title: Combination of therapeutic apheresis and therapeutic ventricular assistance for end-stage heart failure patients.
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.
authors.affiliation: Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Schulte-Eistrup
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ashizawa
authors.forename: Kenji
authors.initials: K
authors.lastname: Nonaka
authors.forename: Seiji
authors.initials: S
authors.lastname: Ichikawa
authors.forename: Tadashi
authors.initials: T
authors.lastname: Motomura
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Murai
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Nosé
mesh_terms: D001781:Blood Component Removal; D002311:Cardiomyopathy, Dilated / Q000628:therapy; D016207:Cytokines / Q000097:blood; D006333:Heart Failure / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D016207:Cytokines