title: Restenosis after arterial injury caused by coronary stenting in patients with diabetes mellitus.
abstract: OBJECTIVE
  To determine whether diabetic patients, when compared with nondiabetic patients, have a higher incidence of restenosis after coronary stenting, and, if so, whether restenosis is attributable to lesion or procedural differences or to a greater biologic tendency for late loss of minimum diameter in diabetic patients.
  
  
  METHODS
  Case series.
  
  
  METHODS
  Tertiary care referral center.
  
  
  METHODS
  Two hundred twenty consecutive patients with coronary artery disease who were referred for placement of a Palmaz-Schatz stent in either a native coronary artery or a saphenous vein graft.
  
  
  RESULTS
  Based on a traditional dichotomous definition of restenosis (> or = 50% stenosis at follow-up), lesions in diabetic patients had a significantly greater restenosis rate (55%) than lesions in nondiabetic patients (20%; P = 0.001). Vessel size, lesion length, pre-procedure lesion severity, procedural outcome, and acute gain (the difference between minimum lumen diameter before and after the procedure) were similar in the diabetic and nondiabetic groups. However, at follow-up, stents in diabetic patients had a smaller lumen diameter (1.66 +/- 1.18 mm) compared with those in nondiabetic patients (2.24 +/- 0.93 mm; P = 0.004), as well as a greater percent stenosis (49% compared with 32%; P = 0.002). Thus, the increased restenosis rate in stents in diabetic patients (55% compared with 20%; P = 0.001) is secondary to increased late loss of minimum lumen diameter (1.66 +/- 1.28 mm compared with 1.23 +/- 0.97 mm; P = 0.04).
  
  
  CONCLUSIONS
  After arterial injury produced by stent placement, diabetic patients have a significantly greater incidence of restenosis because of greater late loss at the treatment site. Because elastic recoil or vasospasm contributes little to stent restenosis, the increased late loss of minimum lumen diameter in diabetic patients suggests that they have a greater predisposition to intimal hyperplasia.
authors.affiliation: Beth Israel Hospital, Boston, Massachusetts.
authors.forename: J P
authors.initials: JP
authors.lastname: Carrozza
authors.forename: R E
authors.initials: RE
authors.lastname: Kuntz
authors.forename: R F
authors.initials: RF
authors.lastname: Fishman
authors.forename: D S
authors.initials: DS
authors.lastname: Baim
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000209:etiology / Q000628:therapy*; D003331:Coronary Vessels / Q000293:injuries*; D048909:Diabetes Complications; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D012008:Recurrence; D015607:Stents / Q000009:adverse effects*