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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 advancement in the field and the interest of interventional cardiologists to win the battle to safely and effectively
treat CTOs. The book continues to serve as a comprehensive guide for both novice and experienced practitioners who seek to enhance their understanding and
skills in the management of CTOs.
The presence of CTOs was initially observed during coronary angiography procedures in the mid-20th
century. In the early days of percutaneous coronary
intervention (PCI), CTOs were considered challenging to treat due to technical difficulties and lack of
suitable equipment and often were referred for surgical 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 percutaneously and its impact on mortality and quality of life.
With the lack of definitive data from randomized
clinical trials, the debate was ongoing. But simultaneously 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 development of specialized guidewires with improved flexibility and penetration power, which allowed for more
successful attempts at crossing CTOs.
In the 1990s, the retrograde approach was introduced 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 saphenous vein grafts expanded the possibilities for CTO
intervention and improved success rates. Finally, dedicated devices and tools were developed specifically
for crossing and treating these challenging lesions.
These devices include CTO-specific guidewires,
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 interventions 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 interventional cardiologists who have extensive experience
in performing CTO interventions.
CTO interventions often require a multidisciplinary approach involving collaboration among interventional cardiologists, imaging specialists, and
cardiac surgeons. A team-based approach ensures
comprehensive evaluation, appropriate patient selection, and optimal treatment strategies for CTO
patients.
To stay updated with the latest advancements and
techniques in CTO interventions, interventional cardiologists in the USA participate in continuing medical education activities. These include conferences,
workshops, case discussions, and comprehensive textbooks, which provide opportunities to learn from
experts and share experiences with peers.
It is important to note that the future of CTO interventions is dynamic and subject to ongoing innovation. 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 visualization and guide treatment strategies, add to this bright
future. Furthermore, the development of novel devices
and tools, including bioresorbable scaffolds and drugeluting 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
x
Foreword xi
interventions. AI algorithms can aid in lesion assessment, procedural planning, and complication management, offering real-time decision support and
enhancing procedural precision.
The third edition of this comprehensive CTO intervention 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 chapter 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 community. 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, acknowledging the critical role of imaging specialists, nurses,
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 editorial management process of this book. Dr. Saito and I
extend our deepest gratitude to all the contributors
who generously shared their expertise and experiences, making this book a comprehensive and valuable 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 stenotic lesion in a coronary artery by balloon dilation.
The key concept at this time was to guide the burstresistant balloon to the lesion site, preceded by a delicate 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 exertional angina pectoris due to a chronic totally
occluded lesion in his right coronary artery. I
reported at an academic conference that I had reopened this patient using a Hartzler LPS (ACS) balloon (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 coronary 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
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 experiences 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 contralateral 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) technical 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.
xii
I
PART 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 total occlusions (CTO) are defined by an
occlusion age of 3 months or greater, with angiographic 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 equipment and strategies, and innovative biologic manipulations [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 angiographic 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 demonstrating 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
“chronic occlusions” in the lower legs [6], (2) Hard
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 neovascular channels was commonly observed at all time
periods, particularly around prominent collections
of inflammatory cells (lymphocytes and macrophages) [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 PART I Pathology, Indications, and Review of Clinical Trials
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
Ca
Ca
MV
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
Necrotic
of the CTO segment (Figure 1.1A). Longer duration (non-bypassed) CTOs in contrast demonstrated more complex features: mainly collagen
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.)
1 deposition and moderate calcification (Figure
1.1B). CTOs with bypass grafts were characterized
by the heaviest calcification (including the adjacent proximal and distal segments) (Figure 1.2C).
Negative remodeling, defined as reduction in the
CTO vessel cross-sectional area relative to the adjacent proximal segment, was least in CTO sections
containing organizing thrombus, followed by calcified sections and proteoglycan-rich thrombus
M
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
MV
Ca
Ca
previously bypassed [14, 15]. Although bypass surgery is well recognized as the superior revascularization strategy in patients with high SYNTAX score
and multivessel disease, there is also a downside of
iatrogenic CTO formation, ultimately creating the
MV
most technically challenging CTOs for percutaneous 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
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.)
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%
CTO formation is coronary artery bypass grafting
[11]. Angiographic follow-up at one year post coronary artery bypass grafting demonstrated ≥1 new
native coronary artery CTO in almost half of the
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
CHAPTER 1 The Pathobiology of CTO 5
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 sizing. Less frequently, protrusion of a necrotic core,
overlapping stents, bifurcation stenting, and stent
fracture with complete disruption were also recognized. Neoatherosclerosis (foamy macrophages,
necrotic core) was present in 25% of these stent
CTO, but neointimal calcification was rarely present, despite a high prevalence of patients with
diabetes and renal failure (Figure 1.2D). These findings highlight a number of differences between denovo and stented coronary CTO.
Current paradigm of CTO evolution
The development of CTOs includes several specific
stages with unique histologic characteristics present 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 syndrome. 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 symptoms [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 chronically occluded artery 3–6 months after MI [21]. In
patients treated with percutaneous coronary intervention (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 relevance to humans, such as non-coronary location, and
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 neovascularization 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 coincides with gradual replacement of proteoglycans by
collagen in the extracellular matrix. Human studies
have shown collagen and calcium accumulation characterize 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 structure 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 structure compared to the proximal cap. This has been part
of the rationale for developing the retrograde
approach to cross the CTO.
6 PART 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 cholesterol-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, particularly within and adjacent to the sites infiltrated by
inflammatory cells (lymphocytes and macrophages). In
some cases, intimal neovascular channels directly communicate with adventitial vasa vasorum. Neovascular
channels were also observed in the vascular medial
layer; the extent of medial neovascularization was proportional to the cellular inflammation in the intimal
plaque. The adventitia of the vessel is usually extensively 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 microvessels 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 microchannels 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 duration coronary occlusions (≤3 months), intimal
plaque calcification was present in 54% of coronary occlusions, but reached 100% in CTO of
>5 years duration [5] (Figure 1.2C). In contrast,
insulin-dependent diabetes mellitus was more frequently 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 indistinguishable 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 simplified 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 calcium-chelating molecules. The formation of hydroxyapatite crystals in this way is now regarded as a
semi-regulated process, and the high phosphate levels
might induce vascular smooth muscle cells to differentiate 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 osteoclastlike cells.
CHAPTER 1 The Pathobiology of CTO 7
Collagen Calcium Proteoglycan FibrinPlaqueMicrovesselsCholesterol
A. CTO <1 year
B.CTO >1 year
C. Calcified CTO
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 components of CTOs and suggested an impact of each on
D. In-stent CTO
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 modification strategies may enable significant improvements
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