IVUS and OCT Assessment of Coronary Artery Disease

© 2018 Indian Heart Journal Interventions | Published by Wolters Kluwer ‑ Medknow 71
Editorial Review
Intravascular Ultrasound and Optical Coherence Tomography
for the Assessment of Coronary Artery Disease and
Percutaneous Coronary Intervention Optimization: The Basics
Vijayakumar Subban, Owen Christopher Raffel1
, Nandhakumar Vasu, Suma M. Victor, Mullasari Ajit Sankardas
Institute of Cardiovascular Diseases, The Madras Medical Mission, Chennai, India, 1
CardioVascular Clinics, St Andrews War Memorial Hospital, Cardiology Program,
The Prince Charles hospital, and University of Queensland, Queensland, Australia
Abstract
Although coronary angiography is the standard method employed to assess the severity of coronary artery disease and to guide
treatment strategies, it provides only two-dimensional image of the intravascular lesions. In contrast with the luminogram obtained by
angiography, intravascular imaging produces cross-sectional images of the coronary arteries of far greater spatial resolution, capable
of accurately determining vessel size as well as plaque morphology, and eliminates some of the disadvantages inherent to angiography,
such as contrast streaming, foreshortening, vessel overlap, and angle dependency. Growing body of literature recommends intravascular
imaging, especially intravascular ultrasound and optical coherence tomography, which can be competently used to answer questions
that arise during daily practice in interventional cardiology such as: Is this stenosis clinically relevant? Which is the culprit lesion? Is
this plaque at high risk for rupture? How can I optimize stent results? Why did thrombosis or restenosis occur in this stent? Patients
with more complex coronary disease likely benefit more from a revascularization approach that includes intravascular imaging. The
aim of this review was to discuss the basic principles of intravascular imaging, characterization of atherosclerosis, optimization of
angioplasty results and to identify technical challenges because of artefacts.
Keywords: Intracoronary imaging, intravascular ultrasound, optical coherence tomography, percutaneous coronary intervention optimization
Introduction
Coronary angiography (CAG) remains the gold standard
for invasive assessment of coronary artery disease (CAD)
and for guiding percutaneous coronary intervention
(PCI). However, it is limited by its poor resolution, angle
dependency, vessel overlap and foreshortening, and
significant inter- and intra-observer variability in assessing
coronary stenoses. Further, CAG is a two-dimensional
luminogram and does not provide adequate information
about the vessel wall and plaque characteristics.[1]
With their ability to produce high-quality cross-sectional
images of the coronary arteries and tissue characterization
capabilities, intravascular imaging (IVI) modalities
compliment CAG in the qualitative and quantitative
assessment of CAD. Further, they also aid in PCI by
providing accurate vessel and lesion dimensions for device
sizing and guiding stent optimization. In addition, IVI
plays an indispensable role in the management of stent
failure. There are four major IVI modalities currently
available for coronary imaging, namely, intravascular
ultrasound (IVUS), optical coherence tomography (OCT),
angioscopy, and near-infrared spectroscopy (NIRS).
This review focuses only on IVUS and OCT: the first part
deals with the basic aspects of IVI including qualitative
and quantitative assessment of CAD, PCI planning, and
post-PCI optimization and the second part focuses on
Address for correspondence: Dr. Vijayakumar Subban,
Department of Cardiology, Institute of Cardiovascular Diseases,
Madras Medical Mission, 4A, Dr. J. Jayalalitha Nagar,
Mogappair, Chennai 600037, Tamil Nadu, India.
E-mail: drkumarvijay@gmail.com
This is an open access journal, and articles are distributed under the terms of the
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows
others to remix, tweak, and build upon the work non-commercially, as long as
appropriate credit is given and the new creations are licensed under the identical terms.
For reprints contact: reprints@medknow.com
How to cite this article: Subban V, Raffel OC, Vasu N, Victor SM,
Sankardas MA. Intravascular ultrasound and optical coherence
tomography for the assessment of coronary artery disease and
percutaneous coronary intervention optimization: The basics. Indian
Heart J Interv 2018;1:71-94.
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Subban, et al.: Coronary intravascular imaging: basics

72 72 Indian Heart Journal Interventions ¦ Volume 1 ¦ Issue 2 ¦ September-December 2018
the utility of IVI during PCI in specific lesion subsets. As
both the imaging systems provide similar information of
different magnitude, they are discussed together and the
differences are highlighted.
Equipment and Principles of Imaging
Intravascular ultrasound
IVUS equipment consists of three components: a
console, an automatic pullback device, and an imaging
catheter. The console houses the imaging engine, which
provides electrical signals to the transducer, receives and
processes the reflected signals, and displays them as a
grayscale reconstruction of the vessel wall. In addition,
it offers tools for quantitative analysis, data exporting in
various formats, and archiving. The automatic pullback
device supports vessel scanning at a constant speed that
enables longitudinal image display and accurate length
measurements. The catheter houses a miniature transducer
at the tip. The transducer contains piezoelectric crystals,
the source of ultrasound waves.[2,3]
IVUS works by the same principle as with any other
ultrasound-based imaging modality. The transducer
receives electric signals from the console and with
electrical stimulation, the piezoelectric crystals in the
transducer expand and contract to produce high-
frequency ultrasound waves. These ultrasound waves are
reflected at the tissue interfaces in the vessel wall. Part of
the reflected ultrasound waves returns to the transducer
and the piezoelectric crystals convert these signals back
to electrical signals. The imaging engine in the console
processes these electrical signals to create grayscale cross-
sectional images of the imaged vessel.[2,3]
There are two basic IVUS catheter designs: mechanical/
rotational and solid state. The mechanical catheters
(OptiCross IVUS catheter, Boston Scientific, Santa Clara,
California; Revolution IVUS catheter, Volcano, Rancho
Cordova, California; ViewIT IVUS catheter, Terumo,
Tokyo, Japan; and Kodama HD IVUS catheter, ACIST
Medical Systems, Eden Prairie, Minnesota) consist of a
single transducer element located at the tip of a flexible
drive cable housed in a protective sheath and operated by
an external motor drive unit. The drive cable rotates the
transducer around the circumference (1800
rpm) and the
transducer sends and receives the ultrasound signals at 1°
increment to form the cross-sectional image. The imaging
catheters operate at a central frequency of 40 MHz
or 60 MHz and are 5F or 6F compatible [Figure 1A].
In the solid-state catheter design (Eagle Eye Catheter,
Volcano), no rotating components are present. There
are 64 transducer elements mounted circumferentially
around the tip of the catheter. The transducer elements
are sequentially activated with different time delays to
produce an ultrasound beam that sweeps around the vessel
circumference. The catheter works at a central frequency
of 20 MHz and is 5F compatible [Figure 1B].[2,3]
With the differences in the design and the operating
frequency, there are some specific advantages and
limitations with each of the catheter designs. The longer
monorail segment provides better trackability to the
solid-state catheter in complex coronary anatomy, and
the central location of the guidewire port eliminates the
guidewire artifact. In addition, the shorter distance from
the catheter tip to the transducer (10
mm in Eagle Eye
Platinum and 2.5
mm in Eagle Eye Platinum ST IVUS
Catheter; Volcano) offers advantage in chronic total
occlusion (CTO) intervention. Further, the catheter does
not have outer sheath so that no air trapping is present
around the catheter and it does not need saline flushing.
No rotating elements are present in the catheter and hence
nonuniform rotational deformity (NURD, mechanical
restrain to the rotation of the catheter resulting in smearing
of the part or whole circumference, described later) does
not occur with solid-state catheter system. However, it is
limited by its lower frequency and the resultant poor near-
field resolution, which produces ring down artifact (bright
halos surrounding the catheter) and loss of imaging details
close to the surface of the catheter. The higher central
frequency with mechanical system offers better resolution
and high-quality images aiding clinical decision-making.
Further, the outer sheath allows precise and controlled
pullback for length and volume assessment. On the
downside, it uses a short monorail system, which limits
its trackability in complex lesions and the guidewire runs
on the side of the transducer, which produces a guidewire
artifact in the image. In addition, the transducer is housed
at 25 mm from the tip, which makes it unsuitable for CTO
imaging. Moreover, the hindrance to the rotation of the
transducer produces NURD, and the air trapping in the
sheath distorts the image quality and needs frequent saline
flushing.[2,3]
Optical coherence tomography
OCT is an optical analog of IVUS and uses near-infrared
light to produce high-resolution cross-sectional images
of the coronary artery. As with IVUS, OCT also forms
images by measuring the echo time delay and intensity
of the backscattered optical signals from the various
interfaces of the vessel wall. However, the speed of light
at 3 × 108
m/s as compared to that of sound at 1500 m/s
makes it impossible to measure the echo time delays of
the reflected light waves with the existing electronics,
and hence, an interferometer is used in OCT to measure
the same. The very high frequency of the light provides
10–15
µ resolution but at the same time limits tissue
penetration to 1–2 mm.[4]
There are two types of OCT systems: Time domain OCT
(TD-OCT) and frequency domain OCT (FD-OCT).
TD-OCT uses broadband light source and the
interferometer splits the light beam into two halves—
sample and reference arms. The sample arm goes to the
patient and is reflected back, whereas the reference arm

Indian Heart Journal Interventions ¦ Volume 1 ¦ Issue 2 ¦ September-December 2018 73
goes to a mirror positioned at a known distance. The
detector combines the reflected signals from the sample
arm and the reference signal and when the path lengths
travelled by both match an interference pattern is created.
The interference pattern is analyzed by the OCT system for
the intensity of backscatter (brightness of the image) and
the echo time delay (depth of the tissue). TD-OCT relies
on varying position of the reference mirror to measure the
echo time delays and sequentially measures the optical
echoes. This limits the rate of image acquisition, and
the maximum pullback speed is approximately 2–3
mm/s
[Figure 2A]. FD-OCT uses a narrow bandwidth light
source that sweeps rapidly between wavelengths 1250–
1350
nm and a fixed reference mirror. The interference
patterns at different wavelengths are processed by Fourier
transformation to provide the amplitude profile and time
delay of the waves reflected from different depths. This
enables FD detector to measure all echo time delays
that forms an A-line at the same time, and the current
generation FD-OCT systems allow image acquisition at
a speed of 38
mm/s [Figure 2B]. This in turn limits the
amount of contrast flush during image acquisition.[4]
Qualitative Analysis
Interaction of ultrasound waves/light photons with
the tissues of the body occurs in the form of reflection,
refraction, attenuation, or scattering. When the sound
waves/light photons encounter a tissue interface, part of
it is reflected from the surface and part of it is allowed
to pass through. The amount of reflection depends on
the impedance change at the interface and the angle
of incidence. The amount of reflection determines the
brightness of the tissue in the image. In case of strong
reflectors, all the signals may be reflected back from the
surface and none of them pass through it, this result in
“shadowing” beyond the leading edge of the structure.
Metal (stent struts and guidewires) is a strong reflector
of both sound and light and causes shadowing in both
the imaging modalities. Calcium reflects ultrasound
waves intensely and causes acoustic shadowing and poor
visibility of deeper structures. However, it reflects light
Figure 1: Types of IVUS catheter systems: (A) Mechanical IVUS system consists of a single transducer element located at the tip of a flexible
drive cable housed in a protective sheath. The drive cable rotates the transducer around the circumference to form the cross-sectional image. The
guidewire passes beside the transducer. (B) In solid-state system, there are 64 transducer elements mounted circumferentially around the tip of the
catheter. The transducer elements are sequentially activated with different time delays to produce an ultrasound beam that sweeps around the vessel
circumference. The guidewire port is located in the center of the transducer. (Figure courtesy: Boston Scientific)
Figure 2: Types of OCT systems: (A) Time domain OCT (TD-OCT). (B) Frequency domain OCT (FD-OCT). TD-OCT uses broadband light source and
relies on varying position of the reference mirror to measure the echo time delays and sequentially measures the optical echoes. This limits the rate
of image acquisition, restricting the maximum pullback speed to approximately 2–3 mm/s. FD-OCT uses a narrow bandwidth light source that sweeps
rapidly between wavelengths 1250 and 1350
nm and a fixed reference mirror. The interference patterns at different wavelengths are processed
by Fourier transformation to provide the amplitude profile and time delay of the waves reflected from different depths. This enables FD detector to
measure all echo time delays that forms an A-line at the same time and this allows very rapid image acquisition. (Figures courtesy: St. Jude Medical)


poorly and allows it to pass through. Hence, it is possible
to measure the thickness of the calcium with OCT
imaging. “Attenuation” is decrease in the signal intensity
when the signals pass through the tissue and occurs
mainly because of absorption by the tissue. Attenuation
determines the penetration depth of the signals: strongly
attenuating tissues have very low penetration depth and
poor visibility of the deeper structures. “Scattering” is
reflection in multiple directions and occurs with small
moving structures, such as red blood cells (RBCs), and
produces a typical appearance of speckling in the image.
During IVUS imaging, prominent speckling occurs with
slow moving or stagnant blood when the catheter is across
a tight stenosis or in a totally occluded vessel, particularly
with high-frequency imaging catheters. With OCT
imaging, RBCs cause intense scattering of the light that
interferes with imaging and hence needs lumen clearance
with contrast flush.[4,5]
Normal coronary artery
A typical IVUS/OCT image has four components: (1) The
catheter: A circular structure inside the lumen. (2) The
guidewire: It appears as a bright spot (IVUS)/arc (OCT)
with a wedge-shaped shadow. Guidewire is visible only
in case of mechanical catheters where it passes beside
the transducer. (3) Echolucent lumen: In an optimally
acquired OCT image, the lumen appears uniformly dark
as the blood is cleared with contrast. In the IVUS image,
blood speckles are visualized in the lumen. (4) The vessel
wall: In a normal adult coronary artery, the vessel wall has
a three-layered architecture. The intimal and adventitial
layers have abundance of collagen and elastin. They reflect
both light and sound waves strongly and appear bright.
The media contains largely smooth muscle cells that
poorly reflect light and sound waves and appears dark.
This gives the vessel wall a three-layered “bright–dark–
bright” pattern. In contrast to IVUS, OCT differentiates
adventitia from the periadventitial tissue [Figure 3].[4]
Characterization of atherosclerosis
With the development of atherosclerosis, plaque
progressively accumulates in intima and its thickness
increases proportionately. The plaque evolves through
various stages that culminate either in thrombosis or
stable lumen narrowing/CTO that in turn results in acute
coronary syndrome (ACS)/sudden death and stable
angina/congestive heart failure, respectively. The updated
morphological classification divides atherosclerotic lesions
into four subtypes: (1) nonatherosclerotic intimal lesions
(intimal thickening and intimal xanthoma); (2) progressive
atherosclerotic lesions (pathological intimal thickening,
fibroatheroma, intraplaque hemorrhage or plaque fissure,
and thin-cap fibroatheroma [TCFA]); (3) lesions with
acute thrombi (plaque rupture [PR], plaque erosion [PE],
and calcified nodule [CN]); (4) healed lesions (healed PR,
PE, or CN). This classification is based on the ex vivo
analysis of coronary specimens derived from patients
who experienced sudden cardiac death or died from
acute myocardial infarction (MI). In vivo characterization
of these abnormalities may help in improving patient
outcomes.[6,7]
IVI modalities produce cross-sectional images of the
coronary arteries and show feature characteristics of
different stages of atherosclerosis and these enable
classification of the atherosclerotic lesions in vivo.
Although grayscale IVUS has been in use for close to
three decades for characterization of atherosclerosis
and assessment of its response to treatment, its lower
resolution limits its utility for this purpose. To improve
the diagnostic accuracy of grayscale IVUS, various tissue
characterization algorithms were introduced by different
IVUS manufacturers based on the analysis of the radio-
frequency data in the reflected ultrasound waves. There
are three such algorithms: virtual histology-IVUS
(VH-IVUS, Volcano), iMap (Boston Scientific), and
integrated backscattered-IVUS (IB-IVUS, Terumo),
which code plaques with different colors based on their
composition. Among these, only VH-IVUS has been
studied extensively.[8]
Advent of OCT with its unsurpassed
resolution dramatically improved assessment of coronary
atherosclerotic lesions in clinical practice.
Grayscale IVUS tissue analysis is based on three basic
features: brightness (compared with the brightness of
Figure 3: Normal coronary artery on IVUS (A-solid-state, B- mechanical) /OCT (C) has 4 components. (1) Imaging catheter (c); (2) Guide wire (gw);
(3) Echolucent lumen (l) and (4) 3-layered vessel wall (i-intima, m-media, a-adventitia). Guide wire artifact is not seen with solid-state systems.
Similarly, due to its low resolution, blood speckles are not commonly observed with solid-state systems

adventitia), attenuation, and shadowing.[2]
VH-IVUS
color codes different tissue types with specific colors: dark
green (fibrous), light green (fibrofatty), white (dense
calcium), and red (necrotic core).[8]
OCT imaging uses five
features: brightness, attenuation, composition, borders,
and texture.[4]
The following section reviews the IVI features of different
subtypes of atherosclerotic lesions. It has followed the
updated classification of atherosclerosis and compared
and contrasted the three different imaging modalities.
Nonatherosclerotic intimal lesions
Nonatherosclerotic lesions are considered to result either
from adaptive response to blood flow (intimal thickening)
or from foam cell accumulations in intima that are
nonprogressive (intimal xanthoma). Intimal thickening
is characterized by areas of thickened intima constituted
by gathering of smooth muscle cells in an extracellular
matrix rich in proteoglycan and no inflammatory cells.
Intimal xanthoma contains superficial macrophage foam
cells as well.[6]
IVI modalities do not clearly differentiate
between these two lesions and use an arbitrary cutoff
value of 300–600
µ of intimal thickness to differentiate
nonatherosclerotic intimal changes from normal coronary
artery (300
µ) and atherosclerotic lesions (600
µ). On
grayscale IVUS, intimal thickening depicts a uniform
signal-rich appearance [Figure 4A]. VH-IVUS defines
it as fibrous or fibrofatty intima with a thickness 600
µ
[Figure 4B]. On OCT imaging, intimal thickening appears
as homogeneous signal-rich intima with a thickness
between 300 and 600 µ and a visibility of media in greater
than or equal to three quadrants [Figure 4C]. In intimal
xanthoma, foamy macrophages produce shadowing of the
light [Figure 4D].[7-9]
Progressive atherosclerotic lesions
Pathological intimal thickening: Pathological intimal
thickening is characterized by lesions with focal
extracellular accumulation of acellular lipid adjacent to
media and a luminal intima that contains smooth muscle
cells embedded in a proteoglycan and collagen-rich matrix.
There may be accumulation of macrophages closer to the
lumen.[6]
Fibroatheromas: Macrophage infiltration of the lipid pools
causes progressive destruction of the extracellular matrix
elements and formation of necrotic core that transforms
pathological intimal thickening into a fibroatheroma.
Early fibroatheromas are characterized by focal loss of
extracellular matrix, whereas late fibroatheromas by
complete depletion of extracellular matrix with large
amounts of free cholesterol and cellular debris. Both
early and late fibroatheromas are covered by thick fibrous
caps.[6]
Thin-cap fibroatheromas: TCFA are a specific type of
fibroatheromas that contain a large necrotic core covered
by a thin fibrous cap (65
µ) with paucity of smooth
muscle cells and large infiltrations of inflammatory cells.
They are also called as “vulnerable plaques”—a precursor
lesion for PR.[6]
The imaging modalities differ in the detection of
various components of pathological intimal thickening
and fibroatheromas. Grayscale IVUS and OCT cannot
differentiate lipid pools from necrotic cores and both
appear as signal-poor areas. IVUS visualizes the entire
thickness of the lipid/necrotic core in the absence of
signal attenuation but with its poor resolution cannot
measure the fibrous cap thickness (FCT). In contrast,
the high resolution of OCT enables it to accurately
assess the FCT but its poor penetration and attenuation
limit visualization of the full thickness of the lipid/
necrotic core. VH-IVUS codes extracellular lipid (light
green) and necrotic core (red) with different colors. On
grayscale IVUS, soft or hypoechoic plaque (a plaque
that is hypoechoic to adventitia) is the terminology
commonly used to define lipid/necrotic core plaques.
Recently, two grayscale IVUS patterns, echo-attenuated
plaque (isoechoic or hypoechoic plaque with deep signal
attenuation) and echolucent plaque (isoechoic plaque
with a well-demarcated zone of intraplaque echolucency)
were validated in an ex vivo study [Figure 5A and B].
Echo-attenuated pattern represented either a large
lipid pool or a necrotic core, whereas echolucent
Figure 4: Non-atherosclerotic intimal lesions. (A) IVUS, (B) VH-IVUS and (C) OCT-intimal thickening (fibrous/fibro-fatty appearing tissue with thickness
300–600µ, arrows). (D) Intimal xanthoma. Signal-rich lumen border with deep signal attenuation and sharp lateral borders suggestive of superficial
macrophage foam cells (star)


pattern was associated with a small lipid pool/necrotic
core. In addition, superficial location of the echo-
attenuation or echolucency was more often associated
with late fibroatheromas, whereas the deeper location
depicted either pathological intimal thickening or early
fibroatheromas.[10]
With VH-IVUS, pathological intimal
thickening is defined as a plaque with predominantly
fibrofatty tissue (15% and occupying 20% of the
circumference) with less of dense calcium (10%) and
necrotic core (10%) [Figure 5C]. Fibroatheroma is
defined as a plaque that contains ≥10% confluent necrotic
core and is further classified into TCFA (necrotic core
is in lumen contact for 30° of circumference) and
thick-cap fibroatheroma (necrotic core is in lumen
contact for 30° of circumference) [Figure 5D and E].[8]
With OCT imaging, lipid pool/necrotic core appears
as a homogenous, signal-poor area with poorly
defined boundaries and fibrous cap as homogenous
signal-rich layer of tissue. Pathological intimal thickening
is characterized as a homogenous, signal-rich plaque
with low signal attenuation, 600 µ thickness, and lipid
or calcium when present, occupies less than one quadrant
[Figure 5F] (OCT defines pathological intimal thickening
and fibrous plaque in a similar manner). Fibroatheroma
is defined as a plaque with greater than or equal to one
quadrant of lipid pool/necrotic core [Figure 5G] and is
further classified into TCFA (FCT65 µ) and thick-cap
fibroatheroma (FCT65
µ) [Figure 5H]. Comparing to
early fibroatheromas, late fibroatheromas are associated
with significant lumen compromise.[7,9]
OCT imaging
also identifies other features of fibroatheromas such
as macrophages (signal-rich spots or bands with deep
signal attenuation, usually occur at the interface between
fibrous cap and necrotic core), microvessels (intraplaque
signal voids measuring 50–300 µ and extending over three
or more frames), cholesterol crystals (signal-rich streaks
Figure 5: Progressive atherosclerotic lesions (A–H) and features of plaque vulnerability for rupture (G–L). (A) Attenuated plaque (blue star).
(B) Echolucent plaque (red star). IVUS does not differentiate between pathological intimal thickening and early/late fibroatheromas. Attenuated plaque
indicates large lipid/necrotic core content. Echolucent plaque indicates smaller lipid/necrotic core content. Superficial location of either indicates
late fibroatheroma and deeper location indicates pathological intimal thickening/early fibroatheroma. (C) VH pathological intimal thickening. (D) VH
Thick-cap fibroatheroma. (E) VH Thin-cap fibroatheroma. (F) OCT pathological intimal thickening/fibrous plaque (lipid/necrotic core more than one
quadrant). OCT imaging does not differentiate between pathological intimal thickening and fibrous plaque. (G) OCT fibroatheroma (lipid/necrotic
core more than one quadrant). (H) OCT thin-cap fibroatheroma (arrow heads indicate thin-fibrous cap). (I) Macrophage accumulation (arrow).
(J) Microvessels (white arrow heads). (K) Cholesterol crystals (arrow). (L) Spotty calcification

with low attenuation), and spotty calcification (small
calciumdepositwithanarc90°)[Figure 5I–L].Although
grayscale IVUS can identify spotty calcification, it
cannot characterize the other structures.[4]
Lesions with acute thrombi
There are three common underlying mechanisms of
coronary thrombosis and ACS, namely, PR, PE, and CN.
Although IVUS can identify CN with high sensitivity, it
has limited sensitivity for detection of PR. In contrast,
OCT identifies both PR and CN with high sensitivity. As
the imaging of endothelium is beyond the resolution of
current OCT systems, the detection of PE is a diagnosis of
exclusion. Hence, it is also referred to as ACS with intact
fibrous cap.
Plaque rupture: PR is the most common mechanism of
coronary thrombosis and results from the disruption of the
fibrous cap overlying a TCFA. On IVUS/OCT imaging, it
is characterized by intraplaque cavity communicating with
the lumen and fibrous cap remnants. [Figure 6A and B]
Plaque erosion: PE is the second common mechanism of
coronary thrombosis and occurs because of disruption
of endothelial layer covering the plaque, and the fibrous
cap remains intact. The underlying plaque type is either
pathological intimal thickening or early fibroatheroma.
OCT-defined PE is classified into two types: definite
erosion—thrombus attached to a visualized intact
fibrous cap [Figure 6C] and probable erosion—irregular
lumen surface with no thrombus or luminal thrombus
in the absence of adjacent superficial calcium or lipid/
necrotic core when the underlying plaque is not visible
[Figure 6D].
Calcified nodules: CN is the least common cause of
coronary thrombosis and usually occurs in the background
of severe coronary calcification. Thrombosis occurs when
nodular calcification breaches the overlying fibrous cap.
On IVUS/OCT imaging, it appears as protruding nodular
calcification with dorsal shadowing [Figure 6E and F].[6,7,11]
Thrombus: IVUS is less sensitive for identification of
thrombus and cannot differentiate between white and
red thrombus.[2]
It usually appears as an intraluminal
pedunculated or lobulated mass with a clear interface
from the underlying lumen surface [Figure 6G]. OCT
imaging clearly differentiates red thrombus from white
thrombus. Red thrombus appears as an intraluminal mass
with high backscatter and high attenuation [Figure 6D],
whereas white thrombus appears as an intraluminal mass
with high backscatter and low attenuation [Figure 6H].[4]
A recanalized thrombus produces a lotus root or Swiss
cheese appearance [Figure 6I and J].[12]
Advanced atherosclerotic lesions
Although the early atherosclerotic lesions are more
prevalent in the real world, the interventionist commonly
encounters advanced atherosclerotic lesions in the
catheterization laboratory, which are better characterized
with current IVI modalities compared to early lesions.
Healed lesions: Episodes of coronary thrombosis from PR,
PE, or CN are very common and they manifest with ACS
only when the thrombus either acutely occludes or narrows
the lumen critically, otherwise, they remain silent. This
nonocclusive thrombus progressively organizes and heals
in due course of time and contributes to lesion progression.
Healed lesions on OCT typically produce a layered pattern
Figure 6: Lesions with thrombus. (A) and (B) Plaque rupture. In (A) OCT clearly shows evidence of fibrous cap rupture with underlying cavity at
3’O clock position. In (B) IVUS shows plaque rupture with underlying cavity containing thrombus (arrow). (C) OCT definitive erosion (intact fibrous
cap with attached red thrombus). (D) OCT probable erosion (large red thrombus with no adjacent necrotic core/lipid or superficial calcium [not
shown in the figure]). (E) and (F) Calcified nodules (2 to 5 O’clock position). (G) IVUS thrombus (intraluminal mass at 3’O clock position). (H) White
thrombus (11 O’clock and 1 O’clock positions). (I) and (J) Recanalized thrombus. (Figure 6F courtesy-Dr. Bahuleyan)


of tissue with different optical densities with or without
underlying necrotic core or calcification [Figure 7A].[6,7]
They
are usually associated with severe lumen narrowing. When
silent thrombosis is occlusive, it evolves into CTO. Early
CTO lesions are characterized by plaques with large necrotic
core, organizing thrombi, and less negative remodeling in
comparison to more fibrous or fibrocalcific appearing tissue
with severe negative remodeling in older CTO lesions.[13]
Fibrous plaque: The nonocclusive thrombus formed during
these silent episodes also propagates both proximally
and distally. When this propagating thrombus heals,
it results in the formation of fibrous plaques.[6]
Fibrous
plaques are recognized by all three imaging modalities. On
grayscale IVUS, it appears as a plaque that is isoechoic to
adventitia [Figure 7B]. On VH-IVUS, it is characterized
by the presence of predominantly fibrous tissue and less
of confluent necrotic core (10%), dense calcium (10%),
or fibrofatty elements (15%) [Figure 7C].[8]
On OCT
imaging, fibrous plaque is defined as a homogenous,
signal-rich plaque with low signal attenuation and 600 µ
thickness [Figure 7D].[4,9]
Fibrocalcific plaque/nodular calcification: Calcification
begins to appear in the early progressive atherosclerotic
lesions. It usually occurs in the form of microcalcification
that results from apoptosis of the smooth muscle cells
and macrophages. In the advanced lesions, the plaque
components, such as collagen, proteoglycan, and necrotic
core, evolve into large calcium deposits. These deposits
usually occur in the form of calcium sheets/plates and
are closer to media. In elderly individuals with tortuous
arteries, these calcium plates fracture to form nodular
calcification surrounded by fibrin deposits.[6]
Calcific plaque
is hyperechoic to adventitia with acoustic shadowing and
reverberations on IVUS imaging [Figure 7E and F].[2]
VH
defines fibrocalcific plaque as a fibrous plaque with 10%
dense calcium and 10% of necrotic core [Figure 7G].[8]
On OCT imaging, calcium appears as a heterogeneous area
of low backscatter with low attenuation and clear borders
surrounded by fibrous tissue [Figure 7H]. Nodular calcium
appears similar to CN but with intact fibrous cap and no
luminal thrombus [Figure 7I].[4]
Artifacts
Artifacts are common with both IVUS and OCT imaging.
They may adversely affect the image quality that limits
identification of the true tissue structures or sometimes
be misinterpreted as pathologies that lead to unnecessary
interventions. The imaging principle for both IVUS and
OCT is the same and in addition, mechanical IVUS
system and OCT systems use drive cable and protective
sheath, and hence share some of the artifacts [Figure 8].
Artifacts common to both IVUS and OCT
Non-uniform rotational deformity: NURD is unique to
mechanical imaging systems. It results from uneven drag
or friction on the drive cable that perturbs its smooth
rotation. It appears as smearing or geometric distortion
in the image that conceals the structures in that part of
the circumference and limits accurate cross-sectional
measurements. It is often due to tortuosity or acute bends
in the artery, tight stenosis, heavy calcification, small
guiding catheter, guiding catheter with multiple curves,
excessive tightening of the hemostatic valve, or defective
imaging catheter [Figure 8A and B].[3,4]
Motion artifacts: Rapid movement of the artery or
the imaging catheter during the acquisition of a single
cross-sectional image causes malalignment along the
Figure 7: Advanced lesions. (A) Healed plaque erosion (layered pattern with no evidence of underlying rupture, arrow). (B–D) Fibrous plaque (OCT
does not differentiate between fibrous plaque and pathological intimal thickening). (E) IVUS superficial calcification. (F) IVUS deep calcification.
(G) VH dense calcium. (H) OCT circumferential calcium plate. (I) Nodular calcification (arrow). (Figure 7I courtesy-Dr.Bahuleyan)

circumference of the image, which is known as sew-up/
seamline artifact [Figure 8B].
The imaging catheter also moves along the longitudinal
axis during cardiac cycle. When this movement is
pronounced, the same structures are visualized repeatedly,
and this precludes accurate length assessment.[3,4]
Obliquity / eccentricity artifact: Cross-sectional imaging
of the vessel occurs perpendicular to the imaging catheter.
When the imaging catheter is in the center of the lumen
and parallel to the long axis of the vessel, it results in a
circular image. However, when the vessel is large in size and
in vessel curvature, the catheter alignment is non-coaxial,
and the resulting image appears elliptical. This makes the
measurements inaccurate [Figure 8C].[4]
Shadow artifact: When ultrasound waves or light photons
encounter strongly reflecting structures, the signals
are reflected from the surface and do not penetrate,
this results in signal dropout or shadowing behind the
structure. Shadowing commonly occurs with guidewires
[Figure 8C] and metallic stent struts. In addition,
air bubbles, red thrombus, blood, and macrophage
accumulations cause shadowing in OCT imaging.
Ultrasound waves do not penetrate calcium and are an
important cause of shadowing during IVUS imaging.
However, calcium allows light photons to pass through
and does not cause shadowing. This allows estimation of
calcium thickness with OCT imaging.[3,4]
Multiple reflections and reverberations: When ultrasound
waves or light photons bump on specular surfaces,
repeated reflections may happen between the transducer
and the reflecting surface. These may form ghost
structures at multiple of the distance between the two
structures.
During OCT imaging, multiple reflections may happen
within the facets of the imaging catheter that produce
circular lines around the catheter [Figure 8D] or with
stent struts [Figure 8E] that result in reverberations. As
calcium is not a strong reflector of light, it does not cause
reverberations. During IVUS imaging, reverberations
occur with stent struts [Figure 8F], calcium [Figure 8G],
guidewires and guide catheters. Multiple reflection
artifacts should not be mistaken for additional interfaces
in the vessel or additional layer of stent struts.[3,4]
Artifacts specific to IVUS imaging
Ring-down artifact: It is a near-field artifact that appears
as luminous halos of different thickness around the
surface of the catheter and hinders evaluation of the
area in the proximity of the catheter [Figure 8H]. It
occurs more commonly with the solid-state catheters
and may be masked electronically by the ring-down
suppression function. Similar artifact may be produced
with the mechanical IVUS catheters by air bubbles
trapped between the transducer and protective sheath
[Figure 8I] and can be resolved by saline flushing.[3]
Figure 8: Artifacts. A-F show artifacts common to IVUS and OCT. (A B) Non-uniform rotational deformity [red stars] and sew up artifact [blue
arrow]. (C) Obliquity artifact, yellow arrow head indicates shadowing artifact from guide wire. (D) Multiple reflection artifact [white arrow head].
(E F) Stent reverberations [yellow arrows]. (G) Calcium reverberation [red arrows]. (H–L) show IVUS specific artifacts. (H) Ring down artifact
[orange arrows]. (I) Air bubble with ring down artifact [white arrows]. (J) Air bubble artifact with poor image quality. (K) Blood speckle artifact. (L)
Side lobe artifact [blue arrow heads]). M–R show OCT specific artifacts. (M) Residual blood artifact [yellow star]. (N) Fold over artifact [blue arrows].
(O) Saturation artifact [white arrow heads] blooming artifact [green arrow]. (P) Proximity artifact [red arrow head] and tangential signal drop-out
[red arrow]. (Q) Merry go round artifact [blue arrow head]. (R) Sunflower artifact [yellow arrow heads]


Air bubble artifact: This artifact is specific to mechanical
catheters. Small air bubbles trapped in the protective
sheath are the most common cause for poor image quality
[Figure 8J]. In addition, they may also produce other
types of abnormalities such as reverberation and ring-
down artifact (see “Ring-down artifact” above). Careful
preparation of the catheter before procedure eliminates
air bubble artifact. During procedure, small air bubbles
may be removed by flushing the catheter with saline.[3]
Blood speckles: Blood speckles when prominent may
obscure the lumen–intima interface [Figure 8K]. This
commonly occurs when IVUS imaging is carried out
across tight stenosis. Contrast or saline flush during
imaging displaces blood and reveals the interface clearly.[3]
Side lobe artifact: IVUS transducer produces multiple
ultrasound beams. Under normal conditions, only the
central high-energy beam (main lobe) takes part in the
image formation, the low-energy beams from the sides (side
lobes) die away. However, when the side lobes encounter
highly reflective surfaces such as calcium or stent struts,
they may also take part in image formation. These false
images when prominent may create an appearance of
dissection flaps [Figure 8L].[3]
Artifacts specific to OCT imaging
Residual blood artifact: Suboptimal vessel flushing causes
signal-rich blood swirls in the lumen that may sometimes
be misinterpreted as red thrombus. In addition, intense
scattering of the light by RBCs causes shadowing
of the underlying structures. This makes vessel wall
characterization extremely difficult [Figure 8M].[4]
Fold over artifact: FD-OCT has a field of view of
approximately 10
mm. When the light is reflected from
areas of vessel beyond this range, aliasing occurs in the
Fourier transformation that gives an appearance of
the far-field area of the vessel folded over in the image
[Figure 8N]. This artifact occurs commonly with large
vessels or at areas of side branches.[4]
Saturation artifact: Saturation artifacts are abnormally
bright A-lines that appear when the high-amplitude
backscattered signals from specular structures such as
stent struts and guidewire saturate the processing limit of
the detector [Figure 8O].[4]
Blooming: Stent struts reflect light intensely and hence only
the leading edge is visible on OCT images. In addition, the
high-signal density at the surface causes a glare or axial
stretching of the stent strut reflections called blooming
[Figure 8O]. This makes it difficult to identify the leading
edge for stent measurements.[4]
Proximity artifact: Proximity artifact refers to artificial
increase in the brightness of the tissues adjacent to an
eccentrically positioned imaging catheter [Figure 8P].[4]
Tangential signal dropout: Tangential signal dropout is
another abnormality resulting from the eccentric catheter
position. When the catheter is close to or in contact with
the vessel wall, the incident light rays are parallel to the
surface of the vessel wall rather than perpendicular to it.
This results in artificial signal attenuation in the deeper
parts of the vessel wall. With a signal-rich surface and
attenuated deeper tissues, this gives a false appearance of
a TCFA [Figure 8P].[14]
Merry-go-round effect: The merry-go-round effect
describes an apparent elongation of stent struts in the
lateral direction. It results from reduced lateral resolution
either from increased distance between the A-lines or
larger diameter beam spot diameter in the far field or
increased scattering of the light in the lumen by RBCs by
incomplete flushing [Figure 8Q].[4]
Sunflower effect: When the OCT catheter is located
eccentrically in a stented vessel, the incident light beam
is not perpendicular to the stent strut and instead it gets
reflected only from the edge of the strut. The resultant
image reconstruction orients the strut perpendicular
to the catheter similar to the orientation of sunflowers
toward the sun. Sunflower effect gives an appearance of
strut malapposition and artificially increases strut-to-
vessel wall distance [Figure 8R].[15]
Quantitative Assessment
Both IVUS and OCT provide accurate cross-sectional
and longitudinal measurements. The basic principle of
quantitative analysis remains same for both the modalities.
IVUS system has its intrinsic distance calibration that
appears as a grid on the image. In contrast, OCT system is
calibrated to the imaging catheter before measurements. In
a native vessel, there are two interfaces: lumen–intima and
media–adventitia external elastic lamina (EEL), whereas
in a stented vessel, there are three interfaces: lumen–
neointima, stent, and EEL. In view of its higher accuracy
and reproducibility, it is recommended to take all the
measurements from the leading edge to leading edge of
the interfaces. The diameter measurements are obtained
through the center of the lumen. Length is estimated from
the automatic pullback (pullback speed × duration of
pullback). The common terminologies and measurements
are summarized in Figure 9.[2,4]
Both the modalities offer automated measurements.
With its high-tissue penetration capacities, IVUS
visualizes entire vessel architecture in most of the cases
except for lesions with calcification and attenuated
plaques. This enables IVUS to assess plaque burden
and positive remodeling. The typical outputs from
IVUS cross-sectional imaging are lumen and external
elastic membrane areas and diameters, plaque burden,
and cross-sectional area (CSA) stenosis. Although the

system provides automatic border tracing, it typically
requires manual correction. Length estimation requires
automatic pullback recording though a newer system
with co-registration function provides length estimation
from manual pullback. In contrast, clear demarcation of
the lumen–intima interface with OCT makes the lumen
measurements truly automatic and accurate. In addition,
the newer lumen profile function provides graphic display
(such as an ideal angiographic view) of frame by frame
lumen measurements over the entire pullback length. This
enables precise understanding of the vessel size, disease
extent, and vessel tapering. Moreover, it automatically
locates the frame with minimal lumen area (MLA) and
once the correct reference vessel frames are manually
located, the system automatically provides the percentage
area/diameter stenosis, the reference vessel dimensions,
and the lesion length to facilitate device sizing.[16]
There are some differences in the measurements between
IVUS and OCT. The OCT compared with IVUS in
a coronary lesion assessment (OPUS-CLASS) study
compared lumen dimensions measured with IVUS and OCT
both in phantom model and human coronary arteries. In the
phantom model, OCT area matched actual dimension of the
phantom (7.45 ± 0.17 vs. 7.45 mm2
) and IVUS area was larger
by8%(8.03 ± 0.58 mm2
;P 0.001).Inthehumanstudy,OCT
measured minimal lumen diameter (MLD) and MLA, which
Figure 9: Quantitative IVUS and OCT assessment


were smaller by 9% (1.91 ± 0.69 vs. 2.09 ± 0.60 mm; P 0.001)
and 10% (3.68 ± 2.06 vs. 3.27 ± 2.22 mm2
; P 0.001),
respectively, when compared to IVUS measurements.[17]
On the basis of these observations, the recent OCT studies
have used newer stent-sizing algorithms to match post-stent
measurements with that of IVUS-guided stent sizing.
Clinical Applications of Intravascular Imaging
The various roles of IVI in clinical practice are
(1) assessment of lesion severity, (2) evaluation of plaque
vulnerability, (3) PCI optimization, and (4) analysis of
stent failure. The following discussion is limited to the
first three aspects, and the analysis of stent failure is
deliberated in the next review.
Assessment of lesion severity
The dilemma arises when interventionists are faced
with management decisions based on angiographically
intermediate stenoses (40%–70%) as angiography does not
predict the significance of these stenoses accurately. This
mandates the use of either IVI or fractional flow reserve
(FFR) for the assessment of lesion severity. IVI has the
potential advantage of not only estimating the lesion
severity but also guiding the intervention of functionally
significant stenoses. With this background, various IVUS/
OCT parameters have been explored for the identification
of flow-limiting stenoses [Tables 1 and 2]. Although
IVUS/OCT MLA predicted the lesion severity in non-
left main coronary artery (non-LMCA) stenosis, the
cutoff value varied from 1.6 to 4
mm2
between different
studies and the accuracy was only modest. This limits the
application of MLA for the assessment of lesion severity
in routine practice.[18-36]
In addition to MLA, the limitation
of flow across a stenosis also depends on various other
parameters such as lesion eccentricity, amount of
myocardium supplied, and length of the lesion, and hence
it is unlikely that a single parameter accurately estimates
the functional significance.[18]
McDaniel et al.[37]
have
proposed an algorithm for IVUS-based assessment of
lesion severity in non-LMCA lesions. An IVUS MLA of
≥4 mm2
has a very high-negative predictive value and most
of the lesions in this area are non-flow limiting. However,
when the MLA is 4
mm2
, the interventionist has to use
either FFR or combination of IVUS parameters such as
area stenosis of 60%–70%, plaque burden of 80%, and
lesion length of 20 mm.
Evaluation of plaque vulnerability
Vulnerable plaque is a plaque, which is prone to produce
clinical events either from rapid progression or from
thrombosis. It is characterized by large lipid content/
necrotic core, thin fibrous cap, expansive remodeling,
inflammation, spotty calcification, intraplaque
hemorrhage, and neoangiogenesis. Identification of such
plaques may guide implementing treatment strategies,
which reduce the future adverse outcomes.[38,39]
IVI
modalities help not only in the identification of these
unstable plaques but also in monitoring their progress with
treatment. Various modalities identify different features
of plaque instability. The resolution of grayscale IVUS
limits it applicability in vulnerable plaque imaging. The
grayscale IVUS features of vulnerability are large eccentric
plaque, positive remodeling, attenuated plaque, spotty
calcification,andintraplaqueecholucency.[10,39]
VH-defined
TCFA is an important predictor of adverse events. In the
PROSPECT (Providing Regional Observations to Study
Predictors of Events in the Coronary Tree) study, TCFA
along with a plaque burden of ≥70% and a lumen area of
≤4 mm2
were associated with clinical events in non-culprit
lesions during follow-up.[40]
OCT with its resolution
capabilities identify the features of vulnerability with high
accuracy. Lesions with OCT-defined TCFA, lipid-rich
plaque, microchannels, spotty calcification, macrophages,
and intraluminal thrombi have been shown to progress
at 7-month follow-up.[41]
However, the natural history of
vulnerable plaque is too complex, with most of the TCFA
stabilize and few thick-cap fibroatheromas transform into
TCFA. Thus, the treatment of atherosclerosis still remains
at the patient level rather than at the plaque level.[42]
Intravascular imaging–guided PCI optimization
Systematic use of IVI before, during, and post-stenting
enhances PCI outcomes. The following discussion
elaborates the optimal use of IVI during different stages
of PCI.
Pre-interventional assessment
Pre-interventional assessment focuses on lesion
characteristics, reference vessel segments, and vessel
proximal to the lesion. Lesion characteristics influence
intervention in two ways: first, with distal embolization
and resultant no-reflow and second, by posing resistance
to stent expansion. Various IVUS (attenuated plaque,
intraplaque echolucency, and positive remodeling),[43]
VH-IVUS (TCFA),[44]
and OCT (TCFA, large lipid core,
and thrombus)[45]
features have been linked with distal
embolization during intervention. The requirement for
lesion preparation depends on the plaque characteristics.
High-pressure pre-dilatation may be avoided and direct
stenting is preferred in the presence of soft plaque or
TCFA to reduce the incidence distal embolization and
no-reflow. However, hard to break fibrous and fibrocalcific
lesions may require pretreatment with cutting balloon
or rotational atherectomy. Further, IVI also helps in
verifying the adequacy of lesion preparation, particularly
in calcified lesions. Imaging of the vessel proximal to the
lesion detects any occult stenosis not identified by CAG.
In addition, it also shows any hindrance to device delivery
such as calcified plaque.
The most important function of pre-procedural imaging
is appropriate device selection, particularly the size of the
stent. No uniform criteria are available for stent sizing with

Table 1:
IVUS
studies
evaluating
anatomical
parameters
for
detecting
ischemia
in
non-left
main CAD
Study
No.
of
patients/
no.
of
lesions
Intermediate
lesion
definition
FFR
cutoff
value
AUC
IVUS
Sensitivity
Specificity
PPV
NPV
MLA/MLD
Diagnostic
accuracy
MLA/MLD
Comment
MLA/MLD
MLA,
mm
2
/
MLD,
mm
MLA/MLD
MLA/MLD
MLA/MLD
Briguori
et al.
[18]
43/53
40%–70%
DS
by
visual
assessment
0.75
-/-
4.0/1.8
92/100
56/66
38/46
96/100
64/79
IVUS
AS
70%
and
LL

10 mm
also
identified
functional
significance
Takagi
et al.
[19]
42/51
-
0.75
3.0/-
83/-
92/-
-
-
-
%AS
also
predicted
functional
significance
Gonzalo
et al.
[20]
56/61
40%–70%
DS
by
QCA
0.80
0.63/0.67
2.36/1.59
67/67
65/65
67/67
65/65
66/66
Simultaneously
compared
with
OCT
Koo
et al.
[21]
252/267
30%–70%
DS
by
visual
assessment
0.80
0.81/-
2.75/-
69/-
65/-
27/-
81/-
67/-
MLA
predicted
functional
significance
only
in
proximal
and
mid-LAD
Kang
et al.
[22]
201/236
30%–75%
DS
by
visual
assessment
0.80
0.80/-
2.4/-
90/-
60/-
37/-
94/-
68/-
In
addition,
LL
with
MLA3.0 mm
2
,
PB,
and
LAD
location
predicted
+ve
FFR
Kang
et al.
[23]
692/784
30%–90%
DS
by
visual
assessment
0.80
0.77/-
2.4/-
84/-
63/-
48/-
90/-
69/-
Subgroup
specific
criteria
(vessel
type,
size,
lesion
location,
and
clinical
setting)
were
inaccurate
to
predict
ischemia
Ben-Dor
et al.
[24]
84/92
40%–70%
DS
by
QCA
0.75
(0.80)
0.76
(0.74)/-
2.8
(3.2)/-
79.7
(69.2)/-
80.3
(68.3)/-
-
-
-
Different
MLA
thresholds
for
different
vessel
size
Naganuma
et al.
[25]
109/132
40%–70%
DS
by
visual
assessment
0.80
0.82/-
2.7/-
79.5/-
76.3/-
58.5/-
89.9/-
-/-
MLA
and
PB
predicted
FFR0.80.
MLA
cutoff
varied
depending
on
the
vessel
size
Waksman
et al.
[26]
350/369
40%–80%
DS
by
visual
assessment
0.80
0.65/-
3.07/-
64/-
65/-
40/-
83/-
-/-
MLA
cutoff
varies
depending
on
the
RVD
Kwan
et al.
[27]
169/169
Single
de
novo
LAD
stenosis
(≥40%
to
100%
by
visual
estimation)
0.80
0.86/-
3.0/-
87.9/-
75.7/
83.7/
81.5/-
82.8/-
Additionally,
PB
and
LL
also
predicted
+ve
FFR
Chen
et al.
[28]
323/323
≥40%
by
visual
estimation
0.80
0.77/-
3.0/-
82.9/-
63.5/-
72.9/-
75.8/-
71.9/-
PB,
LL,
and
LAD
location
also
predicted
+ve
FFR
Cui
et al.
[29]
141/165
40%–70%
DS
by
visual
assessment
0.80
0.71/0.65
3.15/-
71.4/-
69/-
52.6/-
85.3/-
73.6/-
PB
also
predicted
+ve
FFR
Lee
et al.
[30]
94/94
(small
vessels)
30%–75%
DS
by
visual
assessment
0.75
0.87/-
2.0/-
82.4/-
80.8/-
-
-
-
PB
and
LL
also
predicted
+
ve
FFR
Yang
et al.
[31]
206/206
Proximal-
mid
LAD
40%–70%
DS
by
visual
estimation
0.80
0.78
(0.78)/-
3.2
(2.5)/-
85.1
(65.1)/-
66.7
(87.7)/-
PB
and
LL
also
predicted
+
ve
FFR
PPV = positive
predictive
value,
NPV = negative
predictive
value,
DS = diameter
stenosis,
QCA = quantitative
coronary
angiography,
RVD = reference
vessel
diameter,
AS = area
stenosis,
PB = plaque
burden,
LL = lesion
length,
LAD = left
anterior
descending
coronary artery


IVI, and the following may be the best possible approach
without compromising safety.
IVUS: The first step in stent sizing is to identify the
lesion site and relatively disease-free proximal and distal
references. Then the maximum and minimum diameters
of the proximal and distal reference lumens and EEL are
measured and the average diameter of each is calculated.
If pre-dilatation is necessary, a balloon smaller than the
reference lumen diameter is recommended. The stent
diameteristhesameasthatof thereferencelumendiameter
if both the proximal and distal reference diameters are
equal (no vessel tapering) and the reference segments are
disease free. In case of smaller distal reference diameter
(tapering vessel), stent is sized to the distal diameter. When
there is diffuse disease, the reference segment is the zone
with minimal disease (plaque burden 50%) on either
side of the lesion, and the stent selection is based on the
mid-wall diameter of the reference segments (the average
of lumen and EEL diameters), and stent is deployed at low
pressure to avoid edge dissection. Post-dilatation is carried
out with a noncompliant balloon of same diameter as that
of the stent, or additional larger diameter balloon is sized
to the proximal reference diameter if the stent is sized to
the distal reference diameter.[46]
OCT: Lumen-based stent sizing with OCT results in
smaller stent areas compared to that with IVUS, and
hence the recent studies recommend two different
approaches. The Optical coherence tomography compared
with intravascular ultrasound and with angiography to
guide coronary stent implantation (ILUMIEN III) study
used an EEL-based stent-sizing algorithm. When the
reference segments are healthy and the media is clearly
visible all around, maximum and minimum diameters
of EEL are measured and the mean EEL diameter of
each reference is calculated. The smaller of the two
mean EEL diameters is rounded down to the nearest
0.25 to derive the stent diameter (e.g., 2.80
mm round
down to 2.75 mm, [Figure 10]).[47]
When the media is not
clearly visualized the stent sizing is based on the lumen
measurements. In contrast, the optical frequency domain
imaging vs. intravascular ultrasound in percutaneous
coronary intervention (OPINION) study study followed
a lumen-based stent-sizing algorithm. When the reference
segments are healthy, the maximum lumen diameter and
MLD of the proximal and distal segments are measured
and the mean diameter is calculated. The smaller mean
lumen diameter is upsized by 0.25 mm to derive the stent
diameter (e.g., 3.5
mm round up to 3.75
mm). In case
the reference segments are diseased, the stent is sized to
the smaller mean lumen diameter. The distance between
the proximal and distal references provides the length of
the stent.[48]
The current OCT systems with automatic
measurements and lumen profile function make stent
sizing less problematic.
Table 2:
OCT
studies
evaluating
anatomical
parameters
for
detecting
ischemia
in
non-left
main CAD
Study
No.
of
patients/
no.
of
lesions
Intermediate
lesion
definition
FFR
cutoff
value
AUC
OCT
Sensitivity
Specificity
PPV
NPV
Diagnostic
accuracy
Comment
MLA/MLD
MLA,
mm
2
/
MLD,
mm
MLA/MLD
MLA/MLD
MLA/MLD
MLA/MLD
MLA/MLD
Gonzalo
et al.
[20]
56/61
40%–70%
DS
by
QCA
0.80
0.74/0.73
1.95/1.34
82/82
63/67
66/68
80/81
72/73
Simultaneously
compared
with
IVUS
and
better
efficiency
for
RVD
3 mm
Shiono
et al.
[32]
59/62
30%
by
visual
assessment
0.75
0.904/0.917
1.91/1.35
93.5/90.3
77.4/80.6
80.6/84.4
92.3/84.6
85.4/85.5
Additionally
assessed
percent
area
stenosis
Pawlowski
et al.
[33]
48/71
40%–70%
DS
by
visual
assessment
0.80
0.91/0.90
2.05/1.28
75/71
90/84
70.6/68.5
92.6/90.6
87/87
No
relationship
between
FFR
and
lesion
length
Reith
et al.
[34]
46/62
(patients
with
diabetes)
40%–70%
DS
by
QCA
0.80
0.813/0.807
1.59/1.31
75.8/87.9
79.3/72.4
80.6/78.4
74.2/84
77.4/80.6
FFR
predicted
FCT
≤80 µm
Zafar
et al.
[35]
30/41
30%
DS
by
visual
assessment
0.80
0.80/0.76
1.62/1.23
70/70
97/87
89/64
91/90
-/-
High
efficiency
for
RVD
3 mm
Burzotta
et al.
[36]
40/40
30%–80%
DS
by
visual
assessment
0.8
0.83
2.5
64
93
85
AS%
and
plaque
ulceration
independently
predicted
FFR
PPV = positive
predictive
value,
NPV = negative
predictive
value,
DS = diameter
stenosis,
QCA = quantitative
coronary
angiography,
RVD = reference
vessel
diameter,
AS = area
stenosis,
FCT = fibrous
cap
thickness

Post-stent imaging
Post-stent imaging is carried out to assess stent expansion,
apposition, and other parameters of suboptimal stent
deployment such as geographic miss, tissue prolapse,
edge dissection, and hematoma [Figure 11].[49]
The
following sections discusses briefly these various
parameters.
Stent expansion
Stent expansion is the most important parameter of stent
optimizationandiscloselyrelatedtobothin-stentrestenosis
Figure 10: Stent sizing with OCT. Patient presented with chronic stable angina and positive stress test. Coronary angiogram showed tight stenosis
in the proximal left anterior descending coronary artery (A). OCT imaging was acquired following a 2-mm balloon pre-dilatation. In the first step, the
lesion is located on the lumen profile (E) and then the cursor is moved both proximally and distally to identify the disease-free reference segments
(B and D). The average of maximum and the minimum lumen and external elastic lamina (EEL) diameters at each reference segments are measured.
As the reference segments are free of disease, the stent is sized to the distal mean EEL diameter (2.80 mm). The distance between these reference
segments is the length of the stent (14 mm). Hence, a 2.75 × 18 mm stent was chosen
Figure 11: Post percutaneous coronary intervention complications. (A and B) Under expansion. In (A), there is an underlying soft plaque and the
underexpansion is due to underdeployed stent. In (B), underexpansion is due to underlying calcium [blue arrows]. (C) Minor malapposition, (D and E)
major malappositions [double headed white arrows]. (F) Geographic miss–stent landed in the lipid plaque [red star], (G) Minor edge dissection, (H and
I) Major edge dissections. Green arrows in (G–I) indicate dissection flap. (J and K) Intramural hematoma [green stars]. (L) Extramural hematoma [yellow
star]. (M) smooth tissue protrusion [blue arrows], (N) disrupted fibrous tissue protrusion [yellow arrow] and (O) irregular tissue protrusion [red arrow]


and stent thrombosis.[50,51]
Stent expansion has been
defined variously among different studies. It is important
to understand that the quantification of stent expansion
is based on the reference vessel measurements rather than
the vessel wall dimensions at the lesion site [Figure 12]. The
first systematic stent expansion criterion was proposed
in the MUSIC (Multicenter Ultrasound-Guided Stent
Implantation in the Coronaries) trial. It defined adequate
stent expansion as the minimum stent area (MSA)
≥90% of the average reference lumen area or ≥100% of
the smaller reference area when the MSA is 9
mm2
or
MSA ≥80% of the average reference lumen area or ≥90%
of the reference segment with the smaller area when the
MSA is 9 mm.[2,52]
Though the criterion was met in most
of the patients in the IVUS-guided arm of the MUSIC
study, it could not be replicated in the subsequent studies.
Hence, the following modified criteria were used in the
subsequent studies: intra-stent CSA 80% of the average
proximal and distal reference lumen CSA (Restenosis
after Intravascular Ultrasound Stenting [RESIST]
trial[53]
), in-stent MLD ≥80% of the mean proximal and
distal reference lumen diameters (Thrombocyte activity
evaluation and effects of Ultrasound guidance in Long
Intracoronary stent Placement [TULIP] study[54]
), and
in-stent MLA ≥ 90% of distal reference vessel lumen area
(Angiography Versus Intravascular Ultrasound Directed
[AVID] trial[55]
). However, these criteria did not take into
account long lesions and tapering vessels where a big
difference is observed in the proximal and distal reference
vessel dimensions. To overcome this limitation, two other
IVUScriteriahavebeenproposedrecently.Thefirstwasthe
PRAVIO (Preliminary Investigation to the angiographic
Versus IVUS Optimization) criterion, which used media-
to-media dimensions in different segments of the stent to
select the post-dilatation balloon for stent optimization,
and the optimal expansion was defined as the MSA ≥70%
of the CSA of the balloon used for post-dilatation.[56]
The
second was the OCT criterion proposed in the ILUMIEN
III study, which divided stent into proximal and distal
halves and the optimal expansion was defined as the
MSA in each half 90% of the corresponding reference
lumen CSA.[47]
Stringent stent expansion criteria (90%
reference lumen CSA) were difficult to achieve and led
to a high incidence of underexpansion in these studies
(40%–60%). Studies that followed less rigorous expansion
criteria (80% average reference lumen CSA) attained
optimal expansion in most of the patients. In addition, a
recent study showed that a stent expansion of 80% of the
average reference predicted an FFR of 0.90. On the basis
of these observations, the current consensus document
recommends the 80% cutoff value for assessment of
stent expansion [Figure 12].[49]
In most of the studies, IVI was used after stent was
deployed and optimized angiographically, which may be
an important reason for less number of patients achieving
the optimal expansion criteria. The two important factors
that limit optimal stent expansion are fibrocalcific plaques
and undersized/underdeployed stents [Figure 11A and
B]. Systematic pre-procedural IVI provides accurate
information on the plaque morphology and vessel size
so that the lesion can be pretreated adequately and an
Figure 12: Assessment of stent expansion. Quantification of stent expansion is based on reference segment lumen area. Optimal expansion is defined
as the minimal stent area more than 80% of the average reference segment lumen area. Patient was implanted with 2.75 × 18 mm drug-eluting stent in
proximal left anterior descending coronary artery (A). The minimal stent area is 6.6 mm2
(C) and is more than average reference lumen area of 6 mm2
(B+D/2) . The minimal stent area is 110% of the average reference lumen area, and hence, the stent is well expanded. (E) and (F) are longitudinal
two- and three-dimensional views showing well-expanded stent

appropriately sized stent can be implanted, respectively,
which in turn helps in optimal stent expansion.
Malapposition
Malapposition is defined as the lack of contact between
the stent strut and the luminal surface not overlying a
side branch.[2]
Acute malapposition results from one
of the three reasons (1) stent undersizing (2.5
mm stent
implanted in a 3.5 mm vessel), (2) stent under-deployment
(optimally sized stent but deployed at less than nominal
pressure), or (3) underlying resistant plaque. Gross stent
undersizing is very common during PCI for ST-segment
elevation MI (STEMI) and CTO where the vessel is under
spasm and under-filled, respectively. Though IVI helps
in identifying true vessel size in the latter situation, it is
very important to perform all measurements after liberal
administration of intracoronary nitroglycerine to avoid
vessel undersizing. Plaque-related malapposition occurs
when calcified plaque limits symmetrical expansion of
the stent so that part of the stent remains separated from
the vessel wall. Stent expansion and apposition are not
mutually exclusive; a well-expanded stent may still be
malapposed and vice versa.[57]
IVUS identifies malapposition by the presence of blood
speckles behind the stent struts. Low-frequency solid-state
system also provides color Doppler mapping (Chromaflo,
Volcano) of the flow behind the struts. A detailed
assessment of the malapposition area, length, and volume
is also feasible with IVUS.[3]
Higher resolution of OCT makes assessment of
malapposition at the strut level feasible. As stent strut is a
strong reflector of light, OCT shows only the endoluminal
side of the stent strut. In addition, this strong reflection
results in “blooming” on either side of the strut with
the actual strut surface in the middle. Malapposition by
OCT is said to be present when the distance between
the middle of the strut reflection to the lumen surface
exceeds the sum of stent strut and polymer thickness.
It is commonly expressed as the distance from the strut
surface to the surface of the lumen. OCT identifies
even minor degree of malapposition accurately and has
become the modality of choice for assessment of this
abnormality.[57]
The malapposition indicator function
in the newer generation OCT systems automatically
detects and displays malapposed stent struts both in the
cross-sectional and longitudinal views. In addition, it
provides color coding based on the extent of incomplete
stent apposition (ISA) distance. This enables prompt
identification malappositions without scanning through
individual frames.[16]
The incidence of acute malapposition varied between
8% and 42% in IVUS studies and 39% and 100% in OCT
studies. Most of the malappositions were minor and
resolved during follow-up. The resolution resulted from
the neointimal growth behind the stent struts and the
magnitude of malapposition was the main predictor of
this phenomenon.[17,58-67]
In a study by Shimamura et al.,[60]
the acute ISA distance that predicted persistent ISA was
355 μm with everolimus-eluting stent (area under the
curve [AUC] = 0.91) and 285 μm with sirolimus-eluting
stent (AUC = 0.95). In another study, ISA volume of
2.6 mm3
predicted persistent ISA at follow-up.[61]
With the
available evidence so far, acute malapposition has not been
associated with adverse events as long as the stent is well
expanded.[17,58-67]
In contrast to these prospective follow-up
studies, malapposition is an important observation in
patients presenting with stent thrombosis. The ISA
distance and its longitudinal extent ranged between 0.3 and
0.6 mm and 1.0 and 2.1 mm, respectively, in the segments
with thrombus. On the basis of these observations, the
consensus statement recommends against treatment of
malappositions with ISA distance 400 µ and a length of
1 mm.[49]
Although it appears that small malappositions
are innocuous [Figure 11C], every effort should be made
to appropriately size and implant the stent to avoid gross
malappositions [Figure 11D and E].
Geographic miss
Coronary atherosclerosis is a diffuse process and is
mostly angiographically silent. An IVUS study observed
significant plaque burden in the angiographically normal
appearing reference segments.[68]
Reference segment
plaque burden and lumen area have been associated with
increased incidence of stent failure. In ADAPT–DES
(Assessment of Dual Antiplatelet Therapy With Drug-
Eluting Stents) study, a proximal reference segment
plaque burden of 60% was associated with early-
stent thrombosis.[69]
Similarly, in the HORIZONS-AMI
(Harmonizing Outcomes with Revascularization and
Stents in Acute Myocardial Infarction) IVUS sub-study,
residual edge stenosis (a reference segment plaque burden
of ≥70% and a lumen area of 4 mm2
) was associated with
early-stent thrombosis.[70]
In CLI-OPCI (the Centro per
la Lotta contro l’Infarto-Optimisation of Percutaneous
Coronary Intervention) II Study, the reference lumen
area of 4.5
mm2
in the presence of large plaque was
an important predictor of major adverse cardiovascular
events (MACE).[65]
In another OCT study, the presence of
lipid-rich plaque (area 185o
) and small MLA (4.1 mm2
)
predicted edge restenosis at 9–12 month follow-up.[71]
In
IVUS studies evaluating edge restenosis, the reference
segment plaque burden that predicted edge restenosis
varied from 47% to 57% between different stent types.[72,73]
Further, reference segment injury from inappropriate
stent sizing or areas of balloon injury left covered has
also been associated with increased incidence of adverse
events. The current consensus document recommends
stent positioning in reference segments with 50% plaque
burden (IVUS) and absence of lipid-rich plaque (OCT)
[Figure 11F].[49]
The newer IVUS and OCT systems provide
IVI-angiography co-registration function that minimizes
operator errors in accurately identifying landing zones
and may reduce the incidence of geographic miss.[16]


Dissections
Tears in the vessel wall at the edges of the stent result
from landing of the stent in a diseased reference segment,
extension of the balloon beyond the stent, or from
implantation of an oversized stent. Angiographically
detected persistent high-grade edge dissections (National
Heart, Lung, and Blood Institute types B–F) have been
associated with acute-stent thrombosis.[74]
IVI modalities
with their higher resolution detect far more number of
edge dissections that are angiographically invisible.
In a study of systematic post-stenting IVUS imaging,
persistent edge dissections occurred in 9.2% of the
patients and 39% of which were angiographically silent.
Most of the IVUS-detected edge dissections are usually
minor (angiographically silent and no lumen compromise
by IVUS) and can be left alone safely [Figure 11G].[75]
In
contrast, major dissections (IVUS lumen area narrowing
4 mm2
or dissection angle of ≥60°) have been associated
with higher incidence of early-stent thrombosis and need
additional stenting [Figure 11H and I].[70]
In ADAPT-
DES study, a residual lumen area of 5.1 mm2
predicted
adverse outcomes.[76]
OCT identifies edge dissections in still higher number of
the patients. It occurred in 37.8% of the patients in one
study and 84% of them were angiographically silent.
Most of the edge dissections were minor (dissections
with longitudinal length ≤1.75 mm, with 2 concomitant
flaps, flap depth ≤0.52
mm, flap opening ≤0.33
mm, and
not extending deeper than the media layer) and healed on
follow-up.[77]
Similar outcomes were shown in a series of
21 patients with non-flow limiting dissections in another
study.[78]
In a study of 74 patients with ACS treated with
stents, edge dissection with a flap thickness of 0.31 mm
was associated with adverse clinical outcomes.[79]
In
another study, a flap thickness 200 µ and location at the
distal edge were associated with increased incidence of
clinical events.[65]
From these observations, it is evident that the treatment
of edge dissections is based mainly on angiographic
flow compromise. IVI may assist in detecting the further
component of lumen compromise that may not always be
evident angiographically and detecting few of the major
dissections not visible angiographically. The current
consensus document defines significant dissections as
follows: dissection with large residual plaque burden,
lateral extent of 60°, longitudinal extent of 2
mm,
extension into the media, and located at the distal edge.[49]
Intramural hematoma
Intramural hematomas are an extension of dissections
and occur less commonly. Intramural hematoma is
an accumulation of blood within the medial space,
displacing the internal elastic lamina inward and
external elastic lamina outward at the edges of the stent
[Figure 11J and K]. In an IVUS study of 905 patients
involving 1025 coronary arteries, intramural hematoma
was identified in 6.7% of the arteries. It involved the
distal reference segment more frequently (46%) and entry
site was identified in 82% of cases. Angiographically,
it appeared as dissection in 60% of the cases, as a new
lesion in 11% of the cases, and silent in 29% of the cases.
It was associated with high incidence of non-Q wave MI
(26%), need for repeat revascularization, and sudden
death.[80]
IVI not only identifies angiographically occult
hematomas but also reveal the longitudinal extent of it.
The hematomas are treated with additional stenting with
an adequate length extending into the normal appearing
vessel beyond the hematoma. Extramural hematomas
are accumulation of blood with or without contrast in
the periadventitial space [Figure 11L]. They are common
during CTO interventions.
Tissue prolapse
Prolapse of thrombus or plaque material may occur
following stent implantation, especially in patients with
ACS and particularly in those with STEMI.[81]
Presence
of positive remodeling, ruptured plaques, thrombus,
and longer stent lengths increase the incidence of tissue
prolapse.[82]
Though both IVUS and OCT can detect intra-
stent masses, OCT is more sensitive for both detection and
differentiation between different types of materials. Soeda
et al.[64]
divided intra-stent masses into tissue protrusion
(TP) and thrombus and further classified TP into three
categories based on the extent of vessel wall injury: (1)
smooth protrusion: protrusion of plaque with smooth
semicircular arc connecting the adjacent struts without
disruption of the intimal surface probably resulting from
compression of soft plaque by the stent, [Figure 11M]
(2) disrupted fibrous TP: disrupted fragments of
underlying fibrous plaque protruding between stent struts
[Figure 11N], and (3) irregular protrusion: TP with irregular
surface [Figure 11O]. Minor TP is a common finding with
IVI and usually resolves without any consequences.[83]
However, major TP may be associated with adverse
outcomes. A pathological study linked TP with early-stent
thrombosis[84]
and an OCT study correlated extent of TP
with periprocedural myonecrosis.[85]
In another study,
patients with early ST exhibited larger TP volume with
significant lumen narrowing (4 mm2
).[70]
In the study by
Soeda et al.,[64]
irregular TP was an independent predictor
of device-oriented clinical end point. In summary, the
clinical significance of TP is related to ACS presentation,
the amount of prolapse, the extent of lumen compromise,
and the severity of vessel wall injury. Baseline imaging may
identify the underlying vulnerable plaque and thrombus,
which would aid in selecting strategies that reduce the
amount of prolapse and protect the distal vascular bed. In
addition, post-procedural imaging may help in identifying
patients who require additional intervention to prevent
TP-related adverse outcomes.

Clinical Evidence for Intravascular-Guided
Coronary Intervention
IVI has played a tremendous role in understanding the
mechanisms of balloon angioplasty, stent implantation,
and stent failure. This understanding led to the
modification of the stent optimization techniques with
resultant improvement in patient outcomes. However,
the conflicting evidence from randomized trials
comparing IVUS-guided coronary artery stenting with
Table 3: Meta-analysis of trials of IVUS versus angiography-guided BMS and DES implantation
Meta-analysis No. of studies No. of patients Outcome OR (95% CI) P value
Bare metal stent
        Parise et al.[86]
8 RCT 2,193 TVR 0.66 (0.48–0.91) 0.004
Restenosis 0.64 (0.42–0.96) 0.02
MACE 0.69 (0.49–0.97) 0.03
        Casella et al.[87]
5 RCT
4 Registries
2,972 Death and MI 1.13 (0.79–1.61) 0.5
TVR 0.62 (0.49–0.78) 0.00003
Restenosis 0.75 (0.60–0.94) 0.01
MACE 0.79 (0.64–0.98) 0.03
Drug-eluting stent (RCT and registries)
        Zhang et al.[98]
1 RCT
10 Registries
19,619 Death 0.59 (0.48–0.73) 0.001
MACE 0.87 (0.78–0.96) 0.008
ST 0.58 (0.44–0.77) 0.001
MI 0.82 (0.63–1.06) 0.126
       Klersy et al.[99]
3 RCT
9 Observational
18,707 MACE 0.80 (0.71–0.89) 0.001
Death 0.60 (0.48–0.74) 0.001
MI 0.59 (0.44–0.80) 0.001
ST 0.50 (0.32–0.80) 0.007
       Jang et al.[100]
3 RCT
12 Observational
24,849 MACE 0.79 (0.69–0.91) 0.001
Death 0.64 (0.51–0.81) 0.001
MI 0.57 (0.42–0.78) 0.001
TVR 0.81 (0.68–0.95) 0.01
ST 0.59 (0.42–0.82) 0.002
       Ahn et al.[101]
3 RCT
14 Observational
26,503 TLR 0.81 (0.66–1.00) 0.046
Death 0.61 (0.48–0.79) 0.001
MI 0.57 (0.44 -0.75) 0.001
ST 0.59 (0.47–0.75) 0.001
       Steinvil et al.[102]
7 RCT
18 Observational
31,283 MACE 0.76 (0.70–0.82) 0.001
Death 0.62 (0.54–0.72) 0.001
MI 0.67 (0.56–0.80) 0.001
TLR 0.77 (0.67–0.89) 0.005
TVR 0.85 (0.76–0.95) 0.001
ST 0.58 (0.47–0.73) 0.001
Drug-eluting stent (RCT)
       Steinvil et al.[102]
7 RCT 3,192 MACE 0.66 (0.52–0.84) 0.001
TLR 0.61 (0.43–0.87) 0.006
TVR 0.61 (0.41–0.90) 0.013
       Elgendy et al.[103]
7 RCT 3,192 MACE 0.60 (0.46–0.77) 0.0001
TLR 0.60 (0.43–0.84) 0.003
Death 0.46 (0.21–1.00) 0.05
ST 0.49 (0.24–0.99) 0.04
       Bavishi et al.[104]
8 RCT 3,276 MACE 0.64 (0.51–0.80) 0.0001
TLR 0.62 (0.45–0.86) 0.004
TVR 0.60 (0.42–0.87) 0.007
       Shin et al.[105]
3 RCT (second-
generation DES)
2,345 MACE 0.36 (0.13–0.99) 0.04
Cardiac death 0.38 (0.10–1.42) 0.134
MI - 0.026
ST 0.50 (0.13–2.01) 0.320
TLR 0.61 (0.40–0.93) 0.02
OR = odds ratio, CI = confidence interval, BMS = bare metal stent, RCT = randomized controlled trial, TVR = target vessel revascularization,
ST = stent thrombosis, TLR = target lesion revascularisation


angiography-guided stenting hampered the routine use of
IVUS to guide stenting in the catheterization laboratories.
In the seven randomized trials and four meta-analyses
of IVUS versus angiography-guided bare metal stent
published to date, IVUS guidance significantly reduced
in-stent restenosis and repeat revascularization with no
impact on mortality and MI.[86-89]
Though IVUS guidance
has been shown to be beneficial in various registries of
IVUS versus angiography-guided drug-eluting stent
(DES) implantation, in four of the eight randomized
studies till date, it did not translate into better
clinical outcomes. However, these studies were either
underpowered for the primary end points or allowed
significant crossover.[90-97]
With this background, multiple
meta-analyses of these registries and randomized studies
indifferentcombinations(registriesandrandomizedtrials,
randomized trials alone, randomized trials of second-
generation DES alone) have been published over the
past 6 years [Table 3]. Overall, the IVUS-guided strategy
resulted in increase in the length and/or number of stents
used and a larger MLA with no increase in periprocedural
MI. A significant reduction in the incidence of stent
thrombosis, MI, repeat revascularization, and mortality
with IVUS-guided stenting was observed.[98-105]
Further,
in the recent ADAPT-DES study of 3349 all-comer
patient population, the IVUS guidance was associated
with better outcomes in all patient subgroups with major
benefit in patients with ACS and complex lesions.[106]
OCT, with its better resolution and ease of image
interpretation, may be superior to IVUS for stent
optimization. With its recent introduction into routine
clinical practice, no major data are available on its utility
for procedure guidance. Three randomized trials compared
OCT with IVUS for noninferiority. In the trial by Habara
et al.,[107]
OCT resulted in a significantly smaller MSA
compared to IVUS (6.1 ± 2.2 vs. 7.1 ± 2.1 mm2
, P 0.05).
The ILUMIEN III study randomized 450 patients into three
arms of OCT, IVUS, and angiography and used a novel
external elastic membrane-based stent sizing algorithm. The
final MSAs were 5.79, 5.89, and 5.49 mm2
for IVUS-, OCT-,
andangiography-guidedarms,respectively,andOCTmetthe
noninferiority end point with IVUS (Pnoninferiority
= 0.01).[47]
In
the OPINION study, 829 patients were randomly allocated
to either IVUS- or OCT-guided stenting (5.2% vs. 4.9%,
Pnoninferiority
= 0.04).[48]
In the three clinical studies comparing
the outcomes of OCT- versus angiography-based stent
implantation, OCT has been shown to be associated
with either better post-stenting FFR or superior clinical
outcomes [Table 4].[108-110]
The two ongoing major trials are
expected to throw more light on the use of OCT-guided PCI
strategy in complex coronary lesion subsets.[111]
Future Perspectives
Current IVUS systems are limited by lower resolution
(100 µ) and slower pullback speed (0.5–1.0 mm) compared
to the OCT systems. The main challenge in developing
a high-resolution IVUS was compromise in the depth
penetration with increase in the frequency. The first
high-definition IVUS system has been introduced recently
(HDi HD IVUS System, ACIST Medical Systems) for
clinical use. The system provides a resolution of 40
µ
without compromise in the depth penetration. The
pullback speed also improved to 10 mm/s.[112]
The resolution of the FD-OCT systems is suboptimal
for imaging cellular and subcellular structures. The
Massachusetts General Hospital (MGH, Boston,
Massachusetts) has developed a new OCT system
(microoptical coherence tomography [µOCT]) with 10
times higher resolution compared to the present OCT
systems. In the preliminary study of cadaveric coronary
arteries, µOCT provided high-resolution images of
atherogenesis and tissue response to the stents compared
to an FD-OCT imaging system.[113]
Three-dimensional (3D) OCT and stent rendering have
recently been introduced by both the manufacturers
(Abbott Vascular and Terumo, Abbott/St. Jude Medical,
Minneapolis, MN, United States), which has immensely
improved our understanding of stent–vessel wall
interactions during PCI, particularly in complex lesion
subsets such as coronary bifurcation. In addition to the
anatomical information, 3D OCT–based assessment
of flow dynamics and shear stress in future may further
enhance our insight into plaque evolution.[114]
Multimodality imaging system is an exciting new
development in pipeline where the different abilities
Table 4: Trials of OCT versus angiography-guided DES implantation
Trial No. of patients Study design Outcomes
CLI-OPCI[108]
670 Retrospective, multicenter,
observational
OCT was associated with lower incidence of MACE (9.6% vs. 15.1%,
P = 0.034), cardiac death (1.2% vs. 4.5%, P = 0.010), death/MI (6.6%
vs. 13%, P = 0.006) at 1 year
OCT, 335; CAG, 335
DOCTORS[109]
240 (NSTEMI-ACS) Multicenter, randomized OCT-guided group was associated with higher post-procedural FFR
values (0.94 ± 0.04 vs. 0.92 ± 0.05)
OCT, 120; CAG, 120
Jones et al.[110]
123,764 Prospective, multicenter,
observational
OCT guidance was associated with higher procedural success and
lower in-hospital MACE rates. OCT arm (7.7%) was associated with
lower mortality at 4.8-year follow-up compared to IVUS (12.2%) and
CAG (15.7%) guidance
OCT, 1,149; IVUS, 10,971;
CAG, 75,046
DOCTORS = Does optical coherence tomography optimize results of stenting.

of various imaging modalities complement each other,
which may not only improve our understanding of
the disease process but also make the PCI workflow
easier. One of the most promising recent developments
is co-registration of the angiographic images with the
IVUS and OCT images, which may reduce operator
misjudgment in device selection and stent deployment.
The first of multimodality IVI system combining IVUS
with NIRS (TVC Imaging System, Infraredx, Burlington,
Massachusetts) has already been into clinical use, which
has shown to enhance the detection rate of IVUS for lipid
core. FD-OCT does not differentiate lipid from necrotic
core, which may have different prognostic implications.
Addition of near-infrared fluorescence to the FD-OCT
imaging has been shown to improve the identification of
the necrotic core by OCT. The most useful development
may be the combination of the IVUS and OCT imaging.
A variety of designs of integrated IVUS and OCT systems
have been developed and the preclinical studies with these
systems are promising.[115]
IVI, particularly IVUS, has been shown to improve PCI
outcomes in all lesion subsets, particularly the high-risk
subsets such as left main disease. It is used for almost
all the PCI procedures in countries such as Japan and
South Korea. However, cost constraints and need for
expertise limit its widespread application in most of the
catheterization laboratories. With increasing complexity
of the patient and lesion subsets treated with PCI, it is
important for physicians to develop familiarity with
at least one of the IVI modalities to enhance the PCI
outcomes.
Acknowledgement
We would like to thank Ms. Nandhini Livingston,
Ms. Deva Preethi, and Mr. Avinash K. for their technical
support and manuscript editing.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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