A subgroup analysis of the scripps coronary radiation to inhibit proliferation poststenting trial

Introduction: In the Scripps Coronary Radiation to Inhibit Proliferation Po ststenting (SCRIPPS) Trial, Ir-192 Significantly reduced angiographic, ultr asonographic, and clinical endpoints of restenosis. The objective of this a nalysis was to quantitate the impact of patient, lesion and technical chara cteristics on late angiographic outcome. Methods: Patients with restenotic, stented coronary lesions were randomized to receive either Ir-192 or placebo sources. Late luminal loss and loss in dex were calculated for several patient subgroups, including patients with diabetes, in-stent restenosis, multiple previous percutaneous transluminal coronary angioplasty (PTCA) procedures, longer lesion lengths, saphenous ve in grafts, small vessel diameters, and minimum dose exposures < 8.00 Gy. Tw o-factor analysis of variance was used to test for an interaction between p atient characteristics and treatment effect. Results: In the treated group, late loss was particularly low in patients w ith diabetes (0.19 mm), in-stent restenosis (0.17 mm), reference vessel dia meters < 3.0 mm (0.07 mm), and patients who received a minimum radiation do se to the entire adventitial border of at least 8.00 Gy. The loss index in each of these subgroups was similarly low at -0.02, 0.03, -0.02, and 0.03, respectively. By 2-factor analysis of variance, a significant interaction b etween subgroup characteristic and treatment effect (late loss) was found i n patients with in-stent restenosis (p = 0.035), and patients receiving a m inimum dose of 8.00 Gy to the adventitial border (p = 0.009). Conclusion: In this pilot study, patient characteristics associated with a more aggressive proliferative response to injury appeared to confer an enha nced response to radiotherapy. Furthermore, a dose threshold response to Ir -192 was found with an enhanced response occurring when the entire circumfe rence of the adventitial border was exposed to at least 8.00 Gy. (C) 1998 E lsevier Science Inc.