title: Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention.
abstract: BACKGROUND
  With the reduction in restenosis rates by drug-eluting stents, there is new controversy concerning the optimal management of incidental, nontarget lesions identified during percutaneous coronary intervention (PCI). Such lesions have been treated conservatively because of risk of restenosis but now are being considered for PCI to prevent plaque instability. However, the impact of incidental stenoses on future cardiac events remains unknown.
  
  
  RESULTS
  We performed a retrospective cohort study to determine the rate and features of clinical plaque progression using the National Heart, Lung, and Blood Institute Dynamic Registry of consecutive patients undergoing PCI at multiple centers in 1997 to 1998 and 1999. Of 3747 PCI patients, 216 (5.8%) required additional nontarget lesion PCI for clinical plaque progression at 1 year. Fifty-nine percent presented with new unstable angina, and 9.3% presented with nonfatal myocardial infarction. Patients with multivessel coronary artery disease during original PCI were more likely to require nontarget lesion PCI during follow-up (adjusted odds ratio, 1.72 [95% CI, 1.18 to 2.52] for 2 vessels; adjusted odds ratio, 3.37 [95% CI, 2.32 to 4.89] for 3 vessels). Angiographic review showed that the majority (86.9%) of lesions requiring subsequent PCI were < or =60% in severity during original PCI, with the mean lesion stenosis 41.8+/-20.8% at the time of the initial PCI and 83.9+/-13.9% during the recurrent event.
  
  
  CONCLUSIONS
  Approximately 6% of PCI patients will have clinical plaque progression requiring nontarget lesion PCI by 1 year. Greater coronary artery disease burden confers a significantly higher risk for clinical plaque progression.
authors.affiliation: University of Pennsylvania, Philadelphia, PA 19104, USA.
authors.forename: Ruchira
authors.initials: R
authors.lastname: Glaser
authors.forename: Faith
authors.initials: F
authors.lastname: Selzer
authors.forename: David P
authors.initials: DP
authors.lastname: Faxon
authors.forename: Warren K
authors.initials: WK
authors.lastname: Laskey
authors.forename: Howard A
authors.initials: HA
authors.lastname: Cohen
authors.forename: James
authors.initials: J
authors.lastname: Slater
authors.forename: Katherine M
authors.initials: KM
authors.lastname: Detre
authors.forename: Robert L
authors.initials: RL
authors.lastname: Wilensky
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D006328:Cardiac Catheterization; D002317:Cardiovascular Agents / Q000627:therapeutic use; D015331:Cohort Studies; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy; D023903:Coronary Restenosis / Q000453:epidemiology / Q000517:prevention & control; D018450:Disease Progression; D005500:Follow-Up Studies; D006801:Humans; D033162:Incidental Findings; D015993:Life Tables; D009203:Myocardial Infarction / Q000209:etiology* / Q000517:prevention & control / Q000628:therapy; D017202:Myocardial Ischemia / Q000453:epidemiology / Q000209:etiology / Q000628:therapy; D012042:Registries; D012189:Retrospective Studies; D012306:Risk; D015607:Stents
chemical_list: D002317:Cardiovascular Agents