Differentiation of Vulnerable Carotid Plaques by Analysis of Calcium Content and Spectral Curve Slope using Gemstone Spectral Imaging

Author(s):  
Ze-Xin Fan ◽  
Xiao-Qing Li ◽  
Ting-Ting Yang ◽  
Shao-Jie Yuan ◽  
Tian-Tong Niu ◽  
...  

Abstract Growing evidence indicates that vulnerable carotid plaque rupture is an important cause of stroke. However, fewer studies have been conducted to investigate the role of a novel gemstone spectral imaging (GSI) in assessment of vulnerable carotid plaque. In this study, we analyzed GSI data including calcium content of carotid atherosclerotic plaque and spectral curve slope, as well as serum high-sensitivity C-reactive protein (Hs-CRP), monocyte chemotactic protein-1 (MCP-1) levels in patients with carotid atherosclerotic plaque using the GSI-computed tomographic angiography (CTA) and immunoturbidimetry. The patients with unstable plaques demonstrated a significantly lower calcium content and higher spectral curve slope than the stable plaques group. In addition, the patients with unstable plaque showed an increase in Hs-CRP levels and MCP-1 levels compared with the stable plaque and normal controls (NC) group. The alternation in GSI calcium content and spectral curve slope reflects a close link between calcification and plaque instability, while derangement of Hs-CRP and MCP-1 is involved in the formation or development of vulnerable plaques. Taken together, our results strongly support the feasibility of using these serological and newly discovered imaging parameters as multiple potential biomarkers relevant to plaque vulnerability or stroke progression.

Author(s):  
Zheyang Wu ◽  
Chun Yang ◽  
Dalin Tang

It has been hypothesized that mechanical risk factors may be used to predict future atherosclerotic plaque rupture. Much progress has been made in computational modeling, medical imaging, and mechanical analysis for atherosclerotic plaque vulnerability assessment in recent years [1–2]. However, truly predictive methods to predict plaque rupture are currently lacking in the literature and practice. In this paper, we introduce a procedure using computational and statistical models based on serial magnetic resonance imaging (MRI) to quantify sensitivity and specificity of mechanical predictors and their combinations to identify the best candidate for rupture prediction. Serial MRI of carotid plaque from a patient with follow-up scan showing ulceration (rupture) was acquired and the actual appearance of ulceration was used as “gold standard” and validation for the predictive method.


2020 ◽  
Vol 21 (24) ◽  
pp. 9387
Author(s):  
Iraide Alloza ◽  
Andrea Salegi ◽  
Jorge Mena ◽  
Raquel Tulloch Navarro ◽  
César Martin ◽  
...  

Carotid atherosclerotic plaque rupture can lead to cerebrovascular accident (CVA). By comparing RNA-Seq data from vascular smooth muscle cells (VSMC) extracted from carotid atheroma surgically excised from a group of asymptomatic and symptomatic subjects, we identified more than 700 genomic variants associated with symptomatology (p < 0.05). From these, twelve single nucleotide polymorphisms (SNPs) were selected for further validation. Comparing genotypes of a hospital-based cohort of asymptomatic with symptomatic patients, an exonic SNP in the BIRC6 (BRUCE/Apollon) gene, rs35286811, emerged as significantly associated with CVA symptomatology (p = 0.002; OR = 2.24). Moreover, BIRC6 mRNA levels were significantly higher in symptomatic than asymptomatic subjects upon measurement by qPCR in excised carotid atherosclerotic tissue (p < 0.0001), and significantly higher in carriers of the rs35286811 risk allele (p < 0.0001). rs35286811 is a proxy of a GWAS SNP reported to be associated with red cell distribution width (RDW); RDW was increased in symptomatic patients (p < 0.03), but was not influenced by the rs35286811 genotype in our cohort. BIRC6 is a negative regulator of both apoptosis and autophagy. This work introduces BIRC6 as a novel genetic risk factor for stroke, and identifies autophagy as a genetically regulated mechanism of carotid plaque vulnerability.


Author(s):  
Zhongzhao Teng ◽  
Xueying Huang ◽  
Chun Yuan ◽  
Gador Canton ◽  
Fei Liu ◽  
...  

Carotid atherosclerotic plaque (CAP) may rupture without warning and cause acute cardiovascular syndromes such as stroke, which is the No.3 killer in USA and a leading cause of serious disabilities. Available screening and diagnosis techniques are insufficient to identify those victims before the event occurs. Noninvasive methods to identify new and emerging biomarkers to assess plaque vulnerability and predict possible rupture before the fatal event are urgently called for.


2017 ◽  
Vol 26 (7) ◽  
pp. 1535-1540 ◽  
Author(s):  
Yuki Shinohara ◽  
Makoto Sakamoto ◽  
Keita Kuya ◽  
Junichi Kishimoto ◽  
Eijiro Yamashita ◽  
...  

Stroke ◽  
2021 ◽  
Author(s):  
Russell Yanofsky ◽  
Carina Sancho ◽  
Karina Gasbarrino ◽  
Huaien Zheng ◽  
Robert J. Doonan ◽  
...  

Background and Purpose: Unstable carotid plaques are a common cause of ischemic strokes. Identifying markers that reflect/contribute to plaque instability has become a prominent focus in cardiovascular research. The adipokines, resistin and chemerin, and ChemR23 (chemerin receptor), may play a role in carotid atherosclerosis, making them potential candidates to assess plaque instability. However, the expression and interrelationship of resistin and chemerin (and ChemR23) protein and mRNA within the carotid atherosclerotic plaque remains elusive. Thus, we investigated herein, the association between plaque mRNA and protein expression of resistin and chemerin (and ChemR23) and carotid plaque instability in humans, and whether sex differences exist in the relationship between these adipokines and plaque instability. Methods: Human carotid plaques were processed for immunohistochemical/mRNA analysis of resistin, chemerin, and ChemR23. Plaque instability was assessed by gold-standard histological classifications. A semi-quantitative scoring system was used to determine the intensity of adipokine expression on macrophages/foam cells, as well as the percentage of inflammatory cells stained positive. Plaque adipokine protein expression was also digitally quantified and mRNA expression was assessed by qRT-PCR. Results: Resistin and chemerin mRNA expression was 80% and 32% lower, respectively, in unstable versus stable plaques ( P <0.05), while no difference in ChemR23 mRNA expression was observed. In contrast, greater resistin staining intensity and percentage of cells stained positive were detected in unstable versus stable plaques ( P <0.01). Similarly, chemerin and ChemR23 staining intensity and percentage of cells stained were positively associated with plaque instability ( P <0.05). No strong sex-specific relationship was observed between adipokines and plaque instability. Conclusions: This study examined the relationship between resistin, chemerin, and ChemR23, and carotid plaque instability, with a specific analysis at the plaque level. We reported a positive association between plaque instability and protein levels of resistin, chemerin, and ChemR23 but a negative association with resistin and chemerin mRNA expression. This suggests these adipokines exert proinflammatory roles in the process of carotid atherosclerosis and may be regulated via a negative feedback regulatory mechanism.


2020 ◽  
Vol 134 (2) ◽  
pp. 169-192
Author(s):  
Sneha Raju ◽  
Jason E. Fish ◽  
Kathryn L. Howe

Abstract Stroke is the leading cause of serious disability in the world and a large number of ischemic strokes are due to thromboembolism from unstable carotid artery atherosclerotic plaque. As it is difficult to predict plaque rupture and surgical treatment of asymptomatic disease carries a risk of stroke, carotid disease continues to present major challenges with regard to clinical decision-making and revascularization. There is therefore an imminent need to better understand the molecular mechanisms governing plaque instability and rupture, as this would allow for the development of biomarkers to identify at-risk asymptomatic carotid plaque prior to disease progression and stroke. Further, it would aid in creation of therapeutics to stabilize carotid plaque. MicroRNAs (miRNAs) have been implicated as key protagonists in various stages of atherosclerotic plaque initiation, development and rupture. Notably, they appear to play a crucial role in carotid artery thromboembolism. As the molecular pathways governing the role of miRNAs are being uncovered, we are learning that their involvement is complex, tissue- and stage-specific, and highly selective. Notably, miRNAs can be packaged and secreted in extracellular vesicles (EVs), where they participate in cell–cell communication. The measurement of EV-encapsulated miRNAs in the circulation may inform disease mechanisms occurring in the plaque itself, and therefore may serve as sentinels of unstable plaque as well as therapeutic targets.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yu Wang ◽  
Bohong Li ◽  
Yong Jiang ◽  
Runhua Zhang ◽  
Xia Meng ◽  
...  

Background and Aims: YKL-40, an inflammatory biomarker, has been reported to be involved in the process and progression of atherosclerosis. Several studies have investigated the association between YKL-40 and plaque and suggested YKL-40 might be a potential biomarker for plaque instability. This study aimed to investigate the association between YKL-40 and carotid plaque instability.Methods: Based on a community-based study in Beijing from February 2014 to May 2016, 1,132 participants with carotid plaques were enrolled in this study. Data on demographics and medical history were collected through face-to-face interviews, and fasting blood samples were collected and stored. We used ultrasound to evaluate the presence of carotid plaque and its instability. The level of YKL-40 was measured by enzyme-linked immunosorbent assay (ELISA). Multivariate logistic regression analysis was performed to investigate the association between YKL-40 level and carotid atherosclerotic plaque instability.Results: The mean age of the 1,132 participants was 58.0 (52.0–64.0) years, and 560 (49.5%) were male. Unstable plaques were detected in 855 (75.53%) participants. YKL-40 level was classified into four groups according to its quartile: quartile 1: &lt;25.47 ng/mL, quartile 2: 25.47–39.53 ng/mL, quartile 3: 39.53–70.55 ng/mL, quartile 4: ≥70.55 ng/mL. After adjusting for age, sex, smoking, alcohol drinking, medical history, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, homocysteine, high-sensitivity C-reactive protein, and plaque thickness, the top quartiles of YKL-40 level were significantly associated with unstable plaque (quartile 3: OR 2.10, 95% CI 1.29–3.40; quartile 4: OR 1.70, 95% CI 1.04–2.80).Conclusion: This study found that YKL-40 was associated with carotid plaque instability determined by ultrasound. Individuals with high YKL-40 may have a higher risk of unstable carotid plaque.


2012 ◽  
Vol 23 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Arihito Tsurumi ◽  
Yuko Tsurumi ◽  
Osamu Hososhima ◽  
Noriaki Matsubara ◽  
Takashi Izumi ◽  
...  

2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  

Pathological angiogenesis is a critical contributor to atherosclerotic plaque rupture. However, there are few effective theranostic strategies to stabilize plaques by suppressing neovascularization. A polymeric nanosystem using 3 nm manganese...


Sign in / Sign up

Export Citation Format

Share Document