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Vol 19 (2024): Continuous Publishing
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Published online: 2023-08-30

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Iron status and myocardial injury while recovering from acute myocarditis

Paweł Franczuk12, Justyna Maria Sokolska12, Michał Tkaczyszyn12, Paweł Gać34, Aneta Kosiorek1, Katarzyna Kulej-Łyko2, Kamil Aleksander Kobak5, Monika Kasztura6, Alicja Sołtowska78, Joanna Jaroch78, Piotr Ponikowski12, Ewa Anita Jankowska12
DOI: 10.5603/fc.96888

Abstract

Introduction. The pathophysiology of acute myocarditis (MCD) and subsequent recovery involves complex interplay between the virulence of pathogen, host immunity with possible genetic-based immune dysregulation, comorbidities and environmental factors. Precise identification of patients with increased risk of subsequent post-inflammatory cardiomyopathy is challenging. Abnormal iron status not only is a hallmark of immune activation but also plays a role in the development of cardiomyopathy, hence we investigated whether iron indices relate to myocardial injury in patients with acute MCD.

Material and methods. Consecutive patients hospitalized for acute MCD in two cardiology centers were prospectively enrolled. We analyzed clinical characteristics, cardiac magnetic resonance (CMR) findings and biomarkers of myocardial necrosis, neurohormonal activation, inflammation, and comprehensive systemic iron status from index hospitalization and an ambulatory control visit after 6 months. Healthy volunteers were control group.

Results. We enrolled 40 patients hospitalized for acute myocarditis (age: 32 ± 9 years, male gender: 98%). In-hospital serum ferritin correlated with CMR late gadolinium enhancement (LGE) mass (r = 0.537, p < 0.001) and global T2 ratio (r = 0.360, p = 0.03). LGE, regional abnormalities in myocardial T1 relaxation time and elevated extracellular volume persisted after 6 months of recovery in comparison to healthy controls. Persistent LGE mass correlated with lower transferrin saturation and serum iron at the ambulatory visit (r = –0.520, p = 0.03; and r = –0.465, p = 0.04; respectively).

Conclusions. Acute-phase reactant ferritin relates to myocardial injury in the acute phase of MCD, whereas in the recovery phase residual fibrosis is greater in subjects with more profound functional iron deficiency, the latter reflecting, to some extent, systemic low-grade inflammation.

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