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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3734_Библиотеки_им_академика_М_И_Перельмана
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a
Presentation ofAcute Aortic Syndromes
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Fig. 1 Radiating pain in
(a) Stanford type A aortic
dissection (b) Stanford
type B aortic dissection
65
b
Neurologic symptoms are related either to branch vessel obstruction, which may
be expressed as stroke or reduced consciousness when the carotid artery is involved,
and as acute paraplegia when the blood supply to the spinal cord is obstructed. The
latter is more common in distal dissection, but is still rare. Even rarer neurologic
symptoms are caused by a mass effect of the enlarging aorta, and include Horner
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syndrome, from compression of the superior cervical sympathetic ganglion, and
hoarseness, from compression of the left recurrent laryngeal nerve.
S. Trimarchi et al.
Physical Exam
On physical examination, the patient may give a restless, agitated or apprehensive
impression, and appear shocked, cold, clammy, with the sensation of imminent
death. Tachycardia is almost always noted [2]. The rest of the ndings on physical
examination depend on the location and extent of the dissection. While a history of
hypertension is present in about 80% of patients, only 35.7% of type A dissection
patients present with hypertension, while 24.6% are hypotensive, which can be
caused by aortic valve insufciency, cardiac tamponade, or less commonly, coronary occlusion as a result of the dissection [1]. Moreover, if the dissection leads to
malperfusion of the brachiocephalic vessels, brachial cuff pressures may be falsely
depressed. Hypotension is rarely present in type B dissection, and is usually a sign
of aortic rupture with hemothorax or hemoperitoneum.
On auscultation, a new onset diastolic decrescendo murmur points to the pres-
ence of aortic valve insufciency. This is noted in 31.6% of dissections, most of
which are ascending dissections [1]. Prolapse of the cusp due to a single commissure being dissected affects leaet coaptation, which in some cases returns when the
dissection spreads further proximally into the annulus. Aortic insufciency can also
be due to a tear in the aortic root with prolapse of the entire valve. The murmur of
dissection-related aortic valve insufciency is most commonly heard along the right
sternal border (in contrast to pre-existent aortic valve insufciency, which is most
commonly heard along the left sternal border). Auscultation might also reveal a
pericardial rub or distant heart sounds, indicative of cardiac tamponade. Findings of
pleural effusion, especially on auscultation of the left hemithorax, point to distal
aortic rupture.
Obstruction of branch vessels by the dissection ap can lead to weak or absent
peripheral pulses, which is noted in 15.1% of patients [1]. These pulse decits of the
carotid, brachial or femoral arteries are associated with upper or lower extremity
and brain malperfusion, and are associated with an increased risk of mortality [6].
Leg ischemia is a marker of extensive dissection and may be accompanied by compromise of other vascular territories. On the other hand, it is well known that pulse
decits change in nature as the dissection expands distally and produces re-entries.
Spontaneous return of pulses is noted in up to a third of patients with lower extremity malperfusion [7]. Moreover, pulse decits are a quite specic nding and can
thus lead to a swifter diagnosis of dissection. This could explain why pulse decits
do not always lead to higher mortality.
The electrocardiogram is generally normal or shows nonspecic changes, which
is an important way to differentiate the cause of chest pain from myocardial ischemia. However, in proximal dissections extending into the coronary ostia, S-T
Presentation ofAcute Aortic Syndromes
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67
segment and T-wave changes may be observed. Heart block can result from extension of the hematoma into the aortic root, interatrial septum, and atrioventricular node.
Laboratory tests are usually normal, or have non-specic changes. Mild anemia
and mild leukocytosis are not uncommon. In cases of hemothorax, important anemia can be detected. Bilirubin and lactic acid dehydrogenase levels may be increased
due to hemolization of blood trapped within the false lumen. In cases of malperfusion syndrome, metabolic acidosis may be present, and renal malperfusion can lead
to oliguria/anuria and microscopic hematuria. D-dimer is generally highly increased
in acute dissection, so dissection can be reliably ruled out with D-dimer levels
below a cut-off of 500ng/ml [8].
Differences inPresentation ofIntramural Hematoma
andPenetrating Aortic Ulcer
There are few, if any, differences in presentation between intramural hematoma and
aortic dissection [9], although patients with any kind of intramural hematoma
appear less likely to present with pulse decits [10, 11]. Other differences with aortic dissection are that those with type A intramural hematoma are less likely to present with aortic regurgitation, and those with type B intramural hematoma are more
likely to present with chest pain [10, 11]. Penetrating aortic ulcer (PAU) is still
included in the acute aortic syndromes, although the typical PAU patient is elderly
with hypertension, and generally does not present with symptoms, being diagnosed
occasionally after CT scan. In these patients, pain can be present in those with
impending PAU rupture, sudden diameter increase, or frank rupture. Due to the
focal nature of the lesion, the thoracic pain, which is characteristic of all acute aortic
syndromes, is usually not accompanied by signs of aortic valve insufciency, pulse
decits, or neurologic decits [12].
References
1. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, etal.
The international registry of acute aortic dissection (IRAD): new insights into an old disease.
JAMA. 2000;283(7):897–903.
2. Svensson LG, Crawford ES.Aortic dissection and aortic aneurysm surgery: clinical obser-
vations, experimental investigations, and statistical analyses. Part II. Curr Probl Surg.
1992;29(12):913–1057.
3. Evangelista A, Isselbacher EM, Bossone E, Gleason TG, Eusanio MD, Sechtem U, etal.
Insights from the international registry of acute aortic dissection: a 20-year experience of collaborative clinical research. Circulation. 2018;137(17):1846–60.
4. Imamura H, Sekiguchi Y, Iwashita T, Dohgomori H, Mochizuki K, Aizawa K, etal. Painless acute
aortic dissection. Diagnostic, prognostic and clinical implications. Circ J. 2011;75(1):59–66.
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5. Nallamothu BK, Mehta RH, Saint S, Llovet A, Bossone E, Cooper JV, et al. Syncope
in acute aortic dissection: diagnostic, prognostic, and clinical implications. Am J Med.
2002;113(6):468–71.
6. Bossone E, Rampoldi V, Nienaber CA, Trimarchi S, Ballotta A, Cooper JV, etal. Usefulness
of pulse decit to predict in-hospital complications and mortality in patients with acute type A
aortic dissection. Am J Cardiol. 2002;89(7):851–5.
7. Cambria RP, Brewster DC, Gertler J, Moncure AC, Gusberg R, Tilson MD, etal. Vascular
complications associated with spontaneous aortic dissection. J Vasc Surg. 1988;7(2):199–209.
8. Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, etal. Diagnosis of
acute aortic dissection by D-dimer: the international registry of acute aortic dissection substudy on biomarkers (IRAD-bio) experience. Circulation. 2009;119(20):2702–7.
9. Falconi M, Oberti P, Krauss J, Domenech A, Cesareo V, Bracco D, etal. Different clinical fea-
tures of aortic intramural hematoma versus dissection involving the descending thoracic aorta.
Echocardiography. 2005;22(8):629–35.
10. Harris KM, Braverman AC, Eagle KA, Woznicki EM, Pyeritz RE, Myrmel T, etal. Acute aor-
tic intramural hematoma: an analysis from the international registry of acute aortic dissection.
Circulation. 2012;126(11 Suppl 1):S91–6.
11. Tolenaar JL, Harris KM, Upchurch GR Jr, Evangelista A, Moll FL, di Eusanio M, etal. The
differences and similarities between intramural hematoma of the descending aorta and acute
type B dissection. J Vasc Surg. 2013;58(6):1498–504.
12. Coady MA, Rizzo JA, Hammond GL, Pierce JG, Kopf GS, Elefteriades JA.Penetrating ulcer
of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg.
1998;27(6):1006–15. discussion 15-6
S. Trimarchi et al.
Classication Systems ofAcute Aortic
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Syndromes
ArminderS.Jassar, RizwanQ.Attia, andEricM.Isselbacher
Introduction
Acute aortic syndromes (AAS) characterize closely related life-threatening clinical
conditions that include aortic dissection, intramural hematoma, and penetrating aortic ulcer. The suggested etiology of these conditions is pathologically different [1].
Although numerous classication systems have been proposed, rather than exhaustively list them all, the objective of this chapter is to highlight the most commonly
used and most recently described classications that would be of greatest utility for
those caring for patients with AAS.
Anatomic Classication Systems
Stanford andDeBakey Classications
The most commonly used classication system for AAS are the DeBakey and the
Stanford systems [2, 3] (Fig.1). For these, the ascending aorta refers to the part of
the aorta proximal to the brachiocephalic artery, the aortic arch extends from the
brachiocephalic artery to the distal ostium of the left subclavian artery, and the
descending aorta from left subclavian artery to the iliac bifurcation. Stanford type A
dissection involves the ascending aorta and type B the descending aorta distal to the
left subclavian artery (without involvement of the ascending aorta). DeBakey type I
dissection involves the ascending aorta, the aortic arch and the descending aorta;
DeBakey type II is limited to the ascending aorta only. DeBakey type III involves
A. S. Jassar · R. Q. Attia · E. M. Isselbacher (*)
Thoracic Aortic Center, Massachusetts General Hospital, Boston, MA, USA
e-mail: eisselbacher@mgh.harvard.edu
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_6
69© Springer Nature Switzerland AG 2021
70
De Bakey
Stanf
Type I
Type II
Type III
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A. S. Jassar et al.
ord
Fig. 1 Traditional classication of aortic dissection. Schematic drawing of aortic dissection subdivided into DeBakey types I, II, III and Stanford A and B.DeBakey type III may be further differentiated into subtypes IIIa (limited to the thoracic aorta) and IIIb (extending into the abdominal
aorta). (Figure courtesy of 2014 ESC guidelines on the diagnosis and treatment of aortic diseases [
4])
Type A
Type A
Type B
the descending aorta, distal to the subclavian artery. DeBakey type III is further
divided into IIIa (limited to the thoracic aorta) and IIIb (extending into the abdominal aorta).
These two classication systems have stood the test of time and are the most
widely used classication methodologies. The simplicity of the Stanford classication system has made it the most commonly used system by the non-surgical specialties, including those frequently making the initial diagnosis, i.e., radiologists
and emergency medicine physicians. It has the advantage of stratifying treatment
strategy based on the type A or B designation, with type A dissection patients treated
with emergency aortic replacement, while patients with type B dissection are generally managed medically with aggressive blood pressure control unless there is endorgan malperfusion, risk of aortic rupture, uncontrolled hypertension, or uncontrolled
symptoms, in which case intervention can be considered.
Data from the International Registry of Acute Aortic Dissection (IRAD) suggest
that the patients with type A dissection who were treated with surgery have a mortality of 15–23%, whereas those treated medically have a mortality of 56–58% [4,
5]. In most instances, the patients treated medically are those who are thought to
carry a high risk of death prior to the operation and hence not offered surgery.
Longer term survival in surgically managed patients is 97% to 90% at 1 and 3years,
Classication Systems ofAcute Aortic Syndromes
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respectively. The medically managed type A patients who survive the initial hospitalization have survival rates of 88% and 68% at 1 and 3years [5, 6]. Mortality for
type B aortic dissection is 7–10% for patients managed medically, 7–32% for
patients treated with open surgery, and 1.5–8% for patients treated with endovascular techniques [7, 8]. Longer term survival at 1–3years is approximately 77% in the
medical, 85% in the surgical, and 77–98% in the endovascular cohorts [4, 7, 9].
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Dissections oftheAortic Arch: “Non-A, Non-B”
One important limitation of the Stanford and DeBakey classication systems is the
lack of a clear and consistent designation for aortic dissections that involve the aortic arch and the descending aorta but spare the ascending aorta. This has prompted
some authors to coin the term “non-A non-B” dissection [10]. This entity can be
further differentiated into the descending-entry type or the arch-entry type, based on
the location of the intimal tear [11]. There is still debate regarding the optimal management of the non-A non-B dissections. In a series of 101 patients in the IRAD
registry who had retrograde extension of a descending aortic dissection into the
aortic arch, early mortality rate was 9%, 18%, and 13%, for patients treated medically, with open surgical repair, or with endovascular therapies, respectively
(P=0.51) [12, 13]. A favorable early mortality rate was observed in patients with
retrograde extension limited to the arch at 9% vs. into the ascending aorta at 19%,
P=0.14.
In their series of 43 patients with non-A non-B dissection patients, Rylski etal.
found that emergency open or endovascular aortic repair was necessary due to malperfusion or aortic rupture in 29% of the 21 patients with an entry site in the
descending aorta and 36% of the 22 patients with an entry in the aortic arch, with an
in-hospital mortality of 1/6 and 3/8, respectively, of those undergoing aortic repair
[11]. Moreover, at 2 weeks following the dissection, aortic repair was required (due
to new organ malperfusion, rapid aortic growth, aortic rupture, or persistent pain) in
43% of descending-entry and 36% of arch-entry patients. Indeed, by the end of the
4.4 mean years of follow-up, 88% of patients had undergone aortic intervention.
SVS/STS Classication
Recently, the Society for Vascular Surgery (SVS) and the Society of Thoracic
Surgeons (STS) published reporting standards for acute type B dissection and proposed a new anatomic classication system for thoracic aortic dissection. This novel
SVS/STS classication is based on the proximal and distal extent of the dissection
ap at various zones in the aorta (Fig.2). This is akin to the well accepted classication of the aortic arch into zones as proposed by Ishimaru [15]. According to this
schema, the distinction between type A and type B is determined by the location of
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A. S. Jassar et al.
Type
2
1
0
11
3
A
D
4
5
6
7
8
9
10
10
11
Entry tear:
Zone 0
B
PD
Entry tear:
Zone 1≥
I
D
Unidentified
entry tear
involving
Zone 0
Proximal
Extent
0
1
2
3
4
5
6
7
8
9
10
11
12
Distal
Extent
0
1
2
3
4
5
6
7
8
9
10
11
12
Fig. 2 Society for Vascular Surgery/Society of Thoracic Surgeons Aortic Dissection Classication
System. (Courtesy SVS/ STS standards reporting committee [14])
the primary entry tear. Any dissection with an entry tear in zone 0 is classied as
type A.In addition, a subscript is added to denote the most distal zone to which the
dissection extends (A
ing aorta that extends to the infrarenal aorta would be termed A9. Conversely, any
dissection with an entry tear in Zone I or beyond is dened as a type B dissection,
and the proximal and distal extents are denoted by a respective pair of subscripts (B
). For example, a dissection with its intimal tear just distal to the left subclavian
D
artery and extending to the infrarenal aorta would be designated B
ering the proximal and distal extent of a given dissection, any aortic segment that
has true and false lumens, a thrombosed false lumen, or intramural hematoma
(IMH) are to be included. This classication system designates dissections as indeterminate (rather than type A or B) when the location of the entry tear cannot be
determined on diagnostic imaging; and, as with type B dissection, the letter I is followed by a pair of subscripts denoting the proximal and distal extent of the dissection (I
). The SVS and STS also recommend that patients with IMH and penetrating
P, D
atherosclerotic ulcers (PAU) also have the extent of their aortic pathology described
in a similar manner, namely IMH
suggests that after a type A dissection repair, any residual distal dissection should be
designated as such and include similar subscripts, e.g., residual B
). For example, a dissection with an entry tear in the ascend-
D
. When consid-
3, 9
or PAU
P, D
. Finally, the classication scheme
P, D
(Fig.2).
P, D
P,
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While the SVS/STS classication system enables clinicians to accurately dene
the extent of a dissection, the authors acknowledge that this system is not indented
to replace the Stanford or DeBakey classications, which are both simpler and
familiar to the broad medical and surgical community. Indeed, so ingrained is the
clinical distinction between the Stanford type A and B dissections, if a patient presents to an emergency with a dissection that involves the ascending aorta but whose
entry site is in zone 3, a radiology report that were to classify it as a type B rather
than type A dissection could lead to confusion, at the least, and potential mismanagement, at the worst.
Another limitation of the SVS/STS classication system is that although it takes
onto account the location of the entry tear in distinguishing type A from type B dissections, it oddly ignores the location of the entry tear in subtyping type B dissections. Indeed, the location of the entry tear is a key determinant of the feasibility of
endovascular repair of type B dissections. These limitations suggest that there is
ample opportunity to further rene this classication system before it is promoted
for routine clinical use.
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Chronicity-Based Classication ofAortic Dissection
Historically, acute dissection has been considered to be “acute” when a patient presents 14days or fewer from symptom onset and “chronic” when presenting more than
14 days from symptom onset. This distinction has been derived from the seminal
work of Hirst etal. in the 1950s [16], who observed that mortality in untreated patients
with both type A and B dissection signicantly declined after 14days. The estimates
of mortality were 21% at 24h, 49% in the rst 4days, and 74% at 14days from
symptom onset [16]. After 14days, although mortality continued to rise, the curve
attened signicantly during the 2–6-week time frame. Nevertheless, by 3years the
mortality had risen to 95%, indicating that aortic dissection remained lethal well after
entering the “chronic” phase. Since this temporal classication system predated the
current advances in diagnostic imaging and medical, endovascular, and surgical treatment of aortic dissection, several modications have been proposed more recently.
IRAD Classication: Hyperacute, Acute, Subacute andChronic
In a study of over 1800 patients in the IRAD database, Booher etal. [17] examined
time-related survival in patients presenting with acute aortic dissection. The survival estimates were stratied by dissection type (Stanford A vs. B) and treatment
strategy (medical vs. surgical vs. endovascular). The authors noted that survival
continues to decrease signicantly for up to 30days after presentation for both type
A and B dissection and across treatment strategies. Based on the inection points
noted in survival (Fig.3a–c), the time from symptom onset was divided into four
74
Kaplan-Meier Survival Curves
Cumulative SurvivalCumulative SurvivalCumulative Survival
Time from Symptom Onset (days)
a
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Fig. 3 Kaplan-Meier
survival curves for type A
and type B dissection.
(Booher etal. [
17], used
with permission)
1.00
0.90
0.80
A. S. Jassar et al.
Type B
b
0.70
0.60
1.00
(hyperacute)
0
0-24 hours
2-7 days
(acute)
14 8121620
8-30 days
(subacute)
Time from Symptom Onset (days)
Kaplan-Meier Survival Curves
Dissection Type: A
greate than 30 days
(chronic)
24 28 32 36 40 44 48 52 56 60
Log Rank Chi-Sq p<0.001
between management types
Type A
0.80
Surgical Management
0.60
0.40
Medical Management
0.20
0-24 hours
0
(hyperacute)
014812 16 20
c
1.00
8-21 days
2-7 days
(acute)
(subacute)
Time from Symptom Onset (days)
24 28 32 36 40 44 48 52 56 60
Kaplan-Meier Survival Curves
Dissection Type: B
greate than 21 days
(chronic)
Log Rank Chi-Sq p<0.001
between management types
0.95
0.90
0.85
Endovascular Management
Medical Management
0.80
0.75
0.70
0-24 hours
(hyperacute)
014812 16 20
2-7 days
(acute)
8-21 days
(subacute)
24 28 32 36 40 44 48 52 56 60
Surgical Management
greate than 21 days
(chronic)
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