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":"21 1","pages":"247-54"},"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.