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ORIGINAL PAPER
Longitudinal heterogeneity of coronary artery distensibilityin plaques related to acute coronary syndrome
Osamu Sasaki • Toshihiko Nishioka • Yoshiro Inoue • Ami Isshiki • Takashi Akima •
Kentarou Toyama • Aki Koike • Toshiyuki Ando • Mikio Yuhara • Shun-ichi Sato •
Tetsuo Kamiyama • Masato Kirimura • Hiroyuki Ito • Yoshiaki Maruyama • Nobuo Yoshimoto
Received: 9 November 2010 / Accepted: 31 January 2012 / Published online: 10 February 2012
� Springer-Verlag 2012
Abstract
Background How coronary distensibility contributes to
stable or unstable clinical manifestations remains obscure.
We postulated that the heterogeneous plaque distensibility
is associated with unstable clinical presentations in patients
with acute coronary syndrome (ACS).
Methods and results Seventeen and 19 ACS-related and -
unrelated lesions, respectively, were visualized using
intravascular ultrasound imaging with simultaneous intra-
coronary pressure recording. Systolic and diastolic lumen
cross-sectional areas were measured at the lesion site and at
five evenly spaced sites between the proximal and distal
reference sites. The coronary distensibility index and
stiffness index b were calculated for each site and averaged
for each coronary segment. Maximal distensibility index,
standard deviation and the difference between maximal and
minimal distensibility indices within each segment were
significantly higher in the ACS-related than -unrelated
plaques (5.6 ± 2.3 vs. 3.7 ± 1.8, p \ 0.001, 2.1 ± 0.9 vs.
1.1 ± 0.6, p \ 0.001 and 5.3 ± 2.3 vs. 2.8 ± 1.5, p \0.001, respectively). Moreover, the difference in the dis-
tensibility index between the lesion site of ACS-related
plaques and the immediate proximal site was significantly
larger (2.88 ± 2.35 vs. 1.17 ± 1.44, p = 0.022) than that
in ACS-unrelated plaques.
Conclusions Coronary artery distensibility is longitudi-
nally more heterogeneous in ACS-related than-unrelated
plaques, especially between the lesion and the immediate
proximal site.
Keywords Intravascular ultrasound � Compliance �Stiffness index b � Thrombus
Introduction
The major mechanism of acute coronary syndrome (ACS),
including acute myocardial infarction (MI) and unstable
angina, is considered to be intracoronary thrombus for-
mation subsequent to atherosclerotic plaque rupture or
erosion. Rupture-prone vulnerable plaque is characterized
by a thin fibrous cap and a large necrotic core, and pla-
ques rupture when large mechanical stresses develop in
the most fragile portion of the fibrous cap (shoulder
region) [1–3]. Recent intravascular ultrasound (IVUS)
studies have indicated that culprit lesions in ACS are
characterized by large eccentric plaques with an echolu-
cent zone, ulceration, thrombus formation, spotty calcium
deposits and more positive remodeling compared with
culprit lesions in stable angina pectoris or non-culprit
lesions in ACS [4–13], and that culprit coronary artery
walls are more distensible in ACS than in stable angina
[14, 15]. Coronary artery distensibility has been studied
using IVUS imaging and it is reportedly determined by
age, diabetes mellitus, and the size or thickness, eccen-
tricity, composition and remodeling of the imaged plaque
[14–22]. However, how increased vessel distensibility in
the ACS-related coronary artery contributes to unstable
O. Sasaki � T. Nishioka (&) � Y. Inoue � A. Isshiki �K. Toyama � A. Koike � T. Ando � M. Yuhara � S. Sato �T. Kamiyama � M. Kirimura � H. Ito � Y. Maruyama �N. Yoshimoto
Division of Cardiology, Saitama Medical Center,
Saitama Medical University, 1981 Kamoda,
Kawagoe, Saitama 350-8550, Japan
e-mail: nishioka@saitama-med.ac.jp
T. Akima
Division of Cardiology, Saitama City Hospital, Saitama, Japan
123
Clin Res Cardiol (2012) 101:545–551
DOI 10.1007/s00392-012-0424-6
clinical manifestations has not been elucidated. We pos-
tulated that as coronary atherosclerosis gradually advan-
ces, the coronary artery basically stiffens and becomes
rigid due to intimal thickening, fibrosis, calcification and
smooth muscle cell proliferation, and coronary distensi-
bility decreases. However, the development of lipid-rich
atheroma with thin fibrous cap would locally increase
coronary distensibility. Therefore, the difference in coro-
nary distensibility between adjacent sites, especially
between soft atheromatous tissue and relatively hard
sclerotic tissue would increase, and we defined this intra-
plaque difference in coronary distensibility as heteroge-
neity. Furthermore, such heterogeneity might concentrate
mechanical stress at the border between distensible plaque
and relatively stiff tissue, thus leading to the unstable
clinical presentations that arise in patients with ACS.
Therefore, we investigated the longitudinal difference in
coronary distensibility between ACS-related and -unre-
lated plaques using IVUS imaging.
Methods
Study population
We studied 31 patients (28 men and 3 women; mean age
61 years) with stable angina pectoris or ACS who under-
went diagnostic or interventional cardiac catheterization.
None had undergone previous intervention to treat the
target lesion. According to clinical status, ECG findings,
laboratory data and coronary angiographic findings, we
classified these patients into a group with stable angina
pectoris (n = 14) and a group with ACS (n = 17) includ-
ing two with unstable angina, five with ST elevation MI
and 10 with non-ST elevation MI. Culprit lesions of stable
angina were judged from stress myocardial perfusion
imaging and angiographic findings, and those of ACS were
identified from ECG, echocardiography and angiographic
findings. We imaged 17 ACS-related and 19 ACS-unre-
lated lesions using IVUS. The following lesions were
excluded from quantitative analysis: those in which IVUS
images were suboptimal for quantitative measurements
because of heavy intimal calcification (largest arc of cal-
cium, [60�), those in which the proximal reference site
could not be identified due to ostial location of the lesion
and those with a lumen of \1.5 mm2 or which were
occluded (wedged) by the imaging catheter. Our institu-
tional review board approved the study protocol and all
patients provided written informed consent to participate in
all associated procedures.
Standard risk factors as well as current medications were
identified from a review of the medical records of each
patient.
IVUS study protocol
Before coronary intervention, IVUS studies proceeded
using a 2.9/3.2-Fr 30-MHz long monorail imaging catheter
(UltraCross�) or a 2.9-Fr 40-MHz long monorail imaging
catheter (Atlantis�) and an imaging console (ClearView�;
all from Boston Scientific Corporation, Boston, MA).
Thirty-six de novo coronary artery lesions in 31 patients
were imaged by IVUS with simultaneous intracoronary
pressure recording. After angiography, the imaging cathe-
ter was introduced into the target artery through a 6–7-Fr
coronary guiding catheter over a 0.014-in. guidewire. To
prevent possible vasospasm and to maximize vasodilation,
nitroglycerin (100–200 lg) was directly administered into
the coronary artery immediately before IVUS imaging.
After advancing the imaging catheter across the lesion to
the distal portion of the vessel under fluoroscopic guidance,
IVUS imaging proceeded during slow retraction (0.5 mm/s)
of the imaging catheter and intracoronary pressure was
simultaneously recorded. The IVUS images were recorded
on 0.5-in. high-resolution super-VHS videotapes.
Qualitative and quantitative IVUS analysis
Ruptured plaques contained a cavity that communicated
with the lumen and an overlying residual fibrous cap
fragment. A fissure without a cavity communicating with a
true lumen was not included in the analysis [6, 7].
The IVUS images were evaluated offline after the pro-
cedure using an image analysis system. Figure 1 shows that
a coronary segment of interest was defined between two
side branches with a diameter of [1 mm. Systolic and
diastolic external elastic membrane cross-sectional areas
(EEM CSA, mm2) and lumen cross-sectional areas (lumen
CSA, mm2) at the intimal leading edge within this coronary
Fig. 1 Schematic presentation of coronary segment analyzed by
intravascular ultrasound. Coronary segment is defined between two
side branches with diameter [1 mm. Within this coronary segment,
IVUS measurements were taken at lesion site with smallest lumen
area and at five evenly spaced sites. L lesion site, DM distal middle
site, DR distal reference site, M middle site, PM proximal middle site,
PR proximal reference site
546 Clin Res Cardiol (2012) 101:545–551
123
segment were measured at the lesion site with the smallest
lumen CSA and at five evenly spaced sites (proximal ref-
erence site with the largest lumen CSA in the segment
proximal to the lesion site, distal reference site with the
largest lumen CSA in the segment distal to the lesion site,
middle site at the mid portion between both reference sites
and proximal middle site at the mid portion between the
proximal reference and middle sites and distal middle site
at the mid portion between the distal reference and middle
sites). Plaque plus media CSA (mm2) was calculated as
EEM CSA–lumen CSA and plaque burden (%) as plaque
plus media CSA/EEM CSA 9100. Systolic and diastolic
lumen diameters (LD) were calculated assuming that the
cross section was circular.
Coronary artery distensibility
Individual variations in vascular tone were minimized by
administering 100–200 lg of nitroglycerin immediately
before the IVUS study. The largest lumen CSA assessed by
IVUS was determined by tracing the lumen-intima border
at peak systole and the smallest lumen CSA at peak dias-
tole within one cardiac cycle by synchronizing IVUS
images and intracoronary pressure tracing (Fig. 2). Chan-
ges in intracoronary pressure during one cardiac cycle were
measured at the tip of the guiding catheter. Coronary artery
distensibility was defined as the ‘‘distensibility index’’ and
‘‘stiffness index b’’ obtained from the following formulae
as described [13, 14, 17–23].
Distensibility index¼ lumen CSA change=ðfdiastolic lumen CSAÞ= SBP�DBPð Þg�103
Stiffness index b = [ln (SBP/DBP)]/(LD change/diastolic
LD), where SBP and DBP indicate systolic and diastolic
intracoronary pressure and ln is the natural logarithm.
These indices were calculated for each site, the maximal
and minimal values were identified, and then the average
value and standard deviation were calculated for each
coronary segment. Furthermore, differences in coronary
distensibility index and stiffness index b were calculated
between adjacent sites. We defined coronary artery dis-
tensibility as being longitudinally more heterogeneous
when the maximal-minimal value or standard deviation
of these two indices within each coronary segment, or
the difference in these two indices between adjacent sites
significantly differed. Since only patients with ischemic
heart diseases were imaged using IVUS, a normal range
of heterogeneity in coronary artery distensibility was not
accessible and heterogeneity was assessed not as absolute
values but as relative differences between the two
groups.
Statistical analyses
All data are expressed as mean ± standard deviation.
Continuous variables between two groups were compared
using an unpaired t test. Differences in distensibility index
and stiffness index b within the same plaque were com-
pared using the one-way analysis of variance and Fisher’s
PLSD as a post hoc test. Frequencies between two groups
were compared using Fisher’s exact test. Differences were
considered statistically significant at p \ 0.05.
Results
All IVUS studies were completed without vascular com-
plications. Table 1 shows that the baseline characteristics
did not significantly differ between the two study groups.
Fig. 2 Simultaneous recording of IVUS images and intracoronary
pressure tracing. IVUS images were synchronized with intracoronary
pressure at peak (end-systole) and bottom (end-diastole) of pressure
by electrocardiogram monitoring
Clin Res Cardiol (2012) 101:545–551 547
123
Rupture was evident only in four ACS-related plaques
(23.5%) and in one ACS-unrelated plaque (5.3%), and all
rupture sites were located immediately proximal to the
lesion (minimum lumen) sites.
Quantitative IVUS measurements other than coronary
artery distensibility
Table 2 shows the quantitative IVUS results. The ACS-
related and -unrelated plaques did not significantly differ
even in terms of EEM CSA.
Difference in coronary artery distensibility
Table 3 compares the coronary artery distensibility index
and stiffness index b between ACS-related and -unrelated
plaques. The distensibility index was significantly higher at
the lesion site than at other sites in both types of plaques.
However, indices at the lesion site and at five evenly
spaced sites, and the means of these indices in each coro-
nary segment between the proximal and distal reference
sites, did not significantly differ between the groups. The
maximal value, the difference between the maximal and
minimal values and the standard deviation of the distensi-
bility index within each coronary segment were signifi-
cantly higher (5.58 ± 2.37 vs. 3.67 ± 1.78, p = 0.01,
5.26 ± 2.27 vs. 2.76 ± 1.45, p \ 0.001 and 2.13 ± 0.89
vs. 1.13 ± 0.55, p \ 0.001, respectively) and the minimum
stiffness index b was significantly lower (5.1 ± 2.2 vs.
7.1 ± 2.6, p = 0.02) in ACS-related than -unrelated
plaques.
Moreover, the difference in the distensibility index
between the lesion site of ACS-related plaques and the
immediate proximal site was significantly larger
(2.88 ± 2.35 vs. 1.17 ± 1.44, p = 0.022) than that in
ACS-unrelated plaques. The difference in the distensibility
index between the lesion sites of ACS-related plaques and
immediately distal sites did not statistically differ
(p = 0.086) from that in ACS-unrelated plaques. The dif-
ference in the stiffness index b between adjacent sites did
not significantly differ.
Discussion
We showed here that although mean coronary distensibility
did not statistically differ, it was longitudinally more het-
erogeneous in ACS-related than -unrelated plaques, espe-
cially between the lesion and the immediate proximal site.
Table 1 Baseline characteristics of study population
Stable AP
(n = 14)
ACS
(n = 17)
p value
Age* 61.3 ± 9.1 56.5 ± 8.0 ns
Gender (male/female) 13/1 15/2 ns
Coronary risk factors
Hypertension 11 (78.6) 13 (76.4) ns
Diabetes mellitus 5 (35.7) 6 (35.3) ns
Hyperlipidemia 10 (71.4) 10 (58.8) ns
Smoking 6 (31.5) 10 (58.8) ns
Imaged vessel
LAD 11 13 ns
LCx 1 1 ns
RCA 2 3 ns
Medication
Statin 9 (47.4) 7 (41.1) ns
b-Blocker 9 (47.4) 7 (41.1) ns
CCB 7 (36.8) 7 (41.1) ns
Nitrates 13 (68.4) 15 (88.2) ns
ACE inhibitor 3 (15.8) 5 (29.4) ns
ARB 7 (36.8) 7 (41.1) ns
Type of ACS N/A UA 2
NSTEMI 10
STEMI 5
Data are expressed as numbers (%) of patients
ACE angiotensin converting enzyme, ACS acute coronary syndrome,
AP angina pectoris, ARB angiotensin receptor blocker, CCB calcium
channel blocker, LAD left anterior descending coronary artery, LCxleft circumflex coronary artery, NSTEMI non-ST elevation myocar-
dial infarction, RCA right coronary artery, STEMI ST elevation
myocardial infarction, UA unstable angina
* Mean ± standard deviation
Table 2 Quantitative intravascular ultrasound results
ACS-unrelated
plaque (n = 19)
ACS-related
plaque (n = 17)
p value
Proximal reference
Lumen CSA (mm2) 7.5 ± 2.3 7.0 ± 3.4 ns
EEM CSA (mm2) 12.9 ± 3.6 12.4 ± 4.9 ns
P ? M CSA (mm2) 5.4 ± 2.4 5.4 ± 2.7 ns
Plaque burden (%) 40.9 ± 11.3 43.2 ± 12.9 ns
Lesion
Lumen CSA (mm2) 3.7 ± 0.6 3.3 ± 1.0 ns
EEM CSA (mm2) 13.1 ± 3.8 11.3 ± 4.4 ns
P ? M CSA (mm2) 9.4 ± 3.6 8.0 ± 4.3 ns
Plaque burden (%) 69.9 ± 8.9 67.4 ± 14.8 ns
Distal reference
Lumen CSA (mm2) 8.0 ± 3.4 7.3 ± 3.6 ns
EEM CSA (mm2) 13.8 ± 4.9 11.6 ± 4.4 ns
P ? M CSA (mm2) 5.8 ± 2.9 4.3 ± 1.9 ns
Plaque burden (%) 41.2 ± 12.9 37.9 ± 12.1 ns
Data are expressed as mean ± standard deviation
ACS acute coronary syndrome, CSA cross sectional area, EEMexternal elastic membrane, P ? M plaque plus media
548 Clin Res Cardiol (2012) 101:545–551
123
Previous IVUS studies have indicated that coronary
vessels are more distensible in patients with ACS than with
stable angina [14, 15]. Jeremias et al. [14] explained the
association between increased coronary distensibility and
unstable clinical presentation as follows. Greater distensi-
bility might augment positive remodeling by pulsatile
stretch, leading to heightened metalloproteinase activity.
The difference in distensibility might also be related to
matrix changes such as the ratio of collagen to elastin and the
formation of a lipid pool. Differences in endothelial function
between stable and unstable plaques might be reflected in
differences in both remodeling and distensibility. However,
they did not refer to mechanical stress or strain on plaques
that could be the final trigger of plaque rupture. Takano et al.
[15] found that coronary distensibility at the proximal site
near the culprit lesion was greater in angioscopically defined
yellow, than white plaques. They considered that this was
partially due a difference in plaque composition and in
coronary remodeling. They also stated that the border of
normal intima and plaque, namely the ‘‘shoulder region,’’
must be exposed to mechanical stress caused by a difference
in regional distensibility. However, a longitudinal difference
in coronary distensibility within the same coronary plaque
was not described in either of these studies.
The relationship between ‘‘circumferential’’ mechanical
stress and plaque rupture has been extensively investigated
[1–3, 24, 25] and high stresses concentrated in the fibrous
cap, particularly at the junction with relatively normal
tissue (the ‘‘shoulder region’’) causes vulnerability to rup-
ture. Examinations of coronary plaque using intravascular
elastography or palpography have shown very high local
strain values (rate of deformation caused by stress) at the
shoulder regions of plaques [26, 27].
Plaques tend to rupture more frequently in the proximal
or upstream portions than in the distal or downstream por-
tions in the ‘‘longitudinal’’ direction [6, 28–30]. Li et al. [31,
32] found high stress concentrations within the fibrous cap
of a model of longitudinal blood flow and plaque interac-
tion, especially at the shoulder regions at the proximal part
of the plaque. Imoto et al. [33] assessed the distribution of
longitudinal stress within plaques using color mapping
based on computational structural analysis. They found a
concentration of equivalent stress at the tops of hills and
shoulders of homogeneous fibrous plaques and at a local-
ized surface immediately above a lipid core when present.
Gijsen et al. [34] measured local radial strain in vessel walls
using intravascular palpography and found that strain values
were significantly lower at the downstream region of the
plaque than at the upstream, shoulder and throat regions.
Although the regions of concentrated stresses or strains vary
among these studies, they nevertheless reveal significant
longitudinal heterogeneity in mechanical stresses or strains
over coronary plaque. As the ratio of the radial strain to
circumferential tensile stress is equal to the distensibility of
the tissue, this stress–strain relationship implies that an
increase in circumferential stress will cause radial strain to
increase [27, 35]. Although we assessed coronary distensi-
bility without regard to a difference in mechanical stresses
over the plaque, we consider that our findings are consistent
with these previous reports.
Table 3 Comparison of distensibility and stiffness indexes b between ACS-related and unrelated plaques
Distensibility index Stiffness index b
ACS- unrelated ACS-related p value ACS-unrelated ACS- related p value
Proximal reference 2.23 ± 1.35 2.43 ± 2.73 ns 31.3 ± 57.4 7.0 ± 66.6 ns
Proximal middle 1.79 ± 2.25 1.98 ± 2.04 ns 50.8 ± 84.7 19.3 ± 27.1 ns
Middle 1.42 ± 0.80 1.36 ± 1.74 ns 22.1 ± 15.4 37.2 ± 46.6 ns
Distal middle 1.66 ± 1.31 1.08 ± 1.07 ns 30.6 ± 41.8 67.3 ± 82.1 ns
Distal reference 1.50 ± 1.66 1.33 ± 1.12 ns 45.1 ± 121.0 41.6 ± 68.8 ns
Lesion 3.01 ± 2.30* 3.93 ± 2.84* ns 16.9 ± 23.7 12.5 ± 13.1 ns
Mean 2.20 ± 1.74 2.40 ± 0.93 ns 33.4 ± 29.4 34.4 ± 20.5 ns
Maximum 3.67 ± 1.78 5.58 ± 2.37 0.010 101.2 ± 124.7 109.3 ± 92 ns
Minimum 0.91 ± 1.93 0.32 ± 0.23 ns 7.1 ± 2.6 5.1 ± 2.2 0.020
Maximum-minimum 2.76 ± 1.45 5.26 ± 2.27 \0.001 94.1 ± 125.1 104.2 ± 91.5 ns
Standard deviation 1.13 ± 0.55 2.13 ± 0.89 \0.001 39.0 ± 50 243.0 ± 39.8 ns
Lesion–just Proximal 1.17 ± 1.44 2.88 ± 2.35 0.022 48.8 ± 85.0 45.2 ± 72.8 ns
Lesion–just Distal 1.88 ± 1.59 3.42 ± 2.71 0.086 25.4 ± 25.1 53.1 ± 73.8 ns
Data are expressed as mean ± standard deviation
ACS acute coronary syndrome; mean, maximum, minimum and standard deviation are mean, maximal and minimal values and standard
deviation, respectively, of six imaged sites
* p \ 0.05 versus proximal reference, proximal middle, middle, distal middle and distal reference values
Clin Res Cardiol (2012) 101:545–551 549
123
We found here that coronary distensibility was more
longitudinally heterogeneous in ACS-related than -unre-
lated plaques, especially between the lesion and the
immediately proximal region. This heterogeneity might be
due to longitudinal differences in plaque composition as
well as in the types of mechanical stresses affecting the
plaque. Furthermore, such differential heterogeneity in
distensibility could increase mechanical stress at the
shoulder region between the plaque and relatively normal
tissue.
Study limitations
We examined longitudinal differences in coronary disten-
sibility. However, we could not measure circumferential
differences. Intravascular ultrasound elastography or pal-
pography might be more suitable for this purpose [26, 27,
34]. Coronary lesions with a lumen of \1.5 mm2 or those
that were occluded (wedged) by the imaging catheter were
excluded from this study. However, the IVUS catheter
itself might have altered coronary blood flow and trans-
mitted energy. Reflected pulse wave energy might increase
when complex acute longitudinal lesions are present. This
phenomenon might have affected our results. Other factors
such as pressure-characteristics (dp/dt) values, absolute
systolic and diastolic pressure values, flow dynamics,
vessel diameter, segmental vessel pathology (additional
lesions in the same vessel) and myocardial wall stress that
are associated with characteristics of the microcirculation
and myocardial function might also have affected calcu-
lations of the distensibility index and of the stiffness index
b. We analyzed 36 de novo human coronary lesions and
excluded heavily calcified, severely stenotic, restenotic,
post-intervention, ostial and chronic totally occlusive
lesions. Therefore, our findings might not be applicable to
these types of lesions.
Residual thrombus in patients with ACS might have
affected calculations of the distensibility index and stiff-
ness index b. Even thrombectomy does not guarantee
complete removal of a thrombus. All ACS-related lesions
were imaged after the onset of ACS, so the findings might
have been different had we examined vulnerable plaques
beforehand. Most previous studies have the same limita-
tions, except for that of Yamagishi et al. [11] who found
that large eccentric plaques containing an echolucent zone
that can be revealed by IVUS before ACS onset could be at
increased risk for instability.
Conclusions
This study using IVUS demonstrated that coronary dis-
tensibility was longitudinally more heterogeneous in ACS-
related than -unrelated plaques, especially between the
lesion site and the immediate proximal site.
Acknowledgments This study was supported in part by a research
grant from the Japan Foundation of Cardiovascular Research.
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