Utility of high-resolution MR imaging to assess fibrous cap thickness, lipid-rich necrotic core and haemorrhage of carotid atheroma

2009 ◽  
Vol 96 (S1) ◽  
pp. 1-1
Author(s):  
U. Sadat ◽  
V. E. Young ◽  
M. J. Graves ◽  
M. E. Gaunt ◽  
K. Varty ◽  
...  
Keyword(s):  
High Resolution ◽  
Mr Imaging ◽  
Necrotic Core ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness

scholarly journals Research on the correlation between activating transcription factor 3 expression in the human coronary artery and atherosclerotic plaque stability

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
J. Peng ◽  
C. Y. Le ◽  
B. Xia ◽  
J. W. Wang ◽  
J. J. Liu ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Necrotic Core ◽  
Inflammatory Factors ◽  
Lesion Group ◽  
Control Group ◽  
Atherosclerotic Plaques ◽  
Activating Transcription Factor 3 ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness ◽  
Activating Transcription Factor

Abstract Background Activating transcription factor 3 (ATF3) is an early response gene that is activated in response to atherosclerotic stimulation and may be an important factor in inhibiting the progression of atherosclerosis. In this study, we directly measured the expression of ATF3 and inflammatory factors in human coronary atherosclerotic plaques to examine the relationship between ATF3 expression, inflammation and structural stability in human coronary atherosclerotic plaques. Methods A total of 68 coronary artery specimens were collected from the autopsy group, including 36 cases of sudden death from coronary heart disease (SCD group) and 32 cases of acute death caused by mechanical injury with coronary atherosclerosis (CHD group). Twenty-two patients who had no coronary heart disease were collected as the control group (Con group). The histological structure of the coronary artery was observed under a light microscope after routine HE staining, and the intimal and lesion thicknesses, thickness of the fibrous cap, thickness of necrosis core, degree of lumen stenosis were assessed by image analysis software. Western blotting and immunohistochemistry were used to measure the expression and distribution of ATF3, inflammatory factors (CD45, IL-1β, TNF-α) and matrix metalloproteinase-9 (MMP-9) and vascular cell adhesion molecule 1 (VCAM1) in the coronary artery. The Pearson correlation coefficient was used to analyse the correlation between ATF3 protein expression and inflammatory factors and between ATF3 protein expression and structure-related indexes in the lesion group. Results Compared with those in the control group, the intima and necrotic core in the coronary artery were thickened, the fibrous cap became thin and the degree of vascular stenosis was increased in the lesion group, while the intima and necrotic core became thicker and the fibrous cap became thinner in the SCD group than in the CHD group (P < 0.05). There was no or low expression of ATF3, inflammatory factors, VCAM1 and MMP-9 in the control group, and the expression of inflammatory factors, VCAM1 and MMP-9 in the SCD group was higher than that in CHD group, while the expression of ATF3 in the SCD group was significantly lower than that in CHD group (P < 0.05). In the lesion group, the expression of ATF3 was negatively correlated with intimal and necrotic focus thickness, positively correlated with fibrous cap thickness (P < 0.01), and negatively correlated with inflammatory factors, VCAM1 and MMP-9 (P < 0.01). Conclusions The expression of ATF3 may be related to the progression and stability of atherosclerotic plaques, and may affect the structural stability of atherosclerotic plaques by regulating the inflammatory response, thus participating in the regulation of atherosclerotic progression.

High-resolution magnetic resonance imaging of carotid atherosclerotic plaques – a correlation study with histopathology

VASA ◽  
2017 ◽  
Vol 46 (4) ◽  
pp. 283-290 ◽  
Author(s):  
Zhangyong Xia ◽  
Hua Yang ◽  
Xiaochun Yuan ◽  
Jiyue Wang ◽  
Shigang Zhang ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
High Resolution ◽  
Vulnerable Plaque ◽  
Vessel Wall ◽  
Necrotic Core ◽  
Resonance Imaging ◽  
Histopathological Findings ◽  
Fibrous Cap ◽  
High Resolution Mri ◽  
Stable Plaque

Abstract. Background: This study aimed to utilize high-resolution magnetic resonance imaging (MRI) to investigate the characteristics of stable and vulnerable carotid arteriosclerotic plaques, with correlations to histopathological findings. Patients and methods: High-resolution MRI was performed in 817 patients, using three-dimensional magnetic resonance angiography. Plaque composition was evaluated by measuring the areas occupied by calcification, a lipid-rich necrotic core, intra-plaque haemorrhage, and fibrous cap rupture. Plaque morphology was analysed by measuring vessel wall area, thickness, and luminal area at the bifurcation of the common carotid artery. Plaque tissues were sampled during carotid endarterectomy and examined using haematoxylin-eosin, Oil Red O, Masson trichrome staining, and immunohistochemical staining for CD68. Results: Patients were divided into stable plaque group (n = 462) and vulnerable plaque group (n = 355), based on intraoperative observations and postoperative histopathological findings. Compared to the stable plaque group, the vulnerable plaque group exhibited increased vessel wall areas and thickness, and decreased mean luminal areas (P < 0.001). The vulnerable plaque group also had a lower collagen content, a higher lipid content, and higher CD68 expression in plaque tissues on histological examinations (P < 0.01). Incidences of lipid-rich necrotic core (38.1 % vs. 34.3 %), intra-plaque haemorrhage (26.9 % vs. 22.8 %), plaque calcification (45.2 % vs. 40.9 %), and fibrous cap rupture (36.0 % vs 39.8 %) in the plaques were concordant with MRI observations and histopathological findings (p > 0.05). Conclusions: Stable and vulnerable carotid plaques had different morphologies and compositions. High-resolution MRI can assess such differences qualitatively and quantitatively in vivo and provide guidance for risk stratification and management.

Abstract 13: Macrophage Erk5 Activation Induced by Apoptotic Cells and Statins Promotes Efferocytosis and Inhibits Atherosclerosis Formation

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Kyungsun Heo ◽  
Hannah Cushman ◽  
Chang-Hoon Woo ◽  
Masashi Akaike ◽  
Xin Wang ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Cardiac Risk ◽  
Necrotic Core ◽  
High Cholesterol Diet ◽  
Apoptotic Cells ◽  
Phagocytic Capacity ◽  
Fibrous Cap ◽  
Cell Accumulation ◽  
Fibrous Cap Thickness ◽  
Dying Cells

Backgrounds Defective efferocytosis (phagocytic clearance of dying cells) is critically linked to progression of advanced atherosclerotic lesions. Although it has been well known that efferocytosis is processed by molecules including eat-me and find-me signals, it is unclear how efferocytosis becomes defective in advanced lesion. Methods and Results Here, we found that bone marrow-derived macrophages (BMDM) from macrophage-specific ERK5 knockout (ERK5 fl/fl LysM Cre +/- ; ERK5-MKO) mice reduced mRNA and proteins levels of efferocytosis-related signaling molecules such as Mer-tK, C1qa, C1qb, C1qc, Gas6, Mfg-e8, Thbs1, and Anxa1 compared with BMDM from non-transgenic control (NLC) mice. Interestingly, addition of apoptotic cells and pitavastatin activate ERK5 kinase activity and increase opsonins, eat-me and find-me signals, and phagocytic capacity toward apoptotic cells in normal macrophage, but macrophages from ERK5-MKO failed to respond in this manner. ERK5-MKO crossed to LDLR -/- mice and fed a high cholesterol diet for 16-week accelerated atherosclerosis formation with an increased level of apoptotic cell accumulation and necrotic core formation, which was accompanied by a significant reduction in collagen content and fibrous cap thickness. We also found lower levels of expression for Mfg-e8 and Thbs1 in the advanced necrotic core of ERK5-MKO mice compared to NLC mice. Conclusion Our study shows that apoptotic cells and statins-activated ERK5 plays a key role in coordinating the process of efferocytosis. Our results provide a mechanistic understanding of the clinically well-described cardiac risk of acute atherothrombotic events in advanced lesions. 1

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.

Abstract P408: Mesenchymal Stem Cell-derived Angptl4 Improves Endothelial Permeability And Resolution Of Inflammation In Atherosclerosis

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Dong-im Cho ◽  
Yong Sook Kim ◽  
Youngkeun Ahn
Keyword(s):  
Endothelial Permeability ◽  
Necrotic Core ◽  
Vascular Lesions ◽  
Blue Dye ◽  
Vascular Events ◽  
Vascular Integrity ◽  
Fibrous Cap ◽  
Vascular Stability ◽  
Fibrous Cap Thickness ◽  
Inflammatory Molecules

Objective: Given the fundamental contribution of inflammation to atherosclerosis, we studied the effect of ANGPTL4 in regulating vascular lesions during atherosclerosis. Methods and Results: We analyzed plasma levels of ANGPTL4 and found that acute myocardial infarction (AMI) patients with higher levels of ANGPTL4 had fewer vascular events than did patients with lower ANGPTL4 levels ( p <0.05). Moreover, in AMI patients with heart failure (HF) at admission, the recurrence of HF was lower in patients with a higher level of ANGPTL4. We then investigated the therapeutic application of ANGPTL4 in an atherosclerosis model. Apoe-/- mice fed a high-fat diet were injected with PBS or ANGPTL4 protein (2 μg per mouse, i.p. ) three times per week for 7 weeks. En face staining and mRNA analysis showed that plaque size, necrotic core area, lipid accumulation, and inflammatory molecules were greatly reduced in the ANGPTL4 group. Aortic permeability, measured by leakage of Evans blue dye, was significantly decreased in the ANGPTL4 group. The induction of pro-inflammatory mediators was significantly inhibited in endothelial cells, vascular smooth muscle cells, and macrophages by ANGPTL4 treatment. Endothelial Krüppel-like factor 2 (KLF2) and VE-cadherin were restored to contribute to maintenance of vascular integrity by ANGPTL4 treatment. Elevated levels of circulating leptin, interleukin-6, and interleukin-1β were profoundly reduced. Most importantly, the fibrous cap was significant thicker in the ANGPTL4 group than in the PBS group. Conclusions: ANGPTL4 treatment attenuated atherogenesis, which suggests that targeting vascular stability and inflammation may serve as a novel therapeutic strategy to prevent and treat atherosclerosis. More importantly, ANGPTL4 treatment inhibits necrotic core formation in lesions, leading to the formation of more stable plaques as evidenced by increased fibrous cap thickness.

3284Quantification of macrophage presence and identification of thin-cap fibroatheroma by optical coherence tomography image: histopathological validation study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Fujii ◽  
R Kawakami ◽  
T Imanaka ◽  
H Shibutani ◽  
K Kawai ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Predictive Value ◽  
Vulnerable Plaque ◽  
Necrotic Core ◽  
Macrophage Infiltration ◽  
Optical Coherence ◽  
Signal Attenuation ◽  
Fibrous Cap ◽  
Attenuation Ratio ◽  
Fibrous Cap Thickness

Abstract Background Intracoronary optical coherence tomography (OCT) is thought to be capable of identifying a vulnerable, rupture-prone plaque based on the presence of a thin-cap fibroatheroma (TCFA). Moreover, recent studies have reported that OCT may be able to identify macrophage infiltration of the fibrous cap, a key characteristic of vulnerable plaque. Purpose This study evaluated the accuracy of OCT image for characterizing TCFA and identifying macrophage infiltration in comparison with histopathology. Methods A total of 924 focal plaques in 206 coronary arteries from 78 autopsy hearts were examined to compare OCT and histological images. By histology, 16 plaques (1.7%) were classified as TCFAsthat contained a large necrotic core covered by a thin (<65μm) fibrous-cap. Correlating OCT-histological sections were identified and OCT-derived tissue property indexes named normalized standard deviation (NSD) and signal attenuation ratio were applied on the fibrous-cap to identify inflamed fibrous-cap defined as a macrophage percentage >10% by histology. Results With histology as standard, the sensitivity, specificity, and negative-predictive-value of TCFAs were extremely high (more than 90%). However, the positive-predictive-value of TCFAs was only 32%, which indicated a high proportion of false-positives. Most false-positive diagnoses of OCT for TCFAs contained large amounts of foam cell accumulations on luminal surface without necrotic core. Twelve of 16 fibrous-caps were considered as inflamed and the remaining 4 were non-inflamed on histology. However, no significant difference in NSD and signal attenuation ratio were identified between them. There was moderate correlation of the fibrous-cap thickness between OCT and histology (r2 = 0.41 and p<0.01). Conclusions OCT is a promising intracoronary imaging modality for differentiating tissue characteristics (fibrous, calcified, or lipid-rich plaque) and identifying TCFA. However, it is still challenging to precisely identify inflammation, fibrous-cap thickness, and necrotic core in the native coronary artery. Therefore, careful interpretation is required to assess coronary vulnerable plaque by OCT. Acknowledgement/Funding None

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