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Assessment of Coronary Plaque Vulnerability with Optical Coherence Tomography

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Assessment of Coronary Plaque Vulnerability with Optical Coherence Tomography Review Article Acta Cardiol Sin 2014;30:1-9 Assessment of Coronary Plaque Vulnerability with Optical Coherence Tomography Shiro Uemura, Tsunenari Soeda, Yu Sugawara, Tomoya Ueda, Makoto Watanabe and Yoshihiko Saito Several catheter-based imaging modalities have been developed over the past 2 decades for visualizing the morphological features of coronary atherosclerotic plaques that are susceptible to future development of serious cardiovascular events. Optical coherence tomography (OCT) is a new high-resolution intracoronary imaging modality based on near-infrared interferometry, and it has been shown to be able to identify various components of atheromatous plaques. In this review, we examine the histopathology of vulnerable plaques as a target for imaging technology, and discuss the evidence of OCT in identifying vulnerable atherosclerotic lesions in patients with coronary artery disease. Key Words: Coronary artery disease · Optical coherence tomography · Vulnerable plaque It is well recognized that the culprit lesions in pa- image processing. This review focuses on the usefulness tients with acute coronary syndrome (ACS) are usually of OCT for the evaluation of plaque vulnerability in pa- characterized by advanced atherosclerotic changes with tients with coronary artery disease. concomitant thrombus formation.1-3 The term “vulnera- ble plaque” is used to specify a high-risk plaque suscep- tible to the development of either rapid luminal stenosis OCT TECHNOLOGY or occlusive intraluminal thrombus, those lead to cata- strophic cardiovascular events.4-6 Over the past 2 de- OCT is a relatively new high-resolution intraco- cades, considerable effort has been made to identify ronary imaging technology based on near-infrared inter- such high-risk coronary plaques before their rupture for ferometry. The spatial resolution of OCT, nearly 10 mm the prevention of the critical coronary events. In recent on the lateral axis, is almost 10 times greater than that years, catheter-based intravascular imaging techno- of intravascular ultrasound (IVUS). At present, 2 types of logies, especially intravascular optical coherence tomo- OCT systems, time domain (TD)- and Fourier domain graphy (OCT), have shown particular progress. Com- (FD)-OCT, are available for clinical use. TD-OCT is a con- pared with non-invasive or other invasive technologies, ventional type of intravascular device, and this system intravascular OCT has advantages in terms of higher spa- incorporates near infrared light source and optic al com- tial resolution, precise plaque localization, and real-time ponents that operate in a wavelength on 1,310 nm. Rather than using a broadband light source as in con- ventional TD-OCT systems, FD-OCT imaging systems employ a wavelength-swept laser as a light source, and Received: April 17, 2013 Accepted: August 28, 2013 First Department of Internal Medicine, Nara Medical University, this improvement enables faster image acquisition Nara, Japan. speeds and greater scan depths (Table 1). In addition, Address correspondence and reprint requests to: Dr. Shiro Uemura, the higher pull-back speed of FD-OCT can prevent heart First Department of Internal Medicine, Nara Medical University, 840 Shijo-cho Kashihara, Nara Japan 634-8522. E-mail: suemura@ motion artifacts and thus allow precise assessment of naramed-u.ac.jp the longitudinal distribution of plaque components. 1 Acta Cardiol Sin 2014;30:1-9 Shiro Uemura et al. Table 1. Platform comparison between time domain (TD)- and Fourier domain (FD)-optical coherence tomography (OCT) TD-OCT FD-OCT (ILUMIEN OPTIS) Pullback Mode Nominal Survey mode High resolution mode Engine speed 15.6 fps 180 fps 180 fps Pullback speed 2.0 mm/sec 36 mm/sec 18 mm/sec Frame rate 7.8 frames/mm 5 frames/mm 10 frames/mm Pullbacklength 20mm 75mm 54mm Lines/frame 200 500 500 Scan diameter 6.8 mm 10.5 mm 10.5 mm AsshowninFigure1,OCTvisualizes3layerstruc- lesions, which instead showed features such as plaque tures of normal coronary artery as well as plaque com- erosion or calcified nodules. In current clinical practice, ponent of atherosclerotic lesions. The ability of OCT in these non-rupture-type features in baseline lesions are tissue characterization of coronary atherosclerotic also considered to be characteristics of vulnerable coro- lesions has been well validated in clinicopathological nary plaques (Table 2). In clinical setting, OCT is able to studies.7-9 In addition, the drawback points of OCT are visualize plaque morphology possibly agree with au- the relatively shallow depth of light penetration into the topsy findings (Figure 2). Furthermore, recent studies arterial wall in the comparison with ultrasound, and the have shown that vulnerable plaques can develop not necessity of blood removal by contrast medium during only in native coronary arteries but also in the neo- image acquisition. intima after long-term coronary stent implantation.14,15 Table 2. Pathological features of vulnerable plaque PATHOLOGICAL BACKGROUND OF PLAQUE I. Macroscopic features VULNERABILITY Large necrotic or lipid core Luminal thrombus Plaque hemorrhage Medical term “vulnerable plaque” was first used by Spotty calcification Muller et al. in defining the plaque with rupture that is Positive vascular remodeling oneofthetriggersfortheonsetofacutecardiovascular II. Microscopic features disease.10,11 In fact, pathological studies of the victims of Thin fibrous cap covering lipid core sudden cardiac death have revealed that more than 70% Macrophage infiltration of ACS are attributable to the formation of occlusive Plaque neovasculization Endothelial denudation thrombus that is preceded by plaque rupture.3,12,13 How- Smooth muscle cell apoptosis ever, as noted in these autopsy studies, plaque rupture Protease expression is not the sole pathological cause of coronary events; no Endothelial adhesion molecule expression rupture was seen in the remaining 30% of the culprit III. Heat generation FigureA 2. RepresentativeBC OCT findings plaque observed in patients with acute coronary syndrome. (A) Plaque rupture. Arrow indicates disrupted fibrous cap. * Represents space previously contained lipid Figure 1. OCT findings of normal coronary artery. Note. Clear pool. (B) Plaque erosion with thrombus formation (arrow). (C) Calcified differentiation of 3 layers in vessel wall. nodule (arrow). Acta Cardiol Sin 2014;30:1-9 2 OCT Assessment of Plaque Vulnerability Plaque rupture caps,23,24 development of calcification,25 and heat gener- As previously described in the scientific literature, ation.26 Intraplaque new blood vessel formation is an- coronary arterial wall often develops significant athero- other unique morphological feature of TCFA, usually sclerotic changes before the progression of luminal ste- originating from the adventitial vasa vasorum.27,28 Intra- nosis. Figure 3 shows the representative cross-sectional plaque microvessels are immature and leaky due to the OCT images obtained from non-stenotic coronary pla- lack of basement membranes and pericytes,29,30 and que in patients with coronary artery disease (CAD). their deterioration is known to cause intraplaque hemo- Among these complex characteristics, thin-cap fibro- rrhage. This phenomena results in both rapid enlarge- atheroma (TCFA) is known as a vulnerable plaque sub- ment of plaque size and luminal stenosis.31-33 These type which is susceptible to rupture. TCFA is patho- histopathological features observed within TCFA are logically diagnosed when the plaque has a large lipid or candidate targets for coronary artery imaging with the necrotic core (> 40% of total lesion cross-sectional area) goal of detecting plaque vulnerability. However, it and a thin fibrous cap (< 65 mmthick).3,16 An autopsy should also be noted that clinically silent plaque rupture study of ruptured plaques in patients with sudden car- is not rare.33-35 diac death found that 95% of these caps measured < 64 mmthick.3 Notably, a recent computer simulation study Non-rupture type vulnerable plaque showed that fibrous cap thickness and necrotic core size Plaque erosion is characterized pathologically by a are independent determinants for plaque disruption.17 continuous intimal layer without rupture or discon- Additionally, TCFA is frequently accompanied by macro- tinuation, usually accompanied by an intraluminal phage infiltration and matrix metalloproteinase (MMP) thrombus overlying a modestly occlusive plaque, al- expression in the fibrous cap covering the lipid core.18,19 though standard diagnostic criteria have not been de- Many studies have pointed out that high macrophage fined.3,36 Typically, the endothelial cell layer is denuded density is characteristic of lesions vulnerable to rupture. andtheexposedfibrouscapconsistsofsmoothmuscle Ex vivo studies of human coronary artery plaques have cells, rich proteoglycans, and varying numbers of inflam- shown that the density and pattern of macrophage infil- matory cells. Autopsy data have demonstrated that tration at plaque shoulders correlate with degree of plaque erosion is more frequent in women < 50 years of vulnerability.20-22 Chronic inflammation within TCFA also age, and lesions with such erosion are often negatively stimulates smooth muscle cell apoptosis within fibrous remodeled.9 Autopsy studies have shown that 20% to A BCD E FGH Figure 3. Plaque characterization of non-stenotic coronary atherosclerotic lesions with optical coherence tomography. (A) Normal coronary artery. (B) Stable fibrous plaque. (C) Thick cap fibroatheroma, two arrows indicate thickness of
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