P85A proper characterization of myocardial iron load and homeostasis based on serum markers in advanced heart failure

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Correcting iron deficiency with the use of iv iron supplementation in patients with heart failure (HF) with/without anemia may result in clinical improvement, however iron deficiency diagnosis has been solely based on such serum markers as ferritin (FR) and transferrin (TR) saturation (TSAT), being the main criterion for introducing iron supplementation. A proper characterization of iron homeostasis seems important, as the additional iron supplementation could potentially exert a harmful effect related to production of intracellular reactive oxygen species. So the aim of this study was to characterize the relation between myocardial iron (Iron-M), FR (FR-M), transferrin receptor (sTfR-M) and serum iron markers and to compare HF population with relation to Iron-M. FR-M is the main iron storage protein, whereas sTfR-M takes part in iron acquisition.

Methods and Results

Study group 33 patients, left/right ventricle (LV/RV) (LVEDV 245 ± 84 ml; LVESV 189 ± 85 ml; LVEF 22 ± 11%; RVD 32 ± 10 mm), NTproBNP (5464 ± 4825 pg/ml). Serum iron homeostasis assessment: iron, FR, TR/TSAT, sTfR, sTfR/logFR TIBC, UIBC, EPO. Myocardial Iron-M (Instrumental Neutron Activation Analysis, μg/g), FR-M, sTfR-M (ELISA – ng/mg protein) in the explanted failing hearts (FH), compared to non-failing hearts (NFH n=11).

Methods and Results

In multivariate regression analysis/Pearson correlation out of all serum iron markers the independent predictors of myocardial variables were In LV: for Iron-M – sTfR/logFR (R2=0.18 , p=0.04; r=-0.49, p=0.04, respectively); for sTfR-M – sTfR/logFR (R2=0.52, p < 0.0001; r=-0.77, p < 0.0001), for FR-M – FR (R2=0.17 , p=0.03; r=0.42, p=0.03); In RV: for Iron-M – sTfR(R2=0.29, p=0.03, r=-0.44, p=0.03, respectively); for sTfR-M –sTfR/logFR (R2=0.38 , p=0.0005; r=-0.62, p=0.0005); for FR-M – TR (R2=0.24, p=0.009, r=-0.48, p=0.009).

Methods and Results

With regard to Iron-M, patients were divided into reduced (n = 14) and non-reduced Iron-M (n = 19) subgroups. Both subgroups had similar degree of LV/RV dysfunction, NT-proBNP levels. FR-M was lower in reduced than non-reduced Iron-M group (LV –178 ± 80 vs 199 ± 51; p=0.08) and (RV – 159 ± 46 vs 189 ± 39; p=0.024), without differences in sTfR-M.


In HF patients a proper characterization of myocardial iron load and homeostasis, based on serum markers, required TR, FR, sTfR assessment and sTfR/logFR calculation. In low myocardial iron group, decrease in myocardial storage protein FR-M was observed without differences in LV/RV dysfunction degree.

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