Department of Heart Diseases, Wroclaw Medical University, Centre for Heart Diseases, Military Hospital, ul Weigla 5, Wroclaw 50-981, Poland.
Heart Fail Clin. 2010 Jul;6(3):295-304. doi: 10.1016/j.hfc.2010.03.003.
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.
慢性未经治疗的贫血或铁缺乏（ID）可导致心输出量增加、慢性交感神经激活、左心室肥厚和左心室扩张，导致有症状的慢性心力衰竭（CHF）。直到过去十年，人们才对 CHF 过程中出现的贫血和 ID 产生了兴趣。促红细胞生成素信号传导的药物支持或铁代谢的纠正可能会激活分子途径，从而保护心脏，防止心肌重塑，因此成为 CHF 患者的一种新的治疗方法。大部分数据来自实验模型。需要进一步的研究，特别是在临床环境中进行的研究。
