Advances in Intravascular Imaging: New Insights into the Vulnerable Plaque from Imaging Studies

Abstract

The term "vulnerable plaque" denotes the plaque characteristics that are susceptible to coronary thrombosis. Previous post-mortem studies proposed 3 major mechanisms of coronary thrombosis: plaque rupture, plaque erosion, and calcified nodules. Of those, characteristics of rupture-prone plaque have been extensively studied. Pathology studies have identified the features of rupture-prone plaque including thin fibrous cap, large necrotic core, expansive vessel remodeling, inflammation, and neovascularization. Intravascular imaging modalities have emerged as adjunctive tools of angiography to identify vulnerable plaques. Multiple devices have been introduced to catheterization laboratories to date, including intravascular ultrasound (IVUS), virtual-histology IVUS, optical coherence tomography (OCT), coronary angioscopy, and near-infrared spectroscopy. With the use of these modalities, our understanding of vulnerable plaque has rapidly grown over the past several decades. One of the goals of intravascular imaging is to better predict and prevent future coronary events, for which prospective observational data is still lacking. OCT delineates microstructures of plaques, whereas IVUS visualizes macroscopic vascular structures. Specifically, plaque erosion, which has been underestimated in clinical practice, is gaining an interest due to the potential of OCT to make an in vivo diagnosis. Another potential future avenue for intravascular imaging is its use to guide treatment. Feasibility of tailored therapy for acute coronary syndromes (ACS) guided by OCT is under investigation. If it is proven to be effective, it may potentially lead to major shift in the management of millions of patients with ACS every year.

Keywords: Acute coronary syndrome; Atherosclerotic plaque; Interventional ultrasonography; Optical coherence tomography.

Figure 1

A lesion with a necrotic core assessed by VH-IVUS. A fibroatheroma was imaged by grey-scale IVUS (upper row) and VH-IVUS (lower row). VH-IVUS categorizes the tissue into DC, FT, FF, or NC by processing the radiofrequency data of IVUS. In general, a plaque containing >10% of NC is defined as fibroatheroma. When NC is adjacent to the lumen >30 degrees of circumferences on 3 consecutive frames, fibroatherma is defined as VH-TCFA, as proposed in the PROSPECT study. The lesion in the third column contains >10% of NC, but the angle of NC adjacent to the lumen is not >30 degrees. Therefore, the lesion is defined as ThCFA. DC = dense calcium; FT = fibrous tissue; FF = fibrofatty tissue; IVUS = intravascular ultrasound; NC = necrotic core; PROSPECT = Providing Regional Observations to Study Predictors of Events in the Coronary Tree; ThCFA = thick-cap fibroatheroma; VH-IVUS = virtual-histology intravascular ultrasound; VH-TCFA = virtual-histology-derived thin-cap fibroatheroma.

Figure 2

Typical OCT findings representing vulnerable plaques. (A) shows intraluminal thrombus characterized by a mass (*) attached to the wall (9–12 o'clock). (B) shows TCFA characterized by a signal poor region (*) with a thin, signal rich band (white arrow) on the luminal side. (C) shows a fibrous plaque with neovascularization characterized by a tubuloluminal, signal lucent structure (white arrow) within the plaque. OCT = optical coherence tomography; TCFA = thin cap fibroatheroma.

Figure 3

Coronary plaques imaged by angioscopy. Angioscopy allows direct visualization of coronary plaques surface from the luminal side. Plaque characteristics is categorized by color grading: white (grade 0); light yellow (grade 1); yellow (grade 2); or intensive yellow (grade 3). (A) shows white plaque (grade 0) and (B) shows yellow plaque (grade 2). In addition to the color grade, presence of thrombus and plaque disruption can be visualized by angioscopy. (C) shows a plaque rupture with red thrombus.

Figure 4

A lipid-rich plaque imaged by NIRS. A culprit lesion of NSTEMI was examined by NIRS co-registered with grey-scale IVUS. NIRS provides a probability of the presence of lipid ranging from 0 to 1.0 for each pixel occupying 0.1 mm and 1 degree, which is indicated on a map of lumen surface called “chemogram” (Right upper panel). The information of the probability is superimposed on the rim of grey-scale IVUS (A). In the center of grey-scale IVUS and in the right lower panel, “block chemogram” which summarizes the probability value of each 2-mm segment is shown (B). Numbers of pixels of which the probability is >0.6 is expressed as permil, and called LCBI. Max LCBI_4mm is generally used as an indicator of lipid volume (C). IVUS = intravascular ultrasound; LCBI = lipid core burden index; Max LCBI_4mm = Maximal LCBI value within a 4 mm-segment; NIRS = near-infrared spectroscopy; NSTEMI = non-ST-elevation myocardial infarction.

Figure 5

Positive remodeling. EEM area can be measured with IVUS. RI is calculated as the ratio of lesion EEM area divided by that of reference site. Threshold of RI for positive remodeling varies among different studies. In previous IVUS studies, RI >1.05 or 1.00 were predominantly used for the definition of positive remodeling. In this figure, RI is 1.37, which indicates significant positive remodeling. EEM = external elastic membrane; IVUS = intravascular ultrasound; RI = remodeling index.

Figure 6

Macrophage accumulation. Three consecutive frames of a plaque showing macrophage accumulation. Macrophage accumulation is identified by punctate or linear high-signal intensities accompanied by heterogenic shadow (white arrow, frame 304), which cast on the deeper layer of intima. Heterogenic shadow is characterized by frame-by-frame variability (frame 304–306) and sharp radial border between plaque density (triangle, frame 306) and a shadow density (circle, frame 306) within the plaque.

Figure 7

Plaque erosion on OCT. OCT images of a culprit lesion of NSTEMI show “definite” erosion. Definite erosion is defined by OCT as having intact fibrous cap underneath thrombi (arrowheads) that do not preclude plaque characterization behind the thrombus. NSTEMI = non-ST-elevation myocardial infarction; OCT = optical coherence tomography.

Figure 8

Plaque rupture imaged by OCT and IVUS. Plaque rupture in a culprit lesion of STEMI is imaged by OCT (A) and IVUS (B). OCT clearly visualizes disruption of fibrous cap (arrow head) and a thrombus attached to the lumen (white arrow), however circumferential lipid precludes visualization of entire vessel wall. In contrast, IVUS delineate medial layer (yellow arrow) beyond the plaque, whereas microstructure beside the lumen such as a thrombus and plaque rupture are not detectable. IVUS = intravascular ultrasound; OCT = optical coherence tomography; STEMI = ST-segment elevation myocardial infarction.