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J Cardiol 2007 Jun; 49（6）: 313 – 321

Impact of Highly Asymmetric Stent
Expansion After Sirolimus-Eluting
Stent Implantation on TwelveMonth Clinical Outcomes
Masatsugu NAKANO, MD
Kenji WAGATSUMA, MD
Atsushi IGA, MD
Hideo NII, MD
Hideo

AMANO, MD

Mikihito TODA, MD
Junichi YAMAZAKI, MD, FJCC＊
Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
Objectives. This study investigated the impact of highly asymmetric stent expansion after sirolimus-eluting stent（SES）
implantation on clinical outcomes from post procedure to 12 months later.
Methods. Subjects were 118 patients with 171 lesions who underwent SES implantation for angina pectoris and were studied by intravascular ultrasound（IVUS）following the procedure. The stent symmetryindex（minimal stent diameter/maximal stent diameter）at the minimal stent area was calculated by IVUS
analysis. The patients were divided into two groups for comparative study : those with stent symmetryindex ＞
group
（93 patients ; 145 lesions, mean age 66 ± 12 years）− 0.7 were classified into the optimal（O）
and those with stent symmetry index ＜ 0.7 were the sub-optimal（S）
group（25 patients ; 26 lesions, meanage 67 ± 10 years）.
Results. Angiographic follow up after 8 months showed no differences in target lesion revascularization（TLR）（O group : 3.1% vs S group : 3.8%, p ＝ 0.833）. Multivariate analysis identified the post minimal
stent diameter as the independent predictor of TLR（p ＝ 0.038）. The stent symmetry index ＜ 0.7 was not apredictor of TLR（p ＝ 0.887）. Clinical outcomes after 12 months showed both groups had 0% stent thrombosis and there were no differences in deaths（O group : 2.1% vs S group : 4.0%, p ＝ 0.602）.
Conclusions. Highly asymmetric stent expansion after SES implantation may not have a negative
impact on clinical outcomes at 12 months.
──────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2007 Jun; 49（6）: 313−321

Key Words■ Coronary artery disease■ Stent

INTRODUCTION
Some randomized trials such as the SIRIUS trial
have indicated that the sirolimus-eluting stent（SES）
reduces the rate of in-stent restenosis（ISR）and target lesion revascularization（TLR）compared to the■ Intravascular ultrasound■ Prognosis

bare metal stent（BMS）．However, TLR still
occurs after SES implantation at a rate of 4−
5%.1−3）Previous studies have shown that highly
asymmetric stent expansion after BMS implantation with a symmetry index ＜ 0.7 is generally associated with stent underexpansion and that such sub-──────────────────────────────────────────────
東邦大学医療センター大森病院循環器センター 心血管インターベンション室，＊内科 : 〒 143−8541 東京都大田区大森西 6−
11−1
Division of Interventional Cardiology, ＊ Department of Internal Medicine, Cardiovascular Center, Toho University Omori Medical
Center, Tokyo
Address for correspondence : NAKANO M, MD, Division of Interventional Cardiology, Cardiovascular Center, Toho University
Omori Medical Center, Omori-nishi 6−11−1, Ota-ku, Tokyo 143 − 8541 ; E-mail : toho 9686@lily.ocn.ne.jp
Manuscript received December 28, 2006 ; revised January 25 and March 12, 2007 ; accepted March 19, 2007

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optimal stent expansion is a risk factor forincreased incidence of stent thrombosis andISR.4−7）In addition, an in vitro study has reported
that optimization of drug distribution for stentbased delivery requires symmetric expansion of thestent with homogeneous distribution of the struts,
suggesting the importance of achieving symmetric
expansion after stent implantation for drug eluting
stents as well.8）However, much is still unknown
about the impact of highly asymmetric SES expansion on clinical outcomes.
The present study investigated the impact ofhighly asymmetric stent expansion after SES
implantation on clinical outcomes from post procedure to 12 months later.
SUBJECTS AND METHODS
Subjects
A total of 162 consecutive patients with 298
lesions underwent SES implantation for angina
pectoris at our institution from April 2004 to
October 2005. This study included 118 patientswith 171 lesions who underwent intravascular ultrasound（ IVUS）following percutaneous coronary
intervention（PCI）. The subjects were classified
into two groups : those with stent symmetryindex ＞（MSA）site− 0.7 at the minimal stent areafrom IVUS observations formed the optimal or O
group（93 patients, 145 lesions）and those with stentsymmetry index ＜ 0.74）formed the sub-optimal or
S group（25 patients, 26 lesions）. A retrospective
study compared the 12-month clinical outcomes.
One hundred twenty-seven lesions that were notstudied by IVUS after the procedure were excluded
for the following reasons : target lesion with nocoronary dissection in coronary angiography（CAG）
following SES implantation in PCI for a type A
lesion ; 9）side branches of true bifurcated lesions inwhich stent implantation was conducted for bothmain vessel and side branches ; angiographicalslow flow/no-reflow10）after stent implantation ; andthe IVUS catheter was unable to cross over thelesion site.
Procedure and antiplatelet therapy
All subjects underwent SES implantation after
pre-dilation. Determination of stent size and length
was left to the discretion of the operator, and dilation was, in principle, performed under maximum
inflation pressure of 16 atm or more. Antiplatelet
therapy was oral dosage of aspirin 81 or

100 mg/day and ticlopidine 200 mg/day from atleast 1 week prior to the procedure, and theseagents were continued after the procedure for the
lifetime of the patient.
Angiographic analysis
CCIP310（ Catex Co. Ltd.）was used to conduct
quantitative coronary angiography（QCA）
for calculation of lesion site, reference diameter, minimal
lumen diameter（MLD）, and percentage diameter
stenosis（%DS）. Follow-up CAG was performed ata mean of 7.9 ± 1.8 months after the procedure,with binary restenosis within the lesion defined
as %DS ＞− 50% including the 5 mm vessel segments
proximal and distal to the stented segment. Lateloss was calculated by subtracting the follow-up
MLD from the post MLD.2）
Analysis of IVUS images
IVUS studies used a Avanar catheter（Volcano
Co. Ltd.）with the lesion observed at 0.5 mm/sec
using the auto pull back system. IVUS images wererecorded on s-VHS video tape, captured on Netra
IVUS（ScImage Co. Ltd.）and analyzed off-line.11,12）
Using Netra IVUS Dual Roy automatic analysis,
the minimal lumen or stent diameter, maximal
lumen or stent diameter, external elastic membranecross-sectional area（ EEM-CSA）, lumen-CSA,
plaque-CSA（EEM-CSA minus lumen-CSA）were
measured at the MSA site as well as the proximaland distal reference segments.13）The stent symmetry index at the MSA site was calculated by dividing the minimal stent diameter by the maximal
stent diameter（Fig. 1）.4）Stent expansion ratio was
calculated by dividing the MSA by the average reference lumen CSA.4）Lesion calcification was diagnosed when IVUS revealed echoes brighter thanthat of the reference adventitia along with acoustic
shadowing in the back.14）
Other parameters related to IVUS finding
The incidence of calcified lesions behind thestent strut at the MSA site was obtained because
stent asymmetrical expansion is caused by calcification in the target lesion.15）In addition, the meanstent expansion ratio of lesions with stent thrombosis after SES implantation is 0.65,16）so the incidence in lesions with stent expansion ratio ＜ 0.65
was also obtained.

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Impact of Asymmetric Stent Expansion

315

Automatic analysis image

NETRA IVUS image

Fig. 1 Calculation of stent symmetry index
Results from NETRA IVUS Dual Roy automatic analysis.
Minimal SD ＝ 2.1 mm, Maximal SD ＝ 3.1 mm, symmetry index ＝ 0.68.
IVUS ＝ intravascular ultrasound ; SD ＝ stent diameter.

Statistical analysis
Statistical analysis was performed with StatView
5.0（SAS Institute Co. Ltd.）. Data are presented as
frequencies or mean ± SD. Continuous variables
were compared by the unpaired students t-test, andcategorical variables were compared by the χ2
test.13）To identify factors related to TLR after SES
implantation, logistic regression analysis was used.
The variables of univariate logistic regression
analysis were determined by referring to the predictors for TLR indicated in previous reports. 17,18）
Values of p ＜ 0.05 were considered statisticallysignificant. Univariate variables with p ＜ 0.5 andthe stent symmetry index ＜ 0.7 were entered into
the multivariate model to find independent predictors of TLR.19）

Table 1

Patient characteristics
O groupS group（n＝93）（n＝25）

p value

Age（yr）

66±12

67±10

0.703

Male

82（88.1）

24（96.0）

0.250

Diabetes mellitus

47（50.5）12（48.0）

0.821

Hypertension

54（58.1）

17（68.0）

0.368

Hyperlipidemia

40（43.0）8（32.0）0.319

Current smoking

46（49.4）

13（52.0）

0.822

Ticlopidine off

9（9.7）

2（8.0）

0.597

Multivessel disease67（72.0）25（100）0.003

Ejection fraction（%）

61±12

60±12

0.712

Coronary risk factors

Continuous values are mean±SD.（ ）: %.
O＝optimal ; S＝sub-optimal ; Ticlopidine off＝patients
discontinuing ticlopidine within 3 months after the procedure.

RESULTS
Patient characteristics
No differences existed between the two groups inage, sex, coronary risk factors, ejection fraction,and ratio of subjects discontinuing ticlopidine within 3 months following the procedure, but comparedto the O group, the S group had a significantly
higher rate of multivessel disease（O group : 72.0%
vs S group : 100%, p ＝ 0.003 ; Table 1）.

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Angiographical and procedural characteristics
There was no difference in target lesions of thetwo groups, but there were significantly more TypeB2 or C lesions in the S group compared to the O
group（O group : 69.0% vs S group : 92.3%, p ＝0.014）. Regarding lesion morphology, there weresignificantly more calcified lesions in the S groupcompared to the O group（11.7% vs 30.7%, p ＝

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Table 2

Angiographic and procedural characteristics
O groupS group（n＝145）（n＝26）Left main coronary artery3（2.1）

0

0.459

Left anterior descending artery

80（55.2）

14（53.8）

0.900

Right coronary artery

36（24.8）7（27.0）

0.661

Left circumflex artery

26（17.9）5（19.2）0.236

100（69.0）24（92.3）

0.014

Chronic total occlusion

16（11.0）3（11.5）0.940

Calcification

17（11.7）8（30.7）0.011

Diffuse67（46.2）

18（69.2）

0.031
0.100

p value

Target vessel

ACC/AHA classification
Type B2 / C
Lesion morphology

QCA analysis
Reference diameter（mm）

3.0±0.4

3.1±0.5

Pre minimal lumen diameter（mm）

0.83±0.43

0.77±0.32

0.411

Post minimal lumen diameter（mm）

2.99±0.49

2.74±0.24＜0.001

Pre% diameter stenosis（%）

74.3±11.2

73.6±10.3

0.767

Post% diameter stenosis（%）

3.2±14.5

5.5±16.1

0.465

Strategy of stenting
Stent size（mm）

3.0±0.3

3.0±0.4

0.119

Stent length（mm）

26.1±10.829.4±17.2

0.352

Maximal inflation pressure（atm）

17.9±2.1

17.4±2.7

0.287

Stent connecting

35（24.1）

10（38.4）

0.260

Post dilation

58（40.0）12（46.1）

0.557

6（4.1）

1（3.8）

0.945

Use of rotational atherectomy

Continuous values are mean±SD.（ ）: %.
ACC/AHA＝American College of Cardiology/American Heart Association ; QCA＝quantitative coronary angiography ; Stent connecting＝cases of stent implantation by adjoining two or more stents. Other abbreviations
as in Table 1.

0.011）and diffuse lesions（46.2% vs 69.2%, p ＝0.031）. Post MLD from QCA analysis was significantly lower in the S group compared to the O
group（ 2.99 ± 0.49 vs 2.74 ± 0.24 mm, p ＜0.001）. There was no significant difference
between the two groups in strategy of stenting（Table 2）.
Post procedure IVUS analysis
Minimal stent diameter（O group : 2.51 ± 0.45
vs S group : 2.06 ± 0.31 mm, p ＜ 0.001）and lumen
CSA（6.6 ± 2.0 vs 5.7 ± 1.6 mm, p ＝ 0.031）at the
MSA site was significantly smaller in the S groupcompared to the O group. The S group also had asignificantly lower stent expansion ratio（0.91 ±0.22 vs 0.76 ± 0.27, p ＝ 0.002）
and a significantly

higher incidence of stent expansion ratio ＜ 0.65
（8.2% vs 30.1%, p ＝ 0.001）. The incidence of calcified lesions behind the stent strut was significantly higher in the S group than the O group（42.1% vs100%, p ＜ 0.001 ; Table 3）.
Eight-month angiographic results
Follow-up CAG was performed in 131 lesions（90.3%）of the O group and 26 lesions（100%）of
the S group. Follow-up MLD from QCA analysis
was significantly lower in the S group compared to
the O group（O group : 2.89 ± 0.63 vs S group :2.57 ± 0.67 mm, p ＝ 0.020）. No significant difference existed between the two groups in rate of TLR（3.1% vs 3.8%, p ＝ 0.833）, and late loss（0.10 ±0.51 vs 0.17 ± 0.49, p ＝ 0.514 ; Table 4）.
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Table 3

317

Post procedure intravascular ultrasound findings
O groupS group（n＝145）（n＝26）

p value

Reference proximal site
EEM CSA（mm2）19.7±5.5

1.5±5.7

0.128

Lumen CSA（mm2）

8.3±2.7

9.7±3.9

0.089

Plaque CSA（mm ）11.3±4.1

11.9±2.8

0.358

Minimal stent diameter（mm）

2.51±0.45

2.06±0.31＜0.001

Maximal stent diameter（mm）

3.08±0.50

3.12±0.53

0.710

EEM CSA（mm2）17.9±5.1

16.9±3.6

0.231

2Minimal stent area site

Lumen CSA（mm ）6.6±2.0

5.7±1.6

0.031

Plaque CSA（mm2）11.3±4.0

11.2±2.8

0.877

EEM CSA（mm2）14.4±5.4

13.9±5.8

0.668

Lumen CSA（mm2）

6.8±2.9

6.7±2.6

0.870

2Reference distal site

Plaque CSA（mm ）7.6±3.7

7.2±4.2

0.620

Stent symmetry index

0.81±0.05

0.63±0.04＜0.001

Stent expansion ratio

0.91±0.22

0.76±0.27

0.002

Stent expansion ratio＜ 0.65

12（8.2）8（30.1）0.001

Calcification behind struts at MSA site

61（42.1）

26（100）＜0.001

2

Continuous values are mean±SD.（ ）: %.
EEM＝external elastic membrane ; CSA＝cross-sectional area ; MSA＝minimal stent area. Other abbreviations
as in Table 1.

Table 4 Eight-month angiographic results
O group
Number of follow-up lesions

S group p value

131

26

Binary restenosis5（3.8）

1（3.8）

0.994

Target lesion revascularization

4（3.1）

1（3.8）

0.833

QCA analysis
Minimal lumen diameter（mm）
Late loss（mm）

Table 5 Univariate logistic regression analysis forprediction of target lesion revascularization
Odds ratio

95% CI

p value

0.69

0.77 − 6.20

0.740

Diabetes mellitus

8.33

0.95 − 51.4

0.087

Male
Multivessel disease

1.61

0.18 − 8.87

0.672

2.89±0.63 2.57±0.67 0.020

Stent length

1.04

0.94 − 1.06

0.664

0.10±0.51 0.17±0.49 0.514

Reference diameter

0.27

0.04 − 1.93

0.490

Post minimal stent diameter

0.09

0.01 − 0.82

0.031

Minimal stent area

0.61

0.33 − 1.13

0.119

Symmetry index＜ 0.7

1.41

0.15 − 13.1

0.763

Stent expansion＜ 0.65

1.64

0.15 − 13.2

0.666

Continuous values are mean±SD.（
Abbreviations as in Tables 1, 2.

）: %.

Multivariate logistic regression analysis for prediction of TLR showed post minimal stent diameter asmeasured by IVUS was an independent predictor
for TLR（p ＝ 0.038）. Symmetry index ＜ 0.7 was
not a predictor for TLR（p ＝ 0.887 ; Tables 5, 6）.
Twelve-month clinical outcomes
Clinical follow-up at 12 months after SES
implantation was possible for all subjects. The incidence of stent thrombosis and cardiac death during
the observation period was 0% for both groups.
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CI＝confidence interval.

Two patients（2.1%）in the O group died of lungfibrosis and lung cancer. One patient（4.0%）
died ofcerebral infarction in the S group. There was nodifference between the two groups in the incidenceof non-cardiac death（Table 7）.

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Table 6

Nakano, Wagatsuma, Iga et alMultivariate logistic regression analysis forprediction of target lesion revascularization
Odds ratio

95% CI

p value

Post minimal stent diameter 0.05

0.003 − 0.85

0.038

Diabetes mellitus

7.45

0.79 − 71.0

0.077

Minimal stent area

0.93

0.45 − 1.92

0.845

Symmetry index＜0.7

1.27

0.11 − 14.1

0.887

Reference diameter

0.84

0.07 − 10.8

0.893

Abbreviation as in Table 5.

Table 7

Twelve-month clinical outcomesO groupS group

Number of follow-up patients

93

25

Stent thrombosis

00Acute myocardial infarction00

Cardiac death002（2.1%）

1（4.0%）

Non-cardiac deathp value

0.602

Abbreviations as in Table 1.

DISCUSSION
Relationship between highly asymmetric stent
expansion and stent restenosis
Compared to BMS, SES considerably reduces
neointimal hyperplasia after stent implantation.1, 20）
ISR is still evident, however, with a greater focal
pattern of restenosis compared to BMS.21）Several
studies have reported that stent fracture or nonuniform strut distribution may be associated with adecrease in local drug delivery and that this may
affect the incidence of in-stent restenosis after SES
implantation. 19, 22） An in vitro study similarly
reported that local drug underdosing occurred atsites of nonuniform circumferential stent strut distribution.8）Such outcomes suggest that remarkableasymmetrical SES expansion would trigger anincrease of local neointimal hyperplasia by drug
underdosing and may cause stent restenosis.
A study on the association between longitudinal
and tomographic asymmetric stent expansion after
SES implantation and neointimal hyperplasia
reported that asymmetric stent expansion did notseem to affect suppression of neointimal hyperplasia.23）However, the minimum symmetry index inthis study was 0.73, and the asymmetry group was
defined as having symmetry index ＜ 0.86. Thiswas higher than the symmetry index indicated in

the previous studies as a risk factor for ISR or
SAT.4−6）In contrast, our study was conducted on
lesions with a higher degree of local asymmetricstent expansion. However, we did not find any significant differences in late loss or binary restenosis
rate. Moreover, nonuniform strut distribution correlates with more neointimal hyperplasia after SES
implantation, but the mean stent symmetry index of
the restenosis group（mean symmetry index ＝ 0.88）
was higher than the mean stent symmetry index of
our O group（mean symmetry index ＝ 0.81）, whichrevealed no significant difference in comparisonswith that of their no-restenosis group.19）This result
suggests that asymmetric stent distortion may notnecessarily be associated with nonuniform strut distribution.
Several reasons why asymmetric SES implantation may not promote stent restenosis can be surmised : sufficient drug concentration to suppress
neointimal hyperplasia although variation in local
drug concentration occurs through distortion of thestent within the coronary artery blood flow ; nooccurrence of local drug underdosing unless distortion of the stent struts is greater than asymmetrical
distortion or unless stent fracture results ; and alarge volume of neointimal hyperplasia is induced
following completion of sirolimus release after 3
months post procedure due to an oversensitive
inflammatory reaction originating from the presence of metal struts and polymer, which is unrelated to stent asymmetry.19,23,24）
Low values in post minimal stent diameter andpost minimal lumen-CSA are, as for BMS, predictors of ISR or TLR after SES implantation as
revealed by QCA or IVUS analysis.25−27）In addition, as full lesion coverage strategy is recommended for SES implantation,2,3）the total length of thestent has increased. As a result, long stent length isan ISR or TLR predictor specific to SES.18,25）A
study of 670 native coronary artery lesions treatedwith SES showed that the IVUS cut-offs that best
predicted angiographic restenosis after SES implantation were minimal lumen-CSA ＝ 5.5 mm2 andstent length ＝ 40 mm. In subjects satisfying the criteria of lumen-CSA ＞ 5.5 mm2 and a stent length ＜40 mm, the restenosis rate was extremely low at
0.4%.27）In the present study, post minimal stent
diameter was identified as a TLR predictor, but
although the mean post minimal stent diameter was
significantly smaller in the S group compared to theO group, no difference appeared in the TLR rate
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between the two groups. The reasons may involve amean stent length of 40 mm or less and a mean
minimal lumen-CSA of 5.5 mm2 or more in the S
group. From these results, we speculate that TLR
could be avoided even in cases of highly asymmetrical SES expansion if a minimal lumen-CSA isachieved after the procedure and if the total lengthof the stent is not excessive.
Relationship between highly asymmetric stent
expansion and stent thrombosis
Many studies have widely recognized that stentasymmetrical expansion occurs due to calcificationin the target lesion,15, 28, 29）and calcification behindthe stent strut at MSA was observed in all cases in
the S group. What is more, calcification in the target lesion not only causes stent asymmetricalexpansion, but also reduces luminal gain after stentimplantation and causes stent underexpansion.23）The current study also showed the stent
expansion ratio of the S group to be significantly
lower than that of the O group. Stent underexpansion after SES implantation is a risk factor for stent
thrombosis after the procedure and the mean stent
expansion ratio in cases of stent thrombosis was
0.65.16）In the current study, there were a total of 20
lesions with stent expansion ratio ＜ 0.65, but theincidence of stent thrombosis in 12 months after theprocedure was 0%. However, a high volume study
reported that the incidence of stent thrombosis after
SES implantation occurring within 12 months after
the procedure was 1% or less,30, 31）so the incidenceof stent thrombosis was not high. Therefore, it islikely that we did not unexpectedly encounter stent
thrombosis in patients with stent underexpansion
due to the small number of subjects in the present
要study. Moreover, stent underexpansion, residual
stenosis, edge dissection, low MSA values andother indicated predictors of sub-acute stent thrombosis（SAT）
within 30 days after BMS implantation
were confirmed by IVUS to be present in many ofthe patients who had SAT after the SES
procedure.32−34）Therefore, it is believed that there
are no large differences in risk factors for SAT
between SES and BMS.
In contrast, a few reports suggested that there
was no specific IVUS findings in cases with lateangiographic stent thrombosis（LAST）occurring in
the period after 30 days. 33−35）Furthermore, thecauses of LAST may consist of delayed coronary
artery healing and other clinical and procedural risk
factors, 36, 37）suggesting that LAST events may
occur even after optimal stent implantation. As
many studies indicate that the termination of antiplatelet therapy is a risk factor for LAST,30,35,38）
anti-platelet therapy should be continued for as
long as possible regardless of whether stent implantation was optimal or sub-optimal and to conduct
long-term, close observation of progress.
Study limitations
The current investigation was conducted only on
patients undergoing IVUS study after the procedure. Also, IVUS findings were not observed in thechronic period. The number of cases studied wassmall in this single-center non-randomized retrospective study.
CONCLUSIONS
Highly asymmetric stent expansion after sirolimuseluting stent implantation may not have a negative
impact on 12-month clinical outcomes.
約

シロリムス溶出性ステント植え込み術後の高度非対称性ステント拡張が12 ヵ月予後に与える影響
中野

目

雅嗣

我妻

賢司

伊 賀

淳

新居

天野

英夫

戸田

幹人

山]

純一

秀郎

的 : 本研究ではシロリムス溶出性ステント植え込み術後の高度非対称性ステント拡張が術後12 ヵ月の予後に与える影響を検討した.
方

法 : シロリムス溶出性ステント植え込み術後，血管内エコー法を施行しえた狭心症 118 例，

171 病変を対象とした．血管内エコー法解析から術後最小ステント面積部位におけるステント対称
指数（最小ステント長/最大ステント長）を算出し，対象をステント対称指数＞− 0.7 の至適（O）群（93
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Nakano, Wagatsuma, Iga et al

例 ; 145 病変，平均年齢 66 ± 12 歳）とステント対称指数＜ 0.7 の非至適（S）群（25 例 ; 26 病変，平均年
齢 67 ± 10 歳）の 2 群に分け，臨床成績を比較検討した．
結果 : 8 ヵ月後の冠動脈造影の結果，再血行再建術の比率（O 群 3.1% vs S 群 3.8%, p ＝ 0.833）に差はなかった．多変量解析の結果，術後最小ステント径が再血行再建術の独立した予測因子であった（p ＝ 0.038）．ステント対称指数＜ 0.7 は予測因子とならなかった（p ＝ 0.887）．12 ヵ月後の予後においてステント内血栓症発生率は両群とも 0% であり，死亡率（O 群 2.1% vs S 群 4.0%，p ＝ 0.602）に差はなかった.
結論 : シロリムス放出性ステント植え込み術後の高度非対称性ステント拡張は 12 ヵ月予後に負の影響を与えない.

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References
1）Moses JW, Leon MB, Popma JJ, Fitzgerald PJ, Holmes
DR, O Shaughnessy C, Caputo RP, Kereiakes DJ,
Williams DO, Teirstein PS, Jaeger JL, Kuntz RE ; SIRIUS
Investigators : Sirolimus-eluting stents versus standard
stents in patients with stenosis in a native coronary artery.
N Engl J Med 2003 ; 349 : 1315−1323
2）Schofer J, Schlüer M, Gershlick AH, Wijns W, Garcia E,
Schampaert E, Breithardt PG ; E-SIRIUS Investigators :Sirolimus-eluting stents for treatment of patients with longatherosclerotic lesions in small coronary arteries : Doubleblind, randomised controlled trial（E-SIRIUS）. Lancet
2003 ; 362 : 1093−10993）Schampaert E, Cohen EA, Schlüer M, Reeves F, Traboulsi
M, Title LM, Kuntz RE, Popma JJ ; C-SIRIUS Investigators : The Canadian study of the sirolimus-eluting stentin the treatment of patients with long de novo lesions insmall native coronary arteries（ C-SIRIUS）. J Am Coll
Cardiol 2004 ; 43 : 1110−11154）von Birgelen C, Gil R, Ruygrok P, Prati F, Di Mario C, vander Giessen WJ, de Feyter PJ, Serruys PW : Optimized
expansion of the Wallstent compared with the PalmazSchatz stent : On-line observations with two- and threedimensional intracoronary ultrasound after angiographic
guidance. Am Heart J 1996 ; 131 : 1067−10755）Kuntz RE, Safian RD, Carrozza JP, Fishman, RF, Mansour
M, Baim DS : The importance of acute luminal diameter indetermining restenosis after coronary atherectomy or stenting. Circulation 1992 ; 86 : 1827−1835
6）Colombo A, Hall P, Nakamura S, Almagor Y, Maiello L,
Martini G, Gaglione A, Goldberg SL, Tobis JM :Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation
1995 ; 91 : 1676−1688
7）Moussa I, Oi Mario C, Reimers B, Akiyama T, Tobis J,
Colombo A : Subacute stent thrombosis in the era of
intravascular ultrasound-guided coronary stenting without
anticoagulation : Frequency, predictors and clinical outcome. J Am Coll Cardiol 1997 ; 29 : 6−12
8）Hwang CW, Wu D, Edelman ER : Physiological transport
forces govern drug distribution for stent-based
delivery. Circulation 2001 ; 104 : 600−605
9）Ryan TJ, King SB Ⅲ, Bauman WB, Mccallister BD,
Kennedy JW, Smith SC Jr, Kereiakes DJ, Ullyot DJ :Guidelines for percutaneous transluminal coronary
angioplasty : A report of the American College
Cardiology/American Heart Association Task Force on
Assessment of Diagnostic and Therapeutic Cardiovascular
Procedures（ Committee on Percutaneous Transluminal
Coronary Angioplasty）. J Am Coll Cardiol 1993 ; 22 :2033−2054
10）Rezkalla SH, Kloner RA : No-reflow phenomenon.
Circulation 2002 ; 105 : 656−662
11）Yamazaki T, Taniguchi I, Kurusu T, Shimazu Y,
Hashizume Y, Takikawa K, Kuwata M, Onodera T,
Yoshikawa M, Mochizuki S : Effect of amlodipine on vascular responses after coronary stenting compared with anangiotensin-converting enzyme inhibitor. Circ J 2004 ; 68 :328−333
12）Kume T, Akasaka T, Kawamoto T, Watanabe N, Toyota E,
Neishi Y, Sukmawan R, Sadahira Y, Yoshida K :Assessment of coronary intima-media thickness by opticalcoherence tomography : Comparison with intravascularultrasound. Circ J 2005 ; 69 : 903−907
13）Sato H, Iida H, Tanaka A, Tanaka H, Shimodouzono S,
Uchida E, Kawarabayashi T, Yoshikawa J : The decreaseof plaque volume during percutaneous coronary intervention has a negative impact on coronary flow in acute
myocardial infarction : A major role of percutaneous coronary intervention-induced embolization. J Am Coll Cardiol
2004 ; 44: 300−30414）Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF,
Chuang YC, Ditrano CJ, Leon MB : Patterns of calcification in coroary artery disease : A statistical analysis of
intravasucular ultrasound and coroary angiography in 1155
leasions. Circulation 1995 ; 91 : 1959−196515）Albrecht D, Kaspers S, Fussl R, Hopp HW, Sechtem U :Coronary plaque morphology affects stent deployment :Assesment by intracoronary ultrasound.Cathet Cardiovasc
Diagn 1996 ; 38 : 229−23516）Fujii K, Carlier SG , Mintz GS, Yang Y, Moussa I, Weisz
G, Dangas G, Mehran R, Lansky AJ, Kreps EM, Collins M,
Stone GW, Moses JW, Leon MB : Stent underexpansion
and residual reference segment stenosis are related to stent
thrombosis after sirolimus-eluting stent implantation : An
intravascular ultrasound study. J Am Coll Cardiol 2005 ;45 : 995−99817）Suzuki S, Kamihata H, Hata T, Hayashi F, Miura A,
Yoshinaga, M, Karakawa M, Kitaura Y : Success rate of

J Cardiol 2007 Jun; 49（6）: 313 – 321

JC49610下FC

07.6.11 5:14 PM ページ 321

Impact of Asymmetric Stent Expansion
implantation and mid-term outcomes of the sirolimus-eluting stent. Circ J 2007 ; 71 : 15−1918）Ong AT, van Domburg RT, Aoki J, Sonnenschein K,
Lemos PA, Serruys PW : Sirolimus-eluting stents remainsuperior to bare-metal stents at two years : Medium-term
results from the Rapamycin-Eluting Stent Evaluated at
Rotterdam Cardiology Hospital（RESEARCH）registry. J
Am Coll Cardiol 2006 ; 47 : 1356−136019）Takebayashi H, Mintz GS, Carlier SG, Kobayashi Y, Fujii
K, Yasuda T, Costa RA, Moussa I, Dangas GD, Mehran R,
Lansky AJ, Kreps E, Collins MB, Colombo A, Stone GW,
Leon MB, Moses JW : Nonuniform strut distribution correlates with more neointimal hyperplasia after sirolimus-eluting stent implantation. Circulation 2004 ; 110 : 3430−343420）Sousa JE, Costa MA, Abizaid A, Feres F, Seixas AC,
Tanajura LF, Mattos LA, Falotico R, Jaeger J, Popma JJ,
Serruys PW, Sousa A : Four-year angiographic andintravascular ultrasound follow-up of patients treated withsirolimus-eluting stents. Circulation 2005 ; 111 : 2326−
232921）Popma JJ, Leon MB, Moses JW, Holmes DR Jr, Cox N,
Fitzpatrick M, Douglas J, Lambert C, Mooney M, Yakubov
S, Kuntz RE ; SIRIUS Investigators : Quantitative assessment of angiographic restenosis after sirolimus-eluting
stent implantation in native coronary arteries. Circulation
2004 ; 110 : 3773−378022）Sianos G, Hofma S, Ligthart JM, Saia F, Hoye A, Lemos
PA, Serruys PW : Stent fracture and restenosis in the drugeluting stent era. Catheter Cardiovasc Interv 2004 ;61 : 111−11623）Kaneda H, Ako J, Honda Y, Terashima M, Morino Y,
Yock PG, Popma JJ, Leon MB, Moses JW, Fitzgerald PJ :Impact of asymmetric stent expansion on neointimal hyperplasia following sirolimus-eluting stent implantation. Am J
Cardiol 2005 ; 96 : 1404−140724）van der Gissen WJ, Lincoff AM, Schwartz RS, vanBeusekom HM, Serruys PW, Holmes DR Jr, Ellis SG,
Topol EJ : Marked inflammatory sequelae to implantationof biodegradable and nonbiodegradable polymers in
porcine coronary arteries. Circulation 1996 ; 94 : 1690−
169725）Holmes DR Jr, Leon MB, Moses JW, Popma JJ, Cutlip D,
Fitzgerald PJ, Brown C, Fischell T, Wong SC, Midei M,
Snead D, Kuntz RE : Analysis of 1-year clinical outcomesin the SIRIUS trial : A randomized trial of a sirolimus-eluting stent versus a standard stent in patients at high risk forcoronary restenosis. Circulation 2004 ; 109 : 634−64026）Sonoda S, Morino Y, Ako J, Terashima M, Hassan AH,
Bonneau HN, Leon MB, Moses JW, Yock PG, Honda Y,
Kuntz RE, Fitzgerald PJ ; SIRIUS Investigators : Impact offinal stent dimensions on long-term results following
sirolimus-eluting stent implantation : Serial intravascularultrasound analysis from the SIRIUS trial. J Am Coll
Cardiol 2004 ; 43 : 1959−196327）Mitz GS, Weissman NJ : Intravascular ultrasound in the
durg-eluting stent era. J Am Coll Cardiol 2006 ; 48 : 421−

J Cardiol 2007 Jun; 49（6）: 313 – 321

321

429
28）Moussa I, Di Mario C, Moses J, Reimers B, Di Francesco
L, Martini G, Tobis J, Colombo A : Coronary stenting after
rotational atherectomy in calcified and complex lesions :Angiographic and clinical follow-up results. Circulation
1997 ; 96 : 128−136
29）Hoffmann R, Mintz GS, Pompa JJ, Satler LF, Kent KM,
Pichard AD, Leon MB : Treatment of calcified coronary
lesions with Palmaz-Schatz stents : An intravascular ultrasound study. Eur Heart J 1998 ; 19 : 1224−123130）Bavry AA, Kumbhani DJ, Helton TJ, Bhatt DL : Risk ofthrombosis with the use of sirolimus-eluting stents for perucutaneous coronary intervention（from registry and clinical
trial data）. Am J Cardiol 2005 ; 95: 1469−147231）Urban P, Gershlick AH, Guagliumi G, Guyon P, Lotan C,
Schofer J, Seth A, Sousa JE, Wijns W, Berge C, Deme M,
Stoll HP ; e-Cypher Investigators : Safety of coronary
sirolimus-eluting stents in daily clinical practice : One-year
follow-up of the e-Cypher registry. Circulation 2006 ; 113:
1434−1441
32）Cheneau E, Leborgne L, Mintz GS, Kotani J, Pichard AD,
Satler LF, Canos D, Castagna M, Weissman NJ, Waksman
R : Predictors of subacute stent thrombosis : Results of asystematic intravascular ultrasound study. Circulation
2003 ; 108 : 43−4733）Regar E, Lemos PA, Saia F, Degertekin M, Tanabe K, Lee
CH, Arampatzis CA, Hoye A, Sianos G, de Feyter P, vander Giessen WJ, Smits PC, van Domburg RT, Serruys PW :Incidence of thrombotic stent occlusion during the first
three months after sirolimus-eluting stent implantation in
500 consecutive patients. Am J Cardiol 2004 ; 93 : 1271−
127534）Takebayashi H, Kobayashi Y, Mints GS, Garlier SG, Fujii
K, Yasuda T, Moussa I, Mehran R, Dangas GD, Collins
MB, Kreps E, Lansky AJ, Stone GW, Leon MB, Moses
JW : Intravascular ultrasound assessment of lesions withtarget vessel failure after sirolimus-eluting stent implantation. Am J Cardiol 2005 ; 95 : 498−50235）Ong ATL, McFadden EP, Regar E, de Jaegere PP, vanDomburg RT, Serruys PW : Late angiographic stent thrombosis（LAST）events with drug-eluting stents. J Am Coll
Cardiol 2005 ; 45 : 2088−209236）Virmani R, Guagliumi G, Farb A, Musumeci G, Grieco N,
Motta T, Mihalcsik L, Tespili M, Valsecchi O, Kolodgie
FD : Localized hypersensitivity and late coronary thrombosis secondary to a sirolimus-eluting stent : Should we be
cautious ? Circulation 2004 ; 109 : 701−705
37）Joner M, Fine AV, Farb A, Mont EK, Kolodgie FD, LadichE, Kutys R, Skorija K, Gold HK, Virmani R : Pathology ofdrug-eluting stents in humans : Delayed healing and late
thrombotic risk. J Am Coll Cardiol 2006 ; 48 : 193−20238）Park DW, Park SW, Park KH, Lee BK, Kim YH, Lee CW,
Hong MK, Kim JJ, Park SJ : Frequency of and risk factors
for stent thrombosis after drug-eluting stent implantation
during long-term follow-up. Am J Cardiol 2006 ; 98 : 352−
356