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ȣ - 480006 1 |
| Systemic Immunosuppression Inhibits In-Stent Restensis in the Patients with Renal Allograft |
| Cardiovascular Division of Yonsei Cardiovascular Center and Cardiovascular Research Institute, Yonsei University College of Medicine |
| Jae-Hun Jung, Young-Guk Ko, Donghoon Choi, Yangsoo Jang, Won-Heum Shim, Seung-Yun Cho |
Background Cyclosporine, an immunosuppressive agent known to inhibit T-lymphocyte proliferation, 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 Between August 1993 and December 2003, 33 renal transplant patients with 45 coronary lesions and 37 dialysis patients (hemodialysis in 19 and peritoneal dialysis in 18 patients) with 52 lesions underwent coronary stenting using bare metal stents at our center. We followed all patients clinically for mean period of 37±31 months and 40 patients (28 lesions of 20 patients in each groups) angiographically at 14±15 months after coronary intervention.
Results Cyclosporine was combined with glucocorticoids in 32 patients and one patient was received tacrolimus instead of cyclosporine. The baseline clinical and angiographical characteristics were similar and the success rate of procedure was 100% in both groups. In renal transplant group, the mean dose of cyclosporine was 192.5±68 mg/day and the cyclosporine blood level at the time of procedure was 152.9±51.5 ng/mL. The rate of in-stent restenosis was 7.1% (2/28) in renal transplant group and 57.1% (16/28) in dialysis group (p<0.0001). The mean late loss was 0.47±0.57 mm in renal transplant group compared to 1.51±1.09 mm in dialysis group (p=0.004). The overall rate of MACE 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 effects of combined immunosuppressive therapy to inhibit inflammatory reaction and vascular smooth muscle cell proliferation induced by coronary stenting.
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