{'fraction_non_alphanumeric': 0.03333333333333333, 'fraction_numerical': 0.01746031746031746, 'mean_word_length': 5.242574257425742, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
In‐stent restenotic lesions can rupture—A case against plaque sealing

We present a case of plaque rupture located inside a restenotic stent. Intravascular ultrasound defined a lesion with a minimal lumen area (MLA) of 3.59 cm2, plaque burden of 72%, and reference vessel luminal diameter of 4.0 mm with an external elastic membrane lumen cross‐section area of 12.6 mm2. There was a clearly identified plaque rupture, with a flap‐like dissection within the stented segment. Virtual histology intravascular ultrasound confirmed that the adjacent plaque had necrotic core with a thin overlying fibrous cap. The remaining tissue next to the dissection plane was fibrotic. This case illustrates that neointimal hyperplasia may organize into an unstable plaque, with a thin fibrous cap overlying a lipid‐rich necrotic core—a so‐called virtual histology thin‐capped fibroatheroma. As defined in the PROSPECT trial, the in‐stent stenotic lesion in our case conformed to the definition of a high‐risk plaque—it had an MLA <4 mm2, plaque burden was ≥70%, and there was >10% necrotic core. It became unstable and ruptured. The demonstrated findings of this case may sway physicians against sealing hemodynamically nonsignificant unstable plaques. © 2010 Wiley‐Liss, Inc.