Pierce Christopher N, Larson Douglas F
The University of Arizona Graduate Program in Circulatory Sciences, College of Medicine, Sarver Heart Center and University Medical Center, Tucson, AZ, USA.
Perfusion. 2005 Mar;20(2):83-90. doi: 10.1191/0267659105pf793oa.
Mechanical circulatory assist devices (MCADs) are increasingly utilized independently of cardiac transplantation in the management of heart failure. Though MCAD use incorporates inherent mechanical risks, the inevitable onset of chronic anemia, with its associated morbidity and mortality, is also a significant concern. MCAD support has been correlated with elevated plasma levels of inflammatory cytokines TNF-alpha, IL-1beta, and IL-6, which have separately been found to inhibit erythropoietin (Epo)-induced erythrocyte (RBC) maturation. Previous analysis of hematological parameters for MCAD-supported patients concluded that an amplified inflammatory response impedes RBC proliferation and recovery from hemolytic anemia. Additional analysis may bolster this assertion. Hemoglobin concentration (HC), RBC distribution width (RDW), mean cell volume (MCV), and cardiac index were retrospectively analysed for 78 MCAD-supported patients implanted for greater than 30 days at the University of Arizona Health Sciences Center from 1996 to 2002. Analysis confirms that the HC, a conventional marker for anemia, declines with MCAD placement and remains below the clinically defined, minimum normal value. Inversely, the RDW rises above maximum normal measure, signifying an increased fraction of juvenile RBCs. The MCV remains unchanged and within normal limits, demonstrating adequate substrate for RBC formation. MCAD performance also stabilizes as adequate perfusion returns. These results further support our previously published conclusion that a sufficient response of erythropoiesis occurs in reaction to the onset of anemia by an increased production of immature RBCs. However, the cells never fully mature and join circulation. The patient's inflammatory cytokine response to the implanted device most likely mediates the chronic MCAD-induced anemia by inhibition of Epo effects.
机械循环辅助装置（MCADs）在心力衰竭的治疗中越来越多地独立于心脏移植使用。尽管使用MCAD存在固有的机械风险，但慢性贫血不可避免地会出现及其相关的发病率和死亡率，这也是一个重大问题。MCAD支持与血浆中炎症细胞因子TNF-α、IL-1β和IL-6水平升高相关，这些细胞因子已分别被发现可抑制促红细胞生成素（Epo）诱导的红细胞（RBC）成熟。先前对接受MCAD支持患者的血液学参数分析得出结论，放大的炎症反应会阻碍RBC增殖和从溶血性贫血中恢复。进一步的分析可能会支持这一论断。对1996年至2002年在亚利桑那大学健康科学中心植入MCAD超过30天的78例患者的血红蛋白浓度（HC）、红细胞分布宽度（RDW）、平均红细胞体积（MCV）和心脏指数进行了回顾性分析。分析证实，作为贫血的传统标志物，HC随着MCAD植入而下降，并一直低于临床定义的最低正常值。相反，RDW升高至高于最大正常测量值，表明幼稚RBC的比例增加。MCV保持不变且在正常范围内，表明有足够的RBC形成底物。随着足够的灌注恢复，MCAD的性能也会稳定下来。这些结果进一步支持了我们之前发表的结论，即贫血发作时会通过增加未成熟RBC的产生而发生足够的红细胞生成反应。然而，这些细胞从未完全成熟并进入循环。患者对植入装置的炎症细胞因子反应很可能通过抑制Epo作用介导慢性MCAD诱导的贫血。
