Research Assessment #6

Date:​ ​October 24, 2019

Subject:​ ​Treatment of Aortic Dissection Stanford Type A (Contd.)
MLA Citation:

Khayat, M., Cooper, K., Khaja, M., Gandhi, R., Bryce, Y., & Williams, D. (2018, April).
Endovascular management of acute aortic dissection. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5949590/

Analysis

The manifestation of true knowledge transcends a numerical grade and encompasses a

vision for one day applying that knowledge. Such perspectives were consistently accentuated in
my enlightening conversation with Dr.Wael Abo-Auda today. On that account, I aspire to
cultivate that relentless hunger for learning by elaborating on my questions on the endovascular
management of aortic dissections.
Through a deeper dive into this comprehensive article, I was able to attribute the
treatment of Stanford Type A dissections to surgical intervention through the employment of
“hypothermic circulatory arrest” and “cardiopulmonary bypass”. In that sense, I think that the
invasiveness of these procedures in the reconstruction of the true lumen is a testament to the
rapid and extensive nature of a dissection’s prognosis. Furthermore, I was surprised that the role
of endovascular management in Stanford Type A is typically isolated to branch endografts and
retrograde dissections that “extend into the ascending aorta”. Therefore, I think that the criticality
of the location of Stanford Type A has contributed to the historical prevalence of surgical
procedures as the primary course of treatment. On the other hand, the lack of impending rupture
that constitutes uncomplicated type B dissections has enabled treatment, fascinatingly , by
medicine alone. In addition, the popularity of thoracic endovascular aortic repair (TEVAR)
procedures is a reflection of the cognizance towards of progressive complications in rupture. For
me, this provides a perspective on how the potential volatility of dissections can blur the
distinction between complicated and uncomplicated cases. Furthermore, I was exposed to the
significance of diagnostic imaging in gaining an accurate representation of values such as branch
diameter, the location of tears, and angulation when pursuing endovascular management to
restore perfusion and thrombose the false lumen. In essence, I learned that the accumulation of
this information is critical in the development of a custom endograft to accommodate the
redirection of circulation via the true lumen channel to undermine aneurysmal degeneration.
However, I was confused by how retrograde false lumen thrombosis can cause visceral
malperfusion because I initially believed that the thrombosis of the false lumen channel is critical
in reducing the risk of rupture. Does the thrombosis of the retrograde false lumen create
increased branch vessel damage due to increased pressure or are the vessels occluded due to
thrombosis at the arch of the aorta? How do the effects of the closure of the primary tear differ
from those of the thrombosed retrograde channel? How is a dissection flap fenestration effective
despite the sustenance of blood flow to the false lumen and how is rupture/aneurysmal
degeneration then avoided in the long-term?
On that note, I hope to conduct further research on the premise of dissection flap
fenestrations and their effectiveness. I feel that the curiosity and confusion that I have fostered
this week will serve as momentum into my search for answers next week. In addition, I feel that
I’ve continued to be exposed to valuable knowledge regarding the importance of vessel anatomy
and the valuable distinctions of complicated vs.uncomplicated determine the efficacy of
diagnosis and treatment. I’d like to conclude my assessment with a resonating quote from
Dr.Abo-Auda, “ the eye does not see what the mind does not know”.