UMLS:C0018801 - FACTA Search

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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 a common clinical syndrome that may have different causes. Its incidence and prevalence are predicted to rise substantially over the next 10 years. There are therefore major consequences for resource provision, especially in primary care, where most patients are managed. Chronic heart failure is a serious condition with high morbidity and mortality. There is good evidence to show that treatment with angiotensin-converting enzyme (ACE) inhibitors in patients with left ventricular systolic dysfunction improves symptoms and signs, slows progression of heart failure, reduces hospitalisation rates, and improves survival. Despite this evidence, primary care studies show that patients with heart failure are incorrectly diagnosed and inadequately treated. Most patients present in general practice, and because effective treatment relies on a correct diagnosis, this is a key step in the appropriate management of heart failure. The aim of this paper is to review the evidence about the usefulness of signs, symptoms, and investigations in diagnosing heart failure in primary care. To identify relevant studies for this review, four strategies were used: a MEDLINE search from 1993 to January 1998 using the diagnosis search filter; a MEDLINE search from 1993 to January 1998 using the guideline search filter to locate published heart failure guidelines; a search for review articles in the Cochrane Library; and a check of references in the studies identified. The search terms included MeSH terms and the keywords 'heart failure' and 'diagnosis'. All searches were limited to humans and English language articles. Studies were included in this review on the basis of quality and relevance to primary care. The review shows that symptoms and signs are important because they alert clinicians to the possibility of heart failure as a diagnosis. However, they are not sufficiently specific for confirming left ventricular systolic dysfunction. From the evidence available, a patient with suspected heart failure must have objective tests to confirm the diagnosis. These should include an electrocardiogram and, ideally, an echocardiogram. Further research is also needed on the usefulness of signs and symptoms in primary care, as most studies of heart failure have been conducted in secondary care.
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PMID:Diagnosis of patients with chronic heart failure in primary care: usefulness of history, examination, and investigations. 1069 70

Chronic heart failure is associated with multiple pathophysiological alterations and adaptations, such as marked anatomic and biochemical changes of the myocardium, left ventricular dysfunction and dilatation, increased systemic vascular resistance, and activation of neurohumoral and cytokine systems. The use of animal models has provided a new insight into the complex pathogenesis of this syndrome and supplemented clinical experience. However, all of the animal models used have advantages and limitations, and the transfer from experimental to human heart failure needs critical evaluation. The current review will focus upon new aspects of rat and rabbit models of heart failure.
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PMID:Animal models of chronic heart failure. 1081 29

The heart is often refereed to as an "beta-adrenergic organ" because beta-adrenergic agonists are powerful stimulants of cardiac contractility. Catecholamines acting through beta-adrenoceptors produce both positive inotropic and chronotropic effects in human heart. It is now generally accepted that in human heart both beta 1- and beta 2-adrenoceptors coexist. beta-Adrenergic transduction system consist of membrane-bound beta-receptors, the effector enzyme adenylyl cyclase and guanine nucleotide-binding transduction (G) proteins. Repeated long-lasting agonist stimulus evokes homologous or heterologous desensitization of transduction system. Chronic heart failure accompanies with decreased responsiveness to beta-adrenoceptor agonists and is thought to exacerbate the loss of cardiac contractility. Depending on the etiology of heart failure abnormalities of the beta-receptor-G protein-adenylyl cyclase system result from a reduced of beta 1-receptors, uncoupling of beta 1- or beta 2-receptors, alteration of G-protein function, or decreased catalytic subunit activity of adenylyl cyclase and enhanced expression of beta-adrenoceptor kinase. The model most widely used is that of circulating lymphocytes that contain a homogeneous population of beta 2-adrenoceptors. The biochemical and pharmacological properties of human lymphocyte beta 2-adrenoceptors are quite comparable to those of heart beta 2-receptors. The analysis of lymphocyte beta 2-adrenoceptor-adenylyl cyclase system can be used as a model for long-term regulation of human cardiac beta 1- and beta 2-adrenoceptors only if serial changes in response to administration of non-selective beta-adrenergic agonists or antagonists are being investigated. This review concentrates on beta-adrenoceptors in human healthy heart and in heart failure and also on lymphocyte beta 2-adrenoceptors and on the changes of these receptors properties under the influence of some cardiotropic drugs.
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PMID:[Beta-adrenergic receptors of the normal heart and in heart failure]. 1082 33

Chronic heart failure (CHF) is a highly prevalent condition associated with serious morbidity, intense levels of health services use, and shortened survival. It is also a condition for which ameliorative therapies exist. The evidence indicates that there is substantial need to change clinical practice and health care delivery for people with CHF and thereby improve their outcomes. The goal of the Veterans Affairs (VA) Quality Enhancement Research Initiative in CHF (CHF QUERI) is to create measurable, rapid, and sustainable improvements in quality of care and health outcomes of veterans with heart failure. This article describes the current state of knowledge and practice in care for people with CHF. Using the framework of the 5 steps of the QUERI process, we point out the gaps in research and practice that must be filled if the CHF QUERI is to achieve its goal. We relate our recommendations for how the VA can put its research and administrative infrastructure to work to fill the gaps. Lessons learned about CHF in the course of the CHF QUERI will be applicable to all people with heart failure and to all health care systems--VA as well as non-VA--that care for them.
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PMID:Veterans Affairs Quality Enhancement Research Initiative in chronic heart failure. 1084 68

Chronic heart failure (CHF) is associated with activation of the sympathetic nervous system. This activation provides short term haemodynamic support to the failing myocardium, but may be deleterious over longer periods as chronic catecholamine excess appears to contribute to disease progression and increased mortality in this condition. Therefore, blockade of sympathetic activation represents a logical, if somewhat counter-intuitive, approach to the management of the patient with systolic CHF. Pharmacological approaches to blockade of this system include inhibition of central sympathetic outflow (using central sympatholytics, e.g. rilmenidine, moxonidine), blockade of the catecholamine biosynthetic pathway (dopamine beta hydroxylase antagonists) and blockade of the cardiac effects of sympathetic activation (beta-adrenoceptor blocking agents). Beta-blockers have now been extensively studied in patients with symptomatic CHF of the New York Heart Association (NYHA) Class II and III severity. Provided beta-blocker therapy is carefully up-titrated from sub-therapeutic doses and given for at least three to four months, these agents have been associated with favourable long term haemodynamic, functional and mortality outcomes. Furthermore, beta-blockers delay disease progression in CHF by reversing the pathological myocardial remodelling process that accompanies the disease. Non-selective beta-adrenoceptor blocking drugs appear to be of particular benefit in CHF therapy. Myocardial beta2 receptors are down-regulated to a lesser extent than beta1 receptors in CHF, therefore blockade of the beta2 receptor sub-type may assume greater importance in inhibiting the deleterious effects of sympathetic activation on the myocardium in this disease. Newer agents that possess additional vasodilator properties (carvedilol, bucindolol, nebivolol) may be useful in overcoming the initial negative inotropy of the beta-blocking component of the drug, however, it is unlikely that vasodilation contributes greatly to long term clinical benefits. Drugs such as carvedilol are also anti-oxidant, anti-proliferative and have anti-endothelin actions; the clinical significance of these properties is yet to be determined. Unanswered questions remain regarding the use of beta-blockers in heart failure. Ongoing studies are further examining mechanisms underlying the clinical benefits of these agents as well as their therapeutic potential in NYHA Class IV patients, heart failure post-myocardial infarction and patients with asymptomatic left ventricular dysfunction.
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PMID:Sympathetic activation and the role of beta-blockers in chronic heart failure. 1086 14

Chronic heart failure patients often experience significant functional impairments. A better understanding of the biopsychosocial correlates of functional status may lead to interventions that improve quality of life in this population. Social isolation, mood disturbance, low socioeconomic status, and non-White ethnicity were evaluated as possible correlates of impaired functional status in 2,992 U.S. patients with left ventricular ejection fractions (LVEFs) </= 35%. Even after controlling for age and clinical characteristics, all of the psychosocial variables examined were significant predictors of risk for experiencing severe limitations in intermediate and social activities of daily living at 1 year, with adjusted odds ratios in the 1.5-2.0 range. The ability of psychosocial characteristics to predict future functional status was also independent of baseline functional status, comorbid medical conditions, and deterioration in heart failure signs and symptoms over the intervening year. These results suggest that psychosocial factors influence patient functional status even in the later phases of cardiac disease.
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PMID:Psychosocial factors as predictors of functional status at 1 year in patients with left ventricular dysfunction. 1094 Sep 54

Chronic heart failure is an increasing cause of hospital admission in the Netherlands and Belgium. Despite numerous medical treatment modalities, the mortality remains high. Recent placebo-controlled randomized studies suggest that the addition of beta-blockers in stabilized, optimally pretreated patients with chronic heart failure using angiotensin converting enzyme (ACE) inhibitors, diuretics and digitalis, is accompanied by an additional absolute decrease in mortality by about 5% and a relative decrease in mortality by about 35%. Also the number hospitalization frequency decreases. Initially, the beneficial effects of beta-blockers on symptoms are only minor or absent. During the initiation period some clinical deterioration may occur which has to be treated accordingly; these patients are, however, difficult to identify. Initiation has to be done using low doses and should be restricted to stabilized, optimally treated patients. Doses should only be increased every 2 to 4 weeks until target doses are reached. These findings must not be extrapolated automatically to all cases of heart failure, since patients in the trials may differ considerably from those encountered in general practice.
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PMID:[Addition of beta blockers in chronic heart failure]. 1114 1

Chronic heart failure is a multi-etiological cardiovascular disorder with high prevalence and poor prognosis. Medical treatment of dilated cardiomyopathy is aimed at alleviating heart failure symptoms. Diuretics, angiotensin-converting enzyme (ACE) inhibitors and very recently, beta-blockers have been shown to have favorable effects on symptoms, exercise capacity and mortality. Growth hormone (GH) and insulin-like growth factor (IGF)-1 are involved in several physiological processes such as the control of muscle mass and function, body composition and regulation of nutrient metabolism. The role of GH and IGF-1 as modulators of myocardial structure and function is well established. Receptors for both GH and IGF-1 are expressed by cardiac myocytes; therefore, GH may act directly on the heart or via the induction of local or systemic IGF-1, while IGF-1 may act by endocrine, paracrine or autocrine mechanisms. Patients with acromegaly have an increased propensity to develop ventricular hypertrophy and cardiovascular diseases; impaired cardiac efficiency can also be observed in patients with GH deficiency. Animal models of pressure and volume overload have demonstrated up-regulation of cardiac IGF-1 production and expression of GH and IGF-1 receptors, implying that the local regulation of these factors is influenced by hemodynamic changes. Moreover, experimental studies suggest that GH and IGF-1 have stimulatory effects on myocardial contractility, possibly mediated by changes in intracellular calcium handling. Heart failure is due to ventricular dilation with inadequate wall thickening that leads to impaired cardiac performance; therefore, based on previous evidence we would expect beneficial effects from the use of GH in these patients. Several papers have highlighted the positive influence of GH in the regulation of heart development and performance. In patients with GH deficiency, GH administration dramatically improves cardiac function. In small open studies, acute and chronic GH treatment has demonstrated beneficial effects in patients with heart failure due to ischemic or idiopathic cardiomyopathy. Recently, two randomized, placebo-controlled studies did not show any significant GH-mediated improvement in cardiac performance in patients with dilated cardiomyopathy, despite significant increases in IGF-1. Acquired GH resistance might be an important feature of severe heart failure and explain the diverse responses to GH therapy observed in different patients. Whether GH treatment will finally find a place in the treatment of heart failure, and with which modalities, remains to be established.
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PMID:Role of growth hormone in chronic heart failure: therapeutic implications. 1111 May 15

We investigated the hemodynamic effect of regurgitation (or back-flow) due to sudden failure of a rotary blood pump (diagonal pump). Seven healthy sheep (Group C) and 7 with chronic heart failure (Group F) were studied. Chronic heart failure was obtained by intracoronary injection of microspheres several weeks earlier. Left ventricular function and ventricular efficacy were assessed by the pressure-volume relationship. The back-flow through the stopped pump was significantly lower in Group F (2.3 +/- 0.34 L/min) than in Group C (2.8 +/- 0.33 L/min). Mean aortic blood pressure dropped significantly from 68.3 +/- 9.65 to 61.9 +/- 9.75 mm Hg in Group C and from 62.5 +/- 9.12 to 51.5 +/- 9.08 in Group F but remained stable during the 15 min period of pump stop. Parameters of left ventricular contractility (preload recruitable stroke work) dropped significantly in both groups, remained stable during the pump stop, and returned to baseline values 30 min after the end of back-flow. The ventricular efficacy (in terms of energy transfer) was tolerant against this acute volume overload even in the failing hearts. Sudden pump failure of a rotary blood pump leads to an acute depression of the hemodynamic state and myocardial contractility. However, this depression remained stable over 15 min, did not lead to further deterioration of the animals, and was completely reversible.
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PMID:The effect of sudden failure of a rotary blood pump on left ventricular performance in normal and failing hearts. 1111 78

The Na,K-ATPase function appears impaired in human heart failure with dilation; however little is known in animal model with idiopathic dilated cardiomyopathy. We studied Na,K-ATPase isoform composition and activity from cardiomyopathic hamsters of the MS 200 strain with pure dilated cardiomyopathy and compared them with those of healthy Syrian hamsters. 150-day-old male MS 200 Syrian hamsters (n = 16) and sex- and age-matched healthy Syrian hamsters (n = 15) were used. Antibodies specific for the three alpha-isoforms and against the beta1-isoform were used to study Na,K-ATPase isoform expression in ventricular myocardium. Na,K-ATPase activity was quantified in homogenate and membrane fractions. There was no significant change in left ventricular mass. Morphological examination revealed a decreased septum thickness in the dilated cardiomyopathy compared with control hamster. Idiopathic dilated cardiomyopathy in hamsters presented significantly reduced membrane alpha1 and beta1 abundances and reduced Na,K-ATPase activity (-35% vs. healthy control, p<0.05). Chronic heart failure had no effect on the Na,K-ATPase alpha2-subunit protein. We have demonstrated for the first time that dilated cardiomyopathy induces a specific reduction of both membrane alpha1- and beta1-isoform abundance and Na,K-ATPase activity in hamsters similar to those previously reported in human dilated heart failure.
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PMID:Defective activity and isoform of the Na,K-ATPase in the dilated cardiomyopathic hamster. 1135 98

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