Comparison of coronary plaque components between non-culprit lesions in patients with acute coronary syndrome without ST segment elevation and target lesions in patients with stable angina: virtual histology – intravascular ultrasound analysis.

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Norvydas Zapustas1, Ali Aldujeli1, Ramūnas Unikas1

1Hospital of Lithuanian University of Health Sciences Kauno klinikos. Department of interventional Cardiology, Kaunas, Lithuania.

ABSTRACT
Objective: Patients with acute coronary syndrome (ACS) are thought to have multiple vulnerable coronary plaques components, comparing with stable angina (SAP) patients. We compared relationship between coronary plaque components of non-culprit lesions in patients with acute coronary syndrome without ST segment elevation and target lesions in patients with stable angina: virtual histology – intravascular ultrasound (VH-IVUS) analysis.

Methods: We compared virtual histology – intravascular ultrasound findings between 25 ACS without ST segment elevation non-culprit lesions and 22 stable angina target lesions. Using virtual histology – intravascular ultrasound classified the color-coded tissue into four major components: green (fibro-elastic); light green (fibro-fatty); white (dense calcium) and red (necrotic). Planar VH-IVUS analysis at the minimum luminal site in stable angina pectoris patients’ group and non-culprit lesion at ACS without ST segment elevation and volumetric analysis over a 10-mm-long segment centered at the minimum luminal site was performed.

Results. Patients with ACS without ST elevation the plaque burden was significantly smaller (90,8 ±21 mm3 vs. 102,6 ± 28 mm3, p <0,05) compared with SAP patients’ group. Volumetric analysis showed, non-culprit lesions in acute coronary syndrome without ST segment elevation patients had a greater necrotic core volume (19.1 vs. 12.4, mm3, p<0,05) and dense calcium volume  (15.6 vs. 9.6 mm3, p<0.05) and fibro-fatty volume ( 15.8 vs. 15.5, mm3, p>0,05) compared with target lesions in stable angina patients at the minimum lumen site.

Conclusions: In the present study, the VH-IVUS detected necrotic core was significantly larger in atherosclerotic lesions in patients in acute phase of ACS without ST elevation compared to the stable angina subjects and it could be considered a marker of plaque vulnerability.

Keywords: intravascular ultrasound, coronary plaque, plaque components.

Journal of Medical Sciences. November 30, 2020 - Volume 8 | Issue 19. Electronic - ISSN: 2345-0592
151
Medical Sciences 2020 Vol. 8 (19), p. 151-159
Comparison of coronary plaque components between non-culprit
lesions in patients with acute coronary syndrome without ST
segment elevation and target lesions in patients with stable angina:
virtual histology – intravascular ultrasound analysis.
Norvydas Zapustas
1
, Ali Aldujeli
1
, Ramūnas Unikas
1
1
Hospital of Lithuanian University of Health Sciences Kauno klinikos. Department of interventional Cardiology,
Kaunas, Lithuania.
ABSTRACT
Objective: Patients with acute coronary syndrome (ACS) are thought to have multiple vulnerable coronary
plaques components, comparing with stable angina (SAP) patients. We compared relationship between coronary
plaque components of non-culprit lesions in patients with acute coronary syndrome without ST segment elevation
and target lesions in patients with stable angina: virtual histology – intravascular ultrasound (VH-IVUS) analysis.
Methods: We compared virtual histology – intravascular ultrasound findings between 25 ACS without ST
segment elevation non-culprit lesions and 22 stable angina target lesions. Using virtual histology – intravascular
ultrasound classified the color-coded tissue into four major components: green (fibro-elastic); light green (fibro-
fatty); white (dense calcium) and red (necrotic). Planar VH-IVUS analysis at the minimum luminal site in stable
angina pectoris patients’ group and non-culprit lesion at ACS without ST segment elevation and volumetric
analysis over a 10-mm-long segment centered at the minimum luminal site was performed.
Results. Patients with ACS without ST elevation the plaque burden was significantly smaller (90,8 ±21 mm
3
vs.
102,6 ± 28 mm
3
, p <0,05) compared with SAP patients’ group. Volumetric analysis showed, non-culprit lesions
in acute coronary syndrome without ST segment elevation patients had a greater necrotic core volume (19.1 vs.
12.4, mm
3
, p<0,05) and dense calcium volume (15.6 vs. 9.6 mm3, p<0.05) and fibro-fatty volume ( 15.8 vs. 15.5,
mm3, p>0,05) compared with target lesions in stable angina patients at the minimum lumen site.
Conclusions: In the present study, the VH-IVUS detected necrotic core was significantly larger in atherosclerotic
lesions in patients in acute phase of ACS without ST elevation compared to the stable angina subjects and it could
be considered a marker of plaque vulnerability.
Keywords: intravascular ultrasound, coronary plaque, plaque components.
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152
Introduction
Plaque disruption, with superimposed thrombosis, is
the main cause of acute coronary syndromes (ACS)
[1, 2]. Ruptured plaques compose the vast majority
of atherosclerotic lesions associated with acute
thrombi and mor- phological characteristics and
histological composition of these plaques have been
reported in previous studies. Thin- cap
fibroatheroma (TFCA), the lesions most likely to
experience rupture, usually have an extensive
necrotic core and a thin fibrous cap [3, 4].
Recognition of these high risk atheroma plaques (the
so called ‘‘vulnerable’’ plaques) is a challenge for
cardiologists as previous studies have suggested that
leaving these lesions untreated may be associated
with events at follow up [5, 6]. However, an
angiographic study reported that plaque instability is
not merely a local vascular accident but presumably
reflects more generalized pathophysiologic
processes with the potential to destabilize
atherosclerotic plaques through out the coronary tree
[7]). To assess the relevant detail of clinical
syndrome (stable and unstable) and coronary plaque
morphology is more important for the prevention of
ACS. However, the difference of tissue components
of atheromatous plaque in the culprit and non-culprit
lesions between ACS without ST segment elevation
and stable angina pectoris (SAP) has not been fully
clarified by use of Virtual histology-intravascular
ultrasound (VH-IVUS). So the aim of our study is to
assess the tissue characteristics of coronary plaques
between ACS without ST segment elevation of non-
culprit lesions and SAP of culprit lesion.
Subjects and Methods
Study population
A total of 47 patients were enrolled who had
undergone coronary angiography, grayscale and
VH-IVUS in non-culprit lesion in ACS without ST
segment elevation and in target lesion in SAP
patients between January, 2016 and October, 2017
were identified from the Lithuanian University of
Health Sciences VH-IVUS registry database. We
compared VH-IVUS findings between 25 ACS
without ST segment elevation non-culprit lesions
and 22 SAP target lesions. The presence of SAP was
determined according to the 2019 ESC Guidelines
for the diagnosis and management of chronic
coronary syndromes [8] and ACS with non-ST
segment elevation are considered to be closely
related conditions whose pathogenesis and clinical
presentations are similar, but of differing severity
(i.e., they differ primarily in whether the ischemia is
severe enough to cause sufficient myocardial
damage to release detectable quantities of a marker
of myocardial injury, most commonly troponin I).
Once it has been established that no biochemical
marker of myocardial necrosis has been released, the
patient with an ACS may be considered to have
experienced unstable angina, whereas the diagnosis
of non-ST segment elevation myocardial infarction
is established if a marker of myocardial injury has
been released [9].
We excluded patients with ST-segment elevation
myocardial infarction, Thrombolysis in Myocardial
Infarction (TIMI) 0-1 flow, coronary artery bypass
graft lesion, chronic total occlusion, restenosis after
stenting, important systemic disease such as
systemic lupus erythematosus, amyloidosis,
sarcoidosis, human immunodeficiency virus
infection, and malignancies, and so on, or serum
creatinine >2.5 mg/dL. Culprit lesion in ACS
without ST segment elevation patients was defined
as plaques viewed on an angiogram. Target lesion in
SAP patients was defined as a coronary lesion whose
diameter stenosis by quantitative coronary
angiography (QCA) was greatest if the patient had
multivessel disease. Plaques with more than a 30%
diameter stenosis as compared with the reference
diameter by IVUS were included in our study. Each
plaque was separated by at least 5 mm from the edge
of any other plaque or implanted stent edge. The
protocol was approved by the institutional review
board. Hospital records of all patients were reviewed
to obtain clinical demographics and medical history.
Coronary angiography
Coronary angiogram was analyzed with validated a
QCA system. With the outer diameter of the
contrast- filled catheter as the calibration standard,
the reference diameter and minimal lumen diameter
were measured in diastolic frames from orthogonal
projections. Perfusion was evaluated according to
TIMI criteria.
Intravascular ultrasound imaging and analysis
VH-IVUS examination was performed before any
intervention and after the intracoronary
administration of nitroglycerin 0.2 mg using a
motorized transducer pullback system (0.5 mm/s) at
SAP patient group and after the culprit lesion
treatment in ACS without ST segment elevation
group. A 2.9Fr IVUS imaging catheter (Eagle Eye;
Volcano Corporation, Rancho Cordova, California)
incorporated a 20-MHz phased-array transducer.
Conventional gray-scale quantitative IVUS analyses
were performed according to criteria of the clinical
expert consensus document on IVUS to include
external elastic membrane (EEM), luminal, and
plaque and media (P&M; defined as EEM minus
luminal) areas [10]. Plaque burden was defined as
P&M area divided by EEM area. Planar gray-scale
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153
and VH-IVUS analysis was performed at the site of
the minimal luminal area. Volumetric VH-IVUS
analysis was performed along a 10-mm segment
centered on the minimal luminal area; calculations
were made using Simpson’s rule. VH-IVUS analysis
classified and color-coded tissue as green (fibrotic),
yellow-green (fibrofatty), white (dense calcium),
and red (necrotic core) [11;12]. VH- IVUS analyses
are reported in absolute amounts and as percentages
(relative amounts) of plaque area and volume.
Statistical analysis
The Statistical Package for the Social Sciences
(SPSS 17.0) for Windows,(SPSS Inc., Chicago, IL,
USA) was used for all analyses. Continuous
variables were presented as the mean value±1SD;
comparisons were conducted by a Student’s t-test or
nonparametric Wilcoxon test if the normality
assumption was violated. Discrete variables were
presented as percentages and relative frequencies.
Comparisons were conducted by chi-square
statistics or Fisher’s exact test as appropriate.
Multivariate analysis was performed to determine
the independent predictors of TCFA. All variables
with p<0.1 in the univariate analysis were entered
into the multivariate analysis. A p of <0.05 was
considered statistically significant. We also used
Spearman rank correlation is a non-parametric test
that is used to measure the degree of association
between two variables.
Results
A total of 47 patients were enrolled (65.0 ± 11.9
years old ), 25 patients with ACS without ST
segment elevation and 22 stable angina pectoris
patients.
VH-intravascular ultrasound analysis showed that
patients’ group with ACS without ST segment
elevation had statistically significant greater amount
necrotic core and dense-calcium volumes in non-
culprit lesions, compared with stable angina pectoris
patient group by absolute amount and percentage
(fig. 1., fig. 2).
Fig. 1. Athesclerotic plaque components volume.
12.4
9.6
53.4
15.5
19.1
15.6
52.1
15.8
0
10
20
30
40
50
60
Necrotic Dense-calcium Fibro-elastic Fibro-fatty
Volume (mm ³)
Athesclerotic plaque components
Stable angina pectoris ACS without ST elevation
*-p<0,05
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Fig. 2. Athesclerotic plaque components percentage.
In the conventional IVUS analysis the total plaque volume was significantly greater in SAP patients group
compared with patients ACS without ST segment elevation group (fig. 3).
Fig. 3 Total volume of coronary plaque components.
Analyzing the plaque component dependence to the
plaque volume, our results are that non-culprit lesion
of ACS without ST segment elevation group and in
SAP target lesion group necrotic volumes in
atherosclerotic plaque statistically significant
depends to the plaque volume, but it has stronger
relationship in ACS without ST segment elevation
group comparing to the SAP target lesion group (fig.
4.).
Also, our results show that calce-densium
component dependence to the plaque volume in non-
culprit lesion of ACS without ST segment elevation
group are statistically significant comparing with
SAP target lesion group (fig.5.). That shows the non-
culprit lesion of ACS without ST segment elevation
had more vulnerable plaque components comparing
wit SAP patient group.
12.6
12.1
59.8
15.5
17.5
15.1
51.2
16.2
0
10
20
30
40
50
60
70
Necrotic core Dence-calcium Fibro-elastic Fibro-fatty
Percent %
Atherosclerotic plaque components
Stable angina pectoris ACS without ST elevation
*-p<0,05
102.63
90.81
20
40
60
80
100
120
140
Stable angina pectoris ACS without ST
elevation
Total volume of the
coronary plaque
components (mm³)
p>0,05
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Fig. 4. Necrotic component volume dependence to the plaque volume
Fig.5. Dence-calcium component volume dependence to the plaque volume
Also, we find that non-culprit lesion of ACS without ST segment elevation group and target lesion of SAP patient
group fibro-elastic component volume in atherosclerotic plaque strongly, statistically significant depends to the
plaque volume (fig. 6.).
-10
0
10
20
30
40
50
60
70
0 50 100 150 200
Necrotic volume (mm³)
Total volume of the coronary plaque components (mm³)
Stable angina pectoris ACS without ST elevation
r=0,35, p>0,05
r=0,45, p<0,05
r=0,80; p<0,001
r=0,72; p<0,001
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Fig. 6. Fibro-elastic component volume dependence to the plaque volume
Comparing the fibro-fatty plaque component dependence to plaque volume we find that target lesion of SAP
patient group fibro-fatty component volume in atherosclerotic plaque strongly, statistically significant depends to
the plaque volume and there is no correlation between the fibro-fatty component volume in atherosclerotic plaque
in ACS without ST segment elevation group (fig. 7.).
Fig. 7. Fibro-elastic component volume dependence to the plaque volume
0
20
40
60
80
100
120
0 50 100 150 200
Fibro-elastis volume (mm³)
Total volume of the coronary plaque components (mm³ )
Stable angina pectoris ACS without ST elevation
r=0,81, p<0,001
r=0,79, p<0,001
0
10
20
30
40
50
60
70
0 50 100 150 200
Fibro-fatty volume (mm³)
Total volume of the coronary plaque components (mm³)
Stable angina pectoris ACS without ST elevation
r=0,64, p<0,001
r=0,34, p>0,05
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Discussion
The main result of this study is that there is a
significant difference in the structure of the
atherosclerotic plaque in patients with an acute
phase of ACS, without the elevation of ST segments,
compared to the patients with a stable angina. The
first exhibits a significantly higher portion of the
necrotic core, which correlates to the subsequent
research [13,14]. A significantly higher portion of
the necrotic core in the lesions not directly
accountable for the occurrence of ACS supports the
fact that ACS is a multifocal process [13].
By comparing stable and vulnerable plaques, Sano
et al. [15] have established a greater percentage of
the lipid- necrotic component in vulnerable plaques.
Previous pathological studies of vulnerable plaques
after ACS showed that the share of the necrotic core
represents a marker of plaque vulnerability [15].
Kubo et al. [16] used serial IVUS-RF imaging to
investigate the natural evolution of non-obstructive
plaques and showed that in contrast to fibrous and
calcified plaques, which remained unchanged, the
intimal thickening and thick cap fibroatheromas
may evolve to thin cap fibroath- eromas at 12
months follow-up.
Furthermore, in tumors researches, it is well-known
that subpopulations of macrophages present in
atherosclerotic plaques promote angiogenesis [17].
However, these newly formed blood vessels
frequently lack the appropriate structural integrity
and may cause bleeding inside the plaque, which
leads to lesion growth and jeopardizes the stability
of the plaque [18].
Of all parameters pertaining to the vulnerability of
the atherosclerotic plaque, the most significant are
the presence of the necrotic core and a thin fibrous
cap which sep arates it from the lumen (14, 15).
Plaque ruptures are most frequently formed from the
previously angiographically insignificant lesions
(19). Out of all of examined lesions, in our study
only four were angiographically diagnosed as
significant (>70% stenosis). Therefore, an VH-
IVUS analysis may be used for the purpose of
revealing vulner- able lesions (13, 20). The fact that
IVUS-VH has a reduced axial resolution (range:
100-200μm) limits its ability to identify some of
these characteristics (e.g. plaque disrup- tion,
macrophage infiltration) and measure the thickness
of the fibrous cap [21].
These limitations of VH-IVUS may be overcome by
the use of optical coherence tomography (OCT). The
high resolution of OCT enables the identification of
lipid pools and, unlike IVUS-VH, detection of the
internal and exter- nal elastic lamina [22, 23]. OCT
further enables a precise quantification
(measurement) of fibrous cap thickness, enables a
reliable evaluation of the cap disruption and erosion
and can clearly visualize the presence and type of the
thrombus [21, 24]. The limitation of this model is the
reduced axial penetration which may aggravate the
estimate of lipid pool dimensions and the
identification of positive remodeling. For
overcoming these limitations, it has been suggested
that a combined use of VH-IVUS and OCT be used
[25].
Finally, an aggressive lipid defense therapy should
also be administered for the purpose of stabilizing
other plaques, independent of angiographically
significant sten-oses. Possible new episodes of ACS
may be prevented in this manner [26].
Study limitation
This study was a single-center study with a small
number of patients, thus possibly posing a risk of
patient selection bias. Our results of plaque
components were not evaluated by histology or
other diagnostic modalities such as optical
coherence tomography. VH- IVUS cannot
determine the presence of thrombus. Total
occlusions, bifurcation lesions, lesions with severe
angulations, and heavily calcified lesions were
excluded from this study. Therefore, this study
might not represent the whole spectrum of patients
with ACS and patients with SAP.
Conclusion
In the present study, the VH-IVUS detected necrotic
core was significantly larger in atherosclerotic
lesions in patients in acute phase of ACS without ST
elevation compared to the stable angina subjects and
it could be consid- ered a marker of plaque
vulnerability.
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