title: Effect of Angiotensin converting enzyme inhibitors on soluble tumor-necrosis-factor-related apoptosis-inducing ligand levels - association with neointimal hyperplasia in drug eluting stents.
abstract: OBJECTIVE
  To test the hypothesis that angiotensin converting enzyme inhibitors (ACEi) affect soluble tumor-necrosis-factor-related apoptosis-inducing ligand (sTRAIL) and this interaction is associated with less in-drug-eluting-stent (DES) neointimal hyperplasia following percutaneous coronary intervention (PCI).
  
  
  METHODS
  From our database of patients with elective PCI and baseline intravascular ultrasound (IVUS) evaluation of the implanted DES, we randomly selected 60 patients who were prescribed an ACEi and 60 matched controls, who did not receive an ACEi following PCI. All patients underwent coronary angiography and IVUS. sTRAIL was measured in samples from the stented coronary artery and a peripheral vein.
  
  
  RESULTS
  sTRAIL concentration was higher in the ACEi group, both in coronary and peripheral samples: 104 [78-139] pg/ml versus 63 [45-100] pg/ml (P < 0.001) and 99 [73-135] pg/ml versus 69 [49-103] pg/ml (P = 0.002), respectively. There was an inverse association (standardized beta -0.760; P < 0.001) between sTRAIL and lumen area loss in both treatment groups. In the multivariable analysis, log(sTRAIL) was an independent negative predictor of lumen area loss (standardized beta -0.660, adjusted 95% confidence interval -0.722 to -0.466).
  
  
  CONCLUSIONS
  Treatment with ACEi was associated with higher sTRAIL levels and lower lumen area loss in the IVUS evaluation of implanted DES. sTRAIL levels were negatively associated with in-stent neointima hyperplasia in these post-PCI patients.
authors.affiliation: Department of Cardiology, Athens General Hospital "G. Gennimatas", Athens, Greece; Hellenic Center for Disease Control and Prevention, Athens, Greece; Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
authors.forename: Georgios
authors.initials: G
authors.lastname: Giannopoulos
authors.forename: Vasiliki
authors.initials: V
authors.lastname: Panagopoulou
authors.forename: Spyridon
authors.initials: S
authors.lastname: Deftereos
authors.forename: Christos
authors.initials: C
authors.lastname: Angelidis
authors.forename: Periklis
authors.initials: P
authors.lastname: Davlouros
authors.forename: Andreas
authors.initials: A
authors.lastname: Synetos
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Toutouzas
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Alexopoulos
authors.forename: Michael W
authors.initials: MW
authors.lastname: Cleman
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Tousoulis
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003430:Cross-Sectional Studies; D054855:Drug-Eluting Stents; D005260:Female; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D058426:Neointima / Q000000981:diagnostic imaging / Q000473:pathology*; D062645:Percutaneous Coronary Intervention; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000097:blood*; D018084:Ultrasonography, Interventional
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D053221:TNF-Related Apoptosis-Inducing Ligand