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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 frequently observed in patients with chronic heart failure (CHF) and is related to an impaired outcome. The origin of anemia in CHF is diverse and is associated with several factors including renal failure, resistance of the bone marrow to erythropoietin (EPO), hematinic deficiencies, and medication use. Recently, several small-scale clinical trials have shown that EPO treatment might improve clinical parameters in anemic heart failure patients. In addition, several preclinical studies have shown that EPO possesses non-hematopoietic effects. This current review focuses on the etiology, consequences, and treatment of anemia in heart failure patients. The pleiotropic effects of EPO in an experimental setting will also be discussed. Heart Fail Monit 2008;6(1):28-33.
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PMID:Anemia and erythropoietin in heart failure. 1860 19

The triad of chronic kidney disease, heart failure and anemia is well described and frequently encountered in clinical practice. While individually these disease states are associated with significant morbidity and mortality, the presence of the triad portends an even worse prognosis. Anemia is prevalent among cohorts of patients with chronic kidney disease and heart failure, indicating that its presence may serve as a central unifying hypothesis to explain poor outcomes in these populations. Observational and interventional trials of erythropoietin-stimulating agents, however, have had variable results on cardiovascular end points. Data are now emerging that suggest that treating erythropoietin deficiency in and of itself may be as or more important than the absolute levels of hemoglobin attained. Future research in this arena must focus on the optimal dose of erythropoietin administered to hemoglobin level achieved that will result in improved cardiovascular outcomes for patients with heart failure and kidney disease.
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PMID:Chronic kidney disease, heart failure and anemia. 1862 85

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

The recognition of the high prevalence and the independent prognostic role of anemia in heart failure (HF) has contributed to intensification of the search for an effective treatment. A central role of erythropoietin in cardiorenal anemia syndrome has been proposed. Several clinical trials have established the safety and efficacy of erythropoiesis-stimulating agents in correcting anemia in patients with HF. The recognition of the pleiotropic effect of erythropoietin has expanded targets of therapy. The ongoing outcomes trial with darbepoetin alfa will determine the role of this novel therapy in the treatment of HF.
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PMID:Anemia and the potential role of erythropoiesis-stimulating agents in heart failure. 1876 78

Hypertension is an uncommon but significant problem in high-risk neonates and infants, and the spectrum of potential causes is broad. Here, we describe an extremely premature infant (birth weight, 728 g; gestational age, 27 weeks) with multiple complications and hypertension. During admission, umbilical artery catheters were used for a period of time, and he suffered from respiratory distress syndrome, intraventricular hemorrhage, pulmonary hemorrhage, patent ductus arteriosus, pericardial effusion, heart failure, repeated sepsis, anemia, thrombocytopenia, chronic lung disease, and progressive liver damage. He was treated with multiple medications, including erythropoietin, indomethacin, epinephrine, dopamine, aminophylline, multiple antibiotics, amphotericin B, and total parenteral nutrition. Hypertension was first noted when he was 41 days old, with spontaneous remission. It then recurred, reaching higher than 100 mmHg when he was almost 4 months old. After stopping erythropoietin, hypertension subsided for a short period of time and went up again. Multiple factor-related hypertension in this premature infant was considered. Related literature on hypertension in premature infants is reviewed. In conclusion, multiple factors can influence blood pressure and may induce hypertension in high-risk premature infants. Thus, blood pressure should be closely monitored in high-risk premature infants. Judicious use of all medications and interventions are crucial to decrease the incidence of hypertension in high-risk premature infants.
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PMID:Conditions associated with hypertension in a high-risk premature infant. 1881 44

The Insulin-like growth factor-1 (IGF-1) system is dynamic and complex, involving many binding proteins, binding-protein-related proteases, and receptors. It has emerged in time as a powerful defence to life processes of many cytotypes, tissues and systems. Mainly in body metabolism, diabetes and cardiovascular system, but also in brain and kidney, IGF-1 plays a key role in maintaining homeostasis, increasing progenitor cell potential, and improving physiologic performance both in rest and stress conditions. Its vasculoprotective and insulin sensitizing ability exerts a protective role on flow-metabolism coupling and organs function. Therapeutical human use of recombinant human IGF-1 (rhIGF-1) has been widely applied only in Laron syndrome, while being verified in many randomized controlled trials to improve glycemic control in type 1 and type 2 diabetes, and proposed in neurological disease such as amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer disease. Sparse evidence exists moreover about rhIGF-1 use in insulin resistance, burns, catabolic and post-surgery states, acute and chronic renal failure, amyotrophic lateral and multiple sclerosis, brain injury, and immunoincompetence. Along with these data, results are available on cardiovascular benefit of administration of other growth factors, such as erythropoietin and vascular endothelial growth factor, or on cardiovascular side effects of growth factor antagonists such as trastuzumab in cancer therapy. We intended therefore to summarize in this review available human and animals evidence about rhIGF-1 effects on different systems with insights on rhIGF-1 cardiovascular effects. In view of its ability to improve flow-metabolism coupling, IGF-1 could indeed represent a new cardiovascular disease treatment option for many cardiac disorders such as ischemic heart disease and heart failure.
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PMID:Recombinant human insulin-like growth factor-1: a new cardiovascular disease treatment option? 1885 38

Congestive heart failure, chronic kidney insufficiency and anemia are often present in the same patient. We have coined this triad the cardio-renal anemia syndrome. We suggest that congestive heart failure can often cause chronic renal failure, with both diseases producing anemia. The anemia exacerbates the chronic heart failure, which then worsens the chronic renal failure, causing further anemia, in a vicious cycle. Together with early detection and treatment of the chronic heart failure, correction of the associated anemia with a combination of subcutaneous erythropoietin and intravenous iron will often alleviate the chronic heart failure and slow down or stop the progression of the associated chronic kidney insufficiency.
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PMID:The cardio-renal anemia syndrome. 1892 82

In anemic patients with heart failure (HF), erythropoietin-type drugs can elicit clinical improvement. This study examined the effects of chronic monotherapy with darbepoetin-alpha (DARB) on left ventricular (LV) function and remodeling in nonanemic dogs with advanced HF. HF [LV ejection fraction (EF) approximately 25%] was produced in 14 dogs by intracoronary microembolizations. Dogs were randomized to once a week subcutaneous injection of DARB (1.0 microg/kg, n=7) or to no therapy (HF, n=7). All procedures were performed during cardiac catheterization under general anesthesia and under sterile conditions. LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF were measured before the initiation of therapy and at the end of 3 mo of therapy. mRNA and protein expression of caspase-3, hypoxia inducible factor-1alpha, and the bone marrow-derived stem cell marker c-Kit were determined in LV tissue. In HF dogs, EDV and ESV increased and EF decreased after 3 mo of followup. Treatment with DARB prevented the increase in EDV, decreased ESV, and increased EF. DARB therapy also normalized the expression of HIF-1alpha and active caspase-3 and enhanced the expression of c-Kit. We conclude that chronic monotherapy with DARB prevents progressive LV dysfunction and dilation in nonanemic dogs with advanced HF. These results suggest that DARB elicits beneficial effects in HF that are independent of the presence of anemia.
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PMID:Darbepoetin-alpha prevents progressive left ventricular dysfunction and remodeling in nonanemic dogs with heart failure. 1895 19

COPD is a disease that is not confined to the airways and the lungs, but also produces systemic consequences. Muscle weakness is one of these. It is produced by a multitude of factors including deconditioning, systemic inflammation, oxidative stress, nutritional imbalance, reduced anabolic status, systemic corticosteroids, hypoxemia, hypercapnia, electrolyte disturbances, cardiac failure. The most important factors appear to be inactivity and systemic inflammation. Inactivity was shown to be present in patients with COPD from early in the course of the disease on. Systemic inflammation was shown to be predominantly present during COPD exacerbations. IL-6 has the propensity to reduce muscle function in experimental animals. At present there is no evidence of local production of cytokines in the muscle in patients with COPD. Muscle weakness is also important in the clinical course of the disease as it is associated with exercise intolerance, reduced quality of life, enhanced utilization of health care resources and reduced survival. Rehabilitation is the best treatment for muscle weakness and deconditioning in patients with COPD. Indeed, it is the intervention with the largest effect on health status and exercise capacity in these patients. Several factors that may enhance the effects of rehabilitation have been studied. These include: growth hormone/ IGF-I, anabolic steroids, clenbuterol, creatine, anti-cytokine treatment, erythropoietin, oxygen, non-invasive mechanical ventilation and electrical stimulation. Recently, the potential of protease-inhibitors in reversing deconditioning-induced muscle dysfunction was demonstrated. Adjuncts are potentially particularly useful in patients who do not respond to a rehabilitation programme. Analysis of large d-bases demonstrated that about one third of the patients does not respond to rehabilitation. A follow-up study suggests that decline in exercise capacity after a rehabilitation programme is particularly present in these patients and not in the patients with a clear initial response. A better understanding of the factors controlling the response to rehabilitation, may lead to significant advances in this field.
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PMID:Pulmonary rehabilitation 2007: from bench to practice and back. 1898 Jul 25

Anemia is a prevalent comorbidity in chronic heart failure (CHF). As studies have demonstrated close links between anemia and a poorer prognosis, there has been an interest in developing treatment strategies for this condition. Anemia is closely associated with disease severity and may be secondary to multiple modifiable causes; therefore, the initial strategies should always include a thorough search for etiology and should focus on optimizing heart failure treatment. Recently, more specific therapies have been assessed, namely erythropoiesis-stimulating agents and iron supplementation therapy. Studies evaluating erythropoietin in heart failure have demonstrated conflicting results to date, with smaller, single-center studies seeming to show a clinical benefit and larger, multicenter trials demonstrating no significant effect on clinical outcome aside from improvement in selected quality-of-life indices. Similarly, studies evaluating iron therapy alone in anemic patients with heart failure have so far shown promising results with regard to clinical and quality-of-life outcomes, but these studies are limited in that they involved small patient numbers. Ongoing studies such as the Reduction of Events With Darbepoetin Alfa in Heart Failure (RED-HF), Iron Supplementation in Heart Failure Patients With Anemia (IRON-HF), and Ferinject Assessment in Patients With Iron Deficiency and Chronic Heart Failure (FAIR-HF) trials will determine the value of darbepoetin alfa and intravenous iron replacement therapy in anemic CHF patients.
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PMID:Anemia in heart failure: to treat or not to treat? 1902 76


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