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

The prevalence of heart failure is increasing. Anemia is often present, particularly in severe cases. The Fick equation illustrates the relationship between anemia and heart failure. The concepts of cardiorenal syndrome and erythropoietin resistance are parts of the physiopathology. Anemia is associated with a bad prognosis in heart failure. Nevertheless, it is too early to know precisely whether anemia represents a simple marker of severity or if specific treatment, especially with erythropoietin, is useful in terms of morbidity and mortality. Current guidelines recommend the correction of secondary causes when anemia is present in a heart failure patient.
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PMID:[Anemia and heart failure]. 1668 Oct

We did a PubMed and Cochrane Database System review of different studies on the diverse effects of erythropoietin (EPO), focusing mainly on the cardiovascular system. The direct erythropoietic action of EPO is well studied and widely used. Published studies report dramatic improvement in the course of heart failure with EPO treatment. New controlled clinical trials on large and diverse groups of patients are warranted. Antiapoptotic effects of EPO are newly discovered, opening new horizons in both clinical investigation and therapy. The salvage of cardiomyocytes in acute coronary syndromes, limiting the size of myocardial infarction and improving functional recovery, is only one of multiple potential applications of this effect. Derivatives of EPO with selective antiapoptotic properties seem to hold the best prospects for future studies. Heart failure and ischemic heart disease are potential areas where adding EPO to the conventional treatment may be beneficial.
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PMID:Cardiovascular effects of erythropoietin: anemia and beyond. 1678 33

Anemia is more common in patients with diabetes than without diabetes, and the problem is magnified in patients with renal impairment. Diabetic patients with anemia may be at increased risk of adverse outcomes from diabetic retinopathy, nephropathy, neuropathy, and cardiovascular disease. The etiology of anemia in diabetes is multifactorial and includes inflammation, nutritional deficiencies, concomitant autoimmune diseases, drugs, and hormonal changes in addition to kidney disease. Anemia that is associated with erythropoietin deficiency may have prognostic significance for persons with nephropathy or heart failure. In early diabetic nephropathy, damage to the peritubular fibroblasts can occur and lead to erythropoietin deficiency and anemia prior to the loss of filtration. Correction of the anemia not only leads to less fatigue, greater exercise tolerance, and an improved quality of life but also to a reduction in mortality and hospital admissions for congestive heart failure (CHF). Data are accumulating that suggest that treatment of anemia will slow the progression of microvascular and macrovascular complications, including postural hypotension from autonomic neuropathy, retinopathy, and loss of renal function from diabetic nephropathy. Promptly diagnosing and treating anemia in patients with diabetes may result in an improved quality of life and decreased morbidity and mortality.
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PMID:Anemia and the role of erythropoietin in diabetes. 1679 79

We have recently proposed severe cardiorenal syndrome (SCRS), in which cardiac and renal failure mutually amplify progressive failure of both organs. This frequent pathophysiological condition has an extremely poor prognosis. Interactions between inflammation, the renin-angiotensin system, the balance between the nitric oxide and reactive oxygen species and the sympathetic nervous system form the cardiorenal connectors and are cornerstones in the pathophysiology of SCRS. An absolute deficit of erythropoietin (Epo) and decreased sensitivity to Epo in this syndrome both contribute to the development of anemia, which is more pronounced than renal anemia in the absence of heart failure. Besides expression on erythroid progenitor cells, Epo receptors are present in the heart, kidney, and vascular system, in which activation results in antiapoptosis, proliferation, and possibly antioxidation and anti-inflammation. Interestingly, Epo can improve cardiac and renal function. We have therefore reviewed the literature with respect to Epo and the cardiorenal connectors. Indeed, there are indications that Epo can diminish inflammation, reduce renin-angiotensin system activity, and shift the nitric oxide and reactive oxygen species balance toward nitric oxide. Information about Epo and the sympathetic nervous system is scarce. This analysis underscores the relevance of a further understanding of clinical and cellular mechanisms underlying protective effects of Epo, because this will support better treatment of SCRS.
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PMID:Erythropoietin and the cardiorenal syndrome: cellular mechanisms on the cardiorenal connectors. 1688 53

L-carnitine plays an essential role in the beta-oxidation of fatty acids by catalyzing their transport into the mitochondrial matrix. The kidney maintains plasma free L-carnitine levels in the homeostatic range by selective saturable tubular reabsorption. The preferential retention of free L-carnitine over acyl-L-carnitines by the kidney is lost in patients with end-stage renal disease (ESRD). Loss of renal parenchyma as a site of carnitine synthesis, as well as nonselective clearance of L-carnitine by the dialysis procedure lead to dialysis-related carnitine deficiency. Numerous studies investigating whether L-carnitine supplementation will alleviate several dialysis-related symptoms, such as intradialytic hypotension, heart failure, muscle weakness, low exercise capacity, and anemia, have reported conflicting results. Many of these studies suffer from a lack of randomization and control groups, heterogeneity in the administration of L-carnitine, and nonstandardized measures of symptom improvement. More data exist to support the use of L-carnitine in selected anemic dialysis patients with very large erythropoietin requirements in whom extensive examination for reversible causes of anemia was unrevealing.
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PMID:Dialysis-related carnitine disorder. 1689 11

Anemia is a common finding in diabetes, particularly in patients with albuminuria or renal impairment. We recently showed that at least 1 in 5 outpatients with type 1 or type 2 diabetes in tertiary clinics have anemia, in whom it constitutes a significant additional burden. Anemia is associated strongly with an increased risk of diabetic complications including nephropathy, retinopathy, and heart failure. Although a number of factors contribute to an increased prevalence of anemia in diabetes, an uncoupling of hemoglobin concentration and renal erythropoietin synthesis associated with tubular dysfunction appears to be the dominant factor. In our patients with diabetes and anemia, more than three quarters had functional erythropoietin deficiency. This association was most pronounced in patients with renal impairment, in whom nearly half of all patients had anemia. However, 70% of anemic patients without renal impairment also had inappropriately low erythropoietin levels. Consequently, the likelihood of functional erythropoietin deficiency, as a cause of anemia in patients with diabetes, is not dependent on the severity of renal impairment. Although there is a clear rationale for correction of anemia in diabetes, it remains to be established whether this will lead to improved outcomes. Some small studies suggest improvement in cardiac outcomes and hospitalization. It is anticipated that large ongoing studies will help define the optimal approach to the management of anemia in diabetes.
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PMID:The high prevalence of anemia in diabetes is linked to functional erythropoietin deficiency. 1694 65

Anemia, defined as a hemoglobin level of less than 12 g/dL, often is seen in congestive heart failure (CHF). It is associated with an increased mortality and morbidity and increased hospitalizations. Compared with nonanemic patients the presence of anemia also is associated with worse cardiac clinical status, more severe systolic and diastolic dysfunction, a higher beta natriuretic peptide level, increased extracellular and plasma volume, a more rapid deterioration of renal function, a lower quality of life, and increased medical costs. The only way to determine if anemia is merely a marker for more severe CHF or actually is contributing to the worsening of the CHF is to correct the anemia and see if this favorably influences the CHF. In several controlled and uncontrolled studies, correction of the anemia with subcutaneous erythropoietin (EPO) or darbepoetin in conjunction with oral and intravenous iron has been associated with an improvement in clinical status, number of hospitalizations, cardiac and renal function, and quality of life. However, larger, randomized, double-blind, controlled studies still are needed to verify these initial observations. The effect of EPO may be related partly to its nonhematologic functions including neovascularization; prevention of apoptosis of endothelial, myocardial, cerebral, and renal cells; increase in endothelial progenitor cells; and anti-inflammatory and antioxidant effects. Anemia also may play a role in increasing cardiovascular morbidity in chronic kidney insufficiency, diabetes, renal transplantation, asymptomatic left ventricular dysfunction, left ventricular hypertrophy, acute coronary syndromes including myocardial infarction and chronic coronary heart disease, and in cardiac surgery. Again, controlled studies of correction of anemia are needed to assess its importance in these conditions. The anemia in CHF mainly is caused by a combination of renal failure and CHF-induced increased cytokine production, and these can both lead to reduced production of EPO, resistance of the bone marrow to EPO stimulation, and to cytokine-induced iron-deficiency anemia caused by reduced intestinal absorption of iron and reduced release of iron from iron stores. The use of angiotensin-converting enzyme inhibitor and angiotensin receptor blockers also may inhibit the bone marrow response to EPO. Hemodilution caused by CHF also may cause a low hemoglobin level. Renal failure, cardiac failure, and anemia therefore all interact to cause or worsen each other--the so-called cardio-renal-anemia syndrome. Adequate treatment of all 3 conditions will slow down the progression of both the CHF and the chronic kidney insufficiency.
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PMID:The interaction between heart failure and other heart diseases, renal failure, and anemia. 1694 68

Heart failure (HF) is a major disease of the elderly. Since their symptoms of HF are generally light, on admission of the hospitals HF is sometimes in an advanced stage. Therefore, preventive medicine for those with the risk factors of HF is needed as a future strategy of cardiac gerontology. The routine assessment of the HF severity may be performed noninvasively by Nohria's profiles rather than other invasive methods. HF is worsened by the interaction with the co-morbidity factors, such as renal dysfunction and anemia. The interaction between HF and kidney disease (and anemia) is called 'cardiorenal (anemia) syndrome.' Recurrent hospitalization due to HF is common, and the period of hospitalization tends to be long in this syndrome. One of the hopeful therapeutic agents is carperitide, a recombinant human atrial natriuretic peptide. In cardiorenal syndrome, much lower initial doses of carperitide, such as 0.0125 microg/kg/min is recommended for treatment of HF in order to avoid possible worsening of renal dysfunction. In cardiorenal anemia syndrome, supplement of iron, careful blood transfusion in severe cases, administration of recombinant human erythropoietin, should be performed if indicated. However, the possibility of anemia unrelated to HF, such as due to gastrointestinal carcinoma, is also considered in the elderly. In such cases, finding a decrease of serum ferritin preceding that of hemoglobin may contribute to a differential diagnosis of anemia in elderly HF patients. Thus, the therapies considering several features of HF in elderly will contribute to improving quality of life and outcome.
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PMID:[Heart failure in the elderly]. 1723 52

First isolated in the early 1960s, doxorubicin (DOX) remains among the most effective anticancer drug ever developed. However, this drug has proven to be a double-edged sword because it also causes a cardiomyopathy that leads to a form of congestive heart failure that is usually refractory to common medications. It is hoped that a better understanding of the mechanisms underlying DOX's cardiotoxicity will enable development of therapies with which to prevent and/or treat the heart failure it causes. Suggested contributors to DOX-induced cardiomyopathy include formation of reactive oxygen species, apoptosis, inhibited expression of cardiomyocyte-specific genes, and altered molecular signaling. And taking these various contributors into consideration, a variety of approaches aimed at preventing or mitigating the cardiotoxicity of DOX have been tried, but so far, the ability of these treatments to protect the heart from damage has been limited. That said, one recent approach that shows promise is adjuvant therapy with a combination of hematopoietic cytokines, including erythropoietin, granulocyte colony-stimulating factor, and thrombopoietin. We suggest this approach to preventing DOX-induced cardiomyopathy is worthy of serious consideration for clinical use.
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PMID:Doxorubicin-induced cardiomyopathy from the cardiotoxic mechanisms to management. 1732 80

Following an acute myocardial infarction (AMI), early coronary artery reperfusion remains the most effective means of limiting the eventual infarct size. The resultant left ventricular systolic function is a critical determinant of the patient's clinical outcome. Despite current myocardial reperfusion strategies and ancillary antithrombotic and antiplatelet therapies, the morbidity and mortality of an AMI remain significant, with the number of patients developing cardiac failure increasing, necessitating the development of novel strategies for cardioprotection which can be applied at the time of myocardial reperfusion to reduce myocardial infarct size. In this regard, the Reperfusion Injury Salvage Kinase (RISK) Pathway, the term given to a group of pro-survival protein kinases (including Akt and Erk1/2), which confer powerful cardioprotection, when activated specifically at the time of myocardial reperfusion, provides an amenable pharmacological target for cardioprotection. Preclinical studies have demonstrated that an increasing number of agents including insulin, erythropoietin, adipocytokines, adenosine, volatile anesthetics natriuretic peptides and 'statins', when administered specifically at the time of myocardial reperfusion, reduce myocardial infarct size through the activation of the RISK pathway. This recruits various survival pathways that include the inhibition of mitochondrial permeability transition pore opening. Interestingly, the RISK pathway is also recruited by the cardioprotective phenomena of ischemic preconditioning (IPC) and postconditioning (IPost), enabling the use of pharmacological agents which target the RISK pathway, to be used at the time of myocardial reperfusion, as pharmacological mimetics of IPC and IPost. This article reviews the origins and evolution of the RISK pathway, as part of a potential common cardioprotective pathway, which can be activated by an ever-expanding list of agents administered at the time of myocardial reperfusion, as well as by IPC and IPost. Preliminary clinical studies have demonstrated myocardial protection with several of these pharmacological activators of the RISK pathway in AMI patients undergoing PCI. Through the use of appropriately designed clinical trials, guided by the wealth of existing preclinical data, the administration of pharmacological agents which are known to activate the RISK pathway, when applied as adjuvant therapy to current myocardial reperfusion strategies for patients presenting with an AMI, should lead to improved clinical outcomes in this patient group.
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PMID:Reperfusion injury salvage kinase signalling: taking a RISK for cardioprotection. 1754 22


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