Type of publication:Journal article
Author(s):Jubouri M; *Patel R; Tan SZ; Al-Tawil M; Bashir M; Bailey DM; Williams IM
Citation:Annals of Vascular Surgery, 2022 Oct 26 [epub ahead of print]
Abstract:Background: Type B aortic dissection (TBAD) occurs due to an entry tear in the intimal layer of the aorta distal to the origin of the left subclavian artery where blood enters the newly formed false lumen (FL) and extends distally or proximally to form a dissection over an indeterminate length of the aorta which, over time, may eventually rupture. Thoracic endovascular aortic repair (TEVAR) aims to seal off the entry tear proximally with the stent-graft, occluding the origin of the dissection and excluding the FL. Nevertheless, in some cases, the perfusion to the FL is maintained, hindering the aortic remodelling process and increasing the risk of aneurysmal degeneration and rupture, particularly in the abdominal aorta where evidence suggest that remodelling is slower. This review examines the long-term effects of a patent or partially thrombosed FL on clinical outcomes following TEVAR in TBAD, also highlighting the pathological processes behind negative aortic remodelling. Another aim of this review is to provide an overview and appraisal of the currently available techniques for managing a patent or partially thrombosed FL to prevent long-term morbidity occurring. Methods: A comprehensive literature search was performed using several search engines including PubMed, Ovid, Google Scholar, Scopus, and Embase to identify and extract relevant studies. Results: Evidence in the literature show that a partially thrombosed FL is more dangerous than a patent FL due to the occlusion of the distal re-entry tears, impeding outflow and increasing mean arterial and diastolic pressures, whereas the latter is decompressed via distal re-entry sites. FL thrombosis and satisfactory remodelling is sometimes achieved in as few as 40% of patients after TEVAR due to the maintained perfusion of the FL either at the level of the thoracic or abdominal aorta. However, although the thoracic aorta is predominantly covered by the TEVAR stent-graft, poorer remodelling and more dilation is seen in the abdominal aorta. Several techniques are available to embolize the FL, including the Provisional Extension to Induce Complete Attachment, Stent Assisted Balloon Induced Intimal Disruption and Relamination in Aortic Dissection Repair, candy-plug, and Knickerbocker techniques. Conclusions: The management of TBAD is invariably TEVAR to seal off the proximal entry tear while extending the repair distally to completely exclude the FL. A risk of aortic wall dilatation distal to TEVAR stent-graft remains; hence, regular monitoring and accurate imaging are essential. At present, a patent FL can be treated using a range of different endovascular techniques.