title: Markers of inflammation in recipients of continuous-flow left ventricular assist devices.
abstract: Although the newer continuous-flow left ventricular assist devices (CF-LVADs) provide clinical advantages over the pulsatile pumps, the effects of low pulsatility on inflammation are incompletely understood. The objective of our study was to examine the levels of inflammatory mediators in CF-LVAD recipients compared with both healthy control subjects and heart failure patients who were candidates for CF-LVAD support. Plasma levels of chemokines, cytokines, and inflammatory markers were measured in 18 CF-LVAD recipients and compared with those of 14 healthy control subjects and 14 heart failure patients who were candidates for CF-LVADs. The levels of granulocyte macrophage-colony stimulating factor, macrophage inflammatory proteins-1β, and macrophage-derived chemokine were significantly higher in the CF-LVAD group compared with both the heart failure and the healthy control groups, whereas no significant differences were observed between the healthy control subjects and the heart failure groups. Compared with the healthy controls, C-reactive protein, interferon gamma-induced protein-10, monocyte chemotactic protein-1, and interleukin-8 levels were significantly higher in both the CF-LVAD and heart failure groups, but no significant differences were observed between the CF-LVAD recipients and the heart failure patients. Inflammatory markers were elevated in CF-LVAD recipients compared with healthy control subjects and the heart failure patients. Further studies should investigate the clinical implications of elevated levels of inflammation in CF-LVAD recipients.
authors.affiliation: From the *Faculty of Kinesiology and Physical Education, the Graduate Department of Exercise Sciences, University of Toronto, Ontario, Canada; † Division of Cardiovascular Surgery, Peter Munk Cardiac Centre, University Health Network, University of Toronto, Ontario, Canada; and the ‡ Division of Nephrology, University Health Network, University of Toronto, Ontario, Canada.
authors.forename: Liza
authors.initials: L
authors.lastname: Grosman-Rimon
authors.forename: Michael A
authors.initials: MA
authors.lastname: McDonald
authors.forename: Ira
authors.initials: I
authors.lastname: Jacobs
authors.forename: Laura C
authors.initials: LC
authors.lastname: Tumiati
authors.forename: Stacey
authors.initials: S
authors.lastname: Pollock Bar-Ziv
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Shogilev
authors.forename: Amelia G
authors.initials: AG
authors.lastname: Mociornita
authors.forename: Arash
authors.initials: A
authors.lastname: Ghashghai
authors.forename: Andrzej
authors.initials: A
authors.lastname: Chruscinski
authors.forename: David Z I
authors.initials: DZ
authors.lastname: Cherney
authors.forename: Vivek
authors.initials: V
authors.lastname: Rao
mesh_terms: D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D018925:Chemokines / Q000097:blood; D016207:Cytokines / Q000097:blood; D006333:Heart Failure / Q000097:blood* / Q000503:physiopathology / Q000601:surgery*; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011379:Prognosis; D013318:Stroke Volume
chemical_list: D015415:Biomarkers; D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein