Iron and Heart Failure
Autor: | Lauren Goodman, Hossein Ardehali, Jason S. Shapiro, Kambiz Ghafourian |
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Rok vydání: | 2020 |
Předmět: |
FCM
ferric carboxymaltose NTBI non–transferrin-bound iron 0301 basic medicine RCT randomized clinical trial TfR1 transferrin receptor protein 1 medicine.medical_specialty Fpn1 ferroportin 1 heart failure I/R ischemia/reperfusion PGA Patient Global Assessment Disease 030204 cardiovascular system & hematology STATE-OF-THE-ART REVIEW 03 medical and health sciences Route of administration iron deficiency ROS reactive oxygen species 0302 clinical medicine DMT1 divalent metal transporter 1 protein LVEF left ventricular ejection fraction ID iron deficiency Medicine NYHA New York Heart Association Adverse effect Intensive care medicine VO2 peak oxygen uptake chemistry.chemical_classification iron chelation Reactive oxygen species sTfR soluble transferrin receptor business.industry CKD chronic kidney disease TSAT transferrin saturation 6MWT 6-min walk test Iron deficiency medicine.disease Symptomatic relief FGF fibroblast growth factor 3. Good health 030104 developmental biology chemistry Heart failure Concomitant intravenous iron Cardiology and Cardiovascular Medicine business IV intravenous Hb hemoglobin |
Zdroj: | JACC: Basic to Translational Science |
ISSN: | 2452-302X |
DOI: | 10.1016/j.jacbts.2019.08.009 |
Popis: | Highlights • Intravenous iron supplementation provides symptomatic relief in patients with heart failure and concomitant iron deficiency. • The current definition of iron deficiency based on ferritin Summary To date, 3 clinical trials have shown symptomatic benefit from the use of intravenous (IV) iron in patients with heart failure (HF) with low serum iron. This has led to recommendations in support of the use of IV iron in this population. However, the systemic and cellular mechanisms of iron homeostasis in cardiomyocyte health and disease are distinct, complex, and poorly understood. Iron metabolism in HF appears dysregulated, but it is still unclear whether the changes are maladaptive and pathologic or compensatory and protective for the cardiomyocytes. The serum markers of iron deficiency in HF do not accurately reflect cellular and mitochondrial iron levels, and the current definition based on the ferritin and transferrin saturation values is broad and inclusive of patients who do not need IV iron. This is particularly relevant in view of the potential risks that are associated with the use of IV iron. Reliable markers of cellular iron status may differentiate subgroups of HF patients who would benefit from cellular and mitochondrial iron chelation rather than IV iron. |
Databáze: | OpenAIRE |
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