It is unknown whether model of renarrowing after β -radiation for in-stent restenosis(ISR) is influenced by the type of geographic miss(GM). Methods: In 166 ISR treated with Galileo, serial quantitative coronary angiographic analysis was done. Minimal lumen diameters and lengths were measured for(1) stent,(2) peri-stent subsegments subjected to angioplasty with/without irradiation, and(3) irradiation margins. GM was defined as:(Type 1) edge injury within the 32P source dose falloff: 2.0 mm inside and outside the source end marker or(Type 2) overt, nonirradiated injury: beyond the outer 2.0-mm long dose fall-off zone. Results: Restenosis rate was 28.3% at 8.9± 4.5 months with 60% located exclusively outside the stent. Type 1 GM was present in 24.7% of proximal edges, whereas Type 2 in 18.1% . Respective percentages for distal edges were 23.5% and 15.7% . Regardless of presence and type of GM, significant late lumen loss occurred only outside the stent. However, the biggest late lumen loss at the proximal edge was induced by the Type 1 GM(0.65± 0.79, p < 0.001), while proximal Type 2 GM was not associated with edge renarrowing(- 0.04± 0.48, p=NS). Both reference lumen diameter and proximal Type 1 GM influenced restenosis independently(OR 0.47; 95% CI 0.24- 0.90; p=0.023 and OR 2.46; 95% CI 1.12- 5.40; p=0.025). Conclusions: Regardless of presence and type of geographic miss, late lumen loss after β -radiation occurs only outside the stent. However, injury within the proximal 32P dose fall-off but not overt edge injury is associated with the biggest late lumen loss at the respective edge, triggering recurrent restenosis. It is unknown whether model of renarrowing after β -radiation for in-stent restenosis (ISR) is influenced by the type of geographic miss (GM). Methods: In 166 ISR treated with Galileo, serial quantitative coronary angiographic analysis was done. Minimal lumen diameters and lengths were measured for (1) stent, (2) peri-stent subsegments subjected to angioplasty with / without irradiation, and (3) irradiation margins. GM was defined as: (Type 1) edge injury within the 32P source dose falloff : 2.0 mm inside and outside the source end marker or (Type 2) overt, nonirradiated injury: beyond the outer 2.0-mm long dose fall-off zone. Results: Restenosis rate was 28.3% at 8.9 ± 4.5 months with 60% located exclusively outside of the stent. Type 1 GM was present in 24.7% of proximal edges, type 2 in 18.1%. Respective percentages for distal edges were 23.5% and 15.7%. Regardless of presence and type of GM, significant late lumen loss occurred only outside the stent. However, the biggest late lumen loss at the proximal edge was induced by Type 1 GM (0.65 ± 0.79, p <0.001), while proximal Type 2 GM was not associated with edge renarrowing (-0.04 ± 0.48, p = NS). Both reference lumen diameter and proximal Type 1 GM influenced restenosis independently (OR 0.47; 95% CI 0.24- 0.90; p = 0.023 and OR 2.46; 95% CI 1.12-5.40; p = 0.025). Conclusions: Regardless of presence and type of geographic miss, late lumen loss After β -radiation occurs only outside the stent. However, injury within the proximal 32P dose fall-off but not overt edge injury is associated with the biggest late lumen loss at the respective edge, triggering recurrent restenosis.