MANAGEMENT OF ANEMIA
Management of Anemia in Heart Failure
Therapy includes iron, folic acid, blood transfusions, and
erythropoiesis-stimulating agents (ESA)
Iron Therapy
Improves anemia and cardiac function, but also increases oxidative
stress
Significantly reduced LV-end diastolic, end-systolic diameters and LV
mass, associated with decreased filling pressure.
Iron application is controversially debated, but IV iron
administration is mandatory in patients with iron deficiency,
especially if serum ferritin values are below 100 g/L
Erythropoiesis-stimulating agents (ESA)
Improving Hb and LVEF,
functional class and reducing
diuretic doses and LV
remodelling
CARDIOMYOPATHY RELATED TO
CHRONIC TRANSFUSSION
Iron Overload Cardiomyopathy
A secondary form of cardiomyopathy resulting
from the accumulation of iron in the
myocardium mainly because of genetically
determined disorders of iron metabolism or
multiple transfusions
...cont
Described as a dilated cardiomyopathy, and a different forms
of cardiac dysfunction secondary to myocardial iron
deposition
Characterized by LV remodeling with chamber dilatation and
reduced LVEF
A major cause of morbidity, accounts for 1 : 3 deaths in hereditary
hemochromatosis, especially in young male patients
The leading cause of mortality in thalassemia major
A major cause of death in other conditions associated with
secondary iron overload.
Primary hemochromatosis, a
genetically determined
condition leading to iron
overload, is classically
categorized as an infiltrative
cause of restrictive
cardiomyopathy
Secondary hemochromatosis
may lead to severe diastolic LV
dysfunction in the early stages
of the disease, before LVEF is
affected.
Summary
Anemia increases morbidity and mortality in cardiovascular diseases, due
to compensatory consequences of hypoxia, such as a hyperdynamic state
with increased cardiac output, LVH and progressive cardiac enlargement
The main mechanisms of anemia in patients with heart failure are : renal
dysfunction, increased sympathetic and RAAS activity, hemodilution,
absolute or functional iron deficiency, impaired EPO production and
activity, activation of the inflammatory cascade, angiotensin converting
enzyme inhibition and angiotensin receptor blockade, and vitamin B12
and folic acid deficiency
Therapy includes iron, folic acid, blood transfusions, and erythropoiesis
stimulating agents
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