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

The renal community has long recognized that anaemia can impair the quality of life of patients and lead to irreversible cardiac consequences. This review examines anaemia-related outcome studies published after 2001. The profusion of observational studies in non-renal populations in 2002 has made it a remarkable year. One important community cohort study showed that 1 in 10 'healthy' adults has anaemia, an antecedent of the development of cardiovascular disease. Several cross-sectional studies have confirmed that anaemia is common in patients with congestive heart failure (CHF), and its severity correlates positively with the severity of CHF. All recent outcome studies have shown that anaemia is associated with mortality rates beyond those explicable from heart failure severity. A placebo-controlled, randomized trial showed that the normalization of haemoglobin (Hb) levels in anaemic patients with CHF improved peak oxygen uptake and exercise performance. Large clinical trials are required to define the true potential of anaemia therapy in CHF. Most renal guidelines suggest the use of Hb targets that are independent of disease stage or treatment modality. Virtually all the supportive evidence to date has been from haemodialysis populations. Anaemia, which occurs frequently and is often neglected, appears to precede left ventricular hypertrophy and CHF in renal transplant patients. Anaemia may not be an 'innocent bystander' in chronic disease; both components of the term 'anaemia of chronic disease' deserve attention.
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PMID:Anaemia and the heart: what's new in 2003? 1460 94

Anaemia of chronic disease (ACD), with chronically low levels of circulating haemoglobin, is an immune driven abnormality that occurs in many inflammatory diseases, and also in chronic heart failure. Although chronic obstructive pulmonary disease (COPD) is "traditionally" associated with polycythaemia, the systemic inflammation that is now recognised as a feature of COPD makes it a possible cause of ACD. If present in COPD, anaemia could worsen dyspnoea and limit exercise tolerance. Preliminary evidence suggests that anaemia in COPD patients may be more prevalent than expected, concerning 10-15% of patients suffering from severe forms of the disease. A database study conducted in 2,524 COPD patients being prescribed long-term oxygen therapy has shown that a low haematocrit is a strong predictor of survival in this population, before body mass index, and is associated with more hospitalisations and a longer cumulative duration of hospitalisation. COPD patients with low haemoglobin levels have a poorer prognosis than COPD patients with normal haemoglobin levels in the event of acute gastrointestinal bleeding or after elective aneurysm repair. Raising haemoglobinaemia through transfusion decreases minute ventilation and work of breathing in COPD patients. These preliminary evidences point to the need to study the prevalence of anaemia, and its physiological and clinical impact in chronic obstructive pulmonary disease. When this body of knowledge is available, the question of the putative benefits of raising haemoglobinaemia in chronic obstructive pulmonary disease will have to be addressed.
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PMID:The potential impact of anaemia of chronic disease in COPD. 1645 98

Anemia is a common comorbidity in patients with heart failure and affects up to 50% of patients, depending on the definition of anemia used and on the population studied. Presence of anemia and lower hemoglobin (Hgb) concentrations are powerful independent predictors of adverse outcomes in heart failure. Even small reductions in Hgb are associated with worse outcomes. Correction of anemia may be useful in improving heart failure outcomes. However, the causes of anemia in heart failure are not entirely clear. Specific causes of anemia such as hematinic abnormalities are seen only in a minority of subjects. Renal dysfunction and neurohormonal and proinflammatory cytokine activation appear to contribute to anemia of chronic disease in the majority of the patients, resulting in inappropriate erythropoietin production and defective iron utilization. Under normal conditions, reduced tissue oxygenation due to chronic anemia results in non-hemodynamic and hemodynamic compensatory responses to enhance oxygen carrying capacity. Erythropoiesis is the predominant non-hemodynamic response to hypoxia, but because erythropoiesis is defective in heart failure, hemodynamic mechanisms predominate. Hemodynamic responses are complex and involve a vasodilation-mediated high-output state with neurohormonal activation. The high-output state initially helps to increase oxygen transport. However, the hemodynamic and neurohormonal alterations could potentially have deleterious long-term consequences and could contribute to anemia's role as an independent risk factor for adverse outcomes.
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PMID:Heart failure and anemia: mechanisms and pathophysiology. 1823 52

Anemia is common among patients with heart failure (HF) and has been associated with worse prognosis. To date, it is not well known whether correction of anemia in these patients can improve outcome. Proposed modalities for correction of anemia have been either administration of erythropoiesis-stimulating proteins, which appears plausible in patients with concomitant renal failure (so-called cardiorenal syndrome), or iron supplementation, which is particularly attractive in patients with no overt renal failure and chronic disease anemia with some degree of iron deficiency. This article reviews the rationale for anemia correction and the latest randomized clinical trial assessing clinical utility of erythropoiesis-stimulating proteins and/or iron supplementation through oral or intravenous administration in anemic HF patients.
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PMID:Etiology and management of anemia in patients with heart failure: how much iron is missing? 1825 66

The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and intravenous iron (i.v.-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in nutrition, and blood losses during treatment. EPO and i.v.-iron are the mainstays of treatment. Patients with heart failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure patient may aid rational therapy in each case.
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PMID:Iron and anemia in human biology: a review of mechanisms. 1836 95

Anemia is a common comorbidity in patients with heart failure and is associated with worse long-term outcomes. Although the cause of anemia in heart failure is unclear, the weight of evidence suggests that renal dysfunction, along with neurohormonal and proinflammatory cytokine activation in heart failure, favors the development of anemia of chronic disease, with defective iron utilization, inappropriate erythropoietin production, and depressed bone marrow function. Similarly, the mechanisms by which anemia worsens heart failure outcomes are unknown but may be related to increased myocardial workload. If anemia is a mediator and not just a marker of poor outcomes, correcting anemia could become an important and novel therapeutic target to improve long-term outcomes in such patients. Indeed, several small-sized studies have shown the beneficial effects of empirically treating anemia in heart failure patients with recombinant erythropoietin and intravenous iron. However, the ideal threshold at which therapy should be initiated and the extent of correction considered safe and desirable in the individual patient with heart failure need to be known. These issues become more important because of increasing safety concerns that recombinant erythropoietin therapy for treating anemia may be associated with adverse cardiovascular outcomes in patients with chronic kidney disease and may worsen cancer in patients receiving chemotherapy to treat various types of cancer. Therefore, further prospectively designed studies are required to address some of these questions. Fortunately, 2 large mortality morbidity trials, TREAT (Trial to Reduce Cardiovascular Events with Aranesp Therapy) in patients with chronic kidney disease and RED-HF (Reduction of Events with Darbepoetin alfa in Heart Failure) in heart failure patients, are in progress and are likely to provide definitive answers.
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PMID:Anemia and chronic heart failure implications and treatment options. 1868 41

Anemia has been recognized as a very common and serious comorbidity in heart failure, with a prevalence ranging from 10 to 79%, depending on diagnostic definition, disease severity and patient characteristics. A clear association of anemia with worse prognosis has been confirmed in multiple heart failure trials. This finding has recently triggered intense scrutiny in order to identify the underlying pathophysiology and the best treatment options. Etiology is multifactorial, with iron deficiency and cytokine activation (anemia of chronic disease) playing the most important roles. Treatment is aimed at not only restoring hemoglobin values back to normal, but also at improving the patient's symptoms, functional capacity and hopefully the outcome. Iron supplementation and erythropoietin-stimulating agents have been used for this purpose, either alone or in combination. In this review, the recent advances in elucidating the mechanisms leading to anemia in the setting of heart failure are presented and the evidence supporting the use of different treatment approaches are discussed.
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PMID:Anemia in heart failure: pathophysiologic insights and treatment options. 1937 Dec 5

Renal dysfunction and neurohormonal and proinflammatory cytokine activation appear to contribute to anemia of chronic disease in most patients, resulting in inappropriate erythropoietin production and defective iron utilization. Under normal conditions, reduced tissue oxygenation caused by chronic anemia results in non-hemodynamic and hemodynamic compensatory responses to enhance oxygen carrying capacity. Erythropoiesis is the predominant non-hemodynamic response to hypoxia, but because erythropoiesis is defective in heart failure, hemodynamic mechanisms may predominate in chronic severe anemia. Hemodynamic responses are complex and involve a vasodilation-mediated high-output state with neurohormonal activation. The high output state initially helps to increase oxygen transport. However, the hemodynamic and neurohormonal alterations could potentially have deleterious long-term consequences and may contribute to anemia's role as an independent risk factor for adverse outcomes.
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PMID:Pathophysiology of anemia in heart failure. 2063 Apr 2

Anemia is highly prevalent in patients with chronic heart failure (CHF) and is associated with poor clinical outcome. Increased prevalence of anemia in CHF has been linked to advanced age, female gender, renal function impairment, severity of symptoms, and clinical settings. Overall, the anemia of CHF shares many common features with the anemia of chronic disease. Both impaired iron metabolism and inflammatory stress appear to be the key mediators of the anemia of CHF.
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PMID:Mediators of anemia in chronic heart failure. 2063 Apr 3

Over the past few decades, there has been an increase in the number of reports about newly recognized (atypical or unusual) manifestations of Graves' disease (GD), that are related to various body systems. One of these manifestations is sometimes the main presenting feature of GD. Some of the atypical manifestations are specifically related to GD, while others are also similarly seen in patients with other forms of hyperthyroidism. Lack of knowledge of the association between these findings and GD may lead to delay in diagnosis, misdiagnosis, or unnecessary investigations. The atypical clinical presentations of GD include anemia, vomiting, jaundice, and right heart failure. There is one type of anemia that is not explained by any of the known etiological factors and responds well to hyperthyroidism treatment. This type of anemia resembles anemia of chronic disease and may be termed GD anemia. Other forms of anemia that are associated with GD include pernicious anemia, iron deficiency anemia of celiac disease, and autoimmune hemolytic anemia. Vomiting has been reported as a presenting feature of Graves' disease. Some cases had the typical findings of hyperthyroidism initially masked, and the vomiting did not improve until hyperthyroidism has been detected and treated. Hyperthyroidism may present with jaundice, and on the other hand, deep jaundice may develop with the onset of overt hyperthyroidism in previously compensated chronic liver disease patients. Pulmonary hypertension is reported to be associated with GD and to respond to its treatment. GD-related pulmonary hypertension may be so severe to produce isolated right-sided heart failure that is occasionally found as the presenting manifestation of GD.
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PMID:Atypical clinical manifestations of graves' disease: an analysis in depth. 2213 47


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