title: Inverse association of coronary soluble tumor necrosis factor-related apoptosis inducing ligand (sTRAIL) levels to in-stent neointimal hyperplasia.
abstract: OBJECTIVE
  Soluble tumor necrosis factor-related apoptosis inducing ligand (sTRAIL) has been shown to exert protective action against atherosclerosis. The aim of this study was to investigate potential associations of coronary sTRAIL levels with indices of in-stent neointimal hyperplasia.
  
  
  METHODS
  67 patients who underwent percutaneous coronary intervention with drug-eluting stent were followed up at approximately 12 months with determination of coronary sTRAIL concentration, angiography and intravascular ultrasound evaluation of the stent sites.
  
  
  RESULTS
  Mean sTRAIL concentration was 72.2 ± 2.8 pg/ml. sTRAIL was negatively correlated to indices of neointimal hyperplasia and positively correlated to in-stent minimum lumen area (p < 0.001). Neointimal obstruction and maximal in-stent cross-sectional neointima burden in patients in the upper sTRAIL quartile were 3.8 ± 1.2 and 12.6 ± 3.3%, respectively, versus 14.0 ± 0.7 and 49.8 ± 2.7% in the lower quartile (p < 0.001 for both). sTRAIL levels were significantly lower in patients with binary restenosis (48.7 ± 3.0 vs. 75.2 ± 2.9 pg/ml; p < 0.001). In the multivariate analysis, sTRAIL was an independent predictor of neointimal hyperplasia.
  
  
  CONCLUSIONS
  This study demonstrates a negative association of sTRAIL to in-stent neointima formation. The potential pathophysiologic substrate of this effect implicates modulation of apoptosis in various cell types. These observations should prompt further evaluation of the link between sTRAIL and in-stent restenosis.
authors.affiliation: Cardiology Department and Cardiac Catheterization Laboratory, Athens General Hospital 'G. Gennimatas', Greece.
authors.forename: Spyridon
authors.initials: S
authors.lastname: Deftereos
authors.forename: Georgios
authors.initials: G
authors.lastname: Giannopoulos
authors.forename: Vasiliki
authors.initials: V
authors.lastname: Panagopoulou
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Raisakis
authors.forename: Charalambos
authors.initials: C
authors.lastname: Kossyvakis
authors.forename: Andreas
authors.initials: A
authors.lastname: Kaoukis
authors.forename: Vasileios
authors.initials: V
authors.lastname: Tzalamouras
authors.forename: Maria
authors.initials: M
authors.lastname: Mavri
authors.forename: Vlasios
authors.initials: V
authors.lastname: Pyrgakis
authors.forename: Michael W
authors.initials: MW
authors.lastname: Cleman
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D023903:Coronary Restenosis / Q000097:blood* / Q000473:pathology; D003430:Cross-Sectional Studies; D054855:Drug-Eluting Stents; D005260:Female; D005500:Follow-Up Studies; D006083:Graft Occlusion, Vascular / Q000097:blood / Q000473:pathology; D006801:Humans; D006965:Hyperplasia / Q000097:blood; D008297:Male; D058426:Neointima / Q000473:pathology*; D062645:Percutaneous Coronary Intervention; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism* / Q000502:physiology
chemical_list: D053221:TNF-Related Apoptosis-Inducing Ligand