Introduction
Aortic Dissection
Aortic dissection (AD) is a subclass of acute aortic syndromes
encompassing life-threatening aortic pathologies that also include
penetrating atherosclerotic aortic ulcer and intramural haematoma
[1]. The pathology of dissection involves a tear in the aortic
intima where blood circulates from the true lumen (TL) through the entry
tear to the false lumen (FL) that expands over time, which could lead to
either compression of the TL and/or to FL rupture. The tear can also
propagate antegrade (more common) and/or retrograde due to the pulsating
pressure head. This expansion of the FL and propagation of the original
entry tear may result in malperfusion and end-organ ischaemia
(malperfusion syndrome) [2-4]. AD can happen at relatively normal
aortic diameter but the aortic haematoma is likely to expand following
the inception of dissection, with growth rates varying depending on
dissection zone [5].
AD affects an estimated 3-4 people per 100,000 annually, most of whom
are men in their 60s with a history of hypertension and/or diseased
blood vessels. Other predisposing factors leading to AD include genetic
connective tissue disorders such as Marfan and Ehlers-Danlos syndrome,
hereditary vascular disease including Loeys-Dietz syndrome, vascular
inflammation, and trauma [2][3][6]. AD can be further
classified based on anatomy using two universal systems, DeBakey and
Stanford. The DeBakey system is based on the location of the original
entry tear and extent of the dissection [2][7]. Daily and
colleagues [8] at Stanford University developed the Stanford system
and categorised AD into type A and type B depending on whether the
ascending aorta is involved in the tear [2][9]. The Society of
Thoracic Surgery (STS)/Society of Vascular Surgery (SVS) released a more
recent and improved classification system that provides a more
structured and systematic approach to classifying all types of AD. The
reporting standards are similar to those of the Stanford system with
some amendments such as the inclusion of dissection tears that originate
within the arch itself (Figure 1) [10][11]. The current review
will focus specifically on uncomplicated Stanford Type B AD (un-TBAD).
Stanford Type B Aortic Dissection
Stanford Type B AD (TBAD) involves a tear in the aorta distal to the
left subclavian artery (LSA) without any involvement of the ascending
aorta or arch proximal to the LSA (Figure 2). It is equivalent to a
DeBakey III (IIIa and IIIb) dissection [10]. As illustrated in
Figure 1. The STS/SVS system defines TBAD as a dissection with an aortic
entry tear originating in zone 1 or beyond (zones 2-11)
[10][11]. TBAD can be further categorised by time of onset and
presence of complications [2][12]. Different studies report
different time classification of TBAD, however, it is generally accepted
as being acute or chronic. Acute TBAD presents within 14 days of symptom
onset while chronic TBAD is diagnosed 14 days following symptoms. A
subacute phase has been described in some studies as a duration of 15-90
days following symptoms [2][3][12]. The International
Registry of Acute Aortic Dissection divides AD based on time into
hyperacute (symptom onset up to 24 hours), acute (2–7 days), subacute
(8–30 days), and chronic (>30 days) [9][13]. The
dissecting membrane in chronic dissections becomes less compliant, which
appears as a straight line on computed tomography (CT) (Figure 3), while
the more compliant septum in acute dissection present as a wavy line on
CT imaging.
In terms of complications, complicated TBAD (co-TBAD) is associated with
aortic rupture, hypotension/shock, malperfusion, neurological signs,
acute renal failure, recurrent or refractory pain, refractory
hypertension, and/or early aortic dilatation or progression of disease
[2][12]. On the other hand, uncomplicated TBAD (un-TBAD)
comprises about 75% of TBADs and does not present with the above
complications. Since the introduction of thoracic endovascular aortic
repair (TEVAR) for TBAD it has become the gold standard intervention for
co-TBAD. Yet, un-TBAD is still treated conventionally with optimal
medical therapy (OMT), with the exception of acute high-risk cases who
are directly offered TEVAR. It is also important to realise that 20-50%
of un-TBADs will progress to become complicated and eventually require
some intervention [2][9][14]. Historically, un-TBAD was
repaired with open surgery once a diameter-based threshold of repair,
set and challenged as at 5.5 or 6.0 cm, was attained or complications
developed [15-17]. However, TEVAR is gaining increasing popularity
as a treatment option for un-TBAD due to its improved long-term outcomes
in combination with best medical therapy [2][3][18][19].
However, the optimal timeframe for intervention remains to be
established.
TEVAR for un-TBAD: the dilemma of ‘why?’ and ‘when?’
While research is suggesting that endovascular repair of TBAD could be
successfully performed in the subacute and early chronic phases, there
remains concerns about the ability of TEVAR to remodel the aorta (FL
thrombosis, increase in TL dimeter, and decrease in FL diameter) due to
the fact that the dividing septum becomes less compliant over time,
particularly when the chronic phase is reached [15]. This led to a
paradigm shift to assess if performing TEVAR well below the traditional
threshold of intervention in early phase of an un-TBAD would have
greater success in remodelling the distal aorta. Repair in the acute
phase must weigh any purported remodelling benefits against added risks
in the acute phase such as retrograde type A dissection or rupture.
Perhaps there is a point along the continuum between acute un-TBAD at a
relatively small aortic diameter to chronic un-TBAD at 5.5 cm that would
optimise the benefits of TEVAR and mitigate its risks.
Management of Uncomplicated Type B Aortic Dissection
OMT also known as best medical therapy (BMT), has traditionally been the
first line treatment for un-TBAD irrespective of any additional
intervention. Open surgery is associated with increased
morbidity/mortality and subsequently abandoned [1][9]. The
ultimate goal of OMT according to the American College of Cardiology
Foundation (ACCF) involves pharmacological control of BP (systolic BP
< 100-120 mmHg) and HR (<60 b/min) to minimise shear
forces and circumferential strain on the aortic wall and avoid FL
pressurisation [12][20]. Pharmacotherapy includes selective
beta-blockers (first-line), diuretics, calcium channel blockers,
angiotensin-converting-enzyme (ACE) inhibitors, and alpha blockers (less
common) [21]. There is evidence conservative treatment for un-TBAD
has a 10% (30-day) mortality and up to 25% requiring intervention
within 4 years principally due to aortic degeneration [22]. While
TEVAR is the recommended treatment choice as per international
guidelines for co-TBAD, it is still being evaluated for un-TBAD.
Several studies, such as STABLE and STABLE II by Lombardi et al., proved
that TEVAR is highly effective in co-TBAD due to its promotion of
favourable aortic remodelling, false lumen thrombosis, and overall
survival relative to open surgery [23][24]. The INSTEAD,
INSTEAD-XL, and ADSORB randomized control trials investigated the use of
OMT alone for un-TBAD versus the combination of OMT with TEVAR, and
reported on several early and late outcomes. To what extent does TEVAR
offer un-TBAD patients with comparable improvements in clinical outcomes
as those with co-TBAD [22][25-27]?
As mentioned previously, 20-50% of un-TBADs will progress to become
complicated and eventually require complex intervention. Although
un-TBAD may not be symptomatic in the chronic phase but it sometimes
possesses a high risk of progression and development of complications
due to certain physiological and radiological conditions. There high
risk-indicating parameters include total aortic diameter
>44mm, FL diameter >22mm, a patent or partial
thrombosed FL, primary entry tear diameter > 10 mm, and age
of >60. It is vital to identify these cases early on and
intervene accordingly to prevent disease progression
[3][28][29].