2.4. Aortic Remodelling
Aortic remodelling is a term which describes the desirable morphologic
changes in the aortic anatomy following TEVAR. The parameters used to
identify remodelling are false lumen (FL) thrombosis, FL regression,
true lumen (TL) expansion, and maximum aortic diameter stability [1,
27]. Several studies have validated the surveillance of these
morphologic characteristics as significant predictors of outcomes in
TBAD [16, 17, 27, 44]. Whilst there is evidence suggesting
pre-emptive TEVAR in patients with un-TBAD [5, 45], assessment of
aortic remodelling is vital in monitoring the post-procedural course of
the dissection process and predicting outcomes [46, 47].
The FL is the most dangerous element in the process of aortic
dissection. Its patency and hence perfusion (with elevated intraluminal
pressure) contribute to the aortic expansion.. Furthermore, it may
compress the TL and impair the blood flow to distal organs, causing
malperfusion [48-50]. Endo-graft placement by TEVAR seals the
primary entry tear and decreases the pressure within the FL, hopefully
leading to both FL thrombosis and TL expansion [16]. FL thrombosis
has a significant clinical value in the follow-up of patients with
un-TBAD following TEVAR [16, 17]. Any FL thrombosis can be assessed
by the absence of contrast media by a Computerised tomogram. However,
Clough et al. [51] challenged this modality for assessment of FL and
showed that magnetic resonance imaging with a blood pool agent has more
accuracy in detecting thrombosis in FL.
Following TEVAR, the surveillance of FL thrombosis is critical in
evaluating aortic stability and remodelling. Persistent FL perfusion or
aneurysmal expansion might be an indication of stent graft failure, and
warrant further reintervention [52, 53].
Different segments in the dissected thoracic and abdominal aorta exhibit
variable degrees of remodelling. The proximal anatomical zones
demonstrating the greatest favourable remodelling following TEVAR
[54]. The FL thrombosis was shown to be more prominent in the
thoracic dissecting aorta with less remodelling observed in the
abdominal aorta irrespective of the timing of TEVAR [55]. Kamman et
al. [44] showed that FL complete thrombosis in the distal zones
(presented as >20 cm from LSA origin) could be as low as
22%. Similar findings were seen by Yuan et al. [5], who showed a
superior FL thrombosis rate in the thoracic aorta compared to abdominal
segments, especially in patients treated in the chronic phase of the
disease. The overall occurrence of FL thrombosis in the dissected
thoracic aortic segment increases with time after TEVAR [54]. Table
(3) shows the degree of FL thrombosis reported in different studies
according to the follow-up period.