\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[T2A]{fontenc}
\usepackage[ngerman,russian,english]{babel}



\usepackage{float}








\begin{document}

\title{THROMBUS ASPIRATION WITHOUT STENTING IN A PATIENT WITH ANTERIOR STEMI
(REGRESSION AND HEALING OF AN UNSTABLE PLAQUE 24 MONTHS LATER AFTER PCI
ASSESSED BY OCT)}



\author[1]{Avtandil Babunashvili}%
\author[2]{Samir Pancholy}%
\author[1]{Tamara Babunashvili}%
\author[3]{Alexander Prohorov}%
\affil[1]{Center of Endosurgery}%
\affil[2]{Wright Center of Graduate Medical Education}%
\affil[3]{Municipal clinic No7}%


\vspace{-1em}



  
  \date{June 15, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
We report a case of natural healing of a ruptured unstable coronary
plaque using serial OCT examination. Stenting procedure was deferred
based on the angiographic and mainly OCT findings. A healing process of
ruptured plaque without foreign body was studied using OCT at 3, 14 and
24 months after PCI.%
\end{abstract}%



\sloppy


\textbf{THROMBUS ASPIRATION WITHOUT STENTING IN A PATIENT WITH ANTERIOR
STEMI (REGRESSION AND HEALING OF AN UNSTABLE PLAQUE 24 MONTHS LATER
AFTER PCI ASSESSED BY OCT)}

\textbf{Avtandil Babunashvili*, Samir Pancholy\#, Tamara Babunashvili*,
Alexander Prokhorov*}

* Center of Endosurgery, Moscow, Russian Federation

\# Geisinger Commonwealth School of Medicine, The Wright Center for
Graduate Medical Education, Scranton, PA

The work was performed at the Center of Endosurgery

\textbf{Word count} : 3760

\textbf{Short title} : thrombus aspiration without stenting in STEMI
\ldots{}

\textbf{Key words} : acute myocardial infarction, intravascular
visualization, primary PCI, plaque healing

\textbf{Address for correspondence} : 111123, Moscow, Russian
Federation, 62 shosse entuziastov. e-mail:
avtandil.babunashvili@gmail.com

\textbf{ABSTRACT:} We report a case of natural healing of a ruptured
unstable coronary plaque using serial OCT examination. A 41-years old
female patient was admitted with anterior STEMI and a thrombus
containing ostial LAD lesion. After emergency thrombus aspiration the
subsequent stenting procedure was deferred based on the angiographic and
mainly OCT findings. A healing process of ruptured plaque without
foreign body was studied using OCT at 3, 14 and 24 months after PCI.
Endothelization of the ruptured site was found at 3 months and complete
healing of vessel wall and reduction of plaque burden with concomitant
high-intensity statin therapy occurred after 14 months of the initial
procedure. No significant change was found between 14 and 24 months. A
significant decrease of plaque burden and vessel wall regeneration was
determined by OCT in 24 months follow up. In selected cases, OCT-guided
PCI in an ACS patient allows us to defer further instrumentation after
lumen and flow re-establishment, with adequate natural healing of the
ruptured plaque using guideline directed medical therapy.

\textbf{INTRODUCTION:} Atherosclerotic plaque instability and rupture is
the underlying pathophysiology for acute coronary syndrome (ACS).
Previous autopsy and clinical studies have shown that inflammation and
intensive expression of metalloproteinases are key factors for
vulnerability of atherosclerotic plaque 11\textbf{Moreno PR} , Falk E,
Palacios IF, Newell JB, Fuster V, Fallon JT.\textbf{Macrophage
infiltration in acute coronary syndromes. Implications for plaque
rupture.} Circulation, 1994, 90:
775-8.\textsuperscript{,}22\textbf{Zairis MN} , Papadaki OA, Manousakis
SJ, Thoma MA, Beldekos DJ, Olympios CD, Festeridou CA, Argyrakis SK,
Foussas SG. \textbf{C-Reactive protein and multiple complex coronary
artery plaques in patients with primary unstable angina.}
Atherosclerosis 2002,164: 355-9.. Some pathological studies have shown
that ruptured plaques commonly spontaneously heal, and the matrix within
healed plaque contains a proteoglycan-rich mass or collagen-rich scar,
depending on the healing phase33\textbf{Burke AP} , Kolodgie FD, Farb A,
Weber DK, Malcom GT, Smialek J, Virmani R.\textbf{Healed plaque ruptures
and sudden coronary death: Evidence that subclinical rupture has a role
in plaque progression.}Circulation 2001, 103: 934-40.. Moreover, it is
speculated, that repeated silent plaque rupture and subsequent healing
results in an increased plaque burden and percent stenosis. Therefore,
an understanding of the pathology of healing process is of paramount
clinical importance. The healing process of infarct-related plaque has
been previously described using pathologic and angioscopic
examinations44\textbf{Eric van Belle} , Jean-Marc Lablanche, Christophe
Bauters, Natalie Renaud, Eugene P. McFadden, Michel E. Bertrand.
\textbf{Coronary Angioscopic Findings in the Infarct-Related Vessel
within 1 month of Acute Myocardial Infarction. Natural History and the
effect of Thrombolysis.} Circulation 1998, 97: 26-33., with scant data
available using high resolution luminal and transmural imaging.

Contrary to angioscopy, new intracoronary visualization modalities -
Optical Coherence Tomography (OCT) and Intravascular Ultrasound (IVUS)
-- allow us a deep insight in vessel wall and plaque to obtain detailed
information about plaque structure and tissue composition. Given the
high spatial resolution, OCT has been widely used for coronary plaque
characterization,55Uemura S, Ishigami K, Soeda T, Okayama S, Sung JH,
Nakagawa H, Somekawa S, Takeda Y, Kawata H, Horii M, Saito Y.
\textbf{Thin-cap fibroatheroma and microchannel findings in optical
coherence tomography correlate with subsequent progression of coronary
atheromatous plaques.}Eur Heart J. 2012
Jan;33(1):78-85.\textsuperscript{,}66\textbf{Tian J} , Ren X, Vergallo
R, Xing L, Yu H, Jia H, Soeda T, McNulty I, Hu S, Lee H, Yu B, Jang IK.
Distinct morphological features of ruptured culprit plaque for acute
coronary events compared to those with silent rupture and thin-cap
fibroatheroma: a combined optical coherence tomography and intravascular
ultrasound study. J Am Coll Cardiol. 2014 Jun 3;63(21):2209-16.
including detection and detailed morphological description of thin-cap
fibroatheroma (TCFA) and unstable plaque rupture 77\textbf{Hu S} ,
Yonetsu T, Jia H, Karanasos A, Aguirre AD, Tian J, Abtahian F, Vergallo
R, Soeda T, Lee H, McNulty I, Kato K, Yu B, Mizuno K, Toutouzas K,
Stefanadis C, Jang IK. Residual thrombus pattern in patients with
ST-segment elevation myocardial infarction caused by plaque erosion
versus plaque rupture after successful fibrinolysis: an optical
coherence tomography study. J Am Coll Cardiol. 2014 Apr
8;63(13):1336-1338.\textsuperscript{,}88\textbf{Tearney GJ} , Regar E,
Akasaka T, Adriaenssens T, Barlis P, Bezerra HG, Bouma B, Bruining N,
Cho JM, Chowdhary S, Costa MA, de Silva R, Dijkstra J, Di Mario C, Dudek
D, Falk E, Feldman MD, Fitzgerald P, Garcia-Garcia HM, Gonzalo N,
Granada JF, Guagliumi G, Holm NR, Honda Y, Ikeno F, Kawasaki M, Kochman
J, Koltowski L, Kubo T, Kume T, Kyono H, Lam CC, Lamouche G, Lee DP,
Leon MB, Maehara A, Manfrini O, Mintz GS, Mizuno K, Morel MA, Nadkarni
S, Okura H, Otake H, Pietrasik A, Prati F, R\selectlanguage{ngerman}äber L, Radu MD, Rieber J,
Riga M, Rollins A, Rosenberg M, Sirbu V, Serruys PW, Shimada K, Shinke
T, Shite J, Siegel E, Sonoda S, Suter M, Takarada S, Tanaka A, Terashima
M, Thim T, Uemura S, Ughi GJ, van Beusekom HM, van der Steen AF, van Es
GA, van Soest G, Virmani R, Waxman S, Weissman NJ, Weisz G;
International Working Group for Intravascular Optical Coherence
Tomography (IWG-IVOCT).\textbf{Consensus standards for acquisition,
measurement, and reporting of intravascular optical coherence tomography
studies: a report from the International Working Group for Intravascular
Optical Coherence Tomography Standardization and Validation.}J Am Coll
Cardiol. 2012 Mar 20;59(12):1058-72.. Nevertheless, scant data is
available on the natural course of a ruptured plaque leading to acute
coronary syndrome. Rioufol G. et al have used IVUS to demonstrate the
evolution and healing process of spontaneously ruptured atherosclerotic
plaque. The authors evaluated 28 ruptured plaques in 14
patients99\textbf{Rioufol G} , Gilard M, Finet G, Ginon I, Boschat J,
André-Fouët X. Evolution of spontaneous atherosclerotic plaque rupture
with medical therapy: long-term follow-up with intravascular ultrasound.
Circulation. 2004 Nov 2;110(18):2875-80.. According to the study
findings, only half of the ruptured plaques were healed, and the
remodeling index was unchanged or considerably positive with a trend
towards reduction of plaque burden.

It is not known how ruptured plaque and vessel wall at the site of the
culprit lesion evolve in the follow up period. This raises concerns
about treatment issues in terms of the associated risk of thrombosis.
While angioscopy data confirm the presence of thrombus on the culprit
lesion after six months and even up to 18 months1010\textbf{Y. Ueda} ,
M. Asakura, O. Yamaguchi, A. Hirayama, M. Hori, K. Kodama.\textbf{The
Healing Process of Infarct-Related Plaques. Insight of 18 Months of
Serial Angioscopic Follow-up.} JACC 2001, 38, 7: 1916-22., late (18-24
months) follow up is necessary for studying the natural history of
atherothrombosis.

We describe the natural course of ruptured plaque causing an anterior
STEMI, treated without balloon dilatation or stent placement, using OCT
examination over a 24-month follow up. To the best of our knowledge,
this is the first description of the healing process of a ruptured
plaque in vivo by OCT.

\textbf{CASE PRESENTATION:} A 41-years old female patient was admitted
with anterior STEMI diagnosis 2.5 hours after symptom onset. Taking into
consideration the ECG changes (ST elevation in I, aVL, and
V\textsubscript{2}-V\textsubscript{6} leads) and increased Troponin I
level on presentation (more than 15 times the upper limit of normal),
emergency cardiac catheterization was initiated. After intravenous
heparin administration (70 U/kg) coronary arteriography was done through
the distal right radial access. Angiography revealed single vessel
disease with a thrombus containing lesion at the ostium of the left
anterior descending (LAD) artery (Fig. 1).

Taking into account large thrombus burden (Thrombus burden grade (G)
\textgreater{} 2 X Reference vessel diameter (RVD)1111\textbf{Sianos G}
, Papafaklis MI, Serruys PW. \textbf{Angiographic thrombus burden
classification in patients with ST-segment elevation myocardial
infarction treated with percutaneous coronary intervention} . J Invasive
Cardiol. 2010 Oct;22(10 Suppl B):6B-14B.) thrombus aspiration procedure
was performed using a 6F ELIMINATE catheter (Terumo corporation, Japan)
with good immediate result (Fig. 2A). Control angiography revealed
complete disappearance of the filling defect from vessel lumen,
nonsignificant residual stenosis (minimal lumen diameter by QCA =
3.23mm) and antegrade TIMI III flow. A IIb/IIIa inhibitor agent
eptifibatide (Integrillin) was administered and control OCT was
performed thereafter. \selectlanguage{russian}ОСТ revealed arterial lumen without thrombotic
mass and clear signs of a ruptured unstable plaque with disruption of
fibrous cap (defect size was 3.7 X 1.2mm) overlaying a large necrotic
core (Fig. 2B). The plaque extended into the proximal part of left
anterior descending artery (LAD) without involvement of its ostium and
occupied nearly half of the lumen circumference (173.8\selectlanguage{ngerman}°). 3D
reconstruction image showed localization and size of ruptured area in
LAD lumen and its 3D dimensional orientation to the circumflex artery
ostium (Fig. 2C). Mean Luminal Diameter (MLD) at the rupture site by OCT
measurement was 3.2mm (vessel distal reference diameter (VRD) = 3.8mm)
and minimal lumen cross sectional area (CSA) 7.9
mm\textsuperscript{2}(distal reference CSA -- 8.6
mm\textsuperscript{2}). Therefore, area stenosis calculated as distal
reference CSA - minimal lumen CSA/ distal reference CSA was 9\%. Taking
into account the geometry of the vessel lumen, absence of a thrombotic
mass at the plaque rupture site and antegrade TIMI III flow, we decided
not to implant stent. In postintervention period DAPT was continued and
the patient was discharged 10 days after initial admission. Due to
hypercholesterolemia (cholesterol 6.25 mmol/l, LDL = 3.85 mmol/l)
high-intensity statin therapy (Rosuvastatin 40mg once daily) was
prescribed.

After 3 months, control angiography shown good patency of LAD and the
arterial lumen at the site of plaque rupture remained without restenosis
(Fig. 3A). OCT revealed clear signs of an ongoing healing process of
previously ruptured plaque with fibrotic transformation of the plaque,
and a thin layered neointima (90-110 microns) covering its surface.
Plaque burden decreased, but residual necrotic core still persisted
(Fig. 3B). Minimal lumen CSA was 5,97mm\textsuperscript{2}. Despite the
thin neointima covering the ruptured plaque surface, DAPT was continued
for 12 months as recommended by the guidelines.

Angiography at 14 months revealed no restenosis (Fig. 4A). OCT
examination showed complete healing of vessel wall at the site of
previous plaque rupture. Plaque burden was significantly decreased and
transformed into a small sized stable fibrotic plaque (Fig. 4B). Minimal
lumen CSA was 8,2mm\textsuperscript{2}, vessel wall CSA at the point of
minimal lumen CSA was 10.5mm\textsuperscript{2}. Percent atheroma volume
(PAV) and total atheroma volume (TAV) calculated as previously
described1212Bill D Gogas,~Vasim Farooq,~Patrick W Serruys,~Hector M
Garcìa-Garcìa. \textbf{Assessment of coronary atherosclerosis by IVUS
and IVUS-based imaging modalities: progression and regression studies,
tissue composition and beyond.} Int J Cardiovasc Imaging, 2011
Feb;27(2):225-37. were 21.9\% and 27.3mm\textsuperscript{3}respectively.
At 12 months follow up patient had stopped DAPT, continued lipid
lowering therapy and achieved guideline recommended target LDL and HDL
levels.

24 months after initial procedure patient was admitted due to recurrent
angina. Control angiography shown no restenosis in LAD ostium at the
site of thrombus aspiration of without stenting (Fig. 5A) and new lesion
in RCA, which was stented successfully. Repeat OCT evaluation of LAD
ostium revealed stable thick cap fibrotic plaque without lipid core
(Fig. 5, b) occupying 115°(approximately 33\%) of lumen circumference.
No significant vessel wall remodeling occurred in period between 14 and
24 months after primary PCI. Minimal lumen CSA and vessel wall CSA at
the site of previous plaque rupture were 8.6 mm\textsuperscript{2} and
11.0 mm\textsuperscript{2}. Calculated PAV and TAV were 21.8\% and 23.5
mm\textsuperscript{3} respectively.

\textbf{DISCUSSION:} We describe the natural course of an unstable,
ruptured plaque presenting as a STEMI, treated without subsequent
mechanical angioplasty (instrumentation of the plaque) or stenting.
Although the acute phase of the unstable plaque rupture is described
comprehensively1313\textbf{Jacob Fog Bentzon} , Fumiyuki Otsuka, Renu
Virmani, Erling Falk. \textbf{Mechanism of plaque formation and
rupture.} Circ Res, 2014, 114: 1852-1866., the chronic phase or healing
process of ruptured plaque has not been well defined in a live patient.
Many studies describe dynamic changes of atherosclerotic plaque volume
and composition using statin therapy and subsequent serial IVUS
visualization1414\textbf{H. Daida} , T. Dohi, Y. Fukushima, H. Ohmura
and K. Miyauchi. \textbf{The Goal of achieving atherosclerotic plaque
regression with lipid-lowering therapy: Insights from IVUS trials.} J
Atheroscler Thromb, 2019, 26: 592-600.\textsuperscript{,}1515\textbf{M.
Hartmann} , J. Huisman, D. Bose, LO. Jensen, P. Schoenhagen, GS. Mintz,
R. Erbel and C. von Birgelen. \textbf{Serial Intravascular Ultrasound
assessment of changes in coronary atherosclerotic plaque dimensions and
composition: an update.} Eur J of Echocardiography, 2011, 12:
313-321.\textsuperscript{,}1616\textbf{K. Hattori} , Y. Ozaki, TF.
Ismail, M. Okumura, H. Naruse, Sh. Kan, M. Ishikawa, T. Kawai, M. Ohta,
H. Kawai, T. Hashimoto, Y. Takagi, J. Ishii, PW. Serruys, J. Narula.
\textbf{Impact of statin therapy on plaque characteristic as assessed by
serial OCT, Grayscale and Integrated Backscatter-IVUS.}JACC: Cardiovasc
Imaging, 2012, 5(2): 169-77. even in ACS patients\textsuperscript{9},
but none of them report changes and healing process of the ruptured
unstable plaque using a high-resolution imaging modality such as OCT
examination.

The role of plaque healing process in stenosis formation and progression
has been determined in previous studies. Burke AP et al proposed that
scar-like contraction of the healing fibrous tissue may be a cause of
the negative remodeling often seen in severely stenosed arterial
lumen\textsuperscript{3}. Some authors indicate the silent plaque
rupture and subsequent healing as a major mechanism for plaque growth
and chronic stenosis formation1717\textbf{C. Bauters} .\textbf{Silent
coronary plaque rupture.} Archives of cardiovascular diseases, 2008,
101: 79-80.. This suggestion is based on multilayered plaque appearance
consistent with a history of incorporation of organized thrombus formed
on ruptured or eroded plaque\textsuperscript{3}.

Minimal positive remodeling of vessel lumen was detected in our case
between 16 and 24 months of follow up period. Complete endothelization
of a ruptured plaque occurred 3 months after initial PCI, but residual
mass of necrotic core was still observed. Moreover, significant
regression of a plaque burden was confirmed by OCT up to 24 months after
coronary intervention and concomitant high-intensity lipid lowering
therapy. No significant changes were noted in plaque burden, atheroma
composition, vascular geometry and atheroma percent or total volume
between 12 and 24 months after PCI. This could imply that at 12 months,
the ruptured plaque had stabilized and did not change significantly
morphologically in the subsequent period. Interestingly, the classical
three-layered OCT sign of the arterial wall appeared in follow up
accompanied by the process of atherosclerotic plaque regression.

Several studies have shown that lipid lowering therapy with statins is
associated with plaque stabilization and a considerable number of
studies demonstrated plaque regression with statins or non-statin lipid
lowering therapy1818\textbf{M. Banach} , C. Serban, A. Sahebkar, DP.
Mikhailidis, S. Ursoniu, KK. Ray, J. Rysz, PP. Toth, P. Muntner, S.
Mosteoru, HM. Garcia-Garcia, G. Kees Hovingh, JJP. Kastelein, PW.
Serruys and Lipid and Blood Pressure Meta-analysis Collaboration (LBPMC)
Group. \textbf{Impact of Statin Therapy on Coronary Plaque Composition:
a systematic review and meta-analysis of virtual histology intravascular
ultrasound studies.} BMC Medicine 2015, 13:
229-49.\textsuperscript{,}1919\textbf{X. Tang} , Y. Yang, S. Luo, Y.
Zhao, C. Lu, Y. Luo, F. Zhang, H. Xiao. \textbf{The effect of Statin
Therapy on Plaque Regression following Acute Coronary Syndrome: a
meta-analysis of prospective trials.} Coronary Artery Disease, 2016, 27
(8): 636-49.. However, in all these studies IVUS was used as the only
intravascular visualization technique for measuring the atheroma percent
or total volume changes in the follow up period, as well as for
assessment of plaque composition changes. Some authors studied the
plaque healing process using OCT examination\textsuperscript{16} but in
published articles using both imaging modalities only non-culprit
segments were included in the analysis2020\textbf{R. Vergallo} , I.
Porto, D. D'Amario, G. Anniballi, M. Galli, S. Benenati, F. Bendandi, F.
Fracassi, C. Aurigemma, AM. Leone, A. Buffon, F. Burzotta, C. Trani, G.
Niccoli, G. Liuzzo, F. Prati, V. Fuster, I-K. Jang, F.
Crea.\textbf{Coronary Atherosclerosis Phenotype and Plaque Healing in
Patients with Reccurent Coronary Syndromes compared with Patients with
Long-term Clinical Stability. An in Vivo Optical Coherence Tomography
Study.} JAMA Cardiol, 2019, 4(4): 321-9.. Therefore, characteristics of
the healing process of a clinically manifested ruptured unstable plaque
in vivo remained unknown. To our best knowledge, this is a first report
of the serial OCT examination for detailed in vivo assessment of the
plaque regression and a vessel wall regeneration up to 24 months after
initial primary PCI without plaque/stenosis dilatation or stenting.

The guidelines recommend delayed or immediate coronary stenting as a
preferable option compared to balloon angioplasty alone in patients with
STEMI2121\textbf{F-J Neumann} , M. Sousa-Uva, A. Ahlsson, F. Alfonso,
AP. Banning, U. Benedetto, RA. Byrne, JP. Collet, V. Falk, SJ. Head, P.
Juni, A. Kastrati, A. Koller, SD. Kristensen, J. Niebauer. DJ. Richter,
PM. Seferovic, D. Sibbing, GG. Stefanini, S. Windecker, R. Yadav, MO.
Zembala. \textbf{2018 ESC/EACTS guidelines on myocardial
revascularization.} Eur Heart J 2019, 40: 87-165.. Several previous
studies have investigated deferred stenting procedure as an option to
preserve microcirculation option with conflicting
results2222\textbf{Carrick D} , Oldroid KG, McEntegart M, Haig C, Petrie
MC, Eteiba H, Hood S, Owens C, Watkins S, Layland J, Lindsay M, Peat E,
Rae A, Behan M, Sood A, Hillis WS, Mordi I, Mahrous A, Ahmed N, Wilson
R, Lasalle L, Genereux P, Ford I, Berry C. \textbf{A randomized trial of
deferred stenting versus immediate stenting to prevent no- or
slow-reflow in acute ST-segment elevation myocardial infarction
(DEFER-STEMI).} J Am Coll Cardiol 2014; 63:
2088--2098.\textsuperscript{,}2323\textbf{Belle L} , Motreff P, Mangin
L, Range G, Marcaggi X, Marie A, Ferrier N, Dubreuil O, Zemour G,
Souteyrand G, Caussin C, Amabile N, Isaaz K, Dauphin R, Koning R, Robin
C, Faurie B, Bonello L, Champin S, Delhaye C, Cuilleret F, Mewton N,
Genty C, Viallon M, Bosson JL, Croisille P.\textbf{MIMI Investigators.
Comparison of immediate with delayed stenting using the Minimalist
Immediate Mechanical Intervention approach in acute ST-segment-elevation
myocardial infarction: The MIMI study.} Circ Cardiovasc Interv
2016;9:e003388.. The large (deferred vs conventional stent implantation)
multicenter DANAMI 3-DEFER trial showed no statistically significant
difference in the primary clinical outcome between groups in the
follow-up period2424\textbf{Kelbaek H} , Hofsten DE, Kober L, Helqvist
S, Klovgaard L, Holmvang L, Jorgensen E, Pedersen F, Saunamaki K, De
Backer O, Bang LE, Kofoed KF, Lonborg J, Ahtarovski K, Vejlstrup N,
Botker HE, Terkelsen CJ, Christiansen EH, Ravkilde J, Tilsted HH,
Villadsen AB, Aaroe J, Jensen SE, Raungaard B, Jensen LO, Clemmensen P,
Grande P, Madsen JK, Torp-Pedersen C, Engstrom T. \textbf{Deferred
versus conventional stent implantation in patients with ST-segment
elevation myocardial infarction (DANAMI 3-DEFER): An open-label,
randomized controlled trial.} Lancet 2016;387:2199--2206.. Moreover, the
results of two landmark RCTs suggest that the routine use of thrombus
aspiration is not indicated 2525\textbf{Frobert O} , Lagerqvist B,
Olivecrona GK, Omerovic E, Gudnason T, Maeng M, Aasa M, Angeras O,
Calais F, Danielewicz M, Erlinge D, Hellsten L, Jensen U, Johansson AC,
Karegren A, Nilsson J, Robertson L, Sandhall L, Sjögren I, Ostlund O,
Harnek J, James SK: TASTE Trial. \textbf{Thrombus aspiration during
ST-elevation myocardial infarction.} N Engl J Med. 2013 Oct 24;
369(17):1587-97.\textsuperscript{,}2626\textbf{Jolly SS} , Cairns JA,
Yusuf S, Meeks B, Pogue J, Rokoss MJ, Kedev S, Thabane L, Stankovic G,
Moreno R, Gershlick A, Chowdhary S, Lavi S, Niemelä K, Steg PG, Bernat
I, Xu Y, Cantor WJ, Overgaard CB, Naber CK, Cheema AN, Welsh RC,
Bertrand OF, Avezum A, Bhindi R, Pancholy S, Rao SV, Natarajan MK, ten
Berg JM, Shestakovska O, Gao P, Widimsky P, Dzavík V; TOTAL
Investigators. \textbf{Randomized trial of primary PCI with or without
routine manual thrombectomy.} N Engl J Med. 2015 Apr 9;
372(15):1389-98.\textbf{Legends:Fig.1:} Initial arteriography revealed
single vessel disease and a thrombus containing lesion at the LAD ostium
(arrow).\textbf{Fig. 2:} Angiography and OCT immediately after
Interventional procedure: a -- arteriography after thrombus aspiration
shows vessel lumen with minimal residual stenosis (``stent-like''
result) and no signs of a thrombotic mass (arrow). b -- OCT examination
after thrombus aspiration demonstrated unstable plaque with a large
necrotic core (NC) and ruptured fibrotic cap (arrow). No concomitant
thrombus seen along a ruptured plaque. c -- 3D reconstruction of the
ruptured plaque area allows to see location of a rupture in LAD lumen
(arrow) and its relation to the CxA ostium.\textbf{Fig. 3:} Control
angiography and OCT examination after 3 months of the initial PCI
procedure: a -- no restenosis was detected in LAD by angiography at the
site of previous thrombus aspiration without stenting (arrow); b -- OCT
examination shown complete endothelization of a previously ruptured
plaque surface (arrows), but residual necrotic core of the plaque still
persisted (marked by an asterisk).\textbf{Fig. 4:} 14 months follow up
result assessed by angiography and OCT: a -- control angiography shows
LAD without restenosis after initial intervention (arrow). b -- OCT
picture revealed small fibrotic plaque (asterisk) at the site of
previously unstable and ruptured plaque.\textbf{Fig. 5:} Control
arteriography and OCT of the LAD 24 months later: a -- LAD without
restenosis after primary coronary intervention (arrow). b -- Small
stable plaque (asterisk) detected by OCT without significant changes in
plaque size and tissue composition compared to 14-month follow up
result. Classic 3-layered structure of the vessel wall is clearly
visible (media signed by arrows).. Nevertheless, in the high-thrombus
burden subgroup mitigation of the risk of microembolization and
no-reflow provides a rationale for ``bail-out'' thrombus aspiration
procedure. No doubt, that coronary stenting is the technique of choice
during primary PCI in patients with STEMI, however, main question that
arises following the described case is, can we safely defer stent
implantation in STEMI patient? if yes, in which particular situation can
we leave culprit lesion without a stent? Logically, vessel wall healing
process without a foreign body (as a trigger of inflammation) could be
closer to physiology and therefore preferable. This case shows the
potential of OCT based ``stent-free'' strategy with concomitant dual
antiplatelet and high-intensity statin therapy to obtain a satisfactory
short-term and long-term result. Another important point is duration of
dual antiplatelet therapy (DAPT) after initial PCI in ACS patients.
Taking into account the complete endothelization of ruptured plaque
after 3 months, is this OCT finding sufficient basis for shorter DAPT?
This case also highlights the utility of OCT imaging in studying the
natural healing process after a ruptured plaque event leading to a major
clinically relevant presentation.

\textbf{CONCLUSION} : In selected cases the OCT-based ``stent-free''
strategy of primary PCI may be useful to obtain short- and long term
satisfactory result in patients with STEMI. Supposedly, this approach
promotes the natural healing of ruptured plaque and vessel wall without
permanent foreign body in the arterial lumen.

\textbf{ACKNOWLEDGMENT}

We wish to thank all the nurses and technicians of our catheterization
laboratory for their professional contribution and help. We also would
like to express our appreciation to the technical personnel of the
Terumo company for their involvement in this study.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-1/fig-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-2a/fig-2a}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-2b/fig-2b}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-2c/fig-2c}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-3a/fig-3a}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-3b/fig-3b}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-4a/fig-4a}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-4b/fig-4b}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-5a/fig-5a}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/fig-5b/fig-5b}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

