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Chronic Total
Occlusions
A Guide to Recanalization
Third Edition

- V2
^Edited by
Ron Waksman Shigeru Saito

WILEY Blackwell
Chronic Total Occlusions
Chronic Total
Occlusions
A Guide to
Recanalization
T h i rd E d i t i o n

edited by

Ron Waksman
Section of Interventional Cardiology
MedStar Washington Hospital Center
Washington, DC, USA

Shigeru Saito
Heart Center, Cardiology & Catheterization Laboratories
Shonan Kamakura General Hospital
Kamakura City, Japan
This third edition first published 2024
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Library of Congress Cataloging-in-Publication Data
Names: Waksman, Ron, 1952 - editor. | Saito, Shigeru, 1950 - editor.
Title: Chronic total occlusions : A Guide to Recanalization / edited by Ron Waksman, MedStar
Washington Hospital Center, Washington, DC, USA, Shigeru Saito, Shonan Kamakura General
Hospital, Kamakura City, Japan.
Description: Third edition. | Hoboken, NJ : Wiley-Blackwell, 2024. | Includes bibliographical
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Subjects: LCSH: Coronary heart disease. | Arterial occlusions.
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 Contents
List of Contributors, vii
Foreword, x
Preface, xii
Part I Pathology, Indications, and Review
of Clinical Trials
1 The Pathobiology of CTO, 3
Gabby Elbaz-Greener & Bradley H. Strauss
2 Pathology of Chronic Total Occlusions:
Implications for Revascularization, 10
Takao Konishi, Ji Eun Park, Diljon S. Chahal &
Aloke V. Finn
3 Indications and Guidelines of PCI for CTO, 19
Ilan Merdler, Gabriel Maluenda & Ron Waksman
Part II Imaging
4 CT Angiography: Application in Chronic Total
Occlusions, 29
Hidehiko Hara, John R. Lesser, Nicholas Burke &
Robert S. Schwartz
5 IVUS-Guided Recanalization of CTO, 35
Etsuo Tsuchikane
6 Optical Coherence Tomography to Guide the
Treatment of Chronic Total Occlusions, 39
Francesca Maria Di Muro, Giulia Nardi, Niccolò
Ciardetti, Selcuk Kucukseymen, Alessio Mattesini
& Carlo Di Mario
Part III Wires Technology
7 New Coronary Guidewire Technology in Chronic
Total Occlusion Percutaneous Coronary
Interventions, 49
Salman Allana & Emmanouil S. Brilakis
8 Tornus Catheter, 64
Hideaki Kaneda
9 Microcatheters: Characteristics and Use, 69
John D. Hung & James C. Spratt
Part IV Wires Technique
10 CTO Wires: Engineering 101 and Principles of
Wire Manipulation, 83
Rahul Kurup & Luiz Fernando Ybarra
11 Use of Two Wires in the Treatment of CTO, 101
Thierry Lefèvre & Thomas Hovasse
12 Parallel-Wire Techniques, 109
Sudhir Rathore & Takahiko Suzuki
13 Transradial Approach for CTO Lesions, 115
Yutaka Tanaka & Shigeru Saito
14 Subintimal Angioplasty in Coronary CTO, 121
Negar Salehi, Philippe Généreux & George D.
Dangas
15 Antegrade Dissection and Re-Entry
Techniques, 129
Anbukarasi Maran, Carson Keck & Matthew
C. Evans
16 3D Wiring Methods in CTO PCI, 135
Atsunori Okamura
17 Antegrade Fenestration and Re-Entry: An
Alternative Approach to Antegrade Dissection
and Re-Entry, 156
Lorenzo Azzalini & Mauro Carlino
18 Retrograde CTO PCI: Step by Step, 166
Michael Megaly & Ashish Pershad
19 Retrograde CTO Intervention via Vein Grafts, 172
Pavan Reddy & Nelson L. Bernardo
v
vi  Contents
20 Tips and Tricks of the CART and Reverse
CART Technique, 177
Arber Kodra, Chad Kliger, Apurva Patel, Craig
Basman, Tak Kwan & Michael Kim
21 Debulking of CTO, 181
Etsuo Tsuchikane
22 Laser Revascularization in Coronary CTO, 186
On Topaz
23 How to Handle Subintimal Dissections, 203
Pratik B. Sandesara & William J. Nicholson
24 CTO: How to Minimize Contrast-Associated
Acute Kidney Injury, 218
Luis Gruberg
25 Mechanical Support for CTO, 232
Khaldoon Alaswad, Asaad Nakhle, Ankur Gupta,
Katherine J. Kunkel & Mir Babar Basir
26 Stent Grafts to Seal Coronary Perforation, 246
Jasleen Tiwana & Kathleen E. Kearney
27 Complications During Retrograde Approach
for CTO, 250
Yutaka Tanaka & Shigeru Saito
Part V Interesting Cases
28 Interesting Cases I–V, 257
Yutaka Tanaka & Shigeru Saito
Index, 263
 List of Contributors

Khaldoon Alaswad, MD, FACC, FSCAI Niccolò Ciardetti, MD

Henry Ford Hospital & Health System, Detroit, MI, USA Structural Interventional Cardiology
Wayne State University, Michigan, USA Department of Clinical and Experimental Medicine
Careggi University Hospital, Italy
Salman Allana, MD George D. Dangas, MD, PhD
Minneapolis Heart Institute and Minneapolis Heart
Mount Sinai Medical Center, New York, NY, USA;
Institute Foundation
Cardiovascular Research Foundation, New York, NY, USA
Minneapolis, MN, USA
Gabby Elbaz-Greener, MD
Lorenzo Azzalini, MD, PhD, MSc Department of Cardiology, Hadassah Medical Center &
Division of Cardiology The Faculty of Medicine, Hebrew University of Jerusalem
Department of Medicine, University of Washington Jerusalem, Israel
Seattle, WA, USA
Matthew C. Evans, MD
Mir Babar Basir, DO, FACC, FSCAI Medical University of South Carolina
Henry Ford Hospital Charleston, SC, USA
Detroit, MI, USA
Aloke V. Finn, MD
Craig Basman, MD CVPath Institute, Gaithersburg, MD, USA;
Department of Cardiology, Lenox Hill Hospital University of Maryland School of Medicine
New York, NY, USA Baltimore, MD, USA

Nelson L. Bernardo, MD Philippe Généreux, MD

Section of Interventional Cardiology
MedStar Washington Hospital Center
Washington, DC, USA
Emmanouil S. Brilakis,
Minneapolis Heart Institute and Minneapolis Heart
Institute Foundation
Minneapolis, MN, USA
Nicholas Burke, MD
Minneapolis Heart Institute and Foundation
Minneapolis, MN, USA
Mauro Carlino, MD, PhD, MSc
Division of Interventional Cardiology
Cardio-Thoracic-Vascular Department
San Raffaele Scientific Institute
Milan, Italy
Cardiovascular Research Foundation
New York, NY, USA
Luis Gruberg, MD, FACC
Mather Hospital
MD, PhD Donald and Barbara Zucker School of Medicine
New York, NY, USA
Ankur Gupta, MD, PhD
Piedmont Heart Institute
Atlanta, GA, USA
Hidehiko Hara, MD
Minneapolis Heart Institute and Foundation
Minneapolis, MN, USA
Thomas Hovasse, MD
Institut Cardiovasculaire Paris Sud (ICPS)
Massy, France

Diljon S. Chahal, MD
John D. Hung, MBChB, PhD, MRCP
Consultant Cardiologist, Liverpool Heart
University of Maryland School of Medicine
and Chest Hospital
Baltimore, MD, USA
Liverpool University Foundation Trust, UK

vii
viii  List of Contributors

Hideaki Kaneda, MD, PhD Anbukarasi Maran, MD

Okinaka Memorial Institute for Medical Research Medical University of South Carolina
Tokyo, Japan Charleston, SC, USA

Kathleen E. Kearney, MD Carlo Di Mario, MD, PhD, FESC, FACC,

University of Washington Medical Center FSCAI, FRCP
Seattle, WA, USA Structural Interventional Cardiology, Department of
Clinical and Experimental Medicine
Carson Keck, MD Careggi University Hospital, Italy
Medical University of South Carolina
Charleston, SC, USA Francesca Maria Di Muro, MD
Structural Interventional Cardiology, Department of
Michael Kim, MD Clinical and Experimental Medicine
Department of Cardiology, Lenox Hill Hospital Careggi University Hospital, Italy
New York, NY, USA
Alessio Mattesini, MD
Chad Kliger, MD Structural Interventional Cardiology, Department of
Lenox Hill Hospital/Northwell Health Clinical and Experimental Medicine, Careggi University
Hofstra School of Medicine, New York, NY, USA Hospital, Italy

Arber Kodra, MD
Department of Cardiology, Lenox Hill Hospital Michael Megaly, MD, MS
New York, NY, USA Willis Knighton Heart Institute, Shreveport, LA, USA

Takao Konishi, MD Ilan Merdler, MD, MHA

CVPath Institute, Gaithersburg, MD, USA MedStar Washington Hospital Center
Washington, DC, USA
Selcuk Kucukseymen, MD
Structural Interventional Cardiology Asaad Nakhle, MD
Department of Clinical and Experimental Medicine Henry Ford Hospital
Careggi University Hospital, Italy Detroit, MI, USA

Katherine J. Kunkel, MD Giulia Nardi, MD

HonorHealth Scottsdale Shea Medical Center Structural Interventional Cardiology
Scottsdale, AZ, USA Department of Clinical and Experimental Medicine
Careggi University Hospital, Florence, Italy
Rahul Kurup, MD, PhD
South West Sydney Local Health District (Campbelltown William J. Nicholson, MD
and Liverpool Hospitals) and Sydney Medical School Emory Heart and Vascular Center, Division of Cardiology
University of Sydney, NSW, Australia Department of Medicine, Emory University School of
Medicine, Atlanta, GA, USA
Tak Kwan, MD
Department of Cardiology, Lenox Hill Hospital Atsunori Okamura, MD
New York, NY, USA Cardiovascular Center, Sakurabashi Watanabe Hospital,
Osaka, Japan
Thierry Lefèvre, MD, FESC, FSCAI
Institut Cardiovasculaire Paris Sud (ICPS) Ji Eun Park, MD
Massy, France University of Maryland School of Medicine
Baltimore, MD, USA

John R. Lesser, MD
Minneapolis Heart Institute and Foundation Apurva Patel, MD
Minneapolis, MN, USA Department of Cardiology, Lenox Hill Hospital
New York, NY, USA

Gabriel Maluenda, MD Ashish Pershad, MD, MS

MedStar Washington Hospital Center Department of Interventional Cardiology
Washington, DC, USA Chandler Regional Medical Center, Gilbert, AZ, USA
 List of Contributors  ix

Sudhir Rathore, MD Bradley H. Strauss, MD, PhD

Frimley Health NHS Foundation Trust Schulich Heart Centre, Sunnybrook Health Sciences Centre
Surrey, UK University of Toronto, Toronto, ON, Canada

Pavan Reddy, MD Takahiko Suzuki, MD

Toyohashi Heart Centre, Toyohashi, Japan
Section of Interventional Cardiology
MedStar Washington Hospital Center
Washington, DC, USA
Yutaka Tanaka, MD, PhD
Shonan Kamakura General Hospital, Kamakura City, Japan

Shigeru Saito, MD, FACC, FSCAI, FJCC Jasleen Tiwana, MD

Heart Center, Cardiology & Catheterization Laboratories University of Washington Medical Center
Shonan Kamakura General Hospital Seattle, WA, USA
Kamakura city, Japan
On Topaz, MD, FACC, FACP, FSCAI
Negar Salehi, MD Professor of Medicine, Duke University School of Medicine
Mount Sinai Medical Center Durham, NC, USA
New York, NY, USA
Etsuo Tsuchikane, MD, PhD
Pratik B. Sandesara, MD Toyohashi Heart Center, Toyohashi, Japan
Emory Heart and Vascular Center, Division of Cardiology
Department of Medicine, Emory University School of Ron Waksman, MD, FACC
Medicine, Atlanta, GA, USA Section of Interventional Cardiology
MedStar Washington Hospital Center
Robert S. Schwartz, MD Washington, DC, USA
Minneapolis Heart Institute and Foundation
Minneapolis, MN, USA Luiz Fernando Ybarra, MD
London Health Sciences Centre, Schulich School of
James C. Spratt, MD, PhD Medicine & Dentistry, Western University, London, ON
Consultant Cardiologist, Professor of Interventional Canada
Cardiology, St George’s University Hospitals NHS
Foundation Trust, London, UK
 Foreword
Welcome to the world of chronic total occlusion
(CTO) intervention, an exciting and rapidly evolving
field within interventional cardiology. This book is
the third edition within the last 14 years of the popular
Chronic Total Occlusions, a testimonial to the advance-
ment in the field and the interest of interventional car-
diologists to win the battle to safely and effectively
treat CTOs. The book continues to serve as a compre-
hensive guide for both novice and experienced practi-
tioners who seek to enhance their understanding and
skills in the management of CTOs.
The presence of CTOs was initially observed dur-
ing coronary angiography procedures in the mid-20th
century. In the early days of percutaneous coronary
intervention (PCI), CTOs were considered challeng-
ing to treat due to technical difficulties and lack of
suitable equipment and often were referred for surgi-
cal revascularization or medical treatment. However,
the interventional cardiologist was not satisfied with
these alternatives to PCI and strongly believed that
successful revascularization of CTOs can relieve
symptoms, improve cardiac function, and potentially
reduce the need for more invasive procedures like
coronary artery bypass grafting (CABG). Others
questioned the utility of reanalyzing CTO percutane-
ously and its impact on mortality and quality of life.
With the lack of definitive data from randomized
clinical trials, the debate was ongoing. But simultane-
ously skilled operators from around the globe, with
industry support, continued to advance the field and
reported several important breakthroughs through
the past three decades. Among these were the devel-
opment of specialized guidewires with improved flex-
ibility and penetration power, which allowed for more
successful attempts at crossing CTOs.
In the 1990s, the retrograde approach was intro-
duced in the US by Kahn and Hartzler, and in Japan by
the co-editor of this book, Dr. Saito. Navigating and
crossing the occlusion via native collaterals and saphe-
nous vein grafts expanded the possibilities for CTO
intervention and improved success rates. Finally, ded-
icated devices and tools were developed specifically
for crossing and treating these challenging lesions.
These devices include CTO-specific guidewires,
x
microcatheters, and specialized balloon catheters, as
well as devices and techniques to seal perforations.
With the advancement of techniques, devices, and
operator experience, the success rates of CTO inter-
ventions have significantly improved and now stand
in the high 90s success rate, with an acceptably low
rate of procedural complications.
A key to the success of the procedure is adequate
training courses – a dedicated CTO program within
the hospital. These programs comprise skilled inter-
ventional cardiologists who have extensive experience
in performing CTO interventions.
CTO interventions often require a multidiscipli-
nary approach involving collaboration among inter-
ventional cardiologists, imaging specialists, and
cardiac surgeons. A team-based approach ensures
comprehensive evaluation, appropriate patient selec-
tion, and optimal treatment strategies for CTO
patients.
To stay updated with the latest advancements and
techniques in CTO interventions, interventional car-
diologists in the USA participate in continuing medi-
cal education activities. These include conferences,
workshops, case discussions, and comprehensive text-
books, which provide opportunities to learn from
experts and share experiences with peers.
It is important to note that the future of CTO inter-
ventions is dynamic and subject to ongoing innova-
tion. These potential developments hold the promise
of further improving patient outcomes, expanding the
eligibility for CTO interventions, and reducing the
complexity and invasiveness of procedures.
Advancements in imaging techniques, such as the
integration of intravascular ultrasound and optical
coherence tomography to enhance lesion visualiza-
tion and guide treatment strategies, add to this bright
future. Furthermore, the development of novel devices
and tools, including bioresorbable scaffolds and drug-
eluting balloons, may further improve outcomes by
promoting vessel healing and reducing restenosis
rates.
Ongoing innovation in this field is expected to
drive these developments. Artificial intelligence (AI)
is poised to play a crucial role in improving CTO

interventions. AI algorithms can aid in lesion assess-
ment, procedural planning, and complication man-
agement, offering real-time decision support and
enhancing procedural precision.
The third edition of this comprehensive CTO inter-
vention guide aims to provide an in-depth exploration
of the principles, techniques, and tools employed in
the field. Leading experts from around the world have
contributed their knowledge and experience to create
a resource encompassing the entire spectrum of CTO
management. From fundamental physiology and
lesion assessment to procedural planning, equipment
selection, and complication management, each chap-
ter delves into key aspects of CTO intervention,
emphasizing evidence-based practice and innovation
within the CTO community.
Our intent is not only to educate and empower
interventional cardiologists but also to foster a culture
of collaboration and innovation within the CTO com-
munity. In this book, you will find invaluable insights
and pearls of wisdom gained from years of clinical
practice and research. Additionally, we highlight the
importance of a multidisciplinary approach, acknowl-
edging the critical role of imaging specialists, nurses,
Foreword  xi
technicians, and other healthcare professionals in
optimizing patient outcomes.
I would like to extend my special thanks to Jason
Wermers for his guidance and assistance in the edito-
rial management process of this book. Dr. Saito and I
extend our deepest gratitude to all the contributors
who generously shared their expertise and experi-
ences, making this book a comprehensive and valua-
ble resource. We hope that it serves as a guide and
source of inspiration for healthcare professionals
worldwide who are dedicated to improving patient
care through the successful management CTOs.
Ron Waksman, MD, FESC,MSCAI, FACC
Professor of Medicine (Cardiology),
Georgetown University
Associate Director, Cardiology
Director, Cardiovascular Research and
Advanced Education
MedStar Heart and Vascular Institute
MedStar Washington Hospital Center
Washington, DC,
USA
 Preface
The first therapeutic PCI was performed by Dr.
Gruentzig in 1981. The basic idea was to widen a sten-
otic lesion in a coronary artery by balloon dilation.
The key concept at this time was to guide the burst-
resistant balloon to the lesion site, preceded by a deli-
cate atraumatic guidewire. The structure of PCI
balloon catheter consists of several small parts, which
is considered both feasible and best in the current
technology at the time.
The complex procedure of PCI is first broken down
into its component and functional parts. Then, the
aggregate of the parts performs the necessary actions
on the stenotic lesion to achieve a good overall result.
This concept of first breaking it down into parts and
then examining the results as an aggregate of parts is
very important. Smaller units of functional parts are
easier to improve and bring new functionality to. PCI
for chronic total occlusions has also become easier
with the use of improved combinations of functional
components.
The first time I personally performed PCI for a
chronic total occlusion was in 1985 or 1986. The
patient was a man in his 50s suffering from exer-
tional angina pectoris due to a chronic totally
occluded lesion in his right coronary artery. I
reported at an academic conference that I had reo-
pened this patient using a Hartzler LPS (ACS) bal-
loon (2.0 mm), and that six months later, the patient
was still good on angiography. To my surprise, one
of the leading PCI operators at the time stood up
and said, “One-vessel occlusion of the right coro-
nary artery does not affect the prognosis in any
way, and unnecessary PCI is unacceptable”. At that
time, Dr. Gerald Dorros (who was active in
Milwaukee at that time), who was invited to the
conference at that time, stood up and said in front
of everyone, “A young doctor is presenting such a
wonderful treatment, and it is unacceptable for a
xii
doctor not to recognize it.” This was the moment
when I embarked on the long road of PCI for
chronic total occlusion. Looking back, the success
of the PCI of the right coronary CTO at that time
was because I could use a Hartzler LPS balloon
catheter. And what I have learnt from this experi-
ences is that, before opening the door for a new
world, there will be many obstacles, and we have to
overcome them.
At that time, PCI for CTO was performed using
only antegradde approach without contralateral dye
injection. However, as the technique was limited to
that, the success rate was slow to improve even with
the evolution of balloons and wires.
This situation was broken in the 1990s with the
introduction of wires with improved torque control
and penetrating power, the importance of contralat-
eral dye injection was emphasized. Although the
introduction of Intravascular ultrasound (IVUS) in
antegrade approach improved the success rate, the
wire was advanced into the false lumen and could not
enter in the true lumen.
In the 2000s, the retrograde approach was started,
and wires and various devices have been developed to
make this approach easier. With the introduction of
the retrograde approach, more complex CTO lesions
were confronted with PCI than ever before. In the
2010s, Complex high-risk indicated percutaneous
coronary interventions (CHIP-PCI) were started. PCI
for CTO has thus evolved significantly due to (1) tech-
nical developments of operators, (2) introduction of
more sophisticated and advanced devices, and (3)
improved patient’s management strategies This book
documents everything of PCI for CTO from the past
to the future.
Shigeru Saito, MD,
Shonan Kamakura General Hospital.
I PA R T I

Pathology,
Indications, and
Review of Clinical
Trials
 1 CHAPTER 1

The Pathobiology of CTO

Gabby Elbaz-Greener1 & Bradley H. Strauss2,*
1
Department of Cardiology, Hadassah Medical Center & The Faculty of Medicine,
Hebrew University of Jerusalem, Jerusalem, Israel
2
Schulich Heart Centre, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada
* Corresponding author

Introduction “chronic occlusions” in the lower legs [6], (2) Hard

Chronic total occlusions (CTO) are defined by an
occlusion age of 3 months or greater, with angio-
graphic thrombolysis in myocardial infarction (TIMI)
flow grade 0 or 1 [1]. Our current understanding of
CTO development is based on a limited number of
autopsy specimens, imaging studies, and animal CTO
models. CTO constitute the most challenging lesions
in interventional challenge due to the complexity of
the composition and the geometric issues, such as
CTO entry/exit and the overall occlusion length. In
recent years, additional unique features in specific
types of CTO, such as occluded native arteries in
patients with bypass surgery and stent CTO have been
identified. The challenges of CTO PCI have been the
impetus for developing unique interventional equip-
ment and strategies, and innovative biologic manipu-
lations [2, 3].
Human coronary CTO studies
Our current understanding of human coronary
CTO pathology is based on a small number of
autopsy studies. Srivatsa et al. [4, 5] classified angio-
graphic CTOs in 61 patients according to the age of
the occlusions (<1 year vs ≥1 year). The main points
were: (1) Angiographic occlusion did not necessarily
mean histologic occlusion, with 25% of cases demon-
strating antegrade continuity and subtotal occlusion
(90–95% obstructed). Severe, but not completely
obstructive narrowing, may limit contrast reagent
penetration into lesions and thereby overestimate
the difficulty of a successful guidewire crossing.
This was particularly shown in peripheral arterial
fibrocalcific plaques are a common feature in all
CTOs regardless of age, but there is a definite increase
in harder plaques in older CTOs, while softer (mainly
lipid and loose fibrous tissue) plaques are more likely
to be present in CTOs <1 year old, and (3)
Recanalization of the CTO intimal plaques by neo-
vascular channels was commonly observed at all time
periods, particularly around prominent collections
of inflammatory cells (lymphocytes and macro-
phages) [7] (Figures 1.1A, 1.1B; Figures 1.2A, 1.2B).
Katsuragawa et al. [8] examined autopsy specimens
of 10 patients with CTOs, all presumed to be >1 year
old. They reported similar findings, namely loose and
dense fibrous tissue, atheroma, small recanalization
channels, calcification and inflammatory cellular
infiltrates, but no fresh thrombus (Figures 1.1A, 1.1B).
Small recanalization channels, which traversed the
CTO in 4 cases, were correlated with the angiographic
appearance of a tapering entrance into the CTO, a
well-known favorable sign for successful guidewire
crossing [9]. Thus, there is a histologic basis for the
presence of softer tissue components and recanalization
channels with higher angiographic success rates in
guidewire crossing, most frequently evident in CTOs
<1-year duration [5].
Recently, additional histology has been published
for two specific CTO clinical situations: post bypass
and stented coronary lesions.
(1) CTOs in patients with coronary artery bypass
graft:
The Canadian CTO Registry reported that > 50% of
patients with previous bypass surgery undergoing
coronary angiography had a native artery CTO [10].
In fact, the strongest clinical predictor for coronary

Chronic Total Occlusions: A Guide to Recanalization, Third Edition. Edited by Ron Waksman and Shigeru Saito.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
3
4  PA R T I Pathology, Indications, and Review of Clinical Trials
Ca Ca
MV
Necrotic
Figure 1.1A Hematoxylin-eosin stained human coronary
CTO, demonstrating extensive collagen-rich fibrous tissue,
several patches of calcification (Ca), two small microvessels
(MV), and a large necrotic area (necrotic). (Courtesy of Dr.
Jagdish Butany, University Health Network, Toronto, ON,
Canada.)
M
MV
Ca
Ca
MV
Figure 1.1B Elastin-trichrome stained human coronary
CTO, demonstrating fibrous tissue (lighter staining
material inside the lumen), with two distinct areas of
calcification (Ca) and two microvessels (MV). M = media.
(Courtesy of Dr. Jagdish Butany, University Health
Network, Toronto, ON, Canada.)
CTO formation is coronary artery bypass grafting
[11]. Angiographic follow-up at one year post coro-
nary artery bypass grafting demonstrated ≥1 new
native coronary artery CTO in almost half of the
patients. In 7.5% of patients, the native artery and
the graft supplying that territory were both occluded.
In particular, a pre-operative proximal stenosis
>90% identified the highest risk for a subsequent
new CTO. New native artery CTO post bypass had
long-term prognostic significance: 21% of these
cases had died or experienced nonfatal myocardial
infarction or repeated revascularization at a mean of
7.2 years [12].
Sakakura et al. reported on histologic differ-
ences in 95 CTOs in patients with and without
prior coronary artery bypass grafts (CABG) [13].
In this study, short CTO duration was defined by
histology (rather than actual timing), based on
organizing thrombi (fibrin) and proteoglycan-rich
extracellular matrix, particularly in the middle
of the CTO segment (Figure 1.1A). Longer dura-
tion (non-bypassed) CTOs in contrast demon-
strated more complex features: mainly collagen
1 deposition and moderate calcification (Figure
1.1B). CTOs with bypass grafts were characterized
by the heaviest calcification (including the adja-
cent proximal and distal segments) (Figure 1.2C).
Negative remodeling, defined as reduction in the
CTO vessel cross-sectional area relative to the adja-
cent proximal segment, was least in CTO sections
containing organizing thrombus, followed by cal-
cified sections and proteoglycan-rich thrombus
sections, but highest in non-calcified CTO sections
with collagen type I [13]. This predilection for heavy
calcification likely explains the clinical experience of
lowest PCI success rates in CTOs which have been
previously bypassed [14, 15]. Although bypass sur-
gery is well recognized as the superior revasculari-
zation strategy in patients with high SYNTAX score
and multivessel disease, there is also a downside of
iatrogenic CTO formation, ultimately creating the
most technically challenging CTOs for percuta-
neous revascularization, and a pool of no-option,
symptomatic patients.
(2) CTOs in Bare Metal versus Drug Eluting Stents:
In-stent occlusion accounts for approximately 12%
of all coronary occlusion interventions [16, 17]. The
characteristics of chronic stent occlusion (> 3
months post implantation) were described in a
detailed pathological analysis of a series of 56 stent
occlusions (both bare metal stents [BMS] and drug
eluting stent [DES], mainly first generation) [18].
The 5 most common etiologies in order of fre-
quency were (1) acute thrombotic occlusion (>50%
of cases), (2) restenosis (>20%, mainly in BMS
cases), (3) neoatherosclerosis rupture (10%), and
very infrequently, calcified nodules and hypersensi-
tivity reactions. The timing of stent occlusion

relative to stent implantation was 2 years for acute
thrombotic, 4.5 years for restenosis and 7.4 years for
neoatherosclerosis. The contributing factor most fre-
quently identified was a medial tear (60% of cases),
potentially indicative of more aggressive stent siz-
ing. Less frequently, protrusion of a necrotic core,
overlapping stents, bifurcation stenting, and stent
fracture with complete disruption were also recog-
nized. Neoatherosclerosis (foamy macrophages,
necrotic core) was present in 25% of these stent
CTO, but neointimal calcification was rarely pre-
sent, despite a high prevalence of patients with
diabetes and renal failure (Figure 1.2D). These find-
ings highlight a number of differences between de-
novo and stented coronary CTO.
Current paradigm of CTO evolution
The development of CTOs includes several specific
stages with unique histologic characteristics pre-
sent at each stage. The initial acute event leading
to the development of a CTO is in many cases a
ruptured atherosclerotic plaque with bidirectional
thrombus formation [7]. Clinically the arterial
occlusion may develop insidiously with minimal
symptoms or may present as an acute coronary syn-
drome. In patients with minimal or no symptoms,
the timing of the occlusive event cannot be clearly
identified. In fact, the age of approximately 60%
of CTO cases cannot be reliably dated by symp-
toms [10]. In patients with ST segment elevation
myocardial infarction (STEMI) not treated with
reperfusion therapy, an occluded infarct related
artery has been found in 87% of patients within
4 hours, in 65% within 12–24 hours, and in 45%
at 1 month [19, 20]. Up to 30% of patients treated
with thrombolytic therapy alone have a chroni-
cally occluded artery 3–6 months after MI [21]. In
patients treated with percutaneous coronary inter-
vention (PCI) during evolving acute myocardial
infarction (AMI), approximately 6–11% will have
chronic occlusion of an infarct related artery at 6
months, due to either initial treatment failure or
late re-occlusion [22].
Characterization of CTO development in human
studies is problematic since CTOs are often diagnosed
at a very late stage, and data regarding initial stages
in their evolution is lacking. Several animal models,
particularly rabbit and swine, have been developed
to systematically define the development stages of a
CTO [10, 23]. However, these models have certain
characteristics that could potentially limit their rele-
vance to humans, such as non-coronary location, and
C hapter 1 The Pathobiology of CTO 5
the lack of an underlying atherosclerotic substrate or
significant calcification.
Development of CTOs
Acute arterial occlusion due to atherosclerotic
plaque rupture with thrombus formation is likely
a common initiating event, which then triggers an
inflammatory reaction. In a rabbit CTO model,
the freshly formed thrombus contains platelets and
erythrocytes within a fibrin mesh, which is followed
by an invasion of acute inflammatory cells [24].
This early acute inflammatory response (initial
2 weeks) is accompanied by patchy formation of
a proteolycan-enriched extracellular matrix and
myofibroblast infiltration into the thrombotic
occlusion. At the initial part of the intermediate
stage (6 weeks), there is marked negative arterial
remodeling and disruption of the internal elastic
lamina accompanied by intense intraluminal neo-
vascularization and increased CTO ­perfusion. Total
microvessel cross-sectional area increases 2-fold,
along with a nearly 3-fold increase in the size of
individual intraluminal vessels.
However, by 12 weeks, there is a reduction in both
microvessel formation and CTO perfusion, with
further declines at the advanced stage (18–24 weeks).
This progressive decrease in the CTO perfusion coin-
cides with gradual replacement of proteoglycans by
collagen in the extracellular matrix. Human studies
have shown collagen and calcium accumulation char-
acterize the later stages of CTO maturation (Figures
1.1 and 1.2). The density of the fibrocalcific tissue is
highest at the proximal and distal ends of the lesion
compared to the body. Thus, the tissue components
of the CTO evolve over time with remarkable spatial
variability along the length of the CTO. From a
pathobiology standpoint, three specific regions of the
CTO have been proposed:
(1) The proximal fibrous cap is a thickened struc-
ture at the entrance (the proximal end) of the CTO
containing particularly densely packed collagen. It
usually contains types I, III, V, and VI of collagen.
Type IV collagen has also been observed in calcified
tissues [25]. This region represents a distinct physical
barrier to crossing into the CTO.
(2) The distal fibrous cap also contains densely
packed collagen, but is commonly regarded (although
not proven in studies) as a thinner and softer struc-
ture compared to the proximal cap. This has been part
of the rationale for developing the retrograde
approach to cross the CTO.
6  PA R T I Pathology, Indications, and Review of Clinical Trials
(3) The main body of CTO.
As mentioned earlier, human coronary artery autopsy
studies [4, 5, 8] have shown that the lumen of the
CTO in some cases contains organized thrombus.
Recanalization channels were observed in nearly 60%
of lesions. Unlike the preclinical rabbit femoral artery
model, the frequency of lumen recanalization and
sizes of the channels were similar in different CTO
ages. The intimal plaques within the CTO contained
collagen, calcium, elastin, cholesterol clefts, foam
cells, giant cell atherophagocytes, mononuclear cells
(lymphocytes, monocytes), and red blood cells. “Soft”
or cholesterol-laden lesions were more prevalent in
younger CTOs age (< 1 year); the amount of choles-
terol-laden and foam cells declined with advancing
CTO age. Older age CTOs typically contained hard
fibrocalcific lesions (“hard plaque”).
Extensive recanalization of the intimal plaques by
neovascular channels was frequently evident, partic-
ularly within and adjacent to the sites infiltrated by
inflammatory cells (lymphocytes and macrophages). In
some cases, intimal neovascular channels directly com-
municate with adventitial vasa vasorum. Neovascular
channels were also observed in the vascular medial
layer; the extent of medial neovascularization was pro-
portional to the cellular ­inflammation in the intimal
plaque. The adventitia of the vessel is usually exten-
sively revascularized in CTOs of all ages. Again, the
extent of adventitial neovascularization is correlated
to adventitial cellular inflammation. Munce et al. have
shown peripheral artery CTO model in a rabbit that
a large rise in extravascular vessels surrounding the
occluded artery occurred at early time points, which
was followed by a significant increase in intravascular
vessels within the central body of the occlusion [26].
The temporal and geographic pattern of microvessel
formation and the presence of connecting microves-
sels support the thesis that the extravascular vessels
may indeed initiate formation of the intravascular
channels within the center of the occlusion. However,
as the CTO matures beyond 6 weeks, a reduction in
the size and number of central intravascular micro-
channels was demonstrated, suggesting that many of
the vessels in this region become nonfunctional [26].
Intraluminal microvessel formation
(“Recanalization Channels”)
These microvessels generally range in size from 100 to
200 µm, but can be as large as 500 µm [5]. In contrast
to the vasa vasorum which run in radial direction,
these intimal microvessels run within and parallel to
the thrombosed parent vessel [27], and therefore have
particular relevance for crossing of CTOs as a pathway
for guidewire crossing.
Calcification
Calcification, a major predictor of procedure failure
[28–30], seems to be particularly determined
by coronary occlusion duration. In short dura-
tion coronary occlusions (≤3 months), intimal
plaque calcification was present in 54% of coro-
nary occlusions, but reached 100% in CTO of
>5 years duration [5] (Figure 1.2C). In contrast,
insulin-dependent diabetes mellitus was more fre-
quently observed in patients with predominantly
cholesterol laden or mixed CTOs than in those
with fibrocalcific CTOs [5].
Calcification changes range from crystal formation
to tissue that is histomorphologically indistinguish-
able from bone. Calcification is correlated with chronic
kidney disease, diabetes mellitus, and is a consequence
of aging. Our understanding of the balance between
promotion and inhibition of calcification in the CTO
is much more limited.
The process of the CTO calcification is usually sim-
plified into two mechanisms:
(1) Passive process: This requires high concentrations
of tissue calcium and phosphate but is recognized as a
regulated process [31–34]. It was initially considered
that calcium precipitation occurred when apoptotic
cell fragments and cholesterol crystals served as a
crystallization nidus and the calcium and phosphate
concentration approached the salt solubility product
in the presence of a lower concentration of local cal-
cium-chelating molecules. The formation of hydroxy-
apatite crystals in this way is now regarded as a
semi-regulated process, and the high phosphate levels
might induce vascular smooth muscle cells to differ-
entiate into an osteoblastic phenotype resulting in
bone formation.
(2) Active osseous process: This requires recruit-
ment of osteoblasts and osteoclast-like cells into the
atherosclerotic plaque. This process can be triggered
by immunomodulating cytokines, causing local
production of ossification factors such as BMP-2
[34–36], culminating in producing extra osseous
bone tissue inside the media and lumen of CTO.
Similar to skeletal bone, these bone/cartilage-like
structures are subject to resorption by osteoclast-
like cells.

Collagen Calcium Proteoglycan Fibrin
Figure 1.2 CTO pathology variability: longitudinal
arterial section with CTO cross-section.
A. CTO<1 year: Proteoglycan-enriched tissue with
abundant microvessels near center of CTO, surrounded by
recently formed collagen.
B. CTO>1 year: Dense fibrosis tissue, predominantly
collagen, with a few microvessels. Prominent negative
remodeling in the occluded segment relative to adjacent,
non-occluded segment.
C. Calcified CTO: Particularly common in long-standing
CTOs in previous bypassed arteries. Collagen and heavy
calcification are evident throughout, with calcification
Summary
In this chapter we have summarized the key compo-
nents of CTOs and suggested an impact of each on
C hapter 1 The Pathobiology of CTO 7
A. CTO <1 year
B.CTO >1 year
C. Calcified CTO
D. In-stent CTO
Cholesterol Plaque Microvessels
particularly evident in the deeper vessel layers.
Atherosclerotic plaques with necrotic core are present at
the periphery of artery.
D. In-stent CTO: Small rim of proteoglycan-enriched tissue
and microvessels located within the most inner layer of
the CTO. Dense surrounding collagen is main constituent,
both inside and outside stent struts. Cholesterol plaques
also present in deeper vessel layers outside the stent
struts. Fibrin deposits may be present around the stent
struts and occasionally in center of CTO. The medial layer
is compressed by stent struts.
guidewire crossing. Better understanding of the CTO
structure incorporating the imaging techniques with
advances in guidewires and other plaque modifica-
tion strategies may enable significant improvements
8  PA R T I Pathology, Indications, and Review of Clinical Trials
in CTO revascularization. The pathophysiology of
collagen accumulation and calcification in CTO is
now at the frontier of CTO translational to clinical
research. A biologic approach using locally delivered
collagenase to target matrix collagen within CTOs
to enhance guidewire crossing successes with softer
guidewires has encouraging results in initial clinical
trials [2, 3, 37]. These efforts will hopefully contribute
to higher CTO revascularization success rates and a
wider application of percutaneous revascularization
for appropriate cases in the near future.
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 2 CHAPTER 2
Pathology of Chronic Total
Occlusions: Implications for
Revascularization
Takao Konishi1, Ji Eun Park2, Diljon S. Chahal2 &
Aloke V. Finn1,2,*
1
CVPath Institute, Gaithersburg, MD, USA
2
University of Maryland School of Medicine Baltimore, MD, USA
* Corresponding author
Introduction
Chronic total occlusions (CTO) are commonly
observed in daily coronary angiography (CAG),
occurring in 18–31 % of patients with significant
coronary artery disease (CAD) undergoing CAG
[1, 2]. Percutaneous coronary intervention (PCI)
of CTOs remains challenging, with lower success
rates and higher rates of restenosis, as compared to
non-occluded lesions [3, 4]. New techniques,
device-based innovations, increasing operator
experience, and an algorithmic approach has led to
increased success rates with CTO-PCI, with
current success rates approaching 85–94 % in
experienced centers [5, 6]. Incomplete revasculari-
zation for CTOs is associated with higher rates of
death and worse major adverse cardiac events as
compared to complete revascularization in patients
with multivessel coronary artery disease [3, 4, 7].
Understanding the pathology of CTOs can be use-
ful for the CTO-PCI strategy and planning, which
can facilitate the increased success of CTO-PCI. In
this chapter, we will explore the pathological find-
ings of CTOs as they may pertain to successful
procedural outcomes.
Chronic Total Occlusions: A Guide to Recanalization, Third Edition. Edited by Ron Waksman and Shigeru Saito.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
10
Histopathology of chronic total
occlusions, with and without prior
coronary artery bypass grafts
Chronic total occlusions are composed of atheroscle-
rotic and/or thrombotic components that can be com-
posed of multiple layers of different tissues.
Angiographic total occlusions are not always consis-
tent with histologic total occlusions, with one study
showing that only 22 % of all angiographic CTOs cor-
related to a 100 % occlusion on histopathology [8].
This is probably expected given the superior resolu-
tion of histopathology compared to angiography.
In a previous report, we defined CTOs pathologi-
cally as lesions where the lumen area was occupied by
proteoglycan and/or collagen with or without neo-
vascularization and chronic inflammation [9].The
long-duration CTO (LD-CTO) was defined as a
lesion that has a matrix consisting predominantly of
collagen without fibrin in any section of CTOs. The
short-duration CTO (SD-CTO) was defined as a
lesion that has a matrix consisting predominantly of
proteoglycan with fibrin. The pathological character-
istics of the LD-CTO and the SD-CTO are compared
in Figure 2.1 [10].
 C hapter 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 11
Long-duration CTO
(A)
1.0 mm
(B)
500 µm
Figure 2.1 Representative images of long-duration CTO and
short-duration CTO without coronary artery bypass graft. (A
and C) Low-power images of long-duration and short-
duration CTO without coronary artery bypass graft. (B and D)
High-power images of boxed areas in (A) and (C), respectively.
Additionally, we classified CTOs into three groups:
(1) CTO with coronary artery bypass graft (CABG),
defined as having an arterial or venous bypass graft
anastomosed distal to the CTO with a duration over
2 years, (2) LD-CTO without previous CABG, (3)
SD-CTO without previous CABG (Figures 2.1 and
2.2) [10].Morphologically, CTOs with CABG and
SD-CTO tended to be located in the proximal seg-
ment of the artery, whereas only half of LD-CTOs
were located in the proximal vessel. A histologic
comparison of plaque components showed that
both the area of organized thrombus and of necrosis
were greatest in SD-CTO, f­ollowed by LD-CTO, and
CTO with CABG. In c­ ontrast, calcification area was
highest in CTO with CABG, ­followed by LD-CTO,
and SD-CTO. Arterial remodeling was evaluated
using remodeling index [ratio of the internal elastic
lamina (IEL) area in CTO divided by the largest IEL
area in one of the proximal reference sections]. The
Short-duration CTO
(C)
1.0 mm
(D)
500 µm
The matrix is predominantly composed of collagen type I in
(B). The matrix predominantly consists of proteoglycan and
fibrin in (D). CTO, chronic total occlusion. All sections are
stained by Movat Pentachrome. Reproduced with permission
from Sakakura et.al., 2014 / Oxford University Press.
r­emodeling index was the lowest (indicating neg-
ative remodeling) in LD-CTO, followed by CTO
with CABG, and SD-CTO. To summarize, CTOs
with CABG are characterized by c­alcified plaque
and moderate negative remodeling, while LD-CTOs
are characterized by severe negative remodeling and
moderate calcification (Figure 2.3). SD-CTOs are
characterized by abundant organizing thrombi and
necrotic cores, with the least negative remodeling.
These pathological differences between groups are
useful for stratifying the technical difficulty of CTO
lesions, which may aid in patient selection and stra-
tegic approaches to CTO PCI (Figure 2.3).
In addition, the lumen pattern was classified as
abrupt versus tapered, depending on the degree
of n­ arrowing prior to or after the occluded seg-
ment (Figure 2.4). Although there was no statistical
difference in the prevalence of the lumen pattern
between the groups, the abrupt pattern was more
12  PA R T I Pathology, Indications, and Review of Clinical Trials

Vein
Graft

RMB
PRC
P-1 CTO-1 CTO-2

MRC

DRC

CTO-4 CTO-5 CTO-6 CTO-7

PD

CTO-8 CTO-9 CTO-12 D-1

Figure 2.2 A representative case of chronic total occlusion
with coronary artery bypass graft. The radiograph (left)
shows severe calcification of the vein graft as well as a right
coronary artery. P-1 is a proximal segment, and D-1 is the
distal segment. Serial CTO images show severe calcification.
Note: Percent area calcification in CTO-1 is 70 % and CTO-5
shows five microchannels >200 mm in size. The proximal and
distal sections to CTO show 54 and 48 % area calcification,
respectively. CTO, chronic total occlusion; PRC, proximal
right coronary artery; MRC, middle right coronary artery;
RMB, right marginal branch; DRC, distal right coronary
artery; PD, posterior descending artery; P-1, proximal first
section; D-1, distal first section. Reproduced with permission
from Sakakura et.al., 2014 / Oxford University Press.

CTO with CABG LD-CTO SD-CTO

Cholesterol clefts

Necrotic core

Calcified plaque

Collagen

Fibrin

Healed thrombus

Angiogenesis

Negative remodeling ++ +++ −/+

Calcification +++ + / ++ −/+

Lesion difficulty in Most challenging Medium difficulty Least challenging

PCI

Figure 2.3 Lesion characteristics of three types of CTO
lesions. CTO with CABG lesions showed moderate negative
remodeling and severe calcification. LD-CTO is
characterized by collagen rich plaque with severe negative
remodeling and moderate calcification. SD-CTO is
characterized by organized thrombus and fibrin with less
negative remodeling and less calcification in the plaque.
In summary, CTO with CABG is considered the most
challenging lesions, followed by LD-CTO, and SD-CTO in PCI.
Adapted from Sakakura et al,2014.
 C hapter 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 13

(A) Abrupt Pattern Morphology

CTO segment

Proximal Distal
P-1 P-2 P-3 Proximal end of the CTO

P-1 P-2 P-3 CTO (proximal end)

(B) Tapered Pattern Morphology

CTO segment

Proximal Distal
P-1 P-2 P-3 Proximal end of the CTO

P-1 P-2 P-3 CTO (proximal end)

CTO segment

Proximal Distal
Distal end of the CTO D-1 D-2 D-3
CTO (distal end) D-1 D-2 D-3

NC

2.0 mm 2.0 mm 2.0 mm 2.0 mm

Figure 2.4 (A) Representative images of the abrupt
lumen pattern. Adjacent proximal segment and CTO
segment of mid-left anterior descending. Percent stenosis
in P-3, P-2, and P-1 is 71, 80, and 71 %, respectively, and
was assigned to the abrupt lumen pattern. (B)
Representative images of the tapered lumen pattern.
Upper panels: adjacent proximal segment and CTO
segment of mid-right coronary artery. Percent stenosis in
P-3, P-2, and P-1 is 70, 91, and 90 %, respectively; this case
was assigned as the tapered lumen pattern, because of
the gradual opening of the lumen. Lower panels: the
adjacent distal segment and CTO segment of mid-left
anterior descending. Percent stenosis in D-3, D-2, and D-1
is 85, 91, and 95 %, respectively; this case was assigned as
the tapered lumen pattern because of the gradual
opening of the lumen. CTO, chronic total occlusion.
Reproduced with permission from Sakakura et.al., 2014 /
Oxford University Press.

frequently seen in the proximal lumen of the CTO, Pathology of in-stent chronic total
compared with the distal lumen, which may explain occlusion and its difference from
the recent increase in procedural success with the native CTO
retrograde approach which may be more fruit-
In-stent chronic total occlusions (IS-CTO) are also
ful in cases of proximal versus distal lumen occlu-
not uncommonly observed in PCI. The prevalence
sion. Microchannels over 200µm in diameter were
of IS-CTO is estimated to be 5–13 % of all CTOs
rarely observed in all three groups, which may
[12–14]. The major etiologies of IS-CTO are acute
nary guidewires with tapered tip diameters <0.014�
indicate more favorable CTO crossing with coro-
thrombotic occlusion, restenosis, and plaque rup-
ture from neoatherosclerosis [15].A representative
(360 uM) [11].
14  PA R T I Pathology, Indications, and Review of Clinical Trials
case study for each etiology of IS-CTO for bare
metal stent (BMS) and a drug-eluting stent (DES) is
depicted in Figures 2.5–2.7. The frequency of each
etiology of IS-CTO and the major contributing risk
factor for acute thrombotic occlusion are shown in
Figure 2.8. Acute thrombotic occlusion was the most
frequent cause of IS-CTO in both BMS (50 %) and
DES (67 %), with medial tear being the major con-
tributing risk factor for both BMS and DES (56 %
and 69 %, respectively). The second most frequent
cause was restenosis (31 % of BMS; 8 % of DES;
p=0.08). Plaque rupture from neoatherosclerosis was
seen in 9 % of BMS and 4 % of DES. Overall, neointi-
(A)
(B)
Figure 2.5 In-stent CTO due to acute thrombotic
occlusion. Serial cross-sections of BMS (A, a to c are from
the proximal segment, and d and e are from the distal
stent) and zotarolimus-eluting stent (B, a to e), and
corresponding radiographs (f) illustrating the site of the
sectioning, whereas high-power images are shown in g
to i. Both stents had been implanted for 2 years in 2
different patients. Organized thrombus is in direct
mal calcification was minimal in IS-CTO. However,
in BMS, neointimal calcification was observed in 3
lesions with in-stent neoatherosclerotic rupture and
one lesion involving an in-stent calcified nodule. In
the cases with etiologies of acute thrombotic occlu-
sion, restenosis, neointimal erosion, and hypersen-
sitivity, neointimal calcification were not observed.
Thus, it can be said that IS-CTOs differ from native
CTOs, especially in terms of intimal calcifica-
tion, which is seen more frequently in native CTO,
presumably due to a higher prevalence of acute
­
thrombotic occlusion in IS-CTO. In addition, there
was a tendency toward longer length of collagen
contact with the stent struts. Red arrows indicate the
extent of medial tear (in i in A and g to i in B). Black
arrow in h in A indicates persistent fibrin. (All sections
stained by Movat pentachrome.) Thr, organized
thrombus in A and organized and organizing thrombus
in B; BMS, bare-metal stent. Reproduced with permission
from Mori et.al., 2017 / American College of Cardiology
Foundation.
 C hapter 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 15
(A)
(B)
Figure 2.6 Restenosis. Cross-sectional histology of BMS (A)
implanted for 4 years and sirolimus-eluting stent (B)
implanted for 2 years in 2 different patients. Note the
in-stent region in both cases is predominantly occupied by
excessive neointimal formation. In a and g in A, the
neointima is rich in elastic tissue (white arrow) close to the
lumen (illustrated at high power in g) whereas the
peristrut region shows some angiogenesis (asterisk) (g);
whereas c and d show neointimal tissue rich in smooth
muscle cells and proteoglycans and collagen (high-power
and smooth muscle ­cell-rich tissue in the proximal
and distal fibrous caps of the BMS CTOs than in
DES. These findings suggest a similar approach to
IS-CTO as native CTO-PCI, with special attention
to BMS lesions, which may require stiffer wires than
DES lesions. This also suggests that DES when they
occlude may have delayed thrombus organization.
images shown in h and i). B shows restenotic sirolimus-
eluting stent. The lesion consists of smooth muscle cells in
a proteoglycan-rich matrix with interspersed fibrin (white
arrow in c). Total occlusion (defined by 99 % luminal
narrowing) is observed in section d and high-power
images of boxed areas in c and d are shown in g to i. (All
sections stained by Movat pentachrome.) BMS, bare-metal
stent; NI, neointima. Reproduced with permission from
Mori et.al., 2017 / American College of Cardiology
Foundation.
Clinical implications from a
pathological point of view
These histopathologic data suggest that CTOs with
previous CABG are likely the most challenging
lesions mainly because of the severe calcification,
compared to the other types of CTOs, including
16  PA R T I Pathology, Indications, and Review of Clinical Trials
(A)
(B)
Figure 2.7 Neoatherosclerotic rupture. Cross-sectional
histology of BMS (A) implanted for 8 years and paclitaxel-
eluting stent (PES) implanted for 5 years (B) in 2 different
patients. (A) The site of serial sections (a to e) are taken
from the proximal region of the stent as seen in the
radiograph in f. All serial sections in a–e show presence of
in-stent neoatherosclerosis. Note rupture site in c (see
arrow) and corresponding high-power images in g to j. The
arrowhead in a points to the site of foamy macrophage
infiltration, which is highlighted in g, whereas necrotic core
(NC) is observed in b to e. Black arrow indicates rupture site
in c, i, and j. The lumen is occupied by a NC and calcified
(Ca++) plaque (c and i). An organized thrombus is observed
IS-CTO, when considering complete revasculariza-
tion by PCI. Clinically, the procedural success rate
of CTO PCI is lower in patients with prior CABG,
compared to patients without prior CABG [16, 17].
Azzalini et al. showed that the procedural success was
lower in patients who had undergone CABG (81 % vs
87 %; P = 0.001) [16],and Tajti et al. showed that prior
CABG patients had lower procedural success (82 %
in the lumen in c, i, and j. (B) Serial sections (a to e) are
taken from distal portion of PES, shown in the radiograph
in f. Note IS-neoatherosclerosis is observed in b and c.
A necrotic core with a thin cap (arrow) is shown at high
power in g, which is highlighted from boxed area in b.
Similarly, the boxed area from c is shown at high power in h
and highlights the rupture site of the necrotic core with
overlying thrombus (Thr). Neointimal calcification (Ca++)
around stent struts is observed in a to e and can be
appreciated at high power in i. (All sections stained by
Movat pentachrome.) BMS, bare-metal stent. Reproduced
with permission from Mori et.al., 2017 / American College
of Cardiology Foundation.
versus 87 %, P<0.001) [17].This is probably because
of lesion calcification and negative remodeling, which
have been previously associated with higher incidence
of CTO PCI failure [17, 18] and are frequently seen
in CTOs with CABG [10].LD-CTOs are character-
ized by severe negative remodeling and moderate
­calcification, which increase the complexity of PCI.
SD-CTOs are characterized by abundant organizing
 C hapter 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 17

Etiology of In-stent CTO Major Contributing Risk Factor

In-stent Calcified In Acute Thrombotic Occlusion
Edge disease nodule
6% 3%
Neoatherosclerotic Overlapping
rupture 6%
9%
Protrusion of
necrotic core
6%
Medial tear
BMS(n=32) Acute thrombotic 56% Bifurcation
occlusion 50% 19%
Restenosis
31%

Protrusion of
Calcified nodule
Malapposition 6%
6%
P=0.13 P=0.11

Edge disease
4%

Neointimal
erosion
Medial tear
8%
69%

DES(n=24) Hypersensitivity Acute thrombotic

8% occlusion 67%

Neoatherosclerotic
rupture
Overlapping
4%
13%
Restenosis
8% Protrusion of
necrotic core
19%

Figure 2.8 The frequency of each etiology for IS-CTO and
the major contributing risk factor for acute thrombotic
occlusion. Pie chart on the left illustrates the etiology of
in-stent CTO (upper BMS, lower DES), and the pie charts
on the right illustrate the major contributing risk factor
for acute thrombotic occlusion. There were more frequent
acute thrombotic occlusion lesions in DES versus BMS,
whereas restenosis was a more frequent cause of CTO in
BMS versus DES. All other causes were observed in <10 %
of lesions, and the differences did not reach significance.
BMS, bare-metal stent; CTO, chronic total occlusion; DES,
drug-eluting stent.

thrombi and necrotic cores, and the least negative Conclusions

remodeling and calcification. SD-CTOs should be
The detailed understanding of pathological char-
attempted via the antegrade approach because the
acteristics of CTOs can be useful for the proce-
components of such lesions are loose tissue and easier
dural success of CTO-PCI. There are several
to penetrate (Figure 2.3). Since the major etiology
differences between the types of CTO lesions in
of IS-CTO is thrombotic occlusion (Figure 2.8), an
terms of plaque morphologic characteristics,
antegrade approach using direction-controlled wir-
including thrombotic and calcific components,
ing technique can be effective. Because the abrupt
which can be affected by the presence of coronary
lumen pattern was more frequently observed in the
artery bypass grafts, or bare metal versus drug-
proximal lumen, compared to the distal lumen in
eluting stents. This in turn can influence the PCI
CTOs, switching the strategy from the antegrade
strategies used. Furthermore, an abrupt pattern in
approach to the retrograde approach when progress
the proximal lumen and tapered pattern in the
is not made using antegrade approach may facilitate
distal lumen may indicate a favorable retrograde
crossing. Careful review of angiography and coronary
approach to crossing for CTO-PCI. Further
computed tomography, with intravascular imaging
research into the pathological correlates to CTO-
when necessary, is important to predict the compo-
PCI will hopefully continue to lead to higher pro-
nents of plaque in CTOs to aid in determining lesion
cedural success rates.
complexity and strategy to facilitate crossing.
18  PA R T I Pathology, Indications, and Review of Clinical Trials
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 3 CHAPTER 3

Indications and Guidelines

of PCI for CTO
Ilan Merdler, Gabriel Maluenda & Ron Waksman*
MedStar Washington Hospital Center, Washington, DC, USA
* Corresponding author

Introduction Symptom relief

Chronic total occlusions (CTOs) are completely
occluded coronary arteries with no flow and an esti-
mated duration of at least 3 months. They are found in
about one-quarter of patients undergoing coronary
angiography [1, 2]. In recent years, CTO percutane-
ous coronary intervention (PCI) has seen the develop-
ment of enhanced techniques, along with greater
equipment and operator experience, and success rates
of 80% have been reported [3]. However, a 30-day
mortality rate of over 1% and an almost 5% rate of
perforations were also reported [4]. There are 7 widely
accepted principles [5] for CTO-PCI: ischemic symp-
tom improvement as the primary indication, in-depth
planning, microcatheters for optimal manipulation,
combination of antegrade and retrograde approaches,
efficient change of technique, specific CTO-PCI
expertise, and optimum stent expansion. In this chap-
ter, we will discuss the indications and guidelines of
CTO-PCI and the relevant evidence.
Outcome benefits associated with
CTO-PCI
Symptom improvement is the primary indication for
CTO-PCI. Two randomized control trials [6, 7]
(Table 3.1) and several observational trials [3] have
shown improvement in symptoms in these patients.
However, randomized trials have not succeeded in
demonstrating the efficacy of CTO revascularization
for hard endpoints such as mortality, myocardial
infarction, stroke, or heart failure [8]. Thus, the main
indication for CTO-PCI currently is symptom control.
Successful PCI of CTO has been associated with
important symptomatic relief when compared to
failed procedures. In the TOAST-GISE (Total
Occlusion Angioplasty Study-Societa Italiana di
Cardiologia Invasiva) multi-center study conducted
on 369 patients with CTOs > 30 days of duration,
patients with successful CTO-PCI were more fre-
quently free of angina (88.7%) compared to patients
who had an unsuccessful procedure (75%) at 1-year
follow-up (p = 0.008) [9]. The results of the FACTOR
trial (FlowCardia’s Approach to Chronic Total
Occlusion Recanalization), conducted in 125 patients
and based on the Seattle Angina Questionnaire (SAQ)
performed at baseline and 1 month after CTO-PCI,
showed that procedural success was independently
associated with angina relief (SAQ delta among
successful and unsuccessful PCI = 9.5 points,
­
p = 0.019), improved physical activity (SAQ delta
= 13.1 points, p = 0.001), and enhanced quality of life
(SAQ delta = 20.3 points, p < 0.001), which was
greater in symptomatic patients than in asymptomatic
patients [10]. The EuroCTO multicenter trial ran-
domly assigned 396 patients to CTO-PCI versus opti-
mal medical therapy alone. At 1 year, in comparison
with patients randomly assigned to medical therapy
only, CTO-PCI patients had greater improvement in
angina frequency (subscale change difference, 5.23;
95% CI, 1.75–8.71; P = 0.003) and quality of life (sub-
scale change difference, 6.62; 95% CI, 1.78–11.46;
P = 0.007), as assessed with the SAQ [6]. The
IMPACTOR-CTO trial (Impact on Inducible
Myocardial Ischemia of Percutaneous Coronary
Intervention versus Optimal Medical Therapy in

Chronic Total Occlusions: A Guide to Recanalization, Third Edition. Edited by Ron Waksman and Shigeru Saito.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
19
20  PA R T I Pathology, Indications, and Review of Clinical Trials
Table 3.1 Randomized controlled trials in CTO-PCI.
Study n Design CTO success %
DECISION- 834 Multicenter 91
CTO [11]
EuroCTO [6] 396 Multicenter 87
IMPACTOR- 72 Single Center 83
CTO [7]
EXPLORE [12] 304 Multicenter 73
REVASC [13] 205 Single Center 97
Patients with Right Coronary Artery Chronic Total
Occlusion) randomly assigned 94 patients (single
center) with isolated right coronary artery CTO to
CTO-PCI versus optimal medical therapy alone. At 1
year, patients undergoing CTO-PCI had a significant
reduction in ischemic burden and improvement in
6-minute walk distance and quality of life [7]. We
must also mention the randomized DECISION CTO
trial (Drug-Eluting Stent Implantation Versus
Optimal Medical Treatment in Patients with Chronic
Total Occlusion), which did not show an improve-
ment in symptoms for CTO-PCI patients [11].
Left ventricular function
In the past, studies examining changes in ejection
fraction (EF) after CTO-PCI have shown improve-
ment. Left ventricular (LV) angiogram follow-up per-
formed after 6 months of successful recanalization of
CTO in a series of 95 patients found that the EF
increased from 62% to 67% (p < 0.001). No changes in
EF were noted in 8 patients found to have re-occlusion
of the CTO at angiographic follow-up [14]. A sub-
study of 244 patients in the Total Occlusion Study of
Canada (TOSCA) who had ventriculograms at base-
line and at 6-month follow-up found a significant
improvement in EF over time (from 59% to 61%,
p = 0.003). In this series, multivariate analysis revealed
that baseline EF < 60%, duration of occlusion ≤ 6
weeks, and Canadian Cardiovascular Society (CCS)
angina class I or II were independently associated
with an improvement in EF after successful CTO-PCI
[15]. Other studies have suggested that patients who
have never had myocardial infarction (MI) or those
with evidence of residual ischemia or viable myocar-
dium after MI are most likely to benefit from CTO-
PCI [16–18]. In addition, Cheng et al. showed that
wall thickening of myocardium supported by a CTO
vessel improved after CTO-PCI based on a cardiac
magnetic resonance imaging study performed 6
months after successful PCI (from 55% to 68%) [19].
This evidence suggests that imaging techniques to
Follow-up Primary Endpoint Results
4 years Composite of death, MI, No Differences
stroke and revascularization (p = 0.86)
1 year Changes in symptoms Improvement (p = 0.007)
1 year Ischemia Burden Decrease (p < 0.01)
4 months Ejection Fraction on No differences (p = 0.6)
Cardiac MRI
1 year Changes in myocardial No differences (p = 0.57)
wall thickness
assess viability/ischemia may be particularly useful in
determining the role of CTO-PCI in patients with
decreased LV function.
However, newer randomized control studies such
as the EXPLORE trial have shown a different result.
Using cardiac MRI, the EXPLORE study showed no
advantages of CTO-PCI compared with drug treat-
ment at 4 months after the acute event [12].
Arrhythmic events and sudden cardiac
death
CTO of an infarct-related coronary artery has been
associated with higher risk of ventricular arrhythmia
[20]. In patients with CTO, low coronary blood flow
can theoretically create an arrhythmic substrate and
favor the occurrence of ventricular tachycardia. CTO
revascularization might restore blood flow in the area
close to the fibrotic scar and, thus, generate positive
remodeling and reduce ventricular arrhythmias. A
meta-analysis that assessed ventricular arrhythmias in
patients with CTO has shown that CTO is associated
with an increased risk of ventricular arrhythmia and
all-cause mortality [21]. However, not enough studies
are available to address the issue.
Reduction in need for CABG
Successful CTO-PCI appears to be associated with a
significant reduction in the need for surgical revascu-
larization. Freedom from coronary artery bypass
grafting (CABG) was significantly higher among the
317 patients at Emory with successful CTO-PCI at 4
years’ follow-up when compared to the 163 patients
with failed PCI (87% vs 64%, p < 0.0001) [22]. In the
TOAST-GISE study, patients with successful CTO-
PCI had a lower rate of CABG at 1-year follow-up
(2.5% vs 15.7%, p < 0.0001). Multivariate analysis
showed that the only characteristic associated with
event-free survival was CTO-PCI success or failure
[9]. In a 5-year follow-up of 1791 patients who under-
went CTO-PCI in 3 tertiary centers in the USA, South
Korea, and Italy, patients with successful CTO-PCI
 C hapter 3
had significantly lower rates of CABG compared to
patients with failed CTO-PCI (3.2% vs 13.3%, p <
0.001) [23]. Among 100 CTOs in patients with CCS
angina class III or IV despite medical therapy, 47 were
successfully recanalized, and only 7 (15%) underwent
CABG. Among the 45 patients with unsuccessful,
uncomplicated procedures, 16 (36%) surgeries were
required and, among the 8 patients with complicated
procedures, 3 (38%) required CABG [24].
Survival benefit
There is no agreement regarding survival benefit in
CTO-PCI patients. The DECISION-CTO trial, which
assessed all-cause mortality, MI, revascularization,
stroke, and major adverse cardiac events (MACE),
showed no advantages in the PCI group compared to
medical treatment alone [25]. This study excluded
patients with low EF who might have benefited from
PCI. Unlike this trial, data from several registries
showed an increase in survival among patients under-
going successful CTO-PCI [26, 27]. A meta-analysis of
25 studies (28,486 patients) showed that compared with
failed procedures, successful CTO-PCIs were associ-
ated with a lower incidence of death, stroke, and CABG
and less recurrent angina [28]. We must also mention
the REVASC study, which evaluated total mortality, MI,
and repeated revascularization, at 1 year. The CTO-PCI
group in the trial had a lower risk of MACE than the
group with medical therapy alone [13].
Predictors of CTO-PCI success
When considering a CTO-PCI, careful assessment of
the chances of success appears to be particularly impor-
tant, that is, balancing the risk and benefit ratio.
Although an experienced interventionalist may elect to
immediately pursue a CTO-PCI, strong consideration
should be given to deferring “ad hoc” PCI in this situa-
tion to allow for patient discussion and determination
of the appropriate strategy [29]. In this regard, known
clinical and angiographic predictors of CTO-PCI suc-
cess/failure must be carefully analyzed, in addition to
cardiac computed tomography (CT) when indicated.
Angiographic predictors
Several scores were created to estimate the difficulty
of CTO-PCI. The most commonly used is the J-CTO
score, which was created in Japan using a multicenter
registry. It estimates the likelihood of successful ante-
grade guidewire crossing within 30 minutes based on
5 criteria (at least 1 bend of >45° in the CTO entry or
CTO body, occlusion length >20 mm, calcification,
blunt proximal stump, and previously failed attempt)
[30]. This score was validated and is also associated
with 1-year clinical outcomes [31, 32].
Indications and Guidelines of PCI for CTO 21
Other scores include the PROGRESS-CTO score,
the RECHARGE (Registry of Crossboss and Hybrid
Procedures in France, the Netherlands, Belgium, and
United Kingdom) registry score, the CL-score
(Clinical and Lesion related score), the ORA (ostial
location, collateral filling of Rentrop <2, age >75)
score, the weighted angiographic scoring model
(W-CTO score), and the CASTLE score. There are
also cardiac CT angiography-based scores, such as the
CT-RECTOR multicenter registry (Computed
Tomography Registry of Chronic Total Occlusion
Revascularization) score and the Korean Multicenter
CTO CT Registry Score [33–39]. The scores are
mostly based on angiographic findings.
Clinical predictors
Duration of the occlusion appears to be one of the
most important predictors of procedural failure.
Generally speaking, the longer the occlusion dura-
tion, the less likely is recanalization success. Occlusion
duration longer than 3–6 months has been consist-
ently associated with procedural failure [9, 40].
Another important clinical factor that may impact the
ability to recanalize a CTO is the presence of chronic
renal failure, which predicts a worse procedural result
and significantly limits the amount of contrast used
during the intervention [41].
Tomographic predictors
Electrocardiogram-gated cardiac CT has proved to be a
very useful tool for planning CTO-PCI, allowing one to
predict the procedural success/failure likelihood, to pre-
vent possible complications, and to reduce procedural
time, the amount of contrast used, and radiation expo-
sure [42, 43]. Garcia-Garcia et al. identified the follow-
ing predictors for CTO-PCI failure by cardiac CT
performed in 142 patients: length of the occlusion
> 15 mm, severe calcification of the occluded segment,
and blunt-stump of the entry point, particularly if
severely calcified [43]. In addition, cardiac CT allows for
the evaluation of distal vessel characteristics, collateral
vessel distribution, degree of tortuosity of the occluded
segment, and prediction of the best angle for PCI
approach. Unfortunately, due to the amount of required
contrast and radiation associated with cardiac CT, its
use cannot be routinely recommended, but does appear
to be mandatory in patients with unfavorable angio-
graphic anatomy and/or with prior failed CTO-PCI [2].
CTO-PCI techniques – planning the
PCI strategy
Important advances in CTO-PCI technique, includ-
ing dedicated CTO wires, the use of support catheters,
the spread of drug-eluting stent technology, and the
22  PA R T I Pathology, Indications, and Review of Clinical Trials
development of special devices for the “retrograde”
approach, have permitted significant improvements
in CTO-PCI recanalization efficacy and safety.
Whenever collaterals are present, bilateral injections
are recommended to allow for simultaneous ante-
grade and retrograde filling of the target vessel.
General concepts on antegrade and
retrograde techniques
Generally, the antegrade approach is attempted first.
Tapered hydrophilic wires are initially used with the
intention of crossing though microchannels. If this
primary approach fails, progressive wire tip stiffness
should be tried (3–9 g wires) followed by tapered,
hydrophilic 9–20 g wires if this fails. If the wire is
advanced into the subintimal space, it should be left in
place at the time that a second similar wire is used
(“parallel wire” technique). If the second wire moves
subintimally, the first wire is pulled and an attempt to
cross (“see-saw wire” technique) is made [44]. The use
of a microcatheter, placed near the lesion, may be
helpful to increase the support and the penetration
power of the guidewire [5]. The retrograde approach
uses collateral channels to cross the CTO. Septal,
straight channels, with visible connection to the distal
vessel, are ideal for this approach. Atrial and epicar-
dial collaterals are potentially useful but are more pre-
disposed to dissection and perforation. Once the
collateral has been identified, selective injection must
be performed using microcatheters. If the collateral
channel appears to be suitable, a Corsair channel dila-
tor is advanced over the wire. Subsequently, different
techniques (including simple retrograde wire cross,
kissing wire cross, controlled antegrade, and retro-
grade tracking [CART] and reverse CART) can be
attempted to cross the distal CTO cap [45].
In-hospital outcomes using current
CTO-PCI techniques
Using contemporary techniques, the J-CTO Registry
reported a success rate of 88.6% in first-attempt cases in
528 treated CTO lesions of 498 patients [32]. These
results were achieved, however, with a median fluoros-
copy time of 45 minutes and a mean contrast volume of
293 ml. In addition, the frequency of perforation was
7.2% with antegrade approach and 13.6% with retro-
grade approach. Clinically significant tamponade was
seen in only 0.4% collectively [32]. The results of the
multi-center ERCTO (European Registry of Chronic
Total Occlusion) reported an overall success rate of
82.9% of 1983 treated CTO lesions in 1914 patients
(83.2% antegrade vs 64.5% retrograde, p < 0.001) [46].
These results were achieved, however, with a mean
fluoroscopy time of 42.3 minutes and a total contrast
volume of 313 ml. In addition, the frequency of perfo-
ration was 2.1% with antegrade approach and 4.7%
with retrograde approach. The tamponade rate was
only 0.5% [46]. Using techniques from Japan, a study
conducted in two US centers reported the outcomes of
636 consecutive patients undergoing CTO-PCI
between 2005 and 2008, comparing the results of high-
volume operators (>75 total CTO-PCI cases and > 20
retrograde attempts during the study period) to non-
high-volume operators. The overall technical success
was 58.9% for non-high-volume operators and 75.2%
for high-volume operators (p < 0.001) [47]. The techni-
cal success rate did not change for non-high-volume
operators, but for high-volume operators, it increased
to 90% over time (p < 0.001 for trend, 94.4% for retro-
grade and 85.7% for antegrade approach). These results
were achieved with a mean fluoroscopy time of 45 min
and 42 min (p = ns), total contrast volume of 433 ml vs
342 ml (p < 0.001), and cardiac tamponade rates of
0.97% vs 0.82% (p = ns), comparing non-high-volume
and high-volume operators, respectively [47].
Guidelines
The 2018 European Society of Cardiology (ESC)/
European Association of Cardiothoracic Surgery guide-
lines on myocardial revascularization CTO-PCI carry
a class IIA/level of evidence B recommendation:
“Percutaneous recanalization of CTOs should be con-
sidered in patients with angina resistant to medical
therapy or with large area of documented ischemia in
the territory of the occluded vessel” [48]. The 2021
American Heart Association (AHA) guidelines for cor-
onary artery revascularization carry a class 2B/level of
evidence B–R recommendation: “In patients with suit-
able anatomy who have refractory angina on medical
therapy, after treatment of non-CTO lesions, the benefit
of PCI of a CTO to improve symptoms is uncertain” [2].
A summary of the guidelines is shown in Table 3.2.
The AHA guidelines [2] raise some controversy,
and the latest guidelines have downgraded the indica-
tion class from 2A to 2B. As mentioned previously in
this chapter, the 30-day mortality rate is over 1% and
the perforations rate reaches almost 5% [4].
Retrospective data show good outcomes in treating
CTO, but data from randomized controlled trials
(RCTs) do not demonstrate impressive results. The
AHA guidelines, thus, recommend discussing all
options with the patients and explaining all limita-
tions and benefits. The EXPLORE trial [12] and
REVASC trial [13] did not show improvement of EF
compared to medical therapy when treating CTOs.
The EURO CTO Trial [6], which did show a reduc-
tion in angina frequency, was contradicted by the
DECISION-CTO [11] trial. We assume that the
authors of the guidelines have placed equal weight on
 C hapter 3
Table 3.2 Summary of Guidelines.
Guidelines Indication Class Level of Evidence Year
ESC 2A B 2018
AHA 2B B–R 2021
these two trials; however, many criticize the method-
ology of the DECISION-CTO trial (difficulties enroll-
ing patients, most patients from a single center,
non-negligible crossover, etc.) [49]. Also, most real-
world patients are not enrolled in clinical trials. In
order for future guidelines writers to want to increase
the indication level, a reduction in complications
must be demonstrated in future RCTs. Also, evidence
of both symptomatic relief and hard cardiovascular
outcomes must be shown.
Conclusions
Successful CTO recanalization has been shown to be
beneficial by leading to reduced need for CABG,
improved EF, and improved long-term survival.
Nonetheless, the main source of evidence comes from
observational, retrospective, non-randomized series,
with limited information regarding the potential base-
line differences among successful and unsuccessful
cohorts. Therefore, the only current indication,
according to American and European guidelines for
CTO-PCI, is symptomatic relief. Factors associated
with CTO-PCI procedural failure include multi-vessel
disease, presence of bridging collaterals, moderate to
severe calcification, longer CTO length, and longer
CTO duration. Longer stented length and lower mini-
mal lumen diameter following PCI have been shown
to be associated with a higher incidence of binary
restenosis [50]. As technical success improves and
long-term follow-up of patients verifies the benefits of
CTO-PCI, interest in this procedure is expected to
rise. Much of the current evidence is retrospective and
is limited by small patient numbers, but the increasing
enthusiasm is bound to lead to future well-designed
trials that should solidify our knowledge of the factors
important to procedural success and sustained patency.
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II PA R T I I
Imaging
 4 CHAPTER 4

CT Angiography: Application in
Chronic Total Occlusions
Hidehiko Hara*, John R. Lesser, Nicholas Burke &
Robert S. Schwartz
Minneapolis Heart Institute and Foundation, Minneapolis, MN, USA
* Corresponding author

Introduction Since the first generation of MSCT scanners was

Multislice computed tomography (MSCT) has dem-
onstrated high qualitative and quantitative diagnostic
accuracy among various patient populations [1, 2]. It
provides vessel wall plaque morphology and luminal
stenosis quantitation from plaque measurements [3].
Percutaneous coronary intervention (PCI) of the
chronic total occlusion (CTO) remains a significant
interventional problem, but has shown very slow clin-
ical progress. In recent series, procedural success rates
range from 55 to 80%, with the variability reflecting
differences in operator technique and experience,
availability of advanced guidewires, CTO definition,
and case selection [4]. The ability of CT angiography
(CTA) to image plaque and three-dimensional vascu-
lar directions has given rise to the hope that advanced
imaging by CTA may add incrementally to the success
of PCI for CTOs. The present chapter discusses the
present and future for CTA in CTO.
Overview of utility of CT scan to the
coronary artery disease
Quantification of coronary artery calcification was
first reported with electron beam CT (EBCT) [5].
This ability is key since calcification plays a crucial
role in the difficulty of the coronary CTO. Histologic
studies demonstrate an attenuation value of >130 HU
as closely correlated with calcified plaque in the coro-
nary arteries [6]. Additional studies provide evidence
that EBCT underestimates the total coronary plaque
burden. Modern cardiac CT scanners show the extent,
distribution, and location of calcification [7, 8].
introduced in 2000, CT imaging has made rapid
advances. Modern scanners obtain 64 or more slices
in one gantry rotation, and the temporal resolution
has significantly decreased. Evidence for the utility of
CT in coronary artery disease has accumulated over
the years, and recent studies show its high quantitative
and qualitative diagnostic accuracy when compared
against quantitative coronary angiography [2]. It also
has the potential for coronary plaque characterization
in the proximal coronary system, perhaps comparable
to intravascular ultrasound [9]. MSCT has now been
applied to PCI for CTO [10, 11].
Pathology
Pathological features of CTO vary, and depend on the
mechanism of occlusion and its duration. Differential
fibro-atheromatous plaque and thrombus content are
frequent [12]. The acute event is likely plaque rupture,
often causing thrombus formation and vessel occlusion
[13]. Collagen and calcification replace the initial
thrombus and cholesterol esters over time (Figure 4.1).
There may be a hard cap over the proximal and distal
margins of the CTO which is comprised of fibrous tis-
sue. Softer contents often occur between these caps
(Figure 4.2). Proteoglycan is important for CTO lesions.
Age-related changes in intimal plaque composition
from cholesterol laden to fibrocalcific materials are
seen in older CTOs and intimal plaque neovascular
channels derived from the adventitia increase with age
and are strongly associated with intimal cellular inflam-
mation (Figure 4.3). Intimal plaque neovascularization

Chronic Total Occlusions: A Guide to Recanalization, Third Edition. Edited by Ron Waksman and Shigeru Saito.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
29
30  PA R T I I Imaging
Figure 4.1 Human chronic total occlusion showing a
“hard” plaque. Note regions of calcification (Ca, partially
removed by histopathologic preparation process) and
dense fibrous tissue (D). The media (M) and adventitia (A)
are labeled, and the lumen is clearly occluded completely
by the plaque (Elastin stain).
formation is protective against the flow-limiting effects
of intimal plaque growth [14].
How is pathology reflected by CTA
imaging?
Previous investigations showed the importance of
revascularizing CTO. Clinical improvements include
symptoms, exercise tolerance, left ventricular function,
(a)
Figure 4.2 (a) Human chronic total occlusion showing a “soft’ plaque.” Note the cholesterol clefts (CC), where cholesterol
was removed during the histolopathologic preparation. Loose fibrous tissue (FT) is also seen (Hematoxylin/ Eosin stain).
(b) Higher power magnification of (a).
and long-term survival [15–18]. One of the most
important reasons for procedural failure is difficulty of
the guidewire crossing occluded lesions, frequently
experiencing problems due to the three-dimensionality
of its anatomical course visualized using only two-
dimensional conventional coronary angiography
(Figure 4.4).
The increased anatomic accuracy afforded by
MSCT allows excellent resolution, and it may improve
clinical success for PCI of CTO. Moreover, visualiza-
tion and qualification of coronary atherosclerotic
plaque is more difficult than assessing the coronary
lumen narrowing. CTA shows not only the contrast
enhanced lumen but also the vessel wall and athero-
sclerotic plaque (Figure 4.5). The potential for CTA
lies in visualizing important predictors of the CTO
lesion prior to PCI, and include spatial location and
volume of calcification, and occluded lesion length
from accumulation of cholesterol laden or fibrocal-
cific materials [19] (Figure 4.6).
What do we expect to see based on
the CT density and spatial
resolution?
CTA clearly identifies calcified lesions, and it may also
be able to recognize lipid-rich plaque, fibrous plaque,
and the degree of heavy calcification in CTO lesions
according to various calcium scoring regimes. The
most popular scoring was proposed by Agatston, with
calcification defined at a threshold of >130 HU and an
area threshold of >1 mm2. This score was calculated by
(b)
 C hapter 4 CT Angiography: Application in Chronic Total Occlusions
(a)
(c)
Figure 4.3 (a) Low-power view of a human chronic total
occlusion with capillaries and neovascularization.
(A indicates adventitia.) (b) Similar to (a), this
photomicrograph shows an occluded central channel
that has formed neovascular channels. The appearance
multiplying the area of each calcified lesion by peak
plaque density [5]. This score reveals incremental
prognostic value in predicting sudden coronary death
and nonfatal myocardial infarction in asymptomatic
high-risk patients. Moreover, the calcification is an
independent predictor of procedural failure for reca-
nalization in CTO [20]. Identifying calcification is one
of the most important predictors for clinical success.
Extremely heavy calcification causes beam hardening
and partial volume artifacts in the CTO image. Heavy
calcification is associated with a high likelihood of
adverse coronary events, not typically associated with
plaque vulnerability. Moreover, the location of the cal-
cified plaque within CTO is important for procedures
and finding the true lumen within eccentrically calci-
fied plaque. Recently, one study demonstrated the
accuracy of 64-slice MSCT for classifying and quanti-
31
(b)
(d)
of this occlusion suggests it is likely from a prior
thrombotic episode. (c and d) Higher-power views of
the microvascular channels, showing adventitial
capillaries (*) and inflammation (I) around these
channels.
fying plaque volumes in the proximal coronary arter-
ies. The investigators detected not only calcified plaque
but also hypodense spots (lipid pools) that were
defined as structures larger than 2 mm2 revealing a
density of at least 20 HU less than average value of sur-
rounding noncalcified plaque tissue compared with
intravascular ultrasound [9].
Most CT software creates three-dimensional vol-
ume rendered images of the coronary tree, multipla-
nar reconstruction, and maximal intensity projection
images. Accurate roadmaps with good spatial resolu-
tion allow accurate guidewire placement in the
occluded segment, while the lack of visualization of
the course of an occluded artery and its distal lumen
limits the effectiveness of various techniques.
Recent progress in MSCT spatial and temporal
resolution uses decreased slice thickness and faster
32  PA R T I I Imaging

Figure 4.4 Cardiac CTA image of a chronic total occlusion of the right coronary artery. Cross-sections and longitudinal images
are shown, with two regions of stenting. Plaque characterization consists of calcified and noncalcified plaque.

(a) (c)

(b) (d)

Figure 4.5 Similar to Figure 4.4, a cardiac CTA image of a chronic total occlusion showing calcified and noncalcified
plaque. Arrows indicate the chronic total occlusion.
 C hapter 4
Figure 4.6 Conventional angiography image (left panel)
showing a subtotal occlusion (arrowhead) of the mid part
of the right coronary artery, distal to a right ventricular (RV)
branch (arrow). Corresponding CT images using different
rotation times with reduced partial volume effects
and motion artifacts for improved CTO visualization.
One study revealed the complete visualization of cor-
onary routes and plaque characterization in CTO
segments with 16-slice MSCT, providing higher reso-
lution. The investigators conclude that an excellent
PCI success rate for CTO lesions is achieved using
MSCT guidance [11].
Clinical results to date and impact
on the interventional procedure
Several small studies demonstrate favorable results
using MSCT for PCI in patients with CTO. Yokoyama
and co-workers found an overall procedural success
of 91.3% among 23 CTO lesions using MSCT guid-
ance [11]. The investigators treated 23 angiographic
CTO in 22 patients (average age 69 ± 5 years, 17 male),
and 16-slice MSCT was performed prior to PCI. All
coronary routes of the CTO segment were accurately
visualized including markedly angulated CTO lesions
(13%) which could not be detected. Most lesions were
occluded for longer than 3 months (95.7%), and 87%
of those cases received grade 3 collaterals from other
coronary arteries. The lesion length was 15.8 ± 10 mm
and vessel diameter was 2.2 ± 0.4 mm. Calcification
were divided into three groups comprising noncalci-
fied, moderately calcified, and exclusively calcified.
The majority of calcified plaque was located in the
proximal, or both proximal and distal, segments.
MSCT revealed exclusively calcified plaque in 50% of
those lesions. The authors conclude that MSCT
should become a useful tool in PCI of CTO. They
achieved excellent procedural results even with com-
plicated and/or calcified lesions.
CT Angiography: Application in Chronic Total Occlusions 33
image post-processing techniques: volume rendered
(middle panel) and maximum intensity projection (right
panel) images showing the subtotal occlusion (arrowhead)
and RV branch (arrow). (Source: Mollet et al. [3]).
Mollet and de Feyter recently demonstrated
independent predictors of procedural failure of PCI
to the 45 patients with CTO by using 16-slice MSCT
variables [3]. They found that long occlusions and
severe calcification on MSCT coronary angiogram
are important predictors of procedural failure,
while neither variable was identified as an inde-
pendent predictor on conventional CAG. Also, they
pointed out the issue of relatively high radiation
exposure during MSCT previously reported
between 6.7 mSv and 13.0 mSv [21, 22]. MSCT cor-
onary angiography may reduce the procedural time
for PCI of the CTO, because it may suggest a thera-
peutic strategy and the total radiation exposure
dose may be decreased.
In a recent 64-slice MSCT study, Kaneda and Saito
and others demonstrated that technical success was
higher in patients with MSCT imaging than without
imaging (87 vs 80%, respectively) among patients
with scheduled PCI for CTO lesions. They suggested a
difference in procedural success among vessels, where
a 91% (20/22 cases) success rate was achieved in the
left anterior descending and circumflex arteries with
MSCT imaging, whereas motion artifacts limited use
in the right coronary artery. They concluded that
64-slice CT facilitated PCI was a promising adjunctive
modality to the CTO lesions [10].
Future perspectives
MSCT has progressed remarkably within the past
decade. Better temporal and spatial resolution is still
needed. 256-slice CT images are under investigation
[23], and improved new models will likely improve
these numbers.
34  PA R T I I Imaging
Conclusions
MSCT coronary angiography prior to scheduled PCI
of CTO lesions is promising, since this technology
allows not only seeing the true three-dimensional
course of occluded coronary arteries, but also reveals
the characteristics of the occluded segment such as
bending and severe calcification which are independ-
ent predictors of procedural failure. This modality is
still developing and may ease some procedural diffi-
culties, but needs to be further explored especially for
complex coronary intervention such as CTO lesions.
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kuolettavasti haavoitetuksi, niin ettei ole enää parantumisen
toivoakaan. Siinä tapauksessa suostun lyhentämään kärsimyksiäsi.

— Minä tulen kuolettavasti haavoitetuksi tai kerrassaan tapetuksi.

Hän ojensi minulle kätensä, jota minä lujasti puristin. Sen jälkeen
hän oli tyynempi, ja näkyipä hänen silmissään jonkinlaisen taistelu-
ilon välähdyksiäkin.

Kello kolmen tienoissa puolen päivän jälkeen alkoivat vihollisen

kanuunat jo kantaa meidän touvilaitoksiimme asti. Me reivasimme
silloin osan purjeitamme, käännyimme sivuttain Alcestea kohti ja
jatkoimme lakkaamatta tulta, johon englantilaiset pontevasti
vastasivat. Noin tunnin taistelun jälkeen tahtoi kapteenimme, joka ei
tehnyt mitään ennakolta miettimättä, koettaa ryntäystä. Mutta meillä
oli jo kosolta kuolleita ja haavoitettuja, ja jäljelle jäänyt miehistö oli jo
laimentunut; sen lisäksi olivat touvilaitoksemme kärsineet suuria
vaurioita, ja mastotkin olivat pahasti vioittuneet. Samassa kuin me
levitimme jälleen purjeemme lähestyäksemme englantilaista, kaatui
pilalle ammuttu suurmastomme hirmuisella ryskeellä. Alceste käytti
tästä onnettomuudesta syntynyttä hämminkiä heti hyväksensä. Se
liukui laivamme perä puolelle ja lähetti siitä puolen pistoolinkantaman
päästä täyssivuisen linjalaukauksen, joka lävisti fregatti-parkamme
perästä keulaan saakka, meillä kun vielä ei tällä taholla ollut muuta
kuin kaksi pientä tykkiä vastaukseksi. Olin silloin aivan lähellä
Roger'ta, joka juuri hakkautti poikki niitä sivutouveja, jotka vielä
pitivät kaatunutta mastoa hiukan koholla. Tunsin jonkun tarttuvan
kovasti käsivarteeni, käännyn katsomaan ja näen hänen, Roger'n,
makaavan vallan verissään kannella. Hän oli saanut
kartessilaukauksen vatsaansa.

Kapteeni juoksi hänen luoksensa:

— Mitäs nyt on tehtävä, luutnantti? huudahti hän.

— Pitää naulata lippu tuohon mastontynkään ja upottaa laiva

kaikkineen päivineen.

Kapteeni jätti hänet heti, sillä neuvo ei häntä ensinkään

miellyttänyt.

— No, sanoi Roger minulle, muistappa nyt lupauksesi.

— Ei hätää mitään, kyllä sinä voit tuosta parantua.

— Heitä minut mereen! huusi hän hirmuisesti kiroten ja tarttuen

takkini liepeeseen. Näethän, etten voi välttää kuolemaa; heitä minut
nyt mereen, sillä minä en tahdo nähdä lippumme anastamista.

Kaksi matruusia lähestyi häntä aikoen kantaa hänet ruumaan.

— Tykkinne luo, te lurjukset! jyrähytti Roger heille. Ampukaa

kartesseilla ja tähdätkää kannelle. Ja jos sinä nyt syöt sanasi, niin
minä kiroan sinut maailman kurjimmaksi pelkuriksi ja petturiksi!

Hänen haavansa oli varmasti kuolettava. Näin kapteenin kutsuvan

erästä kadettia luoksensa ja käskevän häntä noutamaan lippuamme.

— Anna minulle vielä kerran kätesi, ystävä, sanoin minä Roger'lle.

 Samassa silmänräpäyksessä, jolloin lippumme…

— Kapteeni hoi, valaskala tuulen alla! keskeytti eräs kadetti

juosten luoksemme.

— Valaskala? huudahti kapteeni ilosta loistaen ja jättäen

kertomuksensa sikseen. Vene pian vesille!… Ruuhi mereen!…
Kaikki veneet vesille! — Harppuunat, nuorat tänne! j.n.e., j.n.e.

Enkä minä saanut tietää, miten luutnantti Roger parka päivänsä

päätti.

Etruskilainen vaasi

Auguste Saint-Clair ei ollut ensinkään suosittu n.s. seuraelämässä

pääasiallisesti siitä syystä, ettei hän koettanutkaan miellyttää muita
ihmisiä kuin niitä, jotka häntä itseänsä miellyttivät. Näiden seuraa
hän oikein hakemalla haki, mutta pakeni muita. Muuten hän oli
hajamielinen ja kärsimätön. Italialaisesta teatterista eräänä iltana
lähdettäessä kysyi markiisitar A——— häneltä, mitä hän piti neiti
Sontagin laulusta. »Kyllä, rouva markiisitar», vastasi Saint-Clair
suloisesti hymyillen ja vallan muita asioita ajatellen. Tätä naurettavaa
vastausta ei voinut pitää ujoudesta lähteneenä, sillä hän puhui
muuten ylimyksille, kuuluisille suuruuksille, jopa muodissa oleville
vallasnaisillekin samalla luontevuudella kuin olisi keskustellut jonkun
vertaisensa kanssa. — Markiisitar päätteli, että Saint-Clair oli hirviö,
täynnä hävyttömyyttä ja typeryyttä.
 Rouva B——— kutsui hänet eräänä maanantaina päivällisille. Hän
keskusteli sinä iltana paljon Saint-Clairin kanssa, joka sieltä
lähtiessään selitti, ettei ollut ikinä tavannut rakastettavampaa naista.
Rouva B——— kokoili kuukauden kuluessa henkevyyttä muiden
luona ja anniskeli varastonsa yhden illan kuluessa kotonansa. Saint-
Clair tapasi hänet saman viikon torstaina uudelleen. Sillä kertaa
rouva B——— jo häntä hieman ikävystytti. Seuraavan tapaamisen
jälkeen hän jo päätti, ettei ikinä enää ilmesty hänen salonkiinsa.
Rouva B——— julisti maailmalle, että Saint-Clair oli kerrassaan
seuratapoja ja kasvatusta vailla oleva nuori mies.

Luonteeltaan hän oli helläsydäminen ja rakkautta kaipaava; mutta

siinä iässä, jolloin kovin helposti otetaan halki elämän kestäviä
vaikutuksia, oli hänen liian herkkä tunteellisuutensa joutunut
kumppanien ivan alaiseksi. Hän oli ylpeä, itsestään pitävä, ja arvosti
ihmisten mielipidettä kuin lapset. Siitä lähtien hän koetti peitellä
muilta kaikkea semmoista, mitä piti häpeällisenä heikkoutena. Ja
hän saavuttikin tarkoituksensa, vaikka tämä voitto kävi hänelle
kalliiksi. Hän osasi piilottaa toisilta kaikki liian tunteellisen sielunsa
liikutukset, mutta sulkiessaan ne itseensä hän teki ne vain sata
vertaa vaikeammiksi kantaa. Ihmisten kesken häntä pidettiin
tunteettomana ja välinpitämättömänä, ja yksinäisyys synnytti hänen
levottomassa mielikuvituksessaan kärsimyksiä, jotka olivat sitä
raskaampia, kun hän ei koskaan tahtonut niitä muille uskoa.

Tavata oikea ystävä on todellakin vaikeaa!

Vaikeaa! Onko se edes mahdollista? Onko koskaan ollut kahta

ihmistä, joilla ei ole ollut mitään toisiltansa salattavaa? — Saint-Clair
ei suuresti luottanut ystävyyteenkään, ja sen ihmiset kyllä
huomasivat. Seuraelämän nuoret miehet pitivät häntä kylmänä ja
sulkeutuneena. Ei hän koskaan udellut heidän salaisuuksiaan; mutta
kaikki omat ajatuksensa samoin kuin enimmät tekonsakin hän
myöskin salasi heiltä. Ranskalainen puhuu mielellään itsestään;
tahtomattaan tuli Saint-Clair usein muiden uskotuksi. Hänen
ystävänsä — niinhän me tavallisesti nimitämme henkilöitä, joita pari
kertaa viikossa tapaamme — valittivat, ettei hän luottanut heihin; ja
useimmiten loukkaantuvatkin sellaiset, jotka utelematta uskovat
meille salaisuuksiaan, ellemme vuorostamme kerro omiamme heille.
Arvellaan näet, että tällaisessa lavertelevaisuudessa pitää
molempain mennä yhtä pitkälle.

— Hän on aina haarniskoitta kiireestä kantapäähän saakka, sanoi

kerrankin tuo pulska ratsumestari Alfons de Thémines; en minä ikinä
voisi luottaa siihen pirulliseen mieheen.

— Luulenpa hänessä olevan hieman jesuiittaa, lisäsi siihen Jules

Lambert; eräs henkilö vakuutti kunniasanallaan nähneensä hänen
pari kertaa tulevan Saint-Sulpicen kirkosta. Eihän kukaan tiedä mitä
hän miettii. Minä puolestani en koskaan tunne itseäni varmaksi
hänen seurassaan.

Sitten he erosivat. Alfons tapasi Saint-Clairin kävelemässä Italian-

bulevardilla allapäin ja muista välittämättä. Hän pysähtyi juttelemaan
tuon erakon kanssa, tarttui hänen käsivarteensa, ja ennenkuin he
olivat saapuneet Paix-kadulle, oli hän jo kertonut Saint-Clairille koko
rakkaussuhteensa rva Y:hyn, jonka mies oli niin mustasukkainen ja
raaka.

Samana iltana Jules Lambert menetti pelissä kaikki rahansa. Siitä

huolimatta hän yltyi tanssimaan. Hyörinässä hän sattui tyrkkäämään
erästä miestä, joka niinikään oli rahansa menettänyt ja sen johdosta
tullut huonolle tuulelle. Vaihdettiin muutamia kiivaita sanoja, ja
kaksintaistelu oli seurauksena. Jules pyysi Saint-Clairiä
todistajakseen ja lainasi tältä samassa tilaisuudessa rahaa, jonka
hän on tähän saakka unohtanut maksaa.

Saint-Clair oli kuitenkin mies, jonka kanssa tuli hyvin toimeen.

Hänen vikansa eivät vahingoittaneet muita kuin häntä itseään. Hän
oli kohtelias, usein miellyttäväkin, ja harvoin ikävä. Matkustanut oli
hän paljon ja lukenut paljon eikä hän koskaan puhunut matkoistaan
tai luvuistaan, ellei häntä siihen kehotettu. Muuten hän oli kooltaan
pitkä ja vartaloltaan siro; kasvot olivat jalot ja älykkäät, melkein aina
liian vakavat, mutta hänen hymyilynsä oli leveää ja täynnä suloa.

Unohdin erään tärkeän piirteen. Saint-Clair oli aina huomaavainen

naisille ja etsi enemmän heidän keskustelujaan kuin miesten.
Rakastiko hän? Sitä juuri oli vaikea sanoa. Mutta jos tuo kylmä
olento saattoi tuntea mitään rakkautta, niin oli — se tiedettiin —
kaunis kreivitär Matilde de Coursy ensi sijalla hänen sydämessään.
Tämän nuoren lesken luona hänet nähtiin sangen usein. Ja
seuraavat seikat viittasivat siihen, että heidän välillään oli joku
hellempi suhde: ensinnäkin Saint-Clairin melkein juhlallinen
kohteliaisuus kreivitärtä kohtaan ja päinvastoin; sitten ei hän
koskaan maininnut kreivittären nimeä seurassa, tai jos hänen
suorastaan täytyi se tehdä, tapahtui se aina ilman pienintäkään
ylistystä; edelleen muistettiin Saint-Clairin ennen tutustumistansa
kreivittäreen rakastaneen intohimoisesti soitantoa ja kreivittären taas
sitä ennen yhtä lämpimästi maalaustaidetta. Mutta heti ensi
näkemän jälkeen olivat heidän harrastuksensa vaihtuneet. Ja kun
kreivitär viime vuonna oli matkustanut kylpemään, lähti Saint-Clair
hänen jälkeensä viikkoa myöhemmin.
 Kertojan velvollisuus pakottaa minut ilmaisemaan, että kun
muutamana heinäkuun yönä erään maatalon puutarhaportti avautui
hiukan ennen auringonnousua, astui sieltä ulos mies varovasti kuin
varas, joka pelkää joutuvansa kiinni. Maatalo kuului rouva de
Coursylle, ja sieltä-tulija oli Saint-Clair. Turkiksiin verhoutunut nainen
seurasi häntä portille saakka ja kurottautui hetkeksi katsomaan
häntä, kun hän poistui puiston muuria myöten vievää polkua. Saint-
Clair pysähtyi, silmäsi tutkivasti ympärilleen ja viittasi naista
poistumaan. Valoisassa kesäyössä hän saattoi erottaa nuo kalpeat
kasvot, jotka liikahtamatta pysyivät paikoillaan. Mies palasi jälkiänsä
myöten takaisin, lähestyi naista ja syleili häntä hellästi. Hän aikoi
taivuttaa portilla-seisojaa menemään jo sisälle, mutta tällä näkyi
olevan vielä sata seikkaa juteltavana. Heidän keskustelunsa oli
kestänyt noin kymmenen minuuttia, kun jostakin kuului työhönsä
menevän talonpojan ääni. Suutelo otettiin ja annettiin, portti
sulkeutui, ja muutamalla harppauksella oli Saint-Clair jo polun
päässä.

Hän kulki nähtävästi tuttua tietä. Milloin hän melkein hypähteli

ilosta ja astui juoksujalkaa, rapsien pensaita kepillänsä; milloin hän
taas seisahtui ja asteli verkalleen, katsellen taivasta, jonka itäinen
ranta jo alkoi purppuraisena punoittaa. Lyhyesti, katsoja olisi luullut
häntä hulluksi, joka iloitsi vapauteen-pääsystään. Puolen tuntia
astuttuaan hän saapui pienen, syrjäisen talon portille. Talon hän oli
vuokrannut koko kesäkaudeksi. Hänellä oli oma avain ja hän pääsi
sisälle; siellä hän heittäysi suurelle sohvalle, jolle unohtui
ajattelemaan ja uneksimaan, silmät yhtäänne tuijottavina ja suu
suloisessa hymyssä. Hänen mielikuvituksessaan väikkyi pelkkiä
autuaallisia ajatuksia.
 »Voi, kuinka onnellinen minä olen», hoki hän myötäänsä
itsekseen. »Vihdoinkin olen löytänyt sydämen, joka ymmärtää minun
sydämeni!… — Niin, minä olen löytänyt ihanteeni… Minulla on
samalla kertaa ystävä ja lemmitty… Mikä luonne!.. mikä
intohimoinen sielu!… Ei, hän ei ole rakastanut ketään ennen
minua…» Ja kun turhamaisuus aina sekaantuu tämän maailman
asioihin, mietti hän kohta: »Hän on Pariisin ihanin nainen.»
Mielikuvituksessaan hän kuvaili yhtaikaa kaikki lemmittynsä viehkeät
puolet. — »Kaikkien joukosta hän on valinnut minut. Seuraelämän
hienoimmat miehet kuuluivat hänen ihailijoihinsa. Tuo kaunis ja uljas
husaarieversti, joka ei ole niin kovin tyhmäkään; — tuo nuori kirjailija,
joka maalaa niin sieviä akvarelleja ja näyttelee niin hyvin
pikkunäytelmissä; — ja venäläinen Lovelace, joka on nähnyt
Balkanin ja palvellut Diebitshin johdolla; mutta varsinkin Camille T
———, joka epäilemättä on vilkasälyinen ja jolla on niin hieno
käytöstapa ja sellainen kaunis sapelin arpi otsassa… hän on heidät
kaikki hyljännyt. Vain minut!…» Ja sitten seurasi taas loppulaulu:
»Voi, kuinka onnellinen minä olen!» Hänen täytyi nousta ja avata
ikkuna voidakseen hengittää; sitten hän astuskeli edestakaisin ja
kääntelihe sohvallaan.

Onnellinen rakastaja on melkein yhtä ikävystyttävä kuin

onnettomastikin rakastunut. Eräs ystävistäni, joka usein oli toisessa
tai toisessa näistä kahdesta asemasta, ei voinut muulla tavoin saada
kuulijaa kuin tarjoamalla minulle mainion aamiaisen, jonka kestäessä
hän sai puhua rakkaussuhteistaan; mutta kahvin jälkeen piti hänen
ehdottomasti vaihtaa keskustelualuetta.

Mutta koska minä en voi tarjota aamiaista kaikille lukijoilleni,

säästän heiltä selonteon Saint-Clairin lemmenmietteistä. Eikä
muuten kukaan jaksa aina pilvien tasalla leijailla. Saint-Clair oli
väsynyt, hän haukotteli, ojenteli käsiään ja huomasi ulkona jo olevan
suuren päivän; täytyi kuin täytyikin ajatella hieman nukkumistakin.
Herätessään hän katsahti kelloansa ja huomasi tuskin ehtivänsä
pukeutua ennättääksensä Pariisiin, minne hänet oli kutsuttu
aamiaispäivällisille useiden tuttavien nuorten miesten seuraan…

*****

Oli juuri avattu uusi samppanjapullo, annan lukijan itsensä arvata

monesko järjestyksessä. Riittää, kun hän tietää, että oli jouduttu
siihen tilaan — mikä muuten nuorten miesten aamiaisissa piankin
syntyy — jolloin kaikki tahtovat puhua yhtaikaa ja jolloin hyväpäiset
alkavat pelotella huonompipäisiä.

— Haluaisinpa, sanoi Alfons de Thémines, joka ei koskaan

päästänyt ohitsensa tilaisuutta saada puhua Englannista,
haluaisinpa, että meillä täällä Pariisissa olisi sama tapa kuin
Lontoossa, missä kunkin on esitettävä lemmittynsä malja. Sillä
tavoin saisimme varmasti tietää, kenen vuoksi ystävämme Saint-
Clair huokailee.

Puhuessaan hän täytteli omansa ja naapureittansa lasit.

Hieman hämillään valmistausi Saint-Clair vastaamaan; mutta

Jules
Lambert ehti häntä ennen:

— Minä pidän paljon tästä tavasta, sanoi hän, ja omasta

puolestani siihen suostun. Kaikkien Pariisin ompelijattarien malja! —
huusi hän lasiansa kohottaen — paitsi kolmikymmenvuotiaitten,
silmäpuolten ja ontuvaisten y.m.s.
 — Hurraa! hurraa! huusivat nuoret Englannin ihailijat.

Saint-Clair nousi seisomaan lasi kädessä.

— Hyvät herrat, sanoi hän, minä en suinkaan ole niin

laajasydäminen kuin ystävämme Jules, mutta olen sittenkin
uskollinen. Ja tämä uskollisuus on sitä suurempiarvoinen, kun minä
jo aikoja sitten olen ollut erotettuna ajatusteni morsiamesta. Olenpa
kuitenkin varma siitä, että hyväksytte vaalini, ellette jo olekin
kilpailijoitani. Judit Pastan malja, hyvät herrat! Jospa saisimme pian
jälleen ihailla Euroopan ensimäistä tragedianäyttelijätärtä!

Thémines tahtoi arvostella tätä maljaa, mutta hyvähuudot

keskeyttivät hänet. Tämän iskun torjuttuaan luuli Saint-Clair
saavansa rauhan loppupäiväksi.

Keskustelu kääntyi ensin teattereihin. Näytelmäin sensuroimisesta

päästiin sitten siirtymään politiikkaan, lordi Wellingtonista
englantilaisiin hevosiin ja näistä taas helposti ymmärrettävää tietä
naisiin; nuorista miehistä ovat näet kaunis hevonen ensi sijassa ja
ihana lemmitty toisessa kaksi hartaimmin haluttua omaisuutta.

Ja sitten keskusteltiin keinoista näiden molempain

saavuttamiseksi. Hevosia saa ostamalla ja naisia voi myöskin ostaa,
mutta näistä emme huoli puhua. Tyhjennettyään vaatimattomasti
vähäiset kokemuksensa tällä arkaluontoisella alalla arveli Saint-Clair,
että ensimäinen ehto naisen valloittamiseksi oli muista
erottautuminen vallan erinkaltaiseksi. Mutta oliko olemassa mitään
yleistä kaavaa tälle erinkaltaisuudelle? Hän puolestaan ei sitä luullut.

— Teidän mielipiteenne mukaan, jatkoi Jules, olisi siis ontuvalla ja

kyttyräselkäisellä paremmat edut naisten miellyttämiseksi kuin
suoraselkäisellä ja kasvultaan muidenlaisella!

— Te menette sangen pitkälle, vastasi Saint-Clair, mutta jos niin

vaaditaan, otan puolustaakseni kaikkia johtopäätöksiä, joihin
ehdotukseni voi antaa aihetta. Jos minä esim. olisin kyttyräselkäinen,
niin en minä siltä itseäni lopettaisi, vaan haluaisin tehdä valloituksia
minäkin. Ensistäänkin kääntyisin ainoastaan kahtalaisten naisten
puoleen, nimittäin joko tosi tunteellisten taikka sellaisten — ja heidän
lukunsa on suuri — jotka tahtovat käydä omituisista, eccentric, kuten
englantilainen sanoo. Edellisille minä kuvaisin asemani hirmuisuutta,
luonnon kovuutta minun suhteeni. Koettaisin herättää heissä sääliä
kohtaloani kohtaan ja saattaisin heidät aavistamaan, että voin
rakastaa intohimoisesti. Tappaisin kaksintaistelussa jonkun
kilpakosijoistani ja myrkyttäisin itseni heikolla laudanum-annoksella.
Muutamien kuukausien kuluttua eivät he enää huomaisi kyttyrääni, ja
silloin minä vain odottelisin tunteellisuuden ensimäistä puuskausta.
Mitä taas sellaisiin naisiin tulee, jotka tahtovat käydä omituisista, niin
heidän valloituksensa käy aivan helposti. Saakaa heidät vain
uskomaan varmaksi ja pitäväksi säännöksi, ettei kyttyräselkäisellä
voi olla menestystä; he tahtovat heti osoittaa, ettei tuo yleinen sääntö
pidä paikkaansa.

— Kas, mikä don Juan! huudahti Jules.

— Katkaiskaamme jalkamme, hyvät herrat, lausui eversti Beaujeu,

koska me, onnetonta kyllä, emme ole saaneet kyttyrää
syntymälahjaksemme.

— Minä olen vallan samaa mieltä kuin Saint-Clair, virkkoi Hector

Roquantin, joka oli ainoastaan kolme ja puoli jalkaa pitkä; joka päivä
nähdään kauneimpien ja enimmin liehakoitujen naisten antautuvan
miehille, joista te, pulskat pojat, ette aavista mitään…
 — Hector, nouskaapa, minä pyydän, ja soittakaa meille viiniä,
sanoi
Thémines mitä luonnollisimmalla tavalla.

Kääpiö nousi heti, ja jokainen muisteli hymyillen satua ketusta,

jolta oli häntä leikattu.

— Minä puolestani sanoi Thémines jatkaen keskustelua, näen

joka päivä uusia todistuksia siitä, että tavallinen ulkomuoto — ja
samalla hän loi tyytyväisen silmäyksen vastapäätä olevaa peiliin —
sekä aistikas pukeutuminen ovat juuri se erinkaltaisuus, joka
parhaiten noita sydämettömiä viehättää; — ja nenäänsä
puhaltamalla hän lennätti pois takkinsa rinnustalle pudonneen
pikkuisen leivänmurusen.

— Vielä mitä! huudahti kääpiö. Kauniilla muodolla ja Staubin

tekemällä puvulla valloittaa naisia, joita pidetään viikon päivät ja
jotka jo toisessa näkemässä tuntuvat ikäviltä. Muuta siihen tarvitaan,
jos tahtoo todenteolla tulla rakastetuksi. Siihen pitää…

— Kuulkaahan, keskeytti Thémines, tahdotteko sopivan

esimerkin? Te tunsitte kaikki Massignyn ja tiedätte, mikä hän oli
miehekseen. Tavoiltaan kuin mikähän englantilainen groom ja
puheessa tyhmä kuin aasi… Mutta hän oli kaunis kuin Adonis ja sitoi
kaulaliinansa kuin Brummel. Sanalla sanoen, hän oli ikävin ihminen,
minkä ikinä olen tuntenut.

— Hän oli tappaa minutkin ikävään, sanoi eversti Beaujeu.

Ajatelkaahan, kun minun kerran täytyi matkustaa kaksisataa virstaa
hänen kanssansa!
 — Tiedättekö, puuttui Saint-Clairkin puheeseen, hänen olevan
syypään yhteisen tuttavamme Richard Thornton raukan kuolemaan?

— Mutta ettekö tiedä, että rosvot murhasivat hänet Fondin luona?

kysyi
Jules.

— Oikein; mutta Massigny oli ainakin välillisenä syynä rikokseen,

kuten heti saatte kuulla. Useita matkustajia, joiden joukossa
Thornton, oli päättänyt rosvojen vuoksi matkustaa yhdessä joukossa
Napoliin. Massigny pyysi hänkin päästä karavaanin turviin. Heti sen
kuultuaan jäi Thornton seurasta pois, luullakseni kauhuissaan siitä,
että hänen olisi täytynyt viettää muutamia päiviä Massignyn kanssa
yhdessä. Hän lähti yksin matkalle, ja lopun te tunnette.

— Thornton oli oikeassa, sanoi Thémines. Kahdesta kuolemasta

hän valitsi helpomman. Jokainen olisi hänen sijassaan tehnyt
samoin.

— Te myönnätte siis, jatkoi hän pienen väliajan jälkeen, että

Massigny oli ikävin ihminen maailmassa?

— Myönnetään! huudettiin kuin yhdestä suusta.

— Älkäämme saattako ketään epätoivoon, sanoi Jules,

antakaamme poikkeussija hra N:lle, varsinkin kun hän pääsee
puhumaan politiikasta.

— Te myöntänette kai heti, jatkoi Thémines, että rouva de Coursy,

jos kukaan, on älykäs nainen.

Seurasi lyhyt äänettömyys. Saint-Clair loi silmänsä maahan ja

kuvitteli, että kaikki tarkastivat vain häntä.
 — Kukapa sitä kieltänee? sanoi hän vihdoin kumartaen lautasensa
yli ja näennäisesti suurella uteliaisuudella tutkistellen posliinille
maalattuja kukkasia.

— Minun mielestäni, lausui Jules äänekkäämmin, minun

mielestäni on Pariisissa ainoastaan kolme tosimiellyttävää naista, ja
niistä hän on yksi.

— Tunsin hänen miehensä, sanoi eversti. Hän näytteli minulle

usein vaimoltaan saamiansa erinomaisia kirjeitä.

— Auguste, keskeytti Hector Roquantin, esittäkääpä minut

kreivittärelle. Kerrotaan teidän olevan hänen luonaan poudan ja
sateen aikana.

— Sitten loppusyksyllä, mutisi Saint-Clair, kun hän saapuu takaisin

Pariisiin… Minä… minä en luule hänen välittävän vieraista siellä
maalla.

— Tokko aiotte kuulla minua! huusi Thémines.

— Te ette nähnyt kreivitärtä kolme vuotta takaperin, sillä te olitte

silloin Saksassa, Saint-Clair, jatkoi Alfons de Thémines toivottomalla
tyyneydellä. — Ette voi ajatellakaan, minkälainen hän silloin oli:
ihana, raitis kuin ruusunen, sangen pirteä ja iloinen kuin perhonen.
No, ja tiedättekös, kuka hänen lukuisista ihailijoistaan sai
parhaimmat suosionosoitukset osalleen? Massigny! Maailman
tyhmin ja yksinkertaisin mies pani älykkäimmän naisen pään
pyörälle. Luuletteko jonkun kyttyräselkäisen kykenevän sellaista
tekemään? Joutavia, uskokaa minua, kaunis ulkomuoto, hyvä räätäli
ja kylliksi rohkeutta, siinä kaikki.
 Saint-Clair oli joutunut julmaan asemaan. Hän aikoi tehdä kertojan
suorastaan valehtelijaksi, mutta hän pelkäsi saattavansa kreivittären
maineen vaaraan ja hillitsi itsensä. Hän olisi tahtonut sanoa jotakin
hänen puolustuksekseen, mutta hänen kielensä oli kuin kangistunut.
Huulet värähtelivät suuttumuksesta, ja turhaan hän etsi jotain
syrjäsyytä riidan aiheeksi.

— Mitä! huudahti Jules hämmästyneen näköisenä. Onko rouva de

Coursy antautunut Massignylle! Frailty, thy name is woman!

— Niin, naisen mainehan on niin vähäarvoinen asia, sanoi Saint-

Clair kuivasti ja halveksivasti. Tietysti saa sen tahrata lokaan ja
likaan, kunhan voi olla hieman sukkela… ja…

Puhuessaan hän kauhistuen muisti nähneensä satoja kertoja

kreivittären luona Pariisissa erään etruskilaisen kukkasvaasin
uuninreunustalle. Hän tiesi, että Massigny oli lahjoittanut sen Italiasta
palattuaan, ja — mikä raskauttava asianhaara — tämä vaasi oli
kuljetettu Pariisista tuonne maallekin. Ja kun Matilde irroitti
rintakukkasensa, asetti hän ne joka ilta tuohon etruskilaiseen
vaasiin.

Sanat kuivivat hänen huulillaan; hän näki enää vain yhden esineen
ja ajatteli ainoastaan yhtä asiaa: etruskilaista vaasia!

Kaunis todistus! sanonee kai arvostelija: epäillä lemmittyänsä

senvertaisen asian vuoksi!

Oletteko te koskaan ollut rakastunut, herra arvostelija?

Thémines oli liian hyvällä tuulella loukkaantuaksensa siitä

äänenpainosta, millä Saint-Clair oli hänelle puhunut. Hän vastasi
huolettoman ja hyväsydämisen näköisenä:

— Enhän minä tee muuta kuin toistan mitä yleisesti kerrottiin.

Asiaa pidettiin varmana siihen aikaan kuin te olitte Saksassa.
Muuten minä tunnen rouva de Coursyta sangen vähän enkä ole
kahdeksaantoista kuukauteen käynyt häntä tervehtimässäkään.
Mahdollisesti on juttu vain erehdystä ja Massignyn valeita.
Tullaksemme äskeiseen asiaamme, ja jos mainitsemani esimerkki
olisikin väärä, niin olen minä siltä oikeassa. Te tiedätte kaikki, että
Ranskan älykkäin nainen, jonka teokset…

Samassa aukesi ovi ja sisään astui Teodor Neville. Hän palasi

Egyptistä.

— Teodor! niin pian takaisin! — Ja kysymyksiä sateli häntä

vastaan.

— Toitko muassasi oikean turkkilaisen puvun? kysyi Thémines. Ja

arapialaisen hevosen, ja egyptiläisen groomin?

— Mimmoinen mies se pasha on? uteli Jules. Ja milloin hän

julistautuu itsenäiseksi? Oletko nähnyt lyötävän päätä poikki yhdellä
sapelin iskulla?

— Entäpä almeet? Ovatko Kairon naiset kauniita? tiedusteli

Roquantin.

— Näittekö kenraali L:iä? kysyi eversti Beaujeu; Mitenkä hän on

järjestänyt pashan sotaväen? — Ja antoiko eversti C——— teille
erään sapelin minua vasten?

— Niin, ja pyramiidit? ja Niilin putoukset? ja Memnonin

muistopatsas? ja Ibrahim pasha? y.m.s.
 Kaikki puhuivat yhtaikaa; Saint-Clair ajatteli vain etruskilaista
vaasia.

Teodor oli istuutunut jalat ristissä — hän oli tottunut siihen

Egyptissä eikä ollut vielä päässyt tästä tottumuksestaan täällä
Ranskassa — odotteli, kunnes kysymykset olivat lopussa, ja puhui
sitten kylliksi nopeasti, ettei niin helposti voitaisi keskeyttää,
seuraavaan tapaan:

— Niin, pyramiidit! ne ovat, kunniani kautta, vain regular humbug.

Ne eivät ole niin korkeita kuin luullaan. Strassburgin Münster on
ainoastaan neljä metriä matalampi. Muinaismuistot ihan tunkevat
silmistäni esille. En huoli niistä puhua. Pelkkä hieroglyfin näky jo
saisi minut pyörryksiin. On niin paljon matkailijoita, joita sellaiset
huvittavat! Minä puolestani tutkin tuon Aleksandrian ja Kairon
kaduilla tungeskelevan omituisen ihmisjoukon ulkomuotoja ja tapoja,
turkkilaisten, beduiinien, koptien, fellahien ja mogrebiinien. Tein
kiireessä muutamia muistiinpanoja maatessani sairaalassa. Mikä
ilkeä laitos tuo heidän sairaalansa! Toivon, ettette usko tautien
tarttuvan! Minä se vain polttelin levollisesti piippuani kolmensadan
ruttoa sairastavan potilaan keskellä. Siellä te, eversti, näkisitte
kauniin ratsuväen, joka istuu hyvin hevosen selässä. Näytän teille
joskus sieltä tuomiani mainioita sota-aseita. Minulla on eräs djerid,
joka on ollut kuuluisan Murad beyn oma. Teille, eversti, on minulla
muuan jutaghan ja Augustelle khandjar. Saatte myöskin nähdä
_metshlani, burnus'_ini ja _haikk'_ini. Ja naisia olisin niinikään voinut
tuoda, jos vain olisin tahtonut. Ibrahim pasha lähetti niitä niin paljon
Kreikasta, että niitä sai melkein ilmaiseksi… Mutta äitini tähden…
Pashan kanssa keskustelin paljon. Se on hiivatin älykäs ja
ennakkoluuloton mies. Ette voi uskoa, kuinka hyvin hän tuntee
meidän asioitamme. Hän on, kunniani kautta, perillä ministeristömme
pienimmistäkin salaisuuksista. Minä ammentelin hänen puheistaan
mitä tärkeimpiä tietoja Ranskan puolueasioista… Tällä haavaa
huvittaa häntä erityisesti tilastotiede. Hän tilaa kaikki
sanomalehtemme. Ja voitteko ajatella, hän on hurja
bonapartelainen! Ei hän muusta puhukaan kuin Napoleonista. Voi
mikä suuri mies se Bounabardo! sanoi hän minulle. Bounabardoksi
he Bonapartea nimittävät.

— Giourdina, c'est à dire Jourdain, mutisi aivan hiljaa Thémines.

— Aluksi, jatkoi Teodor, oli Muhamed Ali sangen varovainen minun

suhteeni. Kaikki turkkilaiset ovat, kuten tunnettua, tuiki epäluuloisia.
Hän piti minua, lempo vieköön, vakoilijana tai jesuiittana. Jesuiittoja
hän näet kammoaa. Mutta muutamien näkemien perästä hän
huomasi minun olevan ennakkoluulottoman matkustelijan, joka
halusi tutustua Itämaiden tapoihin, katsantokantoihin ja politiikkaan.
Silloin hän astui kuorestaan ja puhui minulle avosydämisesti. Viime
kerralla, se oli kolmas audienssi, jonka hän suvaitsi minulle myöntää,
uskalsin minä sanoa hänelle: »Minä en ymmärrä, miksei Sinun
Ylhäisyytesi julista itseänsä vapaaksi Portista?» — »Hyvä Jumala,
sanoi hän, eihän minulta tahtoa puutu, mutta pelkäänpä, etteivät
vapaamieliset lehdet, jotka sinun maassasi hallitsevat kaikki,
kannata minua, jos kerran olen julistautunut Egyptistä vapaaksi.»
Pasha on pulska, valkeapartainen ukko eikä naura koskaan. Hän
lahjoitti minulle mainioita sokerileivoksia; mutta eniten kaikista
hänelle antamistani lahjoista hän piti Charlet'n maalaamasta
keisarillisen kaartin pukukokoelmasta.

— Onkohan pasha romantikko? kysyi Thémines.

— Hän ei paljon välitä kirjallisuudesta; mutta te tiedätte, että

arapialainen kirjallisuus on läpeensä romantillista. Eräs heidän
runoilijoistaan, nimeltä Melek Ayatalnefond-Ebn-Esraf, julkaisi
äskettäin kokoelman »Mietelmiä», joiden rinnalla Lamartinen
mietelmät tuntuvat klassilliselta proosalta. Saapuessani Kairoon otin
arapiankielen opettajan, jonka avulla ryhdyin lukemaan Koraania.
Vaikka en monta tuntia ottanutkaan, opin sentään tarpeeksi
oivaltaakseni profeetan kirjoitustavan verrattomat ihanuudet ja
käsittääkseni, kuinka huonoja kaikki meidän käännöksemme ovat.
Kuulkaas, tahdotteko nähdä arapialaista kirjoitusta? Tuo
kultakirjaimilla kirjoitettu sana merkitsee Allah, s.o. Jumala.

Näin sanoen hän näytti kovin ryvettynyttä kirjettä, jonka hän veti
esiin lemuavasta silkkikukkarostaan.

— Kuinka kauan sinä olit Egyptissä? kysyi Thémines.

— Kuusi viikkoa.

Ja matkustelija jatkoi selityksiään setripuusta alkaen iisoppiin

saakka. Saint-Clair pujahti tiehensä melkein heti hänen tultuaan ja
ajoi maatalollensa vievää tietä myöten. Kiihkoisaa laukkaa
ratsastaessaan ei hän voinut seurata oikein tarkasti ajatustensa
kulkua. Mutta epämääräisesti hän tunsi, että hänen onnensa tässä
maailmassa oli iäksi hävitetty, eikä hän voinut kiukkuilla siitä muille
kuin eräälle vainajalle ja tuolle etruskilaiselle vaasille.

Perille päästyään hän heittäysi samalle sohvalle, millä edellisenä

iltana oli niin kauan ja niin suurella nautinnolla rakkauttansa
analyseerannut. Eniten oli häntä hurmannut se rakkaaksi käynyt
ajatus, ettei hänen lemmittynsä ollut muiden naisten kaltainen, ettei
hän ikinä ollut rakastanut eikä koskaan tulisi rakastamaan muita kuin
häntä. Nyt oli tämä kaunis unelma häipynyt surullisen ja julman
todellisuuden tieltä. »Minulla on kaunis lemmitty eikä muuta mitään.
Hän on älykäs: senpävuoksi onkin vielä suurempi rikos, että hän on
voinut rakastaa Massignyta!… Totta on kyllä, että hän nyt rakastaa
minua… koko sielullaan… niinkuin hän voi rakastaa. Samalla lailla
kuin Massignytakin!… Hän on suostunut minun hyväilyihini,
oikkuihini ja epäkohteliaisuuksiini. Mutta minä olen pettynyt. Meidän
molempien sydänten välillä ei ole myötätuntoisuutta. Hänelle on
yhdentekevää, olipa se Massigny tai minä. Poika on pulska, hän
rakastaa minua kauneuteni vuoksi. Minä taas huvitan häntä joskus.
'No niin, rakastakaamme siis Saint-Clairiä', on hän itselleen sanonut,
'koska tuo toinen on kuollut! Ja jos Saint-Clair kuolee tai käy
ikäväksi, niin saammehan nähdä mitä sitten teemme.'»

Luulenpa vakavasti pirun istuvan näkymättömänä kuuntelemassa

onnetonta, joka tällä tavoin itseänsä kiduttaa. Näkyhän on
ihmisvihaajalle huvittava, ja kun uhri alkaa tuntea haavainsa olevan
ummistumassa, on piru heti siinä niitä auki repostelemassa.

Saint-Clair luuli kuulevansa jonkun kuiskuttavan hänen korvaansa:

Kunnia mainio olla on toisen jälkeläisenä…

Hän hyppäsi istualleen ja silmäsi hurjistuneena ympärilleen. Voi,

kuinka hän olisi ollut onnellinen, jos olisi tavannut jonkun huoneessa!
Epäilemättä olisi hän sen heti lopettanut.

Kello löi kahdeksan. Puoli yhdeksän odotti kreivitär häntä. — Jos

hän jäisi pois yhtymisestä? »Todellakin, mitä hupia tuotti hänelle
Massignyn lemmityn tapaaminen?» Hän heittäysi jälleen sohvalleen
ja ummisti silmänsä. »Tahdon nukkua», arveli hän. Puoli minuuttia
hän pysyi liikahtamatta, hyppäsi sitten seisoalleen ja juoksi
katsomaan, kuinka pitkälle aika oli kulunut. »Kunpa se jo olisi puoli
yhdeksän!» mietti hän. »Silloin olisi liian myöhäistä lähteä enää koko