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\begin{document}

\title{Surgical Management of Type A Aortic Dissection After Percutaneous
Coronary Intervention in a Patient with Acute Myocardial Infarction Due
to a Spontaneous Coronary Artery Dissection}



\author[1]{Athanasia Makrygianni }%
\author[1]{Filippos - Paschalis Rorris}%
\author[1]{Lydia  Kokotsaki }%
\author[1]{Konstantinos  Velissarios }%
\author[2]{Mohammad Salmasi}%
\author[2]{Thanos Athanasiou}%
\author[1]{John Kokotsakis}%
\affil[1]{Evangelismos Athens General Hospital}%
\affil[2]{Imperial College London}%


\vspace{-1em}



  
  \date{June 15, 2024}


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\selectlanguage{english}
\begin{abstract}
Type A aortic dissection after percutaneous coronary intervention is a
rare and life-threatening situation. The reported incidence ranges from
0,02\% to 0,6\% of all diagnostic and interventional percutaneous
procedures. We describe a case of aortic dissection after percutaneous
coronary intervention in a patient with acute myocardial infarction from
spontaneous coronary artery dissection. The patient was initially
treated with primary percutaneous coronary intervention of the affected
left coronary artery branches and left main coronary artery.
Conservative management for the aortic dissection proved inadequate due
to increasing diameter of the false lumen and the patient was referred
to our cardiovascular unit for definite surgical management.%
\end{abstract}%



\sloppy


\textbf{INTRODUCTION}

Spontaneous coronary artery dissection is a rare condition defined as an
automatic separation of the coronary artery wall.~ It is not iatrogenic,
not related to trauma or atherosclerotic disease. Women are mostly
affected (\textgreater{}70\%).\textsuperscript{(1)} Two mechanisms
describe SCAD: a ``primary'' rupture of coronary endothelium with
resultant dissection of the coronary artery wall or the rupture of the
``vasa vasorum'' with formation of an intramural hematoma (IMH).
According to angiographic findings, there are three types of SCAD. Type
I: characterized by contrast~dye staining of the arterial wall with
multiple radiolucent lumens. Type II: more diffuse (length
\textgreater{}20mm) and usually presents uniform narrowing of the
coronary vessels. Type III: focal or tubular (\textless{}20 mm) stenosis
that mimics atherosclerosis. \textsuperscript{(2)}

The following case illustrates a case of type II SCAD, and the
subsequent evolution into a type A aortic dissection. The details of
surgical management required to salvage the patient are then described,
including ascending and hemi-arch aortic replacement.

\textbf{CASE PRESENTATION~}

A 59-year-old female smoker with a history of hyperlipidemia was
admitted for ST-segment elevation myocardial infarction (STEMI) in a
peripheral hospital. Transthoracic echocardiography (TTE) revealed
hypokinesis of the lateral wall, however systolic function was preserved
(left ventricular ejection fraction (LVEF) 55\%).

She was immediately transferred to the catheterization laboratory, where
coronary angiography revealed type II spontaneous coronary artery
dissection (SCAD) of the left coronary system, initiating from the
distal part of the left main coronary artery (LMCA) (Figure 1A B,).
Initially stenting of the ramus intermedius was performed. During
stenting manipulations of the first diagonal and left anterior
descending (LAD) artery, the dissection extended retrogradely into the
LM and left coronary sinus (Figure2A). An additional stent was therefore
inserted to the LMCA until its ostium. Specifically, a 3.5mm x 26mm
stent followed by overdistension with a noncompliant balloon 4mm x 2mm
was introduced into the LMCA, with partial protrusion of its foci into
the aortic lumen. Because of the unimpeded flow in the circumflex
coronary artery, the dissection was left unhandled. No apparent residual
stenosis was seen after the procedure (Figure 2B).

The following day, transthoracic echocardiography (TTE) identified a
notable pericardial effusion leading to prompt pericardiocentesis, which
evacuated 540cc of bloody content. An urgent CT angiography revealed an
aortic intramural hematoma \textless{}1cm in size extending
longitudinally along the anterolateral side of the ascending aorta, from
the aortic root up to the origin of the innominate artery (DeBakey type
II). The aorta was 44-45mm in diameter.

Despite attempts to manage this conservatively with strict blood
pressure control on the coronary care unit, a repeat CT scan 12 days
later revealed expansion of the intramural aortic hematoma, and residual
pericardial effusion (Figure 3). Repeat TTE revealed worsening LV
systolic dysfunction (LVEF 40\%) and hypokinesis of the lateral and
anterior-apical cardiac walls, suggesting compromised flow in the left
coronary system. The patient was escalated and transferred to the
cardiothoracic centre for definitive management.

\textbf{Surgical management}

A median sternotomy was performed. Cardiopulmonary bypass was
established by arterial cannulation of the right axillary artery through
an 8mm interposition Dacron graft and venous cannulation with a standard
two-stage venous cannula. The innominate and left common carotid
arteries were freed up with soft tissue dissection and snared (Figure
4A). After cross clamping the ascending aorta, cold crystalloid
(Custodiol) cardioplegia was administered retrogradely through the
coronary sinus as well as antegradely though the right coronary artery
ostium. The dissected ascending aorta was transected and inspected, to
find an entry tear superiorly and laterally of the left main coronary
ostium in close proximity. The LM stent was also visible, protruding
into the aortic lumen (Figure 4B). The crucial decision was made to
preserve the aortic root and seal the entry tear using a single pledged
5-0 polypropylene suture. After reaching 25\textsuperscript{o}C, CPB was
arrested and the aortic cross clamp removed for inspection of the aortic
arch. The origin of the epiaortic vessels as well as the aortic arch
were intact. Unilateral selective antegrade cerebral perfusion was
achieved through right axillary artery cannulation by snaring the
innominate, left common carotid arteries and clamping the origin of left
subclavian artery. A straight tube 28mm Dacron graft was used for
ascending aortic reconstruction with hemiarch replacement. During the
procedure, continuous cerebral oximetry monitoring with a pre-installed
INVOS (Medtronic) was used.

The patient's postoperative course was uncomplicated, and TTE showed no
evidence of left ventricular systolic dysfunction. At 8-month follow-up,
CTA demonstrates no residual aortic dissection and patent coronary
stents (Figure 5).

\textbf{DISCUSSION}

Percutaneous coronary intervention (PCI) in SCAD patients is associated
with high rates of complications. Iatrogenic coronary artery dissection
(ICAD) is very infrequent, but a tremendous complication after coronary
angiography in the general population,
\textless{}0,2\%.\textsuperscript{(3)} Prakash et al. found the
incidence to be 2\% during diagnostic coronary angiography alone and up
to 14,3\% among patients with PCI on SCAD. \textsuperscript{(3)} PCI in
the presence of SCAD is technically more challenging. Maneuvering inside
the coronary arteries can provoke propagation of the dissection ante- or
retrogradely no infrequently, which in turn results in expansion of the
area of myocardial ischemia. Forced~and intense injection of the
contrast medium must~be avoided. \textsuperscript{(4,5)}

Although rare, iatrogenic retrograde extension of the dissection into
the ascending aorta (0,02~--~0,6\% of diagnostic and interventional
percutaneous procedures) is reported.\textsuperscript{(6)} Dunning et
al. have found a significantly increased rate in aortocoronary
dissections in procedures performed for acute myocardial infarction
(AMI) (0,19\%) compared with non-AMI cases
(0,01\%).\textsuperscript{(7,8)} To our knowledge, this is the first
reported case of type A aortic dissection after PCI for AMI due to SCAD.
More frequently, iatrogenic type A aortic dissection involves the right
coronary artery because it is more susceptible to trauma from a guide
catheter than the LM. \textsuperscript{(7)} In our case, the dissection
extended from the LM to the aorta because of preexisting SCAD in the
left coronary artery system.

Aortocoronary dissection is usually suspected at the time of coronary
intervention. According to Dunning et al. criteria, the aortocoronary
dissection is distinguished into three classes: Class I when the aortic
dissection involves the ipsilateral cusp. Class II, when it includes
cusp and extends up to the aorta for less than 40mm and Class III as for
Class II but at length over 40mm. \textsuperscript{(8)} There are no
guidelines for treating aortic dissection caused by
PCI.\textsuperscript{(9)} The best treatment in Classes I and II seems
to be the stenting of the coronary artery, including the respective
ostium trying to seal the entry point of the dissection. Then consider
conservative management with intensive clinical follow-up. Additional
imaging controls are necessary only in unstable patients and if there is
evidence of progression of the lesion. In contract, Class III mandates
more aggressive surgical~management. \textsuperscript{(7,8,10)} In our
case, the presence of abundant pericardial effusion the day after PCI
comprised a high index of suspicion of progression of the known
retrograde aortocoronary dissection. The CT scan revealed a Class III
aortocoronary dissection: dissection with IMH of the ascending aorta
extending from the left coronary sinus to the inferior limit of the
innominate artery origin (Figure 3A). Besides the fact that the patient
was stable and there was no evidence of active flow of contrast media in
the false lumen, the delay of surgery just reconfirmed the necessity of
emergent intervention in Class III aortocoronary dissection. Indeed, as
shown on the revaluation with CT scan on day thirteen, there was an
increase of the aortic hematoma despite the initial invariable CT image
on day eight of hospitalization.

\textbf{CONCLUSION}

Iatrogenic aortocoronary dissection after PCI on AMI patients from SCAD
is a rare complication. The pathology is characterized by the tendency
of evolution and progression as in an acute aortic syndrome. Especially
for more extended dissections of the aorta (over 40mm in length), the
immediate surgical intervention seems to be the most appropriate
treatment. In the case of primary stenting of the left main coronary
artery, if possible, the more conservative surgical management
techniques reduce the risk of major complications generated from the
mobilization of the rigid stented artery.

\textbf{Ethics Statement}

This manuscript and all of its content meet the ethical guidelines and
obtained an ethical waiver from the study institution. Written consent
for submission and publication of this case report including images and
associated text has been obtained from the patient.

\textbf{REFERENCES}

\begin{enumerate}
\tightlist
\item
  Pavlopoulos D, Hamilos M, Kalogerakos P, et al. Spontaneous Coronary
  Artery Dissection in a Woman: Surgical Treatment and Angiographic
  Follow-Up\emph{.} Ann Thorac Surg. 2018;106(3):e133-e135.
\item
  Saw J, Mancini GBJ, Humphries KH. Contemporary Review on Spontaneous
  Coronary Artery Dissection {[}published correction appears in J Am
  Coll Cardiol. 2016 Oct 4;68(14):1606{]}.
\item
  Prakash R, Starovoytov A, Heydari M, Mancini GB, Saw J.
  Catheter-Induced Iatrogenic Coronary Artery Dissection in Patients
  With Spontaneous Coronary Artery Dissection. JACC Cardiovasc Interv.
  2016;9(17):1851-1853.
\item
  Valappil SP, Iype M, Viswanathan S, Koshy AG, Gupta PN, Velayudhan RV.
  Coronary angioplasty in spontaneous coronary artery
  dissection-Strategy and outcomes. Indian Heart J. 2018;70(6):843-847.
\item
  Yip A, Saw J. Spontaneous coronary artery dissection-A review.
  Cardiovasc Diagn Ther. 2015;5(1):37-48.
\item
  Artemiou P, Lukacin S, Kirsch P, et al. Surgical Treatment of a
  Catheter-Induced Iatrogenic Dissection of the Right Coronary Artery
  following Cardiac Catheterization. J Tehran Heart Cent.
  2016;11(1):30-33.
\item
  Baumann S, Behnes M, Sartorius B, et al. Follow-up of iatrogenic
  aorto-coronary ''Dunning'' dissections by cardiac computed tomography
  imaging. BMC Med Imaging. 2017;17(1):64.
\item
  Dunning DW, Kahn JK, Hawkins ET, O'Neill WW. Iatrogenic coronary
  artery dissections extending into and involving the aortic root.
  Catheter Cardiovasc Interv. 2000;51(4):387-393.
\item
  Shah P, Bajaj S, Shamoon F. Aortic Dissection Caused by Percutaneous
  Coronary Intervention: 2 New Case Reports and Detailed Analysis of 86
  Previous Cases. Tex Heart Inst J. 2016;43(1):52-60. Published 2016 Feb
  1.
\item
  Tanasie C, Chandonnet M, Chin A, et al. Catheter-induced aortic
  dissection after invasive coronary angiography: evaluation with MDCT.
  AJR Am J Roentgenol. 2011;197(6):1335-1340.
\end{enumerate}

\textbf{FIGURE LEGENDS}

\textbf{Figure 1:} Different views of the spontaneous coronary artery
dissection during PCI. Elongated uniform stenosis initiating from the
distal part of the left main and extending mainly in the LAD and first
diagonal as well as in the ramus intermedius.

\textbf{Figure 2: (A)} Retrograde extension of the dissection into the
proximal left main coronary artery until its origin in the aorta. A
stent has already been positioned into the ramus
intermedius.\textbf{(B)} Final angiogram after stenting of the LAD, D1
and LM to its origin, with no residual stenosis.

\textbf{Figure 3:} CT angiography imaging showing \textbf{(A)} the
intramural hematoma (red arrow) just proximally to the origin of
innominate artery and \textbf{(B)} the LM stent which protrudes into the
aortic lumen.

\textbf{Figure 4:} Intraoperative images \textbf{(A)} Asc. Ao intramural
haematoma, \textbf{(B)} LM stent protruding into the aortic lumen

\textbf{Figure 5:} 8-month f-up CTA demonstrating \textbf{(A)} no
residual aortic dissection and \textbf{(B)} patent coronary stents.\selectlanguage{english}
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