Management strategies for thoracic stent-graft repair of distal aortic arch lesions: is intentional subclavian artery occlusion a safe procedure?

Abstract

The aim of this retrospective analysis was to assess the clinical consequences after intentional left subclavian artery (LSA) occlusion. Thirty-seven patients, 27 type B dissection and 10 thoracic aneurysm, with short proximal neck (less than 2 cm) underwent endovascular treatment with intentional exclusion of LSA origin. No immediate complications occurred. Mean arterial pressure gradient, between right and left arms, ranged from 15 to 45 mmHg. After a mean follow-up of 43.70 + or - 24.01 months, mild left arm symptoms secondary to flow reduction occurred in eight cases (21.6%) but only one required LSA transposition, after 8 months, for visual impairment. Type II endoleaks from excluded LSA occurred in 10 cases (27.0%): in seven patients, leaks were treated with coils and/or glue embolization; in one case, leak sealed spontaneously; one patient died before leak embolization could occur; one patient refused any further treatment. Intentional exclusion of the LSA may be justified when a longer proximal landing zone in the aortic arch is required.

Biomechanical Changes After Thoracic Endovascular Aortic Repair in Type B Dissection

“…89 In the presence of type II endoleak, the patent branch can be coil embolized, sutured, 89 or treated with glue embolization. 90–92 Type IIIa endoleak is defined as leakage due to junctional separation of the modular components and is a major cause of reintervention, in particular after multistenting with an overlap <5 cm. 84,93 Type IV endoleak is caused by graft wall porosity and is a first-generation stent material problem that seems to have been resolved with the new-generation stent-grafts.…”

Scintigraphic Imaging of Inflammation in the Aortic Wall Using 99mTc-Pyrophosphate

“…To date, the main indication for urgent surgery is the aortic diameter and its increase over time [ 1 , 9 ]. It is believed that surgical treatment is justified in patients with an TA enlarged to >50 mm, who do not suffer from hereditary connective tissue diseases [ 10 , 11 ]. In 30–60% of cases, however, acute aortic syndrome develops in patients with a TA diameter of <50 mm [ 12 – 14 ]; therefore, a search for additional predictors of acute aortic syndrome in patients with TA aneurysm remains relevant.…”

Molecular Imaging of Thoracic Aortic Aneurysm Inflammation: A Review of Clinical and Experimental Studies

“…На сегодняшний день единственным критерием принятия решения о хирургической коррекции является диаметр аорты и скорость ее расширения [2,3,6,13]. Такой подход наиболее оправдан для пациентов с размером аорты более 50 мм, не страдающих наследственными болезнями соединительной ткани [14,15,16]. Несмотря на это, в 30-60% случаев ОАС развивается при диаметре аорты менее 50 мм [17 -22].…”