Adaptive response of the heart to long-term anemia induced by iron deficiency

Naito, Yoshiro; Tsujino, Takeshi; Matsumoto, Mika; Sakoda, Tsuyoshi; Ohyanagi, Mitsumasa; Masuyama, Tohru

doi:10.1152/ajpheart.00463.2008

Cited by 133 publications

(112 citation statements)

References 29 publications

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“…They found that after 20 wk of ID anemia, the rats developed maladapted cardiac hypertrophy with severe left ventricular dysfunction and exhibited signs of decomposition with lung congestion [19] . Dilated ventricles were characterized by myocardial interstitial fibrosis and increased myocardial expression of A-type natriuretic peptide (ANP) and BNP, as well as a reduced myocardial expression of collagen type 3 genes [20] . In the present study, we demonstrated that CKD patients with lower serum hepcidin-25 levels had greater LVMIs and LVMs.…”

Section: Discussionmentioning

confidence: 99%

Hepcidin-25 negatively predicts left ventricular mass index in chronic kidney disease patients

Hsieh

Huang²,

Lee³

et al. 2013

WJN

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AIM:To assess the correlation between the serum hepcidin-25 level and left ventricular mass index. METHODS:This study was a cross-sectional study conducted between March 2009 and April 2010. Demographic and biochemical data, including the serum hepcidin-25 level, were collected for chronic kidney disease (CKD) patients. Two-dimensional echocardiography was performed to determine the left ventricle mass (LVM), left ventricular mass index (LVMI), interventricular septum thickness (IVSd), left ventricle posterior wall thickness (LVPW), right ventricular dimension (RVD), left atrium (LA) and ejection fraction (EF). RESULTS:A total of 146 patients with stage 1 to 5 CKD were enrolled. Serum hepcidin-25 levels were 16.51 ± 5.2, 17.59 ± 5.32, 17.38 ± 6.47, 19.98 ± 4.98 and 22.03 ± 4.8 ng/mL for stage 1 to 5 CKD patients, respectively. Hepcidin-25 level was independently predicted by the serum ferritin level (β = 0.6, P = 0.002) and the estimated glomerular filtration rate (β = -0.48, P = 0.04). There were negative correlations between the serum hepcidin level and the LVM and LVMI (P = 0.04 and P = 0.005, respectively). Systolic blood pressure (BP) was positively correlated with the LVMI (P = 0.005). In the multivariate analysis, a decreased serum hepcidin-25 level was independently associated with a higher LVMI (β = -0.28, 95%CI: -0.48 --0.02, P = 0.006) after adjusting for body mass index, age and systolic BP. CONCLUSION:A lower serum hepcidin level is associated with a higher LVMI in CKD patients. Low hepcidin levels may be independently correlated with unfavorable cardiovascular outcomes in this population.

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Section: Discussionmentioning

confidence: 99%

Hepcidin-25 negatively predicts left ventricular mass index in chronic kidney disease patients

Hsieh

Huang²,

Lee³

et al. 2013

WJN

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“…Studies on iron in rat models of systemic cardiovascular disease have provided inconsistent results, with protective [71] as well as detrimental effects being attributed to iron deficiency [72,73]. Such differences may reflect variations in iron handling between rat strains [71,74].…”

Section: Iron Deficiency As a Potential Therapeutic Target In Ipahmentioning

confidence: 99%

Iron deficiency in pulmonary arterial hypertension: a potential therapeutic target

Rhodes¹,

Wharton²,

Howard³

et al. 2011

Eur Respir J

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Iron deficiency is known to be common and detrimental in chronic left heart failure, where parenteral iron treatment has been shown to improve exercise capacity, New York Heart Association functional class and patient wellbeing. There is now increasing interest in the role of iron in the natural history of pulmonary arterial hypertension (PAH). Iron availability influences the pulmonary vasoconstrictor response to hypoxia and accumulating evidence indicates that iron deficiency is prevalent in idiopathic and heritable forms of PAH, iron status being related to exercise capacity, symptoms and poorer survival in patients with idiopathic PAH (IPAH). Potential mechanisms behind iron deficiency in IPAH include inhibition of dietary iron uptake by the master iron regulator hepcidin. High hepcidin levels underlie the anaemia of chronic disease. Possible stimuli of the observed high levels of hepcidin in IPAH include dysfunctional bone morphogenetic protein receptor type II signalling and inflammation. Iron status may influence outcomes through modulation of the pulmonary circulation as well as myocardial and skeletal muscle function. Two parallel studies, from our centre (Hammersmith Hospital, London, UK) and others in the UK and Amsterdam (the Netherlands), investigating the safety and potential benefit of iron supplementation in patients with PAH are currently under way.

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“…Piloto et al implicated the heart failure as cause of sudden death when was present [10] with brain vascular congestion; left ventricular hypertrophy and elevated hematocrit in rats. Naito et al implicated decreased serum Epo concentration for [11] the cardiac remodeling mechanisms induced by iron deficiency anemia promoting cardiac fibrosis and lung congestion. Kiris et al proved [12] that Epo significantly decreased (P=0.05 versus aortic IR) the focal renoglomerular necrosis, the Bowman's capsule dilatation, the tubular epithelium degeneration, the tubular epithelium necrosis, interstitial tissues inflammatory cells infiltration and the blood vessels congestion upon aortic IR in rats.…”

Section: Discussionmentioning

confidence: 99%

The Erythropoietin Effect on Uterus Congestion after Uterine Ischemia Reperfusion

Tsompos¹,

Panoulis²,

Toutouzas³

et al. 2017

Transl Biomed

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Objective:This experiment investigated the erythropoietin (Epo) effect after uterine ischemiareperfusion (IR) in rats. The effect of Epo was evaluated studying the mean uterine congestion (UC) lesions. Materials and methods:The mean weight of 40 rats used in the study was 247.7 g. The UC lesions were estimated for the groups A and C on 60 min and for the groups B and D on 120 min after reperfusion. Only the groups C and D were administered by Epo.Results: Epo administration non-significantly declined the UC lesions scores by (without lesions) 0.15 (-0.5595137-0.2595137) (p=0.4545). Reperfusion time non-significantly raised the UC lesions scores by (without lesions) 0.15 (-0.5676974-0.3676974) (P=0.5058). However, the combined Epo administration with reperfusion time non-significantly declined the UC lesions scores by (without lesions) 0.0090909 (-0.2577992-0.2396174) (p=0.9414). Conclusions:The Epo administration presented a nonsignificantly declining short-term effect on UC lesions scores. Perhaps, a higher Epo dosage and/or an experimental time lasting longer than 2 hours may reveal more significant efficacies.

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Adaptive response of the heart to long-term anemia induced by iron deficiency

Abstract: Naito Y, Tsujino T, Matsumoto M, Sakoda T, Ohyanagi M, Masuyama T. Adaptive response of the heart to long-term anemia induced by iron deficiency.

Cited by 133 publications

References 29 publications

Hepcidin-25 negatively predicts left ventricular mass index in chronic kidney disease patients

Hepcidin-25 negatively predicts left ventricular mass index in chronic kidney disease patients

Iron deficiency in pulmonary arterial hypertension: a potential therapeutic target

The Erythropoietin Effect on Uterus Congestion after Uterine Ischemia Reperfusion

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