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

In many forms of cardiomyopathic left ventricular (LV) dysfunction, there is a rapid myocardial expression of pro-inflammatory cytokines such as interleukin 1, interleukin 6 and tumour necrosis factor-alpha (TNF-alpha) which mediate, via specific receptors, various processes such as gene expression, cell growth or apoptosis. In the initial stages of myocarditis, the myocardial expression of proinflammatory cytokines appears to be part of an inflammatory process. In many other conditions such as ischaemic cardiomyopathy and chronic LV pressure or volume overload, myocardial expression of proinflammatory cytokines is triggered by an elevation of LV wall stress. Myocardial expression of cytokines contributes to depression of contractile performance and adverse LV remodelling. Cytokine-induced depression of contractile performance appears to result from sphingosine production, which interferes with myocardial calcium handling. In transgenic mice, the rate of progression of LV dilatation appears to correlate with the intensity of myocardial TNF-alpha overexpression. In heart failure patients, cytokine concentrations are elevated not only in the myocardium but also in plasma. Cytokines are, therefore, responsible not only for autocrine and paracrine signalling within the myocardium but also for endocrine signalling throughout the body, especially affecting striated muscle mass with induction of muscle wasting and cachexia. The source of cytokine production in heart failure remains uncertain and several mechanisms have been proposed including endotoxin-induced immune activation due to bowel oedema, myocardial production due to haemodynamic overload and peripheral extramyocardial production due to tissue hypoperfusion and hypoxia. The latter seems to be the most likely mechanism, possibly modulated by the presence of bacterial endotoxins released from the gut. Numerous drugs have meanwhile been shown to influence this cardioinflammatory response to heart failure either by reducing basal levels of cytokines (e.g. amlodipine, pentoxifylline, beta-blockers) or by reducing endotoxin-induced cytokine gene expression (e.g. ouabain, amiodarone, adenosine, angiotensin converting enzyme inhibitors, angiotensin II-receptor blockers). Direct blockade of the deleterious actions of elevated plasma levels of cytokines recently became possible through intravenous infusion of a soluble TNF-alpha receptor fusion protein, which resulted in an increase in exercise tolerance and LV performance.
Heart Fail Monit 2000
PMID:Cytokines and heart failure. 1263 74

Heart failure is an important public health problem and one for which morbidity and mortality remain high despite treatment with angiotensin converting enzyme (ACE) inhibitors. A large number of clinical trials examining the effects of beta-blockers in the treatment of heart failure have now been performed. Two large-scale clinical trials have recently confirmed significant survival benefits with these agents, with effects that are additive to those achieved with ACE inhibitor therapy. These trials have now established beta-blocker therapy as an important part of standard heart failure treatment. The clinical use of beta-blockers in patients with heart failure requires careful translation of the randomized controlled trials into everyday clinical practice. Patient selection is key to the safe use of beta-blockers. Patients who may be suitable for beta-blockade therapy include those with mild-moderate heart failure due to left ventricular systolic impairment, those who are receiving adequate dose of diuretics and ACE inhibitors and those whose clinical condition is stable at the time of initiation of the beta-blocker. Survival benefits have been demonstrated with bisoprolol, carvedilol and metoprolol. Whether different beta-blockers have important clinical differences with regard to clinical end-points is as yet uncertain. beta-Blockers should be initiated at low dose, with titration of dose over several weeks and careful clinical monitoring for potential adverse effects, such as hypotension or worsening congestion. This careful application of the clinical trials into clinical practice will allow the safe use of this effective treatment for patients with chronic heart failure.
Heart Fail Monit 2000
PMID:beta-Blocker therapy in heart failure. 1263 75

There is now conclusive evidence that most patients with heart failure due to left ventricular systolic dysfunction should be treated with angiotensin converting enzyme (ACE) inhibitors and beta-blockers. They will also need diuretics for the control of fluid retention. There is also a powerful case for adding spironolactone to the treatment of patients with more severe symptoms. Many doctors would also use digoxin and, especially if coronary disease is present, aspirin or warfarin. Most patients also have other chronic diseases, such as diabetes, arthritis, depression and dyspepsia, and each of these may provoke the prescription of yet another agent. Many patients will receive prescriptions to treat the side-effects of their therapy. Finding a sure path through the morass of pharmacotherapy is a daunting task. Polypharmacy is having a negative impact on new drug research in an area where there are in fact remarkably few really effective treatments and the therapeutic problem is only partially solved. This paper discusses some of the issues surrounding polypharmacy in heart failure and how to resolve them, using an illustrative case history. It highlights the potential benefits of polypharmacy with effective drugs and the gross over-use of ineffective treatments in heart failure. The major problem with polypharmacy in heart failure is not the heart failure treatment itself, but the drugs for other concomitant conditions, the effectiveness of which is often not supported by an appropriate evidence base and for which alternative, less noxious management strategies often exist. Polypharmacy may be deleterious not only because of the increased potential for side-effects and drug interactions but also because taking unnecessary therapy reduces compliance with effective drugs.
Heart Fail Monit 2000
PMID:Polypharmacy (or polytherapy) in the treatment of heart failure. 1263 76

There are a number of theoretical reasons as to why 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) should be prescribed to patients with chronic heart failure (CHF). These agents are proven to prevent coronary heart disease, the major etiological factor in the development of CHF. Potential additional effects of these agents include inhibition of proinflammatory cytokine activity and other potential beneficial effects on cardiac remodeling. However, there are also possible adverse effects of this strategy, supported by the overriding observation that low plasma lipid levels portend a poorer prognosis in patients with established CHF. Potential mechanisms by which statins may directly confer adverse effects include a reduction in levels of the antioxidant ubiquinone and an increase in blood endotoxin levels, both of which may contribute to CHF disease progression. Given these uncertainties, an answer to the question of whether or not therapy for CHF should include statins requires a definitive clinical trial. The importance of such a trial is further highlighted by the already commonplace usage of statins amongst patients with CHF.
Heart Fail Monit 2003
PMID:Should patients with chronic heart failure be treated with "statins"? 1263 77

Heart failure (HF) is a growing epidemic that not only exerts an enormous burden on the healthcare system but also imparts extremely poor quality of life in the increasing number of patients dying from this fatal syndrome. For the majority of these patients, end-of-life care is clearly suboptimal. It is within this context that this article reviews the case for comparing the prognosis of HF with that of the most common types of cancer. It also summarizes the numerous difficulties in trying to make such comparisons and highlights key comparative data--the majority of which indicate that the prognosis of HF is comparable with that of cancer. Finally, it discusses how these comparisons can highlight the need to extend the type of public health response to HF usually reserved for high profile disease states, such as cancer.
Heart Fail Monit 2003
PMID:Prognosis of patients with heart failure compared with common types of cancer. 1263 78

Over 4.7 million Americans have heart failure, and 50000 new cases of heart failure are diagnosed every year. In addition, a significant proportion of the population may have asymptomatic left ventricular (LV) systolic dysfunction. Population studies estimate that the prevalence of asymptomatic LV dysfunction ranges from 0.9-5.9%. Of these, a substantial number will eventually develop symptomatic heart failure. Diagnosing and treating these patients before they develop symptoms may help to delay or prevent the development of symptomatic heart failure. This review highlights the currently available data on the epidemiology, pathophysiology, diagnosis, and treatment of asymptomatic LV systolic dysfunction.
Heart Fail Monit 2002
PMID:Asymptomatic left ventricular dysfunction: an overlooked part of the continuum of heart failure. 1263 79

It is well known that both atrial and ventricular arrhythmias play a key role in morbidity and overall mortality among patients with heart failure. In addition to pharmacological treatment, up-to-date and evidence-based use of invasive electrophysiology, including implantable cardioverter defibrillator implantation, is recommended in the global management of patients with heart failure. This article will review current clinical indications for invasive electrophysiology, either acknowledged or under evaluation, focusing on the scientific background and some technical and practical aspects. The discussion is organized in an arrhythmia-based manner so that ventricular-, atrial-, and heart transplant-related arrhythmias will be discussed separately.
Heart Fail Monit 2002
PMID:The role of invasive electrophysiology in the management of patients with chronic heart failure. 1263 80

Experimental and clinical studies have recently demonstrated that the growth hormone-insulin-like growth factor-I (GH-IGF-I) system is involved in the regulation of cardiac structure and function. Patients with acromegaly have an increased propensity of developing cardiovascular complications, such as ventricular hypertrophy with interstitial fibrosis. Conversely, patients with GH deficiency can exhibit ventricular dysfunction, increased vascular thickness, and an increased number of atheromatous plaques. In both groups of patients these abnormalities may be partially reverted by normalizing GH-IGF-I levels. In experimental or human chronic heart failure (CHF), GH administration increases ventricular mass and cardiac performance and reduces pulmonary vascular resistance. The mechanism by which this occurs is still unclear, but seems to involve calcium channels and non-endothelium-mediated vasodilatation. Randomized trials studying CHF patients contradict these results, highlighting that, in patients with heart failure, the response to GH therapy appears to be variable, and is probably influenced either by acquired GH resistance or by baseline levels of hormones. Due to the small number of patients examined to date, larger, randomized, controlled studies are needed.
Heart Fail Monit 2002
PMID:Does growth hormone play a role in chronic heart failure? 1263 81

Chronic heart failure (CHF) is associated with an increase in the production and secretion of various regulatory hormones that are initially beneficial, but become deleterious when elevated for prolonged periods. The neurohumoral excitation that occurs in the CHF state is mediated, in part, by abnormal inhibitory cardiovascular reflexes, such as the arterial baroreflex and the cardiopulmonary reflex. In addition, two sympatho-excitatory reflexes have been shown to be enhanced in CHF: the arterial chemoreflex and the cardiac sympathetic afferent reflex. While these reflexes may play a role in the sympatho-excitation of the CHF state, there is an important central modulation of sympathetic outflow by a variety of hormones that are elevated in CHF and have been shown to have neural effects. These include angiotensin II (Ang II), nitric oxide (NO), and endothelin-1. In fact, experimental animal data suggest that a central reciprocal relationship exists between Ang II and NO in their ability to modulate sympathetic outflow. These substances may also participate in the beneficial effects of exercise training in the CHF state. Exercise training lowers sympathetic nerve activity and plasma Ang II, and enhances arterial baroreflex function. This review emphasizes the neurohormonal and reflex regulation of sympathetic outflow in heart failure. While abnormal reflex regulation may predict a poor outcome, new treatment options may emerge from a better understanding of reflex regulation in CHF.
Heart Fail Monit 2002
PMID:Novel mechanisms of sympatho-excitation in chronic heart failure. 1263 82

Heart failure (HF) is an important cause of morbidity and mortality. Obesity is an increasingly prevalent condition that has been associated with increased cardiovascular risk, including increased risk of developing HF. Based on the associations of obesity with cardiac structural and hemodynamic alterations, as well as case reports of reversal of cardiomyopathy with weight loss, obesity has been presumed to have a deleterious effect in patients with HF. However, several recent studies have shown that in patients with established HF, obesity is not associated with increased mortality, but rather is associated with improved survival. Potential mechanisms for cardioprotection in obesity include a diminished activation of the neurohumoral system, an enhanced protection against endotoxin/inflammatory cytokines, and an increased nutritional and metabolic reserve. Further investigations into the relationship between obesity and the progression of HF are necessary. Ultimately, clinical trials are needed to provide definitive guidance to the management of obese and overweight HF patients.
Heart Fail Monit 2002
PMID:The impact of obesity on survival in patients with heart failure. 1263 83


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