title: Elevated CETP activity during acute phase of myocardial infarction is independently associated with endothelial dysfunction and adverse clinical outcome.
abstract: OBJECTIVE
  Recent data suggests that cholesteryl ester transfer protein (CETP) activity may interact with acute stress conditions via inflammatory-oxidative response and thrombogenesis. We investigated this assumption in patients with ST-elevation myocardial infarction (STEMI).
  
  
  METHODS
  Consecutive patients with STEMI (n = 116) were enrolled <24-h of symptoms onset and were followed for 180 days. Plasma levels of C-reactive protein (CRP), interleukin-2 (IL-2), tumor necrosis factor (TNFα), 8-isoprostane, nitric oxide (NOx) and CETP activity were measured at enrollment (D1) and at fifth day (D5). Flow-mediated dilation (FMD) was assessed by ultrasound and coronary thrombus burden (CTB) was evaluated by angiography.
  
  
  RESULTS
  Neither baseline nor the change of CETP activity from D1 to D5 was associated with CRP, IL-2, TNFα, 8-isoprostane levels or CTB. The rise in NOx from D1 to D5 was inferior [3.5(-1; 10) vs. 5.5(-1; 12); p < 0.001] and FMD was lower [5.9(5.5) vs. 9.6(6.6); p = 0.047] in patients with baseline CETP activity above the median value than in their counterparts. Oxidized HDL was measured by thiobarbituric acid reactive substances (TBARS) in isolated HDL particles and increased from D1 to D5, and remaining elevated at D30. The change in TBARS content in HDL was associated with CETP activity (r = 0.72; p = 0.014) and FMD (r = -0.61; p = 0.046). High CETP activity at admission was associated with the incidence of sudden death and recurrent MI at 30 days (OR 12.8; 95% CI 1.25-132; p = 0.032) and 180 days (OR 3.3; 95% CI 1.03-10.7; p = 0.044).
  
  
  CONCLUSIONS
  An enhanced CETP activity during acute phase of STEMI is independently associated with endothelial dysfunction and adverse clinical outcome.
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Luiz Sergio F
authors.initials: LS
authors.lastname: Carvalho
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil; Lipids Laboratory, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Vitor W M
authors.initials: VW
authors.lastname: Virginio
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil; Lipids Laboratory, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Natalia B
authors.initials: NB
authors.lastname: Panzoldo
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Valeria N
authors.initials: VN
authors.lastname: Figueiredo
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Simone N
authors.initials: SN
authors.lastname: Santos
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Rodrigo G P
authors.initials: RG
authors.lastname: Modolo
authors.affiliation: University of Brasília, Brasilia, DF, Brazil.
authors.forename: Joalbo M
authors.initials: JM
authors.lastname: Andrade
authors.affiliation: Escola Superior de Ciencias da Saúde (ESCS), Brasilia, DF, Brazil.
authors.forename: Jose C
authors.initials: JC
authors.lastname: Quinaglia E Silva
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Wilson
authors.initials: W
authors.lastname: Nadruz-Junior
authors.affiliation: Lipids Laboratory, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
authors.forename: Eliana C
authors.initials: EC
authors.lastname: de Faria
authors.affiliation: Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil. Electronic address: andreisposito@gmail.com.
authors.forename: Andrei C
authors.initials: AC
authors.lastname: Sposito
mesh_terms: D000368:Aged; D000792:Angiography; D002097:C-Reactive Protein / Q000378:metabolism; D053480:Cholesterol Ester Transfer Proteins / Q000097:blood*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007376:Interleukin-2 / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D009569:Nitric Oxide / Q000097:blood; D010100:Oxygen / Q000737:chemistry*; D011446:Prospective Studies; D012042:Registries; D017392:Thiobarbituric Acid Reactive Substances / Q000737:chemistry*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014652:Vascular Diseases / Q000473:pathology
chemical_list: C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D007376:Interleukin-2; D008075:Lipoproteins, HDL; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D002097:C-Reactive Protein; D015237:Dinoprost; D010100:Oxygen
keywords: CETP; Endothelial dysfunction; Inflammation; Myocardial infarction; Oxidized HDL