Does myocardial iron load determine the severity of heart insufficiency?

Leszek, Przemysław; Sochanowicz, Barbara; Brzóska, Kamil; Danko, B.; Kraj, Leszek; Kuśmierczyk, Mariusz; Piotrowski, Walerian; Sobieszczańska−Małek, Małgorzata; Rywik, Tomasz; Polkowska-Motrenko, Halina; Kruszewski, Marcin

doi:10.1016/j.ijcard.2015.01.006

Cited by 9 publications

(13 citation statements)

References 9 publications

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“…Furthermore, normal systemic iron stores do not guarantee adequate myocardial iron. Indeed we 3 and others 10 have previously shown that myocardial iron content in explanted human failing hearts may be decreased despite normal systemic iron stores. Furthermore, data concerning iron status in explanted failing hearts are not consistent.…”

Section: Discussionmentioning

confidence: 79%

“…Furthermore, decreased myocardial iron content can occur despite normal parameters of systemic iron turnover. We have previously shown that myocardial iron content in HF patients is lower than expected based on systemic iron turnover parameters (ferritin concentration, transferrin saturation) 3 . To make this even more complex, there can be iron shifts between specific intracellular compartments despite normal myocardial iron content 4 .…”

Section: Introductionmentioning

confidence: 78%

“… 4 even found increased cytosolic iron content in explanted failing hearts. However, others have shown that in myocardial samples from explanted failing hearts 3 , 4 , 12 , 13 myocardial iron content was reduced by up to 30%.…”

Section: Discussionmentioning

confidence: 95%

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Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores

Paterek

Kępska

Sochanowicz

et al. 2018

Sci Rep

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Iron deficiency (ID) commonly occurs in chronic heart failure (HF) and is associated with poor prognosis. Neither its causes nor pathophysiological significance are clearly understood. We aimed to assess iron status and the effect of iron supplementation in the rat model of post-myocardial infarction (MI) HF. Four weeks after induction of MI to induce HF or sham surgery, rats received intravenous iron (ferric carboxymaltose) or saline, 4 doses in 1-week intervals. HF alone did not cause anemia, systemic or myocardial ID, but reduced myocardial ferritin, suggesting depleted cardiomyocyte iron stores. Iron therapy increased serum Fe, ferritin and transferrin saturation as well as cardiac and hepatic iron content in HF rats, but did not increase myocardial ferritin. This was accompanied by: (1) better preservation of left ventricular (LV) ejection fraction and smaller LV dilation, (2) preservation of function of Ca2+ handling proteins in LV cardiomyocytes and (3) reduced level of inflammatory marker, CRP. Furthermore, iron supplementation did not potentiate oxidative stress or have toxic effects on cardiomyocyte function, but increased activity of antioxidant defenses (cardiac superoxide dismutase). Despite lack of systemic or myocardial ID we found evidence of depleted cardiomyocyte iron stores in the rat model of HF. Furthermore we observed positive effect of iron supplementation and confirmed safety of iron supplementation in this setting.

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 78%

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Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores

Paterek

Kępska

Sochanowicz

et al. 2018

Sci Rep

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“…M-Iron load at the cellular level was recently shown to be reduced in the failing heart, without significant changes in the expression of M-FR and M-sTfR1 [ 13 , 14 ]. However, in patients with M-Iron deficiency, M-Iron reduction is accompanied by decreased M-FR expression [ 13 , 14 ].…”

Section: Resultsmentioning

confidence: 99%

“…Myocardial iron (M-Iron) metabolism has also been shown to be strongly related to left ventricle (LV) remodeling in HF [ 13 , 14 ]. Indeed, based on an experimental rat model, we know that ID-anemia leads to molecular heart remodeling and, finally, LV dilatation [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Accurate Noninvasive Assessment of Myocardial Iron Load in Advanced Heart Failure Patients

et al. 2020

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Background. Heart failure patients presenting with iron deficiency can benefit from systemic iron supplementation; however, there is the potential for iron overload to occur, which can seriously damage the heart. Therefore, myocardial iron (M-Iron) content should be precisely balanced, especially in already failing hearts. Unfortunately, the assessment of M-Iron via repeated heart biopsies or magnetic resonance imaging is unrealistic, and alternative serum markers must be found. This study is aimed at assessing M-Iron in patients with advanced heart failure (HF) and its association with a range of serum markers of iron metabolism. Methods. Left ventricle (LV) myocardial biopsies and serum samples were collected from 33 consecutive HF patients (25 males) with LV dysfunction (LV ejection fraction 22 (11) %; NT-proBNP 5464 (3308) pg/ml) during heart transplantation. Myocardial ferritin (M-FR) and soluble transferrin receptor (M-sTfR1) were assessed by ELISA, and M-Iron was determined by Instrumental Neutron Activation Analysis in LV biopsies. Nonfailing hearts ( n = 11 ) were used as control/reference tissue. Concentrations of serum iron-related proteins (FR and sTfR1) were assessed. Results. LV M-Iron load was reduced in all HF patients and negatively associated with M-FR ( r = − 0.37 , p = 0.05 ). Of the serum markers, sTfR1/logFR correlated with ( r = − 0.42 ; p = 0.04 ) and predicted (in a step-wise analysis, R 2 = 0.18 ; p = 0.04 ) LV M-Iron. LV M-Iron load (μg/g) can be calculated using the following formula: 210.24 – 22.869 × sTfR 1 / logFR . Conclusions. The sTfR1/logFR ratio can be used to predict LV M-Iron levels. Therefore, serum FR and sTfR1 levels could be used to indirectly assess LV M-Iron, thereby increasing the safety of iron repletion therapy in HF patients.

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Cardiac iron concentration in relation to systemic iron status and disease severity in non‐ischaemic heart failure with reduced ejection fraction

Hirsch

Tongers

Bode

et al. 2020

European J of Heart Fail

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Aims Low cardiac iron levels promote heart failure in experimental models. While cardiac iron concentration (CI) is decreased in patients with advanced heart failure with reduced ejection fraction (HFrEF), CI has never been measured in non‐advanced HFrEF. We measured CI in left ventricular (LV) endomyocardial biopsies (EMB) from patients with non‐advanced HFrEF and explored CI association with systemic iron status and disease severity. Methods and results We enrolled 80 consecutive patients with non‐ischaemic HFrEF with New York Heart Association class II or III symptoms and a median (interquartile range) LV ejection fraction of 25 (18–33)%. CI was 304 (262–373) μg/g dry tissue. CI was not related to immunohistological findings or the presence of cardiotropic viral genomes in EMBs and was not related to biomarkers of systemic iron status or anaemia. Patients with CI in the lowest quartile (CIQ1) had lower body mass indices and more often presented with heart failure histories longer than 6 months than patients in the upper three quartiles (CIQ2–4). CIQ1 patients had higher serum N‐terminal pro‐B‐type natriuretic peptide levels than CIQ2–4 patients [3566 (1513–6412) vs. 1542 (526–2811) ng/L; P = 0.005]. CIQ1 patients also had greater LV end‐diastolic (P = 0.001) and end‐systolic diameter indices (P = 0.003) and higher LV end‐diastolic pressures (P = 0.046) than CIQ2–4 patients. Conclusion Low CI is associated with greater disease severity in patients with non‐advanced non‐ischaemic HFrEF. CI is unrelated to systemic iron homeostasis. The prognostic and therapeutic implications of CI measurements in EMBs should be further explored.

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Does myocardial iron load determine the severity of heart insufficiency?

Cited by 9 publications

References 9 publications

Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores

Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores

Accurate Noninvasive Assessment of Myocardial Iron Load in Advanced Heart Failure Patients

Cardiac iron concentration in relation to systemic iron status and disease severity in non‐ischaemic heart failure with reduced ejection fraction

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