title: Hemodialysis-induced regional left ventricular systolic dysfunction and inflammation: a cross-sectional study.
abstract: BACKGROUND
  Hemodialysis may acutely induce regional left ventricular (LV) systolic dysfunction, which is associated with increased mortality and progressive heart failure. We tested the hypothesis that hemodialysis-induced regional LV systolic dysfunction is associated with inflammation and endothelial injury. Additionally, we studied whether hemodialysis-induced LV systolic dysfunction is associated with an exaggerated bioincompatibility reaction to hemodialysis.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  105 hemodialysis patients on a thrice-weekly dialysis schedule were studied between March 2009 and March 2010.
  
  
  METHODS
  Plasma indexes of inflammation (high-sensitivity C-reactive protein, pentraxin 3 [PTX3], interleukin 6 [IL-6], and IL-6:IL-10 ratio), bioincompatibility (leukocytes, neutrophils, complement C3, and myeloperoxidase), and endothelial function (soluble intercellular adhesion molecule 1 [ICAM-1], von Willebrand factor, proendothelin, and endothelin) were measured just before dialysis and at 60, 180, and 240 minutes intradialysis.
  
  
  RESULTS
  Hemodialysis-induced regional LV systolic function. Wall motion score was measured by echocardiography at 30 minutes predialysis, 60 and 180 minutes intradialysis, and 30 minutes postdialysis. We defined hemodialysis-induced regional LV systolic dysfunction as an increase in wall motion score in 2 or more segments.
  
  
  RESULTS
  Patients with hemodialysis-induced regional LV systolic dysfunction (n=29 [27%]) had significantly higher predialysis high-sensitivity C-reactive protein, PTX3, IL-6, and lL-6:IL-10 ratio values. Predialysis levels of bioincompatibility and endothelial markers did not differ between groups. Intradialysis courses of markers of inflammation, bioincompatibility, and endothelial function did not differ in patients with versus without hemodialysis-induced regional LV systolic dysfunction.
  
  
  CONCLUSIONS
  Coronary angiography or computed tomography for quantification of coronary calcifications in our patients was not performed; therefore, we could not relate markers of inflammation to the extent of atherosclerosis.
  
  
  CONCLUSIONS
  Patients with hemodialysis-induced regional LV systolic dysfunction have a proinflammatory cytokine profile. There was no indication of an association with an exaggerated bioincompatibility reaction to hemodialysis.
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Solmaz
authors.initials: S
authors.lastname: Assa
authors.affiliation: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Yoran M
authors.initials: YM
authors.lastname: Hummel
authors.affiliation: Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Voors
authors.affiliation: Dialysis Center Groningen, Groningen, the Netherlands.
authors.forename: Johanna
authors.initials: J
authors.lastname: Kuipers
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Dialysis Center Groningen, Groningen, the Netherlands.
authors.forename: Ralf
authors.initials: R
authors.lastname: Westerhuis
authors.affiliation: Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Henk
authors.initials: H
authors.lastname: Groen
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Stephan J L
authors.initials: SJ
authors.lastname: Bakker
authors.affiliation: Department of Laboratory Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Anneke C
authors.initials: AC
authors.lastname: Muller Kobold
authors.affiliation: Department of Cardiothoracic Surgery, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Haemoscan, Groningen, the Netherlands.
authors.forename: Wim
authors.initials: W
authors.lastname: van Oeveren
authors.affiliation: B⋅R⋅A⋅H⋅M⋅S, Hennigsdorf, Germany.
authors.forename: Joachim
authors.initials: J
authors.lastname: Struck
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
authors.forename: Paul E
authors.initials: PE
authors.lastname: de Jong
authors.affiliation: Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Electronic address: c.f.m.franssen@umcg.nl.
authors.forename: Casper F M
authors.initials: CF
authors.lastname: Franssen
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009195:Peroxidase / Q000032:analysis; D006435:Renal Dialysis / Q000009:adverse effects*; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000175:diagnosis* / Q000453:epidemiology
chemical_list: D015415:Biomarkers; C573420:ICAM1 protein, human; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D009195:Peroxidase
keywords: Cardiac stunning; biomarker; echocardiography; hemodialysis; hemodynamic instability; high-sensitivity C-reactive protein (hs-CRP); interleukin 6 (IL-6); left ventricular systolic dysfunction; pentraxin 3 (PTX3); progressive heart failure; proinflammatory cytokine