Abstract 13637: The Best Histopathologic Predictors of DES Restenosis in Human Coronary Autopsy Cases are Media Injury and Inter-Strut Distance
Purpose: BMS restenosis histologically is related to the extent of inflammation induced by media injury and strut penetration into necrotic core (Circulation. 2002;105;2974), yet the mechanisms of DES restenosis remain poorly understood.
Methods: 248 coronary artery lesions with 1st and 2nd generation DES implanted for >30 days were processed at 2-3 mm intervals and histologically evaluated. Of those, restenosis (in-stent >75% x-sectional luminal narrowing or healed total occlusion) was observed 23 lesions (9.3%). Following the exclusion of lesions with acute stent thrombosis and unhealed struts, 65 stented coronary lesions were included where a total of 608 cross-sections including 130 sections from proximal and distal non-stented segments were analyzed. The stented segments were categorized into 4 types of lesion based on the most severe cross-sectional luminal area stenosis per segment, and designated as: i) Patent (<50% x-sectional luminal narrowing, n=22), ii) Intermediate (50-75%, n=20), iii) Severe stenosis without occlusion (>75%, n=14), and vi) Total occlusion (n=9).
Results: There was no significant difference in overall underlying plaque morphologies among study groups. However, detailed examination revealed medial disruption was more frequent for stents with total occlusion while strut penetration into the necrotic core was solely identified in stents without restenosis (Table). Of the measured parameters, notable difference was observed for the normalized maximum inter-strut distance where the degree of separation of stent struts was a significant predictor of restenosis (Table).
Conclusions: Restenosis of DES appears to be independent of strut penetration into necrotic core. However, the extent of inflammation associated with medial injury and the distribution of the anti-proliferative drug (dependent on inter-strut distance) are the best predictors of restenosis.
- © 2011 by American Heart Association, Inc.