Are hematinic deficiencies the cause of anemia in chronic heart failure?

Witte, Klaus K.; Desilva, Ramesh; Chattopadhyay, Sudipta; Ghosh, Justin; Cleland, John G.F.; Clark, Andrew L.

doi:10.1016/j.ahj.2003.11.007

Cited by 114 publications

(94 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This study shows, in accordance with several previous reports, that anemia is frequent in chronic HF patients and associated with a lower exercise capacity [1][2][3][4][5][6]. Indeed, the prevalence of anemia we observed (26%) is in agreement with what has been reported previously (between 10 and 55%) [4].…”

Section: Discussionsupporting

confidence: 83%

“…The latter depends on hemoglobin, which reduction negatively affects the arterial oxygen concentration. Furthermore several reports showed that, in chronic HF patients, anemia is associated with low exercise capacity [5,6]. In principle, it is possible to calculate the amount of peak _ VO 2 loss due to anemia if hemoglobin arterial oxygen saturation is normal, and if peak exercise cardiac output and peak exercise oxygen extraction are known.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2010

View full text Add to dashboard Cite

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

show abstract

Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

View full text Add to dashboard Cite

show abstract

“…This mismatch between erythropoietin and haemoglobin may be because erythropoietin production is impaired in CHF or because there is erythropoietin resistance in the bone marrow (or both) [6,10,[16][17][18][19][20][21][22]. The chronic renal impairment that often accompanies CHF may also play a role, as a part of the pathophysiological ''vicious cycle'' that has been named the cardio-renal-anaemia syndrome [29].…”

Section: Erythropoietin In Chfmentioning

confidence: 99%

“…Surprisingly, although we know much about the prevalence and prognostic importance of anaemia in these patients, we know very little about its causation. We think the aetiology of anaemia in CHF is multifactorial, with impaired iron metabolism, bone marrow suppression by pro-inflammatory cytokines, inadequate erythropoietin production and blunted response to erythropoietin in the bone marrow among the suspected culprits [6,10,[16][17][18][19][20][21][22]. Other potential candidates include renal dysfunction, salt and water retention causing haemodilution and the use of drugs such as antiplatelet and anticoagulant agents which increase the risk of blood loss from the gastrointestinal tract [6,10,[16][17][18][19][20][21][22].…”

Section: Aetiology As a Basis For Treatmentmentioning

confidence: 99%

Approaches to the treatment of anaemia in patients with chronic heart failure

Murphy

McMurray

2008

Heart Fail Rev

View full text Add to dashboard Cite

“…The etiology of anemia in HF patients is thought to be multifactorial. Hemodilution (Androne et al 2003), chronic inflammation (Weiss and Goodnough 2005), renal dysfunction (Eschbach 2002), hemolysis (Kliger et al 2013), gastrointestinal bleeding (Holleran et al 2013), bone marrow dysfunction (Westenbrink et al 2010), resistance to erythropoietin (van der Meer et al 2008), hematinic deficiencies including vitamin B12, folic acid, and functional iron deficiency (FID) (Witte et al 2004;Opasich et al 2005) are thought to be etiological factors of anemia in HF patients. Especially, absolute and FID have been reported to be an important factor and a new term, cardiorenal-iron deficiency syndrome was proposed (Macdougall et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

Ohno¹,

Hanawa²,

Jiao³

et al. 2015

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n = 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting monocrotaline that causes pulmonary hypertension. The monocrotaline-treated rats displayed liver congestion with increase of hepcidin expression at 4 weeks after monocrotaline injection, followed by anemia and functional iron deficiency observed at 5 weeks. We conclude that liver congestion induces hepcidin production, which may result in anemia and functional iron deficiency in some patients with heart failure.

show abstract

Are hematinic deficiencies the cause of anemia in chronic heart failure?

Cited by 114 publications

References 30 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

Approaches to the treatment of anaemia in patients with chronic heart failure

Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

Contact Info

Product

Resources

About