The introduction of the drug-eluting stent (DES) has contributed to a significant reduction in in-stent restenosis and repeat revascularization.^1,2 However, despite the use of the DES, percutaneous coronary intervention (PCI) of diffuse long coronary lesions still remains challenging because the prevalence of in-stent restenosis and stent thrombosis remains high compared with short-length coronary lesions.^3,4

Intimal hyperplasia and resulting restenosis limit the efficacy of coronary stenting. We studied a coronary stent coated with the antiproliferative agent paclitaxel as a means of preventing restenosis. We conducted a multicenter, randomized, controlled, triple-blind study to evaluate the ability of a paclitaxel-eluting stent to inhibit restenosis. At three centers, 177 patients with discrete coronary lesions (<15 mm in length, 2.25 to 3.5 mm in diameter) underwent implantation of paclitaxel-eluting stents (low dose, 1.3 μg per square millimeter, or high dose, 3.1 μg per square millimeter) or control stents. Antiplatelet therapies included aspirin with ticlopidine (120 patients), clopidogrel (18 patients), or cilostazol (37 patients). Clinical follow-up was performed at one month and four to six months, and angiographic follow-up at four to six months. Technical success was achieved in 99 percent of the patients (176 of 177). At follow-up, the high-dose group, as compared with the control group, had significantly better results for the degree of stenosis (mean [±SD], 14±21 percent vs. 39±27 percent; P<0.001), late loss of luminal diameter (0.29±0.72 mm vs. 1.04±0.83 mm, P<0.001), and restenosis of more than 50 percent (4 percent vs. 27 percent, P<0.001). Intravascular ultrasound analysis demonstrated a dose-dependent reduction in the volume of intimal hyperplasia (31, 18, and 13 mm³, in the high-dose, low-dose, and control groups, respectively). There was a higher rate of major cardiac events in patients receiving cilostazol than in those receiving ticlopidine or clopidogrel. Among patients receiving ticlopidine or clopidogrel, event-free survival was 98 percent and 100 percent in the high-dose and control groups, respectively, at one month, and 96 percent in both at four to six months. Paclitaxel-eluting stents used with conventional antiplatelet therapy effectively inhibit restenosis and neointimal hyperplasia, with a safety profile similar to that of standard stents.

OBJECTIVE—Despite the popularity of coronary stenting in coronary artery disease (CAD), restenosis remains a challenging clinical problem. This study evaluated the efficacy of rosiglitazone for preventing in-stent restenosis in type 2 diabetic patients. RESEARCH DESIGN AND METHODS—We conducted a prospective, randomized, case-controlled trial involving 95 diabetic patients with CAD who were randomly assigned to either the control or rosiglitazone group (48 and 47 patients, respectively). Quantitative coronary angiography (QCA) was performed at study entry and again at 6-month follow-up. The primary end point was the restenosis rate, which was determined by QCA. RESULTS—Eighty-three patients (45 patients with 55 lesions in the control group and 38 patients with 51 lesions in the rosiglitazone group) completed follow-up angiography. Rosiglitazone treatment for 6 months reduced fasting insulin concentration. The high-sensitivity C-reactive protein concentration was significantly reduced in the rosiglitazone group compared with that in the control group (from 2.92 ± 1.98 to 0.62 ± 0.44 mg/l, P < 0.001 vs. from 2.01 ± 1.33 to 1.79 ± 1.22 mg/l, P = NS). However, the baseline and follow-up glucose and lipid concentrations were not different between two groups. The rate of in-stent restenosis was significantly reduced in the rosiglitazone group compared with the control group (for stent lesions: 17.6 vs. 38.2%, P = 0.030). The rosiglitazone group had a significantly lower degree of diameter stenosis (23.0 ± 23.4% vs. 40.9 ± 31.9%, P = 0.004) compared with the control group. CONCLUSIONS—We demonstrated that treatment with rosiglitazone significantly reduces in-stent restenosis in diabetic patients with CAD who underwent coronary stent implantation.