Combination of therapeutic apheresis and therapeutic ventricular assistance for end-stage heart failure patients.

S. Schulte-Eistrup, S. Ashizawa, K. Nonaka, S. Ichikawa, T. Motomura, N. Murai, Y. Nosé
{"title":"Combination of therapeutic apheresis and therapeutic ventricular assistance for end-stage heart failure patients.","authors":"S. Schulte-Eistrup, S. Ashizawa, K. Nonaka, S. Ichikawa, T. Motomura, N. Murai, Y. Nosé","doi":"10.1046/J.1526-0968.2002.00444.X","DOIUrl":null,"url":null,"abstract":"Dilated cardiomyopathy is a cardiac disease of unknown origin which is characterized by the gradual development of cardiac failure associated with four-chamber dilatation of the heart. Heart transplantation has been considered as the last resort for this disease. However, some patients who received support with a ventricular assist device (VAD) as a bridge-to-transplantation and then recovered without transplantation have been reported. This new concept of treating heart failure is termed bridge-to-recovery. A VAD can inhibit the heart failure compensatory mechanisms by extreme ventricular unloading. Also, heart failure is a complex neurohormonal/autocrine-paracrine syndrome, and these mechanisms consecutively lead to inflammatory response by proinflammatory cytokines; interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Furthermore, the existence of anti-beta1-adrenoceptor autoantibodies (A-beta1-AABs) in a patient with dilated cardiomyopathy has been reported. These proinflammatory cytokines and this antibody accelerate a ventricular remodeling and a contractile dysfunction over the long term. Apheresis can also inhibit the vicious cycle in heart failure by removing the factors that are produced by activated neurohormonal/autocrine-paracrine compensatory mechanisms. Therefore, we propose that the combined therapies, therapeutic VAD and therapeutic apheresis, will provide a prominent outcome for a patient who is suffering from end-stage heart failure.","PeriodicalId":79755,"journal":{"name":"Therapeutic apheresis : official journal of the International Society for Apheresis and the Japanese Society for Apheresis","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Therapeutic apheresis : official journal of the International Society for Apheresis and the Japanese Society for Apheresis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1046/J.1526-0968.2002.00444.X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

Abstract

Dilated cardiomyopathy is a cardiac disease of unknown origin which is characterized by the gradual development of cardiac failure associated with four-chamber dilatation of the heart. Heart transplantation has been considered as the last resort for this disease. However, some patients who received support with a ventricular assist device (VAD) as a bridge-to-transplantation and then recovered without transplantation have been reported. This new concept of treating heart failure is termed bridge-to-recovery. A VAD can inhibit the heart failure compensatory mechanisms by extreme ventricular unloading. Also, heart failure is a complex neurohormonal/autocrine-paracrine syndrome, and these mechanisms consecutively lead to inflammatory response by proinflammatory cytokines; interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Furthermore, the existence of anti-beta1-adrenoceptor autoantibodies (A-beta1-AABs) in a patient with dilated cardiomyopathy has been reported. These proinflammatory cytokines and this antibody accelerate a ventricular remodeling and a contractile dysfunction over the long term. Apheresis can also inhibit the vicious cycle in heart failure by removing the factors that are produced by activated neurohormonal/autocrine-paracrine compensatory mechanisms. Therefore, we propose that the combined therapies, therapeutic VAD and therapeutic apheresis, will provide a prominent outcome for a patient who is suffering from end-stage heart failure.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
治疗性离心分离与治疗性心室辅助联合治疗终末期心力衰竭患者。
扩张型心肌病是一种病因不明的心脏疾病,其特征是逐渐发展为心力衰竭,并伴有心脏四室扩张。心脏移植被认为是治疗这种疾病的最后手段。然而,也有一些患者接受了心室辅助装置(VAD)作为移植的桥梁,然后在没有移植的情况下恢复。这种治疗心力衰竭的新概念被称为康复之桥。VAD可通过极端心室卸荷抑制心力衰竭代偿机制。此外,心力衰竭是一种复杂的神经激素/自分泌-旁分泌综合征,这些机制连续导致促炎细胞因子的炎症反应;白细胞介素-1 α (IL-1 α)、白细胞介素-1 β (IL-1 β)、白细胞介素-2 (IL-2)、白细胞介素-6 (IL-6)和肿瘤坏死因子- α (tnf - α)。此外,在扩张型心肌病患者中存在抗β -肾上腺素能受体自身抗体(a - β - aabs)的报道。这些促炎细胞因子和抗体长期加速心室重塑和收缩功能障碍。单采也可以通过去除激活的神经激素/自分泌-旁分泌代偿机制产生的因素来抑制心力衰竭的恶性循环。因此,我们建议联合治疗,治疗性VAD和治疗性离心分离术,将为患有终末期心力衰竭的患者提供一个突出的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Presidential Address: PRESIDENTIAL ADDRESS Fluctuations in the peripheral blood leukocyte and platelet counts in leukocytapheresis in healthy volunteers. Mobilization factors of peripheral blood stem cells in healthy donors. Cytokine removal by plasma exchange with continuous hemodiafiltration in critically ill patients. In vitro evaluation of newly developed adsorbent for selective removal of glycosylated low-density lipoprotein.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1