Interventional Cardiology. Группа авторов

causes a signal‐rich area overlying a signal‐poor region in an area of adaptive intimal thickening. (f) Bubble in the catheter causes a shadow on the vessel wall (arrow). (g) Multiple reflections. (h) Fold‐over artifact.

      Blooming artifact is the effect of intense signal generated by the reflection of light [10]. This is most commonly caused by stent struts, which appear thicker. Bubble artifact is the result of air bubbles in the catheter sheath. Bubbles also form in the silicon lubricant used to reduce friction between the sheath and the revolving optic fiber in TD‐ OCT systems [11]. Bubbles can attenuate the signal along a region of the vessel wall, and images with this artifact are unsuitable for tissue characterization (Figure 9.1f). Multiple reflections are caused by the reflected surface of catheters creating one or more circular line within the image (Figure 9.1g). Strut orientation artifacts appears when the OCT catheter resides close to a stented artery wall, imaging metal coronary stents deployed appear as a bending of stent struts toward the imaging catheter. This so‐called sunflower effect occurs when the catheter occupies an eccentric position within the vessel lumen and the struts appear as a straight line [12]. Fold‐over artifact is more specific to FD‐OCT systems. It occurs when the vessel is larger than the ranging depth, thus it is typically observed in large vessels or side branches. Consequently, the vessel might appear to be folded over in the image (Figure 9.1h).

Normal coronary vessel anatomy

With the exception of the left main stem, coronary arteries are muscular arteries and are histologically organized into three layers. The intima consists of a lining layer of endothelial cells supported by a subendothelial layer [13], which is exceedingly thin at birth and grows progressively with age, eventually reaching OCT resolution limits [14]. In OCT, the intima can be visualized as a signal‐rich luminal layer. The intimal thickens with age, and nearly all adult coronaries display an extent of intimal thickening [15]. There is no established cut‐off for the identification of pathologic intimal thickening; however, some authors use, rather arbitrarily, a cut‐off of 300 μm to identify intimal thickening, and above 600 μm for pathologic intimal thickening in the absence of a lipid pool or calcified region >1 quadrant [16]. The medial layer is a signal‐poor region isolated from the intimal layer and the adventitia by the brighter lines of the internal and the external elastic membrane, respectively [17]. The adventitia is recognized as a heterogeneous high signal outer layer.

      Plaque characterization

Atherosclerotic plaque components can be categorized by utilizing various optical properties of different tissues (Figure 9.2). Fibrous plaques are identified as homogenous, highly backscattering, low attenuation lesions. The emitted light is absorbed more intensely by lipids which leads to a high level of posterior signal attenuation; plaques appear as low backscatter regions with poor delineation of the external contour. Calcifications are also regions of low backscatter (signal poor), but they let light filter rather than absorb it, so that they maintain well‐delineated external borders. However, differentiation of signal‐poor areas is not always straightforward and calcium can be misinterpreted as lipids, particularly if the calcification is situated deep in the vessel wall.

Figure 9.2 Plaque characterization with optical coherence tomography. (a) Normal coronary anatomy organized in three layers. (b) Lipid‐rich plaque; note possible macrophage accumulations around 3 o’clock. (c) Lipid‐rich plaque in a saphenous vein graft. (d) Fibrous plaque. (e) Calcification extending deep into the vessel wall between 4 and 11 o’clock. Outer border of the calcification cannot be delineated. (f) Calcification between 12 and 4 o’clock. (g) Thrombus protruding into the lumen. (h) Neovascularization (arrows).

      An early ex vivo study established a sensitivity and specificity ranging 71–79% and 97–98% for fibrous plaques, 95–96% and 97% for fibro‐calcific plaques, and 90–94% and 90–92% for lipid‐rich plaques with low inter‐observer and intra‐observer variability [18]. Other studies showed less impressive results, with only 45% of lipid‐laden atheromas identified, with higher but still suboptimal identification success in fibro‐calcific and fibrous plaques (68% and 83%, respectively) [19]. Misinterpretation in this study was mainly caused by low OCT signal penetration, which precluded the detection of lipid pools or calcium behind thick fibrous caps and by misclassification of calcium deposits for lipid pools and vice versa [19]. Furthermore, artifacts such as superficial shadowing and tangential signal dropout can produce images with signal‐poor regions covered by a thin signal rich layer mimicking thin‐cap fibroatheromas (TCFA). Rather than relying only on subjective visual interpretations, algorithms based on the optical attenuation coefficient to classify plaques quantitatively have been proposed; however, as yet, these algorithms are not sufficiently robust to be used in the clinical setting [20].

      OCT imaging can also demonstrate thrombi as protrusions or floating masses. Red and white thrombi can be identified via the differences in attenuation intensity, with red thrombi showing high attenuation and complete wall shadowing and white thrombi appearing as low attenuation intraluminal masses or layers [21].

      Vulnerable plaque assessment

      Imaging in acute coronary syndromes (ACS) includes ruptured plaques and histomorphologic features that can be detected by OCT (superficial lipids, fibrous cap thickness as well the presence of macrophages and neovascularization).

A semi‐quantitative definition of the presence of superficial lipids in ≥2 quadrants is used to describe lipid‐rich plaques in OCT studies [21]. However, low penetration depth prevents accurate evaluation of the lipid core thickness. Pathologic studies reported that ruptured plaques harbor a thin fibrous cap being <65 μm in 95% of ruptured plaques [22]. Using OCT, the fibrous cap can be detected as a high signal homogeneous band covering the lipid‐rich core. OCT was shown to provide accurate measurement of fibrous cap thickness (FCT) ex vivo [23]; previous studies demonstrated thinner fibrous caps in patients with ACS [21,24]. A study that aimed to evaluate the relationship between FCT and plaque rupture in vivo found that in 95% of ruptured plaques, the thinnest FCT was <80 μm and so the investigators proposed this value as an alternative in vivo threshold [25].

      The progression of atherosclerosis and plaque vulnerability is critically affected by macrophages, identified as high signal regions appearing either distinct or confluent punctate visually. With dedicated software, OCT‐derived indices can be used to identify macrophages [26]. Nonetheless, macrophages should only be considered in the presence of a fibroatheroma, because there have not yet been any studies to confirm macrophages on normal vessel walls or intimal hyperplasia. In addition, high speckle from microcalcifications or cholesterol crystals can also appear similar to macrophages [27].

      Plaque neovascularization is considered as a feature of vulnerable plaques. These microvessels are inherently fragile and leaky, giving rise to local extravasation of plasma proteins and erythrocytes [28]. OCT reveals these vessels as small black holes in the atherosclerotic plaque [29]. The presence of these microchannels is associated with vulnerable features such as thin fibrous cap and positive remodeling [30]. In a larger study, microchennels characterized culprit lesions of patients with ACS, and were not present in non‐culprit lesions of patients with ACS or in stable patients [31]. Another study found no difference in the prevalence of microchannels in ACS and non‐ACS patients; however, the closest distance from the lumen to the microchannel was shorter in ACS subjects than in non‐ACS [32].

      OCT imaging over time can provide insights on the efficacy of the therapeutic strategies for plaque stabilization. In an initial study, patients on preceding