title: Glycaemic control and restenosis after percutaneous coronary interventions in patients with diabetes mellitus: a report from the Insulin Diabetes Angioplasty study.
abstract: OBJECTIVE
  We investigated the impact of glucose control on target lesion restenosis after PCI in patients with type 2 diabetes.
  
  
  METHODS
  Ninety-three consecutive patients with type 2 diabetes accepted for PCI were randomised to intensified glucose control based on insulin (I-group; n=44) or to continue ongoing glucose-lowering treatment (C-group; n=49).The treatment target was a FBG of 5-7 mmol/L and HbA1c <6.5%. Information on target lesion restenosis after six months was available in 82 patients.
  
  
  RESULTS
  At baseline HbA1c and FBG did not differ between the I- and C-groups, respectively (HbA1c: 6.5 vs. 6.5%; p=1.0 and FBG: 7.0 vs. 7.3 mmol/L; p=0.3). After six months there was no significant change in HbA1c or FBG in either group (change in HbA1c: -0.2 vs.-0.1%; p=0.3 and in FBG: +0.2 vs. -0.3 mmol/L; p=0.3 in the I- and C-groups, respectively). Target lesion restenosis at six months did not differ, I vs. C = 41 and 44% (p=0.8). Independent predictors for restenosis were previous myocardial infarction (OR 8.0, 95% CI 2.5-25.7; p=<0.001) and FBG at baseline (OR for an increase by 1 mmol/L = 1.4, 95% CI 1.1-1.9; p=0.015).
  
  
  CONCLUSIONS
  Restenosis was predicted by baseline FBG suggesting that it would be of interest to target glucose normalisation in future trials. Intensified insulin treatment did not influence the rate of restenosis indicating that the main focus should be on lowering glucose rather than the tool to normalise glucose.
authors.affiliation: Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. camilla.hage@karolinska.se
authors.forename: Camilla
authors.initials: C
authors.lastname: Hage
authors.forename: Anna
authors.initials: A
authors.lastname: Norhammar
authors.forename: Lars
authors.initials: L
authors.lastname: Grip
authors.forename: Klas
authors.initials: K
authors.lastname: Malmberg
authors.forename: Nondita
authors.initials: N
authors.lastname: Sarkar
authors.forename: Bertil
authors.initials: B
authors.lastname: Svane
authors.forename: Lars
authors.initials: L
authors.lastname: Rydén
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000295:instrumentation; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D023921:Coronary Stenosis / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000628:therapy*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D005215:Fasting / Q000097:blood; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D018570:Risk Assessment; D012307:Risk Factors; D015607:Stents; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; C517652:hemoglobin A1c protein, human