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Seminar

Acute aortic dissection


Thierry Carrel, Thoralf M Sundt 3rd, Yskert von Kodolitsch, Martin Czerny

Although substantial progress has been made in the prevention, diagnosis, and treatment of acute aortic dissection, Lancet 2023; 401: 773–88
it remains a complex cardiovascular event, with a high immediate mortality and substantial morbidity in individuals Published Online
surviving the acute period. The past decade has allowed a leap forward in understanding the pathophysiology of this January 11, 2023
https://doi.org/10.1016/
disease; the existing classifications have been challenged, and the scientific community moves towards a nomenclature
S0140-6736(22)01970-5
that is likely to unify the current definitions according to morphology and function. The most important
Department of Cardiac Surgery,
pathophysiological pathway, namely the location and extension of the initial intimal tear, which causes a disruption of University Hospital Zurich,
the media layer of the aortic wall, together with the size of the affected aortic segments, determines whether the Zurich, Switzerland
patient should undergo emergency surgery, an endovascular intervention, or receive optimal medical treatment. The (Prof T Carrel MD); Division of
Cardiac Surgery,
scientific evidence for the management and follow-up of acute aortic dissection continues to evolve. This Seminar
Massachusetts’ General
provides a clinically relevant overview of potential prevention, diagnosis, and management of acute aortic dissection, Hospital, Harvard Medical
which is the most severe acute aortic syndrome. School, Boston, MA, USA
(T M Sundt 3rd MD);
Introduction 100 000 person-years). Incidence of overt acute aortic Department of Vascular
Medicine, German Aortic
In this Seminar, we summarise current knowledge dissection was higher (4·4 per 100 000 person-years) than Center, University Heart &
about prevention, diagnosis, and treatment of people in penetrating aortic ulcer (2·1 per 100 000 person-years) Vascular Center Hamburg,
with acute aortic dissection.1–6 We focus on preoperative, and intramural haematoma (1·2 per 100 000 person- Hamburg, Germany
(Y von Kodolitsch MD MBA);
perioperative, and postoperative management, leaving years). Differences were observed according to race and Department of Cardiovascular
detailed surgical techniques only briefly covered. ethnicity. Acute aortic dissection most frequently involved Surgery, University Heart
Acute aortic syndrome refers to signs and symptoms in the ascending aorta (58·4%), and intramural haematomas Center Freiburg, Bad
people with acute chest pains due to a sudden aortic wall were more common in the descending aorta (76·2%).12 In Krozingen, Germany
(M Czerny MD MBA); Faculty of
lesion (figure 1).7–9 Intramural haematoma is often the International Registry of Acute Aortic Dissection Medicine, Albert Ludwig
considered an early stage of acute aortic dissection that (IRAD), two-thirds of patients presented with type A University Freiburg, Freiburg,
requires the same treatment, especially when located in thoracic aortic dissection and one-third with type B Germany (M Czerny)
the ascending aorta. However, in some instances (aortic thoracic aortic dissection. The peak incidence was Correspondence to:
diameter ≤45 mm, thickness of haematoma ≤10 mm, observed around age 60 years.13 Prof Thierry Carrel, Department
of Cardiac Surgery, University
absence of significant haemopericardium, and aortic
Hospital Zurich, Zurich 8091,
insufficiency), intramural haematoma can be treated Acute aortic dissection as cause of out-of-hospital Switzerland
conservatively with blood pressure control and monitoring cardiac arrest and incidence at autopsy [email protected]
through repeated imaging, especially in people older than The true incidence of acute aortic dissection is
80 years and individuals at high risk.7,8 Penetrating aortic underestimated because an unknown number of people
ulcers occur most often within an atherosclerotic aorta, die before reaching a hospital and mortality might be
mainly in the aortic arch and descending aorta (90% of the attributed to another cardiovascular event.14 In a
cases). Large penetrating aortic ulcers might be best
treated by endovascular stent-grafts while conservative
treatment is justified for small lesions.7 Acute aortic Search strategy and selection criteria
dissection is the most severe form of acute aortic This work is a narrative review based on the knowledge of the
syndrome and will be the topic of this Seminar. authors. We searched PubMed, MEDLINE, and Embase with
the terms “aortic dissection”, “acute”, and “chronic” alone,
Epidemiology and combined with “prevention”, “diagnosis”, and
In vivo incidence “treatment”. We mainly selected full-text articles, reviews, and
The reported incidence of acute aortic dissection varies meta-analyses published in the past 3 years through to the
greatly, from three to 16 individuals per 100 000 per year, end of August, 2022, but did not exclude some commonly
depending on study designs and geographical referenced and highly regarded older publications. We also
characteristics.10 A systematic review and meta-analysis reviewed major society guidelines and expert consensus
showed that the pooled incidence of thoracic aortic documents. The articles were categorised with relevance to
aneurysms as a predisposing condition of acute aortic epidemiology and risk factors, prevention, classification,
dissection was 5·3 per 100 000 individuals per year and clinical diagnosis and immediate management, treatment
the prevalence was 0·16%.11 strategies, and long-term follow-up. One particularity of this
A study of the Rochester Epidemiology Project in the disease is that very few randomised studies are available
general population found an overall age-adjusted and regarding optimal treatment; this is due to the disease
sex-adjusted incidence of acute aortic syndrome of requiring urgent treatment, and the individual presentation
7·7 per 100 000 person-years. Incidence was higher for and complexity of the disease.
men (10·2 per 100 000 person-years) than women (5·7 per

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Seminar

IMH PAU AAD


had an aortic diameter of at least 5·5 cm.13,22,23 Therefore,
it is advisable to refer patients with the size of the aorta
exceeding 4·5 cm to a cardiovascular specialist for serial
imaging, especially when they have first-degree relatives
with thoracic aortic aneurysm or dissection.

Sex and ethnicity


In the IRAD database, two-thirds of the people are men;
FL
TL
Black patients present more often with type B thoracic
* aortic dissection, are younger, and more frequently have
DM arterial hypertension (up to 90%), diabetes, or cocaine
abuse, or a combination of these.13 Women are often
TL
FL affected later in life than men, and their health outcomes
are worse.24,25 Pregnant women with connective tissue
Figure 1: Main types of acute aortic syndrome disease are at an increased risk of acute aortic dissection.26
The three main pathologies that might cause acute aortic syndrome: IMH in the ascending aorta (asterisk) without Type A thoracic aortic dissection is more common during
visible lesion of the inner aortic layers (left); PAU (red arrows) in the descending aorta with a transmural lesion and the third trimester, whereas type B thoracic aortic
a localised subadventitial haematoma (middle); and AAD (right) with an intimal rupture and the dissecting
membrane separating the native aortic lumen in a TL and FL. For each acute aortic syndrome, a corresponding
dissection is more frequent in the post-partum period.26
CT scan image is presented. IMH=intramural haematoma. PAU= penetrating atherosclerotic ulcer. AAD=acute
type A aortic dissection. DM=dissection membrane. TL=true lumen. FL=false lumen. Socioeconomic status
Low socioeconomic status might explain why some
systematic review, type A thoracic aortic dissection was individuals more often present with acute aortic
suggested to be the cause of out-of-hospital cardiac arrest dissection than with stable aneurysm.27,28 Possible
in up to 7% of cases and type B thoracic aortic dissection explanations include reduced access to medical care and
in up to 0·5% of cases. Death following out-of-hospital therefore less prophylactic imaging, less awareness of
cardiac arrest due to acute aortic dissection was 100%.15,16 risk factor control, and work environments with higher
This finding should alert the medical community to physical and emotional stress, when compared with
keep the threshold for emergency aortic imaging low in patients with high socioeconomic status.
case of acute thoracic pain, especially when acute
coronary syndrome has been excluded. Aortic risk factors
Increased aortic length has been identified as a risk factor
Early diagnosis and risk factors for acute aortic for acute aortic events and is reported to be as important
dissection as aortic diameter.29–32 Typical values are available via the
For the Aortic Calculator see Early diagnosis of heritable thoracic aortic diseases is Aortic Calculator29 to calculate the risk of acute aortic
www.aorticcalculator.com widely believed to save lives by preventing acute dissection by combination of aortic diameter with length
complications such as acute aortic dissection.17 In the and the individual’s height.
See Online for appendix appendix (p 1) we summarise current knowledge about Invasive assessment of increased aortic stiffness and
signs and indicators of Marfan syndrome, Loeys-Dietz central haemodynamic parameters predict future thoracic
syndrome, and non-syndromic heritable thoracic aortic aortic aneurysm expansion.33 The anatomy of the aortic
diseases.18–21 arch and abnormal aortic flow patterns have been explored
The role of specific risk factors (appendix p 2) that as potential risk factors for acute aortic dissection. A
might cause acute aortic syndrome is not fully elucidated, gothic aortic arch, defined by a larger vertical distance
but conditions associated with increased aortic wall stress from the origin of the innominate artery to the top of the
(eg, arterial hypertension) and with aortic media arch, together with angulation and tortuosity, is typically
abnormalities (eg, bicuspid aortic valve, connective tissue associated with a turbulent flow pattern, and a risk factor
diseases, and inflammatory diseases of the aorta) might for type B thoracic aortic dissection.34,35
play a significant part. According to the IRAD, increased
aortic diameter is more relevant for type A thoracic aortic Drugs
dissection, but the lack thereof does not imply safety Drugs have been discussed as a risk factor of aortic
because acute aortic dissection might occur in a normal- aneurysms and dissection. A meta-analysis demonstrated
sized or moderately dilated aorta.22 The effect of risk increased odds of aortic aneurysm, dissection, or rupture
factors differs for type A and type B thoracic aortic in patients under current treatment with fluoroquinolones
dissection. Most conspicuously, enlarged aortic diameter compared with non-user counterparts.36 Future research is
is an important determinant for the risk of acute aortic needed to elucidate the pathophysiological mechanisms
dissection in the ascending aorta, and was believed to and the plausibility of this association. Cytostatic drugs
have a similar effect in the descending aorta; however, and immunosuppressants, including glucocorticoids,
only 18·4% of patients with type B acute aortic dissection might increase the risk of thoracic aneurysms and acute

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Seminar

aortic dissection, so clinical caution might be required


after transplantation and in patients with cancer.37 An Panel: Conditions and behaviours with the option to
increased risk for acute aortic dissection might exist better evaluate the risk or prevent acute aortic dissection
in athletes using anabolic steroids,38 and in patients • Bicuspid aortic valve disease
following intake of amphetamine, ecstasy, or cocaine.39,40 • Aortic coarctation (ie, operated or non-operated)
The risk factors for aortic aneurysm progression and acute • Marfan syndrome
aortic dissection are summarised in the appendix (p 2). • Loeys-Dietz syndrome
• Vascular Ehlers-Danlos syndrome
Prevention of acute aortic dissection • Non-syndromic heritable thoracic aortic diseases
Conditions with the option to prevent acute aortic • Turner syndrome
dissection • Pregnancy
Congenital cardiovascular malformations such as a • Arterial hypertension, especially if uncontrolled
bicuspid aortic valve and aortic coarctation, regardless • Dyslipidaemia
of surgical or interventional correction, monogenic • Smoking
hereditary thoracic aortic diseases such as Marfan • Obstructive sleep apnoea
syndrome, Loeys-Dietz syndrome, vascular Ehlers-Danlos • Autoimmune disorders (eg, Takayasu, Behçet, Ormond, or
syndrome, and non-syndromic hereditary thoracic aortic giant-cell arteritis)
diseases, and chromosomal disorders such as Turner • Infectious diseases (eg, syphilis or tuberculosis)
syndrome, are conditions with a definite risk for acute • Catheter intervention
aortic dissection. In these conditions, early diagnosis with • Aortic manipulations (eg, cross clamping and tangential
screening of family members, monitoring of aortic clamping, and aortotomy)
growth, preventive medications, and elective surgery for • Anastomotic sites or patch aortoplasty
aortic sizes that reach the critical diameter specified in • Strong isometric exercises, weightlifting, or Valsalva
the guidelines2,3 are effective in preventing acute aortic manoeuver
dissection. The guidelines also recommend control of • Deceleration trauma
common cardiovascular risk factors such as arterial
Modified from Kodolitsch et al.20
hypertension and dyslipidaemia, and smoking cessation
to reduce the risk for acute aortic dissection.3 A meta-
analysis found that obstructive sleep apnoea is associated arterial disease in patients with a history of aneurysm,
with a 60% increased risk of acute aortic dissection.41 This aortic dissection, or sudden death. Screening first-degree
was confirmed in an investigator-initiated study with relatives of patients with thoracic aortic aneurysm and
patients with Marfan syndrome42 (panel). dissection might identify a familial form in which relatives
have a 50% chance of carrying the mutation or disease in
Lifestyle and medication the family.3 Once a familial form of thoracic aortic
Exertion and emotion have been identified as inciting aneurysm or acute aortic dissection is suspected, the
events for acute aortic dissection.43 Although patients are guidelines recommended referral to a geneticist for family
often unable to adhere to recommendations to refrain screening and molecular testing.3 These recommendations
from physical or mental stress, this association should be were difficult to implement in clinical practice because
mentioned, and awareness encouraged. they referred only to monogenetic conditions such as
Regarding chronic arterial hypertension, guidelines Marfan syndrome, Loeys-Dietz syndrome, arterial
emphasise the role of antihypertensive medications in tortuosity thoracic aortic aneurysm, and acute aortic
keeping blood pressure below 140/90 mm Hg.3 A syndrome. Meanwhile, health insurance data have shown
population-based retrospective cohort study confirmed that that aortic dissection aggregates in families and that a
long-term use of β blockers, angiotensin-converting family history is a strong risk factor for aortic dissection,
enzyme inhibitors, or angiotensin 2 receptor blockers were independent of the presence of heritable thoracic aortic
associated with long-term benefits for aortic dissection.44 syndromes.18,48 Experts now recommend aortic imaging
These are first-line agents for blood pressure control, and clinical examination of family members of patients
because they slow aortic root diameter growth and reduce with aortic aneurysm or dissection who are younger than
aortic events in randomised clinical trials, in Marfan 60 years or 60 years and older without atherosclerosis or
syndrome or Ehlers-Danlos syndrome.44–47 There is no hypertension.18
evidence to support the prophylactic use of antihypertensive
drugs in normotensive patients with chronic thoracic aortic Clinical diagnosis, biomarkers, and imaging
disease of cause other than connective tissue disease.3 Clinical pretest probability of acute aortic dissection
Prompt diagnosis and therapy are the only factors critical
Family screening and genetic testing to acute aortic dissection survival. Especially in type A
In 2014, the European Society for Cardiology (ESC) thoracic aortic dissection, time is death because delays
guidelines recommended evaluating the family history of between door and surgical knife reduce survival.49 The

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Seminar

American Heart Association has integrated clinical signs such as non-ST-elevation myocardial infarction,
and symptoms into an Aortic Dissection Detection Risk pulmonary embolism, or pneumo­ thorax (figure 2).
Score (ADD-RS)2 which has recently been confirmed to Nevertheless, the limited availability of D-dimers and
be accurate.49 Nevertheless, acute aortic dissection might other potential biomarkers in the acute setting and the
cause highly unspecific symptoms (appendix pp 3–4). scarcity of prospective studies preclude any
In step 1 of the ADD-RS, acute aortic dissection should recommendation regarding their utility.2,3
be considered in patients with chest, back, or abdominal
pain; syncope; stroke; or mesenteric, myocardial, or limb Definitive imaging of acute aortic dissection
ischaemia. Delay or misdiagnosis of acute aortic Rapid access to a CT angiogram is of paramount
dissection is common in patients with features of many importance because timely diagnosis of acute aortic
other cardiovascular diseases (figure 2).13,50,51 dissection is essential for survival. Electrocardiogram-
In step 2 of the ADD-RS, patients with clinical triggered CT angiography is the best imaging to rule in or
suspicion of acute aortic dissection should be screened rule out acute aortic dissection. It might also detect the
for 12 high-risk features, including five predisposing presence of aortic rupture and pericardial and pleural
conditions, three pain features, and four examination effusion. Non-gated scans can lead to misdiagnosis due to
findings. In patients younger than 60 years not motion artifact (false positive). CT scanning can also
previously diagnosed with genetic aortopathy, additional distinguish between dissection and intramural
indicators for genetic aortopathy could be examined haematoma, with arguments being made by some for
(appendix p 1). non-operative management of type A intramural
In step 3, the ADD-RS counts all 12 high-risk features. haematoma with favourable imaging characteristics (total
In patients with high probability of acute aortic dissection diameter <5 cm, intramural haematoma thickness <1 cm,
(ADD-RS score >1), the guidelines recommend or absence of giant ulcer). Contrast imaging might also be
immediate definitive imaging, which should usually be useful in detecting malperfusion with absence of flow in
CT angiography in patients who are stable, and the visceral vessels or differential enhancement of the
transoesophageal echocardiography in patients who are true and false lumen with implications for viscera
unstable, with instability defined by very severe pain, perfused by either. The extension of dissection into the
tachycardia, tachypnoea, hypotension, cyanosis, or shock, brachiocephalic vessels and femoral vessels might also
or a combination of these.2,3 In patients with a high have implications for options for perfusion during
likelihood of acute aortic dissection, the ESC supports a cardiopulmonary bypass for repair of the dissection. CT
definitive diagnosis of type A thoracic aortic dissection in scanning is quicker than MRI because image acquisition
the presence of intimal tear, aortic regurgitation, or time is shorter.
pericardial effusion, or a combination of these, on Transthoracic echocardiography has a lower sensitivity
transthoracic echocardiography. than CT angiography, but is useful to demonstrate aortic
dilatation and dissection flaps, to search for pericardial
D-dimers, transthoracic echocardiography, and chest effusion and aortic regurgitation, and to evaluate cardiac
radiography function. Echocardiography is accordingly an essential
There are no definitive data or convincing algorithms component of intraoperative management.
for step 3 of the diagnostic work-up of patients with
low (ADD-RS score 0) or intermediate probability of Classifications of acute aortic dissection
acute aortic dissection (ADD-RS score 1), and there is no The first stage of the pathophysiological pathway of all
blood test or marker that is accurately able to predict types of acute aortic dissection is an intimal tear in the
aortic dissection. However, studies have confirmed the aortic wall. The tear leads to a bleeding within and
diagnostic value of D-dimers,52 transthoracic echocardio­ along the aortic wall resulting in the separation of the
graphy,53 and chest radiography in the evaluation of different layers and the development of two, and
acute aortic dissection.49,54 In particular, D-dimers sometimes more than two, perfused channels within
greater than 500 ng/mL, transthoracic echocardiography the aorta. The location of the primary tear is the most
with direct (intimal tear, false lumen) or indirect important determinant for the further clinical evolution
evidence of acute aortic dissection (eg, aortic diameter of an acute aortic dissection, and longitudinal
>40 mm, aortic regurgitation, pericardial effusion or propagation of the dissecting process might occur both
tamponade, or pleural effusion), and chest radiographs in the antegrade and retrograde direction (figure 3).55 It
with evidence of mediastinal enlargement support is important to note that what is often referred to as the
definitive imaging for acute aortic dissection. It is primary entry tear should not be assumed to be the
argued that D-dimers, transthoracic echocardiography, most proximal tear as it might not have been the initial
and chest radiography might delay the diagnosis of site of the dissection.
acute aortic dissection; however, in patients with low or The classical definition of acute aortic dissection is at
intermediate probability of acute aortic dissection, these an alphabetical level from proximal to distal, regardless
examinations are often needed for alternative diagnoses of the location of the primary intimal tear, being Stanford

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Seminar

A B
STEP 1 Suspicion of AAD

Consideration of AAD with Features of patients with missed or delayed Acute chest pain: ECG <10 min
• Chest, back, or abdominal pain diagnosis
• Syncope • Features of acute coronary syndrome, stroke, or
• Central nervous, mesenteric, myocardial, or limp pulmonary embolism
STEMI
ischaemia ? • Atypical pain (not sudden or painless)
• Features of congestive heart failure
• Previous cardiac surgery
• Initial presentation to a non-tertiary care hospital
• Fever Haemodynamic
No ADD-RS No
• Female sex instability with or without
≥1
cardiogenic shock

STEP 2 ADD-RS Yes Yes


High-risk predisposing conditions Causes for concern in previously unknown genetic
(1) Marfan or other heritable aortic diseases aortopathy
(2) Family history of aortic disease ? • Seven signs of Marfan syndrome
Yes TTE No
(3) Aortic valve disease • Visible signs of Loeys-Dietz syndrome with criteria for AAD
(4) Recent aortic catheter or surgery • Associates of non-syndromic genetic aortopathy
(5) Thoracic aortic aneurysm
?
+ No
CTA with AAD Coronary angiography
High-risk chest, back, or abdominal pain features Other risk conditions
(6) Abrupt onset • BAV or CoA
(7) Severe pain intensity • Weightlifting or deceleration trauma
(8) Ripping or tearing quality • Anabolics, sildenafil, or fluorchinolone
• Autoimmune or infectious disease
+ • Cocaine or amphetamine
• Sleep apnoea
High-risk examination findings
• Pregnancy
(9) Asymmetry of pulse or systolic blood pressure
(>20 mm Hg)
(10) Focal neurological deficit
(11) Murmur of aortic regurgitation
(12) Shock state or hypotension

STEP 3 Diagnostic evaluation

Yes ADD-RS Transthoracic echocardiography of the proximal aorta


CTA for AAD >1 • Intimal flap, false lumen flow
• Aortic diameter enlargement
No ? • Aortic regurgitation
• Bicuspid aortic valve
Yes D-dimer • Pericardial effusion
CTA for AAD ≥500 ng/mL • Pleural effusion
• Cardiac tamponade
No

Yes TTE
CTA for AAD with or without Mediastinal widening on chest radiography
CXR ? • Maximum width >80 mm at the level of the aortic
knob
• Ratio of mediastinum to chest width >0·25
No • Subjective evaluation with suboptimal images

STEP 4 Definitive diagnosis

No Alternative Yes
CTA for AAD diagnosis Consider clarification of alternative diseases
established?

Figure 2: Recommended algorithms in case of suspicion and strong suspicion of acute aortic dissection
(A) Algorithm in case of suspected AAD reproduced from Hiratzka et al.3 (B) Algorithm in case of strong suspicion of ST-elevation myocardial infarction (but AAD not fully excluded). AAD=acute aortic
dissection. ECG=electrocardiogram. STEMI=ST elevation myocardial infarction. ADD-RS=Aortic Dissection Detection Risk Score. TTE=transthoracic echocardiography. CTA=computer tomography
angiography. BAV=bicuspid aortic valve. CoA=coarctation of the aorta. CXR=chest x-ray.

type A if the ascending aorta is involved (historically involvement deserve specific attention.56 Figure 4
DeBakey type I and type II), and Stanford type B if the summarises the classifications of acute aortic dissection.
descending aorta is involved (historically DeBakey type
IIIa or type IIIb). In this Seminar, we discuss the term Type A aortic dissection
non-A non-B thoracic aortic dissection because we are Type A thoracic aortic dissection means that the ascending
convinced that the different types of aortic arch aorta is dissected with the primary entry tear located

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Seminar

within the aortic root or the ascending aorta. When the


ascending aorta is dissected but the primary entry tear is
in the aortic arch or in the descending aorta, it is called a
retrograde type A thoracic aortic dissection.57 The attrition
rate of type A thoracic aortic dissection is estimated to be
2% per hour. The three main reasons for the attrition rate
consist of cardiac tamponade due to rupture or ongoing
transudation, new aortic regurgi­ tation with rapidly
developing heart failure, and organ malperfusion, mainly
in the myocardial, cerebral, and visceral circulation.

Type B aortic dissection


Acute aortic dissection involving the descending aorta
without (Stanford type B or DeBakey type IIIa) or with
(Stanford type B or DeBakey type IIIb) extension in the
abdominal aorta is classified as type B thoracic aortic
dissection. The ascending aorta and the aortic arch are
always free of disease. Acute type B thoracic aortic
dissection might stabilise as an uncomplicated form or
evolve into a complicated form. The ESC guidelines
define complicated type B thoracic aortic dissection by the
presence of persistent or recurrent pain, medication-
resistant hypertension, and early aortic expansion,
malperfusion, or signs of rupture including haemothorax,
and increasing periaortic and mediastinal haematoma.3
Because the distinction between the uncomplicated
Figure 3: Typical type A aortic dissection with primary entry tear in the aortic and complicated forms has far-reaching therapeutic
arch
From the primary intimal tear, the aortic dissection might propagate in an consequences, it is important to note that these criteria
antegrade fashion (yellow arrow) or retrograde fashion (red arrow). are not based on data but on what was perceived to
be a broad consensus, and that persistent pain and
De Bakey I II IIIa IIIb Non-A Non-B uncontrolled hypertension leave room for subjective
Stanford A A B B interpretation.
A systematic review of the morphological signs of
complicated type B thoracic aortic dissection found that
aortic size (>40 mm) at presentation predicted adverse
events and total false lumen thrombosis protected against
such events.58 A higher number of re-entry tears is
protective against false channel expansion,59,60 whereas a
shorter distance between the primary tear and the left
subclavian artery offspring predicted aortic growth in
uncomplicated type B thoracic aortic dissection.61 All
other morphological signs yielded controversial and
conflicting results.

Type non-A non-B aortic dissection


The clinical course of non-A non-B acute aortic dissection
is fundamentally different from type B thoracic aortic
dissection.56,62 The intimal tear is localised beyond the
ascending aorta and the dissection is limited to the aortic
arch, or the tear is located in the descending aorta and
Figure 4: Classification of the different types of aortic dissection
extends in a retrograde way into the arch.56,62,63 When
Historical DeBakey classification (types I, II, and III), and the modified Stanford classification (type A, type B,
and type non-A non-B). Type A describes involvement of the ascending aorta with the entry tear (red arrows) retrograde extension stops in the aortic arch, it is a non-A
in the ascending or in the aortic arch or descending aorta with retrograde propagation. Type B describes non-B dissection, when it extends into the ascending aorta,
involvement of the descending aorta with entry tear distally to the left subclavian artery, with distal extension it becomes a retrograde type A thoracic aortic dissection.
either limited to the thoracic or involving both the thoracic and the abdominal aorta. Type IIIa describes
a limited dissection to the thoracic aorta, whereas type IIIb describes more distal extension into the abdominal
Patients with a primary entry tear within the aortic arch are
aorta. In type non-A non-B, the ascending aorta is always free from disease. The intimal tear is located either in the at highest risk of developing rupture, retrograde type A
aortic arch or in the descending aorta with retrograde expansion limited to the arch. thoracic aortic dissection, or end-organ malperfusion.62

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All three types might occur as acute, subacute, or A B


chronic events, where the term subacute is used when
the initial event is older than 2 weeks and chronic
when it is older than 3 months. This timeline is defined DM
according to current guidelines.64

Anatomical and clinical description of acute F


aortic dissection and risk assessment T
Standardised anatomical descriptors (eg, Type-Entry-
T F F T
Malperfusion classification and DISSECT) and anatomy-
based risk scores (eg, the German Registry for Acute
Aortic Dissection Type A [German registry]) are
Figure 5: Malperfusion in acute aortic dissection
increasingly used for a more precise description of the (A) Possible mechanisms of malperfusion. The dissecting membrane extends with the aortic branch and might
disease, for initial clinical triage, risk assessment, and for cause malperfusion through narrowed or thrombosed true lumen, or thrombosis of the aortic branch (left).
planning the intervention.49,63,65 These classi­fications are Compression of T by F while the dissecting membrane bulge out in front of an aortic branch (right).
(B) Pathological specimen of the abdominal aorta in a case with severe visceral and peripheral malperfusion
considered complementary to the more established consecutive of acute type A aortic dissection. Intact aortic wall (red arrow) and dissected aortic wall with adventitial
Stanford classification. Although the Type-Entry- layer only (yellow arrow). T=true aortic lumen. F=false aortic lumen. DM=dissecting membrane.
Malperfusion classification might be helpful in the
emergency room, DISSECT is more complex and useful from detachment of the valve commissures from the
for scientific purposes (appendix pp 5–7). aortic wall through the dissection itself or from
The German registry risk score can be used incomplete valve closure due to sudden dilatation of the
preoperatively to enable prediction of 30-day mortality risk aortic root or because of prolapse of the dissecting
in patients undergoing surgery for type A thoracic aortic membrane through the valve.
dissection.66 This score uses easily retrievable parameters
based on clinical assessment and CT scan; initial Malperfusion
validations have confirmed its accuracy (appendix p 8). Symptomatic and subclinical malperfusion occurs in
40–50% of patients and might lead to coronary, cerebral,
Complications of acute aortic dissection spinal, visceral, renal, and lower extremity ischaemia.13,68,69
Pain, uncontrollable hypertension, and aortic rupture Malperfusion occurs when the true lumen of an aortic
Severe therapy-resistant pain is frequently observed in branch vessel is obstructed by haematoma or thrombosis
acute aortic dissection. It is frequently accompanied by expansion in the false lumen, or by the dissecting
uncontrollable arterial hypertension and both conditions membrane itself. When the dissecting membrane is fixed
might lead to rapid aortic rupture. independent of the cardiac cycle, it is termed static.
Dynamic malperfusion occurs when the membrane is
Pericardial effusion and cardiac tamponade floating in front of the branch or extends into a branch,
Pericardial effusion is common in acute aortic dissection, with dynamic obstruction and resultant changing
but cardiac tamponade might develop under two different pressures in the true and false lumen during the cardiac
presentations with similar consequences; namely, cycle (figure 5). Finally, thrombosis of a branch caused by
hypotension, shock, and need for resuscitation. The first is low flow and embolism might also result in malperfusion.
frank rupture with haemorrhage into the pericardial space, Coronary malperfusion might lead to coronary
which is observed in 6–10% of cases. The second is ischaemia at presentation and requires special attention
continuous transudation through the suddenly more to intraoperative myocardial protection and liberal
permeable aortic wall, which occurs in up to 40% of cases.13 indication for coronary revascularisation in case of
It is important to note the difference between these persistent myocardial dysfunction following aortic
two conditions, because drainage of pericardial effusion repair.
might stabilise the haemodynamics, and allow a safer The location of the primary entry tear is a key point for
transfer or more stable induction of anaesthesia. Drainage the development of malperfusion: visceral and renal
might be life-saving, but it is rarely used because of the ischaemia occur significantly less often when the tear is
common belief that drainage will result in exsanguination. in the ascending aorta, and more often when it is located
Haemodynamic recovery is the rule, but close monitoring in the distal aortic arch or the proximal descending
of the blood pressure is necessary when fluid is evacuated aorta.63,70 Timely diagnosis and treatment of malperfusion
because blood pressure rises substantially.67 are key elements for survival.71,72

Aortic regurgitation Treatment strategies


Acute aortic regurgitation perceived as a new diastolic Initial medical management and transfer
murmur is the most frequent cardiac complication of Decreasing aortic wall stress by heart rate and blood
type A thoracic aortic dissection. This event might result pressure control is the most important goal in the initial

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management of acute aortic dissection. This decrease in At present, cardiopulmonary bypass is conducted with
stress is achieved by administering analgesia with opioids moderate (26–30°C) hypothermia, whereas deep
that have a beneficial effect on anxiety and respiratory hypothermia (18°C) was more common in the past.
distress, or anti-impulse treatment, which is important Arterial cannulation occurs peripherally (via subclavian
when intravenous β blockers are used to obtain a heart or femoral artery) or centrally via direct aortic cannulation
rate of 60 beats per min, or calcium-channel blockers if using Seldinger’s technique and ultrasound to place the
β blockers are contraindicated.3,72,73 Additional use of other cannula into the true aortic lumen.4,82 Circulatory arrest is
vasodilators should only be considered after heart rate recommended to allow direct inspection of the aortic
control if the systolic blood pressure remains more than arch, resection of the tear if present at this level, and the
120 mm Hg. Reflex tachycardia should be avoided because most complete replacement of the ascending aorta with
it increases the aortic wall stress. the distal anastomosis at the level of the proximal aortic
Whenever possible, the patient should be referred to an arch. This requires brain protection realised with
institution known for a large volume of elective and unilateral antegrade cerebral perfusion through the
emergency surgical and endovascular aortic procedures, subclavian line or with bilateral cerebral perfusion using
because a higher case load is a significant predictor of two perfusion catheters into the carotid arteries.
improved survival in such conditions.74
Treatment of type B dissection
Treatment of type A dissection Non-operative treatment is considered as standard in
Immediate surgery is the gold standard in most patients patients presenting with type B thoracic aortic dissection
with type A thoracic aortic dissection.4 Decision making with maximal analgesia and strict control of blood
around treatment includes repair complexity, durability, pressure;2,3,83 this often allows the patients to survive the
and risk of death, especially in acute unstable patients. early phase and be discharged, but their subsequent
Resection or closure of the intimal tear is the key element history is largely unknown. However, in a mid-term
in ensuring a good outcome.70 A primary entry tear in follow-up analysis, two-thirds of these individuals did not
the ascending aorta is addressed by ascending aortic improve following medical therapy because of
replacement using a vascular graft with the proximal aneurysmal degeneration, and the 6-year intervention-
anastomosis performed at the level of the sinotubular free survival was 41%.84 Therefore, the natural history of
junction and a limited replacement of the concavity of what is initially called an uncomplicated type B thoracic
the aortic arch with a circular open distal anastomosis. aortic dissection might be daunting for the clinicians.
This technique is particularly indicated in case of
normally functioning aortic valve and normal-sized Uncomplicated type B thoracic aortic dissection
aortic root. It is sufficient in most cases, but a limited Following the acute phase, and depending on the wall
initial approach with short ascending graft might result quality and the long-term control of blood pressure,
in more complex redo-procedures later in life, since aortic diameter remains stable or increases.85 Randomised
subsequent endovascular arch repair would need a studies are not available, but a group of experts from the
sufficient landing zone in the previous ascending Society of Thoracic Surgeons and the American
graft.75–77 In pre-existing aortic root dilatation, a more Association for Thoracic Surgery recently summarised
radical approach including root replacement with the current treatment evidence for patients with type B
coronary reimplantation (Bentall procedure) must be thoracic aortic dissection.6 Thoracic endovascular aortic
considered. In patients younger than 50 years with repair has been increasingly proposed to promote
enlarged aortic root, valve-sparing aortic root replacement favourable long-term aortic remodelling and mitigate
(David or Yacoub type of repair) is an ideal, but more aneurysm formation.83,85,86 5-year survival analysis showed
complex procedure that should be performed in a favourable trend towards thoracic endovascular aortic
experienced centres only.78 repair in these patients.87–89 The general principle of
When the primary entry tear is in the proximal intervention is to exclude the primary entry tear in the
descending aorta and extends retrogradely into the acute phase and restore a normal blood flow into the true
ascending aorta, a more extensive approach (namely the aortic lumen. Although coverage of the primary entry
frozen elephant trunk technique) allows exclusion of the tear is often sufficient, stent-graft extension might be
tear and total aortic arch replacement.79 The frozen necessary to treat residual true lumen collapse.
elephant trunk consists of a hybrid prosthesis. The stent- The INSTEAD trial90 prospectively compared
graft part of the prosthesis is inserted in an antegrade prophylactic thoracic endovascular aortic repair and
fashion into the true lumen of the descending aorta, optimal medical treatment with optimal medical treatment
which will stabilise the dissected descending aorta and alone in stable patients with uncomplicated type B thoracic
has potential to reverse malperfusion. The proximal aortic dissection. Morphological evidence of favourable
surgical graft is used to repair the aortic arch. In addition, aortic remodelling was observed more frequently in
frozen elephant trunk facilitates later endovascular steps patients who received thoracic endovascular aortic repair
on the downstream aorta.80,81 plus optimal medical treatment (91·3%) compared with

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optimal medical treatment alone (19·4%), but no difference


in mortality was observed at 2 years. In the INSTEAD-XL
trial,91 patients were monitored up to 5 years and thoracic
endovascular aortic repair plus optimal medical treatment
was associated with improved aorta-specific survival and
less disease progression. This observation influenced ESC
guidelines to recommend thoracic endovascular aortic
repair be considered in uncomplicated type B thoracic
aortic dissection to prevent early and late complications.3
The ADSORB trial92 compared the same treatment options,
but the primary endpoint was a combination of incomplete
or no false lumen thrombosis, aortic dilatation, or aortic
rupture at 1 year. Thrombosis of the false lumen after
thoracic endovascular aortic repair was frequently
associated with a reduction of its diameter, leading to a
favourable aortic remodelling, but no long-term outcome
has been available.

Complicated type B thoracic aortic dissection


An interdisciplinary consensus has suggested the
following factors as signs of complicated type B thoracic Figure 6: Long-term imaging following surgical repair of type A aortic
aortic dissection: persisting pains and hypertension dissection
despite full treatment, rapid increase of aortic size, The CT shows a significant increase in the overall diameter of the descending
aorta with a very narrowed true lumen (red arrow) and an important expansion
periaortic haematoma and haemorrhagic pleural effusion of the false lumen with residual perfusion (blue arrow). Part of the false lumen is
in two subsequent CT scans suggestive of impending already thrombosed (yellow arrow). This patient was scheduled for operative
rupture, and malperfusion indicated by impending thoracoabdominal repair 6 years following composite-graft replacement of the
organ failure.93,94 aortic root and ascending aorta.
Complicated type B thoracic aortic dissection requiring
more active treatment occurs in up to 30–40% of patients, aortic dissection, but this approach has not yet been
and timely diagnosis is a key element for a successful broadly recognised.101
outcome. Among them, one-third of patients might have
the most dangerous complication, visceral ischaemia, Treatment of chronic type B thoracic aortic dissection
which is strongly associated with in-hospital mortality.94,95 Due to improved early outcomes, chronic dissection of the
The IRAD registry reported increasing rates of thoracic descending aorta is increasingly observed in two distinct
endovascular aortic repair in patients with a complicated groups of patients: those in whom a type A thoracic aortic
type B thoracic aortic dissection (from 35% between 1996 dissection has been successfully operated, but a flap
and 2001, to 68% between 2008 and 2013).13,68,95 The persists distal to the initial repair; and those who survived
presence or the creation of a sufficient proximal landing acute type B thoracic aortic dissection. Management of
zone (>2·5 cm), using bypass or transposition of the left chronic type B thoracic aortic dissection includes blood
subclavian artery, might be necessary for stable anchoring pressure control, repeated imaging, and repair of late
of a stent-graft.96 Coverage of the left subclavian artery complications before emergencies occur.6,44,102 Blood
without revascularisation is a significant factor for stroke.97 pressure control and repeated imaging are straightforward,
If no landing zone is present or cannot be gained by left whereas the timing of thoracic endovascular aortic repair
subclavian artery bypass or transposition, rerouting of the or surgical repair of a chronic type B thoracic aortic
supra-aortic vessels combined with thoracic endovascular dissection requires more attention.103,104
aortic repair, branched thoracic endovascular aortic repair, Y N
Post-type A aortic arch and descending aorta aneurysmal
Illustration: 20TLGH_3609_1
or frozen elephant trunk are alternative strategies. 94,98,99
Fast Track
In degeneration is not uncommon, and chronic type B thoracic
some cases, theEditor:
provisional extension to induce complete aortic dissection also tends to evolve to thoracoabdominal
attachment technique Text typed
(PETTICOAT) and stent-assisted aneurysm (figure 6).103 Furthermore, some patients might
Author:
balloon-induced intimal disruption and relamination
Image redrawn in present with consequences of endoleaks following early
Illustrator: Matteo Simonetti
aortic dissection repair (STABILISE) techniques might thoracic endovascular aortic repair.
Illustrator check
help to induce a more complete remodelling of the distal Limited post-dissection aneurysms of the descending
Date started:
aorta to a stent-graft. 89,100 04/01/2021 Proofreader sustained
PETTICOAT obliterates check aorta might be managed by open repair, thoracic
abdominal false lumen flow and pressurisation despite endovascular aortic repair, or by thoracic endovascular
successful stent-graft sealing of the thoracic entry tear. aortic repair plus false lumen occlusion techniques.104–107
Branch stenting and fenestration to stabilise the flap Thoracic endovascular aortic repair is a valid alternative
has been reported as primary strategy for type B thoracic to surgery, especially in people with limited disease and

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favourable anatomy, and in people classified as being at rupture.113,114 Recently, most patients with descending-entry
high risk for surgery. and arch-entry non-A, non-B dissection undergo aortic
The aim of treatment remains closure of the primary repair within 2 weeks of dissection onset.53,59 This approach
entry tear, which can usually be achieved by thoracic endo­ allows a more radical treatment of the disease and is more
vascular aortic repair. This approach treats the pathology complex than supracoronary repair in type A thoracic
at its origin. The window of opportunity is open for at least aortic dissection, but seems reasonable, especially in
1 year after the index event. When the pathophysiology patients with connective tissue disease deemed fit enough
changes from a dynamic dissection to a static aneurysm, to undergo the procedure.115
treatment becomes more complex. Number and size of
communications between lumina play a major role in Endovascular interventions of acute aortic dissection
post-dissection aneurysm development. type A
However, thoracic endovascular aortic repair has Endovascular treatment of type A thoracic aortic dissection
technical and anatomical limitations, even though it might with current technologies remains an exceptional
have a lower mortality and complication rate. Coverage of procedure. It is still experimental, and most often used as
the complete dissected aorta with distal sealing of the flap compassionate care.116 The aortic root remains difficult for
because of re-entries in the abdominal aorta might be endovascular purposes because the proximal landing
challenging because of narrowing and stiffness of the zone is close to the coronary ostia and the aortic valve, and
membrane. This can be addressed by balloon fracture of the distal landing zone might require additional actions to
the membrane or by innovative devices for false lumen preserve blood flow in the supra-aortic branches.117
occlusion and tapered grafts.107–109 Finally, exclusion of the However, ascending thoracic endo­vascular aortic repair
primary tear and coverage of the proximal descending combined with transcatheter aortic valve replacement as
aorta is effective and sufficient in most patients with a well as thoracic endovascular aortic repair with custom-
watchful waiting strategy for downstream segments.110 made grafts might represent future options.
Thoracoabdominal aneurysms (from the left subclavian
artery to the aortoiliac bifurcation) with a size greater Contraindications to surgery in type A thoracic aortic
than 5·5–6 cm or a growth rate greater than dissection and delayed repair
0·5–1 cm per year might be treated surgically in patients Although immediate surgical repair of type A thoracic
who are found to be fit enough to withstand such a major aortic dissection is almost always indicated, a sound
procedure.111 Besides aortic size, symptoms such as back clinical judgement with a full appreciation of the patient’s
pain or chronic malperfusion (eg, abdominal angina or condition (ie, age, comorbidities, and additional disease
renal failure) might represent indications for repair too. limiting the life expectancy) is mandatory, especially
Open thoracoabdominal aortic repair is a recognised in the presence of stroke or coma, severe myocardial
surgical approach, usually performed on left-heart bypass infarction requiring high-dose vasopressors, mechanical
with mild hypothermia and cerebrospinal fluid drainage. resuscitation before surgery, and liver failure due to
Despite acceptable results (mortality around 7·5% and malperfusion.118 Postponing aortic repair might be a wise
paraplegia rate of 3% in experienced centres), open surgery decision in such patients. In patients with manifest
for post-dissection thoracoabdominal aneurysm repair is malperfusion judged not amenable to aortic repair,
increasingly being replaced by endovascular strategies. endovascular fenestration or stenting of a compromised
This replacement results in aortas full of stent-grafts, often aortic branch only might be a valid alternative to restore
with persistent false lumen perfusion,104,106 and late adequate perfusion of the malperfused organ. 119,120
outcomes of thoracic endovascular aortic repair studies are However, even in such instances, thoracic aortic repair is
heterogeneous regarding endpoints.6 For this reason, not absolutely contraindicated.121
preserving skills in open repair should be mandatory in
centres of references. Selection bias, dissimilar cohorts, Conservative treatment of limited iatrogenic type A
and the absence of outcomes beyond 5 year makes thoracic aortic dissection
comparison of series and techniques difficult. Type A thoracic aortic dissection as a complication
of a transcatheter valve replacement or percutaneous
Treatment of non-A non-B dissection coronary intervention is a rare iatrogenic complication.
Non-A, non-B acute aortic dissection is the most There are few reports so far, but a conservative approach
challenging type of acute aortic dissection regarding the seems justified in patients with a limited dissection
treatment strategy.112,113 Non-operative treatment of a within the aortic root, and in selected cases with more
non-A, non-B thoracic aortic dissection was originally distal propagation.122,123
thought to be reasonable (similar to type B thoracic aortic
dissection); recent experience advises surgical repair with Outcome, long-term management, and screening
a frozen elephant trunk prosthesis to eliminate the Outcome
primary intimal tear in the arch: the most frequent Early outcome following repair of type A thoracic aortic
indications being severe organ malper­fusion and aortic dissection is highly variable and in-hospital mortality is

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highly dependent on clinical presentation and patient A phenomenon called distal stent-graft induced new
risk profiles.13 Although the average hospital or 30-day entry (dSINE), observed following repair of type B
mortality is reported to be between 15% and 25%, thoracic aortic dissection using thoracic endovascular
experienced aortic centres have reported early mortality aortic repair, has recently gained the attention of the
of 5–8%.124–126 Significant bias might impact results, research community.131 In dSINE, the distal end of a
including selection bias in indications to surgery, survival stent-graft causes erosion and rupture of the dissecting
bias related to transfer, or treatment bias in the technique membrane, which remains asymptomatic; the conse­
and extent of the repair. Observations regarding quence is the formation of new entry tears, which might
surgeons’ and institutions’ performances are important lead to rapid diameter increase. Retrograde type A
for quality improvement. thoracic aortic dissection is the morphological proximal
In the UK National Adult Cardiac Surgical Audit mirror to dSINE, without more clinical impact.132 It might
dataset, multivariable logistic regression analysis happen at the proximal end of a stent-graft and would be
showed that age, left-ventricular function, previous called in analogy proximal stent-graft induced new entry
cardiac surgery, preoperative resuscitation, concomitant (pSINE). pSINE might happen for several reasons: gothic
coronary bypass because of myocardial ischaemia, arch anatomy, stent-graft oversizing and ballooning,
centre, and high-volume surgeons were strong deter­ deploy­ment under high systolic pressure, and landing in
minants of outcome following type A thoracic aortic a still diseased or dissected aorta.
dissection repair.74,127,128 Perioperative stroke plays a major
role in worsening results. The Nordic Consortium for Control of risk factors after acute aortic dissection
type A thoracic aortic dissection database demonstrated a Control of cardiovascular risk factors is of utmost
30-day mortality of 27·1% in patients with stroke versus importance for patients who have recovered from acute
13·6% in patients without stroke, and 5-year mortality of aortic dissection. Although β blockers and calcium-
42·9% in patients with stroke versus 25·6% in patients channel blockers are indicated in the acute situation,
without stroke.129 control of blood pressure (with targeted systolic values
Results following treatment for type B thoracic aortic <120 mm Hg) with other anti-hypertensive drugs is
dissection have also considerably improved. Predictors of very efficient in reducing long-term mortality after
death are hypotension or shock, and branch vessel type A, respiratory type B thoracic aortic dissection.133
involvement. In a review of 1500 patients, in-hospital Lipid profile optimisation, smoking cessation, and
mortality was 13% within the IRAD, with most deaths all other atherosclerosis risk-reduction measures are
occurring during the first 7 days;103 in-hospital mortality also recommended, although evidence is still lacking.
of patients receiving thoracic endovascular aortic repair Without surveillance, acute aortic dissection is associated
was twice that of those managed medically. This finding with notable re-admission due to aortic-related and other
is not surprising since these were patients presenting cardiovascular complications, as well as lower quality of
with a complicated dissection. life scores.

Long-term management, control of risk factors, and Screening of relatives


screening In addition to long-term prophylactic measures,
Acute aortic dissection is not a single event, but a life­long screening of first-degree relatives is recommended to
disease. Treatment of the acute event alone might not be rule out family members with an existing pathology of
successful, and long-term surveillance is required to the aorta or aortic valve. Testing is guided by a thorough
detect complications and avoid emergencies in treated medical and family history, and physical and imaging
and untreated aortic segments. examinations. More specific genetic testing is advisable
Surveillance imaging for any acute aortic dissection is for patients and their families with a particular
thought to provide benefit regardless of temporal or risk phenotype, a syndromic presentation, and for those with
stratification or even treatment applied. The current 2010 a family history of dissection.134,135
American Heart Association/American College of
Cardiology guidelines for thoracic aortic disease call for Management of patients with type A thoracic aortic
CT angiography or MRI of the thoracic aorta at discharge, dissection
and at months 1, 3, 6, and 12 post dissection, with annual An increasing number of patients with type A thoracic
imaging thereafter, if stable.2,102 Unfortunately, contem­ aortic dissection receive antiplatelet treatment or
porary epidemiological studies have shown that oral anticoagulation (coumadin or novel oral
approximately 50% of patients are lost to follow-up by anticoagu­lation). This hampers perioperative
28 months post dissection; such non-compliance with the haemostatic management. Jiang and colleagues136
guidelines is concerning, because 38% of patients with studied the effects of antiplatelets on outcome following
medically treated type B thoracic aortic dissection were surgical repair of type A thoracic aortic dissection.
found to have become complicated and required Patients taking antiplatelets received significantly more
intervention during the follow-up period.130 packed red blood cells, plasma, and platelet transfusion.

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Antiplatelets were an independent predictor of mortality 24 h/day, improving electronic communications between
(26% vs 10%; odds ratio 6·8).136 emer­gency room physicians and centres of excellence,
Preoperative anticoagulation also increases peri­ assuming a consistent reporting according to inter­
operative bleeding risk.137 Sromicki and colleagues137 national standards, and promoting translational
showed that novel oral anticoagulation intake was research.145,146 The treatment for aortic dissection should
associated with greater need for blood products as be the same as for myocardial infarction, with a door-to-
compared with patients without anticoagulation and diagnosis and operative intervention time considered a
those with older forms of anticoagulants that could quality metric. Overall, improving quality of care and
quickly be reversed, and had worse survival (p=0·001), satisfaction of the patients and referring doctors should
whereas this was not observed in patients taking be the overriding motivation to develop an aortic centre.
coumadin (p=0·994). Operative mortality was 14% overall, Improvements in the organisation, resource allocation,
53% in the novel oral anticoagulation group, and 30% in utilisation, and efficiency of delivering care will finally
the coumadin group. Intraoperative filtration systems lead to increased activity.
might efficiently retrieve some of these medications Contributors
during cardiopulmonary bypass.138 In stable patients TC, YvK, and MC contributed to the conceptualisation of the review,
without pericardial effusion, a 12–24 h delay might and the formal analysis of the published literature. TMS and YvK
conducted the review, and TMS and MC provided supervision. TC wrote
reverse pre-existing anticoagulation. the original draft, and TMS made corrections to the original draft.
All authors contributed to the development of the methodology and
Future developments editing. TC provided the resources and YvK contributed to the validation.
More knowledge is needed to better understand the Declaration of interests
mechanisms in the aortic wall.139 Progressive loss of TC, TMS, and YvK declare no competing interests. MC is a consultant for
smooth muscle cells within the aortic wall has been Terumo Aortic, Medtronic, NEOS, and Endospan, received speaking
honoraria from Cryolife Jotec and Bentley, and is a shareholder and
demonstrated to be a crucial feature of acute aortic co-founder of TEVAR and Ascense Medical. TEVAR and Ascense Medical
dissection, because it contributes to aortic wall weakening are academy-based start-ups founded by qualified experts in the field of
with consecutive degeneration, aneurysm, and eventually cardiothoracic and vascular surgery, and are research-oriented spinoffs with
dissection.140 Cell death is controlled by various pathways an interest in animal experimentation to improve current technologies for
the treatment of cardiac and aortic diseases. At this stage, both entities are
and understanding the molecular mechanisms of smooth far away from being relevant companies or competitors since they neither
muscle loss is essential to develop preventive have commercial products nor pre-released products on the market.
pharmacological therapies.141 Among interventions to The main actual interest is directed at the level of conceptual designs to
maintain the integrity of the aortic wall, maintenance of improve the compliance of vascular substitutes or to facilitate device
delivery. To allow full scientific liberty in the experimental research, MC has
nitric oxide homoeostasis and control of potential disease no function on the board of these companies (strategical level), nor does he
mediators is an interesting option and could be further fulfil any position at the operational level. MC also serves in a leading role
investigated.142 in the committees for aortic guidelines of national and international
societies (ie, European Association of Cardio-thoracic Surgery, and German
Machine learning is rapidly evolving in the evaluation
Society for Thoracic and Cardiovascular Surgery) that both considered this
of aortic disease, with algorithms for segmental aortic founding membership role and shareholding as uncritical.
analysis, detection of pathology, monitoring the size of
Acknowledgments
the aorta, and risk stratification.143 These algorithms allow We thank Nadja Baltensweiler (Ebikon, Lucern, Switzerland) for the
in-depth assessment of flow dynamics and simulation drawing of figures 1 and 2 and Klaus Oberli (Bern, Switzerland) for the
with four-dimensional flow MRI. Other possibilities of drawing of figure 6.
artificial intelligence include screening from routine References
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