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.