Heart failure and anemia: mechanisms and pathophysiology

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Abstract
Anemia is a common comorbidity in patients with heart failure and affects up to 50% of patients, depending on the definition of anemia used and on the population studied. Presence of anemia and lower hemoglobin (Hgb) concentrations are powerful independent predictors of adverse outcomes in heart failure. Even small reductions in Hgb are associated with worse outcomes. Correction of anemia may be useful in improving heart failure outcomes. However, the causes of anemia in heart failure are not entirely clear. Specific causes of anemia such as hematinic abnormalities are seen only in a minority of subjects. Renal dysfunction and neurohormonal and proinflammatory cytokine activation appear to contribute to anemia of chronic disease in the majority of the patients, resulting in inappropriate erythropoietin production and defective iron utilization. Under normal conditions, reduced tissue oxygenation due to chronic anemia results in non-hemodynamic and hemodynamic compensatory responses to enhance oxygen carrying capacity. Erythropoiesis is the predominant non-hemodynamic response to hypoxia, but because erythropoiesis is defective in heart failure, hemodynamic mechanisms predominate. Hemodynamic responses are complex and involve a vasodilation-mediated high-output state with neurohormonal activation. The high-output state initially helps to increase oxygen transport. However, the hemodynamic and neurohormonal alterations could potentially have deleterious long-term consequences and could contribute to anemia’s role as an independent risk factor for adverse outcomes.