Erythropoietin treatment in patients with chronic heart failure: a meta-analysis

Meer, van der Peter; Groenveld, Hessel F.; Januzzi, James L.; Veldhuisen, van Dirk

doi:10.1136/hrt.2008.161091

Cited by 117 publications

(75 citation statements)

References 31 publications

(41 reference statements)

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“…Several studies have focused on the effect of anemia correction, usually by iron and erythropoietin or darbopoietin, on exercise performance, measured either by peak _ VO 2 , exercise tolerance or by distance walked at the 6 min walking test, in both HF and non-HF patients [21][22][23][24][25][26][27][28][29]. However, only four [21][22][23] reports all based on small studies, showed the effect of anemia correction on peak exercise _ VO 2 in HF patients, with discordant findings.…”

Section: Discussionmentioning

confidence: 97%

Relationship of resting hemoglobin concentration to peak oxygen uptake in heart failure patients

et al. 2010

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Anemia is frequent in chronic heart failure (HF). To calculate what change in peak oxygen uptake ( _ VO 2 ) should be expected in the event of changes in hemoglobin concentration, we studied the correlation between peak _ VO 2 and hemoglobin concentration in a large HF population. We carried out retrospective analysis of all cardiopulmonary exercise tests (CPET) performed in our HF Clinic between June 2001 and March 2009 in HF patients who had a resting hemoglobin concentration measurement taken within 7 days of the CPET. We collected 967 CPETs, 704 tests were considered maximal and analyzed. We identified 181 patients (26%) as anemic. Peak _ VO 2 was lower (P < 0.001) in anemic patients (971 ± 23 ml/min) compared with nonanemic (1243 ± 18 ml/min). The slope of the _ VO 2 vs. hemoglobin ratio was 109 ml/min/g/dl at peak exercise. This correlation remained significant also when several confounding variables were analyzed by multivariate analysis. As an average, each gram of hemoglobin accounts, at peak exercise, for 109 ml/min change in _ VO 2 which is equivalent to 0.97 ml/min/kg. Therefore, in HF patients anemia treatment should increase _ VO 2 by 109 ml/min for each g/dl of hemoglobin increase. Am. J. Hematol. 85:414-417, 2010. V

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Section: Discussionmentioning

confidence: 97%

Relationship of resting hemoglobin concentration to peak oxygen uptake in heart failure patients

et al. 2010

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“…They found that patients treated with ESAs had a 47% reduction in HF related hospitalizations. They did not find a difference in mortality between the two groups, or any increase in risk of hypertension or venous thrombosis in the ESAs treated arms, 83 but the sample size may have still been too small. 83 Silverberg reported on an analysis of 10 RCTs.…”

Section: Dovepressmentioning

confidence: 94%

“…They did not find a difference in mortality between the two groups, or any increase in risk of hypertension or venous thrombosis in the ESAs treated arms, 83 but the sample size may have still been too small. 83 Silverberg reported on an analysis of 10 RCTs. These studies succeeded in raising mean hemoglobin to 12 to 13 g/dL, with no adverse effects and some benefits.…”

Section: Dovepressmentioning

confidence: 94%

Managing anemia in patients with chronic heart failure: what do we know?

Sandhu

Soman²,

Hudson³

et al. 2010

VHRM

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Anemia is common in patients with chronic heart failure (HF) with an incidence ranging from 4% to 55% depending on the studied population. Several studies have highlighted that the prevalence of anemia increases with worsening heart failure as reflected by New York Heart Association classification. Additionally, several epidemiological studies have highlighted its role as a prognostic marker, linking it to worse outcomes including; malnutrition, increased hospitalizations, refractory heart failure and death. The pathophysiology of anemia is multifactorial and related to various factors including; hemodilution, iron losses from anti-platelet drugs, activation of the inflammatory cascade, urinary losses of erythropoietin and associated renal insufficiency. There are a host of epidemiological studies examining HF outcomes and anemia, but only a few randomized trials addressing this issue. The purpose of this article is to review the literature that examines the interrelationship of anemia and congestive HF, analyzing its etiology, impact on outcomes and also the role of associated kidney disease as well as cardiorenal syndrome both as a marker of morbidity and mortality.

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“…In a recent meta-analysis of seven of these randomized trials of erythropoietic agents in CHF patients, including 363 treated patients and 287 controls, there was a significantly lower risk for CHF hospitalization (RR, 0.59; p ϭ .006) [69]. No differences occurred in mortality or in the incidence of hypertension, venous thrombosis, pulmonary embolus, cerebrovascular disorder, myocardial infarction, or other cardiovascular events [69].…”

Section: The Effect Of Treating Anemia On Chfmentioning

confidence: 99%

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

2009

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In treating moderate to severe anemia of chronic kidney disease (CKD), oral iron is effective only in a minority of nondialysis patients. Intravenous iron is more effective and can raise levels of hemoglobin even without the use of erythropoiesis-stimulating agents (ESAs). Unfortunately, the current assays of iron status that are presently widely available are not especially helpful in predicting response. In patients on dialysis, i.v. iron is effective over a wide range of serum ferritin from <100 ng/ml to 800 ng/ml. None of the three available randomized controlled trials comparing oral with i.v. iron showed evidence of nephrotoxicity caused by i.v. iron.Iron deficiency is a risk factor for thrombocytosis and should, wherever possible, be avoided. Optimal coadministration of iron may reduce the risk for ESA-driven cardiovascular events. Increased total body iron stores (imperfectly reflected by serum ferritin levels in CKD) do not appear to be related to such events or hospitalization in CKD; it is unclear what other risk factors and mechanisms need to be considered.In the appreciable proportion of patients with both renal and cardiac dysfunction, management is further complicated by a vicious circle (which can be characterized as cardiorenal anemia syndrome) in which CKD, heart failure, and anemia exacerbate each other. In such patients, correction of anemia appears to improve cardiac function and quality of life without a greater risk for adverse events. The Oncologist 2009;14(suppl 1):22-33

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Erythropoietin treatment in patients with chronic heart failure: a meta-analysis

Cited by 117 publications

References 31 publications

Relationship of resting hemoglobin concentration to peak oxygen uptake in heart failure patients

Relationship of resting hemoglobin concentration to peak oxygen uptake in heart failure patients

Managing anemia in patients with chronic heart failure: what do we know?

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

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