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178 PART IV Wires Technique
Figure 20.1 The CART Technique. A cartoon showing the
(A) The antegrade guide catheter in place (i), antegrade
wire in the subintima and the balloon inflated over the
retrograde wire also the subintimal space (ii); (B) passage
advantage of this technique is that it minimizes subintimal tracking through the CTO lesion. However, it
is not always possible to negotiate a retrograde balloon
inside the occlusion due to friction between the balloon
and the vessel wall. Switching to a different balloon or
advancing the wire as deeply as possible into the subintima may help in these scenarios [10].
Recently, the CART technique has been largely
replaced with the reverse CART although it is still used
in some cases of ostial occlusions, heavily calcified occlusions, and when the retrograde equipment is not long
enough to reach the antegrade guide catheter. Table 20.1
highlights the main procedural differences between the
two techniques. The reverse CART technique consists of
dilating the subintimal space of the CTO lesion with the
balloon inflated over the antegrade guidewire, creating a
space into which the retrograde guidewire is advanced
with the help of a microcatheter such as a 150 cm long
Corsair catheter (Figure 20.2) [2]. With inflation of the
balloon over the antegrade guidewire, the true lumen is
moved aside so that the two subintimal spaces become
one common subintimal space. There should not be any
gap between the antegrade balloon and retrograde
microcatheter during the formation of this common
space.
Another adaptation of the CART technique involves
the use of intravascular ultrasound (IVUS) [11]. IVUS
is useful to estimate the precise size of antegrade
balloon that can lead to medial disruption. Furthermore,
it checks the disruption of the media and the creation of
a common subintimal space. IVUS is also useful to
determine the position of the retrograde guidewire in
the subintimal space especially in scenarios where it is
challenging to maneuver the retrograde wire. For
of the antegrade wire from the true lumen through the
subintimal space (i) and into the distal true lumen around
a deflated retrograde balloon (ii).
example, when the knuckle wire technique is used to
enter the subintimal space through to the true lumen, it
is a good idea to check wire position with IVUS to
avoid subintimal stenting. Lastly, IVUS can be used to
confirm wire position after successful crossing of a
CTO, especially in cases of aorto-ostial lesions to ensure
that the stent will be placed within the lumen of the
vessel. Short-tipped IVUS probes are better as the space
into the occlusion may be limited.
Another technique for difficult crossing scenarios
is to deploy a stent from the antegrade true lumen into
the subintimal space formed by antegrade balloon
inflation. This may create a path for the retrograde
wire to go through [12]. A safer way to do this may be
with guide extenders such as the Guideliner (Vascular
Solutions Inc) or Guidezilla (Boston Scientific, USA)
catheters delivered antegrade to provide a continuous
conduit to the antegrade guide. Unlike a stent, the
guide extension device may be removed or repositioned once there is failure of connection between the
antegrade and retrograde true lumen [13].
The advent of the Gaia wires, with more penetration power and good torque, has ushered in a more
contemporary adaptation of the reverse CART technique where in antegrade preparation is initiated
before retrograde wiring. When antegrade and retrograde guidewires come together in the vessel, a
smaller antegrade balloon (~2.0 mm) is inflated close
to the distal end of CTO. The shoulder of the inflated
balloon is then punctured by the Gaia wires. With
quick deflation of the antegrade balloon, the Gaia
guidewire penetrates the membrane between the different spaces. This reduces the length of subintimal
stenting that is needed [14].
Table 20.1 “Comparison of CART vs REVERSE CART”
Comparison of CART vs REVERSE CART
CART Reverse Cart
Wiring Antegrade Retrograde
Guidance Fluoroscopy Fluoroscopy + IVUS
Retrograde Reentry Retrograde Balloon Antegrade Balloon
CHAPTER 20 Tips and Tricks of the CART and Reverse CART Technique 179
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Figure 20.2 The Reverse CART technique. CTO of the
proximal RCA crossed after (A) Antegrade 2.5
balloon inflated and (B) Pilot 200 guidewire enters true
lumen with the help of a Corsair microcatheter. (C) The
mm
Another tip for the reverse CART technique
involves the inflation of both an antegrade and a retrograde balloon, in a kissing fashion, to create confluent subintimal space. The antegrade balloon is then
kept inflated and punctured by the retrograde guidewire which is advanced while the punctured antegrade balloon is retracted [1].
Finally, in cases of difficulty in navigating the retrograde wire, knuckle wire technique can be used to
enter subintimal space and into the true lumen [2]. A
Fielder XTR, Sion black, Pilot 200, and the Gladius
wire are good for this technique. An IVUS check of
wire positions is always safe before the entry of retrograde wire into antegrade guiding to avoid serious
problems of subintimal stenting at ostial RCA or left
main coronary artery (LMCA), respectively [15].
Once the CTO is crossed via the CART or reverse
CART technique, the retrograde wire is exchanged for
an externalization wire [16]. Several workhorse guidewires come in ≥ 300cm lengths and could be used as
the externalized wire. Often, an RG3 (Asahi Intecc;
330 cm long, 0.010″) or R350 (Vascular Solutions;
350cm long, 0.013″) are used. The Fielder FC 300 cm
can also be used. To complete the externalization of a
wire, the original retrograde wire is navigated into the
antegrade guide. This could be aided by guide
extenders. Once retrograde guidewire enters the antegrade guide, a trapping balloon is inflated within the
antegrade guide next to the wire to allow the delivery
of the retrograde microcatheter into the antegrade
guide. The retrograde wire is then removed while the
retrograde microcatheter is kept in place within the
antegrade guide. The wire to be externalized is
inserted through the microcatheter to the hub of the
antegrade guide. Retrograde wire should then be
pushed out of the antegrade guide. The copilot is
reconnected to the antegrade guide without flushing
to avoid a hydraulic dissection. The retrograde wire
antegrade guide is wired by the retrograde wire and
the Corsair microcatheter is then advanced in the
antegrade guide to allow for a wire exchange to an
externalization wire.
may fail to enter the guide in cases of aorto-ostial
lesions or of extremely tortuous vessels or whenever
there is poor retrograde wire control. In these cares, a
snaring device like the Ensnare (EN Snare; Merit
Medical Systems, South Jordan, USA) can be useful.
Larger snares such as an 18×30 mm EN Snare, which
is 6F compatible are preferred [16]. The snare is introduced into the antegrade guide and opened in the
aorta to capture the externalized wire. Once the wire
is externalized the PCI can be completed over the
externalized wire once the retrograde microcatheter
has been withdrawn into the collateral artery.
Technical and procedural success rates of CTO PCI
have risen tremendously over few years, because of
operator experience, improved equipment, and refinements of retrograde approaches such as the CART and
reverse CART techniques. Further technical improvements are necessary to simplify the techniques making
them more widely used. This will ensure continued
success for these complex interventions.
References
1 Surmely JF, Tsuchikane E, Katoh O et al. New concept for
CTO recanalization using controlled antegrade and retrograde subintimal tracking: the CART technique. J Invasive
Cardiol 2006; 18: 334–338.
2 Matsuno S, Tsuchikane E, Harding SA, Wu EB, Kao HL,
Brilakis ES, Mashayekhi K, Werner GS. Overview and
proposed terminology for the reverse controlled antegrade and retrograde tracking (reverse CART) techniques.
EuroIntervention 2018; 14: 94–101.
3 Kandzari DE. The challenges of chronic total coronary
occlusions: an old problem in a new perspective. J Intervent
Cardiol 2004; 17: 259–267.
4 Srivatsa S, Edwards WD, Boos CM et al. Histologic corre-
lates of angiographic chronic total coronary artery occlusions: influence of occlusion duration on neovascular
channel patterns and intimal plaque composition. J Am
Coll Cardiol 1997; 29: 955–963.
180 PART IV Wires Technique
5 Stone GW, Kandzari DE, Mehran R et al. Percutaneous
recanalization of chronically occluded coronary arteries:
a consensus document: part I. Circulation 2005; 112:
2364–2372.
6 Suzuki T, Hosokawa H, Yokoya K et al. Time-dependent
morphologic characteristics in angiographic chronic
total coronary occlusions. Am J Cardiol 2001; 88:
167–169.
7 Khan MF, Wendel CS, Thai HM, Movahed MR. Effects of
percutaneous revascularization of chronic total occlusions
on clinical outcomes: a meta-analysis comparing successful
versus failed percutaneous intervention for chronic total
occlusion. Catheter Cardiovasc Interv 2013; 82: 95–107.
8 Wu EB, Tsuchikane E, Ge L, Harding SA, Lo S, Lim ST,
Chen JY, Lee SW, Qian J, Kao HL et al. Retrograde versus
antegrade approach for coronary chronic total occlusion
in an algorithm-driven contemporary Asia pacific multicenter registry: comparison of outcomes. Heart Lung
Circ 2019; 29: (6)894-903 pii:S1443-9506(19)31329-0.
9 Hoye A, van Domburg RT, Sonnenschein K, Serruys PW.
Percutaneous coronary intervention for chronic total
occlusions: the Thoraxcenter experience 1992-2002. Eur
Heart J 2005; 26: 2630–2636.
10 Surmely JF, Katoh O, Tsuchikane E et al. Coronary septal
collaterals as an access for the retrograde approach in the
percutaneous treatment of coronary chronic total occlusions. Catheter Cardiovasc Interv 2007; 69: 826–832.
11 Wu EB, Tsuchikane E, Lo S, Lim S, Ge L, Chen J.
Retrograde algorithm for chronic total occlusion from
the Asia Pacific Chronic Total Occlusion club. Asian
Interv 2018; 4: 98–107.
12 Dash D. Guidewire crossing techniques in coronary
chronic total occlusion intervention: A to Z. Indian Heart
J 2017; 68: 410–420.
13 Huang Z, Zhang B, Chai W, Ma D, Liao H, Zhong Z,
Wang F, Lin J. Usefulness and safety of a novel modification of the retrograde approach for the long tortuous
chronic total occlusion of coronary arteries. Int Heart J
2017; 58: 351–356.
14 Dash D. Iteration of reverse controlled antegrade and ret-
rograde tracking for coronary chronic total occlusion
intervention: a current appraisal. Kor Circ J 2020; 50:
867–879.
15 Ito S, Suzuki T, Ito T. Novel technique using intravascular
ultrasound-guided guidewire cross in coronary intervention for uncrossable chronic total occlusions. Circ J 2004;
68: 1088–1092.
16 Grantham JA. The final steps of the retrograde tech-
nique: wire externalization, stenting, and wire removal.
Interv Cardiol Clin 2012; 1(03): 345–348.
21
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CHAPTER 21
Debulking of CTO
Etsuo Tsuchikane
Toyohashi Heart Center, Toyohashi, Japan
Higher patency and freedom from restenosis after
successful recanalization of chronic total occlusions
(CTOs) were greatly increased by the implantation of
DES [1–4]. Despite its positive treatment outcomes,
the delivery of DES in complex anatomy involving
severely calcified and eccentric lesions still remains
challenging. In this chapter, we discuss indications
and techniques of plaque debulking in the DES era,
illustrated by case examples. By the end of the chapter,
the readers will have learned the role of plaque debulking in modern interventional cardiology.
Indications of plaque debulking
The management of heavily calcified lesions represents a formidable challenge for an interventional cardiologist. From a technical standpoint, the geometry
and rigidity of these morphologies often prevent
optimal device delivery and deployment. To overcome such unfavorable lesion subsets, a plaque debulking strategy should be considered. Rotational
atherectomy (RA) and directional coronary atherectomy (DCA) are two of the most common devices
used for plaque debulking in CTO-PCI (percutaneous
coronary interventions). In addition, a newly introduced plaque debulking system, Silverhawk, is considered to be promising in the use of CTO-PCI.
RA involves the use of a high-speed diamond tip
drill that pulverizes the thrombus into microscopic
particles. DCA involves the use of a catheter tip
equipped with a bladed rotor that cuts away the plaque
and the debris is collected in a tiny container. The
SilverHawk Plaque Excision System comprises an
atherectomy device that is threaded through the
lumen of the artery. It comprises a tiny rotating blade
that scrapes the plaque from the lesion and the
scraped material is collected in a chamber in the
device’s tip and is removed from the patient.
Rotational atherectomy
Rotational atherectomy (RA) is used to remove the
plaque by debulking the atherosclerotic material producing millions of microparticles assumed to be
smaller than red blood cells. It facilitates lesion and
device success for a massive plaque with severe calcification. The massive plaque burden in CTO is considered to interfere with full stent expansion and/or
accelerates in-stent neointimal proliferation after
stent expansion.
Plaque debulking of CTO lesions requires careful
case selection. For example, RA should be avoided if a
conventional wire passes through the subintima.
Intravascular ultrasound (IVUS) examination may be
helpful in determining whether RA is suitable. Cases
in which RA is contraindicated include patients with
severe congestive heart failure or severe vessel tortuosity. Furthermore, the RA technique is considered to
be an important factor for procedural success. Because
CTO lesions have a massive plaque burden and insufficient pre-procedural antegrade flow, the rotating
burr should be advanced carefully to prevent the noreflow phenomenon. Careful case selection and an
efficient procedural technique are essential to achieve
successful results without major complications.
Optimal stent deployment may not be possible
unless satisfactory dilatation of the lesion is achieved
and the lesion is made more compliant. Such a lesion
preparation of a severely calcified plaque is assumed
to facilitate stent delivery and symmetrical stent
expansion resulting in more homogeneous drug
delivery. Since RA helps maximize lesion preparation,
restenosis can be prevented by achieving the full
expansion of the drug-eluting stents (DES) in highly
calcified lesions.
To perform RA, a 1.5 mm over-the-wire balloon or
a 3-Fr infusion catheter is used as a RotaWire (Boston
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.
181
182 PART IV Wires Technique
Scientific, Natick, MA) instead of the conventional
guidewire. Predilatation with a 1.5 mm balloon is
performed when necessary. The Rotablator (RotaLink
PLUS, Boston Scientific) burr size is determined and
increased according to the vessel size if necessary.
IVUS imaging should be used to determine the burr
size. High-speed RA is preferred because drug-eluting
stents should be implanted after the atherectomy. For
a case example see Figure 21.1.
Directional coronary atherectomy
Directional coronary atherectomy (DCA), developed
to excise obstructive coronary atheromas, is the only
available device in which the operator decides the
direction of plaque excision. Although pre-stent
plaque debulking by DCA may reduce the rate of
restenosis in complex cases [5, 6], there have been few
studies on debulking strategies with respect to CTO
[6]. In addition, morphological characteristics of
CTO are not always suitable for DCA. Hence, DCA
plays a very limited role in the DES era. In current
clinical practice, we consider DCA only for younger
patients with ostial CTO of the left anterior descending artery (LAD). In this case, optimal plaque debulking is aimed at preventing DES implantation so as to
terminate dual anti-platelet therapy within the first
month.
To perform DCA, the use of an IVUS catheter is
essential. Suitable lesions for DCA were selected on
Figure 21.1 A long CTO in a severely calcified right coronary
artery (a): Although the occlusion was successfully crossed
using a tapered stiff wire (Confianza, Asahi Intecc, Japan),
any 1.5 mm balloon may not cross the lesion (b). A
penetration catheter (Tornus, Asahi Intecc, Japan) was
introduced; however, it could not overcome the most
constricted point of the vessel (arrow in c). Thus, to facilitate
the passage of the balloon beyond this point, another stiff
wire (Miraclebros 12, Asahi Intecc, Japan) was extended
along the first wire to “crush” the tight plaque (d). After the
successful passage of the second wire, a third stiff wire was
introduced because the balloon was still not able to cross the
constricted point even after the plaque was crushed by the
second wire (three wires in e). After withdrawal of two
wires, a 1.5 mm balloon finally crosses the lesion (f) and an
antegrade flow was obtained (g). This technique should be
called the “Crushing plaque technique.” To ensure vessel
dilatation and the passage of DES, RA was performed using a
1.25 mm burr (h) and a 1.75 mm burr (i). After vessel
modification by RA (j), three Cypher stents were immediately
delivered without any friction resistance along with full
expansion leading to a successful angiographic result (k).
CHAPTER 21 Debulking of CTO 183
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the basis of angiographic and IVUS findings and the
patient’s clinical condition. DCA should not be performed in lesions located in vessels that are smaller
than 2.8
mm as assessed by on-line quantitative coronary angiography, lesions with an arc of superficial
calcium greater than 180° as assessed by IVUS, restenotic lesions after stenting or DCA, nonprotected left
main trunk lesions, aorto-ostial lesions, bypass graft
lesions, thrombotic lesions, or cases of acute myocardial infarction. For a case example see Figure 21.2.
The SilverHawk Plaque Excision
System
The SilverHawk Plaque Excision System recently
received approval for peripheral application in the
United States and for both coronary and peripheral
applications in Europe. This device consists of two
components: a low-profile catheter and a palm-sized
drive unit. All device functionality is controlled by a
single on/off thumb-switch that resides on the drive
unit. A tiny blade on the tip of the catheter rotates
when activated and removes the plaque from the
arterial wall. After each pass, the cutter extends
through the nose cone to pack the tissue and maximize
the storage capacity of the collection chamber. The
device can be used to treat very long segments of vessels and can remove 100–200g or more of plaque.
Because CTO presents with a massive plaque burden,
the use of the device can be expected to optimize the
treatment outcome in contemporary CTO-PCI.
Unfortunately, the device has not received approval in
Japan, but it will be applicable in the use of CTO-PCI.
Orbital atherectomy
Orbital atherectomy system (OAS) has also been
introduced for plaque modification, particularly for
calcified plaque in PCI. Although there are still
limited data on the efficacy for CTO interventions,
Figure 21.2 Ostial LAD CTO with mild calcification (a/b).
After confirming the entrance of CTO using an IVUS
catheter inserted into the left circumflex artery (LCx), the
lesion was successfully crossed by an intermediate wire
(Miraclebros 3) (c). The pre-dilatation IVUS image with a
1.5 mm balloon showed a mild calcified massive plaque
burden at the ostium of the LAD that might allow plaque
debulking by DCA (d); however, there was a superficial
calcified plaque in the proximal LAD that could possibly
obstruct the passage of the nose cone of the delivery
(DCA) catheter. To facilitate its passage, RA using a
2.0 mm burr was performed prior to DCA (e). After RA,
IVUS-guided DCA debulking was performed (f), and the
plaque was successfully excised at the LAD ostium (g) to
prevent its shift to LCx after DES implantation. A 3.0 mm
Cypher was implanted in mid-LAD (h) and a 3.5 mm
Cypher was implanted in the ostial LAD as a noncrossover
stent to the left main trunk (i) with successful
angiographic results (j/k). Final IVUS image confirmed fully
expanded stent struts without any plaque shift to LCx (l).
184 PART IV Wires Technique
OAS may play the role of a reasonable treatment
option for complex calcified lesions, such as calcified
CTOs [7]. Further clinical investigations will be
required.
Outcome of CTO-PCI
In the bare metal stent (BMS) era, plaque debulking
played a significant role in the reduction of restenosis
by minimizing massive plaque burden in CTOs [8, 9].
However, the role of plaque debulking in the DES era
has been limited to facilitate device and lesion success.
The higher incidence of procedure-related events may
restrict the use of plaque debulking to certain lesion
subsets, as demonstrated by the DOCTORS
(Debulking Of CTO with Rotational or directional
atherectomy before Stenting) study conducted in
Japan [10]. This study, which was conducted in the
bare metal stent era, was a multi-center, prospective,
randomized trial to evaluate the efficacy of pre-stent
debulking of CTOs. The primary endpoint of this
study was the angiographic restenosis rate at 6 months.
Secondary endpoints were the procedure-related
event rate and the major adverse cardiac event
(MACE) rate at 1 year. Procedure-related events
included MACEs within 30 days (death, Q-wave myocardial infarction, coronary arterial bypass grafting,
target vessel revascularization, or sub-acute thrombosis), procedural failures (flow disturbance, residual
stenosis, or failed device delivery), and procedural
complications (perforation, temporary no-flow, or
non-Q-wave myocardial infarction). In this study, the
incidence of procedure-related events in the debulking group was significantly higher than that in the
nondebulking group (18.1 vs 9.4%, p = 0.04), despite
the fact that patients in the debulking group tended to
have a lower binary restenosis rate than those in the
nondebulking group (23.8 vs 34.6%, p = 0.072).
Role of plaque debulking in CTO-PCI
Optimal stent deployment may not be possible unless
satisfactory dilatation of the lesion is achieved and it is
made more compliant [5]. In such cases, RA still plays a
significant role in patients with severe calcification to
facilitate success and achieve full expansion of the stent
apposed to the vessel wall. The goal of lesion preparation in these patients is to facilitate stent delivery,
reduce plaque shift, and allow optimal stent expansion
[6]. Leaving an unexpanded stent in the arterial wall in
a calcified lesion is likely to be associated with restenosis [11]. Clavijo et al. reported the effect of RA on
heavily calcified coronary lesions treated with DES in
150 consecutive patients (69 patients who underwent
DES implantation without atherectomy and 81 patients
in whom atherectomy was required to facilitate DES
implantation). The clinical success rates were equivalent
in both patient groups, and no differences in in-hospital outcomes were observed between the groups. At 6
months, the target lesion revascularization rate was
4.9% in the DES-alone group and was 4.2% in the
group that underwent DES with RA (p = ns). Sirolimuseluting stents performed well in patients with complex
heavily calcified coronary lesions, with a relatively low
event rate [12]. Although no significant differences
were observed in this study, the results indicate a
significant role of pre-stent lesion modification by RA
in optimizing DES implantation in CTO with heavily
calcified coronary lesions that otherwise do not permit
full stent expansion.
To determine the efficacy of plaque removal by
directional atherectomy before DES implantation for
bifurcated lesions, a multi-center, nonrandomized,
prospective trial was conducted in Japan in which 99
patients were enrolled. Angiographic follow-up was
performed in 89 patients (90% follow-up rate) at a
mean follow-up period of 259 ± 79 days. Restenosis
rates of the main and side-branch were 1.1% (1/89)
and 3.4% (3/89), respectively, and the total restenosis
rate, the primary endpoint of this study, was 4.5%
(4/89). One-year clinical follow-up was accomplished
in 96 patients (97% of the entire cohort). There were
no incidences of death, coronary arterial bypass
grafting, or myocardial infarction in these patients.
No stent thrombosis was observed. However, TLR was
required in the main branch of one patient (1%) and
in the side-branch of another (1%) [13]. Directional
atherectomy provides the best anatomical conditions
for optimal and simple DES implantation because it
removes the massive atherosclerotic plaque of CTOs
located in the ostium of the LAD. In CTOs without a
left main lesion, atherectomy enables implantation of
a DES in the ostium of the LAD without plaque shift
to the circumflex artery. In patients with a left main
lesion, crossover stenting beyond the circumflex
artery with the kissing balloon technique can be conducted after directional atherectomy for the distal left
main LAD and its ostium. These simple DES implantations may reduce the higher restenosis rates of the
side-branch, which are commonly observed in the
current stenting techniques.
On the other hand, we should always keep in mind
the procedural risk of plaque modification in CTOPCI. The PROGRESS CTO Registry reported that
rotational and/or orbital atherectomy significantly
increased peri-procedural risk [14]. Therefore, the use
of atherectomy devices before DES implantation in
CTO-PCI should be very carefully determined
depending on patients’ clinical information and lesion
morphology.
Conclusion
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In the DES era, the role of plaque debulking is limited
to certain complex morphologies that are not satisfactorily treated with conventional angioplasty alone.
Lesion preparation with plaque debulking before DES
implantation may be an appropriate method for
improving device and lesion success without compromising the clinical outcome.
References
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recurrence in chronic total coronary occlusions by paclitaxel-eluting stents. J Am Coll Cardiol 2004; 44: 2301–2306.
Migliorini A, Moschi G, Vergara R et al. Drug-eluting
2
stent-supported percutaneous coronary intervention for
chronic total coronary occlusion. Catheter Cardiovasc
Interv 2006; 67: 344–348.
3
Nakamura S, Muthusamy TS, Bae JH et al. Impact of siroli-
mus-eluting stent on the outcome of patients with chronic
total occlusions. Am J Cardiol 2005; 95: 161–166.
4 Hoye A, Tanabe K, Lemos PA et al. Significant reduction
in restenosis after the use of sirolimus-eluting stents in the
treatment of chronic total occlusions. J Am Coll Cardiol
2004; 43: 1954–1958.
5 Palmer ND, Nair RK, Ramsdale DR. Treatment of calcified
ostial disease by rotational atherectomy and adjunctive
cutting balloon angioplasty prior to stent implantation. Int J
Cardiovasc Intervent 2004; 6: 134–136.
CHAPTER 21 Debulking of CTO 185
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stenting. Rev Cardiovasc Med 2004; 5(suppl 2): S16–S21.
7 Lee MS, Shlofmitz RA, Shlofmitz E et al. Procedural and
long-term ischemic outcomes of tight subtotal occlusions treated with orbital atherectomy: an ORBIT II subanalysis. Cardiovascular Revasc Med 2019; 20: 563–568.
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Braden GA, Young TM, Love WM et al. Rotational ather-
ectomy of chronic total coronary occlusion is associated
with very low clinical rates: the treatment of choice. J Am
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9
Tsuchikane E, Otsuji S, Awata N et al. Impact of pre-stent
plaque debulking for chronic total occlusions on restenosis reduction. J Invasive Cardiol 2001; 13: 584–589.
Tsuchikane E, Suzuki T, Asakura Y et al. and DOCTORS
10
Investigators. Debulking of chronic coronary total occlusions with rotational or directional atherectomy before
stenting. Int J Cardiol 2008; 125: 387–403.
11
Hadjimiltiades S, Tsikaderis D, Louridas G. Rotational
ablation of unexpandable sirolimus-eluting stent. J Invasive
Cardiol 2005; 17: 116–117.
12 Clavijo LC, Steinberg DH, Torguson R et al. Sirolimus-
eluting stents and calcified coronary lesions: clinical outcomes of patients treated with and without rotational
atherectomy. Catheter Cardiovasc Interv 2006; 68: 873–878.
Tsuchikane E, Aizawa T, Tamai H et al. and PERFECT
13
Investigators. Pre-drug eluting stent debulking of bifurcated
coronary lesions. J Am Coll Cardiol 2007; 50: 1941–1945.
14 Xenogiannis I, Karmpaliotis D, Alaswad K et al. Usefulness
of atherectomy in chronic total occlusion interventions
(from the PROGRESS-CTO Registry). Am J Cardiol 2019;
123: 1422–1428.
22
CHAPTER 22
Laser Revascularization in
Coronary CTO
On Topaz
Professor of Medicine, Duke University School of Medicine, Durham, NC, USA
Introduction
The presence of coronary CTO (Chronic Total
Occlusion) as demonstrated by coronary angiography
or autopsy is a testimonial to progression of critical
atherosclerotic vascular obstruction in a de-novo
lesion or in-stent restenosis. The finding of CTO represents as well clinical management challenges, and,
in particular, dilemmas of lesion and vessel revascularization options. The histopathology of CTO
includes calcifications, fibrotic tissue, and organized
thrombus which constitute a complex, flow obstructing morphology. These lesion components carry a
marked impact on the planning and execution of
potential revascularization strategies. The clinical
manifestations of coronary CTO are caused by severe
impairment to tissue perfusion distal to the lesion and
the consequential burden and damage to the myocardium. The classic clinical features associated with
CTO include angina pectoris, acute or chronic coronary syndrome in the form of angina pectoris or myocardial infarction, congestive heart failure, and
arrhythmias. Performance of percutaneous revascularization of CTO entails five critical steps: vessel
engagement; lesion crossing; debulking recanalization
through the obstruction; enlargement of lumen diameter; and facilitation of subsequent stenting.
Cardiovascular lasers of various wavelengths produce
intense electromagnetic energy that interacts favorably with absorbing bio-tissues. Upon absorption of
the laser irradiation the targeted atherosclerotic
plaques are morphologically transformed and modified through mechanisms of vaporization and
removal. The intent of this chapter is to describe the
usefulness of the laser technology in revascularization
of coronary CTO.
CTO prevalence
CTO occlusions are prevalent in patients with coronary artery disease, by some estimates in at least
15–20 % of cases. Most cases of coronary CTO are
detected and assessed during diagnostic coronary arteriography. A large size Canadian academic registry
included over 1600 patients with angiographic proven
CTO [1]. The majority were men (81%), and 87% had
significant angina pectoris corresponding to Canadian
Cardiovascular Society Class 2–4. Patients with STEMI
(ST-segment Elevation Myocardial Infarction) or with
previous CABGS (Coronary Artery Bypass Surgery)
were excluded from the analysis. The patients were
about equally divided into acute coronary syndrome
(excluding STEMI) and stable angina. Noteworthy, Q
waves were only detected in 25% of the territory supplied by the artery that contained a CTO. Data on left
ventricular function was limited to 71% of the enrollees, of whom 84% exhibited mild to normal LV
function. The prevalence of CTO was 14.7% among
the patients who underwent diagnostic coronary angiography, and reached 18.2% in patients with atherosclerotic disease causing 50% or more diameter
stenosis in at least one coronary vessel. Interestingly,
multiple CTOs were identified in nearly 20% of the
patients.
CTO histopathology
The histopathology and morphology of severe atherosclerotic lesions, in particular CTO stenoses, accounts
for their rigidity and noncompliance toward revascularization attempts [2]. It directly correlates with the
success or failure of devices assigned for CTO revascularization. Over time, CTO lesions exhibit distinct
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.
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CHAPTER 22 Laser Revascularization in Coronary CTO 187
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structural compositions. Yalonetsky and colleagues
recently defined three morphologic elements occupying the length of CTO: (1) a proximal thickened
fibrous cap, (2) an organized thrombus in the main
body of the CTO and, (3) fibrous cap at the distal end
of the occlusive plaque [3].
The cardinal role and deleterious impact of calcium
deposits through the entire length of CTOs are well recognized. The presence of calcium increases the complexity and risk of CTO-PCI mainly through resistance
to guidewire crossing, encroachment on balloon dilatation, restriction to debulking and impediment on stent
delivery and deployment [4, 5]. A multivariate analysis
covering the landmark study titled Japanese CTO-PCI
Expert Registry found that calcification was a strong
predictor of procedural failure, with odds ratio 3.264;
confidence interval 1.739–6.125; p<0.001 [6].
Intriguingly, a retrograde approach to CTO recanalization faces similar constrains from calcium embedded
in the CTO lesion as reported in another large size
Japanese multicenter study which was conducted from
2009–2012 to include 5984 CTO-PCI procedures, of
which 1276 interventions (21
%) were performed
through the retrograde approach. The investigators
evaluated the predictive factors for failure of the retrograde approach after successful collateral channel
crossing [7]. While success was obtained in 89.4 % of
patients whose collaterals were successfully crossed,
multivariate analysis demonstrated that lesion calcification was an independent predictor of retrograde
CTO-PCI failure (odds ratio 1.347, 95% confidence
interval, 1.06–1.717, p=0.014). In the United States,
outcome analysis of 755 consecutive CTO-PCI procedures in 734 patients from 2012–2016 demonstrated
that in 9% of participants, operators encountered following successful guidewire application a CTO that
rendered balloon uncrossable. These lesions were more
likely to contain moderate-severe calcification than
balloon crossable lesions [8].
The CTO lesions commonly contain layers of organized thrombus of various ages. Microchannels commonly recanalize the organized thrombus within the
CTO [9]. As a result, while the angiographic hallmark
of CTO is 100% stenosis, the histopathology demonstrates that about 50% of these lesions are, in fact, less
than 100% occluded [10]. From a revascularization
perspective, intriguingly, the intra CTO thrombus on
one hand contributes to the formation of total occlusion and cessation of antegrade flow, yet, on the other
hand, can permit guidewire crossing [11]. The latter
stems from the creation of microvascular recanalization channels within the CTO thrombus which provide delicate anatomic conduits through which a
guidewire can be manipulated to penetrate and
advance across the entire plaque. In contradistinction,
the rigid calcium deposits and fibrotic tissue within
the proximal and distal segments of the CTO build a
formidable anatomic barrier to guidewire penetration
and crossing [3, 12].
CTO – clinical relevance
The clinical manifestations of coronary CTO reflect
the presence of severely impaired tissue perfusion
distal to the index lesion and resultant ischemic
damage to the perfused myocardium. They include
ischemia, angina pectoris, myocardial infarction,
congestive heart failure, arrhythmias, palpitations,
and atrioventricular node conduction abnormalities.
The SCAAR (Swedish Coronary Angiography and
Angioplasty Registry) study demonstrated that CTO
patients were at higher risk of death than that of nonCTO patients at a mean follow up of 3.2 years,
independent of the severity of the underlying coronary artery disease [13]. CTO continue to be identified as the strongest independent predictor of
incomplete revascularization after PCI and a major
reason behind the management selection of bypass
surgery over PCI [14]. CTO lesions have also been
shown to worsen 1-year mortality rates in patients
presenting with acute STEMI compared to patients
with multivessel disease but without CTO [15, 16].
Moreover, in patients with systolic heart failure the
presence of CTO is similarly associated with increased
adjusted mortality in 1 year [17]. These observations
were recently corroborated by a landmark Canadian
study of 10-year follow-up of 1964 consecutive CTO
patients that documented overall mortality of 33%,
despite receiving contemporary medical therapy [18].
Merits of CTO-PCI revascularization
Revascularization of CTO is recognized as one of the
“last frontiers” in interventional cardiology [19]. Long
experience denotes that CTO-PCI commonly encounters complex target morphology that exerts marked
resistance to guidewire crossing and standard balloon
application [20, 21]. The procedure related difficulties
arise from the presence of interspersed layers and
deposits of fibrotic tissue, calcifications, thrombus,
and atherosclerotic material in the CTO [11, 22]. The
abovementioned Canadian academic study [1] reference, conducted just 2 decades ago, reported that the
majority of patients who were managed with coronary
revascularization in fact were referred for CABGS
(Coronary Artery Bypass Surgery) while only 10.7%
underwent CTO-PCI. However, since then, especially
during the last decade, a growing recognition of the
clinical merits granted by CTO-PCI had been globally
shared by leading interventionalists and professional
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