Contact Address:
Dr. A. Mohammed Idhrees MCh, FAIS
Cardio Thoracic and Vascular Surgeon
Institute of Cardiac and Aortic Disorders
SRM Institutes for Medical Science (SIMS Hospitals)
Chennai, India – 600 026
Phone: +919962268787
E-Mail:a.m.idhrees@gmail.com
Key Words: Aortic dissection, false lumen, TEVAR, complicated
Uncomplicated Stanford type B aortic dissection (UnTBAD) constitutes
more than two-thirds of the type B aortic dissection. The present
recommended management of UnTBAD is optimum medical management. On the
other hand, intervention is warranted in patients with complicated
Stanford type B aortic dissection (CoTBAD). It is documented that nearly
one-fourth of the patients who were initially diagnosed with UnTBAD may
progress to CoTBAD (1,2). Further, there is evidence that the aorta in
40% of UnTBAD develop dilatation within a period of 18 months (3,4). To
avoid these complications and progression of the natural disease, it has
been suggested to identify the ‘high risk’ subset of patients. Alexander
et al (5) in their review have enumerated a battery of risk factors to
identify these ‘high risk’ patients. They strongly recommended‘timely prophylactic TEVAR intervention’ in these patients.
This brings us to a juncture where many questions are left unanswered
with limited literature. ‘How to categorise high and low-risk
patients?’. ‘What are the flow dynamics and pathophysiology of the Type
B aortic dissection?’. ‘What patient factors contribute to the
progression of the disease?’. ‘Is there a possible way to stop the
progression of the disease?’.
The progression of the pathology in these patients is dependent on the
flow dynamics involving the intimo-medial dissection flap and entry
tear. Unfortunately, this factor is not entirely understood. The
intimo-medial dissection flap is thin and fragile in acute conditions
while it is more mature and fibrosed in chronic aortic dissection. The
margins of entry tears in acute dissection are thin and free-floating
fragile, while that in chronic dissections are well defined with a
fibrosed rim. To complicate the flow dynamics further, the aorta lies in
three different axes with varying degrees of concavity and convexity at
the level of the aortic arch. The elastic property of the aorta in
varying between patients and between different segments in a patient.
Apart from these, patient factors like age, ethnicity, gender, genetic
association, and comorbidities like hypertension, and diabetes mellitus
also influence the flow dynamics (7). All these factors have a complex
interaction and influence the progression of the disease from UnTBAD to
CoTBAD.
We have incontrovertible evidence that patent false lumen (FL) is an
important factor for future complications including dilated false lumen
compressing the true lumen, aortic dilation, malperfusion and rupture.
At the turn of this century, Fattori et al in their research has shown
that the growth rate of the descending aorta is substantially higher
with a patent false lumen (3.7mm/year as compared to 1.1mm/year).
Further, it is demonstrated that the growth rate of the aorta is
significantly reduced in patients where complete false lumen thrombosis
is achieved (8,9). The patency of the FL is directly related to the size
of the entry tear and its location. A larger entry tear will direct more
blood to the FL keeping it patent. This eventually may lead to true
lumen collapse; higher wall stresses in FL causing aortic dilatation.
Additionally, the proximal location of the entry tear tends to raise the
diastolic pressure in FL, a tendency toward aortic dilatation (10).
Hence all our efforts would be directed to achieving false lumen
thrombosis in type B aortic dissection. Optimum medical management may
achieve this in most of these UnTBAD. But unfortunately, it is not in
‘all’ patients. A proper subset of patients does not respond to this
medical management. In other words, these patients are ‘allowed’ to
progress from UnTBAD to CoTBAD under the banner of ‘medical
management’. It is imperative to take the bull by its horn. Recently,
the long-term clinical benefits of thoracic endovascular aortic repair
in UnTBAD have been enumerated (11). Though larger randomised trials are
warranted, with the limited evidence available, these patients have to
be categorised based on laboratory, radiological and clinical parameter.
The identified ‘high-risk patients’ have to have a lower threshold for
prophylactic aortic intervention