An important role for VCAM-1, but not for ICAM-1 in restenosis following coronary stent implantation
1Department of Cardiology, İzmir Atatürk Training and Research Hospital, İzmir, Turkey
2Clinic of Cardiology Atatürk Education and Research Hospital, İzmir-Turkey
3Department of Cardiology İzmir Atatürk Training and Research Hospital, İzmir, Turkey
4Department of Biochemistry Atatürk Teaching Hospital, İzmir, Turkey
5Department of Cardiology and, Atatürk Teaching Hospital, İzmir, Turkey
Anatol J Cardiol 2010; 10(5): 405-409 PubMed ID: 20929696 DOI: 10.5152/akd.2010.137
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Abstract

Objective: In this study, we evaluated the possibility that, levels of circulating adhesion molecules following direct stent implantation may be a marker of restenosis. Methods: This prospective, observational study investigated levels of circulating intercellular (ICAM-1), and vascular cell (VCAM-1) adhesion molecules in 15 patients with stable angina pectoris before and after coronary stent implantation for single vessel-single lesion disease in proximal left anterior descending artery. All patients received bare-metal stents. Patients underwent repeat coronary angiography for detection of restenosis at 6 month. Continuous data between patients with and without restenosis were compared using Mann-Whitney U test. Repeated measurements were compared using Wilcoxon T test. Categorical data were compared using Chi-square statistics. Results: Baseline ICAM-1 and VCAM-1 concentrations before percutaneous coronary intervention (PCI) were 4.89±2.28 and 46.35±22.96 ng/ml respectively. Levels of ICAM and VCAM increased nonsignificantly 24 hours after PCI (5.01±2.35 ng/ml and 52.57±19.40 ng/ml, respectively). Six patients (40%) developed restenosis within 6 months. Mean stent length, mean stent diameter, and mean dilatation pressure were comparable in patient groups with and without restenosis. Levels of plasma VCAM-1 measured before and after PCI did not change significantly in patients without restenosis. However, these levels increased significantly in the group of restenosis. At 6 months, patients who developed restenosis, had higher VCAM-1 levels, as compared to baseline values (from 45.1±21.0 to 57.2±14.3 ng/ml, p<0.05). Plasma levels of pre and post PCI ICAM-1 did not differ significantly between groups with and without restenosis. Conclusion: These results suggest a more dominant role for VCAM-1, but not for ICAM-1 in development of restenosis following coronary stent implantation.