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limited damage to the aortic media, medical management with serial hemodynamic
monitoring, imaging, and follow-up is appropriate.
H. Chaudry et al.
Percutaneous Coronary Stenting or Endovascular Repair
When the dissection originates from an entry point within a coronary artery and
there is compromise to the ow or extension into the aortic arch, most reports favor
management with percutaneous coronary stenting to seal the entry point which is
usually located at the coronary ostium (Fig.1b). One review of 67 cases of iatrogenic
aortic dissections, found that 28 (42%) rapidly progressed to the ascending aorta if
a stent-based sealing technique was not performed promptly [15]. The authors
propose that in all cases where there is dissection into the coronary sinus, the ostium
should be sealed immediately to prevent further propagation of the dissection.
Moreover, if the ostial stenting failed to halt the dissection progression, it did not
compromise the chances of surgical success [15].
Based on historical experience of 9 patients with aortocoronary dissections by
Dunning et al., class I and II iatrogenic aortic dissections were all successfully
managed with coronary stenting of the entry point whereas more extensive (class
III) iatrogenic aortic dissections or patients with hemodynamic instability or
ischemia of one of the aortic branches were referred to surgery with poor outcomes
[2]. More recently, a retrospective analysis of 74 patients from the Registry on
Aortic Iatrogenic Dissection (RAID) found that after a median follow-up of
51.2months, only 2 deaths were recorded in patients treated conservatively. There
were 15 (20%) patients with Dunning class III dissections and only 3 patients were
referred for cardiac surgery (2 for aortic surgery and 1 for coronary artery bypass
grafting). The remaining 71 cases were treated successfully with either conservative
management or PCI [3]. These results suggest that even Dunning class III iatrogenic
aortic dissections may be managed with coronary stenting to immediately seal the
entry site with favorable outcomes.
Several different stent types have been used to manage iatrogenic aortic dissections. These include bare-metal stents, drug-eluting stents, covered stents, and a
covered stent/drug-eluting stent combination [15–19]. A bare-metal stent may be
appropriate in cases with extensive aortic dissections that may require early surgical
intervention. However, current generation drug eluting stents with biocompatible
polymers can also be considered based on studies showing early thromboresistance
and higher rates of long-term patency compared to bare metal stents. While covered
stents will completely seal the entry point of dissection, their use is not generally
required, and drug-eluting stents are likely to be sufcient in most cases. Some
authors recommend intravascular ultrasound (IVUS) guided coronary stenting to
ensure complete coverage of the dissection and exact placement of the stent to
entirely cover the coronary ostium [17]. Optical coherence tomography (OCT) is
usually avoided due to the need for contrast injection into the coronary and fear of
extension of dissection.
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233
Surgical Repair
Urgent surgical intervention has been necessary in only small minority of previously reported cases of catheter-induced iatrogenic aortic dissections. This is in
contrast to spontaneous aortic dissections of the ascending aorta that often require
urgent surgical attention due to degeneration of the media that facilitates extensive
propagation. High-risk features that should prompt consideration of surgical referral include dissections with signicant extension into the aortic arch (Dunning class
III), those that involve the aortic branches, or failure of entry sealing with a stent. In
addition, patients with signicant valvular dysfunction and those in which the coronary artery involved is unsalvageable with stenting or in which coronary artery
bypass grafting is indicated should also be considered for surgical management.
The goal of surgery is to perform resection of the aortic intimal tear and as much of
the dissected aorta as possible, without resulting in excessive operative risk [20].
Surgical resection of the ascending aorta with or without the aortic arch (when
involved) is considered the gold standard for patients with spontaneous type A dissection, and this approach has been extended to patients presenting with iatrogenic
aortic dissections [20]. Of note, in comparison to spontaneous aortic dissections, the
surgical repair of catheter-induced dissection may be riskier, especially in the setting of coronary ischemia and following PCI with full anticoagulation and antiplatelet therapy.
Surveillance
In most cases of catheter-induced iatrogenic aortic dissections where surgical repair
is not required, serial imaging with either CT or MRI is needed to monitor the progression of the dissection. The optimal interval between scans has not yet been
established. In one series that evaluated the use of multidetector CT (MDCT) in
follow-up of catheter-induced aortic dissections, the most common follow-up pattern was MDCT immediately after the occurrence of aortocoronary dissection, followed by repeat imaging at 48hours and 1week [14]. The authors proposed repeat
follow-up CT after 1–2months in patients with more extensive class III dissections.
In case reports of aortocoronary dissection evaluated with CT, time to resolution of
the aortic dissection ranged from 48hours to 3months [14].
Prognosis
Historically, iatrogenic aortic dissections have been noted to have a generally poor
prognosis similar to that of spontaneous aortic dissections (35% vs 24%,
respectively), with type A aortic dissections carrying about a 35% mortality despite
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H. Chaudry et al.
regardless of underlying mechanism. It was also noted that the mortality rate was
higher (37%) for iatrogenic type B aortic dissections when compared to spontaneous
aortic dissection (10%), with the majority of type B dissections (87%) occurring as
a consequence of cardiac catheterization procedures [1]. In contrast, Dunning etal.
found that patients with limited (Dunning class I and II) dissection had good
prognosis with more extensive dissections (Dunning class III) portending a worse
outcome.
Based on data from more recent case reports the short- and long-term prognosis
of catheter-induced aortic dissections may be more favorable than previously
reported [3, 4, 11, 15]. This is likely due to the success of aortocoronary stenting
techniques to quickly seal and halt rapid propagation of a dissection. In 5-year
follow-up data from the RAID analysis of 74 patients with iatrogenic aortic
dissections, there were no long-term complications such as dissection progression,
myocardial ischemia, or dissection recurrence in the 72 (97%) patients that survived
the acute injury. The authors noted only 2 deaths with a 2.7% mortality in this case
series [3]. Similarly, one other series of 18 cases showed a 0% mortality at 1-month
follow-up, including cases of extensive dissections requiring urgent surgical
intervention [4]. This is in contrast to spontaneous aortic dissections, especially of
the ascending aorta (type A) where acute mortality has been reported close to 25%.
The authors point out that an acute retrograde type A aortic dissection presents a
more favorable prognosis than spontaneous type A dissections that tend to be
antegrade in nature with a higher likelihood of propagation.
Conclusion
Iatrogenic aortic dissection is a rare complication of catheter-based procedures,
with relatively better outcomes compared with spontaneous aortic dissections. The
low event rate had limited our knowledge in regard to the best approach in managing
different types of catheter-induced aortic dissections. However, the majority of
cases can be adequately managed through conservative or percutaneous approaches,
with surgical intervention deemed necessary in a small proportion of these
cases.DisclosuresJ Dawn Abbott has received research funding with no personal
compensation from AstraZeneca, Bristol Myers Squibb, Abbott, Sinomed, CSL
Behring, Biosensors Research USA.
Funding
None.
References
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2. Dunning DW, etal. Iatrogenic coronary artery dissections extending into and involving the
aortic root. Catheter Cardiovasc Interv. 2000;51(4):387–93.
Catheter-Induced Aortic Dissection
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3. Nunez-Gil IJ, etal. Incidence, management, and immediate- and long-term outcomes after iat-
rogenic aortic dissection during diagnostic or interventional coronary procedures. Circulation.
2015;131(24):2114–9.
4. Gómez-Moreno S.Iatrogenic dissection of the ascending aorta following heart catheterisation:
incidence, management and outcome. EuroIntervention. 2006;2(2):197. –EOA
5. Vega MR.Aortic dissection—exceedingly rare complication of coronary angioplasty. Catheter
Cardiovasc Diagn. 1997;42(4):416.
6. Perez-Castellano N, et al. Dissection of the aortic sinus of Valsalva complicating coronary
catheterization: cause, mechanism, evolution, and management. Catheter Cardiovasc Diagn.
1998;43(3):273–9.
7. Carter AJ, Brinker JA. Dissection of the ascending aorta associated with coronary angiogra-
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8. El Sabbagh A, etal. Angiographic success and procedural complications in patients undergo-
ing retrograde percutaneous coronary chronic total occlusion interventions: a weighted metaanalysis of 3482 patients from 26 studies. Int J Cardiol. 2014;174(2):243–8.
9. Carlson RG, Lillehei CW, Edwards JE.Cystic medial necrosis of the ascending aorta in rela-
tion to age and hypertension. Am J Cardiol. 1970;25(4):411–5.
10. El-Haress M, etal. Iatrogenic acute ascending aortic dissection with intramural hematoma
during coronary artery stenting: a case report. Front Surg. 2017;4:2.
11. Nunez-Gil IJ, etal. Type a iatrogenic aortic dissection following catheterization without coro-
nary involvement: long-term prognosis. Rev Esp Cardiol (Engl Ed). 2015;68(3):254–5.
12. Alfonso F, etal. Aortic dissection occurring during coronary angioplasty: angiographic and
transesophageal echocardiographic ndings. Catheter Cardiovasc Diagn. 1997;42(4):412–5.
13. Hartnell GG. Imaging of aortic aneurysms and dissection: CT and MRI.J Thorac Imaging.
2001;16(1):35–46.
14. Tanasie C, etal. Catheter-induced aortic dissection after invasive coronary angiography: evalu-
ation with MDCT.AJR Am J Roentgenol. 2011;197(6):1335–40.
15. Carstensen S, Ward MR.Iatrogenic aortocoronary dissection: the case for immediate aortoos-
tial stenting. Heart Lung Circ. 2008;17(4):325–9.
16. Lindsay A, etal. Complications of percutaneous coronary intervention the survival handbook.
London: Springer; 2016. p. XIII, 310 p.109 illus., 52 illus. in color
17. Abdou SM, Wu CJ.Treatment of aortocoronary dissection complicating anomalous origin
right coronary artery and chronic total intervention with intravascular ultrasound guided stenting. Catheter Cardiovasc Interv. 2011;78(6):914–9.
18. Danzi GB, etal. Retrograde dissection during percutaneous coronary intervention: sealing of
the entry site by covered stent implantation. BMJ Case Rep. 2012;2012
19. Gorog DA, Watkinson A, Lipkin DP.Treatment of iatrogenic aortic dissection by percutaneous
stent placement. J Invasive Cardiol. 2003;15(2):84–5.
20. Leontyev S, etal. Iatrogenic type a aortic dissection during cardiac procedures: early and late
outcome in 48 patients. Eur J Cardiothorac Surg. 2012;41(3):641–6.
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Aortic Intramural Hematoma
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NeelR.Sodha andFrankW.Sellke
Introduction
Acute aortic syndromes (AAS) represent a spectrum of aortic pathologies including
aortic dissection, penetrating atherosclerotic ulcer (PAU), and intramural hematoma
(IMH). Originally described by Krukenberg in 1920, an aortic intramural hematoma
has been dened as “dissection without intimal tear that results from hemorrhage
within the aortic wall” [1]. The etiology of, or even the very existence of an aortic
intramural hematoma as a distinct pathologic entity from classic aortic dissection,
remains controversial. Some physicians believe an acute intramural hematoma
results from spontaneous rupture of vasa vasorum within the aortic wall, resulting
in bleeding within the tunica media, whereas others believe the imaging and surgical ndings associated with an intramural hematoma are the result of a small undetectable intimal tear with subsequent thrombosis, and thus feel an IMH should be
referred to as a thrombosed-type aortic dissection [2]. Proponents for the former
(IMH as a distinct entity), argue that an intimal defect is often not identied at the
time of surgery, and the variability in terms or risk factors and clinical behavior differ signicantly from classic aortic dissection, thus supporting IMH as distinct from
dissection. Proponents of the latter (IMH as a variant of classic aortic dissection),
argue that enhanced imaging and distal inspection of the aorta at the time of surgery
may often identify intimal defects which may be missed on initial evaluation [2, 3].
Given the debate as to the existence of IMH as a distinct acute aortic syndrome, it is
understandable that management remains controversial as well.
N. R. Sodha (*)
Division of Cardiothoracic Surgery, Alpert Medical School, Brown University,
Providence, Rhode Island, USA
e-mail: nsodha@lifespan.org
F. W. Sellke
Cardiothoracic Surgery, Alpert Medical School, Brown University,
Providence, Rhode Island, USA
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_16
237© Springer Nature Switzerland AG 2021
238
Normal IMH
IMH
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N. R. Sodha and F. W. Sellke
Classication of acute aortic intramural hematoma is identical that used for aortic dissection. Most commonly, the Stanford classication system as described by
Daily and colleagues is used in the clinical setting, with Stanford Type A and B
dened as “type A involvement of the ascending aorta, and type B are dened as
those limited to the descending aorta with primary intimal tear usually within 2 to
5cm of the left subclavian artery” [4]. Recent updates from the Society of Thoracic
Surgeons and Society for Vascular Surgery provide for more granular reporting of
acute aortic syndromes with Type A lesions described as the primary tear originating in the ascending aorta, Type B lesions with the primary tear originating in the
aortic arch or descending aorta, with additional subscripts to describe the extent of
pathology depending on zone [5]. Updated classication schemes such as non-A/
non-B or Type C are not in widespread clinical use [6, 7] (Fig.1).
Presentation
Data from the International Registry of Acute Aortic Dissection (IRAD) suggest
both Type A and Type B acute intramural hematomas are far less common than
ab c
TL
Penetrating
de f
Aortic Ulcer
Ath
TL TL TL FL
Ath
Fig. 1 Schematic representation of acute aortic syndromes. (a) Normal, (b) Intramural hematoma—Crescenteric, (c) Intramural hematoma—Circumferential, (d) Penetrating aortic ulcer, (e)
Aortic dissection, (f) Aortic dissection. TL True Lumen, Ath Atheroma, IT Intimal tear, FL False
lumen. Adapted from Maslow A, Atalay, M, Sodha N. Intramural Hematoma. J Thorac and
Cardiovasc Anesth. 2018;32:1341–1362
Crescentic
TL TL
Aortic
Dissection
IT
FL
Circumferential
Aortic
Dissection
Aortic Intramural Hematoma
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239
classic aortic dissection, with IMH accounting for less than 10% of acute aortic
syndromes [8]. Patients with an acute IMH tend to be about 8years older than those
with acute dissection, averaging near 70years of age at presentation, and while
more common in men than in women, IMH patients trended to a more even distribution between males and females relative to aortic dissection [8]. Arterial hypertension has been more commonly identied as a risk factor for IMH relative to
dissection and in contrast with aortic dissection, where Type A is more common
than Type B by an approximately 3:1 ratio, Type B IMH is more common than Type
A IMH (42% Type A, 58% Type B). Chest pain is the most common presenting
symptom for both Type A and B IMH, and is present in approximately 80% of
patients, whereas back pain is less common in patients with Type A IMH, but presents with equal frequency to chest pain in patients with Type B IMH.Pain is generally abrupt in onset and severe, but is less commonly described as radiating.
Neurologic manifestations, pulse decits and aortic valve regurgitation are less
commonly present relative to aortic dissection [8]. Laboratory analysis is of little
value in establishing a diagnosis of intramural hematoma, but may aid in excluding
other etiologies of chest pain [9]. Interestingly, aortic intramural hematomas are
more likely to present with effusion or pericardial tamponade relative to aortic dissection, possibly related to the location of an IMH relative to the adventitial wall.
This nding is thought to be a marker for potential rupture [10]. The above ndings
highlight the difculty of diagnosing an intramural hematoma on history or examination alone, as symptoms may be non-specic and mimic other cardiovascular
pathology. Rather than elucidate a diagnosis, the presentation ndings discussed
above and complaints of acute onset chest pain or back pain should raise the suspicion for an acute aortic syndrome and guide the appropriate initial management and
diagnostic evaluation (Table1).
When considering an acute intramural hematoma as a diagnosis based on presentation or imaging, it is essential consider aortitis in the differential diagnosis, as this
rare entity may mimic an acute IMH on imaging. On history, aortitis may present
with a more chronic or subacute onset of pain relative to an acute IMH.Constitutional
symptoms such as fevers, arthralgias and myalgias may be present. A leukocytosis
or elevation of inammatory markers such as erythrocyte sedimentation rate (ESR)
of C-reactive protein (CRP) may be present, but are non-specic. CT imaging may
be non-specic and unable to differentiate between the two entities, in which case
magnetic resonance imaging on weighted T2 sequences or FDG-PET scanning may
provide the diagnosis. As surgical intervention for acute aortitis may result in poor
outcomes, consideration of this diagnosis in all patients with possible intramural
hematoma is essential [11, 12] (Table2).
The diagnostic imaging for evaluation of acute aortic syndromes, including acute
intramural hematoma is discussed in detail elsewhere in the textbook (see Chapter
on Imaging for Acute Aortic Dissection, Intramural Hematoma, and Penetrating
Atherosclerotic Ulcer). Briey, plain lm radiographs/chest x-rays are generally
non-diagnostic [8]. Optimal imaging in the stable patient should include computed
tomography. Specically, a non-contrast CT of the chest, abdomen and pelvis
should be obtained followed by a contrast-enhanced CT angiogram of the chest,
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Comparison between acute aortic syndromes
Table 1
Layer
Lesion
affected Demographics Presentation Location Appearance Complication
IMH Medial
layer
AD 58–63 y AAS Ascending >
Intimal
tear
Intimal
ap
Medial
false
lumen
AA Intima Asymptomatic Ascending >
Media 50–60 y Compression
Adventitia Males Fistula related No dual lumen Fistula
PAU Intimal
layer
ULP Intimal
layer
65–70 y AAS Descending
HTN Circumferential
Males Varying length Dissection
Iatrogenic No intimal ap Aneurysm
Trauma No false lumen
HTN
CTD Intimal ap Peripheral
Coarctation Dual lumen:
Bicuspid AoV Low-ow false
Pregnancy False > True
Trauma
• Iatrogenic
of proximal
structures
70 y AAS Descending
Males Crater-like
HTN No intimal ap Embolization
Tobacco No dual lumen Dissection
CAD No false lumen Rupture
COPD
Asymptomatic Distal Arch
65 y Outpouchings
Males Intima into
> Ascending
> Arch
Descending
Descending
>>> Arch
>>> Arch
>>
Ascending
Proximal
descending
>>>
Ascending
and Distal
Descending
Crescentic
thick
thick
True/false
lumen
lumen
Dilation Rupture
No intimal ap Embolization
No false lumen
Irregular
surface
protrusion
Single
Contrast-lled
across
medial layer
No connections
with
Aortic branches
Rupture
ischemia
Embolization
Aneurysm
Rupture
IMH
Aneurysm
Aneurysm
Regression
(continued)
Aortic Intramural Hematoma
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Table 1 (continued)
Layer
Lesion
affected Demographics Presentation Location Appearance Complication
IBP Medial
layer
Abbreviations: AA aortic aneurysm, AAS acute aortic syndrome, AD aortic dissection, AoV aortic
valve, CAD coronary artery disease, COPD, chronic obstructive pulmonary disease, CTD connective tissue disorder, HTN hypertension, IBP intramural blood pool, IMH intramural hematoma,
PAU penetrating atherosclerotic (aortic) ulcer, ULP ulcer-like projection
Adapted from Maslow A, Atalay, M, Sodha N.Intramural Hematoma. J Thorac and Cardiovasc
Anesth. 2018;32:1341–1362 2018
60–62 y Asymptomatic Descending
Males No
>>> Arch
>>
Ascending
Multiple pools
medial layer
communication
Near branch
vessels
Disappear
241
abdomen, and pelvis. Non-contrast imaging is essential in establishing a diagnosis
of an intramural hematoma as a hyperdense area of cresenteric thickening will be
visible on these studies. Particular attention should be paid to the location of the
IMH, aortic diameter, IMH thickness, presence of a pericardial effusion, and the
presence of contrast pools or ulcer-like projections, as each of these ndings may
play a key role in surgical decision-making. Transesophageal echocardiography can
be utilized in the emergent setting for the unstable patient, whereas MRI/MRA may
play a role in the stable patient in whom the diagnosis is uncertain [13] (Table3).
Management
Once the diagnosis of an acute aortic intramural hematoma has been conrmed,
immediate medical therapy should be initiated, regardless of whether surgical intervention is planned. Invasive hemodynamic monitoring should be performed with an
arterial line and sufcient large-bore intravenous access should be obtained in case
of abrupt hemodynamic deterioration. Anti-impulse therapy–systemic arterial blood
pressure control combined with reduction in the contractile force of the myocardium, expressed as the change in pressure over time (dP/dt)—should be initiated
immediately to reduce the risk of progression to frank dissection or rupture. If the
heart rate allows and severe aortic regurgitation is not present, rst-line treatment
includes the use of beta-adrenergic blockers to reduce systemic blood pressure to
less than 120mmHg systolic and to a heart rate to 60–70 beats per minute. Thereafter,
addition of a systemic vasodilator to further reduce arterial blood pressure should be
initiated, but should not be used in isolation due to potential reex tachycardia from
the reduction in mean arterial pressure [14].
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Presentation of
Table 2
intramural hematoma
Table 3 Adverse outcomes and predictors
Adverse outcomes Hospital/30-d mortality 10–30% 4–20%
Predictors of adverse
outcome
Adapted from Maslow A, Atalay, M, Sodha N.Intramural Hematoma. J Thorac and Cardiovasc
Anesth. 2018;32:1341–1362
Sign/Symptom Type A IMH Type B IMH
Age (y) >65 >65
Aortic pain (%) >90 >90
Chest pain (%) 82.5 77.3
Back pain (%) 41 78.7
Abdominal pain (%) 13.1 36.8
Radiating pain (%) 45.9 35.3
Acute onset pain (%) 86.7 82.6
Hypertension (%) 32.2 58.6
Hypotension (%) 11.9 2.3
Aortic regurgitation (%) 25–35 <10
Pulse decit (%) 15 <10
Renal complications (%) <10 <10
Pericardial effusion (%) ≤70 <5
Tamponade (%) ≤50 <5
Coronary ischemia (%) ≤30 ≤20
Hemodynamic instability (%) ≤20 <5
Adapted from Maslow A, Atalay, M, Sodha N. Intramural
Hematoma. J Thorac and Cardiovasc Anesth
IMH Type A
Long-term mortality ≤40% 4–14%
Progression, AA, AD,
rupture
Surgery ≤50% < 10%
Persistent pain X X
Hemodynamic instability X X
Pleural effusion X X
Pericardial effusion X X
Para-aortic hematoma X X
Echolucency X X
Rapid aortic growth >5mm/y > 5mm/y
Intimal tear (ULP/FID) X X
PAU-related IMH Uncommon > 10mm depth
MAD >45 to
Wall thickness >10 to 15mm > 10 to 15mm
≤90% Up to 50%
>60mm
Intramural Hematoma
Type B
> 40 to >60mm
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