How should anemia be managed in heart failure?

Anemia often coexists with heart failure, especially in New York Heart Association classes II to IV. The multiple causes include:

Deficiency states (iron, vitamin B12, folic acid).

Cardiac cachexia.

Renal failure.


Deficiency states

Frequent malnutrition is compounded by malabsorption of proteins, vitamins, and minerals due to visceral venous congestion (decreased enzyme synthesis, intestinal mucosa edema).

Cardiac cachexia

The hypercatabolic state known as cardiac cachexia is characterized by factors such as low cardiac output and consequent tissue hypoxia, muscle deconditioning, malnutrition, hormone activation (cortisol, adrenergic system), and the elevation of proinflammatory cytokines such as interleukin (IL)-l, -2, and -6, tumor necrosis factor (TNF)-oc, soluble TNF receptors, and abnormal growth factor. Cytokines in particular have been attracting great interest. There is experimental evidence that they have numerous biological effects, at both the peripheral and myocardial levels. They inhibit protein synthesis and accelerate protein catabolism. They cause oxidative stress and consequent cellular dysfunction. They stimulate apoptosis, in both cardiac and endothelial cells. In particular, TNF appears to cause bone marrow depression and interfere with erythropoiesis. Although the stimuli that precipitate the cytokine cascade are poorly characterized, a direct relationship has been shown between IL-6, TNF, and heart failure severity.

Increased cytokine expression may precipitate progression to cachexia.

Renal failure

In advanced heart failure, renal failure is often due to hypoperfusion and ischemia, with a decrease in erythropoietin production and hence in erythropoiesis.


Silent blood loss occurs mainly in the gastrointestinal tract due to microlesions and the frequent use of antiplatelet agents and anticoagulant drugs.


Anemia exacerbates clinical status and is an independent predictor of adverse outcome in heart failure. It decreases the myocardial oxygen supply, encourages ischemia, and depresses already compromised contractile function. It also decreases peripheral oxygenation, facilitating organ damage, and hence compounding symptoms such as asthenia and dyspnea. Anemia can in addition trigger a hyperdynamic circulatory state and burden a myocardium already overloaded by increased adrenergic tone with reflex tachycardia. Anemia is a risk factor for ventricular remodeling in hypertensive patients: circulating hemoglobin levels correlate closely with left ventricular mass in dialyzed patients. Even partial correction of anemia by erythropoietin administration can partially regress ventricular hypertrophy and enhance systolic function.

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