{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T05:54:18Z","timestamp":1793426058869,"version":"4.5.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"16","license":[{"start":{"date-parts":[[2025,2,5]],"date-time":"2025-02-05T00:00:00Z","timestamp":1738713600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100001003","name":"Boehringer Ingelheim","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001003","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004312","name":"Eli Lilly Company","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004312","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Comprehensive Heart Failure Centre, University of W\u00fcrzburg, Germany","award":["01EO1004"],"award-info":[{"award-number":["01EO1004"]}]},{"DOI":"10.13039\/100007277","name":"Atherothrombosis Research Unit, Icahn School of Medicine at Mount Sinai","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007277","id-type":"DOI","asserted-by":"publisher"}]},{"name":"University Center for Cardiovascular Science"},{"DOI":"10.13039\/501100012680","name":"University of Hamburg-Eppendorf, Germany","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100012680","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,4,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Sodium-glucose cotransporter 2 inhibitors (SGLT2i) impact iron metabolism in patients with heart failure but mechanisms are incompletely understood. This post hoc analysis explored interrelations between iron homeostasis, cardiac structure\/function, exercise capacity, haematopoiesis, and sympathetic activity at baseline, and the effects of 6-month treatment with empagliflozin vs. placebo by anaemia status in EMPATROPISM-FE study participants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Myocardial iron content (MIC, estimated by cardiac magnetic resonance T2* imaging), left ventricular (LV) volumes and LV ejection fraction (LVEF), exercise capacity, laboratory iron markers (LIM), haemoglobin\/haematocrit, erythropoietin, and plasma norepinephrine were determined at baseline and 6 months.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>At baseline, 24\/80 participants (30%) had anaemia (haemoglobin &amp;lt; 13\/&amp;lt;12\u2005mg\/dL in men\/women). Patients with vs. without anaemia had higher T2* (indicating lower MIC, P &amp;lt; .001), lower peak oxygen consumption (VO2max, P = .024) and hepcidin (P = .017), and higher erythropoietin (P = .040) and norepinephrine (P = .016). Across subgroups, lower MIC correlated with higher LV volumes (P &amp;lt; .01) and norepinephrine (P &amp;lt; .001), and lower LVEF (P &amp;lt; .01), VO2max (P &amp;lt; .001) and haemoglobin\/haematocrit (P &amp;lt; .001). Associations with LIM were poor (all P &amp;gt; .10). Empagliflozin increased MIC (P &amp;lt; .012), improved exercise capacity, and activated haematopoiesis. Changes in LIM and norepinephrine suggested progressive systemic iron depletion and sympatholysis. LV reverse remodelling was greater in individuals with anaemia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Dysregulated cellular iron uptake\/availability may be a shared mechanism in myocardial structural\/functional impairment, reduced exercise capacity, and restricted haematopoiesis in heart failure, which are worse in patients with anaemia, and improve with empagliflozin. Empagliflozin increases MIC and decreases norepinephrine. Given this inverse association, sympatholysis may help explain the diverse cardiac and systemic benefits from SGLT2i therapy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Trial Registration<\/jats:title>\n                    <jats:p>NCT03485222 (www.clinicaltrials.gov).<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehae917","type":"journal-article","created":{"date-parts":[[2025,2,5]],"date-time":"2025-02-05T10:48:37Z","timestamp":1738752517000},"page":"1507-1523","source":"Crossref","is-referenced-by-count":21,"title":["Anaemia predicts iron homoeostasis dysregulation and modulates the response to empagliflozin in heart failure with reduced ejection fraction: the EMPATROPISM-FE trial"],"prefix":"10.1093","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7491-7637","authenticated-orcid":false,"given":"Christiane 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Mannheim, Faculty of Medicine Mannheim of the University of Heidelberg , Mannheim ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1408-8958","authenticated-orcid":false,"given":"Carlos G","family":"Santos-Gallego","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai, Cardiovascular Institute , New York, NY ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan Antonio","family":"Requena-Ibanez","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai, Cardiovascular Institute , New York, NY ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3379-2641","authenticated-orcid":false,"given":"Tanja","family":"Zeller","sequence":"additional","affiliation":[{"name":"University Center of Cardiovascular Science, University Heart and Vascular Center, University Hospital Hamburg-Eppendorf, and German Center of Cardiovascular Research, Partner Site Hamburg\u2013Kiel\u2013L\u00fcbeck , Hamburg ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3694-4559","authenticated-orcid":false,"given":"Christoph","family":"Maack","sequence":"additional","affiliation":[{"name":"Comprehensive Heart Failure Center W\u00fcrzburg, University and University Hospital W\u00fcrzburg , Am Schwarzenberg 15, 97078 W\u00fcrzburg ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6386-0313","authenticated-orcid":false,"given":"Javier","family":"Sanz","sequence":"additional","affiliation":[{"name":"Icahn School of Medicine at Mount Sinai, Cardiovascular Institute , New York, NY 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