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].