2.3.1. Late Endoleaks 
Late or secondary endoleaks are defined as endoleaks occurring 30-days post-TEVAR [23]. Of the five endoleak types described, type I endoleak occurs when the blood flows alongside the graft’s proximal (Ia) or distal (Ib) attachments to the arterial wall. Type II endoleak describes a backward flow from a single (IIa) or multiple (IIb) side branches as the intercostal or lumbar arteries into the false lumen [24, 25]. Type I and Type II endoleaks are the most commonly observed endoleaks during later follow-up after TEVAR in un-TBAD [8, 12, 21, 26].
Some endoleaks such as type Ia and Ib can eventually resolve on their own without any need for re-intervention [12, 27]. However, some endoleaks persist and will perfuse the FL, leading to progressive aortic expansion due to endotension created
An earlier study by Xu et al. reported 3 deaths from thoracic aortic rupture due to overlooked endoleaks in patients managed with TEVAR in the chronic phase of dissection [28]. However, recent studies focusing on intervention in the acute phase showed no endoleak-specific mortality. This might be attributed to the use of renovated grafts and technologically advanced practice. Table (2) summarizes the reported incidence of endoleaks after TEVAR in several studies identified.
Time from symptom onset of a TBAD to intervention with TEVAR has not shown any association with endoleak development, for example, Xie et al. [8] reported no significant difference in incidence of endoleak between acute and subacute intervention groups. Endoleaks can be treated with careful monitoring if no significant increase in aortic diameter is observed. Still, re-intervention should be considered in those with perfusion of the FL or an unsealed primary entry tear due to the high risk of aortic rupture and associated mortality. Further improvement in stents and practice might be able to decrease the incidence of endoleak and yield more satisfying outcomes.
2.3.3. Retrograde Type A aortic dissection (RTAD)
Retrograde type A aortic dissection (RTAD) is a life-threatening complication which is defined by Estrera et al. as a dissection originating distal to the ascending aorta but extending backwards with a retrograde flap into the ascending aorta [27, 29]. Iatrogenic proximal Stent graft induced new entry (SINE) is a potential aetiology of RTAD following TEVAR for unTBAD [12, 28]. Though it has a rare incidence that ranges between 1.33%-3.17% [27, 30, 31], it has a high mortality rate (42%) [27].
RTAD post-TEVAR can present acutely during the TEVAR, however, most can take several months to present [27, 31, 32]. RTAD must be suspected during follow-up in acute-onset or recurrent chest pain cases [31]. However, it may present silently and be discovered incidentally on follow-up imaging [32, 33]. A meta-analysis by Chen et al. [34], included both complicated and uncomplicated dissections and showed that patients treated with proximal bare stent were more likely to have RTAD than those treated with proximal non-bare stent-grafts . (2.31% vs. 1.24%; RR=2.06; 95% CI, 1.22–3.50). This was contradicted later by Ma et al. [31], indicating no significant difference in the incidence of RTAD between proximal bare and non-bare stent-graft groups (Bare: 3.4% vs. non-bare 2.8%, P= 0.64).
Ma et al. [31] also showed a very high mortality rate associated with RTAD; 7 out of 27 (25%) patients had aorta-related sudden death due to rupture or cardiac tamponade. In contrast, five other deaths occurred postoperatively due to multiple organ failure. The mortality rate in this study was (44.4%) which further validated the results of Eggebrecht et al., who reported a mortality rate of 42% [27, 31].
Dissection characteristics, grafting procedure, and genetics were shown to influence the incidence of RTAD after TEVAR in patients with TBAD. Demographics, however, were not associated with an increased risk of RTAD. Still, patients with Marfan syndrome experienced more complications and were at a higher risk of developing RTAD (OR: 3.7; 95%CI 1.09-12.75) [31].
An ascending thoracic aortic diameter > 4 cm ( 47% in RTAD vs. 21% in no-RTAD patients, P=.05) [32] and a proximal aortic tear on the concave surface of the arch [35] were shown to be dissection-related predisposing factors for RTAD. Further, the FL tended to be consistently larger at the levels of the left subclavian artery in patients with RTAD (RTAD patients: 3.2 mm; no-RTAD patients 2.2 mm ; P=.3), [32].
Stent-graft-related risks included a proximal landing zone 1 or 2, which can induce a proximal new re-entry tear [32]. In addition, stent-graft size < 165 mm was reported to be predictive of RTAD following TEVAR (OR:2.99; 95% CI 1.35-6.64) [31].
There is a reported increased risk of RTAD in patients undergoing TEVAR in the acute rather than the chronic stage of dissection. (RR: 1.81; 95% CI, 1.04-3.14) [31], this result can be explained by the fragility of the aortic wall during the acute phase. However, this concept was challenged recently in 2 studies that showed that the intervention timing did not influence the incidence of RTAD in their TBAD study population [8, 32].
RTAD is a very serious complication following TEVAR that often necessitates further high risk procedures such as total arch replacement and a frozen elephant trunk (An et al. 2018). Accurate stent-graft oversizing and play a vital role in minimizing the risk of RTAD in un-TBAD patients undergoing TEVAR [36]. The reported risks come from separate studies with variable sample sizes, putting them at a greater risk of under- or over-estimating effects. Yet, these should be considered carefully so that patients may benefit from more focused care.