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

Cardiovascular impairment is frequent during the neonatal period and can be expression of malformative or not-malformative pathology. In both conditions the clinical presentation is often dramatic with cyanosis and/or heart failure. The neonatologist has to make differential diagnosis as soon as possible, because cardiac malformations in the neonatal period are usually ductus arteriosus-dependent and can worsen suddenly after its closure. Since colour Doppler-echocardiography is not available in all the neonatal units in order to be helped in the diagnosis, it is very important that neonatologists learn to use the indications obtained with a careful physical examination and with some simple instrumental tests, as chest X-ray, electrocardiogram and blood gas analysis. In this article a review is made of the most frequent heart malformations associated with cyanosis and/or heart failure during the neonatal period (complete transposition of the great arteries, Fallot's tetralogy, tricuspid and pulmonary atresia, aortic coarctation, interventricular septal defect, persistence of ductus arteriosus) and the most common neonatal pathologic conditions simulating congenital heart diseases (persistence of fetal circulation, neonatal transitory myocardial ischemia, hypervolemia, hypoglycemia, hypocalcemia). Some clinical, instrumental and laboratory findings that could be useful for the diagnosis in absence of echocardiography are also reported.
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PMID:[The newborn with cardiological problems. The dilemma between malformative and non-malformative pathology]. 1275 55

Ethyl alcohol (ethanol) is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. The basic enzyme involved in its oxidation is alcohol dehydrogenase. Another important metabolic pathway is the Microsomal Ethanol-Oxidizing System (MEOS). Toxic effect on basic cell functions is produced both by ethanol and acetic aldehyde, its oxidation product which accounts for most of the acute and delayed effects of ethanol toxicity. In acute ethanol intoxication's the CNS symptoms are the first to manifest. Ethanol affects the CNS functions mainly through stimulating opiate and benzodiazepine receptors and a number of neurotransmitters. However, the attempts to diminish the toxic effects of ethanol on CNS by blocking the affected receptors have proved to be ineffective. In acute poisoning a basic essential is to sustain vital functions by following the principles of intensive care. Each case of acute ethanol intoxication must be subject to neurological examination for possible cerebro-cranial traumas. The diagnostics and treatment procedures should take account of the possible symptoms: convulsions, respiratory and cardiac failure, hypoglycemia, hypothermia, and severe gastric dysfunction. Vital signs monitoring and control of acid-base and water-electrolyte balance are a must. The toxic properties of ethanol metabolites can be particularly hazardous to patients treated with disulfiram. The patients who develop "antabuse response" should be given immediately iron and vitamin C intravenously.
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PMID:[Biological and toxic effects of ethanol: diagnostics and treatment of acute poisonings]. 1456 85

Lipopolysaccharide (LPS) produces varied systemic metabolic effects. We studied the effects of LPS on the cardiac fatty acid profile and its relationship to energy metabolism and inflammatory mediators that included TNF-alpha and nitric oxide synthase (NOS) in 10-day-old neonatal rat pups. Rat pups received an i.p. injection of LPS after a 4-hour starvation period, followed by collection of blood and cardiac tissue 4 h following LPS administration. Compared to controls, LPS induced significant hypoglycemia and hyperlactacidemia, suggesting the development of endotoxic shock. The result was a significant depression in total fatty acid levels as well as non-esterified fatty acid in the cardiac tissue of the LPS-treated pups. In addition, LPS-treated pups also showed a significant increase in TNF-alpha, NOS levels with a depressed redox state and energy metabolism in cardiac tissue. These observations suggest that endotoxic shock in 10-day-old rat pups induces a systemic inflammatory response with a depression in fatty acid metabolism that may contribute to myocardial failure.
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PMID:LPS-induced changes in myocardial markers in neonatal rats. 1459 43

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.
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PMID:The management of the diabetic patient with prior cardiovascular events. 1466 2

Heart failure affects nearly 5 million Americans and is associated with high morbidity and mortality rates. It is now recognized that activation of multiple neurohormonal systems is intrinsic in the pathophysiology of heart failure. Patients with diabetes mellitus are at high risk for heart failure, and some of the complications of diabetes (e.g., insulin resistance) contribute to the development and progression of heart failure, partly because of their effects on neurohormonal systems. Pharmacologic intervention directed toward these systems (i.e., angiotensin-converting enzyme [ACE] inhibition, use of aldosterone antagonists, and beta-adrenergic blockade) has been shown to decrease the morbidity and mortality associated with heart failure. Despite this knowledge, ACE inhibitors, aldosterone antagonists, and beta-blockers are grossly underused, and deaths and hospitalizations due to heart failure have steadily increased. Guidelines for the management of heart failure recommend the use of ACE inhibitors and beta-blockers in patients with mild, moderate, or severe disease. Aldosterone antagonists are recommended in severe heart failure, and recent data also support their use in mild to moderate heart failure. Concerns about the increased incidence of hypoglycemia, worsening dyslipidemia, and decreased insulin sensitivity with beta-blocker use may be preventing physicians from prescribing these agents for patients with diabetes with heart failure. Although evidence from earlier clinical trials justifies some of these concerns, newer vasodilating beta-blockers (e.g., carvedilol) have been shown to have a neutral or positive effect on dyslipidemia and insulin resistance. beta-Blockade in conjunction with ACE inhibition should be standard therapy for all patients with diabetes who have heart failure. Furthermore, early in-hospital initiation of neurohormonal intervention can provide earlier benefit to these patients.
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PMID:Managing the patient with diabetes mellitus and heart failure: issues and considerations. 1501 65

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

This analysis compares the safety and tolerability of pioglitazone (a thiazolidinedione), metformin (a biguanide), and gliclazide (a sulfonylurea). Data collected from four 1-year, double-blind studies comparing treatment of over 3700 patients with type 2 diabetes with pioglitazone, metformin, or gliclazide have been combined to provide comparative tolerability and safety profiles. All treatments were well tolerated with approximately 6% of patients withdrawing from treatment because of side-effects. The side-effects profile varied between treatments, with pioglitazone being associated with edema, metformin with gastrointestinal side-effects, and gliclazide with hypoglycemia. Cardiovascular outcome was similar with all treatments, with no excess reports of cardiac failure with pioglitazone treatment. Both pioglitazone and gliclazide resulted in mean weight gain, whilst with metformin there was mean weight loss. Mean liver enzyme values decreased with pioglitazone and to a lesser extent with metformin. With gliclazide, mean liver enzyme values increased. The expected small decreases in mean hemoglobin and hematocrit seen with pioglitazone also occurred with metformin and to a lesser degree with gliclazide. The results show that all three drugs are safe, but that tolerability profiles vary. Each treatment provides an alternative therapy for type 2 diabetes, dependent on the particular needs of individual patients.
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PMID:Safety and tolerability of pioglitazone, metformin, and gliclazide in the treatment of type 2 diabetes. 1600 75

The range of therapeutic modalities to treat type 2 diabetes mellitus has broadened in recent years. Biguanides and thiazolidinediones are the two currently available classes of anti-hyperglycemic agents with insulin-sensitizing properties. Thiazolidinediones, in particular, have received much attention, not only for the well documented hepatotoxicity of troglitazone that led to its removal from the market in 2000, but also for the emerging data that support the beneficial effects of the thiazolidinedione class of drugs on beta-cell rejuvenation and cardiovascular risk reduction. In the US, thiazolidinediones are indicated either as monotherapy or in combination with a sulfonylurea, metformin, or insulin in cases where diet, exercise, and a single drug fail. In contrast, the UK National Institute for Clinical Excellence included in its re-appraisal of 'glitazones' in August 2003 the continued exclusion from licensed use in the UK of combination therapy with thiazolidinediones and insulin. When added to insulin therapy, thiazolidinediones appear to effectively lower glucose levels and reduce insulin dosage in clinical trials involving individuals with poorly controlled type 2 diabetes. However, weight gain, hypoglycemia, and fluid retention pose problems in certain patients. The fluid retention may exacerbate or even precipitate congestive heart failure, which usually necessitates discontinuation of the drug. Risk stratification and careful management of patients at risk for heart failure, including those taking insulin concomitantly, allow healthcare providers to safely administer combination therapy with thiazolidinediones in patients with type 2 diabetes. Hepatic toxicity with currently available thiazolidinediones has been found to be minimal overall.
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PMID:Thiazolidinediones and insulin: rationale for use and role of combination therapy in type 2 diabetes mellitus. 1605 38

Diabetes mellitus is a chronic progressive disease that results in microvascular and macrovascular complications. Diabetes is a significant independent risk factor for heart failure, and there are a substantial number of patients with diabetes and heart failure. Neurohormonal activation plays an important pathophysiologic role in insulin resistance, diabetes, cardiovascular events, and progression of heart failure. Pharmacologic intervention in these neurohormonal systems (ie, angiotensin-converting enzyme [ACE] inhibition, aldosterone antagonism, and beta-adrenergic blockade) has been shown to decrease the morbidity and mortality of diabetes and of heart failure. Despite this knowledge, ACE inhibitors, aldosterone antagonists, and beta-blockers are grossly underutilized, and deaths and hospitalizations due to heart failure have steadily increased. Guidelines for the management of heart failure recommend the use of ACE inhibitors and beta-blockers in patients with mild, moderate, and severe heart failure with or without diabetes. Aldosterone antagonists are recommended in severe heart failure and recent data also support their use in mild to moderate heart failure. Concerns about increased incidence of hypoglycemia, worsening dyslipidemia, and decreased insulin sensitivity with beta-blockers may be preventing physicians from prescribing these agents for their patients with diabetes who have heart failure. Beta-blockade, in conjunction with ACE inhibition and aldosterone antagonism, should be standard therapy for all patients with diabetes and heart failure. Furthermore, every effort should be made to ensure that eligible patients are treated with these evidence-based, guideline-recommended, life-prolonging therapies.
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PMID:An approach to heart failure and diabetes mellitus. 1609 44

Although beta-adrenoceptor antagonists (beta-blockers) have effects on metabolism via their mechanism as blockers of adrenergic stimulation, most interest in the metabolic effects of beta-blockers is caused by their effect on glucose metabolism. Strict metabolic control and management of cardiovascular risk factors in patients with diabetes mellitus has proven to be of great importance in the improvement of prognosis. Beta-blockers are necessary tools for the treatment of heart failure and hypertension. The use of beta-blockers in patients with diabetes mellitus has been controversial because of fear of deterioration of metabolic control of glucose and lipids and blunting of the symptoms of hypoglycemia. Currently, it appears that there is a beneficial metabolic effect with the third-generation beta-blocker carvedilol. Comparisons have been made between the second-generation beta-blocker metoprolol and carvedilol, with a clear advantage for carvedilol in terms of metabolic control. In the GEMINI (Glycemic Effects in Diabetes Mellitus: Carvedilol-Metoprolol Comparison in Hypertensives) trial, a decrease of 9.1% (p = 0.004) in insulin resistance, compared with baseline values, was seen in patients treated with carvedilol, whereas no significant difference was seen in the group of patients treated with metoprolol. Additionally, an increase in glycosylated hemoglobin of 0.15% from baseline was seen in the metoprolol group (p < 0.001) compared with no significant change in the carvedilol group. These findings indicate that, as carvedilol exerts favorable effects on glucose metabolism compared with metoprolol, patients with diabetes mellitus could benefit from treatment with carvedilol rather than metoprolol. The mechanisms behind these findings are not yet fully understood. Several mechanisms have been suggested, and special interest has been paid to the investigation of the potential beneficial role of the beta2- and alpha1-adrenoceptor-blocking effects of carvedilol, along with its known antioxidant properties.
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PMID:Metabolic effects of beta-adrenoceptor antagonists with special emphasis on carvedilol. 1691 22


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