Aim: 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.
Methods: 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.
Results: 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).
Conclusion: 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.