title: [Inflammatory mediators in patients with biventricular assist device systems].
abstract: We studied the plasma levels of TNF-alpha, IL-6, IL-8 and soluble adhesion molecules (sE-Selectin, sL-Selectin, sVCAM-1) immediately before and during mechanical circulatory support with a Biventricular Assist Device System (BVAD-"Berlin Heart") in comparison to patients with chronic heart failure (NYHA classes II/III) and patients with coronary artery disease with normal ventricular function. Additionally, the biocompatibility of the membranes used in the "Berlin Heart" was tested in vitro. IL-6 and IL-8 but not TNF-alpha could only be detected in patients with cardiogenic shock immediately before starting circulatory support. Furthermore, plasma concentrations of soluble adhesion molecules were statistically significantly elevated in patients with cardiogenic shock compared to patients with coronary artery disease. This picture of a systemic inflammatory response syndrome without significant level of TNF-alpha looks quite similar to that seen in patients following trauma and severe operations. During mechanical circulatory support plasma levels of cytokines and soluble adhesion molecules dropped to low levels in patients, who were successfully maintained on BVAD. By contrast, we have found persistently elevated levels of these mediators in patients with fatal outcome. This seems not to be the result of individual distinct response of blood cells to contact with the artificial surfaces of the device. In summary, our data suggest the development of a systemic inflammatory response syndrome may be due to hypoxia during cardiogenic shock. Persistence of systemic inflammation suggests failing of the mechanical support. Therefore, the monitoring of inflammatory mediators may be relevant as a prognostic marker in these patients (disappearance of peripheral hypoxia).
authors.affiliation: Institut für Medizinische Immunologie, Universitätsklinikum Charité, Berlin.
authors.forename: D
authors.initials: D
authors.lastname: Hasper
authors.forename: M
authors.initials: M
authors.lastname: Hummel
authors.forename: W D
authors.initials: WD
authors.lastname: Döcke
authors.forename: F X
authors.initials: FX
authors.lastname: Kleber
authors.forename: S B
authors.initials: SB
authors.lastname: Felix
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
authors.forename: H D
authors.initials: HD
authors.lastname: Volk
mesh_terms: D000328:Adult; D000368:Aged; D015815:Cell Adhesion Molecules / Q000097:blood; D003327:Coronary Disease / Q000276:immunology / Q000628:therapy*; D005260:Female; D006333:Heart Failure / Q000276:immunology / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008422:Materials Testing; D008567:Membranes, Artificial; D008875:Middle Aged; D011379:Prognosis; D012770:Shock, Cardiogenic / Q000276:immunology / Q000628:therapy*; D018746:Systemic Inflammatory Response Syndrome / Q000175:diagnosis / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D008567:Membranes, Artificial; D014409:Tumor Necrosis Factor-alpha
vernacular_title: Inflammatorische Mediatoren bei Patienten mit biventrikulären Assist-Device-Systemen.