Molecular changes in myocardium in the course of anemia or iron deficiency.
Chronic untreated anemia or iron deficiency (ID) can result in an increased cardiac output, chronic sympathetic activation, left ventricular hypertrophy, and left ventricular dilation, leading to symptomatic chronic heart failure (CHF). Only in the past decade has there been an increase in interest in anemia and ID occurring in the course of CHF. The pharmacologic support in erythropoietin signaling or the correction in iron metabolism may activate molecular pathways that can protect the heart and prevent myocardial remodeling, and hence become a novel therapeutic approach in patients with CHF. Most of the data come from experimental models. Further studies, in particular performed in clinical settings, are warranted.
Jankowska
Ewa A
EA
Department of Heart Diseases, Wroclaw Medical University, Centre for Heart Diseases, Military Hospital, ul Weigla 5, Wroclaw 50-981, Poland. ewa@antro.pan.wroc.pl
Ponikowski
Piotr
P
D018798:Anemia, Iron-Deficiency / Q000209:etiology* / Q000473:pathology; D004921:Erythropoietin; D006333:Heart Failure / Q000209:etiology* / Q000517:prevention & control; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000517:prevention & control; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D012307:Risk Factors
D004921:Erythropoietin