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      Noninvasive Imaging Estimation of Myocardial Iron Repletion Following Administration of Intravenous Iron: The Myocardial‐IRON Trial

      research-article
      , MD, PhD 1 , 2 , , , MD, PhD 1 , 2 , , MD 1 , , MD, PhD 3 , , MD, PhD 4 , , MD, PhD 5 , , MD, PhD 6 , , MD, PhD 7 , , MD, PhD 7 , , MD 1 , , MD 1 , , MD 3 , , MD 5 , , MD 6 , , MD 1 , 2 , , MD 1 , 2 , , MD, PhD 1 , 2 , , MD 1 , , MD, PhD 2 , 8 , 9 , , MD, PhD 10 , , MD, PhD 11 , , MD, PhD 1 , 2 , , MD, PhD 1 , 2 , , MD, PhD 12 , 13 , 14 , , MD, PhD 2 , 8 , 9 , , the Myocardial‐IRON Investigators*
      Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
      John Wiley and Sons Inc.
      cardiac magnetic resonance, ferric carboxymaltose, heart failure, iron deficiency, myocardial iron, Cardiomyopathy, Magnetic Resonance Imaging (MRI), Pharmacology, Treatment

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          Abstract

          Background

          Intravenous ferric carboxymaltose ( FCM) improves symptoms, functional capacity, and quality of life in heart failure and iron deficiency. The mechanisms underlying these effects are not fully understood. The aim of this study was to examine changes in myocardial iron content after FCM administration in patients with heart failure and iron deficiency using cardiac magnetic resonance.

          Methods and Results

          Fifty‐three stable heart failure and iron deficiency patients were randomly assigned 1:1 to receive intravenous FCM or placebo in a multicenter, double‐blind study. T2* and T1 mapping cardiac magnetic resonance sequences, noninvasive surrogates of intramyocardial iron, were evaluated before and 7 and 30 days after randomization using linear mixed regression analysis. Results are presented as least‐square means with 95% CI. The primary end point was the change in T2* and T1 mapping at 7 and 30 days. Median age was 73 (65–78) years, with N‐terminal pro‐B‐type natriuretic peptide, ferritin, and transferrin saturation medians of 1690 pg/mL (1010–2828), 63 ng/mL (22–114), and 15.7% (11.0–19.2), respectively. Baseline T2* and T1 mapping values did not significantly differ across treatment arms. On day 7, both T2* and T1 mapping (ms) were significantly lower in the FCM arm (36.6 [34.6–38.7] versus 40 [38–42.1], P=0.025; 1061 [1051–1072] versus 1085 [1074–1095], P=0.001, respectively). A similar reduction was found at 30 days for T2* (36.3 [34.1–38.5] versus 41.1 [38.9–43.4], P=0.003), but not for T1 mapping (1075 [1065–1085] versus 1079 [1069–1089], P=0.577).

          Conclusions

          In patients with heart failure and iron deficiency, FCM administration was associated with changes in the T2* and T1 mapping cardiac magnetic resonance sequences, indicative of myocardial iron repletion.

          Clinical Trial Registration

          URL: http://www.clinicaltrials.gov. Unique identifier: NCT03398681.

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          Most cited references20

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          Intravenous iron reduces NT-pro-brain natriuretic peptide in anemic patients with chronic heart failure and renal insufficiency.

          Our objective was to evaluate in a double-blind, randomized, placebo-controlled study possible modifications in NT-pro-brain natriuretic peptide (NT-proBNP) and C-reactive protein (CRP) levels together with clinical and functional parameters, in a group of anemic patients with chronic heart failure (CHF) and chronic renal failure (CRF) receiving intravenous iron therapy, without recombinant human erythropoietin (rhEPO), versus placebo. Chronic heart failure and CRF associated with absolute or relative iron deficiency anemia is a common problem. This situation is linked with a variable inflammatory status. Both NT-proBNP and CRP are recognized markers for left ventricular dysfunction and inflammatory status, respectively. In this double-blind, randomized, placebo-controlled study, modifications in NT-proBNP and CRP level and clinical and functional parameters, in anemic patients with CHF and CRF receiving intravenous iron therapy, without rhEPO, versus placebo were evaluated. Forty patients with hemoglobin (Hb) <12.5 g/dl, transferrin saturation <20%, ferritin <100 ng/ml, creatinine clearance (CrCl) <90 ml/min, and left ventricular ejection fraction (LVEF) < or =35% were randomized into 2 groups (n = 20 for each). For 5 weeks, group A received isotonic saline solution and group B received iron sucrose complex, 200 mg weekly. Minnesota Living with Heart Failure Questionnaire (MLHFQ) and 6-min walk (6MW) test were performed. NT-pro brain natriuretic peptide and CRP were evaluated throughout the study. No patients received erythroprotein any time. After 6 months follow-up, group B showed better hematology values and CrCl (p < 0.01) and lower NT-proBNP (117.5 +/- 87.4 pg/ml vs. 450.9 +/- 248.8 pg/ml, p < 0.01) and CRP (2.3 +/- 0.8 mg/l vs. 6.5 +/- 3.7 mg/l, p < 0.01). There was a correlation initially (p < 0.01) between Hb and NT-proBNP (group A: r = -0.94 and group B: r = -0.81) and after 6 months only in group A: r = -0.80. Similar correlations were observed with Hb and CRP. Left ventricular ejection fraction percentage (35.7 +/- 4.7 vs. 28.8 +/- 2.4), MLHFQ score, and 6MW test were all improved in group B (p < 0.01). Additionally, group B had fewer hospitalizations: 0 of 20 versus group A, 5 of 20 (p < 0.01; relative risk = 2.33). Intravenous iron therapy without rhEPO substantially reduced NT-proBNP and inflammatory status in anemic patients with CHF and moderate CRF. This situation was associated with an improvement in LVEF, NYHA functional class, exercise capacity, renal function, and better quality of life.
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            Iron Deficiency in Heart Failure

            Iron deficiency is an extremely common comorbidity in patients with heart failure, affecting up to 50% of all ambulatory patients. It is associated with reduced exercise capacity and physical well-being and reduced quality of life. Cutoff values have been identified for diagnosing iron deficiency in heart failure with reduced ejection fraction as serum ferritin, <100 μg/l, or ferritin, 100 to 300 μg/l, with transferrin saturation of <20%. Oral iron products have been shown to have little efficacy in heart failure, where the preference is intravenous iron products. Most clinical studies have been performed using ferric carboxymaltose with good efficacy in terms of improvements in 6-min walk test distance, peak oxygen consumption, quality of life, and improvements in New York Heart Association functional class. Data from meta-analyses also suggest beneficial effects for hospitalization rates for heart failure and reduction in cardiovascular mortality rates. A prospective trial to investigate effects on morbidity and mortality is currently ongoing. This paper highlights current knowledge of the pathophysiology of iron deficiency in heart failure, its prevalence and clinical impact, and its possible treatment options.
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              Myocardial iron content and mitochondrial function in human heart failure: a direct tissue analysis

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                Author and article information

                Contributors
                yulnunez@gmail.com
                abayesgenis@gmail.com
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                13 February 2020
                18 February 2020
                : 9
                : 4 ( doiID: 10.1002/jah3.v9.4 )
                : e014254
                Affiliations
                [ 1 ] Cardiology Department Hospital Clínico Universitario de Valencia Universidad de Valencia INCLIVA Valencia Spain
                [ 2 ] CIBER Cardiovascular Universitat Jaume I Castellón Spain
                [ 3 ] Cardiology Department Hospital General de Castellón Universitat Jaume I Castellón Spain
                [ 4 ] Internal Medicine Department Hospital de Manises Manises Spain
                [ 5 ] Cardiology Department Hospital General Universitario de Valencia Valencia Spain
                [ 6 ] Cardiology Department Hospital Universitario La Fe de Valencia Valencia Spain
                [ 7 ] Unidad de Imagen Cardiaca (ERESA) Hospital Clínico Universitario de Valencia Valencia Spain
                [ 8 ] Cardiology Department and Heart Failure Unit Hospital Universitari Germans Trias i Pujol Badalona Spain
                [ 9 ] Universitat Autonoma de Barcelona Barcelona Spain
                [ 10 ] Hospital Clínico Universitario de Valencia Universidad de Valencia INCLIVA Valencia Spain
                [ 11 ] Nephrology Department Hospital Clínico Universitario de Valencia Universidad de Valencia INCLIVA Valencia Spain
                [ 12 ] Department of Cardiology Hospital del Mar Barcelona Spain
                [ 13 ] Heart Diseases Biomedical Research Group IMIM (Hospital del Mar Medical Research Institute) Barcelona Spain
                [ 14 ] Department of Medicine Universitat Autònoma de Barcelona Barcelona Spain
                Author notes
                [*] [* ] Correspondence to: Julio Núñez, MD, PhD, Cardiology Department, Hospital Clínico Universitario de Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain. E‐mail: yulnunez@ 123456gmail.com Antoni Bayés‐Genís, MD, PhD, Cardiology Department and Heart Failure Unit, Hospital Universitari Germans Trias i Pujol, Badalona, Spain. Universitat Autonoma de Barcelona, Barcelona, Spain. E‐mail: abayesgenis@ 123456gmail.com
                [†]

                A complete list of the Myocardial‐IRON Investigators can be found in the Appendix at the end of the article.

                Article
                JAH34791
                10.1161/JAHA.119.014254
                7070181
                32067585
                b6be4790-c67f-4b10-b8c2-0b0c7a4c5410
                © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 18 September 2019
                : 19 December 2019
                Page count
                Figures: 4, Tables: 2, Pages: 12, Words: 7545
                Funding
                Funded by: Vifor Pharma , open-funder-registry 10.13039/501100006484;
                Funded by: Sociedad Española de Cardiología
                Categories
                Original Research
                Original Research
                Heart Failure
                Custom metadata
                2.0
                18 February 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.6.1 mode:remove_FC converted:04.03.2020

                Cardiovascular Medicine
                cardiac magnetic resonance,ferric carboxymaltose,heart failure,iron deficiency,myocardial iron,cardiomyopathy,magnetic resonance imaging (mri),pharmacology,treatment

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