Stress Concentrations of Vulnerable Plaques With a Composite Variable Core

2010 ◽  
Author(s):  
Eyass Massarwa ◽  
Aronis Ze’ev ◽  
Rami Eliasy ◽  
Rami Haj-Ali ◽  
Shmuel Einav
Keyword(s):  
Plaque Rupture ◽  
Necrotic Core ◽  
Intraplaque Hemorrhage ◽  
Plaque Morphology ◽  
Rapid Progression ◽  
Stress Concentrations ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Vulnerable Plaques ◽  
Life Threatening

Vulnerable plaques are inflamed, active, and growing lesions which are prone to complications such as rupture, luminal and mural thrombosis, intraplaque hemorrhage, and rapid progression to stenosis. It remains difficult to assess what factors influence the biomechanical stability of vulnerable plaques and promote some of them to rupture while others remain intact. The rupture of thin fibrous cap overlying the necrotic core of a vulnerable plaque is the principal cause of acute coronary syndrome. The mechanism or mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to a life threatening athero-thrombotic lesion are not fully understood. It has been widely assumed that plaque morphology is the major determinant of clinical outcome [1, 2]. Thin-cap fibroatheroma with a large necrotic core and a fibrous cap of < 65μm was describes as a more specific precursor of plaque rupture due to tissue stress.

Influence of Microcalcifications on Stress Development Within a Vulnerable Plaque’s Cap

2011 ◽  
Author(s):  
Ze’ev Aronis ◽  
Erez Kanka ◽  
Eyass Massarwa ◽  
Rami Haj-Ali ◽  
Shmuel Einav
Keyword(s):  
Mechanical Characteristics ◽  
Plaque Rupture ◽  
Intraplaque Hemorrhage ◽  
Rapid Progression ◽  
Stress Concentrations ◽  
Coronary Syndrome ◽  
Vulnerable Plaques ◽  
Material Fatigue ◽  
Mechanical Factors ◽  
As Stress

Vulnerable plaques are inflamed, active, and growing lesions which are prone to complications such as rupture, luminal and mural thrombosis, intraplaque hemorrhage, and rapid progression to stenosis. Despite major advances in the prevention and treatment of this disease, it remains the leading cause of morbidity and mortality worldwide, accounting for 30% of all deaths globally [1]. The importance of stress/strain distribution is now well recognized in vascular pathophysiology, specifically in the mechanisms of plaque rupture. Finite element modeling (FEM) and advanced fluid structure interaction (FSI) studies can better characterize coronary stenosis coupling constitutive equations. Mechanical factors such as stress concentrations within a plaque (material fatigue), lesion characteristic (location, size, and composition), and flow patterns are involved in rupture of plaques. Assessment of local mechanical characteristics caused by plaque structure is important for identifying vulnerable plaques and may improve final estimation of the risk for coronary syndrome.

Analysis of Biomechanical Forces Influencing Atherosclerotic Plaque Vulnerability

2009 ◽  
Author(s):  
Ze’ev Aronis ◽  
Shmuel Einav
Keyword(s):  
Atherosclerotic Plaque ◽  
Intraplaque Hemorrhage ◽  
Western World ◽  
Plaque Morphology ◽  
Rapid Progression ◽  
Heart Attacks ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Life Threatening ◽  
Biomechanical Forces

Cardiovascular disease has long been the leading cause of death in the western world: over 1.4 million heart attacks are suffered every year, more than half of which prove fatal. Vulnerable plaques are inflamed, active, and growing lesions which are prone to complications such as rupture, luminal and mural thrombosis, intraplaque hemorrhage, and rapid progression to stenosis. The rupture of thin fibrous cap overlying the necrotic core of a vulnerable plaque is the principal cause of acute coronary syndrome. The mechanism or mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to a life threatening athero-thrombotic lesion are not fully understood. It has been widely assumed that plaque morphology is the major determinant of clinical outcome [1, 2].

Abstract T MP29: Contrast-Enhanced Ultrasound is Useful for Detection of Vulnerable Plaques

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Rie Motoyama ◽  
Kozue Saito ◽  
Shuichi Tonomura ◽  
Hatsue I Ueda ◽  
Hiroharu Kataoka ◽  
...  
Keyword(s):  
High Intensity ◽  
Necrotic Core ◽  
Intraplaque Hemorrhage ◽  
Contrast Enhanced Ultrasound ◽  
Histopathological Findings ◽  
Rapid Acquisition ◽  
Fibrous Cap ◽  
Vulnerable Plaques ◽  
Contrast Enhanced ◽  
Active Inflammation

Background and Purpose: Vulnerable plaques of carotid arteries are characterized as the presence of large necrotic core, intraplaque hemorrhage (IPH), intraplaque neovascularization (IPN), and active inflammation with thin fibrous cap. MRI is widely used for the qualitative evaluation of the plaques in vivo and the high-intensity plaques (HIP) on magnetization-prepared rapid acquisition with gradient echo (MPRAGE) images indicate containing necrotic cores with IPH, which indicates vulnerable plaques. However, we encounter the symptomatic cases without the presence of HIP on MPRAGE in clinical practice. Recent studies showed the efficacy for the evaluation of IPN using contrast-enhanced ultrasound (CEUS). We aimed to assess the vulnerability of the plaques without high intensity on MPRAGE images using CEUS. Methods: Between July 2010 and June 2014, we enrolled 69 patients with internal carotid artery stenosis who underwent carotid endarterectomy (CEA) and preoperatively examined CEUS and MRI (MPRAGE). All plaques were evaluated with CEUS and the contrast effects were classified semi-quantitatively (grade 0: absent, 1: small, 2: large, 3: extensive). We also divided the plaques into two groups (HIP group or non-HIP group) based on the signal intensity of the plaques on MPRAGE images. The results of MRI and CEUS were compared with histopathological findings of CEA specimens. Results: Fifty-eight plaques of all 69 patients showed HIP (41 were symptomatic), and eleven plaques were non-HIP (five were symptomatic: amaurosis fugax in three, cerebral infarction in two). In non-HIP group, symptomatic plaques were more enhanced (three in grade 2, two in grade 3) than asymptomatic plaques (one in grade 0, five in grade 1) using CEUS. Histopathological findings of all five CEA specimens from symptomatic patients showed that extensive IPN, large necrotic core, and active inflammation with thin fibrous cap which indicated vulnerable plaques, but small amount of IPH. These histological findings were compatible with the results of CEUS and MRI findings. Conclusion: CEUS may be useful for diagnosis of vulnerable plaques without high intensity on MPRAGE images.

scholarly journals Necrotic core thickness and positive arterial remodeling index: emergent biomechanical factors for evaluating the risk of plaque rupture

2008 ◽  
Vol 295 (2) ◽  
pp. H717-H727 ◽  
Author(s):  
Jacques Ohayon ◽  
Gérard Finet ◽  
Ahmed M. Gharib ◽  
Daniel A. Herzka ◽  
Philippe Tracqui ◽  
...  
Keyword(s):  
Plaque Rupture ◽  
Necrotic Core ◽  
Plaque Morphology ◽  
Arterial Remodeling ◽  
Plaque Instability ◽  
Fibrous Cap ◽  
Remodeling Index ◽  
Core Thickness ◽  
Fibrous Cap Thickness ◽  
Biomechanical Factors

Fibrous cap thickness is often considered as diagnostic of the degree of plaque instability. Necrotic core area (Corearea) and the arterial remodeling index (Remodindex), on the other hand, are difficult to use as clinical morphological indexes: literature data show a wide dispersion of Corearea thresholds above which plaque becomes unstable. Although histopathology shows a strong correlation between Corearea and Remodindex, it remains unclear how these interact and affect peak cap stress (Capstress), a known predictor of rupture. The aim of this study was to investigate the change in plaque vulnerability as a function of necrotic core size and plaque morphology. Capstress value was calculated on 5,500 idealized atherosclerotic vessel models that had the original feature of mimicking the positive arterial remodeling process described by Glagov. Twenty-four nonruptured plaques acquired by intravascular ultrasound on patients were used to test the performance of the associated idealized morphological models. Taking advantage of the extensive simulations, we investigated the effects of anatomical plaque features on Capstress. It was found that: 1) at the early stages of positive remodeling, lesions were more prone to rupture, which could explain the progression and growth of clinically silent plaques and 2) in addition to cap thickness, necrotic core thickness, rather than area, was critical in determining plaque stability. This study demonstrates that plaque instability is to be viewed not as a consequence of fibrous cap thickness alone but rather as a combination of cap thickness, necrotic core thickness, and the arterial remodeling index.

Macrophage infiltrates in coronary plaque erosion portend a worse cardiovascular outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Vulnerable Plaque ◽  
Cardiac Death ◽  
Cox Regression ◽  
Plaque Rupture ◽  
Culprit Lesion ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion

Abstract Background Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS). Inflammatory activation is considered a key mechanism of plaque instability in patients with plaque rupture through the release of metalloproteinases and the inhibition of collagen synthesis that in turns lead to fibrous cap degradation. However, the clinical relevance of macrophage infiltration has never been investigated in patients with PE. Purpose In our study, we aimed at assessing the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site and in non-culprit segments along the culprit vessel was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. In particular, culprit lesion analysis demonstrated that patients with PE with MØI had a significantly thinner fibrous cap [median (IQR) 100 (60–120) μm vs. 160 (95–190) μm, p&lt;0.001], higher prevalence of thrombus [41 (80.4%) vs. 64 (62.7%), p=0.028], lipid plaque [39 (76.5%) vs. 50 (49.0%), p&lt;0.001], TCFA [20 (39.2%) vs. 14 (13.7%), p=0.001], and a higher maximum lipid arc [median [IQR] 250.0° (177.5°-290.0°) vs. 190.0° (150.0°-260.0°), p=0.018) at the culprit lesion compared with PE without MØI. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p=0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression model, PE with MØI [HR=2.95, 95% CI (1.09–8.02), p=0.034] was an independent predictor of MACEs. Conclusion Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with a more aggressive phenotype of coronary atherosclerosis with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up. These findings are of the utmost importance in the era of precision medicine because clearly show that macrophage infiltrates may identify patients with a higher cardiovascular risk requiring more aggressive secondary prevention therapies and a closer clinical follow-up. Prognosis Funding Acknowledgement Type of funding source: None

scholarly journals Potential relationship between high wall shear stress and plaque rupture that cause acute coronary syndrome: insights from optical coherence tomography based computational fluid dynamic simulation

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Fukuyama ◽  
H Otake ◽  
F Seike ◽  
H Kawamori ◽  
T Toba ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Shear Stress ◽  
Acute Coronary Syndrome ◽  
Wall Shear Stress ◽  
Plaque Rupture ◽  
Optical Coherence ◽  
Lumen Area ◽  
Segmental Analysis ◽  
Coronary Syndrome ◽  
Fibrous Cap

Abstract Background The direct relationship between plaque rupture (PR) that cause acute coronary syndrome (ACS) and wall shear stress (WSS) remains uncertain. Methods From the Kobe University ACS-OCT registry, one hundred ACS patients whose culprit lesions had PR documented by optical coherence tomography (OCT) were enrolled. Lesion-specific 3D coronary artery models were created using OCT data. Specifically, at the ruptured portion, the tracing of the luminal edge of the residual fibrous cap was smoothly extrapolated to reconstruct the luminal contour before PR. Then, WSS was computed from computational fluid dynamics (CFD) analysis by a single core laboratory. Relationships between WSS and the location of PR were assessed with 1) longitudinal 3-mm segmental analysis and 2) circumferential analysis. In the longitudinal segmental analysis, each culprit lesion was subdivided into five 3-mm segments with respect to the minimum lumen area (MLA) location at the centered segment (Figure. 1). In the circumferential analysis, we measured WSS values at five points from PR site and non-PR site on the cross-sections with PR. Also, each ruptured plaque was categorized into the lateral type PR (L-PR), central type PR (C-PR), and others according to the relation between the site of tearing and the cavity (Figure. 2). Results In the longitudinal 3-mm segmental analysis, the incidences of PR at upstream (UP1 and 2), MLA, and downstream (DN1 and 2) were 45%, 40%, and 15%, respectively. The highest average WSS was located in UP1 in the upstream PR (UP1: 15.5 (10.4–26.3) vs. others: 6.8 (3.3–14.7) Pa, p&lt;0.001) and MLA segment in the MLA PR (MLA: 18.8 (6.0–34.3) vs. others: 6.5 (3.1–11.8) Pa, p&lt;0.001), and the second highest WSS was located at DN1 in the downstream PR (DN1: 5.8 (3.7–11.5) vs. others: 5.5 (3.7–16.5) Pa, p=0.035). In the circumferential analysis, the average WSS at PR site was significantly higher than that of non-PR site (18.7 (7.2–35.1) vs. 13.9 (5.2–30.3) Pa, p&lt;0.001). The incidence of L-PR, C-PR, and others were 51%, 42%, and 7%, respectively. In the L-PR, the peak WSS was most frequently observed in the lateral site (66.7%), whereas that in the C-PR was most frequently observed in the center site (70%) (Figure. 3). In the L-PR, the peak WSS value was significantly lower (44.6 (19.6–65.2) vs. 84.7 (36.6–177.5) Pa, p&lt;0.001), and the thickness of broken fibrous cap was significantly thinner (40 (30–50) vs. 80 (67.5–100) μm, p&lt;0.001), and the lumen area at peak WSS site was significantly larger than those of C-PR (1.5 (1.3–2.0) vs. 1.4 (1.1–1.6) mm2, p=0.008). Multivariate analysis demonstrated that the presence of peak WSS at lateral site, thinner broken fibrous cap thickness, and larger lumen area at peak WSS site were independently associated with the development of the L-PR. Conclusions A combined approach with CFD simulation and morphological plaque evaluation by using OCT might be helpful to predict future ACS events induced by PR. Funding Acknowledgement Type of funding source: None

Abstract 102: Cd98 Modulates Atherosclerotic Plaque Morphology by Regulating Smooth Muscle Cell Proliferation via the P-38 Map Kinase Pathway

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Sara McCurdy ◽  
Yvonne Baumer ◽  
Franz Hess ◽  
William A Boisvert
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Atherosclerotic Plaque ◽  
Necrotic Core ◽  
Plaque Morphology ◽  
Fibrous Cap ◽  
Plaque Area

Smooth muscle cells (SMC) are known to migrate and proliferate to form a stabilizing fibrous cap that encapsulates atherosclerotic plaques. It has been shown that CD98hc, a transmembrane protein with a known role in amino acid transport and integrin signaling, is involved in proliferation and survival of various cell types including SMC. Based on these data, we hypothesized that CD98hc deficiency selectively in SMC would have pathogenic effects on atherosclerosis development and plaque composition. To test this, we utilized mice with SMC-specific deletion of the CD98hc ( CD98hc fl/fl SM22Cre + ) to determine the effects of CD98hc deficiency on SMC function in the context of atherosclerosis. We performed in vitro proliferation and survival/apoptosis assays to investigate the role of CD98hc in the proliferation and survival of primary mouse aortic vascular smooth muscle cells. We found that VSMC isolated from whole aortas of CD98hc -/- animals displayed approximately 60% reduced cell counts compared to control (41 ± 8.2% of control) after 5 days in culture. EdU assays in vivo showed a defect in the ability of CD98hc -/- SMC to proliferate, with 25% reduction in EdU-positive VSMC compared to controls (2.3 ± 0.2% vs 3 ± 0.2%). In addition, caspase-3 staining of SMC in vitro displayed a 41% increase in propensity of CD98hc -/- SMC to undergo apoptosis compared to controls (7.9 ± 0.6% vs 5.6 ± 0.5%). Furthermore, the absence of CD98hc in SMC caused a sharp increase in phosphorylated p-38, which was partially abrogated towards control levels when the cells were treated with PDGF-BB to induce proliferation. Long-term atherosclerosis study using SMC-CD98hc -/- /LDLR -/- mice showed that atherosclerotic plaque morphology was altered with increased necrotic core area (25.8 ± 1.9% vs 10.9 ± 1.6% necrotic core area per plaque area) due to a reduction in infiltration of SMC within the plaque (2.1 ± 0.4% vs 4.3 ± 0.4% SM22α positive area per plaque area) compared to control LDLR -/- mice. These data support an important role for CD98hc and its regulation of p-38 MAP kinase signaling in aortic vascular smooth muscle cell proliferation and survival. We conclude that CD98hc is critical for the formation of fibrous cap that is important in maintaining the stability of atherosclerotic plaque.

Abstract 2559: Reflectance, Fluorescence, and Raman Spectroscopy Identify Features of Vulnerable Atherosclerotic Plaque In Vivo Including a Thin Fibrous Cap, Necrotic Core or Superficial Foam Cells, and Thrombus

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Obrad R Šćepanović ◽  
Maryann Fitzmaurice ◽  
Arnold Miller ◽  
Chae-Ryon Kong ◽  
Ramachandra R Dasari ◽  
...  
Keyword(s):  
Raman Spectroscopy ◽  
Early Detection ◽  
Ex Vivo ◽  
Foam Cells ◽  
Necrotic Core ◽  
Histopathological Analysis ◽  
Artery Wall ◽  
Fibrous Cap ◽  
Vulnerable Plaques

Early detection and treatment of vulnerable atherosclerotic plaques, the lesions most prone to rupture, is critical to reducing patient mortality associated with cardiovascular disease. The combination of reflectance, fluorescence, and Raman spectroscopy - termed multimodal spectroscopy (MMS) - provides complementary and depth-sensitive information about tissue composition. We assessed the hypothesis that MMS can detect morphological features of vulnerable plaque: thin fibrous cap (TFC), necrotic core (NC), superficial foam cells (SFC), intralesional hemorrhage (IH), and thrombus. Methods. In vivo and ex vivo MMS spectra were collected from 12 patients undergoing peripheral vascular surgeries. The data collection was facilitated by means of a novel MMS probe catheter and a portable clinical instrument developed in our laboratory. During carotid endarterectomies, MMS spectra were collected in vivo from the intimal surface of the plaque with the probe held normal to the artery wall. During femoral bypasses, MMS spectra were collected in vivo either through the proximal anastomosis site from the posterior artery wall or adjacent to the incision. A tissue specimen was excised for additional MMS spectral collection ex vivo. Histopathological analysis was performed by a blinded cardiovascular pathologist to assess the vulnerability of each spectrally evaluated tissue site using a quantitative index based on the dimension or severity of the following: TFC, NC, SFC, IH, and thrombus. Across the total set of 76 evaluated tissue locations, MMS is shown to have the ability to detect vulnerability features including a TFC, NC or SFCs, and thrombus. A TFC is detected by measuring the relative amount of collagen assessed by fluorescence, a large NC or SFCs are detected through the combination of beta-carotene absorption and the Raman spectral signature of lipids, and thrombus is detected through its Raman signature. The results indicate that rupture-prone vulnerable plaques could be detected with a sensitivity of 96% and specificity of 72%. In conclusion, these encouraging results will help bring MMS into the clinical arena as a powerful, catheter-based diagnostic technique for early detection of vulnerable plaques.

scholarly journals Studying the Factors of Human Carotid Atherosclerotic Plaque Rupture, by Calculating Stress/Strain in the Plaque, Based on CEUS Images: A Numerical Study

2020 ◽  
Vol 14 ◽  
Author(s):  
Zhenzhou Li ◽  
Yongfeng Wang ◽  
Xinyin Wu ◽  
Xin Liu ◽  
Shanshan Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Principal Stress ◽  
Plaque Rupture ◽  
Maximum Principal Stress ◽  
Intraplaque Hemorrhage ◽  
Pulsatile Blood Flow ◽  
Carotid Artery Plaque ◽  
Fibrous Cap ◽  
Luminal Stenosis

Carotid plaque neovascularization is one of the major factors for the classification of vulnerable plaque, but the axial force effects of the pulsatile blood flow on the plaque with neovessel and intraplaque hemorrhage was unclear. Together with the severity of stenosis, the fibrous cap thickness, large lipid core, and the neovascularization followed by intraplaque hemorrhage (IPH) have been regarded as high-risk features of plaque rupture. In this work, the effects of these factors were evaluated on the progression and rupture of the carotid atherosclerotic plaques. Five geometries of carotid artery plaque were developed based on contrast-enhanced ultrasound (CEUS) images, which contain two types of neovessel and IPH, and geometry without neovessel and IPH. A one-way fluid-structure interaction model was applied to compute the maximum principal stress and strain in the plaque. For that hyper-elastic and non-linear material, Yeoh 3rd Order strain energy density function was used for components of the plaque. The simulation results indicated that the maximum principal stress of plaque in the carotid artery was higher when the degree of the luminal stenosis increased and the thickness of the fibrous cap decreased. The neovessels within the plaque could introduce a 2.5% increments of deformation in the plaque under the pulsatile blood flow pressure. The IPH also contributed to the increased risk of plaque rupture that a gain of stress was 8.983, 14.526, and 34.47 kPa for the plaque with 50, 65, and 75%, respectively, when comparing stress in the plaque with IPH distributed at the middle to the shoulder of the plaque. In conclusion, neovascularization in the plaque could reduce the stability of the plaque by increasing the stress within the plaque. Also, the risk of plaque rupture increased when large luminal stenosis, thin fibrous cap, and IPH were observed.

scholarly journals Optical Coherence Tomography Imaging in Acute Coronary Syndromes

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Takashi Kubo ◽  
Yasushi Ino ◽  
Takashi Tanimoto ◽  
Hironori Kitabata ◽  
Atsushi Tanaka ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
High Resolution ◽  
Acute Coronary Syndromes ◽  
Plaque Rupture ◽  
Vasa Vasorum ◽  
Optical Coherence ◽  
Coronary Syndrome ◽  
Vulnerable Plaques ◽  
Coronary Syndromes

Optical coherence tomography (OCT) is a high-resolution imaging technique that offers microscopic visualization of coronary plaques. The clear and detailed images of OCT generate an intense interest in adopting this technique for both clinical and research purposes. Recent studies have shown that OCT is useful for the assessment of coronary atherosclerotic plaques, in particular the assessment of plaque rupture, erosion, and intracoronary thrombus in patients with acute coronary syndrome. In addition, OCT may enable identifying thin-cap fibroatheroma, the proliferation of vasa vasorum, and the distribution of macrophages surrounding vulnerable plaques. With its ability to view atherosclerotic lesions in vivo with such high resolution, OCT provides cardiologists with the tool they need to better understand the thrombosis-prone vulnerable plaques and acute coronary syndromes. This paper reviews the possibility of OCT for identification of vulnerable plaques in vivo.

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