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

Severe obesity with co-morbidity such as diabetes mellitus, cardiac failure, obesity hypoventilation, degenerative bone diseases and increased incidence of malignancy give rise to shorter life expectancy and have an impact on quality of life. This results in higher costs of health care and work absence. Surgical procedures have become commonplace in the therapy of morbid obesity because of the infrequent success of medical treatment. We performed a horizontal gastroplasty by laparoscopic adjustable silicon gastric banding (LASGB) on 60 patients between 1. 11. 1995 and 28. 2. 1997. The average excess above normal weight was 62 kg, the median BMI (Body-Mass-Index) was 46.44 kg/m2. Fifty-nine procedures were performed by the laparoscopic method and one with an open technique. The average postoperative hospital stay was five days. Due to dorsal slipping or pouch enlargement the procedure had to be repeated on 6 patients (10%). The median loss of weight in the first three months was 14.78 kg, after six months 24.14 kg and after nine months 35.1 kg. Insulin treatment for three patients suffering diabetes mellitus could be discontinued-in addition blood sugar levels in six patients normalised. Two patients with obstructive sleep-apnea syndrome no longer needed a nocturnal Nasal-Continuous-Positive-Airway-Pressure-(nCPAP-)Therapy. To provide a better quality of life to this group of patients, the gastric banding is a suitable method for carefully evaluated and followed patients. In addition improved ability to work and reduction of health care costs due to co-morbidity and joint diseases have a positive economic impact.
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PMID:[Surgical therapy of morbid obesity: indications, technique of laparoscopic gastric banding and initial results]. 941 44

Insulin-like growth factor I (IGF-I) enhances myofibrillar development in cardiomyocytes of rats in culture and in vivo. In addition, IGF-I has vasodilatory effects and improves cardiac function in healthy volunteers. This study was conducted to evaluate the acute hemodynamic effects of IGF-I in patients with chronic heart failure Eight patients with chronic heart failure were randomized to receive recombinant human IGF-I (60 micrograms/kg) or placebo, i.v., over 4 h in a cross-over, double blind study on 2 consecutive days. Electrocardiogram as well as systemic hemodynamics were continuously monitored over 7 h by flow-guided thermodilution and radial artery catheters. IGF-I was well tolerated by all patients, and no pathological changes on electrocardiogram were recorded. Compared with placebo, IGF-I increased the cardiac index by 27 +/- 3.7% (+/- SE; P < 0.0005) and the stroke volume index by 21 +/- 5.6% (P < 0.05), and decreased systemic vascular resistance by 28 +/- 4.4% (P < 0.0002), right atrial pressure by 33 +/- 9.0% (P < 0.003), and pulmonary artery wedge pressure by 25 +/- 6.1% (P < 0.03). Mean systemic and pulmonary artery pressure as well as heart rate and pulmonary vascular resistance were not significantly influenced by IGF-I treatment. Insulin and C peptide levels were decreased by IGF-I, whereas glucose and electrolyte levels remained unchanged. Urinary levels of norepinephrine decreased significantly (P < 0.05) during IGF-I infusion. Thus, acute administration of IGF-I in patients with chronic heart failure is safe and improves cardiac performance by afterload reduction and possibly by positive inotropic effects. Further investigations to establish whether the observed acute effects of IGF-I are maintained during chronic therapy appear to be warranted.
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PMID:Acute cardiovascular effects of insulin-like growth factor I in patients with chronic heart failure. 974 22

Hypertension is a very important cardiovascular risk factor and directly leads to major atherosclerotic cardiovascular diseases, including coronary artery disease, stroke cardiac failure and peripheral artery disease. Hypertension tends to cluster with other atherogenic risk factors like dyslipidemia, insulin resistance, obesity and others. The association between hypertension and dyslipidemia is very frequent and the risk is more than additive and its possible pathogenesis may be of a common mechanism. Insulin resistance is the main cause of both risk factors. Endothelium dysfunction is present in arterial hypertension and dyslipidemia and the pathogenesis of atherosclerosis. The treatment of hypertensive patients must be individualized to accommodate both the concomitant dyslipidemia and other atherogenic factors.
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PMID:[Hypertension and dyslipidemia]. 988 66

Long-lasting problem on the differentiation of adenohypophyseal cell, which prepares them for their specific tasks (somatotropic, lactotropic ect.), becomes elucidated after recognition of the differentiational effect of transcription factor Pit-1. Expression of that factor in somatotrops results in STH secretion, contrary to lactotrops producing prolactin. Subclinical hypothyreosis (increased TSH with normal T3 and T4) endangers vessel not because of hypercholesterolemia, but because of changes in the dynamics of the blood flow. The idea of cardiotropic effect of thyroidal hormones is supported by the finding that administration of trijodthyronine to children after the surgical correction of heart malformations (cardiopulmonary bypass) improves myocardial function--it elevates cardiac output and decreases requirements on the intensive care. Receptors for hormones in tissues are flexible, they can be "heterooligomers" for dopamine and somatostatin. Mutations of mineralocorticoid receptor may cause hypertension in pregnancy and progesterone receptors have several isoforms. Receptors can be also activated by short exposition to a hormone. Glucocorticoids have probably also membrane receptors. Diabetes mellitus "type I" needn't to be immunogenic and DM type II not only results from down-regulation of receptors and subsequent insulin resistance, but it can be also caused by defects in insulin secretion. Insulin has receptors in the brain and participates in the appetite regulation. The attempt to use "desensibilisation" by peroraly administered insulin in patients with immunogenic DM had no effect. Stress affects memory mechanisms, heavy emotional stress during gravidity can bring congenital malformations. The decrease of mental functions in aged women depends on the level of free estradiol (the fraction, which is not bound to plasma proteins). Activation of dopaminergic neurons can be achieved by neurotropic growth factors. Nesiritide is a recombinant brain natriuretic hormone successfully tested in heart failure. The role of leptin in the appetite regulation in man is still not clear, other signalling molecules may have also an effect, e.g., ghrelin, which primarily stimulates STH secretion and brings about weight gain. Sildenafil influences nitrergic neurons elsewhere than in penis, for example it has positive effects in patients with oesophageal achalasia.
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PMID:[Endocrinology 1999-2000]. 1128 21

Insulin resistance is an important risk factor for the development of hypertension, atherosclerotic heart disease, left ventricular hypertrophy and dysfunction, and heart failure. It reflects a disturbance of glucose metabolism and potentially worsens metabolic efficiency of both skeletal muscle and cardiac muscle. The exact mechanisms of insulin resistance are not known, but the finding of significant insulin resistance occurring as a consequence of heart failure raises interesting possibilities as to its pathogenesis. While sympathetic nervous system overactivity can acutely reduce insulin sensitivity, it is not clear to what extent, in stable optimally treated chronic heart failure (CHF), the neurohormonal overactivity of this syndrome is the major cause of insulin resistance. Other potential mechanisms include the loss of skeletal muscle bulk, impaired endothelial function and reduced skeletal muscle blood flow, and a possible direct action of proinflammatory cytokines such as tumour necrosis factor-alpha. The consequences of insulin resistance in heart failure are not known, but the severity of the abnormality appears to parallel symptomatics and exercise limitation in this condition, and, in particular, be related to the impairment of gross skeletal muscle function. While specific therapies to correct insulin resistance in CHF have not been evaluated, there are several exciting possibilities on the horizon. Several nonpharmacological therapies have been shown to increase insulin sensitivity in patients with normal left ventricular function, and if these benefits could be duplicated in CHF, they may offer symptomatic benefit. These include weight reduction in the obese, regular exercise training and the use of dietary manipulation such as low-fat, high-fibre diets. Drug treatments with positive effects on insulin sensitivity include some angiotensin converting enzyme-inhibitors as well as newer drug groups, such as the glitazones and moxonidine, a centrally active agent with effects on the recently described imidazoline I-1 receptor that inhibits central sympathetic tone. The role of these agents in reversing the insulin resistance of chronic heart failure warrants further investigation.
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PMID:Insulin resistance in chronic heart failure. 1134 20

The leading cause of death among patients with diabetes is cardiovascular disease with approximately 80% of all deaths being attributed to coronary heart disease. Acute myocardial infarctions (AMIs) in patients with diabetes are associated with an increased rate of reinfarction than those without diabetes. Following AMI, patients with diabetes are more likely to develop severe heart failure. The Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) clinical trial examined the relationship between intensive insulin and conventional therapy following AMI. Results of the DIGAMI study clearly identify the need for tight glucose control following AMI in improving clinical outcomes and mortality.
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PMID:Glycemic control and heart disease. 1138 66

Insulin resistance and hyperinsulinemia have been observed in over 70% of the nonobese, nondiabetic subjects with essential hypertension (HT). Alpha-1 blockers, ACE-antagonists, long-acting Ca blockers including nifedipine CR, some form of beta-blockers, tilisolor, which is reported to increase blood flow, improve insulin sensitivity when blood pressure is better controlled. Decrease of serum potassium during insulin sensitivity test and intraplatelet free Ca2+ concentration is positively and negatively correlated with insulin sensitivity, respectively. Blood pressure is correlated with insulin resistance, which is also observed in secondary HT. The resistance is correlated with salt sensitivity as well as impaired nocturnal fall of blood pressure. These suggest the possible association of insulin resistance with altered intracellular cation metabolism. Insulin resistance and associated hyperinsulinemia have been observed in effort as well as vasospastic angina pectoris (VSAP), atherothrombotic cerebral infarction, and in ASO without obesity, HT, or diabetes, suggesting the resistance resulting from endothelial dysfunction. Insulin resistance has been observed in heart failure and is correlated with angiotensin II. Resistance is also observed in hypertrophic cardiomyopathy and is partially correlated with TNF-alpha. These results indicate that insulin resistance seem to be multifactorial. An effort to normalize insulin sensitivity is crucial to eliminate multiple risk factors as well as to prevent the progression of atherosclerotic vascular lesions.
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PMID:Multifactorial insulin resistance and clinical impact in hypertension and cardiovascular diseases. 1187 61

In the past decade, expected in-hospital length of stay (LOS) after carotid endarterectomy (CEA) has decreased from 4 days to 1. Long LOS is associated with known complications and factors affecting severity of the patient's condition. Factors affecting an intermediate stay of 2 to 4 days need further clarification. The vascular registry at Jobst Vascular Center includes data on manifestation of disease; cardiovascular history; operation and discharge dates; surgeon; surgical details such as patching, shunting, and completion arteriography; and complications. Univariate chi-square and ANOVA and multivariate logistic regression were applied to analyze 635 CEAs performed in 1998, 1999, and 2000. Statistical significance was at a p value less than 0.05 (two-sided). Overall morbidity rate was 8.2% with three (0.5%) in-hospital neurologic complications and one death for a 0.16% mortality rate. Fifty-eight percent of the patients were discharged in 1 day. Patients staying 1 day were 3 years younger. Female gender and prior cerebrovascular accident were factors extending LOS to 2 and 3 days. History of angina, heart failure, valve disease, and vein patch or no patch contributed to LOS of 3 or 4 days. Completion arteriography had an association with LOS of 2 days. The relative percentage of patients with complications increased with LOS. No significant relationship was found for symptoms, smoking, myocardial infarction, atrial fibrillation, cardiac revascularization, or surgeon. Insulin-treated diabetes mellitus, cardiac risk factors, cerebrovascular accident, and vein patch or no patch correlated with prolonged hospitalization. Factors were identified that may alter a clinical pathway designed for discharge 1 day after CEA. Focused management of patients with cardiac and cerebrovascular accident history or requiring vein patch and a better understanding of CEA in women may further increase the percentage of patients discharged 1 day after CEA.
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PMID:Factors related to short length of stay after carotid endarterectomy. 1247 32

We investigated whether insulin resistance in patients with chronic heart failure (CHF) is associated with impaired insulin signalling in skeletal muscle and whether exercise training would lead to an improvement in insulin signalling, concomitant with enhanced insulin action. Fourteen men with CHF due to idiopathic dilated cardiomyopathy, with mild-to-moderate limitation of physical activity and a left-ventricular ejection fraction of less than 45 %, were studied before and after either a 5 month exercise training programme (n = 7) or standard care (n = 7). Seven healthy men participated as controls. Whole-body insulin-stimulated glucose uptake was determined by the euglycaemic hyperinsulinaemic clamp technique and skeletal muscle biopsy samples were obtained before and after the insulin infusion for insulin signalling measurements. Insulin-stimulated glucose uptake was 20 % lower in CHF patients versus healthy subjects. Physiological hyperinsulinaemia increased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 by approximately 2.5-fold, IRS-1-associated phosphatidylinositol 3-kinase (PI-3-kinase) activity by approximately 2-fold and Akt (protein kinase B) phosphorylation by approximately 3-fold, with similar responses between healthy subjects and CHF patients. Insulin-mediated glucose uptake was not altered in patients after standard care, whereas exercise training elicited a 25 % increase in glucose uptake. Neither standard care nor exercise training altered insulin-stimulated tyrosine phosphorylation of IRS-1, IRS-1-associated PI-3-kinase activity or Akt phosphorylation. In conclusion, the CHF patients demonstrated impaired insulin-stimulated glucose uptake, despite normal signal transduction in skeletal muscle at the level of IRS-1, PI-3-kinase and Akt. Of clinical relevance is the finding that exercise training improves glucose uptake. However, these changes in insulin action after exercise training appear to be independent of enhanced insulin signalling at the level of IRS-1, PI-3-kinase or Akt.
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PMID:Insulin signalling and resistance in patients with chronic heart failure. 1274 Apr 26

Insulin is a hormone that possesses several therapeutic properties, some of which are only partially known and not definitely appreciated. Insulin appears to be an attractive therapeutic tool in several cardiovascular diseases and particularly in chronic heart failure (CHF). Insulin, in fact, exerts a direct effect on biological properties of myocytes by increasing the transmembrane glucose transport through glucose-specific insulin-regulated receptors, whose gene expression is down-regulated since the initial stages of myocyte hypertrophy. In addition, a hormonal antiapoptotic molecular effect has also been reported. These effects explain, at least in part, the observed improvement in ejection fraction and cardiac output in CHF patients when given insulin. Vasodilation is the most remarkable peripheral effect of insulin that seems to be due to a direct activity on vascular smooth muscle cells and, more remarkably, on an increased release of endothelium-derived relaxing factors, such as nitric oxide and vasodilator prostaglandins. In accordance with most recent clinical observations, this endothelial modulatory activity is not limited to the systemic circulation but involves also the pulmonary one and the alveolar-capillary interface, resulting in a facilitation of the alveolar gas diffusion. Such an effect on alveolar gas diffusion appears to play a major role in CHF patients. The present review focuses on the pathophysiological mechanisms underlying the insulin benefits, and emphasizes the hormone therapeutic applicability in a CHF setting.
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PMID:[Cardiocirculatory effects of insulin in patients with heart failure]. 1284 74


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