{'fraction_non_alphanumeric': 0.027710843373493974, 'fraction_numerical': 0.01536144578313253, 'mean_word_length': 5.027223230490018, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, '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}}
Aortic False Lumen Thrombosis and Remodeling: The Paradigm for Endovascular Repair of Aortic Dissection

The use of thoracic endovascular aortic repair (TEVAR) in the treatment of aortic dissections holds promise of reducing aneurysmal degeneration and achieving false lumen thrombosis by covering the aortic entry tear to halt antegrade flow. In the INSTEAD trial (Investigation of Stent-Grafts in Aortic Dissection), .90% of the patients in the stent-graft cohort experienced false lumen thrombosis at 1 year. The subanalysis of aortic dissection patients in the RESTORE (Relay Endovascular Registry for Thoracic Disease) registry showed complete/ partial thrombosis of the false lumen in 40%/ 60%, 63%/37%, 68%/32%, and 100% of patients at 1, 6, 12, and 24 months, respectively. However, the false lumen flow that often persists in the lower thoracic and abdominal aorta due to re-entry tears or intimal fenestrations is retrograde in orientation, and the significance of these small distal fenestrations remains unknown. Notably, patients with incomplete false lumen thrombosis are at risk of progression over time due to aneurysmal degeneration. Intimal tears that extend beyond the ascending aorta into the arch or descending aorta pose a significant surgical challenge and are present in as many as 30% of acute type A dissections. In patients with DeBakey type I dissections, the residual dissected aorta in the arch and descending thoracic aorta has a tendency to dilate over time. Reported risk factors of late aortic dilatation are false lumen patency and the size of the false lumen relative to that of the true lumen. In both type B and postoperative type A patients, the risk of late aortic events is higher for the patients with a patent false lumen, large initial aortic diameter, large false lumen relative to the true lumen, Marfan syndrome, and young age. Park et al. followed 122 patients with residual distal dissection after proximal repair for DeBakey type I dissection. In early postoperative computed tomograms, they found that the thoracic false lumen was patent in 85 (69.7%) patients, and the abdominal false lumen was patent in 111 (91.0%) patients. In 3-year follow-up, the thoracic aortic false lumen remained patent in . 80% of patients. In nearly half of patients (47.5%), the descending aorta dilated by .1 cm in the followup period. Shrinkage of the thoracic false lumen occurred in 30% of patients, of whom 96% had thrombosis of the false lumen. In TEVAR for aortic dissection, theory now holds that scaffolding the distal thoracoabdominal aorta restores flow to malperfused branch vessels and induces positive aortic remodeling, diminishing potential late dilatation. To that end, the STABLE procedure was developed to augment endograft closure of the primary entry tear (type B dissections) with bare metal Z stenting of the true lumen distally or, for type A dissections, open surgical intervention plus adjunctive retrograde proximal endograft deployment with bare metal Z stenting beyond the resected aorta. The extent of bare-metal Z stenting is determined by the distal extension of the dissection and any branch vessel or true lumen compromise. Placement of the dissection stent also facilitates subsequent intervention of malperfused branch vessels. The expansion of the true