Myocardial iron content by T2 Star cardiac magnetic resonance and serum markers of iron metabolism in patients with heart failure

Pereira, Guilherme Augusto Reissig; Foppa, Murilo; Eifer, Diego André; Beck‐da‐Silva, Luís

doi:10.2459/jcm.0000000000001263

Cited by 3 publications

(1 citation statement)

References 12 publications

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“…However, in the absence of superior markers, our research team opted to use it as a supplementary endpoint to the actual incidence of VT/VFs recorded in patients' CIEDs. Finally, direct assessment of the effect of IV FCM on intramyocardial iron content, as assessed through cardiac magnetic resonance (CMR) techniques, could have been an invaluable additional endpoint to this study, 31 as it would provide direct insights into the mechanism through which IV FCM improves patient outcomes. Theoretically, restitution of myocardial iron content leading to better metabolic status and thusly improved function and electrochemical stability would be directly observable with this method 19 .…”

Section: Discussionmentioning

confidence: 99%

Iron therapy and severe arrhythmias in HFrEF: rationale, study design, and baseline results of the RESAFE‐HF trial

et al. 2023

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Aims The Iron Intravenous Therapy in Reducing the burden of Severe Arrhythmias in HFrEF (RESAFE‐HF) registry study aims to provide real‐word evidence on the impact of intravenous ferric carboxymaltose (FCM) on the arrhythmic burden of patients with heart failure with reduced ejection fraction (HFrEF), iron deficiency (ID), and implanted cardiac implantable electronic devices (CIEDs). Methods and results The RESAFE‐HF (NCT04974021) study was designed as a prospective, single‐centre, and open‐label registry study with baseline, 3, 6, and 12 month visits. Adult patients with HFrEF and CIEDs scheduled to receive IV FCM as treatment for ID as part of clinical practice were eligible to participate. The primary endpoint is the composite iron‐related endpoint of haemoglobin ≥ 12 g/dL, ferritin ≥ 50 ng/L, and transferrin saturation > 20%. Secondary endpoints include unplanned HF‐related hospitalizations, ventricular tachyarrhythmias detected by CIEDs and Holter monitors, echocardiographic markers, functional status (VO 2 max and 6 min walk test), blood biomarkers, and quality of life. In total, 106 patients with a median age of 72 years (14.4) were included. The majority were male (84.9%), whereas 92.5% of patients were categorized to New York Heart Association II/III. Patients' arrhythmic burden prior to FCM administration was significant—19 patients (17.9%) received appropriate CIED therapy for termination of ventricular tachyarrhythmia in the preceding 12 months, and 75.5% of patients have frequent, repetitive multiform premature ventricular contractions. Conclusions The RESAFE‐HF trial is expected to provide evidence on the effect of treating ID with FCM in HFrEF based on real‐world data. Special focus will be given on the arrhythmic burden post‐FCM administration.

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Section: Discussionmentioning

confidence: 99%

Iron therapy and severe arrhythmias in HFrEF: rationale, study design, and baseline results of the RESAFE‐HF trial

et al. 2023

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Iron deficiency and supplementation in heart failure

Lakhal-Littleton,

Cleland

2024

Nat Rev Cardiol

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Iron deficiency in myocardial ischaemia: molecular mechanisms and therapeutic perspectives

Corradi,

Masini,

Bucciarelli

et al. 2023

Cardiovascular Research

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Systemic iron deficiency (SID), even in the absence of anemia, worsens the prognosis and increases mortality in heart failure (HF). Recent clinical-epidemiological studies, however, have shown that a myocardial iron deficiency (MID) is frequently present in cases of severe HF even in the absence of SID and without anemia. In addition, experimental studies have shown a poor correlation between the state of systemic and myocardial iron. MID in animal models may lead to severe mitochondrial dysfunction, alterations of mitophagy and mitochondrial biogenesis, with profound alterations in cardiac mechanics and the occurrence of a fatal cardiomyopathy, all effects prevented by intravenous administration of iron. This shifts the focus to the myocardial state of iron, in the absence of anemia, as an important factor in prognostic worsening and mortality in HF. There is now epidemiological evidence that SID worsens prognosis and mortality also in patients with acute and chronic coronary heart disease, and experimental evidence that MID aggravates acute myocardial ischemia as well as post-ischemic remodeling. Intravenous administration of ferric carboxymaltose or ferric dextrane improves post-ischemic adverse remodeling. We here review such evidence, propose that MID worsens ischemia/reperfusion injury, and discuss possible molecular mechanisms, such as chronic hyperactivation of HIF1-α; exacerbation of cytosolic and mitochondrial calcium overload, amplified increase of mitochondrial [NADH]/[NAD+] ratio, and depletion of energy status and NAD+ content with inhibition of sirtuin 1-3 activity. Such evidence now portrays iron metabolism as a core factor not only in heart failure, but also in myocardial ischemia.

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Myocardial iron content by T2 Star cardiac magnetic resonance and serum markers of iron metabolism in patients with heart failure

Cited by 3 publications

References 12 publications

Iron therapy and severe arrhythmias in HFrEF: rationale, study design, and baseline results of the RESAFE‐HF trial

Iron therapy and severe arrhythmias in HFrEF: rationale, study design, and baseline results of the RESAFE‐HF trial

Iron deficiency and supplementation in heart failure

Iron deficiency in myocardial ischaemia: molecular mechanisms and therapeutic perspectives

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