Levels of Hematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline partially explain the occurrence of anemia in heart failure

Autor: Adriaan A. Voors, Ruud M.A. van de Wal, Erik Lipsic, Edo Vellenga, Regien G. Schoemaker, B. Daan Westenbrink, Peter van der Meer, Dirk J. van Veldhuisen, Wiek H. van Gilst
Přispěvatelé: Guided Treatment in Optimal Selected Cancer Patients (GUTS), Stem Cell Aging Leukemia and Lymphoma (SALL), Cardiovascular Centre (CVC), Schoemaker lab, Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)
Jazyk: angličtina
Rok vydání: 2005
Předmět:
Male
Heart disease
Myocardial Ischemia
heart failure
Angiotensin-Converting Enzyme Inhibitors
Blood Pressure
Gastroenterology
Ventricular Function
Left
RECEPTOR ANTAGONIST
Reference Values
Ejection fraction
biology
PROLIFERATION
anemia
Growth Inhibitors
Echocardiography
ENALAPRIL
Female
Cardiology and Cardiovascular Medicine
Oligopeptides
Glomerular Filtration Rate
medicine.drug
ERYTHROPOIETIN
medicine.medical_specialty
Anemia
Peptidyl-Dipeptidase A
RISK-FACTOR
Physiology (medical)
Internal medicine
medicine
Humans
Enalapril
Hematinic
cardiovascular diseases
Aged
business.industry
ANGIOTENSIN-CONVERTING-ENZYME
MORTALITY
Angiotensin-converting enzyme
angiotensin
medicine.disease
hematopoiesis
POLYMORPHISM
Endocrinology
Erythropoietin
POSTTRANSPLANTATION ERYTHROCYTOSIS
Heart failure
biology.protein
peptides
CREATININE CLEARANCE
business
Zdroj: Circulation, 112(12), 1743-1747. LIPPINCOTT WILLIAMS & WILKINS
ISSN: 0009-7322
Popis: Background— Anemia is common in patients with chronic heart failure (CHF) and is associated with a poor prognosis. However, only a minority of patients with CHF have impaired renal function or underlying hematinic deficiencies. It has been shown that inhibition of the renin-angiotensin system is associated with the development of anemia. The aim of the present study was to determine possible mechanisms linking anemia to renin-angiotensin system activity in CHF patients. Methods and Results— We initially evaluated 98 patients with advanced stable CHF who were treated with ACE inhibitors (left ventricular ejection fraction, 28±1%; age, 69±1 years; 80% male), 10 of whom had an unexplained anemia (normal hematinics and no renal failure). These 10 anemic patients were matched with 10 nonanemic patients in terms of age and left ventricular ejection fraction. Serum ACE activity was 73% lower in anemic CHF patients compared with nonanemic CHF patients ( P =0.018). Moreover, serum of these patients inhibited in vitro the proliferation of bone marrow–derived erythropoietic progenitor cells of healthy donors by 17% ( P =0.003). Levels of the hematopoiesis inhibitor N -acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is almost exclusively degraded by ACE, were significantly higher in anemic CHF patients and were clearly correlated to erythroid progenitor cell proliferation ( r =−0.64, P =0.001). Conclusions— Serum ACE activity is markedly lower in anemic CHF patients, and serum of these patients inhibits hematopoiesis. The clear correlation between Ac-SDKP and proliferation of erythroid progenitor cells suggests an inhibitory role of Ac-SDKP on hematopoiesis in CHF patients, which may explain the observed anemia in patients treated with ACE inhibitors.
Databáze: OpenAIRE
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