Myocardial iron homeostasis in advanced chronic heart failure patients

Abstract

BackgroundAlthough, correction of iron deficiency and/or anemia in heart failure (HF) with iron seems promising, little is known about myocardial iron load and homeostasis. Moreover iron supplementation indications are solely based on iron serum markers. The purpose was to assess myocardial iron (M-Iron), ferritin (M-FR), transferrin receptor (M-sTfR) in HF in relation to serum Iron markers. Methods and resultsStudy group 33 patients, left/right ventricle (LV/RV) (LVEDV 245±84ml; LVESV 189±85ml; LVEF 22±11%; RVD 32±10mm), NTproBNP (5464±4825pg/ml).Iron homeostasis assessment serum: iron, FR, transferrin/saturation (TSAT), sTfR; myocardial: M-Iron (Instrumental Neutron Activation Analysis, μg/g), M-FR, M-sTfR (ELISA – ng/mg protein) in the explanted failing hearts (FH), compared to non-failing hearts (NFH n=11).In FH as compared to NFH, M-Iron was reduced in RV (174±45 vs 233±97, respectively, p=0.07), LV (189±58 vs 265±119, p=0.04), without significant changes in M-FR/M-sTfR. Out of all serum iron markers only sTfR was negatively correlated with M-Iron in either ventricle (RV r=−0.44, p=0.03, LV r=−0.38, p=0.07).With regard to serum iron status, based on TSAT, patients were divided into two subgroups: reduced (TSAT<15%; n=11) and not-reduced serum iron (TSAT≥15%; n=22). Both subgroups had similar grade of LV/RV dysfunction, NT-proBNP levels. M-FR was lower in TSAT<15% than in TSAT≥15% (LV −31±26 vs 46±29; p=0.07) and (RV –24±24 vs 43±29; p=0.02), without differences in M-Iron and M-sTfR. ConclusionsIn HF, M-Iron levels were reduced. Serum iron markers did not reflect M-Iron levels, except for serum sTfR. In reduced serum iron group, decrease in myocardial storage protein M-FR was observed.