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

Anemia is a major problem in patients with chronic kidney insufficiency. The development of recombinant human erythropoietin has enabled physicians to correct this anemia. Although anemia has not been considered to be a common or important contributor to congestive heart failure, anemia of any cause can lead to cardiac damage and eventually congestive heart failure. Our joint renal-cardiac heart failure team found that anemia was indeed very common in congestive heart failure and was associated with severe, medication-resistant cardiac failure. Correction of the anemia with erythropoietin and intravenous iron led to a marked improvement in patients' functional status and their cardiac function, and to a marked fall in the need for hospitalization and for high-dose diuretics; renal function usually improved or at least stabilized. Subsequent investigations by others have confirmed many of our observations. We call this interrelationship between congestive heart failure, chronic kidney insufficiency, and anemia the Cardio-Renal Anemia syndrome. Treatment of the anemia in congestive heart failure may prove vital in preventing progression of both the heart failure and the associated renal disease.
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PMID:The role of anemia in congestive heart failure and chronic kidney insufficiency: the cardio renal anemia syndrome. 1546 79

Anemia is highly prevalent in patients with chronic heart failure (HF) and is associated with poor clinical outcomes. Multiple mechanisms contribute to anemia in chronic HF, and subnormal compensatory rise in endogenous erythropoietin levels in response to anemia is one contributory factor. Randomized trials with recombinant human erythropoietin therapy in anemic patients with chronic kidney disease and concomitant heart disease have demonstrated a reduction in left ventricular hypertrophy but variable effects on clinical outcome. Preliminary clinical trials in anemic patients with chronic HF demonstrate that erythropoietin therapy is well tolerated and associated with short-term clinical improvement. The optimum target hemoglobin, erythropoietic agent, and dosing regimen, and the role of iron supplementation in patients with chronic HF, are not known. Additional studies are needed to determine the safety and efficacy of long-term erythropoietic therapy in chronic HF patients.
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PMID:Mechanisms and treatment of anemia in chronic heart failure. 1547 Mar 2

Despite advances in the treatment of heart failure (HF) over the past decade, the prognosis remains poor. Anemia is a well-recognized comorbidity in many chronic conditions, but its role in HF has only recently been recognized. Anemia is significantly related to symptoms, exercise capacity, and prognosis in HF; it has been identified as an independent risk factor for mortality in those with left ventricular dysfunction. When HF patients have concomitant renal disease, they invariably become anemic owing to erythropoietin deficiency. In chronic HF patients without renal disease, erythropoietin levels may be elevated in response to anemia, but not adequately increased to overcome it. Some degree of erythropoietin resistance may also be present because of elevated plasma levels of cytokines. Several studies in anemic HF patients have shown positive outcomes using erythropoietin and iron supplementation therapy to increase hemoglobin concentrations to more normal levels. This article reviews the current information available regarding anemia in HF and discusses the clinical implications and treatment of this syndrome.
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PMID:Anemia in heart failure: implications, management, and outcomes. 1552 75

The cytokine erythropoietin (EPO) protects the heart from ischemic injury, in part by preventing apoptosis. However, EPO administration can also raise the hemoglobin concentration, which, by increasing oxygen delivery, confounds assignment of cause and effect. The availability of EPO analogs that do not bind to the dimeric EPO receptor and lack erythropoietic activity, e.g., carbamylated EPO (CEPO), provides an opportunity to determine whether EPO possesses direct cardioprotective activity. In vivo, cardiomyocyte loss after experimental myocardial infarction (MI) of rats (40 min of occlusion with reperfusion) was reduced from approximately 57% in MI-control to approximately 45% in animals that were administered CEPO daily for 1 week (50 microg/kg of body weight s.c.) with the first dose administered intravenously 5 min before reperfusion. CEPO did not increase the hematocrit, yet it prevented increases in left ventricular (LV) end-diastolic pressure, reduced LV wall stress in systole and diastole, and improved LV response to dobutamine infusion compared with vehicle-treated animals. In agreement with the cardioprotective effect observed in vivo, staurosporine-induced apoptosis of adult rat or mouse cardiomyocytes in vitro was also significantly attenuated ( approximately 35%) by CEPO, which is comparable with the effect of EPO. These data indicate that prevention of cardiomyocyte apoptosis, in the absence of an increase in hemoglobin concentration, explains EPO's cardioprotection. Nonerythropoietic derivatives such as CEPO, devoid of the undesirable effects of EPO, e.g., thrombogenesis, could represent safer and more effective alternatives for treatment of cardiovascular diseases, such as MI and heart failure. Furthermore, these findings expand the activity spectrum of CEPO to tissues outside the nervous system.
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PMID:A nonerythropoietic derivative of erythropoietin protects the myocardium from ischemia-reperfusion injury. 1567 Nov 58

Heart failure (HF) in elderly patients is associated with more diffuse symptoms and signs due to the presence of other noncardiac comorbidities. This can cause difficulties in assessing the correct diagnosis and initiating appropriate therapy. The four most frequently occurring noncardiac comorbidities and therapies used to treat them are discussed in the present paper. Hypertension is an important precursor of HF, and is still the most common risk factor for HF in the general population. About 50% of patients with untreated hypertension will develop HF. Pressure overload leads to the development of left ventricular hypertrophy (LVH) and diastolic dysfunction. Diabetes, which occurs in about 20-30% of patients with HF, is an important comorbidity resulting in morphological and metabolic disturbances affecting myocardial blood flow and hormonal regulation leading to a poor outcome and necessitating aggressive conventional treatment. Chronic obstructive pulmonary disease (COPD), occurs in approximately 20-30% of heart failure patients, and may complicate HF treatment, it is therefore important to recognize and treat it effectively. Finally, the early detection of anemia, which occurs in 20-30% of HF patients, is important since it is associated with functional impairment and increased mortality and morbidity. Combined treatment with erythropoietin and intravenous iron has shown beneficial effects on clinical symptoms and morbidity. In conclusion early detection of concomitant diseases in patients with HF is important and should be considered carefully when initiating therapy.
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PMID:Frequent non-cardiac comorbidities in patients with chronic heart failure. 1571 70

Recently there has been considerable interest in the associations between blood hemoglobin (Hb) level, renal function, and cardiovascular disease. Anemia is a common feature of end-stage renal disease, but it also accompanies lesser degrees of chronic kidney disease (CKD). The degree of anemia roughly approximates the severity of CKD. Anemia seen in diabetes has been linked to diabetic nephropathy; however, diabetes itself affects the hematologic system in several ways. Anemia is associated with left ventricular hypertrophy, cardiovascular morbidity, progressive loss of kidney function, and poor quality of life. Anemia seems to act as a mortality multiplier; that is, at every decrease in Hb below 12 g/dL, mortality increases in patients with CKD, cardiovascular disease, and those with both. Unlike blood transfusion, treatment of anemia with exogenous erythropoietin in patients with cardiorenal disease has shown promise in reducing morbidity and in improving survival and quality of life. Increasing the Hb level from less than 10 g/dL to 12 g/dL has resulted in favorable changes in left ventricular remodeling, improved ejection fraction, improved functional classification, and higher levels of peak oxygen consumption with exercise testing. Clinical trials are underway to test the role of erythropoietin in patients with CKD and in patients with heart failure.
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PMID:The deadly triangle of anemia, renal insufficiency, and cardiovascular disease: implications for prognosis and treatment. 1574 20

Diuretics, ACE inhibitors and betablockers form the cornerstone of pharmacological treatment of chronic heart failure (CHF), while angiotensin receptor blockers are gaining ground. However, despite optimal treatment CHF remains a syndrome with poor prognosis. For this reason, a large number of new agents have been developed as add-on treatment over the last few years. Vasopeptidase inhibitors, moxonidine, endothelin antagonists, vasopressin antagonists, and selective aldosterone antagonists, are some of the new agents that were designed to interfere with different neurohormonal pathways. Immunomodulating agents, growth hormone, caspase inhibitors, adrenomedullin, and erythropoietin have different modes of action, which in general are less understood. Although most of the agents exhibited efficacy in preclinical trials, the clinical results have not always been similarly positive. The results of trials involving vasopeptidase inhibitors, endothelin antagonists, immunomodulating agents, and growth hormone have been disappointing. Other compounds like caspase inhibitors, adrenomedullin, and vasopressin antagonists are still at the early stages of development. Currently, the two most promising agents seem to be erythropoietin and the selective aldosterone receptor blocker eplerenone. In the present article an overview of new pharmacological developments for CHF is given, and the clinical value of these developments is discussed.
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PMID:New pharmacological strategies in chronic heart failure. 1577 Apr 37

Mechanical circulatory assist devices (MCADs) are increasingly utilized independently of cardiac transplantation in the management of heart failure. Though MCAD use incorporates inherent mechanical risks, the inevitable onset of chronic anemia, with its associated morbidity and mortality, is also a significant concern. MCAD support has been correlated with elevated plasma levels of inflammatory cytokines TNF-alpha, IL-1beta, and IL-6, which have separately been found to inhibit erythropoietin (Epo)-induced erythrocyte (RBC) maturation. Previous analysis of hematological parameters for MCAD-supported patients concluded that an amplified inflammatory response impedes RBC proliferation and recovery from hemolytic anemia. Additional analysis may bolster this assertion. Hemoglobin concentration (HC), RBC distribution width (RDW), mean cell volume (MCV), and cardiac index were retrospectively analysed for 78 MCAD-supported patients implanted for greater than 30 days at the University of Arizona Health Sciences Center from 1996 to 2002. Analysis confirms that the HC, a conventional marker for anemia, declines with MCAD placement and remains below the clinically defined, minimum normal value. Inversely, the RDW rises above maximum normal measure, signifying an increased fraction of juvenile RBCs. The MCV remains unchanged and within normal limits, demonstrating adequate substrate for RBC formation. MCAD performance also stabilizes as adequate perfusion returns. These results further support our previously published conclusion that a sufficient response of erythropoiesis occurs in reaction to the onset of anemia by an increased production of immature RBCs. However, the cells never fully mature and join circulation. The patient's inflammatory cytokine response to the implanted device most likely mediates the chronic MCAD-induced anemia by inhibition of Epo effects.
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PMID:Inflammatory cytokine inhibition of erythropoiesis in patients implanted with a mechanical circulatory assist device. 1591 45

Anemia is common in subjects with chronic heart failure, and correction of anemia improves quality of life and exercise capacity in both men and women. The definition of anemia is sex-specific, but enrollment criteria of studies examining the effects of recombinant human erythropoietin in chronic heart failure to date have not taken sex into account. Indeed, it is unknown whether sex-specific differences of hemoglobin values observed in normal individuals are maintained in subjects with chronic disease and volume overload states. Given the significant treatment implications for sex-specific differences in hemoglobin values, the authors analyzed data for 260 subjects consecutively admitted with decompensated chronic heart failure. In a multivariate regression analysis controlling for serum creatinine and age, female sex was independently associated with lower hemoglobin. When deciding upon initiation of treatment in this population, sex-specific targets should be applied.
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PMID:Anemia, chronic heart failure, and the impact of male vs. female gender. 1594 33

Cardiovascular disease (CVD) is a significant complication in chronic kidney disease (CKD) and a major cause of death in dialysis patients. Clinical studies have shown that anaemia is associated with reduced survival in patients with renal disease, heart failure or both. There is also evidence that, even in otherwise healthy individuals, anaemia is independently associated with an increased risk of CVD. The body adapts to anaemia by increasing cardiac output, which may result in cardiac remodelling and progression of left ventricular (LV) growth. Indeed, low haemoglobin (Hb) has been identified as an independent risk factor for LV growth in CKD patients, suggesting that there is a direct link between anaemia and adverse cardiac outcomes. This suggests that correction of anaemia with recombinant human erythropoietin (rhEPO; epoetin) may improve prognosis. Partial correction of anaemia produces partial regression of LV hypertrophy, while complete correction of anaemia can help to prevent LV dilatation in haemodialysis patients with normal LV volumes. Moreover, in non-dialysis patients with advanced CVD, pilot studies showed that a moderate increase in Hb improved cardiac function and reduced hospitalization rates. In addition, consistent epoetin treatment before the start of dialysis was associated with a reduced risk of developing cardiac disease in CKD patients. In contrast, in dialysis patients with advanced cardiac disease, Hb normalization increased mortality risk. Therefore, early correction of anaemia appears important. The Cardiovascular risk Reduction by Early Anaemia Treatment with Epoetin beta (CREATE) study is investigating whether this approach is associated with a measurable reduction in cardiovascular risk.
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PMID:Managing a fateful alliance: anaemia and cardiovascular outcomes. 1595 21


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