This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Hage, C. Articles by Rydén, L. Search for Related Content PubMed Articles by Hage, C. Articles by Rydén, L. Social Bookmarking                         What's this?

Glycaemic control and restenosis after percutaneous coronary interventions in patients with diabetes mellitus: a report from the Insulin Diabetes Angioplasty study

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, camilla.hage{at}karolinska.se

Anna Norhammar

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

Lars Grip

Molecular and Clinical Medicine, Sahlgrenska University Hospital, Göteborg, Sweden

Klas Malmberg

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

Nondita Sarkar

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

Bertil Svane

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

Lars Rydén

Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

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.

Key Words: percutanous coronary intervention • diabetes mellitus • restenosis • blood glucose • insulin

Diabetes and Vascular Disease Research, Vol. 6, No. 2, 71-79 (2009)
DOI: 10.1177/1479164109336042


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?