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  • Title: Iron Deficiency in Heart Failure with Reduced Ejection Fraction: Pathophysiology, Diagnosis and Treatment.
    Author: Pereira GAR, Beck-da-Silva L.
    Journal: Arq Bras Cardiol; 2022 Mar; 118(3):646-654. PubMed ID: 35319614.
    Abstract:
    Iron deficiency (ID) is an important comorbidity in heart failure with reduced ejection (HFrEF) and is highly prevalent in both anemic and non-anemic patients. In HFrEF, iron deficiency should be investigated by measurements of transferrin saturation and ferritin. There are two types of ID: absolute deficiency, with depletion of iron stores; and functional ID, where iron supply is not sufficient despite normal stores. ID is associated with worse functional class and higher risk of death in patients with HFrEF, and scientific evidence has indicated improvement of symptoms and quality of life of these patients with treatment with parenteral iron in the form of ferric carboxymaltose. Iron plays vital roles such as oxygen transportation (hemoglobin) and storage (myoblogin), and is crucial for adequate functioning of mitochondria, which are composed of iron-based proteins and the place of energy generation by oxidative metabolism at the electron transport chain. An insufficient generation and abnormal uptake of iron by skeletal and cardiac muscle cells contribute to the pathophysiology of HF. The present review aims to increase the knowledge of the pathophysiology of ID in HFrEF, and to address available tools for its diagnosis and current scientific evidence on iron replacement therapy. A deficiência de ferro (DF) ou ferropenia é uma importante comorbidade na insuficiência cardíaca com fração de ejeção reduzida (ICFER) estável, e muito prevalente tanto nos anêmicos como não anêmicos. A ferropenia na ICFER deve ser pesquisada por meio da coleta de saturação de transferrina e ferritina. Há dois tipos de ferropenia na IC: absoluta, em que as reservas de ferro estão depletadas; e funcional, onde o suprimento de ferro é inadequado apesar das reservas normais. A ferropenia está associada com pior classe funcional e maior risco de morte em pacientes com ICFER, e evidências científicas apontam melhora de sintomas e de qualidade de vida desses pacientes com tratamento com ferro parenteral na forma de carboximaltose férrica. O ferro exerce funções imprescindíveis como o transporte (hemoglobina) e armazenamento (mioglobina) de oxigênio, além de ser fundamental para o funcionamento das mitocôndrias, constituídas de proteínas à base de ferro, e local de geração de energia na cadeia respiratória pelo metabolismo oxidativo. A geração insuficiente e utilização anormal de ferro nas células musculares esquelética e cardíaca contribuem para a fisiopatologia da IC. A presente revisão tem o objetivo de aprofundar o conhecimento a respeito da fisiopatologia da ferropenia na ICFER, abordar as ferramentas disponíveis para o diagnóstico e discutir sobre a evidência científica existente de reposição de ferro. Iron deficiency (ID) is an important comorbidity in heart failure with reduced ejection (HFrEF) and is highly prevalent in both anemic and non-anemic patients. In HFrEF, iron deficiency should be investigated by measurements of transferrin saturation and ferritin. There are two types of ID: absolute deficiency, with depletion of iron stores; and functional ID, where iron supply is not sufficient despite normal stores. ID is associated with worse functional class and higher risk of death in patients with HFrEF, and scientific evidence has indicated improvement of symptoms and quality of life of these patients with treatment with parenteral iron in the form of ferric carboxymaltose. Iron plays vital roles such as oxygen transportation (hemoglobin) and storage (myoblogin), and is crucial for adequate functioning of mitochondria, which are composed of iron-based proteins and the place of energy generation by oxidative metabolism at the electron transport chain. An insufficient generation and abnormal uptake of iron by skeletal and cardiac muscle cells contribute to the pathophysiology of HF. The present review aims to increase the knowledge of the pathophysiology of ID in HFrEF, and to address available tools for its diagnosis and current scientific evidence on iron replacement therapy.
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