scholarly journals Possibilities of Ultrasound Dopplerography in Detecting Instability of Atherosclerotic Plaque of Carotid Arteries

2019 ◽  
Vol 6 (3) ◽  
pp. 36-43
Author(s):  
D. E. Zaitsev ◽  
G. E. Trufanov

Background. Studying the possibilities of ultrasound diagnosis of atherosclerotic lesions of the carotid arteries to determine the treatment tactics of patients with various types of atherosclerotic plaques.Objective. Assessment of the possibilities of ultrasonic triplex research in identifying signs of instability of atherosclerotic plaques of the carotid arteries.Design and methods. The study included 360 patients aged from 28 to 95 years old who were admitted to the St. Petersburg State Budgetary Health Institution “Mariinskaya Hospital” with diagnoses of transient ischemic attack and acute cerebrovascular accident. All patients underwent an ultrasound visualization of the brachiocephalic arteries. Results. Most patients had atherosclerotic plaques of the carotid arteries with a stenosis of up to 75 % and had signs of instability with varying degrees of severity (according to triplex ultrasound). However, it was not possible to reliably assess the presence of hemorrhage in the plaque using a single imaging method.Conclusion. The data obtained indicate the complexity and ambiguity of the studied question. Further detailed examination of the signs of atherosclerotic plaque instability is required using various diagnostic imaging techniques.

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Siqin Zhaorigetu ◽  
Chien-An A Hu ◽  
Warren Laskey ◽  
Brian Walton

Background: We recently demonstrated that apolipoprotein L6 (ApoL6) regulates apoptosis and autophagy in atherosclerotic lesions, implying that ApoL6 is an important factor that causes plaque instability and a potential therapeutic target for treating atherosclerosis. To further investigate the role of ApoL6 in atherogenesis in vivo , the expression of ApoL6 was knocked down by the liposome-siRNA strategy in the aorta tissue of ApoE -/- mouse. Methods: Liposomal siRNAs were prepared by using the thin-film hydration method and were labeled with quantum dots (QD). ApoE -/- mice were intravenously injected twice in 1 week with either liposomal control siRNA-QD or liposomal ApoL6 siRNA-QD. We harvested aortic tissue from mice and used immunofluorescence staining to analyze the expression of ApoL6 in atherosclerotic plaque. Results: Immunofluorescence analysis showed that expression of ApoL6 was elevated in the atherosclerotic plaque and partially co-localized with a macrophage marker CD68 in ApoE -/- mouse. The results suggest a link between ApoL6 and macrophages in the pathobiology of atherosclerotic lesions ( Fig. A and B ). Confocal microscopy images showed that liposomal ApoL6 siRNA significantly reduced ApoL6 expression (green punctures) in atherosclerotic plaques as compared with liposomal control siRNA (Fig. C) . Conclusion: We established a silencing model of ApoL6 in cardiovascular system of ApoE -/- mouse using liposome-mediated siRNA delivery system. The intravenous injection of liposomal ApoL6 siRNA silences ApoL6 expression in the aortas of ApoE -/- mice and may protect against the development of atherosclerosis.


Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Xihai Zhao ◽  
Huilin Zhao ◽  
Feiyu Li ◽  
Jie Sun ◽  
Ye Cao ◽  
...  

Introduction Rupture of vulnerable atherosclerotic plaques in the intracranial and extracranial carotid arteries could trigger ischemic stroke. However, the incidence of high risk atherosclerotic lesions in these vascular beds is not well known. This study sought to investigate the incidence of high risk atherosclerotic lesions in intracranial and extracranial carotid arteries in stroke patients using magnetic resonance (MR) imaging. Methods Seventy-five patients (mean age 62.7 years, 56 males) with acute ischemic stroke underwent MR imaging for index carotid arteries, assigned as the same side as the brain lesions, with a Philips 3.0T MR scanner. Intracranial carotid MR angiography was performed using 3D TOF sequence with FOV of 23 × 23 cm 2 , matrix of 256 × 256, and a slice thickness of 1mm. The multi-contrast vessel wall images (3D TOF, T1W, T2W, and MP-RAGE) were acquired for extracranial carotid arteries with FOV of 14 × 14 cm 2 , matrix of 256 × 256, and slice thickness of 2 mm. The intracranial artery includes middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA). The extracranial carotid artery was divided into internal carotid artery (ICA), bulb, and common carotid artery (CCA). Luminal stenosis for each intracranial and extracranial carotid segment was measured and graded (normal or mild = 0-29%, moderate =30-69%, severe=70-99%). Normalized wall index (NWI = wall area/total vessel area × 100%), and presence/absence of calcification, lipid-rich necrotic core (LRNC), and intraplaque hemorrhage (IPH) and/or fibrous cap rupture in each extracranial carotid segment were determined. Results MCAs developed more severe stenotic lesions (24.6%), followed by extracranial carotids (16.5%), PCAs (5.4%), and ACAs (4.1%) in stroke patients ( Figure 1 A). For extracranial carotid arteries, ICAs showed the largest plaque burden as measured by NWI (44.3%±13.1%), followed by bulbs (39.4%±13%), and CCAs (37%±6.8%). Compared to CCAs, ICAs and bulb regions had more LRNCs (38.4% and 49.3% for ICA and bulb respectively) and IPH and/or rupture (11% and 9.6% for ICA and bulb respectively) ( Figure 1 B). Conclusions In patients with acute ischemic stroke, high risk atherosclerotic plaques can be found in both intracranial and extracranial carotid arteries, particularly in the MCA, ICA and bulb regions. Compared to extracranial carotid arteries, intracranial arteries develop more high risk lesions. The findings of this study suggest the necessity for early screening to detect high risk atherosclerotic lesions in these carotid vascular beds prior to cerebravascular events.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mihaela G Ionita ◽  
Gerard Pasterkamp ◽  
Dominique deKleijn

Objectives : Atherosclerosis is a chronic, complex inflammatory process and is the underlying cause of stroke and myocardial infarction due to rupture of the atherosclerotic plaque leading to acute occlusion of the artery in the brain or heart. Macrophages, infiltrating atherosclerotic lesions, abundantly express Mrp8 and Mrp14. Recently Mrp8, Mrp14 and the complex Mrp8/14 have been identified as endogenous ligands of Tlr-4.The role of Tlr-4 in the development and progression of the atherosclerotic plaque is well recognized and it is associated with a rupture-prone plaque phenotype. Expression of Mrps in human plaques and its relation to plaque phenotype is unknown. For this, we investigated the levels of Mrp8, Mrp14 and Mrp8/14 complex in a large number of human atherosclerotic plaques. Methods and results : Mrp8, Mrp14 and Mrp8/14 were quantified by ELISAs in human carotid endarterectomy specimens (186 patients) and plaque phenotype was determined by immunohistochemistry. Mrp levels were higher in the unstable (58 fibro-atheromatous, 64 atheromatous) compared to the stable (64 fibrous) plaques: Mrp8 p = 0.001 ; Mrp14 p = 0.001 ; Mrp8/14 p = 0.01 . Concomitantly, Mrp8, Mrp14 and Mrp8/14 were associated with characteristics of unstable plaques: more macrophages ( p = 0.024; p = 0.002; p = 0.076 ), less smooth muscle cells ( p = 0.041; p = 0.001; p = 0.074 ), larger lipid core ( p = 0.001; p = 0.001; p=0.004 ), less collagen ( p = 0.440; p = 0.011; p = 0.372 ). Furthermore, Mrp plaque levels were positively correlated with the pro-inflammatory cytokines (IL-6 and IL-8) and matrix metalloproteinsases (MMP2, MMP8 and MMP9) plaque levels. EDA, marker of stable plaques, was negatively associated with Mrps plaque levels. Histological analysis revealed that Mrps are expressed by a subgroup of plaque macrophages localized in the plaque cap and shoulder, the most rupture-prone sites of an atherosclerotic plaque. Conclusions: We show that Mrp8, Mrp14 and Mrp8/14 are strongly associated with the histological characteristics and inflammatory status of human rupture-prone plaques and identify Mrps as a potential marker for rupture-prone plaques.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Z Mamasaidov ◽  
A K Baatyrbekova ◽  
M T Duishenalieva ◽  
S T Ryskulova ◽  
S S H Mamasaidova ◽  
...  

Abstract Objective To study the association of serum cytokine concentrations (tumor necrosis factor-alpha (TNF-a) and interleukin-10 (IL-10)) with ultrasonic characteristics of atherosclerotic plaque and signs of its instability. Materials and methods We examined 166 patients (mean age 56.3±6.1 years). We used the generally accepted classification of Gray-Weale AC et al.(1988) to describe the structural characteristics of atherosclerotic plaque (ASP) and to determine local hemodynamic defects. There were 3 groups of patients. The 1st group included 48 patients with homogeneous hyperechoic plaques, the 2nd group included 56 patients with predominantly hyperechoic ASP (more than 50% of sites), the 3rd group included 13 patients with anechoic, low ultrasound density of ASP or with predominantly hypoechoic average density ASP (more than 50% of sites with average density). The control group consisted of 39 patients with essential hypertension (EH) without atherosclerotic lesions of the carotid arteries. All patients were subjected to general clinical examinations (measuring height, weight, waist, systolic and diastolic blood pressure, calculating body mass index), laboratory tests (lipid profile, fasting glucose, creatinine with glomerular filtration rate (eGFR), fibrinogen, TNF-a and IL-10). Mass determination of TNF-a and IL-10 was carried out by the method of enzyme-linked immunosorbent assay and ultrasound doppler sonography of the carotid arteries, common carotid artery scanned in longitudinal section using a wideband linear sensor with a frequency of 3–11 MHz, the image was synchronized with the R wave on the ECG). Results Patients of the 1st (7,26±0,64 pg/ml) and 2nd groups (8,93±0,98 pg/ml) who do not have ultrasonic signs of ASP instability TNF-a was significantly lower than in patients of the 3rd group (10,51±2,23 pg/ml, p<0,001) with ultrasound signs of ASP instability. Similar results were obtained in terms of the level of IL-10. The level of IL-10 in patients of the 1st and 2nd groups, having reached 14,7±3,5 pg/ml and 14,4±2,7 pg/ml, was significantly lower in comparison with patients of the 3rd group (17,1±5,3 pg/ml, p<0,025 and p<0,017, respectively). The logistic regression analysis showed that the independent factors associated with the presence of ultrasonic signs of ASP instability in patients with EH are: age (HR-1,20; 95% CI 1,03–1,38; p<0,02), concentration of triglycerides (HR-4,05; 95% CI 1,90–8,64; p<0,001) and TNF-a (HR-2,72; 95% CI 1,44–5,15; p<0,02). The influence of other factors, including IL-10, on the instability of ASP was less significant (p>0,05). Further statistical analysis showed that in patients with level of TNF-a more than 10 pg/ml, the risk of detecting an unstable ASP increased almost in 7 times (HR 6,81; 95% CI 2,17–21,6). Conclusions Increasing the concentration of tumor necrosis factor-alpha above 10 pg/ml is an independent risk factor for unstable atherosclerotic plaques in patients with essential hypertension


2020 ◽  
Vol 21 (11) ◽  
pp. 3946 ◽  
Author(s):  
Wioletta Olejarz ◽  
Dominika Łacheta ◽  
Grażyna Kubiak-Tomaszewska

Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases responsible for tissue remodeling and degradation of extracellular matrix (ECM) proteins. MMPs may modulate various cellular and signaling pathways in atherosclerosis responsible for progression and rupture of atherosclerotic plaques. The effect of MMPs polymorphisms and the expression of MMPs in both the atherosclerotic plaque and plasma was shown. They are independent predictors of atherosclerotic plaque instability in stable coronary heart disease (CHD) patients. Increased levels of MMPs in patients with advanced cardiovascular disease (CAD) and acute coronary syndrome (ACS) was associated with future risk of cardiovascular events. These data confirm that MMPs may be biomarkers in plaque instability as they target in potential drug therapies for atherosclerosis. They provide important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification.


Author(s):  
D. E. Zaitsev ◽  
A. S. Lepekhina ◽  
G. E. Trufanov

Aim. To assess the ultrasonography role for diagnosis of atherosclerotic lesions of the extracranial carotid arteries.Material and methods. The study was conducted on the basis of the St. Petersburg Mariinsky Hospital. A total of 855 patients who were admitted to the regional vascular center due to ischemic stroke or transient ischemic attack were examined. The mean age of the patients was 68 years (min 18, max 107). All patients underwent ultrasound of the carotid arteries.Results. In 570 (66,6%) patients with neurological symptoms (according to clinical and neurological examination), hemodynamically insignificant carotid artery lumen stenosis up to 70-75% was revealed. Ultrasound imaging in all patients revealed signs of atherosclerotic plaque (ASP) instability in various combinations, except for hemorrhage. It was not possible to clearly visualize the finished hemorrhage in the ASP structure.Conclusion. Despite the high informative value of ultrasound, it is not possible to answer all clinical questions with its single use. At the moment, there is no classification of instability signs, reflecting the ASP embolism risk. It needs for paternal change the management of asymptomatic patients. More detailed study of ASP destabilization using various visualization methods is necessary.


2017 ◽  
Vol 95 (1) ◽  
pp. 51-56
Author(s):  
Evgeniy A. Praskurnichiy ◽  
I. I. Aleksandrova ◽  
T. V. Kostycheva ◽  
A. N. Knyazev

Aim. To study the character, prevalence, and typological structure of atherosclerotic changes in major arteries by multislice computed tomography in patients with various metabolic disorders. Material and Methods: Carotid arteries of 78 patients with metabolic syndrome or type 2 diabetes mellitus and without carbohydrate metabolism disorders were examined by multislice computed tomography. Results: The study revealed various types of atherosclerotic plaques differing in the composition of lipid, lipid-fibrotic and calcium components. The latter were especially well expressed in diabetes. Conclusion. All types of atherosclerotic plaques are roughly equally represented in the structure of atherosclerotic lesions of carotid arteries in patients with metabolic syndrome in the absence of type 2 diabetes. Diabetic patients had vascular lesions with especially high density of atherosclerotic plaques.


2021 ◽  
Author(s):  
Paula González-López ◽  
Carla Ares-Carral ◽  
Andrea R. López-Pastor ◽  
Jorge Infante-Menéndez ◽  
Tamara Gonzalez-Illanes ◽  
...  

Abstract Background: Cardiovascular diseases (CVDs) are the main cause of death in first world countries, being atherosclerosis, a recurring process underlying their apparition. MicroRNAs (miRNAs) are small non-coding RNAs that modulate the expression of their target proteins. Therefore, they have emerged as key players in diseases like cancer, diabetes, or CVDs.Methods: Apolipoprotein E-deficient (ApoE-/-) mice fed a standard type diet (STD) or high fat diet (HFD) for 8 and 18 weeks was compared to wild type (WT) STD-fed groups for the same time. 18 miRNAs were selected (from pubmed and GEO database) for their possible role in promoting atherosclerosis and were analysed by RT-qPCR in the aorta from the experimental model. Afterwards, the altered miRNAs in the aorta from 18 weeks-ApoE-/- mice were studied in human healthy aortic samples, human early aortic atherosclerotic plaques, and human advanced carotid atherosclerotic plaques. Results: From the 18 miRNAs analyzed, miR-155-5p was overexpressed and miR-143-3p was downregulated in mouse and human atherosclerotic lesions. In addition, a significant decrease of protein kinase B (AKT), target of miR-155-5p, and an increase of insulin-like growth factor type II receptor (IGF-IIR), target of miR-143-3p, were noted in aortic roots from ApoE-/- mice and in carotid plaques from ACA patients. Finally, both miRNAs were studied on vascular endothelial and smooth muscle cell lines. The overexpression of miR-155-5p reduced AKT levels and its phosphorylation in vascular smooth muscle cells. MiR-143-3p overexpression decreased IGF-IIR reducing apoptosis in vascular cells. Conclusions: Our results suggest that miR-155-5p and miR-143-3p may be implicated in insulin resistance and plaque instability by the modulation of their targets AKT and IGF-IIR, contributing to the progression of experimental and human atherosclerosis.Trial Registration: authorization numbers PFS09-007 and PI1442016.


Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Zhong-Song Shi ◽  
Jin-Shan Wang ◽  
Xiang-Song Zhang ◽  
Xiao-Bing Jiang ◽  
Dong-hong Liu ◽  
...  

Purpose: The imaging modality 18 F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET) has been recently used to identify inflammation in the atherosclerotic plaque. Increased uptake of 18 F-FDG in human atherosclerotic plaque on PET may predict plaque vulnerability, however, there is a lack of histological validation for PET imaging. The aim of this study is to evaluate the association of plaque vulnerability with FDG uptake on serial PET/CT scans in a swine model. Methods: Twenty carotid atherosclerotic models was induced in 10 miniswines using partial ligation and high cholesterol diet, and a minimum 70% stenosis was confirmed by carotid angiography. Serial 18 F-FDG PET/CT scans were performed at 0, 4, 8 and 12 weeks. MR scan for imaging-histologic correlation was performed at 12 weeks, and carotid artery sections were obtained for histopathological examination. The atherosclerotic lesions of AHA type IV to VI were defined as advanced plaques. Carotid arteries were evaluated for increased FDG uptake with a maximum standardized uptake value (SUV) and target-to-backgroud ratio (TBR). The association of carotid plaque vulerability with the serial FDG uptake was analyzed. Results: Various stages of atherosclerotic plaques were found in carotid segments from 20 carotid arteries. Most advanced plaque had the feature of vulnerability. FDG uptake in 100 carotid plaques were analyzed. Compared with carotid segments without atherosclerosis, significantly higher FDG uptake was observed in carotid segments with atherosclerosis at 4, 8 and 12 weeks (P<0.001). Mean TBR was significantly higher in advanced plaque group than in early atherosclerosis group at 4, 8 and 12 weeks (P<0.01). Maximum SUV was significantly higher in advanced plaque group than in early atherosclerosis group at 12 weeks (P<0.01), whereas this did not reach statistical significance at 4 and 8 weeks. FDG uptake increased continuously in both groups of advance plaque and early atherosclerosis. Conclusion: Increased plaque metabolism revealed by PET persists with time and is associated with the complexity of carotid atherosclerotic plaque in a swine model. FDG PET/CT may be useful for identification of plaque vulnerability and monitoring the progress of atherosclerotic lesions.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Tiewei Li ◽  
Xiaojuan Li ◽  
Yichuan Feng ◽  
Geng Dong ◽  
Yuewu Wang ◽  
...  

Matrix metalloproteinase-9 (MMP-9) belongs to the MMP family and has been widely investigated. Excessive MMP-9 expression can enhance extracellular matrix degradation and promote plaque instability. Studies have demonstrated that MMP-9 levels are higher in vulnerable plaques than in stable plaques. Additionally, several human studies have demonstrated that MMP-9 may be a predictor of atherosclerotic plaque instability and a risk factor for future adverse cardiovascular and cerebrovascular events. MMP-9 deficiency or blocking MMP-9 expression can inhibit plaque inflammation and prevent atherosclerotic plaque instability. All of these results suggest that MMP-9 may be a useful predictive biomarker for vulnerable atherosclerotic plaques, as well as a therapeutic target for preventing atherosclerotic plaque instability. In this review, we describe the structure, function, and regulation of MMP-9. We also discuss the role of MMP-9 in predicting and preventing atherosclerotic plaque instability.


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