title: Previous cytomegalovirus infection and restenosis after coronary stent placement.
abstract: BACKGROUND
  Reactivated cytomegalovirus may promote neointima formation after percutaneous coronary interventions by facilitating cell cycle progression through inhibition of the eukariotic tumor suppressor protein p53. This prospective study sought to investigate the effect of previous cytomegalovirus infection on restenosis after coronary stenting.
  
  
  RESULTS
  In 551 consecutive patients with successful stent placement, we determined cytomegalovirus IgG titers. Primary and secondary end points were the rate of angiographic restenosis at 6 months and the rate of target vessel reintervention at 1 year, respectively. Three hundred forty patients (62%) had a positive cytomegalovirus IgG titer. We obtained angiographic follow-up in 82% of all patients. Angiographic restenosis rate was 28.7% in patients with positive cytomegalovirus titers and 34.6% in patients with negative titers (P=0.18). Between the groups with and without positive cytomegalovirus titers, there were no significant differences in late lumen loss (1.16+/-0.90 mm and 1.23+/-0.86 mm, respectively, P=0.44). Target vessel reintervention was performed in 16.8% of the patients with positive cytomegalovirus titers and in 17.5% of those without (P=0.82). Even after correction for potential confounding variables by multivariate analysis, positive cytomegalovirus titers did not manifest as a predictor of angiographic restenosis (adjusted odds ratio [95% confidence interval], 0.78 [0.52 to 1.19]).
  
  
  CONCLUSIONS
  Previous cytomegalovirus infection does not carry an increased risk of restenosis after stenting.
authors.affiliation: 1. Medizinische Klinik, Deutsches Herzzentrum, Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Munich, Germany.
authors.forename: F J
authors.initials: FJ
authors.lastname: Neumann
authors.forename: A
authors.initials: A
authors.lastname: Kastrati
authors.forename: T
authors.initials: T
authors.lastname: Miethke
authors.forename: J
authors.initials: J
authors.lastname: Mehilli
authors.forename: G
authors.initials: G
authors.lastname: Pogatsa-Murray
authors.forename: W
authors.initials: W
authors.lastname: Koch
authors.forename: M
authors.initials: M
authors.lastname: Seyfarth
authors.forename: A
authors.initials: A
authors.lastname: Schömig
mesh_terms: D000368:Aged; D000914:Antibodies, Viral / Q000097:blood; D015331:Cohort Studies; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000209:etiology / Q000628:therapy; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D003587:Cytomegalovirus / Q000235:genetics / Q000276:immunology; D003586:Cytomegalovirus Infections / Q000150:complications* / Q000821:virology; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D012008:Recurrence; D012307:Risk Factors; D015607:Stents
chemical_list: D000914:Antibodies, Viral; D004279:DNA, Viral; D007074:Immunoglobulin G