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8 PART 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. Finn
1
CVPath Institute, Gaithersburg, MD, USA
2
University of Maryland School of Medicine Baltimore, MD, USA
* Corresponding author
1,2,
*
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 revascularization 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 useful for the CTO-PCI strategy and planning, which
can facilitate the increased success of CTO-PCI. In
this chapter, we will explore the pathological findings of CTOs as they may pertain to successful
procedural outcomes.
Histopathology of chronic total
occlusions, with and without prior
coronary artery bypass grafts
Chronic total occlusions are composed of atherosclerotic and/or thrombotic components that can be composed of multiple layers of different tissues.
Angiographic total occlusions are not always consistent with histologic total occlusions, with one study
showing that only 22 % of all angiographic CTOs correlated to a 100 % occlusion on histopathology [8].
This is probably expected given the superior resolution of histopathology compared to angiography.
In a previous report, we defined CTOs pathologically as lesions where the lumen area was occupied by
proteoglycan and/or collagen with or without neovascularization 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 characteristics of the LD-CTO and the SD-CTO are compared
in Figure 2.1 [10].
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
CHAPTER 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 11
Long-duration CTO
Short-duration CTO
(A)
1.0 mm
(B) (D)
(C)
500
1.0 mm
µm500 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 shortduration 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 segment 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 contrast, 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
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 negative 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 strategic approaches to CTO PCI (Figure 2.3).
In addition, the lumen pattern was classified as
abrupt versus tapered, depending on the degree
of narrowing prior to or after the occluded segment (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 PART I Pathology, Indications, and Review of Clinical Trials
CTO-9CTO-8
D-1CTO-12
CTO with CABG
LD-CTO
SD-CTO
Vein
Graft
RMB
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
PRC
MRC
DRC
PD
P-1 CTO-2CTO-1
CTO-5CTO-4
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-6
CTO-7
Cholesterol clefts
Necrotic core
Calcied plaque
Collagen
Fibrin
Healed thrombus
Angiogenesis
Negative remodeling+++++ − / +
Calcication +++
Lesion difculty in
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
Most challengingMedium difculty Least challenging
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.
+ / ++
− / +
CHAPTER 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 13
Tapered Pattern Morphology(B)
Abrupt Pattern Morphology
(A)
CTO segment
P-1
CTO (distal end)
P-1
Proximal
Proximal
Proximal
Distal end of the CTO
D-1
P-2
P-2
CTO segment
Proximal end of the CTO
P-3P-2P-1
P-3
CTO segment
Proximal end of the CTO
P-3P-2P-1
P-3
D-2
D-3
D-1
D-2
Distal
CTO (proximal end)
Distal
CTO (proximal end)
Distal
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
frequently seen in the proximal lumen of the CTO,
compared with the distal lumen, which may explain
the recent increase in procedural success with the
retrograde approach which may be more fruitful in cases of proximal versus distal lumen occlusion. Microchannels over 200µm in diameter were
rarely observed in all three groups, which may
indicate more favorable CTO crossing with coronary guidewires with tapered tip diameters <0.014�
(360 uM) [11].
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.
Pathology of in-stent chronic total
occlusion and its difference from
native CTO
In-stent chronic total occlusions (IS-CTO) are also
not uncommonly observed in PCI. The prevalence
of IS-CTO is estimated to be 5–13 % of all CTOs
[12–14]. The major etiologies of IS-CTO are acute
thrombotic occlusion, restenosis, and plaque rupture from neoatherosclerosis [15].A representative
14 PART I Pathology, Indications, and Review of Clinical Trials
(B)
(A)
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 contributing 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-
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 occlusion, restenosis, neointimal erosion, and hypersensitivity, neointimal calcification were not observed.
Thus, it can be said that IS-CTOs differ from native
CTOs, especially in terms of intimal calcification, 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
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
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.
CHAPTER 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 15
(B)
(A)
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 sirolimuseluting 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 PART I Pathology, Indications, and Review of Clinical Trials
(B)
(A)
Figure 2.7 Neoatherosclerotic rupture. Cross-sectional
histology of BMS (A) implanted for 8 years and paclitaxeleluting 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
++
) plaque (c and i). An organized thrombus is observed
(Ca
IS-CTO, when considering complete revascularization 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 characterized by severe negative remodeling and moderate
calcification, which increase the complexity of PCI.
SD-CTOs are characterized by abundant organizing
CHAPTER 2 Pathology of Chronic Total Occlusions: Implications for Revascularization 17
19%
BMS(n=32)
DES(n=24)
Etiology of In-stent CTO
Major Contributing Risk Factor
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Neoatherosclerotic
rupture
9%
Edge disease
Restenosis
31%
6%
In-stent Calcied
nodule
3%
Acute thrombotic
occlusion 50%
P=0.13 P=0.11
Edge disease
4%
Neointimal
erosion
8%
Hypersensitivity
8%
Neoatherosclerotic
rupture
4%
Restenosis
8%
Acute thrombotic
occlusion 67%
In Acute Thrombotic Occlusion
Overlapping
6%
Protrusion of
necrotic core
6%
Medial tear
56%
Medial tear
Malapposition
69%
Protrusion of
necrotic core
Bifurcation
19%
6%
Protrusion of
Calcied nodule
6%
Overlapping
13%
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
thrombi and necrotic cores, and the least negative
remodeling and calcification. SD-CTOs should be
attempted via the antegrade approach because the
components of such lesions are loose tissue and easier
to penetrate (Figure 2.3). Since the major etiology
of IS-CTO is thrombotic occlusion (Figure 2.8), an
antegrade approach using direction-controlled wiring technique can be effective. Because the abrupt
lumen pattern was more frequently observed in the
proximal lumen, compared to the distal lumen in
CTOs, switching the strategy from the antegrade
approach to the retrograde approach when progress
is not made using antegrade approach may facilitate
crossing. Careful review of angiography and coronary
computed tomography, with intravascular imaging
when necessary, is important to predict the components of plaque in CTOs to aid in determining lesion
complexity and strategy to facilitate crossing.
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.
%
Conclusions
The detailed understanding of pathological characteristics of CTOs can be useful for the procedural success of CTO-PCI. There are several
differences between the types of CTO lesions in
terms of plaque morphologic characteristics,
including thrombotic and calcific components,
which can be affected by the presence of coronary
artery bypass grafts, or bare metal versus drugeluting stents. This in turn can influence the PCI
strategies used. Furthermore, an abrupt pattern in
the proximal lumen and tapered pattern in the
distal lumen may indicate a favorable retrograde
approach to crossing for CTO-PCI. Further
research into the pathological correlates to CTOPCI will hopefully continue to lead to higher procedural success rates.
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