LAUSR

Long-term effect of carotid stenting (CAS) on the stabilization of the plaque is not well described. The interaction among the late stent expansion, neointimal hyperplasia, and lipid core might explain stabilization of the plaque and low long-term incidence of stroke after CAS. To assess long-term change in the lipid signal, stent, and luminal dimensions and restenosis after CAS with the multimodality intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) imaging. We performed follow-up NIRS-IVUS imaging in patients who underwent CAS at our institution. Of the 112 patients (120 carotid arteries) who had NIRS-IVUS during CAS, 96 were alive at the time of the study, and 52 (58 carotid arteries) agreed to participate on the study. The lipid signal of the stented segment was calculated from the NIRS-derived chemogram (a spectroscopic map) as the lipid core burden index (LCBI, a dimensionless number from 0 to 1000). Volumetric calculations were performed using dedicated software with the automated lumen and stent detection and manual corrections. Median time from CAS to the follow-up examination was 31 months (range 5–56). The mean (± SD) LCBI significantly decreased from 32±56 to 17±27 (p=0,002). The mean stent volume significantly increased from 717±302 mm3 to 1019±429 mm3 (p<0,001) with mean stent expansion 43±24%. The mean luminal volume increased from 717±302 mm3 to 760±359 mm3 (p=0,025) due to the mean in-stent restenosis (ISR) 26±15% of the stent volume. Significant increase in the mean minimal stent area (MSA) (from 11,1±3,0 mm2 to 15,0±3,5 mm2, p<0,001) was not observed in the minimal luminal area (MLA) (from 11,1±3,0 mm2 to 11,4±4,4 mm2, p=0,098) due to the ISR. Significant restenosis (reduction of MLA ≥50% from baseline) was present in 7 stents. During nearly three years of the follow-up after CAS the lipid signal decreased suggesting stabilization of the plaque. Significant late stent expansion was balanced with substantial neointimal hyperplasia therefore the late luminal gain was only modest in volume and nonsignificant at the site of MLA. There was a major variability in the rate of the late stent expansion and restenosis.