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Updated: Jul 20, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Systemic immunosuppressive therapy inhibits in-stent restenosis in patients with renal allograft
Jae-Hun Jung1, Pil-Ki Min, Jong-Youn Kim
1Cardiovascualr Division, Department of Internal Medicine, Kangnam Sacred Heart Hospital, Hallym University Medical Center, Seoul, South Korea.
Background:
Cyclosporine is used routinely for prophylaxis for renal allograft rejection. In experimental animal studies, cyclosporine had been shown to inhibit smooth muscle cell proliferation during the arterial response to injury. We investigated whether systemic immunosuppression may inhibit in-stent restenosis in renal transplant patients undergoing coronary stenting.
Methods:
From 1993 to 2003, 33 renal transplant patients with 45 coronary lesions and 37 dialysis patients with 52 lesions underwent coronary stenting using bare metal stents at our center. We followed all patients clinically for a mean period of 37 +/- 31 months and 40 patients angiographically at 14 +/- 15 months after coronary intervention. Cyclosporine was combined with corticosteroids in 32 patients and one patient received tacrolimus instead of cyclosporine.
Results:
The baseline clinical and angiographical characteristics were similar and the success rate of the procedure was 100% in both groups. In renal transplant group, the mean dose of cyclosporine was 192.5 +/- 68 mg/day and the blood cyclosporine level at the time of procedure was 152.9 +/- 51.5 ng/mL. The rate of in-stent restenosis was 7.1% in renal transplant group and 57.1% in dialysis group (P < 0.0001). The mean late loss was 0.47 +/- 0.57 mm in renal transplant group when compared with 1.51 +/- 1.09 mm in dialysis group (P = 0.004). The overall rate of major adverse cardiac events (MACEs) was 6.1% in renal transplant group and 35.1% in dialysis group (P < 0.0001).
Conclusions:
Renal transplant patients receiving combined immunosuppressive agents showed markedly low rates of in-stent restenosis and MACE after coronary revascularization with stent. We consider that this result may be related to the ability of combined immunosuppressive therapy to inhibit inflammatory reaction and vascular smooth muscle cell proliferation induced by coronary stenting.
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