A Willfort-Ehringer1, R Ahmadi2, A Gessl3, M E Gschwandtner2, A Haumer2, W Lang4, E Minar2, S Zehetmayer5, H Ehringer2. 1. Department of Medical Angiology, General Hospital of Vienna, University of Vienna Medical School, Waehringer Guertel 18-20, 1090, Vienna, Austria. andrea.willfort.@akh-wien.ac.at. 2. Department of Medical Angiology, General Hospital of Vienna, University of Vienna Medical School, Waehringer Guertel 18-20, 1090, Vienna, Austria. 3. Department of Endocrinology and Metabolism, General Hospital of Vienna, University of Vienna Medical School, Vienna, Austria. 4. Department of Neurology, General Hospital of Vienna, University of Vienna Medical School, Vienna, Austria. 5. Department of Medical Statistics, General Hospital of Vienna, University of Vienna Medical School, Vienna, Austria.
Abstract
AIMS/HYPOTHESIS: We studied the influence of initial hyperglycaemia on neointimal proliferation within carotid Wallstents. METHODS:A total of 112 patients were followed by duplex sonography after carotid stenting for 24 months. Patients were assigned to three groups: non-diabetic subjects (group A) and diabetic patients, who were assigned according to their baseline HbA(1)c values, to group B1(HbA(1)c<or=6.5%) or group B2 (HbA(1)c>6.5%). RESULTS: At baseline the groups did not differ with respect to other vascular risk factors and residual stenosis on angiograms. The maximal thickness of the layer between the stent and the perfused lumen was measured at the duplex follow-ups. At 3 months the typical ultrasonic structure of the neointima was clearly discernible. From this point on, group B2 differed significantly ( p<0.001) compared with B1 and A with respect to the maximal thickness of neointima and the time course of its ingrowth: group A vs B1 vs B2 was 0.51+/-0.39 vs 0.52+/-0.33 vs 0.56+/-0.35 at 3 months, 0.91+/-0.27 vs 0.90+/-0.38 vs 1.14+/-0.48 at 6 months, 1.02+/-0.24 vs 0.97+/-0.34 vs 1.21+/-0.44 at 12 months and 1.09+/-0.23 vs 1.10+/-0.31 vs 1.23+/-0.37 at 24 months. CONCLUSION/ INTERPRETATION: Initial hyperglycaemia seems to be a predictor of more pronounced neointimal proliferation after carotid stenting independent of diabetes. As intimal hyperplasia is known to be responsible for stent restenosis, strict optimisation of the hyperglycaemic state should be aimed at before elective carotid artery stenting.
RCT Entities:
AIMS/HYPOTHESIS: We studied the influence of initial hyperglycaemia on neointimal proliferation within carotid Wallstents. METHODS: A total of 112 patients were followed by duplex sonography after carotid stenting for 24 months. Patients were assigned to three groups: non-diabetic subjects (group A) and diabeticpatients, who were assigned according to their baseline HbA(1)c values, to group B1(HbA(1)c<or=6.5%) or group B2 (HbA(1)c>6.5%). RESULTS: At baseline the groups did not differ with respect to other vascular risk factors and residual stenosis on angiograms. The maximal thickness of the layer between the stent and the perfused lumen was measured at the duplex follow-ups. At 3 months the typical ultrasonic structure of the neointima was clearly discernible. From this point on, group B2 differed significantly ( p<0.001) compared with B1 and A with respect to the maximal thickness of neointima and the time course of its ingrowth: group A vs B1 vs B2 was 0.51+/-0.39 vs 0.52+/-0.33 vs 0.56+/-0.35 at 3 months, 0.91+/-0.27 vs 0.90+/-0.38 vs 1.14+/-0.48 at 6 months, 1.02+/-0.24 vs 0.97+/-0.34 vs 1.21+/-0.44 at 12 months and 1.09+/-0.23 vs 1.10+/-0.31 vs 1.23+/-0.37 at 24 months. CONCLUSION/ INTERPRETATION: Initial hyperglycaemia seems to be a predictor of more pronounced neointimal proliferation after carotid stenting independent of diabetes. As intimal hyperplasia is known to be responsible for stent restenosis, strict optimisation of the hyperglycaemic state should be aimed at before elective carotid artery stenting.
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