Heart Failure and Anemia
Content
Heart failure and anemia: mechanisms and pathophysiology.
Anand IS1.
Author information
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.
Anand IS1.
Author information
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.
