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38
Tab le 4 Recommendations for Reporting of Bifurcation Analyses
Standard reporting of bifurcation analyses
Item Recommendation
Angiographic views Acquire angiograms on at least three matching views at baseline, final
Angulation Report two-dimensional angulations between MV and SB, including a. the
Restenosis
intervention, and follow-up (attempt to: no vessel overlap, minimal target
segment foreshortening, display widest bifurcation angle)
“take-off” angle between the proximal MV to the SB, and b. the “carina angle”
between the distal MV and the SB
1. A single restenosis rate should be provided for the MV and for the SB
(suggestion to use the
bifurcation trials)
2. An overall restenosis rate should be reported for the entire bifurcation lesion
Medina
classification (17) as primary endpoint for
COSTA ET AL.
Segmental Analysis Describe QCA parameters in the subsegmental areas of the bifurcation
Additional reporting Results should further be reported based on the target lesion location, the
Source
: Adapted from Ref. 29.
(Figure 11)
Medina
classification (17), and on the specific treatment strategy of the
bifurcation PCI
Intravascular Ultrasound
IVUS is routinely used to clarify angiographic ambiguity in many clinical scenarios. In general,
IVUS is more useful incomplex lesions where optimization ofacute results iscritical to improve
long-term outcome (33). In bifurcation lesions, IVUS provides valuable baseline and iterative
information regarding plaque distribution, particularly in relation to the SB ostium, vessel size,
and appropriateness of stent expansion particularly at the SB ostium [Fig. 13(A) to 13(C)].
Furukawa et al. (6) demonstrated that the presence and severity of ostial SB plaque as
observed by IVUS is the most important predictor of SB occlusion after bifurcation PCI. In
Figure 11 QCA analysis method proposed for coronary bifurcation including subsegmental analysis in three
distinct locations at the proximal MV, distal MV, and SB.
Source
: Adapted from Ref. 29.

CORONARY ARTERY BIFURCATION LESIONS
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39
Before stenting
2-D
3-D
Figure 12 Illustrations demonstrating distal angle measurements in 3-D reconstruction models of coronary
bifurcations: (A) distal RCA bifurcation and (B) proximal LAD bifurcation.
After stenting Before stenting
2-D
3-D
After stenting
(B)(A)
this study, the SB ostium was assessed by an IVUS pullback from distal to proximal MV and
was classified according to the IVUS findings into group 1, angiographic ostial stenosis due
to atherosclerotic plaque visualized only in the MV (n = 61); and group 2, angiographic ostial
stenosis due to atherosclerotic plaque involving the SB ostium. There were no differences in
baseline SB reference diameter (1.75 ± 0.48 mm) and percent diameter stenosis between the
groups. After MV stenting, group 2 had significantly higher frequency of SB deterioration
(defined as final TIMI flow ≤2) compared to group 1 (35% vs. 8.2%, p = 0.003). Also, the
presence ofeccentric and diffuse plaque in the MVaround the SB ostium significantly increased
SB deterioration.
The question whether IVUS pullback in the MV is sufficient to characterize the degree
of SB ostium involvement, compared to an IVUS pullback from the SB, is important and the
data suggest that it is not (Fig. 14). Van der Waal and colleagues (34) performed IVUS pullback
in the MV and the SB in bifurcation lesions. They studied three segments: (a) distal segment,
measured 3 mm distal to the bifurcation (MV and SB); (b) bifurcation carina,measured3mm
starting atthe first framein which thedistal branch (MVor SB) wasvisualized and endedwhere
the LAD assumed a circular shape; and (c) proximal MV (LAD), measured 3 mm proximal to
the bifurcation carina. This study showed the following: (i) IVUS measurements of the proximal
MV differed significantly between the MV versus the SB pullback; (ii) the mean vessel area and
mean vessel diameter at the carina were significantly larger during MV pullback compared to
SB pullback; and (iii) there was no relationship between the IVUS measurements at different
bifurcation segments and the 3-D bifurcation angle.
Nonetheless, IVUS interrogation of bifurcation lesions may be challenging because the
image in the carina usuallyappears oval or irregular in shape. Standardized IVUS methodology
for bifurcation analysis has not been considered in previous IVUS and bifurcation consensus
documents. Thus, the findings from van der Waal et al. study strengthen the recommendation
for performance of IVUS pullbacks from both the MV and the SB for assessment of bifurcations
rather than one pullback, as two pullbacks allow better understanding of the geometry of the
bifurcation, especially the SB ostium. One of the authors of this chapter (Marco Costa, MD,
personal communication) proposed an IVUS methodology for bifurcation lesions as depicted in
Figure 15. It includes performance of quantitative analysis in four distinct segments including
proximal MV,distal MV, SB, and carina. The carina was defined within 5 mm from the bifurcation
point and calculated as the average of value obtained from IVUS pullbacks from both the MV
and the SB.

40
COSTA ET AL.
Virtual Histology and Optical Coherence Tomography
Although IVUS has provided valuable insights into our understanding of bifurcation anatomy
and its response to intervention, IVUS imaging does not have the required resolution to provide insights into bifurcation plaque vulnerability. Recent studies using virtual histology (VH)
and optical coherence tomography (OCT) have shed light on these issues. A study by Gonzalo
et al. (35) evaluated the in vivo frequency and distribution of high-risk plaques at bifurcations
using a combined plaque assessment with IVUS-VH and OCT. IVUS-VH and OCT analysis
of coronary bifurcations was performed in 30 patients (103 lesions). All lesions were considered nonsignificant by angiographic criteria and had a MLA >4.0 mm
2
. The lesions were
(a)
(b)
(c)
LAD
(d)
(A)
Figure 13 Examples of IVUS cross-sectional images assessing coronary bifurcations. (A)—(a, b) Angiograms
demonstrating proximal LAD/Diagonal bifurcation lesion: SB ostium involvement not visualized in (a), better
assessed in (b). (c) SB ostium (pullback from SB) demonstrating significant amount of plaque located opposite
to the flow divider. (d) Distal reference of the SB. (B)—(a) angiogram demonstrating proximal LAD/Diagonal
bifurcation lesion: Note that the MV has moderate stenosis by angiography. (b) MV proximal reference (IVUS).
(c) MV minimum lumen area with large plaque burden (IVUS). (d) MV distal reference(IVUS). (e)SB ostium(IVUS).
(f) SB distal reference (IVUS). (C) LAD/Diagonal bifurcation post-double stenting implant (“crush” technique).
(a, b) Final angiograms demonstrating optimal angiographicresult. (c) SBdistal reference. (d) SB ostium minimum
stent area with significant stent underexpansion compared to distal reference.
(
Continued on pages 41 and 42
)

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41
analyzed at three cross-section locations: (a) proximal rim of the ostium (first frame proximal
to the SB take-off); (b) in-bifurcation (frame with the larger SB ostial diameter); and (c) distal
rim of the SB ostium (first frame distal to the SB take-off) (Fig. 16). The authors predefined
the following characteristics for identifying high-risk plaque morphology: (a) fibroatheroma
(FA)-–the presence of more than 10% confluent necrotic core covered by a fibrous cap thicker
than 65 m; (b) calcified FA (CaFA)-–FA with more than 10% of confluent dense calcium;
(c) IVUS-VH/OCT-derived thin capped FA (TCFA)-–more than 10% confluent necrotic core at
the lumen covered by a fibrous cap <65 m; and (d) IVUS-VH/OCT-derived calcified TCFA
(CaTCFA)-–TCFA with more than 10% of confluent dense-calcium.
Overall, themean area ofnecrotic coreand the mean percentage of necrotic core decreased
from proximal to distal location. Conversely, the mean cap thickness was lower in the proximal
rim and increased from proximal to distal location. The distribution of FA, CaFA, TCFA, and
CaTCFA plaque components were 8.4%, 14.7%, 10.5%, and 5.3% in the proximal rim; 4.9%,
14.6%, 7.8%, and 5.8% in the in-bifurcation; and 5.3%, 13.7%, 3.2%, and 2.1% in the distal rim;
respectively. In addition, thin caps (<65 m) were more often located in the proximal rim
(e)
(f)
LAD
(a)
b
c
d
(b)
(c)
f
e
(d)
(B)
Figure 13
(Continued)
(
Continued on page 42
)

42
COSTA ET AL.
(a)
(b)
(c)
(d)
LAD
(C)
Figure 13
(a)
(b)
MV
(Continued)
SB
(c)
MV
SB
Figure 14 Angiography of an LAD/diagonal
bifurcation lesion (a), illustrating the observation
that IVUS pullback in the main vessel (b) is not
adequate for accurate imaging of the SB ostium
compared to direct imaging of the SB (c).

CORONARY ARTERY BIFURCATION LESIONS
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MB Carina MT
43
MT
Carina (5 mm)
SB
MB
A
B
SB Carina MT
Figure 15 Proposed IVUS methodology for evaluation of coronary bifurcation lesions.
Figure 16 (
cross-sections using virtual histology and optical coherence tomography.
See color insert
) An illustration of the proximal rim, in-bifurcation, and distal rim of bifurcation
Source
: Adapted from Ref. 35.

44
COSTA ET AL.
(A)
Figure 17 Illustration of MSCT extraction of the cross-section of a LAD bifurcation analyzed from the 3-D
dataset: (A) plane through the mother and side branches of the bifurcation of interest; (B) imaging plane;
(C) plane magnification, star indicates the flow divides and the arrows (D and E) indicate the position of the
cross-sections; (D) cross-section of the distal MV; (E) cross-section of the SB; (F) cross-section division into
quadrants according to expected WSS level, as demonstrated in (D and E).
(B) (C)
(D)
(E)
Source
(F)
Pericardial
side
Myocardial
side
: Adapted from Ref. 36.
compared to the in-bifurcation and distal rims (44.1% vs. 41.2% vs. 14.7%). Furthermore, highrisk lesions had significantly greater vessel area and plaque burden, but similar lumen area
compared to non–high-risk lesions.
Multislice Computed Tomography (MSCT)
The introduction of MSCT presentsa greatopportunity to study and categorize the 3-D structure
of coronary bifurcation anatomy (Fig. 17).
A study by van der Giessen et al. (36) assessed the plaque distribution and morphology
near bifurcations with 64-slice computed tomography in relation to wall shear stress distribution. In this analysis, plaque distribution was evaluated in two locations: distal LM-LAD/LCx
and LAD/Diagonal. Analysis was performed at a plane where both the MV and the SB were
visible and the distal angle was maximal. Overall, 28 patients (65 lesions) with suspected CAD
underwent MSCT evaluation. Plaques were more often found in low wall shear stress regions
(62–72%) compared to high wall shearstress regions(31–38%). Another study byKawasaki et al.
(37) investigated bifurcation angles in 209 patients undergoing 64-MSCT because of symptoms
of angina. In this study, the prevalence of “steep” (proximal) angle (<110 degrees) was significantly higher in the LM (26%) compared to non-LM locations (p < 0.05), demonstrating that
MSCT can clarifythe 3-D structure of coronary bifurcation and may provide useful information
for bifurcation PCI strategy. Finally, a study by Rodriguez-Granillo et al. (38), investigating the
differences in plaque burden at different segments of the LM bifurcation and its relationship
with the bifurcation angle in 50 patients undergoing 40-row MSCT analysis, demonstrated that
>90% of plaques were located opposite to theflow divider,localized at the ostial LAD.Also, the
median distal angle was 88.5 degrees (diseasedLAD hadsignificantly increasedangle compared
to nondiseased LAD; p = 0.018).
THE LEFT MAIN CORONARY ARTERY BIFURCATION: A DIFFERENT ANIMAL
The bifurcation anatomy of the distal left main coronary artery (LMCA) is different from that of
non-LMCA bifurcations with respect to vessel size (larger) and proximal and distal angles.
Although the MEDINA classification is also used to classify LMCA bifurcation lesions, it
provides limited insight in terms of actionable information. The LMCA perfuse most of the

CORONARY ARTERY BIFURCATION LESIONS
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(A)
(B)
Figure 18 MSCT imaging demonstrating plaque location within the LM bifurcation.
45
ventricular myocardium (68.8% of the cardiac muscle mass and 79% of the left ventricular cardiac muscle mass) (39). The anatomy of the LMCA has been described in detail by Reig and
Petit (40). In this study, the average length of the LMCA was 10.8 mm. Short (<5 mm), medium
length (>5mmto<15 mm), and long (>15 mm) LMCA was observed in 7.4%, 73.7%, and
18.9% of the study population, respectively.
was 4.86 mm.
Although the LMCA often ends with a bifurcation (the LAD and the LCx), it
The average diameter of the LMCA at midpoint
does divide into three or more branches in more than one-third (38%) of the cases. The average
angle between the LAD and the LCx is
∼90 degrees (86.7
degrees). Correlation between the
angle and the length of LM, with the longest LM having the largest angle of division, has also
been reported. Autopsy has also limitations in assessing bifurcation since it does not consider
the natural dynamic of the bifurcation along the cardiac cycle. Recently, a 4-D (X, Y, Z axes
+ time) assessment by MSCT has been developed for assessing coronary bifurcation anatomy
more quantitatively, considering the movement of the heart (Fig. 18).
SUMMARY
The complexity of performing PCI in coronary bifurcation lesions is simply due to the operator
efforts to maintain optimal patency of the SB while optimally treating the MV. These efforts
are well justified because side branch compromise can lead to myocardial injury. The dominant
viewpoint ofrelying exclusivelyon theMedina classificationto characterizebifurcation anatomy
in practice and clinical trials may be misguided! The Medina classification fails to capture key
bifurcation anatomicelements (SB ostium lesion severityand length, SB angulation andSB size)
that have been shown to increase the risk of SB compromise during bifurcation PCI. In other
words, this classification is not designed to identify the “at risk” bifurcations where the chances
of SB compromise during PCI is highest. Although improvements in angiographic methods
of bifurcation anatomy characterization are important other imaging modalities are needed to
further enhance our understanding of bifurcation anatomy. In clinical practice, physician operators should make individual judgments regarding technique choice based on comprehensive
analysis of bifurcation anatomy that allow the identification of “at risk” bifurcations that may
need tailored treatment techniques. With respect to the ongoing efforts to build a more relevant
evidence-base for treatment of coronary bifurcation lesions more focus should be placed on
inclusion of “at risk” bifurcations as defined by comprehensive anatomic analysis.

46
COSTA ET AL.
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