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Fig. 11 Intraoperative
photograph after the
descending thoracic aorta
has been clamped and
opened, showing a Grade
III blunt traumatic aortic
injury from inside of the
aortic lumen
Fig. 12 Dacron
replacement of the injured
segment of the descending
thoracic aorta
B. L. Tjaden and A. L. Estrera
post- TEVAR at 1month, 6months, 12 months, and yearly thereafter. If there are
any doubts about the integrity of the aorta outside of the area of endograft coverage
(for example, periaortic hematoma or intramural hematoma extending into the distal
thoracic aorta beyond the TEVAR), earlier imaging may be indicated.DisclosuresDr.
Estrera is a consultant for W.L.Gore. Dr. Tjaden has no disclosures.
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B. L. Tjaden and A. L. Estrera
Catheter-Induced Aortic Dissection
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HannahChaudry, MarwanSaad, andJ.DawnAbbott
Terminology
Aortic dissection occurs when an injury to the intima, or innermost layer of the
aorta, results in a tear, allowing blood to accumulate between the intimal and medial
layers of the vessel wall. This split between the layers of the vessel wall results in a
dissection ap separating a true and false lumen. Aortic dissection often occurs
spontaneously in aortas that are dilated or in which the integrity of the media is
compromised. They can also, however, occur in the setting of diagnostic or
interventional procedures where a catheter or device manipulation results in injury
to the intima with resultant bleeding into the vessel wall. Iatrogenic aortic dissection
refers to an aortic dissection that results as a consequence or complication of
invasive procedures such as a diagnostic cardiac catheterization, percutaneous
coronary interventions (PCI), or cardiac surgery. Catheter-induced iatrogenic aortic
dissections are those in which a coronary catheter is responsible for inducing the
initial injury in the vessel wall and often occurs as an extension or propagation of a
coronary artery dissection. In 2002, the International Registry of Aortic Dissection
(IRAD) reported 34 cases of iatrogenic aortic dissections among 723 patients with
aortic dissections in the registry at the time. Of these, 19 (2.6%) occurred after
major surgery and 14 (2%) were catheter-derived following coronary angiography
or intervention [1].
H. Chaudry · M. Saad · J. D. Abbott (*)
Cardiovascular Institute, Warren Alpert Medical School, Brown University,
Providence, RI, USA
e-mail: Jabbott@lifespan.org
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_15
225© Springer Nature Switzerland AG 2021
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H. Chaudry et al.
Incidence
Catheter-induced aortic dissections are rare. The incidence has been reported at
around 0.02–0.06% of all invasive cardiac procedures [2–5] with the incidence
being higher in PCIs than diagnostic catheterizations (0.06 to 0.07% vs 0.008 to
0.02%, respectively) [6, 7]. One case series noted an even higher incidence of 0.12%
following PCI as compared to 0.01% following diagnostic coronary angiography
[4]. Iatrogenic aortic dissections also occur more frequently in the setting of urgent
PCI for acute myocardial infarction (AMI) with an incidence of 0.19% [2] and
following PCI for chronic total occlusions (CTO) with an incidence of as high as
1.9% [8].
Risk Factors
Previous studies have identied risk factors for iatrogenic catheter-induced aortic
dissection; however, these are limited to case reports due to the rarity of the event.
Clinical risk factors that have been described include older age, diabetes,
hypertension, atherosclerotic burden, calcication of the aortic root as well as
history of prior coronary artery bypass grafting [1, 4, 6]. Atherosclerosis is thought
to predispose vessels to plaque ulceration when manipulated, which then serves as
an entry site for blood ow between the layers of the vessel wall. This link between
acute plaque rupture and inammation may be a factor in the apparent increased
susceptibility of patients with AMI to coronary dissection with propagation to the
aorta [2]. Additionally, any condition resulting in weakness in the media of the
vessel wall carries a higher risk of developing an aortic dissection in general,
however, these have not necessarily been linked to the development of an iatrogenic
aortic dissection in the current literature. This point highlights the differences in the
pathophysiology between spontaneous aortic dissections and those that are
iatrogenic and is also reected in the difference in management strategies between
these two conditions. The classic risk factors for spontaneous aortic dissections
include; history of aortic aneurysm, Marfan syndrome, Ehlers-Danlos syndrome,
bicuspid aortic valve, unicuspid valve as well as cystic medial necrosis [2]. The role
of cystic medial necrosis is controversial since low grades of degeneration are nonspecic and occur with advancing age [2, 9].
Several procedural characteristics have been associated with iatrogenic aortic
dissection. These types of dissections have been noted to occur more frequently
during coronary artery engagement (specically the right coronary artery) and
balloon dilation, where there is more risk of traumatic damage to the intima [3, 4].
Certain types of catheters (e.g., the Amplatz catheter) have also been reported in a
disproportionate number of catheter-induced dissections [2–4]. In addition,
Catheter-Induced Aortic Dissection
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over- vigorous hand injection of contrast is a potential contributing factor, and care
must be taken to minimize further injection to prevent propagation once a dissection
is identied [6]. Engagement of the right coronary artery (RCA), as well as treatment of chronic total occlusion (CTO), poses an increased risk for catheter-induced
aortic dissection [2–4, 6]. In an IRAD report of 74 consecutive iatrogenic dissections, 97% occurred during engagement of a vessel with 57% being the RCA.The
dissections were catheter induced in 92% of cases. It is unclear whether technical or
anatomical differences between the RCA and left main coronary artery (LM) are
responsible for this difference but it is proposed that the larger ostium of the LM, as
well as the decreased angulation at which it is engaged, may decrease the risk of
aortocoronary dissection.
227
Mechanism
Iatrogenic catheter-induced aortic dissection most often involves the ostium of a
coronary artery and may extend variably in an antegrade or retrograde fashion. Few
studies have reported isolated aortic dissection without coronary artery involvement
[10, 11]. Antegrade aortic dissections usually occur with an entry point inside a
coronary artery and extend in the same direction of blood ow in the true lumen. In
contrast, retrograde dissections extend in the opposite direction to blood ow in the
true lumen. Due to the fact that blood ow is pulsatile in the same direction as an
antegrade dissection, these often remain patent for a longer period, while retrograde
dissections usually seal off quicker due to the opposite nature of blood ow.
Antegrade dissections can also propagate down coronary vessels resulting in acute
vessel closure. Retrograde aortic dissections related to coronary injury can result
from a traumatic injury of the coronary artery with the catheter itself or during
balloon/stent ination. Most retrograde iatrogenic aortic dissections originating
from the coronary ostia remain limited to the coronary sinus or are conned to the
ascending aorta (Stanford type A; DeBakey types 1 or 2) [2, 6, 7]. This is
predominantly due to the anatomy of the sinus of Valsalva which has a high content
of collagenous bers near the aortic annulus and is bordered by the thickened supravalvular ridge [6]. Figure1, panel A represents a case of right aortocoronary dissection extending to the aortic root and ascending aorta, as evident with contrast
staining within the aortic wall; panel B: a coronary stent graft was used to seal the
entry site with halting of the extension of the dissection in the same patient. Figure2,
panel A represents a second case of proximal RCA dissection from guide catheter
manipulation; panel B demonstrates the dissection extending retrogradely to the
aortic root; panel C: a drug-eluting stent was used to seal the dissection entry site;
panel D: Near complete resolution of the contrast staining in the aortic wall with
sealing the dissection entry site.
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ab
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H. Chaudry et al.
Fig. 1 (a) Iatrogenic aortic dissection caused by post-dilatation with non-compliant balloon after
stent placement; (b) Sealing off the dissection entry using a JOMED
®
coronary graft stent
Clinical Presentation
The presenting signs and symptoms of iatrogenic aortic dissection vary from that of
spontaneous aortic dissection [1]. Patients with iatrogenic aortic dissection are more
likely to present with indolent hemodynamic instability, often with hypotension or
shock. A review of 723 patients with aortic dissection from the IRAD database
showed that patients with iatrogenic aortic dissection are less likely to present with
abrupt symptoms (35% vs 87%) and more likely to have no chest or back pain (25%
vs 1%) compared with those with spontaneous aortic dissection. Patients with
iatrogenic aortic dissection were also more likely to have hypotension (30% vs 9%)
and develop cardiac complications such as myocardial ischemia (36% vs 5%) or
infarction (15% vs 3%). Aortic regurgitation was less frequent (11% vs 34%) and
fewer patients with iatrogenic aortic dissections had a visualized intimal ap (46%
vs 60%) or patent false lumen on imaging (48% vs 75%) compared with those with
spontaneous aortic dissection.
Diagnosis
Catheter-induced aortic dissection is most often recognized on angiography during
the index cardiac procedure, but often subsequently need to be evaluated with noninvasive imaging such as transesophageal echocardiogram (TEE), computed
tomography/angiography (CT/CTA) or magnetic resonance imaging/angiography
(MRI/MRA).
Catheter-Induced Aortic Dissection
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ab
cd
229
Fig. 2 (a) Proximal RCA dissection from guide catheter manipulation; (b) demonstrates the dissection extending retrogradely to the aortic root; (c) a drug-eluting stent was used to seal the dissection entry site; (d) Near complete resolution of the contrast staining in the aortic wall with
sealing the dissection entry site
Coronary Angiography
Iatrogenic aortic dissection presents on coronary angiography as persistence of contrast dye staining around the aortic root (Figs.1a and 2b). In 2000, Dunning etal.
proposed a classication system (Table1) for iatrogenic aortic dissections based on
the extent of aortic involvement seen on coronary angiography. Class I includes dissections in which the contrast staining is limited to the ipsilateral coronary cusp;
Class II, where contrast extends within 40mm up the aortic wall; and Class III,
where contrast extends to greater than 40mm up the aortic wall [2]. While Classes
I and II are typically medically managed or treated with stenting of the entry point;
Class III dissections may necessitate immediate surgical intervention and are associated with higher mortality [2, 3].
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Table 1 Dunning Classication
Dunning Class Aortic Involvement
I Dissection limited to ipsilateral cusp only
II Dissection extending <40mm up the aortic wall
III Dissection extending >40mm up the aortic wall
H. Chaudry et al.
Non-invasive Imaging
Any aortic dissection with evidence of hemodynamic compromise should be evaluated with transthoracic echocardiogram (TTE) to evaluate for extension into the
pericardium with pericardial effusion and to rule out cardiac tamponade. In addition, the aortic valve should be evaluated for acute aortic incompetence. TEE can be
performed urgently in the catheterization laboratory to identify an aortic dissection
ap and evaluate aortic valve function [12]. In most cases, following initial management, urgent imaging with CT or MRI should be performed to determine if there is
any residual dissection, evaluate its extent, and for follow-up. There is no consensus
as to which imaging technique is preferred. CT has the advantage of rapid, easy
acquisition with high sensitivity and specicity, however, it exposes the patient to
contrast dye and radiation. MRI, on the other hand, lacks exposure to radiation with
high sensitivity and specicity but is time-consuming, and hence may be more suitable for long-term follow-up rather than during the acute situation [13, 14]. Both
contrast and non-contrast CT imaging should be obtained in order to differentiate
between retained contrast from cardiac catheterization vs contrast from CT scan.
Fig.3: Computed tomography of the chest without contrast in a patient with catheter-induced aortic dissection from RCA percutaneous intervention revealing contrast staining in the aortic wall in relation to RCA (arrows).
Management
Given the rarity of catheter-induced iatrogenic aortic dissection, there are no randomized trials to guide appropriate therapy or inform prognosis. Therefore, most
treatment decisions are based on data from previously published care reports and
case series of iatrogenic aortic dissections.
Although most spontaneous Stanford type A aortic dissections are treated surgically, several case reports have demonstrated that iatrogenic aortic dissections can
be successfully treated by quick sealing of the entry point of the dissection within
the coronary vessel [1–4, 7, 15].
Several factors affect management strategies when addressing catheterinduced iatrogenic aortic dissections. These include the hemodynamic stability
of the patient, propagation and extent of the aortic injury, presence of aortic
valvular incompetence, presence of pericardial effusion or cardiac tamponade,
Catheter-Induced Aortic Dissection
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Fig. 3 Computed
tomography of the chest
without contrast in a
patient with catheterinduced aortic dissection
from RCA percutaneous
intervention revealing
contrast staining in the
aortic wall in relation to
RCA (arrows)
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and the condition of the involved coronary artery [16]. Current options for management of catheter-induced aortic dissections include a conservative approach
with careful surveillance, percutaneous stenting of the dissection entry point,
and surgery.
Medical Management
All patients with identied iatrogenic aortic dissections should have immediate
hemodynamic evaluation. As previously mentioned, TTE should be performed to
evaluate for the presence of pericardial effusion or valvular dysfunction. Acute
hemodynamic optimization should initially take precedence with an attempt at
containing and preventing dissection propagation. Further contrast injections should
be avoided. Beta-blockers and vasodilators are the mainstays for treatment of
spontaneous aortic dissections, and while it may be of limited use in acutely unstable
patients, it should be considered in those with stable hemodynamics and small
contained dissection, as well as in the follow-up period [16].
Conservative management with watchful waiting has been described with good
results for retrograde iatrogenic aortic dissections that are small and contained to
the sinus of Valsalva (Dunning class I) and the involved coronary remains with good
ow [3, 4]. Additionally, a review of 14 cases with dissection of the descending
aorta/arch, without coronary involvement found that if the dissection is small
without progression on follow-up imaging, a conservative approach is acceptable
and results in good outcomes [3, 11]. In the presence of low-risk dissections with
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