title: The systemic inflammatory response in coronary artery bypass grafting: what is the role of the very low ejection fraction (EF < or = 30%)?
abstract: OBJECTIVE
  Patients with depressed left ventricular function are more susceptible to develop postoperative complications after cardiac surgery. The aim of the present study was to examine the effect of severe left ventricular dysfunction on the activation of systemic inflammatory reaction during and after coronary artery bypass grafting (CABG).
  
  
  METHODS
  Clinical prospective study; 32 selected patients underwent CABG; 16 patients had depressed left ventricular function before the operation (low ejection fraction [EF] <30%)--Low EF group (study group). Sixteen patients had normal left ventricular function (normal EF, >50%)--Normal EF group (control group). The levels of inflammatory mediators TNF-alpha, IL-6, IL-8 and IL-10 were measured preoperatively, during and after cardiopulmonary bypass (CPB) and 24 hours postoperatively.
  
  
  RESULTS
  Higher levels of almost all of inflammatory mediators were detected in patients with depressed left ventricular function compared with patients of normal EF group. IL-6 levels were found statistically significant higher in Low EF group before the induction of anesthesia (P=0.039) and after the administration of protamine (P=0.02). IL-8 levels were found statistically significant higher in Low EF group before the induction of anesthesia (P=0.05), 30 min after the start of CPB (P=0.02), after the administration of protamine (P=0.015) and 24 hours after the end of the operation (P=0.05). No statistically significant differences were demonstrated between the 2 groups of study relative to TNF-alpha and IL-10.
  
  
  CONCLUSIONS
  A greater activation of systemic inflammatory reaction occurred in patients with depressed left ventricular function than in patients with normal cardiac function when they underwent CABG with extracorporeal circulation.
authors.affiliation: Department of Cardiac and Thoracic Surgery, University Hospital of Ioannina, School of Medicine, Ioannina, Greece. hkarfis@yahoo.gr
authors.forename: E A
authors.initials: EA
authors.lastname: Karfis
authors.forename: G
authors.initials: G
authors.lastname: Papadopoulos
authors.forename: M
authors.initials: M
authors.lastname: Matsagas
authors.forename: D
authors.initials: D
authors.lastname: Pantazi
authors.forename: M
authors.initials: M
authors.lastname: Lekka
authors.forename: I
authors.initials: I
authors.lastname: Kitsiouli
authors.forename: S
authors.initials: S
authors.lastname: Siminelakis
authors.forename: C
authors.initials: C
authors.lastname: Anagnostopoulos
authors.forename: G
authors.initials: G
authors.lastname: Drossos
mesh_terms: D000368:Aged; D001026:Coronary Artery Bypass / Q000009:adverse effects; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D013318:Stroke Volume; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000503:physiopathology
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10