Cardiology Department, Fondazione IRCCS Policlinico S Matteo, Pavia, Italy.
Int J Cardiol. 2011 Feb 17;147(1):124-31. doi: 10.1016/j.ijcard.2009.10.028. Epub 2009 Nov 10.
Mortality and morbidity after acute myocardial infarction (AMI) remain high even when myocardial reperfusion is successful. Erythropoietin (EPO) protects against experimental MI.
The aim of this single-centre study was to investigate the effects of short-term high-dose erythropoietin on peripheral blood cells (PBCs) and infarct size in 30 patients with a first uncomplicated AMI undergoing percutaneous coronary intervention (PCI) who were randomly assigned to treatment with EPO (33 × 10(3)IU before PCI, and 24 and 48 h after admission), or placebo. We considered short-term CD34+ cell mobilisation, quantitative PBC gene expression in the apoptotic, angiogenic and inflammatory pathways, and enzymatically estimated infarct size. Echocardiographic and cardiac magnetic resonance studies were performed in the acute phase and six months later.
CD34+ cell mobilisation 72 h after admission was greater in the EPO-treated patient group (93 cells/μl [36-217] vs 22 cells/μl [6-51]; p = 0.002), who also showed higher expression of the anti-apoptotic AKT and NFkB, the pro-angiogenic VEGFR-2, and the EPO-R genes, and lower expression of the pro-apoptotic CASP3 and TP53 and pro-inflammatory IL12a genes. Moreover, they showed smaller infarct size (30% reduction in CK-MB release; p = 0.025), and a favourable pattern of left ventricular remodelling.
Short-term high-dose EPO administration in patients with AMI treated by PCI and standard anti-platelet therapy increases the levels of circulating CD34+ cells, shifts PBC gene expression towards anti-apoptotic, pro-angiogenic and anti-inflammatory pathways, and decreases infarct size. The clinical relevance of these results needs to be confirmed in specifically tailored trials.
即使心肌再灌注成功，急性心肌梗死（AMI）后的死亡率和发病率仍然很高。促红细胞生成素（EPO）可保护实验性心肌梗死。
这项单中心研究的目的是探讨短期大剂量促红细胞生成素对 30 例首次接受经皮冠状动脉介入治疗（PCI）的无并发症 AMI 患者外周血细胞（PBC）和梗死面积的影响，这些患者被随机分为 EPO 治疗组（PCI 前 33×103IU，入院后 24 和 48 小时）和安慰剂组。我们观察短期 CD34+细胞动员、凋亡、血管生成和炎症途径的定量 PBC 基因表达，以及酶法估计梗死面积。在急性期和 6 个月后进行超声心动图和心脏磁共振研究。
入院后 72 小时 EPO 治疗组的 CD34+细胞动员增加（93 个细胞/μl [36-217] 比 22 个细胞/μl [6-51]；p=0.002），EPO 治疗组还显示出抗凋亡 AKT 和 NFkB、促血管生成 VEGFR-2 和 EPO-R 基因的表达更高，以及促凋亡 CASP3 和 TP53 和促炎 IL12a 基因的表达更低。此外，他们的梗死面积较小（CK-MB 释放减少 30%；p=0.025），左心室重构呈有利模式。
在接受 PCI 和标准抗血小板治疗的 AMI 患者中短期大剂量 EPO 给药可增加循环 CD34+细胞的水平，使 PBC 基因表达向抗凋亡、促血管生成和抗炎途径转移，并减少梗死面积。这些结果的临床相关性需要在专门设计的试验中得到证实。
