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

Cardiovascular complications are the most common causes of morbidity and mortality in diabetic patients. Coronary atherosclerosis is enhanced in diabetics, whereas myocardial infarction represents 20% of deaths of diabetic subjects. Furthermore, re-infarction and heart failure are more common in the diabetics. Diabetic cardiomyopathy is characterized by an early diastolic dysfunction and a later systolic one, with intracellular retention of calcium and sodium and loss of potassium. In addition, diabetes mellitus accelerates the development of left ventricular hypertrophy in hypertensive patients and increases cardiovascular mortality and morbidity. Treating the cardiovascular problems in diabetics must be undertaken with caution. Special consideration must be given with respect to the ionic and metabolic changes associated with diabetes. For example, although ACE inhibitors and calcium channel blockers are suitable agents, potassium channel openers cause myocardial preconditioning and decrease the infarct size in animal models, but they inhibit the insulin release after glucose administration in healthy subjects. Furthermore, potassium channel blockers abolish myocardial preconditioning and increase infarct size in animal models, but they protect the heart from the fatal arrhythmias induced by ischemia and reperfusion which may be important in diabetes. For example, diabetic peripheral neuropathy usually presents with silent ischemia and infarction. Mechanistically, parasympathetic cardiac nerve dysfunction, expressed as increased resting heart rate and decreased respiratory variation in heart rate, is more frequent than the sympathetic cardiac nerve dysfunction expressed as a decrease in the heart rate rise during standing.
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PMID:Diabetes mellitus and cardiac function. 954 31

Serum coenzyme Q10 (CoQ10: 2-(3,7,11,15,19,23,27,31,35,39-decamethyl-2,6,10,14,18,22,26,30,34 ,38 -tetracontadecaenyl)-5,6-dimethoxy-3-methyl-1,4-benzoquinone, CAS 303-98-0) and cholesterol levels were measured to assess the effect of cholesterol-lowering therapy in patients with non-insulin-dependent diabetes mellitus (NIDDM). Twenty healthy volunteers, 97 NIDDM patients and 2 patients with familial hypercholesterolemia were studied. None had overt heart failure or any other heart disease. Mean serum CoQ10 concentrations were significantly (p < 0.01) lower in diabetic patients with normal serum cholesterol concentrations, either with or without administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA RIs) including simvastatin (normal: 0.91 +/- 0.26 (mean +/- SD) mumol 1(-1); diabetic with HMG-CoA RI: 0.63 +/- 0.19; diabetic without HMG-CoA RI: 0.66 +/- 0.21). CoQ10 concentrations were higher (1.37 +/- 0.48, p < 0.001) in diabetic patients with hypercholesterolemia. Simvastatin or low density lipoprotein apheresis decreased serum CoQ10 concentrations along with decreasing serum cholesterol. Oral CoQ10 supplementation in diabetic patients receiving HMG-CoA RI significantly (p < 0.001) increased serum CoQ10 from 0.81 +/- 0.24 to 1.47 +/- 0.44 mumol 1(-1), without affecting cholesterol levels. It significantly (p < 0.03) decreased cardiothoracic ratios from 51.4 +/- 5.1 to 49.2 +/- 4.7%. In conclusion, serum CoQ10 levels in NIDDM patients are decreased and may be associated with subclinical diabetic cardiomyopathy reversible by CoQ10 supplementation.
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PMID:Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. 1033 51

The accumulating body of data indicate that the occurrence of diabetic cardiomyopathy is an independent phenomenon from macroangiographic changes in coronary arteries and hypertension. Results from animal studies, human histological results and clinical observations provided support for this phenomenon. Although the clinical symptoms have been identified, however, the pathogenesis of diabetic cardiomyopathy is uncertain. The definition of diabetic cardiomyopathy describes both specific defects in the myocytes from diabetics and associated changes in the heart which have developed during the course of diabetes. The following defects in myocytes have been identified and are postulated to contribute to diabetic cardiomyopathy: The changes in carbohydrates metabolism, in fatty-acid metabolism, calcium and potassium transport, microvascular narrowing and micro aneurysms, hypertrophy, defects in collagen structure, myocardial fibrosis and perivascular fibrosis, abnormalities in conducting system, the decrease in the function of autonomic nerves. The clinical presentation of diabetic cardiomyopathy lead to the description of two phases of the disease. First, asymptomatic diabetic subjects with subclinical abnormalities of the left-ventricular diastolic function, measured by Doppler echocardiography. In the second phase--clinically evident diabetic cardiomyopathy is described by congestive cardiac failure without evident arteriosclerotic changes in coronary arteries and hypertension. Diabetic cardiomyopathy can be diagnosed early after the onset of diabetes mellitus and is independent phenomenon from late diabetic complications. The main cause of mortality in diabetic subjects is largely due to macroangiopathic changes in the coronary arteries (evaluated by coronarography), not the heart failure.
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PMID:[Diabetic cardiomyopathy. Pathophysiology and clinical implications]. 1129 28

Many diabetic patients suffer from cardiomyopathy, even in the absence of vascular disease. This diabetic cardiomyopathy predisposes patients to heart failure and mortality from myocardial infarction. Evidence from animal models suggests that reactive oxygen species play an important role in the development of diabetic cardiomyopathy. Our laboratory previously developed a transgenic mouse model with targeted overexpression of the antioxidant protein metallothionein (MT) in the heart. In this study we used MT-transgenic mice to test whether an antioxidant protein can reduce cardiomyopathy in the OVE26 transgenic model of diabetes. OVE26 diabetic mice exhibited cardiomyopathy characterized by significantly altered mRNA expression, clear morphological abnormalities, and reduced contractility under ischemic conditions. Diabetic hearts appeared to be under oxidative stress because they had significantly elevated oxidized glutathione (GSSG). Diabetic mice with elevated cardiac MT (called OVE26MT mice) were obtained by crossing OVE26 transgenic mice with MT transgenic mice. Hyperglycemia in OVE26MT mice was indistinguishable from hyperglycemia in OVE26 mice. Despite this, the MT transgene significantly reduced cardiomyopathy in diabetic mice: OVE26MT hearts showed more normal levels of mRNA and GSSG. Typically, OVE26MT hearts were found to be morphologically normal, and elevated MT improved the impaired ischemic contractility seen in diabetic hearts. These results demonstrate that cardiomyocyte-specific expression of an antioxidant protein reduces damage to the diabetic heart.
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PMID:Overexpression of metallothionein reduces diabetic cardiomyopathy. 1175 38

1. Electrical remodelling of the ventricle is a common pathogenic feature of cardiovascular disease states that lead to heart failure. Experimental data suggest this change in electrophysiological phenotype is largely due to downregulation of K(+) channels involved in repolarization of the action potential. 2. Voltage-clamp studies of the transient outward current (I(to)) in diabetic cardiomyopathy support a metabolic mechanism for K(+) channel downregulation. In particular, I(to) density is significantly increased in diabetic rat isolated ventricular myocytes treated in vitro with insulin or agents that activate pyruvate dehydrogenase. Recent data suggest this mechanism is not limited to diabetic conditions, because metabolic stimuli that upregulate I(to) in diabetic rat myocytes act similarly in non- diabetic models of heart failure. 3. Depressed I(to) channel activity is also reversed by experimental conditions that increase myocyte levels of reduced glutathione, indicating that oxidative stress is involved in electrical remodelling. Moreover, upregulation of I(to) density by activators of glucose utilization is blocked by inhibitors of glutathione metabolism, supporting the premise that there is a functional link between glucose utilization and the glutathione system. 4. Electrophysiological studies of diabetic and non-diabetic disease conditions affecting the heart suggest I(to) channels are regulated by a redox-sensitive mechanism, where glucose utilization plays an essential role in maintaining a normally reduced state of the myocyte. This hypothesis has implications for clinical approaches aimed at reversing pathogenic electrical remodelling in a variety of cardiovascular disease states.
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PMID:A metabolic mechanism for cardiac K+ channel remodelling. 1190 72

Heart failure is an important problem for the growing number of persons afflicted with diabetes. Not only is HF more prevalent than in the non-diabetic population but also it carries a graver prognosis. Diabetic cardiomyopathy adds to the already increased risks for developing HF with hypertension and coronary heart disease, leading to systolic and diastolic dysfunction. As LV function deteriorates, increases in RAS and SNS activation may lead to progressive HF and premature death. The greater prevalence and increased mortality risk in diabetic patients supports the role of aggressive HF diagnosis and management, even in asymptomatic patients. Treatment strategies already established for HF have been shown to be effective in the diabetic population, including ACE inhibitors and beta-blockers. There is evidence that glycemic control is also important in improving clinical outcomes. The adverse effects of beta-blockade on carbohydrate and lipid metabolism and vasoconstriction may be circumvented by the use of carvedilol.
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PMID:Treatment of heart failure in patients with diabetes: clinical update. 1191 48

Accumulation of long-chain fatty acids in the heart has been proposed to play a role in the development of heart failure and diabetic cardiomyopathy. Several animal models with increased cardiomyocyte lipid accumulation suggest a link between the accumulation of lipid, cardiomyocyte cell death and the development of cardiomyopathy. In this review, we discuss the mechanism through which fatty acid accumulation may contribute to the development or progression of heart failure by initiation of apoptotic cell death. Long-chain saturated fatty acids induce apoptosis through a mechanism involving the generation of reactive intermediates. Reactive intermediate production occurs in concert with de novo ceramide synthesis, but ceramide production is not required for cell death. Cardiomyocyte dysfunction and death from reactive intermediates generated by long-chain saturated fatty acids may contribute to the pathogenesis of human heart disease.
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PMID:Mechanisms of lipoapoptosis: implications for human heart disease. 1200 39

The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.
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PMID:[Diabetic cardiomyopathy: concept, heart function, and pathogenesis]. 1215 93

Diabetes mellitus is a strong risk factor for the development of cardiovascular disease, and is associated with a worse prognosis. The incidence of congestive heart failure is higher in diabetic patients, although the reasons for this increased rate are debated (higher incidence and severity of coronary heart disease and arterial hypertension, or a true diabetic cardiomyopathy). The treatment of heart failure in diabetic patients does not differ from that of non-diabetic patients, although recent studies of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers offer interesting new perspectives.
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PMID:[Prevention and treatment of congestive heart failure in diabetic patients]. 1238 94

Our aim is to summarize and discuss the recent literature linking diabetes mellitus with heart failure, and to address the issue of the optimal treatment for diabetic patients with heart failure. THE STUDIES LINKING DIABETES MELLITUS (DM) WITH HEART FAILURE (HF) : The prevalence of diabetes mellitus in heart failure populations is close to 20% compared with 4 to 6% in control populations. Epidemiological studies have demonstrated an increased risk of heart failure in diabetics; moreover, in diabetic populations, poor glycemic control has been associated with an increased risk of heart failure. Various mechanisms may link diabetes mellitus to heart failure: firstly, associated comorbidities such as hypertension may play a role; secondly, diabetes accelerates the development of coronary atherosclerosis; thirdly, experimental and clinical studies support the existence of a specific diabetic cardiomyopathy related to microangiopathy, metabolic factors or myocardial fibrosis. Subgroup analyses of randomized trials demonstrate that diabetes is also an important prognostic factor in heart failure. In addition, it has been suggested that the deleterious impact of diabetes may be especially marked in patients with ischemic cardiomyopathy. TREATMENT OF HEART FAILURE IN DIABETIC PATIENTS : The knowledge of the diabetic status may help to define the optimal therapeutic strategy for heart failure patients. Cornerstone treatments such as ACE inhibitors or beta-blockers appear to be uniformly beneficial in diabetic and non diabetic populations. However, in ischemic cardiomyopathy, the choice of the revascularization technique may differ according to diabetic status. Finally, clinical studies are needed to determine whether improved metabolic control might favorably influence the outcome of diabetic heart failure patients.
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PMID:Influence of diabetes mellitus on heart failure risk and outcome. 1255 46


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