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(a)
(c)
(b)
(d)
(e)
(B)
Figure 4 (
Continued
)
CORONARY ARTERY BIFURCATION INTERVENTIONS
Tab le 3 Quantitative Angiographic Measurements: RCTs of ES Vs. PS
NORDIC BBK CACTUS
Elective Provisional Elective Provisional Elective Provisional
(
N
= 206) (N= 207) (N= 101) (N= 101) (N= 177) (N= 173)
Main vessel
Reference (mm) 3.3 ± 0.41 3.3 ± 0.41 3.08 ± 0.40 3.08 ± 0.38 2.85 ± 0.33 2.74 ± 0.35
Lesion length (mm) 7.5 ± 7.5 8 ± 8.3 21.7 ± 7.5 20.9 ± 8.2 15.8 ± 8.7 14.7 ± 8.2
Diameter
stenosis (%)
Side branch
Reference (mm) 2.6 ± 0.3 2.6 ± 0.4 2.39 ± 0.31 2.38 ± 0.37 2.3 ± 0.31 2.16 ± 0.33
Lesion length (mm) 6.4 ± 4.7 6.0 ± 4.8 10.4 ± 4.1 9.9 ±4.2 5.9 ± 4.7 5.7 ± 4.2
Diameter
stenosis (%)
Bifurcation morphology
True bifurcations NA 75% 94%
No SB disease NA 25% 6%
Bifurcation angle <70 48–50 NA
50 ± 25 52 ± 24 54.9 ± 24.3 54.9 ±24.3 68 ± 12 69 ± 12
47 ± 26 46 ± 2 53.1 ± 23.5 54.4 ± 22.3 63 ± 12 61 ± 13
9
was associated with large periprocedural MI (15% vs. 1.1%; p = 0.02). The rate of MI after SBO
depends on the size of the myocardial territory supplied by the SB and the definition of MI,
hence the wide variability in the reported rate of procedural MI after SBO (7–27%) (17–20).
Furthermore, the concept of “threatened” SB morphologies is important because the incidence of SBO varies widely accordingly to varying morphologies that are also not reflected in
the Medina classification (18,21). In the study by Aliabadi and colleagues (18), SBO occurred in
7.9% of patients without threatened SB morphology versus 80% of patients with threatened SB
morphology [Fig. 5(A) and 5(B)].
The fact that the rate of SBO in the PS arms of the RCTs (10–12) was very low could
mean one of two things: either that the operators, technology, and techniques have improved
so much that the concept of “at risk” bifurcations have become irrelevant and does not impact
SB occlusion rates or that the patients with “at risk” bifurcations were not well represented in
these trials. We propose the latter possibility. In fact, a recent study by Gil et al. (22) have shown
a functional occlusion rate of 17% in consecutive patients treated with PS despite the fact that
only one-thirdof the study population hadtrue bifurcations. Therefore, we think that PS should
not be the default strategy in “at risk” bifurcations that involve a large SB. A case in point is the
patient in Figure 6. This patient has a proximal LAD bifurcation lesion involving a moderate
size diagonal branch. Provisional stenting of this lesion was adopted, although this patient
does not fit the profile of those patients enrolled in the RCTs (SB with severe ostial lesion and
approximately a 90-degree angulation). Despite a jailed wire technique, the SB occluded after
deploying the MV stent and the operator was not able to salvage it despite prolonged attempts
with several wires. The patient suffered an STEMI. In hindsight, did the evidence-base apply to
this patient? The answer is no.
SUMMARY
The currently available evidence-base pertaining to treatment of bifurcation lesions is not adequate to inform decision making in all patients with bifurcation lesions, hence a gap still exists
between the evidence-base and patient-centered decision making. Although meta-analyses of
the existingRCTs improve the statistical powerof the data,they do notsolve the problem of trial
design (23,24). The reason for the gap between “evidence-base” and patient-centered decision
making is thatthe research methodology used in the RCTsdoes not simulate the questionsasked
in practice.This position shouldnot be construed tothe effect that clinicalresearch isdestined to
be disconnected from clinical practice, but it meant to emphasize that clinical research can only
provide answers to the questions that we pose and within the framework we apply. Physicians
10
1a. 1b. 2b.2a.
(A)
100
80
MOUSSA AND COLOMBO
2d.2c.
60
40
20
Side branch occlusion (%)
0
Threatened
morphology
(n=35)
p < 0.0001
Nonthreatened
morphology
(n=189)
(B)
Figure 5 The concept of “threatened” SB morphologies. (A)(
ized by SBs with >50% ostial narrowing, where the origin is completely spanned by either the diseased segment
of the index lesion (1a) or arises adjacent to, but is partially contiguous with, the diseased index lesion (1b). (
panel
) Nonthreatened SB morphologies includes four subtypes: SBs without (2a) or with ostial narrowing (2b) that
were incidentally covered by stents that extended beyond the diseased segment of the index lesion; disease-free
SB arising just adjacent to the diseased segment of the parent vessel (2c); SBs without ostial disease arising from
parent vessel lesion spanning the entire origin of the SB (2d). (B) Comparison of the incidence of SBO based
on threatened versus nonthreatened morphology. The incidence of SBO was significantly higher in threatened
morphologies (80%) than in nonthreatened morphologies (7.9%).
initiate their inquiry for solutions from the demands of the patient’s particular condition and
not from the demand for generalizable knowledge, and their goal is just as specific: to treat the
Left panel
Source
) threatened SB morphologies character-
Right
: Adapted from Ref. 18.
patient’s illness, not to test the therapy.
To generate an evidence-base that can be used to guide decision making in patients with
“complex bifurcation lesions,” a RCT should
(a) include patients with complex “at risk” bifurcations, that is, patients with true bifurcation
lesions involving moderate-to-large side branches with severe SB ostial stenosis (not 50–60%
stenosis) and/or complex bifurcation angles;
(b) utilize a randomization strategy that simulate clinical practice, that is, on one hand, all
patients will be allocated to PS; on the other hand, the operator will triage patients to PS or
EDS based on predefined anatomic criteria.
(c) Operators participating in these trials should possess familiarity and skills in performing
a variety of double stenting techniques.
Surely, this would be a complex trial design, but so is clinical decision making! Until such
a RCT is performed, clinicians should individualize decision making based on the particulars
of patient’s bifurcation anatomy.
CORONARY ARTERY BIFURCATION INTERVENTIONS
(A) (B)
11
(C)
(D)
Figure 6 Coronary angiography in RAO cranial (A) and LAO cranial (B) projections, illustrating a midLAD/diagonal bifurcation lesion (0,1,1). Note the severity and length of the SB ostial lesion; (C)a3.0mm×
28 mm DES deployed in the mid-LAD with a jailed wire in the diagonal branch; (D) coronary angiography in
the RAO cranial projection poststent deployment demonstrating compromised flow in the diagonal branch (with
chest pain and ST elevation); (E) failure to re-wire the diagonal branch after using multiple wires over 20 minutes; (F) diagonal branch occlusion (with chest pain and ST elevation); (G, H) five-month follow-up coronary
angiography in RAO cranial (G) and LAO cranial (H) projections, illustrating persistent occlusion of the diagonal
branch. (
Continued on page 12
)
12
MOUSSA AND COLOMBO
Figure 6 (
Continued
)
CORONARY ARTERY BIFURCATION INTERVENTIONS
13
REFERENCES
1. YamashitaT, Nishida T,Adamian MG,et al. Bifurcation lesions: two stents versusone stent:immediate
and follow-up results. J Am Coll Cardiol 2000; 35:1145–1151.
2. Al Suwaidi J, Berger PB, Rihal CS, et al. Immediate and long-term outcome of intracoronary stent
implantation for true bifurcation lesions. J Am Coll Cardiol 2000; 35(4):929–936.
3. Lefevre T, Louvard Y, Morice MC, et al. Stenting of bifurcation lesions: classification, treatments, and
results. Catheter Cardiovasc Interv 2000; 49(3):274–283.
4. Al Suwaidi J, Yeh W, Cohen HA, et al. Immediate and one-year outcome in patients with coronary
bifurcation lesions in the modern era (NHLBI dynamic registry). Am J Cardiol 2001; 87:1139–1144.
5. Cervinka P, Stasek J, Pleskot M, et al. Treatment of coronary bifurcation lesions by stent implantation
only in parent vessel and angioplasty in side branch: immediate and long-term outcome. J Invasive
Cardiol 2002; 14(12):735–740.
6. Assali AR, Teplitsky I, Hasdai D, et al. Coronary bifurcation lesions: to stent one branch or both?
J Invasive Cardiol 2004; 16(9):447–450.
7. Costa RA, Moussa I. Percutaneous treatment of coronary bifurcation lesions in the era of drug-eluting
stents. Minerva Cardioangiol 2006; 54(5):577–589.
8. Pan M, de Lezo JS, Medina A, et al. Rapamycin-eluting stents for the treatment of bifurcated coronary
lesions: a randomized comparison of a simple versus complex strategy. Am Heart J 2004; 148:857–864.
9. Colombo A, Moses JW, Morice MC, et al. Randomized study to evaluate sirolimus-eluting stents
implanted at coronary bifurcation lesions. Circulation 2004; 109:1244 –1249.
10. Steigen TK, Maeng M, Wiseth R, et al. Randomized study on simple versus complex stenting of
coronary artery bifurcation lesions: the Nordic bifurcation study. Circulation 2006; 114:1955–1961.
11. Ferenc M, Gick M, Kienzle RP, et al. Randomized trial on routine vs. provisional T-stenting in the
treatment of de novo coronary bifurcation lesions. Eur Heart J 2008; 29:2859–2867.
12. Colombo A, Bramucci E, Sacc`a S, et al. Randomized study of the crush technique versus provisional
side-branch stenting in true coronary bifurcations. The CACTUS (Coronary Bifurcations: Application
of the Crushing Technique Using Sirolimus-Eluting Stents) study. Circulation 2009; 119:71–78.
13. Medina A, Suarez de Lezo J, Pan M. A new classification of coronary bifurcation lesions. Rev Esp
Cardiol 2006; 59(2):183.
14. Movahed MR.Coronary arterybifurcationlesion classifications,interventional techniques,and clinical
outcome. Expert Rev Cardiovasc Ther 2008; 6(2):261–274.
15. Meier B, Gruentzig AR, King SB, et al. Risk of side branch occlusion during coronary angioplasty. Am
J Cardiol 1984; 53(1):10–14.
16. Arora RR,Raymond RE,Dimas AP,et al.Side branch occlusionduring coronaryangioplasty: incidence,
angiographic characteristics, and outcome. Cathet Cardiovasc Diagn 1989; 18(4):210–212.
17. Chaudhry EC, Dauerman KP, Sarnoski CL, et al. Percutaneous coronary intervention for major bifurcation lesions using the simple approach: risk of myocardial infarction. J Thromb Thrombolysis 2007;
24(1):7–13.
18. Aliabadi D, Tilli FV, Bowers TR, et al. Incidence and angiographic predictors of side branch occlusion
following high-pressure intracoronary stenting. Am J Cardiol 1997; 80:994–997.
19. Bhargava B, Waksman R, Lansky AJ, et al. Clinical outcomes of compromised side branch (stent jail)
after coronary stenting with the NIR stent. Cathet Cardiovasc Intervent 2001; 54:295–300.
20. Paez L, Moreno R, Alcocer A, et al. Side branch occlusion during direct stent implantation. Incidence
and related factors. Arch Cardiol Mex 2005; 75(3):252–259.
21. Furukawa E, Hibi K, Kosuge M, et al. Intravascular ultrasound predictors of side branch occlusion in
bifurcation lesions after percutaneous coronary intervention. Circ J 2005; 69(3):325–330.
22. Gil RJ, Vassilev D, Formuszewicz R, et al. The Carina angle—new geometrical parameter associated
with periproceduralside branch compromise and thelong-term results incoronary bifurcation lesions
with main vessel stenting only. J Interv Cardiol 2009; 22(6):E1–E10. Epub 2009 Aug 20.
23. Niccoli G, Ferrante G, Porto I, et al. Coronary bifurcation lesions: to stent one branch or both? A
meta-analysis of patients treated with drug eluting stents. Int J Cardiol 2010; 139(1):80–91. Epub 2008
Nov 22.
24. Zhang F,Dong L, Ge J. Simple versus complexstenting strategy for coronary artery bifurcation lesions
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July 29, 2009]. Heart 2009; 95(20):1676–1681.
2
Coronary Artery Bifurcation Lesions:
Anatomy 101
Ricardo A. Costa
Instituto Dante Pazzanese de Cardiologia & Cardiovascular Research Center, S˜ao Paulo, Brazil
Hiroyuki Kyono and Marco Costa
Harrington-McLaughlin Heart and Vascular Institute, University Hospitals, Case Western Reserve University,
Cleveland, Ohio, U.S.A.
Mary E. Russell
Ascent Translational Sciences, Inc., Carlisle, Massachusetts, U.S.A.
Issam D. Moussa
Cardiac Catheterization Laboratory, New York Presbyterian Hospital–Weill Medical College of Cornell University,
New York, New York, U.S.A.
INTRODUCTION
PCI in coronary bifurcation lesions continue to be a focus of debate and interest because of its
complexity with respect to obtaining an optimal result in the main vessel (MV) while maintaining adequate patency of the side branch (SB). This procedural complexity is responsible for the
fact that bifurcation PCI is associated with higher incidence of procedural complications and
worse clinical outcomes compared with non-bifurcation PCI.
Even though several technical approaches have been advocated for bifurcation PCI, the
risk of SBcompromise isstill amajor concernthat drives new innovations and new techniquesin
this space. Although angiographic SB compromise is not always hemodynamically significant
when assessed physiologically (1), it can result in periprocedural myocardial infarction. The
causes and consequences of SB compromise during bifurcation PCI depend on well-defined
bifurcation anatomic characteristics (2–6), size of the territory supplied by the SB, and the
physiologic severity of the flow compromise in the SB. Therefore, defining and understanding
bifurcation anatomy is critical for the success of any bifurcation PCI strategy.
This chapter reviews the following:
r
Defining coronary bifurcation anatomy
r
Bifurcation classification schemes: advantages and limitations
r
The bifurcation anatomic features that affect the frequency and severity of SB compromise
r
Novel imaging modalities of coronary bifurcations
DEFINING CORONARY BIFURCATION ANATOMY
What is a Coronary Bifurcation Lesion?
A coronary bifurcation encompasses three distinct anatomical segments: proximal MV (including the bifurcation carina), distal MV, and SB [Fig. 1(A)]. The bifurcation carina (or MV-SB
“transition zone”) is considered to be the core of the coronary bifurcation anatomy and is
delimited proximally by the inflection point of the MV and SB and distally by the takeoff of
both distal branches. In general, each coronary bifurcation presents with an unique anatomy
represented by (a) conical shape connecting proximal and distal segments; (b) different vessel
diameters at each segment location, that is, larger proximal MV reference diameter compared
with smaller reference diameter in distal branches; (c) negative remodeling at the SB ostium;
(d) proximal to distal vessel diameter tapering; and (e) nonuniform geometrical distribution of
(A)
(a)
(b)
(d)
(c)
(e)
(B)
Figure 1 (A) Coronary bifurcation lesion (LAD/Diagonal). (B)(
of coronary plaque in a bifurcation lesion. (a) Longitudinal section of trifurcation (left main/LAD/Ramus intermedicus/CX). There are atherosclerotic plaques in the lateral wall, while the flow divider regions are spared (b). (c)
Longitudinal section taken in the region of LCM/left obtuse marginal bifurcation. Note, severe luminal narrowing
located at, and proximal to, the bifurcation. Low shear regions show atherosclerotic plaque development including
necrotic core formation whereas flow divider regions show minimal intimal thickening (d, e).
from Ref. 7. Courtesy of Virmani R et al. (C)(
(red) and outer vessel wall (green) of the left main coronary artery, left main bifurcation, left anterior descending
coronary artery (LAD), and circumflex coronary artery (a). Detailed view of the left main bifurcation (white box)
demonstrating the blood flow pattern in the lumen with an area (
side of the LAD (b), where lower values of computed endothelial shear stress (c) and increased plaque thickness
(d) are found.
Source
: Adapted from Ref. 9.
See color insert
See color insert
) Three-dimensional reconstruction of the lumen
arrow
) of disturbed slow recirculating flow on the
) Representative histologic images
Source
: Adapted
(
Continued on page 16
)
16
COSTA ET AL.
(a)
(b)
(c) (d)
(C)
Figure 1 (
See color insert)(Continued)
atherosclerotic plaque that can involve one, two, or all three anatomical segments, sparing the
flow divider [Fig. 1(B)] (7).
Histopathological studieshad demonstrated greater deposits of elastictissue surrounding
the SB ostium compared to other locations in the coronary tree, which could partially explain
the elastic recoil and spasm frequently seen at this location.
Coronary bifurcation lesions are
typically defined by the presence of a stenosis of at least 50% within 3 mm of a bifurcation
carina and may be found in every segment of the coronary tree with a side branch involved.
Atherosclerotic plaques are usually localized in vascular regions with low wall shear stress. In
onary bifurcations, it has been shown that the outer wall is exposed to low wall shear stress
cor
compared to the flow divider, where high wall shear stress is present [Fig. 1(C)] (8,9).
Ex Vivo Characterization of Coronary Bifurcation Lesions
A study by Russell et al. (10) reported an ex vivo characterization of coronary bifurcation
lesions, evaluating the intersections of coronary bifurcations by measuring vessel diameters,
angles, and shapes at the SB ostium in human coronary arteries with a combination of a microscope (Smartscope MVP100) and computer program (Gage-X metrology software) specifically cal-
ibrated for video-based inspection and measurement (34-fold magnification). In this experiment,
retrograde polymer injection was performed to create casts of the human coronary tree in 23
human adult cadavers to characterize the anatomy of the SB vessels relative to the MV. This
experiment demonstrated a complex and asymmetric geometry at the MV-SB transition zone
(carina) of the bifurcation. The major forms of asymmetry included curvilinear junctions, taper-
ing diameters, and an elliptical SB takeoff rather than spherical or round forms [Fig. 2(A)]. This
study demonstrated the following:
1. Vessel tapering is more pronounced in the SB compared to the MV (2.5-fold greater). The
relative reduction in vessel diameter within the bifurcation length in the MV (proximal to
distal) was 17% compared to 30% in the SB [Fig. 2(B]).
CORONARY ARTERY BIFURCATION LESIONS
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
MB proximal
b
f
e
a
MB distal
i
h
g
c
(A)
17
d
SB
(B)
(C)
Figure 2 (A) Schematic illustration demonstrating differentsegments and/orspots withinthe bifurcations (derived
from Russell et al.): a, region defined as
inflexion and distally (laterally) by the take-off of both distal branches; b, proximal MV axis or centerline, used as
landmark to assess proximal angle or “take-off” angle (between b and d); c, distal MV axis or centerline, used
as landmark to assess distal angle or “carina” angle (c and d); d, SB axis or centerline, used as landmark to
assess both “take-off” and “carina” angles; e, point where all axis or centerlines from the three segments of the
bifurcation meet (“point of bifurcation”), landmark for assessing bifurcation angles (intersection angles); f and g,
proximal and distal transition angles (“obtuse” angles), defined as the initial angle in the MV–SB transition zone
as measured from the MV; h, SB “ostium” diameter (defined as the distance between the inflection points of
the MV and SB on the proximal and distal sides; i, SB ostium diameter typically measured by QCA and IVUS.
(B) Cast of a human coronary bifurcation demonstrating the location for vessel diameter measurement. Overall,
the mean vessel diameters at proximal MV, distal MV, and SB were the following according to each myocardial
territory— LMCA: 4.46 ± 0.97 mm, 2.91 ± 0.44 mm, and 2.81 ± 0.46 mm; LAD/Diagonal (1st major branch):
3.06 ± 0.40 mm, 2.47 ± 0.31 mm, and 2.10 ±0.22 mm; for LCx/OM (1st major branch): 2.95 ± 0.51 mm, 2.46 ±
0.38 mm, and 2.07 ±0.25 mm; for RCA-PDA/PLSA: 2.58 ± 0.48 mm, 2.21 ±0.41 mm, and 1.79 ±0.11 mm. SB
ostium: 2.45 ± 0.71 mm,2.36 ±0.54 mm, and 2.17 ± 0.37 mm; for the LAD, LCX and RCA locations, respectively.
(C) Location of transitional and intersection angles at coronary bifurcations. (D) Plots of measurements of transitional and intersection angles at coronary bifurcations. (E) SB ostium geometry.
carina
(or MV–SB transition zone), delimited proximally by the MV–SB
Source
: Adapted from Ref. 10.
(
Continued on page 18
)
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