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

Major causes of anaemia in pregnancy in tropical Africa are malaria, iron deficiency, folate deficiency and haemoglobinopathies: now there is added also the acquired immune deficiency syndrome (AIDS). Anaemia is often multifactorial, with the different causes interacting in a vicious cycle of depressed immunity, infection and malnutrition. Anaemia progresses through 3 stages: compensation, with breathlessness on exertion only; decompensation, with breathlessness at rest and haemoglobin (Hb) below about 70 g/litre; cardiac failure, with Hb below about 40 g/litre. Without treatment, over half of the women with haematocrit less than 0.13 and heart failure die. Maternal anaemia, malaria and deficiencies of iron and folate cause intrauterine growth retardation, premature delivery and, when severe, perinatal mortality. Surviving infants have low birthweights, immune deficiency and poor reserves of iron and folate. They have entered already the vicious cycle of infection, malnutrition and impaired immunity. Treatment with blood transfusions is even more hazardous since the advent of AIDS, and should be limited to saving the life of the mother. Treatment of malaria is complex as chloroquine-resistant strains are now common. Prevention remains relatively easy with proguanil and supplements of iron and folic acid and is highly cost-effective in the improvement of maternal and infant health; it is more important than ever as it avoids the unnecessary exposure of women and infants to HIV transmitted through blood transfusion.
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PMID:Tropical obstetrics and gynaecology. 1. Anaemia in pregnancy in tropical Africa. 269 76

In Eisenmenger's syndrome a central left-to-right shunt in the heart, a congenital anomaly, leads to pulmonary hypertension which subsequently causes the shunt to be reversed. The hypoxaemia resulting from a right-to-left shunt is compensated by an increase of the haemoglobin concentration due to a rise of the haematocrit. In adult patients not operated (adequately), the symptoms are the consequence of the erythrocytaemia and an increased haemorrhagic diathesis. In the long run heart failure develops. Phlebotomy is indicated for patients with haematocrits higher than 0.65 with signs of hyperviscosity and is also advised before non-cardiac surgery to improve coagulation parameters. Phlebotomy should be performed slowly (500 ml in 30-45 min) with simultaneous volume replacement. Excessive phlebotomy causes iron deficiency and spherocytosis which increase viscosity as well as the risk of CVA. Treatment consists of iron supplementation. Anticoagulation is indicated only in case of atrial fibrillation or mechanical valves. The use of acetylsalicylacid or NSAIDs is relatively contraindicated, because of abnormal haemostasis in these patients. During treatment with ACE inhibitors and other vasodilators, hypovolaemia should be avoided, because at a lower systemic blood pressure the right-to-left shunt increases and a potentially fatal cyanosis may occur.
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PMID:[Eisenmenger syndrome in adults]. 1032 Dec 57

An association between moderate anemia and poor perinatal outcomes has been found through epidemiologic studies, although available evidence cannot establish this relation as causal. Anemia may not be a direct cause of poor pregnancy outcomes, except in the case of maternal mortality resulting directly from severe anemia due to hypoxia and heart failure. Preventing or treating anemia, whether moderate or severe, is desirable. Because iron deficiency is a common cause of maternal anemia, iron supplementation is a common practice to reduce the incidence of maternal anemia. Nevertheless, the effectiveness of large-scale supplementation programs needs to be improved operationally and, where multiple micronutrient deficiencies are common, supplementation beyond iron and folate can be considered. High hemoglobin concentrations are often mistaken as adequate iron status; however, high hemoglobin is independent of iron status and is often associated with poor health outcomes. Very high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxygen delivery to tissues and cerebrovascular complications. Epidemiologic studies have also found an association between high maternal hemoglobin concentrations and an increased risk of poor pregnancy outcomes. Evidence does not suggest that this association is causal; it could be better attributed to hypertensive disorders of pregnancy and to preeclampsia. The pathophysiologic mechanism of these conditions during pregnancy can produce higher hemoglobin concentrations because of reduced normal plasma expansion and cause fetal stress because of reduced placental-fetal perfusion. Accordingly, higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications, not necessarily as a sign of adequate iron nutrition, because iron supplementation does not increase hemoglobin higher than the optimal concentration needed for oxygen delivery.
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PMID:Significance of an abnormally low or high hemoglobin concentration during pregnancy: special consideration of iron nutrition. 1087 93

During the last decades efforts regarding dietary iron supply focused mostly on the prevention of deficiencies, especially during growth and pregnancy. Correspondingly, homeostatic mechanisms increase intestinal iron absorption in iron deficiency, but its downregulation at high intake levels seems insufficient to prevent accumulation of high iron stores at high intake. There is no regulated iron excretion in overload. Excess of pharmaceutical iron may cause toxicity and therapeutic doses may cause gastrointestinal side effects. Chronic iron excess, e.g. in primary and secondary hemochromatosis, may lead to hepatic fibrosis, diabetes mellitus and cardiac failure. Chronic intake of 50-100 mg Fe/day of highly bioavailable iron with home-brewed beer in sub-Saharan Africans lead to cirrhosis and diabetes. Applying a safety factor of 2 would lead to an upper safe level of 25-50 mg Fe/day for this endpoint of conventional iron toxicity. However, beyond this kind of damage iron is known to catalyze the generation of hydroxyl radicals from superoxide anions and to increase oxidative stress which, in turn, increases free iron concentration. This self-amplifying process may cause damage to lipid membranes and proteins, which relates radical generation and organ damage after ischemia-reperfusion events to available free iron in clinical and experimental settings. Correspondingly, epidemiological studies as well as observations in heterozygotes for hereditary hemochromatosis suggest that the risk of atherosclerosis and acute myocardial infarction is related to body iron stores, though there is conflicting epidemiological evidence as well. The most recent and best controlled studies, however, support the hypothesis that iron stores are related to cardiovascular risk. Iron-amplified oxidative stress may also increase DNA damage, oxidative activation of precancerogens and support tumor cell growth. This is supported by experimental, clinical and epidemiological observations. Due to these mechanisms high iron stores may present a health hazard. Though this has not been finally proven, available evidence strongly recommends not to increase iron intake beyond physiological requirements. To avoid iron deficiency symptoms, on the other hand, care must be taken to meet recommended daily intake.
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PMID:Safety aspects of iron in food. 1142

Anemia can be the cause of heart failure, but also its consequence. The pathogenesis of anemia in chronic heart failure (CHF) has yet to be fully elucidated, but is likely to be complex. Epidemiologic studies suggest that kidney dysfunction (by reducing the erythropoietic response to anemia), inflammation (by inducing erythropoietin resistance), decreased body mass index, old age, female gender, and poor clinical status may be important factors in the development of anemia in CHF. Intestinal malabsorption, chronic aspirin use, and proteinuria predisposes to iron deficiency. Proinflammatory cytokines are likely to play a significant role in anemia in CHF by generating the "anemia of chronic illness" that is a hallmark of inflammatory conditions. Few studies have investigated the mechanisms of anemia in CHF. There is a need for such studies.
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PMID:Anemia in chronic heart failure: pathogenetic mechanisms. 1500 93

Anemia and renal dysfunction (RD) are frequent complications seen in chronic heart failure (HF). However, the prevalence and interaction of these co-morbidities in a representative population of outpatients with chronic HF is poorly described. In this study, it was sought to determine the association between RD and anemia in patients with HF enrolled in a community-based HF program. Nine hundred fifty-five patients with HF due to left ventricular systolic dysfunction were investigated for the prevalence of anemia and its cause and followed for a median of 531 days. Anemia was defined as hemoglobin < 12.0 g/dl in women and < 13.0 g/dl in men. RD was defined as a calculated glomerular filtration rate of < 60 ml/min. The prevalence of anemia was 32%. Fifty-three percent of patients with and 27% of those without anemia had > or = 1 test suggesting hematinic deficiency. The prevalence of RD was 54%. Forty-one percent of patients with and 22% of patients without RD had anemia, with similar proportions associated with iron deficiency in the presence or absence of RD. Anemia and RD independently predicted a worse outcome, and this effect was additive. In conclusion, in outpatients with chronic HF, anemia and RD are common and co-exist but confer independent prognostic information. A deficiency of conventional hematinic factors may cause about 1/3 of anemia in this clinical setting.
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PMID:Anemia, renal dysfunction, and their interaction in patients with chronic heart failure. 1686 30

Anemia is common in patients who have both heart failure and chronic kidney disease, and there is an association between anemia and progression of both diseases. The main causes of anemia are deficient production of erythropoietin (EPO), iron deficiency, and chronic disease with endogenous EPO resistance. EPO has been successfully used for over a decade to treat anemia in patients with chronic kidney disease. Less obvious are the safety and efficacy of EPO treatment in patients with both heart failure and renal disease. Up to 10% of patients receiving EPO are hyporesponsive to therapy and require large doses of the agent. Several mechanisms could explain resistance to endogenous and exogenous EPO. Proinflammatory cytokines antagonize the action of EPO by exerting an inhibitory effect on erythroid progenitor cells and by disrupting iron metabolism (a process in which hepcidin has a central role). EPO resistance might also be caused by inflammation, which has a negative effect on EPO receptors. Furthermore, neocytolysis could have a role. As resistance to exogenous EPO is associated with an increased risk of death, it is important to understand how cardiorenal failure affects EPO production and function.
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PMID:Mechanisms of Disease: erythropoietin resistance in patients with both heart and kidney failure. 1809 27

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

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

We carried out retrospective analysis of 219 case histories of patients with chronic heart failure admitted to a general medical hospital. Anemia (hemoglobin level below 130 g/l in men and below 120g/l in women) was found in 23.3% of cases. Anemia was classified as iron deficiency in 23.5% and as B12 deficiency in 3.9% of patients. In 3.9% of patients other definite causes of anemia were found and in 68.6% origin of anemia was not determined. However at least in some of the latter patients disturbed kidney function could play some role in anemia genesis.
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PMID:[Prevalence and structure of anemia in patients with chronic heart failure in a therapeutic hospital]. 1946 16


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