Why the study?
Does intensified glucose control based on insulin reduce target lesion restenosis after PCI in patients with type 2 diabetes?
Does intensified glucose control based on insulin reduce target lesion restenosis after PCI in patients with type 2 diabetes?
Intensified insulin treatment did not reduce target lesion restenosis after PCI in patients with type 2 diabetes, although baseline fasting blood glucose was an independent predictor of restenosis.
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.
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Hage et al. (2009) studied this question.
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