Hydrocortisone reduces restenosis after stenting of small coronary arteries.

Stenting of small coronary arteries has been limited by high rates of restenosis, and restenosis after stenting has chiefly been attributed to inflammatory reactions resulting in cell proliferation and intimal hyperplasia. In order to suppress this inflammatory process, we examined the effects of hydrocortisone, an antiinflammatory agent, on restenosis after stenting in a nonrandomized retrospective registry. The study population consisted of 193 patients treated at two hospitals, who underwent stent implantations in coronary arteries of reference diameter <3 mm between February 1999 and September 2001. Target lesions included complex, restenotic, diabetic, or chronic total lesions and types of implanted stents were Multi-Link, S-series, and gfx stents. Effect of intravenous administration of hydrocortisone (200 mg) before stenting was compared to control patients who did not receive this treatment. There was no significant difference of early outcomes between the hydrocortisone group and the control group. On angiographic follow-up at 6 months after stenting, the rate of restenosis was significantly lower in patients treated with hydrocortisone as compared with control group (22.8% vs 37%, respectively; P < 0.05). The revascularization rate of target lesion at 6 months was also significantly lower in the treated group (16.5% vs 29%, respectively; P < 0.05). These results suggest that preprocedural intravenous administration of hydrocortisone reduces restenosis after stenting of small coronary arteries. Prospectively controlled trials will be necessary to confirm this preventive effect of hydrocortisone on coronary in-stent restenosis.

The effect of hydrocortisone on reducing rates of restenosis and target lesion revascularization after coronary stenting less than 3 mm in stent diameter.

OBJECTIVE: Stenting of small coronary arteries has always been limited by high rates of restenosis, and restenosis has mainly been attributed to inflammatory reactions resulting in cell proliferation and intimal hyperplasia. Based on our experience for several years, we retrospectively investigated the effect of hydrocortisone on reducing in-stent restenosis. PATIENTS AND METHODS: Study population consisted of consecutive 166 patients, 221 lesions, who electively underwent stent implantations stent diameter less than 3 mm into coronary arteries between February 1999 and October 2002. We intravenously administered hydrocortisone before the procedure to 40 patients for preventing allergic reactions due to contrast material, and the effect of hydrocortisone on reducing restenosis was retrospectively compared with 126 patients who did not receive this treatment. RESULTS: There was no significant difference in the prevalence of diabetes mellitus, hyperlipidemia, or hypertension between the two groups. There was no significant difference in the type of lesion, length of stent, balloon/artery ratio, or initial success rate between the two groups, but stent diameter was significantly smaller in the hydrocortisone group compared with the control group. On six-month angiographic follow-up, the restenosis rate was significantly lower in the hydrocortisone group compared with the control group (16.2% vs 34.0%, respectively), and the target lesion revascularization rate was also significantly lower in the hydrocortisone group compared with the control group (13.2% vs 27.5%, respectively). CONCLUSION: These results suggest that intravenous administration of hydrocortisone reduces in-stent restenosis of small coronary arteries. Prospectively controlled trials will be necessary to confirm this preventive effect of hydrocortisone.