypertrophy, necrosis, and apoptosis, and increases interstitial tissue. The pathophysiology of diabetic cardiomyopathy is incompletely understood. It appears that metabolic perturbations such as hyperlipidemia, hyperinsulinemia, hyperglycemia, and changes in cardiac metabolism are involved in cellular consequences leading to increased oxidative stress, interstitial fibrosis, myocyte death, and altered intracellular ions transient and calcium homeostasis. Clinically, an early detection of asymptomatic diastolic dysfunction is possible. When patients develop signals and symptoms of heart failure, isolated diastolic dysfunction is usually detected. Systolic dysfunction is a late finding. Treatment of heart failure due to diabetic cardiomyopathy is not different from myocardiopathies of other etiologies and must follow the guidelines according to ventricular function, whether diastolic or diastolic and systolic impairment.
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PMID:[Diabetic cardiomyopathy]. 1750 22

Obesity is a well-known risk factor for the development of type 2 diabetes mellitus and cardiovascular disease. Importantly, obesity is not only associated with lipid accumulation in adipose tissue, but also in non-adipose tissues. The latter is also known as ectopic lipid accumulation and may be a possible link between obesity and its comorbidities such as insulin resistance, type 2 diabetes mellitus and cardiovascular disease. In skeletal muscle and liver, lipid accumulation has been associated with the development of insulin resistance, an early hallmark of developing type 2 diabetes mellitus. More specifically, accumulation of intermediates of lipid metabolism, such as diacylglycerol (DAG) and Acyl-CoA have been shown to interfere with insulin signaling in these tissues. Initially, muscular and hepatic insulin resistance can be overcome by an increased insulin production by the pancreas, resulting in hyperinsulinemia. However, during the progression towards overt type 2 diabetes, pancreatic failure occurs resulting in reduced insulin production. Interestingly, also in the pancreas lipid accumulation has been shown to precede dysfunction. Finally, accumulation of fat in the heart has been associated with cardiac dysfunction and heart failure, which may be an explanation for diabetic cardiomyopathy. Taken together, we conclude that evidence for deleterious effects of lipid accumulation in non-adipose tissue (lipotoxicity) is strong. However, while ample human data is available for skeletal muscle and the liver, future research should focus on lipid accumulation in the pancreas and the heart.
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PMID:Lipid accumulation in non-adipose tissue and lipotoxicity. 1822 98

Obesity is associated with heart failure. Recognition of subclinical left ventricular (LV) dysfunction may permit the initiation of therapy to prevent the development of heart failure. In this study of anthropometric, biochemical, and echocardiographic measurements in 295 healthy overweight subjects, we sought to investigate the effect of insulin resistance and severity of obesity on LV function and to establish a strategy for detection of LV dysfunction using metabolic and echocardiographic measurements. Correlates of subclinical dysfunction (defined from myocardial deformation in a matched group of 98 slim controls) were sought, and receiver operator characteristic curves for clinical and laboratory parameters were performed to identify optimal cutoffs to permit an effective diagnostic strategy. Subclinical impairment of LV function (average strain<18%) was present in 124 subjects (42%), and 52% of severely obese patients (body mass index [BMI]>35 kg/m2). Independent correlates of strain were BMI (beta=-0.25, p<0.0001), fasting insulin (beta=-0.22, p<0.001), and age (beta=-0.18, p<0.003). In patients with a BMI<35 kg/m2, subclinical impairment was uncommon in the absence of hyperinsulinemia. Using a BMI<35 kg/m2 and an insulin level<13 mIU/L to select patients for further testing allowed echocardiography to be avoided in 35% of subjects in whom the prevalence of LV dysfunction was low. In conclusion, obesity and insulin resistance are important contributors to LV dysfunction, a deleterious effect of hyperinsulinemia on LV performance is particularly seen in overweight and moderately obese subjects, and the combination of BMI, fasting insulin, and echocardiography appears optimal for efficient identification of subclinical LV dysfunction in overweight and obese subjects.
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PMID:Use of body weight and insulin resistance to select obese patients for echocardiographic assessment of subclinical left ventricular dysfunction. 1843 67


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