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

Chronic heart failure is one of the main causes of death in western countries. Despite state-of-the-art treatment including angiotensin-converting enzyme inhibitors, beta-blockers, and spironolactone, survival and relief from symptoms still are unacceptably poor in patients with chronic heart failure. The present article gives an overview of current limitations in the treatment of heart failure and points out possible treatment options in the future. It seems possible to reduce or at least delay progression of heart failure by adding drugs that interfere with novel pathophysiologic aspects in heart failure activation of the neuroendocrine system, including catecholamines, angiotensin II, cytokines, and endothelins, as well as alteration of calcium homeostasis and energy depletion.
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PMID:Current limitations in treatment of heart failure: new avenues and treatment options. 1184 68

Chronic heart failure is a common condition with a poor prognosis, usually associated with poor exercise tolerance and debilitating symptoms despite optimal modern therapy. Standard therapy includes diuretics, digoxin, angiotensin-converting enzyme inhibitors (ACEIs) and beta-blockers. Despite this, many patients remain symptomatic, and interest is high as to whether the angiotensin receptor blockers (ARBs) would offer further advantage to a patient already receiving quadruple therapy. In addition, some patients are intolerant of ACEIs, and for this group the ARBs seem a logical choice. This article reviews the evidence for the use of ARBs as a class in heart failure concentrating on clinical recommendations and clinical needs and evidence rather than purely on statistical issues of significance in trials. The trials to date have demonstrated clearly similar hemodynamic effects to those seen with ACEIs and variety of ancillary benefits such as improvements in endothelial function, anti-thrombotic effects, and effects on neurohormonal inhibition. There is consistent evidence of a preservation of exercise tolerance when patients with heart failure are crossed over from stable ACEI therapy, and when added to ACEIs exercise tolerance appears to increase with ARBs. In terms of major outcomes, the two largest trials, Elite-II and Val-Heft, demonstrate that angiotensin receptor blockers probably have a clinical role in improving mortality and morbidity as an alternative to ACEIs in those patients unable to tolerate these agents, which remain, however, the first choice in unselected patients with heart failure. There is a worrying suggestion of a negative interaction when ARBs are added to beta-blockers, which is a reason for caution in using the ARBs, not a reason not to use beta-blockers.
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PMID:Angiotensin type-1 receptor blockers in heart failure. 1200 79

Plasma aldosterone escape is found during long-term ACE inhibitor therapy of chronic heart failure. Evidence for aldosterone production in cardiovascular tissues raised the question of whether aldosterone escape occurs or not in these tissues. Rats with infarction-induced chronic heart failure were treated with enalapril (20 mg/kg/d) and losartan (15 mg/kg/d) for 20 weeks. Untreated chronic heart failure and sham-operated rats were used as positive and normal controls, respectively. Ex vivo mesenteric artery and heart perfusion, high performance liquid chromatography, and RIA for aldosterone were performed. Chronic heart failure due to myocardial infarction was associated with tissue-specific activation of cardiovascular aldosterone synthesis. In the mesenteric artery, enalapril significantly inhibited aldosterone production compared to untreated, chronic heart failure rats, and losartan lowered aldosterone production to that of sham rats. In myocardium, enalapril failed to significantly inhibit aldosterone production, and losartan significantly inhibited aldosterone production compared to untreated, chronic heart failure rats. These results provide the first evidence that long-term ACE inhibition therapy induces aldosterone escape in myocardium but not in mesenteric artery of chronic heart failure. The angiotensin II subtype 1 receptor blocker losartan tranquilized aldosterone levels in the cardiovascular tissues of chronic heart failure rats.
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PMID:Effects of long-term enalapril and losartan therapy of heart failure on cardiovascular aldosterone. 1203 45

Chronic heart failure is associated with pathophysiologic alterations in myocardial and vascular function. Accompanying these changes are increased oxidative stress and modulation of the nitric oxide pathway. The role of the nitric oxide(.) pathway in heart failure and the effect of its interaction with reactive oxygen species are complex, with diverse pathophysiologic implications in both the heart and the peripheral vasculature. This review discusses current information regarding the nitric oxide(.) pathway in heart failure and its relationship with increased oxidative stress.
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PMID:The nitric oxide pathway and oxidative stress in heart failure. 1204 82

Chronic heart failure is a complex clinical syndrome in which abnormal vascular endothelial function has been shown to occur at both the experimental and clinical levels. Alterations in endothelial function may contribute to the increased vasomotor tone and to the vascular remodeling process observed in patients with chronic heart failure. Reduced shear stress, increased activity of the various vasoconstricting neurohormonal systems, and increased levels of proinflammatory cytokines promote endothelial dysfunction in chronic heart failure. This article summarizes the major mechanisms implicated in the pathophysiology of abnormal endothelial function in chronic heart failure, as well as the novel therapeutic interventions aimed at reducing endothelial dysfunction in patients with the syndrome.
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PMID:Endothelial dysfunction in chronic heart failure: clinical and therapeutic implications. 1206 18

It is hypothesized that the moisture incorporated into canola meal (CM) during desolventization, as sparge steam, promotes toasting. Elimination of toasting of CM would result in higher digestible amino acid content, but it is not known if it is required to reduce anti-nutritional factors. Therefore, the objectives of this study were to determine if suspending the use of sparge steam would prevent toasting and to study the effects of toasting on broiler chicken performance. Conventional toasted CM (TCM) and a hexane laden, nontoasted CM (NTCM) were collected from a commercial crushing plant. NTCM was desolventized in a research desolventizer/toaster without the use of sparge steam, producing a yellow-colored meal. The meals were fed to broiler chickens from 0 to 39 d and replaced 0, 20, 40, 60, 80, and 100% of the soybean meal (SBM) in wheat-based diets. Elimination of toasting increased broiler weight from 0.606 and 2.148 to 0.618 and 2.181 kg at 19 and 39 d of age, respectively. The feed ratio (0 to 19 d) increased from 0.637 to 0.642, but toasting did not affect mortality. Total mortality and chronic heart failure between 19 and 39 d increased with level of CM addition from 5.2 to 13.9% and 1.9 to 9.6%, respectively. Chronic heart failure in males, but not females, was increased from 3.3 to 17.4% with increasing CM level. In conclusion, desolventization without sparge steam produced a nontoasted meal and improved broiler growth and feed efficiency in comparison to TCM. Therefore, NTCM could be fed to broiler chickens.
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PMID:The effects of toasting canola meal on body weight, feed conversion efficiency, and mortality in broiler chickens. 1207 49

The purpose of the work presented here was to investigate the responses mediated by alpha-adrenoceptors and also contractility of vascular smooth muscle in large peripheral vessels following doxorubicin (DXR)-induced heart failure. Cardiac failure was induced by DXR injection. Thirty saline-treated (normal group) and 30 DXR-treated rabbits (1 mg/kg administered intravenously twice weekly for 8 weeks) were studied. Chronic heart failure was confirmed by echocardiography and later also by histopathology. The DXR-treated hearts were subdivided by ejection fraction >40 or <40 into non-failing (control) and failing (test) groups. Animals were sacrificed by overdose with pentobarbitone sodium (i.v. injection). Arteries and veins were carefully removed with as little connective tissue as possible and placed in cold physiological salt solution. The arterial and venous rings were mounted in 10 ml isolated organ baths, maintained at 37 degrees C and gassed with 95% O(2) plus 5% CO(2). The rings were then placed under different resting tensions. After initial application of tension tissues were left to equilibrate for a 60-min period. Then all preparations were contracted with KCl (Krebs solution, Na free and high KCl, 125 mM) and allowed to contract for 5-10 min. Following complete washout with normal Krebs, an additional 30 min equilibration period was allowed. Then cumulative concentration-response curves to noradrenaline (NA) obtained by increasing the concentration of the agonist in half-log increments. In contraction responses to NA the renal artery and aorta were the most sensitive preparations (pD(2) values: 5.75 and 5.36, respectively). Compared with control, in DXR-treated rabbits, maximum response (E(max)) of NA was not modified in the aorta; renal and saphenous arteries, renal and saphenous veins, whereas it was significantly lower in the vena cava. Compared with control rabbits, in DXR-treated rabbits the pD(2) of NA was significantly increased in the thoracic aorta whereas there was no significant difference between groups in the other studied vessels. Contraction to KCl showed no significant difference between two groups. These results suggest that the sympathetic regulation of vascular contraction is impaired by DXR-induced heart failure through reduction in the alpha-adrenoceptors.
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PMID:Effects of noradrenaline and KCl on peripheral vessels in doxorubicin induced model of heart failure. 1210 Sep 71

Chronic heart failure is no longer a mere cardiac entity, but involves several, initially adaptive and later detrimental, neurohumoral compensatory mechanisms. Peripheral manifestations of the disease, such as endothelial dysfunction, skeletal muscle changes, and disturbances in ventilatory control, are major determinants of symptoms. The independent prognostic value and the relevance of cachexia on morbidity of patients with chronic heart failure have only recently been recognised. Altered body composition in heart failure patients is reflected in the early loss of muscle tissue but affects all tissue compartments in case of cardiac cachexia. Recently, a new portfolio of biologically active molecules, termed cytokines, have been shown to play an important role in the development and progression of both cardiac and peripheral abnormalities. Similar to other chronic illnesses, covered in the remainder of this issue, a low-grade chronic inflammatory process may be of particular relevance in the development of tissue wasting in these patients. Whereas the presence of immune activation in chronic heart failure is now widely accepted, as well as the prognostic relevance of chronic inflammation, the site and the source of cytokine production remain the object of intense research. Although the inciting event is located in the heart, cross-talk between the myocardium on the one hand, and the immune system, peripheral tissues and organs on the other hand, will lead to the overproduction of proinflammatory cytokines and, inevitably, to their detrimental effects. The specific problems related to heart failure progression and inflammatory activation are described in this review.
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PMID:Chronic heart failure: an example of a systemic chronic inflammatory disease resulting in cachexia. 1216 8

Chronic heart failure (CHF) impairs quality of life (QoL) much stronger than other chronic diseases. The objective of this evaluation was to assess the effect of a new integrated comprehensive outpatients rehabilitation program on somatic parameters and quality of life in 51 patients with stable CHF. After rehabilitation, left ventricular ejection fraction, NYHA class, and parameters of sub-maximum and maximum exercise capacity improved significantly between 11 and 20%, and 6-minute walking distance by 58% on average (p < 0.0001). Non-disease specific QoL (Short Form-36 questionnaire) improved in only 2 of 8 subscales (physical functioning [effect size 0.38, p < 0.001], and role functioning [effect size 0.17, p < 0.05]), and a mental component score [effect size 0.47, p < 0.0001]. Disease-specific QoL (Minnesota Living with Heart Failure questionnaire) improved in terms of sum score [effect size 0.24, p < 0.0001], and physical component score [effect size 0.35, p < 0.0001]. Improvement in exercise capacity correlated significantly with improvements in parameters of disease-specific QoL.
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PMID:[Stress tolerance and quality of life--effect of a comprehensive ambulatory rehabilitation program for patients with chronic heart failure]. 1236 20

Chronic heart failure is an enormous and growing public health problem and is reaching epidemic proportions. Its economic impact is dramatic; two thirds of expenses are for hospitalizations and relatively little is being spent for medications and outpatient visits. Most of the hospitalizations, deaths and costs are incurred by a relatively small minority of patients who may be described as having "complex", "advanced", "refractory" or "end-stage" heart failure; however, in essence they are patients who have severe symptoms and/or recurrent hospitalizations and/or emergency department visits despite maximal oral therapy. Many of the recommendations regarding the management of these patients are based more on experience than on evidence from controlled trials. This, because such patients require an individualized therapy which limits their inclusion in large trials and because support is less easily available when testing specific strategies than when testing specific agents. Improving the treatment of this group of patients by optimizing their medical regimen, aggressive monitoring and providing early intervention to avert heart failure can reduce their morbidity, mortality and costs of care. Refractory heart failure is not a single disease and it is extremely unlikely that all patients should be treated in a similar manner; before selecting the appropriate therapy, the clinician must categorize and profile the patient. The first step should be a re-evaluation of the previous treatment because many patients are treated suboptimally. It is also important to identify reversible or precipitating factors. For patients with advanced heart failure, the initial goal of therapy is to improve symptoms; the next goal is to maintain the improvement and to prevent later deterioration. The appropriate treatment plan will reflect the presence of comorbidities, the patients' history regarding previous responses to therapy, their own expectations with regard to daily life. The most common symptoms causing hospitalizations are those related to congestion; the distinction between the rising filling pressures and low cardiac output puts the focus on the adjustment of further medical therapy. The persistence of congestion confers a worse prognosis and urgency for the consideration of surgical therapies. It has been repeatedly shown that in case of heart failure, fewer hospitalizations and lower costs are necessary after referral to programs that provide multidisciplinary care. This care includes heart failure physician specialists with specifically trained clinical nurses. Other important components of a comprehensive management program for advanced heart failure are patient education, rehabilitation and the availability of adequate social service. We have entered a difficult era marked by a collision course between increasing scientific discoveries and restricted resources; a better care for heart failure, integrating improved medical practice with the necessity of bearing the financial pressures in mind, constitutes a great opportunity for medicine.
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PMID:[Refractory heart failure. Models of hospital, ambulatory, and home management]. 1240 39


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