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Table of Contents
EDITORIAL REVIEW
Year : 2018  |  Volume : 1  |  Issue : 2  |  Page : 71-94

Intravascular ultrasound and optical coherence tomography for the assessment of coronary artery disease and percutaneous coronary intervention optimization: The basics


1 Institute of Cardiovascular Diseases, The Madras Medical Mission, Chennai, India
2 CardioVascular Clinics, St Andrews War Memorial Hospital, Cardiology Program, The Prince Charles hospital, and University of Queensland, Queensland, Australia

Date of Web Publication13-Dec-2018

Correspondence Address:
Dr. Vijayakumar Subban
Department of Cardiology, Institute of Cardiovascular Diseases, Madras Medical Mission, 4A, Dr. J. Jayalalitha Nagar, Mogappair, Chennai 600037, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IHJI.IHJI_32_18

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  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


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

How to cite this URL:
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 [serial online] 2018 [cited 2019 Sep 16];1:71-94. Available from: http://www.ihji.org/text.asp?2018/1/2/71/247452




  Introduction Top


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 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 Top


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 (1800rpm) 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 1]A. 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 1]B.[2],[3]
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)

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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 (10mm in Eagle Eye Platinum and 2.5mm 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 25mm 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 10–15µ resolution but at the same time limits tissue penetration to 1–2mm.[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 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 2–3mm/s [Figure 2]A. FD-OCT uses a narrow bandwidth light source that sweeps rapidly between wavelengths 1250–1350nm 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 38mm/s [Figure 2]B. This in turn limits the amount of contrast flush during image acquisition.[4]
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 2–3mm/s. FD-OCT uses a narrow bandwidth light source that sweeps rapidly between wavelengths 1250 and 1350nm 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)

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  Qualitative Analysis Top


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 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]
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

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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 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 300–600µ of intimal thickness to differentiate nonatherosclerotic intimal changes from normal coronary artery (<300µ) and atherosclerotic lesions (>600µ). On grayscale IVUS, intimal thickening depicts a uniform signal-rich appearance [Figure 4]A. VH-IVUS defines it as fibrous or fibrofatty intima with a thickness <600µ [Figure 4]B. On OCT imaging, intimal thickening appears as homogeneous signal-rich intima with a thickness between 300 and 600µ and a visibility of media in greater than or equal to three quadrants [Figure 4]C. In intimal xanthoma, foamy macrophages produce shadowing of the light [Figure 4]D.[7],[8],[9]
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)

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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 (<65µ) 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 5]A and B. Echo-attenuated pattern represented either a large lipid pool or a necrotic core, whereas echolucent 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 5]C. 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 5]D 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],[ >600µ thickness],[ and lipid or calcium when present],[ occupies less than one quadrant [Figure 5]F (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 5]G and is further classified into TCFA (FCT<65µ) and thick-cap fibroatheroma (FCT>65µ) [Figure 5]H. 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 50–300µ and extending over three or more frames), cholesterol crystals (signal-rich streaks with low attenuation), and spotty calcification (small calcium deposit with an arc <90°) [Figure 5]I–L. Although grayscale IVUS can identify spotty calcification, it cannot characterize the other structures.[4]
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

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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 6]A and B]
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)

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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 6]C 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 6]D.

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 6]E 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 6]G. OCT imaging clearly differentiates red thrombus from white thrombus. Red thrombus appears as an intraluminal mass with high backscatter and high attenuation [Figure 6]D, whereas white thrombus appears as an intraluminal mass with high backscatter and low attenuation [Figure 6]H.[4] A recanalized thrombus produces a lotus root or Swiss cheese appearance [Figure 6]I 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 of tissue with different optical densities with or without underlying necrotic core or calcification [Figure 7]A.[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]
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)

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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 7]B. 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 7]C.[8] On OCT imaging, fibrous plaque is defined as a homogenous, signal-rich plaque with low signal attenuation and >600µ thickness [Figure 7]D.[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 7]E and F].[2 VH defines fibrocalcific plaque as a fibrous plaque with >10% dense calcium and <10% of necrotic core [Figure 7]G.[8] On OCT imaging, calcium appears as a heterogeneous area of low backscatter with low attenuation and clear borders surrounded by fibrous tissue [Figure 7]H. Nodular calcium appears similar to CN but with intact fibrous cap and no luminal thrombus [Figure 7]I.[4]


  Artifacts Top


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].
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]

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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 8]A 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 circumference of the image],[ which is known as sew-up/seamline artifact [Figure 8]B.

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 8]C.[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 8]C 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 8]D or with stent struts [Figure 8]E 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 8]F, calcium [Figure 8]G, 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 8]H. 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 8]I and can be resolved by saline flushing.[3]

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 8]J. 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 8]K. 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 8]L.[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 8]M.[4]

Fold over artifact: FD-OCT has a field of view of approximately 10mm. 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 8]N. 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 8]O.[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 8]O. 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 8]P.[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 8]P.[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 8]Q.[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 8]R.[15]


  Quantitative Assessment Top


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]
Figure 9: Quantitative IVUS and OCT assessment

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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. 7.45mm2) and IVUS area was larger by 8% (8.03±0.58mm2; P < 0.001). In the human study, OCT measured minimal lumen diameter (MLD) and MLA, which were smaller by 9% (1.91±0.69 vs. 2.09±0.60mm; P < 0.001) and 10% (3.68±2.06 vs. 3.27±2.22mm2; 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 ofIntravascular Imaging Top


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 [Table 1] and [Table 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 4mm2 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],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[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 ≥4mm2 has a very high-negative predictive value and most of the lesions in this area are non-flow limiting. However, when the MLA is <4mm2, 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 >20mm.
Table 1: IVUS studies evaluating anatomical parameters for detecting ischemia in non-left main CAD

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,
Table 2: OCT studies evaluating anatomical parameters for detecting ischemia in non-left main CAD

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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, and intraplaque echolucency.[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 ≤4mm2 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 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 diameter is the same as that of the reference lumen diameter 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., 2.80mm round down to 2.75mm, [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 0.25mm to derive the stent diameter (e.g., 3.5mm round up to 3.75mm). 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.
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 (2.80mm). The distance between these reference segments is the length of the stent (14mm). Hence, a 2.75×18mm stent was chosen

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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.
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]

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Stent expansion

Stent expansion is the most important parameter of stent optimization and is closely related to both in-stent restenosis 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 <9mm2 or MSA ≥80% of the average reference lumen area or ≥90% of the reference segment with the smaller area when the MSA is >9mm.[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 IVUS criteria have been proposed recently. The first was the 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]
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 2.75×18mm drug-eluting stent in proximal left anterior descending coronary artery (A). The minimal stent area is 6.6mm2 (C) and is more than average reference lumen area of 6mm2 (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

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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 11]A 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 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 (2.5mm stent implanted in a 3.5mm 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],[59],[60],[61],[62],[63],[64],[65],[66],[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 2.6mm3 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],[59],[60],[61],[62],[63],[64],[65],[66],[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 0.6mm and 1.0 and 2.1mm, respectively, in the segments with thrombus. On the basis of these observations, the consensus statement recommends against treatment of malappositions with ISA distance <400µ and a length of <1mm.[49] Although it appears that small malappositions are innocuous [Figure 11]C, every effort should be made to appropriately size and implant the stent to avoid gross malappositions [Figure 11]D 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 <4mm2) 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 <4.5mm2 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 (<4.1mm2) 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 11]F.[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 11]G.[75] In contrast, major dissections (IVUS lumen area narrowing <4mm2 or dissection angle of ≥60°) have been associated with higher incidence of early-stent thrombosis and need additional stenting [Figure 11]H and I].[70] In ADAPT-DES study],[ a residual lumen area of <5.1mm2 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 ≤1.75mm, with <2 concomitant flaps, flap depth ≤0.52mm, flap opening ≤0.33mm, 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 >0.31mm was associated with adverse clinical outcomes.[79] In another study, a flap thickness >200µ 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 >2mm, 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 11]J 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 11]L. 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 11]M (2) disrupted fibrous TP: disrupted fragments of underlying fibrous plaque protruding between stent struts [Figure 11]N, and (3) irregular protrusion: TP with irregular surface [Figure 11]O. 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 (<4mm2).[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 Top


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 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],[87],[88],[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],[91],[92],[93],[94],[95],[96],[97] With this background, multiple meta-analyses of these registries and randomized studies in different combinations (registries and randomized trials, 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],[99],[100],[101],[102],[103],[104],[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]
Table 3: Meta-analysis of trials of IVUS versus angiography-guided BMS and DES implantation

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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±2.1mm2, 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 5.49mm2 for IVUS-, OCT-, and angiography-guided arms, respectively, and OCT met the 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],[109],[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]
Table 4: Trials of OCT versus angiography-guided DES implantation

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  Future Perspectives Top


Current IVUS systems are limited by lower resolution (100µ) and slower pullback speed (0.5–1.0mm) 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 <40µ without compromise in the depth penetration. The pullback speed also improved to 10mm/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 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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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