title: Impact of endothelial activation on infective and inflammatory complications after cardiac surgery in type II diabetes mellitus.
abstract: OBJECTIVE
  Altered endothelial response has been described in diabetics after cardiac surgery. Infections and inflammatory organ damage often complicate the postoperative course. We evaluated endothelial/cytokine response (ECR) after cardiac surgery and its role on infective/inflammatory complications of type II diabetic patients.
  
  
  METHODS
  Perioperative ECR of 60 diabetic patients (Group A) undergoing cardiopulmonary bypass was compared to that of 60 non-diabetics (Group B). Hemodynamics, endothelial markers [vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1)], pro-inflammatory (IL-2, IL-6, IL-8) and anti-inflammatory cytokines (IL-10) were analyzed preoperatively (T0), at time of aortic declamping (T1), at ITU admission (T2), at 12 h (T3) and 24 h (T4) postoperatively. Postoperative infective/inflammatory complications were registered, and the related ECR was analyzed.
  
  
  RESULTS
  Hemodynamics were comparable. No differences were found in perioperative IL-6 (p = 0.776) and IL-8 (p=0.660) between the 2 groups. However, the diabetics showed significantly higher endothelial activation (VEGF p = 0.0001, p = 0.0001 since T1 to T3; MCP-1 p = 0.0001, p<0.007 at T1, T3 and T4) with lower IL-10 (p = 0.0001, p<0.05 at T2, T3, T4) and lower IL-2 secretion (p = 0.0001, p < 0.0001 at T1, T2). Infections developed in 23.3% of the diabetics; inflammatory complications in 13.3%. Those developing infections showed significantly lower IL-2 (p = 0.042; p = .021 at T1 and T2) than patients without infections, whereas those with complicated inflammatory lung or renal injury had higher MCP-1 leakage (p = 0.006) with lower IL-10 (p = 0.005).
  
  
  CONCLUSIONS
  The diabetics showed higher endothelial activation and lower antiinflammatory response to CPB compared to non-diabetics. Infections in diabetic patients correlated with depressed IL-2, while inflammatory complications correlated to higher endothelial activation and lower anti-inflammatory cytokine secretion.
authors.affiliation: Cardiac Surgery Unit, Division of Cardiac Surgery, University of Verona, Verona, Italy. frankono@libero.it
authors.forename: Francesco
authors.initials: F
authors.lastname: Onorati
authors.forename: Antonino S
authors.initials: AS
authors.lastname: Rubino
authors.forename: Aldo
authors.initials: A
authors.lastname: Cuda
authors.forename: Daniela
authors.initials: D
authors.lastname: Foti
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Sica
authors.forename: Francesco
authors.initials: F
authors.lastname: Santini
authors.forename: Elio
authors.initials: E
authors.lastname: Gulletta
authors.forename: Attilio
authors.initials: A
authors.lastname: Renzulli
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood; D016009:Chi-Square Distribution; D003141:Communicable Diseases / Q000276:immunology* / Q000503:physiopathology; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D042783:Endothelial Cells / Q000276:immunology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007378:Interleukins / Q000097:blood; D007558:Italy; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology* / Q000503:physiopathology / Q000517:prevention & control; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D018836:Inflammation Mediators; D007378:Interleukins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A