title: Effects of atorvastatin on systemic inflammatory response after coronary bypass surgery.
abstract: OBJECTIVE
  Systemic inflammatory response occurs frequently after coronary artery bypass surgery, and it is strongly correlated with the risk of postoperative morbidity and mortality. Recent studies demonstrate that treatment with statin is associated with a significant and marked decrease in inflammation-associated variables such as the C-reactive protein, cytokines, and adhesion molecules. Therefore, we investigated the effects of preoperative atorvastatin treatment on systemic inflammatory response and perioperative morbidity after cardiopulmonary bypass.
  
  
  METHODS
  Double-blinded, placebo-controlled, randomized study.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Forty patients were randomized to treatment with atorvastatin (20 mg/day, group A, n=20) or placebo (group B, n=20) 3 wks before surgery.
  
  
  METHODS
  Three-week treatment by atorvastatin 20 mg/day.
  
  
  RESULTS
  Postoperative serum levels of both interleukin-6 and interleukin-8 increased significantly over baseline, but the peak levels observed 4 hrs postoperatively were significantly lower in the atorvastatin group. In the same fashion, CD11b expression on neutrophils was significantly lower in the statin group at 4 and 24 hrs postoperatively. Finally, neutrophil-endothelial adhesion was significantly reduced in the statin patients compared with controls. The operation time, blood loss, need for inotropic support, intubation time, and length of intensive care unit or hospital stay did not differ significantly between the two groups. The systemic inflammatory response syndrome score on postoperative days 1 and 2 was comparable in both groups.
  
  
  CONCLUSIONS
  Pretreatment with atorvastatin significantly reduces cytokine release and neutrophil adhesion to the venous endothelium in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass.
authors.affiliation: Interdisciplinary Center for Biomedical Research, University Campus BioMedico di Roma, Italy. m.chello@unicampus.it
authors.forename: Massimo
authors.initials: M
authors.lastname: Chello
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Patti
authors.forename: Dario
authors.initials: D
authors.lastname: Candura
authors.forename: Stefano
authors.initials: S
authors.lastname: Mastrobuoni
authors.forename: Germano
authors.initials: G
authors.lastname: Di Sciascio
authors.forename: Felice
authors.initials: F
authors.lastname: Agrò
authors.forename: Massimiliano
authors.initials: M
authors.lastname: Carassiti
authors.forename: Elvio
authors.initials: E
authors.lastname: Covino
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000069059:Atorvastatin; D001026:Coronary Artery Bypass; D016207:Cytokines / Q000097:blood; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D018375:Neutrophil Activation / Q000187:drug effects; D011183:Postoperative Complications / Q000097:blood / Q000188:drug therapy*; D011758:Pyrroles / Q000627:therapeutic use*; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000188:drug therapy*
chemical_list: D016207:Cytokines; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin