In-stent restonosis is an important limitation for coronary stenting. The cause of in-stent restenosis is neointimal hyperplasia developed from smooth muscle and matrix. We aimed to investigate the association between urotensin II (U-II) and in-stent restenosis after coronary stenting, which causes endothelial and muscle proliferation and accumulation of collagen.Total 153 patient was enrolled to the study who meet criteria for angiographic indication underwent coronary artery angiography. All patients have history undergone for coronary stent implantation 3 to 9 months ago. In-stent restenosis is identified as ≥50% narrowing inside the stent. In-stent restenosis was observed in 73 and remaining of 80 patients revealed no critical lesion in stent on angiographic evaluation. Plasma level measurement of U-II was performed in all subjects.Urotensin II levels were found to be significantly higher in Group I compared to Group II (1.44±0.74 ng/mL and 1.21±0.59 ng/mL, respectively, P=0.03). In a subgroup analysis, U-II levels were significantly higher in group I than group II in patients treated with bare metal stent (BMS) (1.50±0.76 ng/mL and 1.18±0.56 ng/mL, P=0.016); however, there was not significant change in patients treated with drug-eluted stent (1.26±0.64 ng/mL and 1.27±0.63 ng/mL, P=0.9). Multivariate statistical significance: negative correlation was found between in-stent restenosis and renin-angiotensin-system (RAS) blocker usage (P=0.040) and right coronary artery (RCA) lesion interventions (P=0.018).This study revealed high plasma U-II level might be accepted as a risk factors for in-stent restenosis with BMS. In-stent restenosis is less developed after RCA interventions and taking drug of RAS blockages. Our study findings need to be confirmed in further studies.
