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Pathophysiology, Classication andPrinciples ofManagement ofAcute Aortic…
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14
Fig. 14.3 Zones of graft
attachment in the aorta and
iliac arteries [36]
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0
2 cm
3
4
5
6
7
8
9
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Mid-point of
descending
thoracic aor
(approx. T6)
In 65% of cases of dissection, the intimal tears occur in the ascending aorta, 20%
in the descending aorta, 10% in the arch, with 5% starting in the abdominal aorta.
There is a male:female ratio of 5:1 with a peak incidence of 50–60years for proximal dissections, and 60–70years for distal dissection [37].
14.8.2 Intra-mural Haematoma (IMH) (Class 2 Dissection)
IMH typically occurs in patients with extensive atherosclerotic disease and makes
up 5–20% of AAS cases. Several papers have reported that IMH may spontaneously
regress (<10%), however a signicant proportion progress to true dissection
(16–47%) [38]. Occurring in greater prevalence in Asian populations, IMH makes
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M. Hamilton
up 30–40% of AAS in Asian series [39]. It is dened as a circular or crescentshaped thickening >5mm of the aortic wall with the absence of dissecting membrane, intimal disruption or false lumen ow [5] (Fig.14.2).
IMH is usually visualised on CT as a crescent-shaped or concentric thickening of
the aortic wall, with attenuation consistent with haematoma. It may involve a longer
segment of aorta than classical dissection. It appears as a “dissection without intimal tear”, and was previously described as such—however it is now recognised that
there may be small atherosclerotic plaque ruptures in the wall of the vessel that are
related to the proximal extent of the IMH [40]. It has also been suggested that there
may be focal rupture of vasa vasorum in the aortic wall which causes IMH, however
with the advent of newer multi-detector CT arrays, previously invisible intimal
defects are now being recognised [40]. This leads to the proposition that a ruptured
vasa vasorum leads to increased focal transmural pressure and consequent “retrograde” rupture of a pre-existing aortic plaque and intimal disruption [41].
Anatomically, IMH presents as Type A (Ascending aorta or arch, in 30% and
10% of cases respectively), or Type B (distal to the subclavian, 60% of cases). Type
A presentations are more common in Asian series [39]. Symptomatic Type A IMH
is associated with a high mortality when managed medically (55%), and the argument can probably be made that surgical intervention is appropriate in this cohort.
The answer is not so clear in asymptomatic lesions, where mortality with medical
management is lower (in-hospital mortality rates of 7% and 5year survival of 90%).
Unfortunately a signicant proportion (45%) of cases go on and develop complications over 5years [42].
Two subtypes of IMH are recognised;
1. Type I showing a smooth aortic intima, with an aortic diameter <3.5cm and a
wall thickness <0.5cm. The mean longitudinal extent of these lesions is less
than 11cm.
2. Type II lesions occur in the setting of thoracic aortic atherosclerosis and are
associated with calcium deposits, rough aortic luminal margins and aortic dilata-
tion to >3.5cm. The aortic wall thickness is substantially greater than Type I at
>1.3cm with a range of 0.6–4cm.
IMH seems to be associated with a lower risk of malperfusion syndromes than
classical TAD, although complications are common. Between 28 and 47% of IMH
progress to overt false luminal dissection. Early aneurysm formation or contained
rupture develops in 20–45% of patients [
43].
Predictors of progression to TAD include recurrent or persisting pain and presence of PAU.Some IMH may improve spontaneously with medical management
only (particularly in Asian series). Younger ages, smaller aortic diameter (<4–4.5cm)
and thinner haematoma (<1cm) confer better prognosis [33, 44] and may allow non
operative treatment with close observation. In one series, a 30-fold increase in progression to rupture was demonstrated if the aortic diameter was greater than 40mm,
and wall thickness >1cm was associated with a nine-fold risk of progression [45].
IMH has been shown to progress and develop new lesions in a short space of time
(24–48h) so that diligent clinical assessment and repeat imaging is required [4].
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The location of the IMH is also prognostic, with IMH in the ascending aorta having
a high risk of progression to frank dissection. This usually mandates repair.
Exceptions to this seem to be Japanese and Korean series where there is a more
benign course with Type A IMH treated with BP control, bed rest and serial imaging [46].
Recent advances in understanding of the contribution of genetic inuences on
matrix metalloproteinase (MMP) concentrations, elastin and collagen turnover and
risk of syndromal AAS, suggest that the genotypic differences between Asian and
European groups explains the differences in prognosis, progression and prevalence in IMH.
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14.8.3 Penetrating Aortic Ulcer (Class 4 Aortic Dissection)
Penetrating aortic ulcer is dened as ulceration of an aortic atherosclerotic plaque
penetrating through the internal elastic lamina into the aortic media. It is also classied as Class 4 Aortic Dissection [5]. PAUs are predominantly distributed in the
descending thoracic aorta (62%) and abdominal aorta (31%), with only around 7%
in the arch [47, 48]. Ascending aortic PAU are less common but are occasionally
seen in association with a Type A IMH.It appears that for a given aortic diameter,
the presence of symptomatic PAU confers a worse prognosis than for classical
TAD [49].
PAU comprises around 2.3–7.6% of acute aortic syndromes. In a series of 15
patients, 40% suffered aortic rupture, compared to a rate of 7.3% for Type A dissection and <4% for Type B. PAU is consequently considered to be a morbid
pathology when present [49]. Approximately 18% of PAU patients present with
symptoms consistent with AAS [47] and rupture rates in symptomatic PAU are
around 38% [39, 49].
A recent paper by Gabel etal. [50] identied a large number of asymptomatic
PAU patients found incidentally on contrast enhanced imaging. The disease progression to symptomatic PAU, or rupture in this previously asymptomatic cohort
was only 30%, with 10% undergoing late surgical intervention. They also found that
early referral of asymptomatic incidentally discovered PAU for intervention led to
better long-term outcomes. This aligns with another study by Nathan [47] which
demonstrated a low rupture rate of 4.1% for PAU, and a long term operative intervention rate of 13%. There is radiological progression in approximately 17% of
asymptomatic patients, and 43% of symptomatic patients. Thirty-six percent of
symptomatic PAU in this series progressed to needing repair. This suggests that
incidentally discovered, asymptomatic PAU can safely be monitored and managed
medically, with diligent radiological and clinical follow up.
PAU tends to occur in patients with extensive aortic atherosclerotic disease and
in an older population than those affected by Type 1 dissection (a mean age of
77years compared to 54 Type A dissection and 67 for Type B) [49]. Other risk factors include the presence of aortic aneurysm, smoking, chronic obstructive
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pulmonary disease, and coronary artery disease [4]. It appears that the pathological
lesion (haemorrhage through an atherosclerotic plaque) is limited in its extent
around the aorta by the transmural inammation of extensive surrounding atherosclerosis. Penetration through and dissection towards the adventitia can occur in the
setting of medial penetration of the localised plaque haemorrhage.
Both IMH and PAU are recognised to be endpoints of a degenerative aortic
pathology, and largely occur in the descending thoracic aorta. In one series [51],
90% of IMH and PAU were conned to the descending aorta. Their presence in the
ascending aorta however has the same implications as any other Type A dissection,
with commensurately higher morbidity and mortality.
Although such focal pathology as IMH and PAU seem ideally suited to treatment
by endovascular means, it is probable that most patients in these groups with pathology in the descending aorta do not require intervention, unless they full criteria that
would categorise them in a treatment group for classical TAD (rupture/aneurysm
etc.). The presence of aneurysmal dilatation is a strong predictor of the requirement
for intervention in the future. A recent interdisciplinary consensus document [52] has
laid out an approach to both IMH and PAU, including imaging and treatment options.
M. Hamilton
14.9 Prognosis ofAAS
Data from IRAD demonstrates approximately 25% of medically managed stable
type B dissection patients will die within 3 years, with a substantial proportion
(30–60%) being aortic related deaths [53]. Overall, 5year mortality of Type B TAD
is 30–40% [54]. This includes death related to complications from aortic surgery in
a delayed fashion. The group most likely to suffer complications leading to death
were patients over 66years of age and those with an initial presenting aortic diameter over 40mm [55]. False lumen diameters of >22mm have been shown to indicate a poorer long term prognosis, as well as echocardiographic or intra-vascular
ultrasound (IVUS) demonstration of entry tears >10mm in diameter [56]. There has
been a recent cohort study that also suggested that left ventricular hypertrophy may
be an independent indicator of increased risk of all-cause mortality in uncomplicated type B aortic dissection (TBAD) [57].
Refractory hypertension in patients with TBAD has been shown to denote a worse
long-term outcome, with mortality rates of 35.6% in poorly controlled versus 1.5%
in well controlled cohort of medically managed patients [58]. This difference did not
however seem to be signicant in patients treated with TEVAR (3.7 versus 9.1%).
In-hospital mortality of complicated versus uncomplicated TBAD is signicantly different, with complicated cases having a mortality of 50% compared to
10% of uncomplicated cases [26]. Age greater than 70years and hypotension or
shock on presentation have been shown to be signicant independent predictors of
mortality in TAD.As many as 40% of initially uncomplicated TAD managed medically will proceed to develop complications or aneurysm formation over time [59].
Once aortic diameter reaches 60mm, rupture rates approximate 30% perannum [29].
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STABLE-1 [60] reported acceptable 5 years mortality (comparable with that
seen in IRAD) and low paraplegia rates in treatment of complicated TAD (either
acute or non-acute) with TEVAR, with high rates of thoracic segment false lumen
thrombosis and positive remodeling both within and beyond the stented segment.
Abdominal aortic false lumen thrombosis was not as common as in the thoracic
aorta, however positive remodeling was still seen in the abdominal aorta. Nonetheless
thoracic aortic growth was still seen in 35% of chronic TBAD (cTBAD) cohort, and
19% of the non-acute group during post-intervention follow-up. Abdominal aortic
growth was seen in 52% and 24% respectively during post intervention follow up.
The authors propose that this is related to inammatory changes occurring in the
acute group. Along with many longer term TAD studies, there was a 20% dropout
rate, and this leads to inherent aws in data interpretation, however the data overall
suggests that prognosis can be improved by the use of TEVAR in cTBAD in both
the acute and non-acute phases out to 5years.
It is also important to realise there is a signicantly increased risk of non-aortic
cardiovascular death and morbidity in the AAS cohort, with a 2.4 increased risk of
fatal cardiac events, and a 3 times risk of developing a rst time non-fatal cardiac
event compared to non AAS matched controls [61]. This is presumably due to the
baseline higher cardiovascular morbidity and disease burden of these patients.
14.10 Diagnostic Imaging
14.10.1 Computed Tomography
The rapid acquisition times, ECG gating and post-processing of high resolution CT
angiography has made it the imaging modality of choice [62]. It allows excellent
spatial anatomical visualisation of the aorta and planning for intervention with sensitivity and specicity approaching 100% [62]. There are also some CT features
which may suggest an increased risk of later aneurysmal degeneration or complications [63], including features of the false lumen, diameter, entry tear, multiple false
Table 14.3 Comparative diagnostic ability of imaging techniques for aortic dissection
TOE CT MRI Aortography
Sensitivity ++ ++ +++ ++
Specicity +++ ++ +++ ++
Classication +++ ++ ++ +
Intimal ap +++ – ++ +
Aortic regurgitation +++ – ++ ++
Pericardial effusion +++ ++ ++ –
Branch vessel involvement + ++ ++ +++
Coronary artery involvement ++ + + +++
TOE Trans-oesophageal echocardiogram
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lumens and visceral vessels perfused from the false lumen. The main concerns are
the relatively high radiation dose, the use of iodinated contrast, and radiation risks
in pregnant women. In non ECG-gated CTA there is the possibility of false positive
scans due to pulsation artefact, particularly in the ascending aorta (Table14.3) [64].
M. Hamilton
14.10.2 Trans Oesophageal Echocardiography (TOE)/Trans
Thoracic Echocardiography (TTE)
There has been extensive interest in the utilisation of echocardiography for initial
assessment, and ongoing surveillance of AAS [65]. TTE has the advantage of being
rapid and being able to be performed at the bedside. This may have signicant utility in patients who are too unstable to transfer to CT [66]. It offers excellent imaging
of the ascending aorta and root via the right parasternal and suprasternal views and
in well trained hands is able to view IMH and dissection. In the modern era of contrast enhanced harmonic echocardiography, sensitivity and specicity for Type A
dissection is 93 and 97% respectively with TTE.It is, however, limited in its views
of the descending aorta (sensitivity and specicity of 84 and 94%) [67], and TOE
offers superior imaging of the ascending, descending aorta and the arch. However,
it is not straightforward to use TOE in the awake patient. The sizing of the aorta is
accurate and reproducible (more so than IVUS) [68], and false and true lumens may
be dened and ow assessed [69]. It is also useful in the intra-operative setting,
allowing modications in procedure with greater sensitivity than aortography alone
[68]. There is evidence that low ow endoleaks are more apparent on TOE than on
angiography alone, and that when used along with IVUS it plays an important role
in ensuring appropriate true luminal placement of wires and catheters.
There is also an ongoing role for TTE and TOE in surveillance and assessment
of aortopathies such as MFS [70] and Turner Syndrome, where it can be utilised to
assess size, wall compliance and elasticity, and aid in prediction of long-term risk of
complications [71, 72]. Limitations of the use of TOE include some difculty visualising the carotid and innominate origins on occasion and the inability of ultrasound to penetrate PTFE stent grafts due to the relative impermeability of this
material to ultrasound waves. Also, TTE is not able to reliably image the descending
thoracic aorta (although it may demonstrate an abdominal aortic dissection ap,
particularly in TTE windows achieved from the abdomen).
14.10.3 Magnetic Resonance Imaging (MRI)
There is currently no role for the routine utilisation of MRI in the diagnosis or investigation of AAS in unstable or hyperacute patients [73]. There have been improvements in 4D and contrast enhanced Magnetic Resonance Angiography (MRA)
which allow imaging of complex TAD [74] and may be predictive of degeneration
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of aortic anatomy. Analogous to TOE, time resolved (4D) MRA can demonstrate
ow in each lumen and may be useful for surveillance for this reason.
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14.10.4 Intravascular Ultrasound (IVUS)
IVUS can display both true and false lumen anatomy, particularly the relationship
of visceral or arch branches to the site of dissection. It has been utilised to assist in
the placement of grafts in multi-channel aortic dissections [75], and can demonstrate dynamic or static malperfusion syndromes [69], along with assisting in
assessment of dissection ap mobility (and hence likelihood of improved remodeling after treatment) [27]. The adjunctive intraoperative use of IVUS may reduce the
procedural dose of radiation and iodinated contrast [76]. It has been shown to be
able to guide stent graft size selection, particularly in the setting of AAS, where
shocked patients may have signicant alterations in aortic diameter with resuscitation, and hence alterations in landing zone diameter [77]. Limitations of IVUS
include that eccentric placement of the IVUS catheter within the aorta limits visualisation of the distant wall of the aorta. Also, the relatively high cost of IVUS units
and their consumables reduces their cost-effectiveness when compared with TOE.
14.10.5 Biochemical Markers
D-Dimer [78] has been shown to be elevated in AAS, with levels over 500 ng/mL
being associated with increased severity and extent of AAS [39] and possibly may
have some prognostic implications [79]. D-dimer levels <500ng/mL can reliably rule
out classical TAD within 6h of symptom onset, however this marker cannot reliably
exclude IMH or PAU, or indeed TAD where the false lumen is not fenestrated [64].
There has been some concern about the high rate of false negatives with D-Dimer
(9/113) [80] in IMH and it should not be solely relied upon to exclude TAD.C-Reactive
Protein (CRP) elevation is seen in TAD [56] and there is some suggestion that the
peak CRP level may be predictive of increased risk of complications of TAD [81].
Interleukin-11 (IL-11), MMP-9 and Platelet-derived Growth factor (PDGF) have
all been demonstrated to be upregulated in AAS [7, 82, 83], however the only biomark-
ers that are routinely available for diagnosis or exclusion of AAS are D-dimer and CRP.
14.11 Principles ofTreatment ofAAS
The basic principles of treatment for AAS remain appropriate rst line medical
therapy in all instances. This includes adequate analgesia, provision of beta blockers
and addition of further supplemental antihypertensives. Recent data suggests that
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M. Hamilton
medical therapy may not in itself be enough to reduce long term mortality, however
delayed TEVAR for TAD is still safe and feasible [66]. Unfortunately best medical
therapy does not always result in optimal management of blood pressure and heart
rate, and refractory hypertension has been shown in the IRAD data to be associated
with a worse long-term outcome [58]. Optimal blood pressure targets are still
debated, but it is accepted that a target in the range of 130–140mmHg systolic is
reasonable [5]. Lower limits (<130mmHg) have been shown to reduce 90day aortic
related adverse events in some studies [84], and in the absence of a contraindication,
these lower limits are probably optimal.
Multiple agents may be considered appropriate for initial medical therapy. A
reasonable approach to the initial medical management of AAS is shown in
Table14.4 [85]. Longer term medical management of AAS patients is also important, given the increased risk of non-aortic events such as myocardial infarction,
stroke, heart failure and cardiac death in this cohort [61].
The traditional indications for surgical/endovascular treatment of dissection
remain—Type A TAD, either classical, IMH or PAU requires surgery in otherwise
t candidates. Persistently symptomatic or ruptured TBAD, IMH or PAU require
surgical/interventional treatment, as do those patients who are unable to be managed optimally with medical treatment. There is suggestion from IRAD that patients
with refractory hypertension may be more appropriately dealt with by TEVAR than
medical management due to lower all-cause mortality when stented versus medically managed [58].
However, it is apparent that TBAD in its different variations now requires a more
tailored approach to consideration of intervention, particularly in light of recent
evidence that endovascular treatment of the uncomplicated but high-risk Type B
dissection may be benecial. The INSTEAD [66], INSTEAD-XL [86] and ADSORB
[87] trials have all shown to some degree either an improvement in aortic remodel-
ing [66] or a decrease in aortic-related mortality (INSTEAD-XL, ADSORB) in the
Table 14.4 Medical therapies commonly used in aortic dissection (analgesia, heart rate control,
blood pressure control) (based on (Strayer, 2017 #85)
Drug Dose
Fentanyl 1–2mcg/kg bolus (may need to be repeated), then 0.5–2mcg/kg/h (titrate
Labetolol 10–50mg bolus, then 0.5–4mg/min infusion
Metoprolol 0.1mg/kg titrated every 5–10min (1–2mg/min), up to three doses
Esmolol 500mcg/kg bolus, then 50–200 mcg/kg/min (can repeat bolus if titrating up
Clonidine 75–300mcg 3–6h up to max 750mcg/day (useful in very anxious patient)
Hydralazine 5–10mg IV slow injection. Repeat after 20min if desired BP not achieved.
Morphine 0.1mg/kg bolus (may need to be repeated), then 0.1mg/kg/h
Nitroprusside 0.3mcg/kg/min, maximum of 10mcg/kg/min (risk of reex tachycardia and
loading dose and infusion to pain/ sedation levels
infusion)
Infusion rate 200–300mcg/min (e.g. useful addition to beta-blocker if further
reduction in HR undesirable)
metabolic complications with cumulative dose)
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longer term compared to best medical therapy. It is now therefore reasonable to
consider TEVAR for patients with asymptomatic non-ruptured but “high risk” TAD.
Decision making around these high-risk features is not entirely clear. A number
of perceived high risk features are laid out in a review of current management of
TAD by Alfson etal. [88]. These include features such as large entry tear, aortic
diameter >40mm, patent false lumen with partial thrombosis, false lumen diameter
>22 mm (at upper descending aorta), number of intercostal arteries and visceral
perfusion from the false lumen. Rapid aortic expansion or increase in size of IMH
or PAU are also high-risk features.
Best medical therapy, surveillance and follow-up in congenital and genetic aortic
diseases is well codied in an article by Bradley etal. [89]—this is useful for the
vascular surgeon who may also be involved in the care of the paediatric patient with
syndromal aortic disease.
14.12 Summary
Acute aortic syndrome is associated with high morbidity and mortality. There are a
number of discrete but interlinked pathological processes that predispose individuals to AAS, and the prevalence of AAS is much higher in particular populations
such as those with congenital aortic or valvular disease, and connective tissue disorders such as Marfan or Loeys-Deitz syndromes.
Early aggressive medical management, and decision-making regarding intervention based on well validated classication systems and guidelines improves outcomes, and there is emerging evidence that suggests that even stable patients with
uncomplicated thoracic aortic dissection may benet from endovascular management of their dissection to improve long term outcomes.
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M. Hamilton
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