To see the other types of publications on this topic, follow the link: Potentiel de plaque.
Journal articles on the topic 'Potentiel de plaque'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Potentiel de plaque.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Tiengo, Cesare, Jenny Deluca, Anna Belloni-Fortina, Roberto Salmaso, Flavia Galifi, and Mauro Alaibac. "Occurrence of Squamous Cell Carcinoma in an Area of Lichen Simplex Chronicus: Case Report and Pathogenetic Hypothesis." Journal of Cutaneous Medicine and Surgery 16, no. 5 (September 2012): 350–52. http://dx.doi.org/10.1177/120347541201600513.
Full textAbstract:
Background: Lichen simplex chronicus is a common skin disorder characterized by circumscribed, lichenified, pruritic plaque secondary to local repetitive trauma, notably rubbing and scratching. Objective: We describe a case of a squamous cell carcinoma arising in a patient with a long-lasting history of lichen simplex chronicus and discuss the potential role of the microenvironment in predisposing the malignant transformation. Conclusion: Here we propose a hypothesis in which rubbing and scratching contribute to an excess of inflammatory mediators, which in turn may lead to alterations in the processes of keratinocyte proliferation and differentiation. Renseignements de base: Le lichen simplex chronique est une affection cutanée courante caractérisée par une plaque pruritique lichénifiée circonscrite consécutive à des traumatismes locaux répétés, notamment le frottement et le grattage. Objectif: Nous décrivons un cas de carcinome squameux chez un patient présentant depuis longtemps des antécédents de lichen simplex chronique, et nous discutons du rôle potentiel du micro-environnement dans la prédisposition de la transformation maligne. Conclusion: Nous proposons ici une hypothèse selon laquelle le frottement et le grattage contribuent à un excès de médiateurs inflammatoires, lesquels peuvent à leur tour venir modifier les processus de prolifération et de différenciation des kératinocytes.
2
Troquet, J., and Ph Lambin. "Répartition du potentiel électrocinétique imposée par un dipôle de courant excentré dans une plaque conductrice rectangulaire partiellement cloisonnée." Revue de Physique Appliquée 20, no. 6 (1985): 423–35. http://dx.doi.org/10.1051/rphysap:01985002006042300.
Full text
3
Li, Hongbo, Hui Huang, Yun Luan, Niu Liu, Hui Gao, and Huijuan Sun. "Contrast-Enhanced Ultrasonography Characteristics in the Evaluation of Different Nature of Carotid Artery Plaques." Journal of Medical Imaging and Health Informatics 10, no. 3 (March 1, 2020): 688–92. http://dx.doi.org/10.1166/jmihi.2020.2919.
Full textAbstract:
To investigate the value of contrast-enhanced ultrasonography (CEUS) in the evaluation of neovascular density in plaques with different carotid atherosclerosis. 97 patients with carotid plaques were observed by conventional ultrasound from January 2016 to December 2018. The CEUS test was used to grade and quantify the new blood vessels in the plaque. The results showed of the 97 patients with 101 plaques, 49 were soft plaques, 45 were mixed plaques, and 7 were hard plaques. CEUS clearly showed the continuity of plaque fibrous caps and found plaque ulcers that were easily missed by conventional ultrasound. The lower the echo of the plaque, the more obvious contrast enhancement in the plaques. Quantitative analysis of CEUS showed the peak time of soft plaques was shorter and the peak intensity of soft plaques was higher compared with mixed plaques. The difference was statistically significant (P <0.01). The results displayed that carotid CEUS is a convenient and intuitive new technology that can better help analyze plaque morphology and determine and quantify the extent of neovascularization in plaque. It can be used for clinical evaluation of potential cerebrovascular risk and also provides an accurate and reproducible detection method for clinical efficacy evaluation.
4
Hafiane, Anouar. "Vulnerable Plaque, Characteristics, Detection, and Potential Therapies." Journal of Cardiovascular Development and Disease 6, no. 3 (July 27, 2019): 26. http://dx.doi.org/10.3390/jcdd6030026.
Full textAbstract:
Plaque development and rupture are hallmarks of atherosclerotic vascular disease. Despite current therapeutic developments, there is an unmet necessity in the prevention of atherosclerotic vascular disease. It remains a challenge to determine at an early stage if atherosclerotic plaque will become unstable and vulnerable. The arrival of molecular imaging is receiving more attention, considering it allows for a better understanding of the biology of human plaque and vulnerabilities. Various plaque therapies with common goals have been tested in high-risk patients with cardiovascular disease. In this work, the process of plaque instability, along with current technologies for sensing and predicting high-risk plaques, is debated. Updates on potential novel therapeutic approaches are also summarized.
5
Kovanen, P. T. "Mast cells and degradation of pericellular and extracellular matrices: potential contributions to erosion, rupture and intraplaque haemorrhage of atherosclerotic plaques." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 857–61. http://dx.doi.org/10.1042/bst0350857.
Full textAbstract:
Mast cells are present in advanced human atherosclerotic plaques, where they are thought to exert multiple effects on their neighbouring cells and on the extracellular matrix of the plaque. Extensive efforts at delineating their role(s) in atherosclerotic plaques have unravelled mechanisms by which plaque mast cells may render advanced atherosclerotic plaques susceptible to erosion, rupture or intraplaque haemorrhage and so modulate their stability. In these mechanisms, the key effector molecules are mast-cell-derived neutral proteases and pro-inflammatory cytokines. These effector molecules are synthesized and stored in the cytoplasmic secretory granules of mast cells and, once the mast cells are activated to degranulate, are released into the microenvironment surrounding the activated mast cells. In the plaques, the key target cells are endothelial cells and smooth muscle cells and their pericellular matrices. In addition, the various components of the extracellular matrix of the plaques, notably collagen, are degraded when the released mast cell proteases activate matrix metalloproteinases in the plaques. By rendering the plaque susceptible to erosion, to rupture or to intraplaque haemorrhage, the mast cells may contribute to the onset of acute atherothrombotic complications of coronary atherosclerosis, such as myocardial infarction.
6
Tang, Dalin, Chun Yang, Jie Zheng, Pamela K. Woodard, Jeffrey E. Saffitz, Gregorio A. Sicard, Thomas K. Pilgram, and Chun Yuan. "Quantifying Effects of Plaque Structure and Material Properties on Stress Distributions in Human Atherosclerotic Plaques Using 3D FSI Models." Journal of Biomechanical Engineering 127, no. 7 (July 29, 2005): 1185–94. http://dx.doi.org/10.1115/1.2073668.
Full textAbstract:
Background: Atherosclerotic plaques may rupture without warning and cause acute cardiovascular syndromes such as heart attack and stroke. Methods to assess plaque vulnerability noninvasively and predict possible plaque rupture are urgently needed. Method: MRI-based three-dimensional unsteady models for human atherosclerotic plaques with multi-component plaque structure and fluid-structure interactions are introduced to perform mechanical analysis for human atherosclerotic plaques. Results: Stress variations on critical sites such as a thin cap in the plaque can be 300% higher than that at other normal sites. Large calcification block considerably changes stress/strain distributions. Stiffness variations of plaque components (50% reduction or 100% increase) may affect maximal stress values by 20–50 %. Plaque cap erosion causes almost no change on maximal stress level at the cap, but leads to 50% increase in maximal strain value. Conclusions: Effects caused by atherosclerotic plaque structure, cap thickness and erosion, material properties, and pulsating pressure conditions on stress/strain distributions in the plaque are quantified by extensive computational case studies and parameter evaluations. Computational mechanical analysis has good potential to improve accuracy of plaque vulnerability assessment.
7
Teng, Zhongzhao, Aart J. Nederveen, Aad Van der Lugt, Jonathan H. Gillard, and Lambert Speelman. "MRI-based biomechanical parameters for carotid artery plaque vulnerability assessment." Thrombosis and Haemostasis 115, no. 03 (2016): 493–500. http://dx.doi.org/10.1160/th15-09-0712.
Full textAbstract:
SummaryCarotid atherosclerotic plaques are a major cause of ischaemic stroke. The biomechanical environment to which the arterial wall and plaque is subjected to plays an important role in the initiation, progression and rupture of carotid plaques. MRI is frequently used to characterize the morphology of a carotid plaque, but new developments in MRI enable more functional assessment of carotid plaques. In this review, MRI based biomechanical parameters are evaluated on their current status, clinical applicability, and future developments. Blood flow related biomechanical parameters, including endothelial wall shear stress and oscillatory shear index, have been shown to be related to plaque formation. Deriving these parameters directly from MRI flow measurements is feasible and has great potential for future carotid plaque development prediction. Blood pressure induced stresses in a plaque may exceed the tissue strength, potentially leading to plaque rupture. Multi-contrast MRI based stress calculations in combination with tissue strength assessment based on MRI inflammation imaging may provide a plaque stress-strength balance that can be used to assess the plaque rupture risk potential. Direct plaque strain analysis based on dynamic MRI is already able to identify local plaque displacement during the cardiac cycle. However, clinical evidence linking MRI strain to plaque vulnerability is still lacking. MRI based biomechanical parameters may lead to improved assessment of carotid plaque development and rupture risk. However, better MRI systems and faster sequences are required to improve the spatial and temporal resolution, as well as increase the image contrast and signal-to-noise ratio.
8
Biasi, Giorgio M., Paolo M. Mingazzini, Lucia Baronio, Maria Rosa Piglionica, Stefano A. Ferrari, Tarek S. Elatrozy, and Andrew N. Nicolaides. "Carotid Plaque Characterization Using Digital Image Processing and its Potential in Future Studies of Carotid Endarterectomy and Angioplasty." Journal of Endovascular Therapy 5, no. 3 (August 1998): 240–46. http://dx.doi.org/10.1177/152660289800500309.
Full textAbstract:
Purpose: To corroborate the validity of a computerized methodology for evaluating carotid lesions at risk for stroke based on plaque echogenicity. Methods: The records of 96 carotid endarterectomy patients (59 men; median age 69.5 years, range 52 to 83) with stenoses > 50% were studied retrospectively. Forty-one patients (43%) had been symptomatic preoperatively. All patients had undergone computed tomography (CT) to detect infarction in the carotid territory and a duplex scan to measure carotid stenosis. Plaque echogenicity was analyzed by computer, expressing the echodensity in terms of the gray scale median (GSM). The incidence of CT-documented cerebral infarction was analyzed in relation to symptomatology, percent stenosis, and echodensity. Results: Symptoms correlated well with CT evidence of brain infarction: 32% of symptomatic patients had a positive CT scan versus 16% for asymptomatic plaques (p = 0.076). The mean GSM value was 56 ± 14 for plaques associated with negative CT scans and 38 ± 13 for plaques from patients with positive scans (p < 0.0001). However, there was no difference in the GSM value between plaques with > or < 70% stenosis. Furthermore, the incidence of CT infarction was 40% in the cerebral territory of carotid plaques with a GSM value < 50 and only 9% in those with a GSM > 50 (p < 0.001). Conclusions: Computerized analysis of plaque echogenicity appears to provide clinically useful data that correlates with the incidence of cerebral infarction and symptoms. This method of analyzing plaque echolucency could be used as a screening tool for carotid stent studies to identify high-risk lesions better suited to conventional surgical treatment.
9
Ma, Wei, Xinyao Cheng, Xiangyang Xu, Furong Wang, Ran Zhou, Aaron Fenster, and Mingyue Ding. "Multilevel Strip Pooling-Based Convolutional Neural Network for the Classification of Carotid Plaque Echogenicity." Computational and Mathematical Methods in Medicine 2021 (August 18, 2021): 1–13. http://dx.doi.org/10.1155/2021/3425893.
Full textAbstract:
Carotid plaque echogenicity in ultrasound images has been found to be closely correlated with the risk of stroke in atherosclerotic patients. The automatic and accurate classification of carotid plaque echogenicity is of great significance for clinically estimating the stability of carotid plaques and predicting cardiovascular events. Existing convolutional neural networks (CNNs) can provide an automatic carotid plaque echogenicity classification; however, they require a fixed-size input image, while the carotid plaques are of varying sizes. Although cropping and scaling the input carotid plaque images is promising, it will cause content loss or distortion and hence reduce the classification accuracy. In this study, we redesign the spatial pyramid pooling (SPP) and propose multilevel strip pooling (MSP) for the automatic and accurate classification of carotid plaque echogenicity in the longitudinal section. The proposed MSP module can accept arbitrarily sized carotid plaques as input and capture a long-range informative context to improve the accuracy of classification. In our experiments, we implement an MSP-based CNN by using the visual geometry group (VGG) network as the backbone. A total of 1463 carotid plaques (335 echo-rich plaques, 405 intermediate plaques, and 723 echolucent plaques) were collected from Zhongnan Hospital of Wuhan University. The 5-fold cross-validation results show that the proposed MSP-based VGGNet achieves a sensitivity of 92.1%, specificity of 95.6%, accuracy of 92.1%, and F1-score of 92.1%. These results demonstrate that our approach provides a way to enhance the applicability of CNN by enabling the acceptance of arbitrary input sizes and improving the classification accuracy of carotid plaque echogenicity, which has a great potential for an efficient and objective risk assessment of carotid plaques in the clinic.
10
Liu, Wu, Jenna May Kim, Benjamin K. Young, Ravinder Nath, Zhe Chen, Roy H. Decker, Melvin A. Astrahan, and Renelle Pointdujour-Lim. "Novel Eye Plaque Designs for Brachytherapy of Iris and Ciliary Body Melanoma and the First Clinical Application." Ocular Oncology and Pathology 5, no. 3 (October 11, 2018): 220–28. http://dx.doi.org/10.1159/000493269.
Full textAbstract:
Background: While traditional eye plaque brachytherapy can be used for the treatment of iris melanoma, it faces challenges of poor patient tolerability due to cornea-plaque touch caused by radius of curvature mismatch and potential dosimetric inaccuracy from incomplete coverage. We present novel plaque designs and the first clinical application of the plaques for iris melanoma. Methods: Two dome-shaped plaques (EP2132 and EP1930) were designed to vault above the cornea to treat tumors of the iris and ciliary body. Image-based treatment planning of the first 2 clinical cases using the EP2132 plaque covered the tumor base plus a 2 mm margin and the involved ciliary body with at least 75 Gy to the tumor apex. Results: The tumors decreased in size following treatment. The patients tolerated the treatment well. There was no adverse event associated with the traditional iris plaques, such as decreased vision, pain, corneal edema, glaucoma, or cataract. Conclusion: The novel dome-shaped plaques for the treatment of iris melanoma provide effective dose distribution, improved surgical maneuverability, and increased tolerability for the patient. This plaque model can be used to treat iris melanoma of various sizes, configurations, and locations, including the ciliary body. The need for a customized plaque platform for each patient is minimized.
11
Lenti, Massimo, Emanuela Falcinelli, Marcella Pompili, Paola De Rango, Valentina Conti, Giuseppe Guglielmini, Stefania Momi, Teresa Corazzi, Giuseppe Giordano, and Paolo Gresele. "Matrix metalloproteinase-2 of human carotid atherosclerotic plaques promotes platelet activation." Thrombosis and Haemostasis 111, no. 06 (2014): 1089–101. http://dx.doi.org/10.1160/th13-07-0588.
Full textAbstract:
SummaryPurified active matrix metalloproteinase-2 (MMP-2) is able to promote platelet aggregation. We aimed to assess the role of MMP-2 expressed in atherosclerotic plaques in the platelet-activating potential of human carotid plaques and its correlation with ischaemic events. Carotid plaques from 81 patients undergoing endarterectomy were tested for pro-MMP-2 and TIMP-2 content by zymography and ELISA. Plaque extracts were incubated with gel-filtered platelets from healthy volunteers for 2 minutes before the addition of a subthreshold concentration of thrombin receptor activating peptide-6 (TRAP-6) and aggregation was assessed. Moreover, platelet deposition on plaque extracts immobilised on plastic coverslips under high shear-rate flow conditions was measured. Forty-three plaque extracts (53%) potentiated platelet aggregation (+233 ± 26.8%), an effect prevented by three different specific MMP-2 inhibitors (inhibitor II, TIMP-2, moAb anti-MMP-2). The pro-MMP-2/TIMP-2 ratio of plaques potentiating platelet aggregation was significantly higher than that of plaques not potentiating it (3.67 ± 1.21 vs 1.01 ± 0.43, p<0.05). Moreover, the platelet aggregation-potentiating effect, the active-MMP-2 content and the active MMP-2/pro-MMP-2 ratio of plaque extracts were significantly higher in plaques from patients who developed a subsequent major cardiovascular event. In conclusion, atherosclerotic plaques exert a prothrombotic effect by potentiating platelet activation due to their content of MMP-2; an elevated MMP-2 activity in plaques is associated with a higher rate of subsequent ischaemic cerebrovascular events.
12
Yanofsky, Russell, Carina Sancho, Karina Gasbarrino, Huaien Zheng, Robert J. Doonan, Fanny Jaunet, Samantha Steinmetz-Wood, John P. Veinot, Chi Lai, and Stella S. Daskalopoulou. "Expression of Resistin, Chemerin, and Chemerin’s Receptor in the Unstable Carotid Atherosclerotic Plaque." Stroke 52, no. 8 (August 2021): 2537–46. http://dx.doi.org/10.1161/strokeaha.120.030228.
Full textAbstract:
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.
13
Ospel, Johanna M., Nishita Singh, Martha Marko, Mohammed Almekhlafi, Dar Dowlatshahi, Josep Puig, Andrew Demchuk, et al. "Prevalence of Ipsilateral Nonstenotic Carotid Plaques on Computed Tomography Angiography in Embolic Stroke of Undetermined Source." Stroke 51, no. 6 (June 2020): 1743–49. http://dx.doi.org/10.1161/strokeaha.120.029404.
Full textAbstract:
Background and Purpose— Embolic stroke of undetermined source (ESUS) constitutes a large proportion of acute ischemic stroke. It is crucial to identify possible stroke etiologies in this patient subgroup to individually tailor secondary stroke prevention strategies. This study aimed to assess the prevalence of carotid plaques causing <50% stenosis in ESUS patients on computed tomography angiography and the association of these plaques with ipsilateral strokes. Methods— Patients from INTERRSeCT—a multicenter prospective study of patients with acute ischemic stroke—were included in this study if their stroke etiology was not large artery atherosclerosis (>50% stenosis), and neck computed tomography angiography was obtained. Degree of stenosis (<30% versus 30%–50%), maximum plaque thickness, degree of plaque calcification (<50% versus ≥50%), plaque irregularity, ulceration, hypodensity, carotid web, and focal vessel outpouching were assessed for both carotid arteries on computed tomography angiography. Prevalence of carotid plaques with <50% stenosis (nonstenotic plaques), ipsilateral and contralateral to the stroke, in ESUS patients was determined and compared with non-ESUS patients. Features of these plaques with versus without ipsilateral stroke in ESUS patients were compared. Uni- and multivariable logistic regression was performed to determine associations between nonstenotic carotid plaque, plaque characteristics, and ipsilateral stroke in ESUS patients. Results— Four hundred forty-six patients were included in the study (median age, 73 years; 218 men), 138 of which were ESUS patients (median age, 70 years; 61 men). Nonstenotic carotid plaques (with <50% stenosis) were present in 54 of 138 (39.1%) ESUS patients. Twelve (8.7%) patients had bilateral carotid plaques. Forty (60.6%) of these plaques were ipsilateral and 26 (39.4%) contralateral to the side of the stroke ( P =0.004). Nonstenotic carotid plaques were significantly associated with ipsilateral strokes (adjusted odds ratio, 1.83 [95% CI, 1.05–3.18]). Conclusions— In patients with ESUS, nonstenotic carotid plaques were significantly more common on the side of the ischemic stroke, suggesting that these plaques could be a potential stroke etiology in patients in whom the ischemic stroke is classified currently as ESUS.
14
Shinohara, Masakazu, Tomoya Yamashita, Hideto Tawa, Masafumi Takeda, Naoto Sasaki, Tomofumi Takaya, Ryuji Toh, et al. "Atherosclerotic plaque imaging using phase-contrast X-ray computed tomography." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H1094—H1100. http://dx.doi.org/10.1152/ajpheart.01149.2007.
Full textAbstract:
Reliable, noninvasive imaging modalities to characterize plaque components are clinically desirable for detecting unstable coronary plaques, which cause acute coronary syndrome. Although recent clinical developments in computed tomography (CT) have enabled the visualization of luminal narrowing and calcified plaques in coronary arteries, the identification of noncalcified plaque components remains difficult. Phase-contrast X-ray CT imaging has great potentials to reveal the structures inside biological soft tissues, because its sensitivity to light elements is almost 1,000 times greater than that of absorption-contrast X-ray imaging. Moreover, a specific mass density of tissue can be estimated using phase-contrast X-ray CT. Ex vivo phase-contrast X-ray CT was performed using a synchrotron radiation source (SPring-8, Japan) to investigate atherosclerotic plaque components of apolipoprotein E-deficient mice. Samples were also histologically analyzed. Phase-contrast X-ray CT at a spatial resolution of 10–20 μm revealed atherosclerotic plaque components easily, and thin fibrous caps were detected. The specific mass densities of these plaque components were quantitatively estimated. The mass density of lipid area was significantly lower (1.011 ± 0.001766 g/ml) than that of smooth muscle area or collagen area (1.057 ± 0.001407 and 1.080 ± 0.001794 g/ml, respectively). Moreover, the three-dimensional assessment of plaques could provide their anatomical information. Phase-contrast X-ray CT can estimate the tissue mass density of atherosclerotic plaques and detect lipid-rich areas. It can be a promising noninvasive technique for the investigation of plaque components and detection of unstable coronary plaques.
15
Van Houte, J., C. Sansone, K. Joshipura, and R. Kent. "In vitro Acidogenic Potential and Mutans Streptococci of Human Smooth-surface Plaque Associated with Initial Caries Lesions and Sound Enamel." Journal of Dental Research 70, no. 12 (December 1991): 1497–502. http://dx.doi.org/10.1177/00220345910700120501.
Full textAbstract:
Samples of human dental plaque were pooled from several "white spot" smooth tooth surface areas as well as from several clinically-sound tooth surface areas in each of 12 caries-positive college students. Each of the two samples from each subject was used for the determination of: (1) pH-lowering potential in vitro involving dispersed plaque suspensions, excess glucose supply, and a 60-minute test, and (2) the proportions of mutans streptococci and lactobacilli. When all subjects were considered, plaques from "white spot" areas, as compared with samples from sound surface areas, were characterized by significantly higher proportions of mutans streptococci, a lower starting ("resting") pH, a faster rate of pH drop between pH 6.0 and 5.0, and a lower minimum pH of the suspension; the lactobacillus proportions were generally very low in both types of plaques. For individual subjects, however, the proportions of mutans streptococci in plaque associated with "white spot" areas showed a wide range (0.001-10.0%), and samples with high as well as low levels of these micro-organisms could exhibit a high rate of pH drop and a low pH minimum. This suggests that, besides mutans streptococci and lactobacilli, other bacteria capable of acidogenesis at a low pH may contribute to the high pH-lowering potential exhibited by many plaques.
16
Rombouts, Miche, Rachid Ammi, Ilse Van Brussel, Lynn Roth, Benedicte Y. De Winter, Sven R. Vercauteren, Jeroen M. H. Hendriks, et al. "Linking CD11b+Dendritic Cells and Natural Killer T Cells to Plaque Inflammation in Atherosclerosis." Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/6467375.
Full textAbstract:
Atherosclerosis remains the leading cause of death and disability in our Western society. To investigate whether the dynamics of leukocyte (sub)populations could be predictive for plaque inflammation during atherosclerosis, we analyzed innate and adaptive immune cell distributions in blood, plaques, and lymphoid tissue reservoirs in apolipoprotein E-deficient (ApoE−/−) mice and in blood and plaques from patients undergoing endarterectomy. Firstly, there was predominance of the CD11b+conventional dendritic cell (cDC) subset in the plaque. Secondly, a strong inverse correlation was observed between CD11b+cDC or natural killer T (NKT) cells in blood and markers of inflammation in the plaque (including CD3, T-bet, CCR5, and CCR7). This indicates that circulating CD11b+cDC and NKT cells show great potential to reflect the inflammatory status in the atherosclerotic plaque. Our results suggest that distinct changes in inflammatory cell dynamics may carry biomarker potential reflecting atherosclerotic lesion progression. This not only is crucial for a better understanding of the immunopathogenesis but also bares therapeutic potential, since immune cell-based therapies are emerging as a promising novel strategy in the battle against atherosclerosis and its associated comorbidities. The cDC-NKT cell interaction in atherosclerosis serves as a good candidate for future investigations.
17
Ledder, Ruth G., Tejal Madhwani, Prem K. Sreenivasan, William De Vizio, and Andrew J. McBain. "An in vitro evaluation of hydrolytic enzymes as dental plaque control agents." Journal of Medical Microbiology 58, no. 4 (April 1, 2009): 482–91. http://dx.doi.org/10.1099/jmm.0.006601-0.
Full textAbstract:
The plaque-control potential of commercially available amylase, lipase and protease was evaluated by observing their effects on coaggregation and on bacterial viability within various plaque microcosms. A quantitative coaggregation assay indicated that protease significantly inhibited the extent of coaggregation of Actinomyces naeslundii and Streptococcus oralis (P <0.05) and of Porphyromonas gingivalis and S. oralis. Amylase significantly (P <0.05) increased the coaggregation of A. naeslundii versus Fusobacterium nucleatum and A. naeslundii versus P. gingivalis. Concomitant challenge of constant-depth film fermenter-grown plaques with the enzymes did not result in detectable ecological perturbations (assessed by differential culture and denaturing gradient gel electrophoresis). Similar dosing and analysis of multiple Sorbarod devices did not reveal increases in bacterial dispersion which could result from disaggregation of extant plaques. A short-term hydroxyapatite colonization model was therefore used to investigate possible enzyme effects on early-stage plaque development. Whilst culture did not indicate significant reductions in adhesion or plaque accumulation, a vital visual assay revealed significantly increased aggregation frequency following enzyme exposure. In summary, although hydrolytic enzymes negatively influenced binary coaggregation, they did not cause statistically significant changes in bacterial viability within plaque microcosms. In contrast, enzyme exposure increased aggregation within extant plaques.
18
Kumric, Marko, Josip A. Borovac, Dinko Martinovic, Tina Ticinovic Kurir, and Josko Bozic. "Circulating Biomarkers Reflecting Destabilization Mechanisms of Coronary Artery Plaques: Are We Looking for the Impossible?" Biomolecules 11, no. 6 (June 14, 2021): 881. http://dx.doi.org/10.3390/biom11060881.
Full textAbstract:
Despite significant strides to mitigate the complications of acute coronary syndrome (ACS), this clinical entity still represents a major global health burden. It has so far been well-established that most of the plaques leading to ACS are not a result of gradual narrowing of the vessel lumen, but rather a result of sudden disruption of vulnerable atherosclerotic plaques. As most of the developed imaging modalities for vulnerable plaque detection are invasive, multiple biomarkers were proposed to identify their presence. Owing to the pivotal role of lipids and inflammation in the pathophysiology of atherosclerosis, most of the biomarkers originated from one of those processes, whereas recent advancements in molecular sciences shed light on the use of microRNAs. Yet, at present there are no clinically implemented biomarkers or any other method for that matter that could non-invasively, yet reliably, diagnose the vulnerable plaque. Hence, in this review we summarized the available knowledge regarding the pathophysiology of plaque instability, the current evidence on potential biomarkers associated with plaque destabilization and finally, we discussed if search for biomarkers could one day bring us to non-invasive, cost-effective, yet valid way of diagnosing the vulnerable, rupture-prone coronary artery plaques.
19
Antonacci, Giuseppe, Ryan M. Pedrigi, Avinash Kondiboyina, Vikram V. Mehta, Ranil de Silva, Carl Paterson, Rob Krams, and Peter Török. "Quantification of plaque stiffness by Brillouin microscopy in experimental thin cap fibroatheroma." Journal of The Royal Society Interface 12, no. 112 (November 2015): 20150843. http://dx.doi.org/10.1098/rsif.2015.0843.
Full textAbstract:
Plaques vulnerable to rupture are characterized by a thin and stiff fibrous cap overlaying a soft lipid-rich necrotic core. The ability to measure local plaque stiffness directly to quantify plaque stress and predict rupture potential would be very attractive, but no current technology does so. This study seeks to validate the use of Brillouin microscopy to measure the Brillouin frequency shift, which is related to stiffness, within vulnerable plaques. The left carotid artery of an ApoE −/− mouse was instrumented with a cuff that induced vulnerable plaque development in nine weeks. Adjacent histological sections from the instrumented and control arteries were stained for either lipids or collagen content, or imaged with confocal Brillouin microscopy. Mean Brillouin frequency shift was 15.79 ± 0.09 GHz in the plaque compared with 16.24 ± 0.15 ( p < 0.002) and 17.16 ± 0.56 GHz ( p < 0.002) in the media of the diseased and control vessel sections, respectively. In addition, frequency shift exhibited a strong inverse correlation with lipid area of −0.67 ± 0.06 ( p < 0.01) and strong direct correlation with collagen area of 0.71 ± 0.15 ( p < 0.05). This is the first study, to the best of our knowledge, to apply Brillouin spectroscopy to quantify atherosclerotic plaque stiffness, which motivates combining this technology with intravascular imaging to improve detection of vulnerable plaques in patients.
20
Evans, Nicholas R., Jason M. Tarkin, Elizabeth PV Le, Rouchelle S. Sriranjan, Andrej Corovic, Elizabeth A. Warburton, and James HF Rudd. "Integrated cardiovascular assessment of atherosclerosis using PET/MRI." British Journal of Radiology 93, no. 1113 (September 1, 2020): 20190921. http://dx.doi.org/10.1259/bjr.20190921.
Full textAbstract:
Atherosclerosis is a systemic inflammatory disease typified by the development of lipid-rich atheroma (plaques), the rupture of which are a major cause of myocardial infarction and stroke. Anatomical evaluation of the plaque considering only the degree of luminal stenosis overlooks features associated with vulnerable plaques, such as high-risk morphological features or pathophysiology, and hence risks missing vulnerable or ruptured non-stenotic plaques. Consequently, there has been interest in identifying these markers of vulnerability using either MRI for morphology, or positron emission tomography (PET) for physiological processes involved in atherogenesis. The advent of hybrid PET/MRI scanners offers the potential to combine the strengths of PET and MRI to allow comprehensive assessment of the atherosclerotic plaque. This review will discuss the principles and technical aspects of hybrid PET/MRI assessment of atherosclerosis, and consider how combining the complementary modalities of PET and MRI has already furthered our understanding of atherogenesis, advanced drug development, and how it may hold potential for clinical application.
21
Ganji, Morsaleh, Valentina Nardi, Megha Prasad, Kyra L. Jordan, Melanie C. Bois, Federico Franchi, Xiang Y. Zhu, et al. "Carotid Plaques From Symptomatic Patients Are Characterized by Local Increase in Xanthine Oxidase Expression." Stroke 52, no. 9 (September 2021): 2792–801. http://dx.doi.org/10.1161/strokeaha.120.032964.
Full textAbstract:
Background and Purpose: XO (xanthine oxidase) is a key enzyme of uric acid metabolism and is thought to contribute to oxidative pathways that promote atherosclerotic plaque progression, yet its role in plaque destabilization is not well elucidated. We hypothesized that XO is expressed in carotid plaque from symptomatic patients in association with cardiovascular risk factors. Methods: Patients were stratified by symptoms, defined as presentation with an ipsilateral cerebral ischemic event. Carotid atherosclerotic plaques were obtained from 44 patients with symptomatic plaque and 44 patients without ischemic cerebral events. Protein expression of XO was evaluated by immunohistochemical staining and the percentage of cells expressing XO and CD68 (macrophage marker) compared between the groups. Biochemical and demographic cardiometabolic risk factors of study participants also were measured. Results: Carotid atherosclerotic plaques from symptomatic patients were associated with significantly higher XO expression versus asymptomatic plaque (median [interquartile range]: 1.24 [2.09] versus 0.16 [0.34]; P <0.001) and with significantly higher circulating uric acid levels (mean±SD: 7.36±2.10 versus 5.37±1.79 mg/dL; P <0.001, respectively). In addition, XO expression in atherosclerotic carotid plaque was inversely associated with serum high-density lipoproteins cholesterol levels ( P =0.010, r =−0.30) and directly with circulating uric acid levels ( P <0.001, r =0.45). The average percentage of macrophages that expressed XO was significantly higher in symptomatic versus asymptomatic plaques (median [interquartile range]: 93.37% [25] versus 46.15% [21], respectively; P <0.001). Conclusions: XO overexpression in macrophages is associated with increased serum uric acid and low high-density lipoproteins cholesterol levels and may potentially have a mechanistic role in carotid plaque destabilization. The current study supports a potential role for uric acid synthesis pathway as a target for management of carotid atherosclerosis in humans.
22
Polonskaya, Yana V., Elena V. Kashtanova, Ivan S. Murashov, Aleksei V. Kurguzov, Evgeny V. Sadovski, Nikolay A. Maslatsov, Ekaterina M. Stakhneva, Alexander M. Chernyavskii, and Yuliya I. Ragino. "The Influence of Calcification Factors and Endothelial-Dysfunction Factors on the Development of Unstable Atherosclerotic Plaques." Diagnostics 10, no. 12 (December 11, 2020): 1074. http://dx.doi.org/10.3390/diagnostics10121074.
Full textAbstract:
Background: This study aimed to evaluate changes in markers of calcification and of endothelial dysfunction during the development of calcification and instability of atherosclerotic plaques and to identify associations of calcification factors with the formation of unstable plaques. Methods: We analyzed 44 male patients with coronary atherosclerosis who underwent endarterectomy in coronary arteries during coronary bypass surgery. The endarterectomy material (intima/media) was examined using histological and biochemical methods, and the stability and calcification degree of atherosclerotic plaques were assessed. In homogenates of the tissue samples and in blood, concentrations of osteoprotegerin, osteocalcin, osteopontin, osteonectin, monocyte-chemoattractant protein type 1 (MCP-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), and E-selectin were determined by enzyme immunoassays. Results: Unstable atherosclerotic plaques proved to be calcified more frequently (80.4% of plaques) than stable ones (45.0%). Osteonectin, E-selectin, and sVCAM-1 levels were lower in unstable plaques and plaques with large calcification deposits. Osteocalcin content increased with the increasing size of the calcification deposits in plaque. Blood osteocalcin concentration directly correlated with osteocalcin concentration in atherosclerotic plaques and was higher in the blood of patients with calcified plaques in coronary arteries. Conclusions: The results provide the basis for further research on the suitability of osteocalcin as a potential biomarker of an unstable calcified atherosclerotic plaque in a coronary artery.
23
Larmann, Jan, Tim Frenzel, Martina Schmitz, Anke Hahnenkamp, Philipp Demmer, Stephan Immenschuh, Uwe J. F. Tietge, Christoph Bremer, and Gregor Theilmeier. "In Vivo Fluorescence-mediated Tomography Imaging Demonstrates Atorvastatin-mediated Reduction of Lesion Macrophages in ApoE-/- Mice." Anesthesiology 119, no. 1 (July 1, 2013): 129–41. http://dx.doi.org/10.1097/aln.0b013e318291c18b.
Full textAbstract:
Abstract Background: Macrophage recruitment into atherosclerotic plaques drives lesion progression, destabilization, and rupture. Chronic statin treatment reduces macrophage plaque content. Information on dynamics of macrophage recruitment would help assessing plaque vulnerability and guiding therapy. Techniques to image macrophage homing to vulnerable plaques in vivo are scarcely available. The authors tested if noninvasive fluorescence-mediated tomography (FMT) can assess plaque-stabilizing effects of short-term high-dosage atorvastatin. Methods: Macrophages from green-fluorescent-protein-transgenic mice were labeled with a near-infrared fluorescent dye and were injected IV in apolipoprotein E-deficient mice (n = 9) on Western diet 7 days after guidewire-injury of the carotid artery. FMT-scans, 2 and 7 days thereafter, quantified macrophage recruitment into carotid artery plaques. Atorvastatin was tested for macrophage adhesion, proliferation, and viability (n = 5 to 6) in vitro. Fourteen mice received atorvastatin or vehicle for 4 days after 16 weeks on Western diet. FMT assessed macrophage recruitment into aortic and innominate artery lesions. Means (±SD)% are reported. Results: Double-labeled macrophages were recruited into carotid artery lesions. FMT resolved fluorescence projecting on the injured carotid artery and detected a signal increase to 300% (±191) after guidewire injury. Atorvastatin reduced macrophage adhesion to activated endothelial cells by 36% (±19). In a clinically relevant proof-of-concept intervention, FMT-imaging detected that 4 days atorvastatin treatment reduced macrophage recruitment by 57% (±8) indicating plaque stabilization. Immunohistochemistry confirmed reduced macrophage infiltration. Conclusions: FMT optical imaging proved its high potential for clinical applicability for tracking recruitment of near-infrared fluorescent-labeled macrophages to vulnerable plaques in vivo. FMT-based quantification of macrophage recruitment demonstrated rapid plaque stabilization by 4-day atorvastatin treatment in apolipoprotein E-deficient mice.
24
Hao, Hiroyuki, Koji Iihara, Hatsue Ishibashi-Ueda, Fumio Saito, and Seiichi Hirota. "Correlation of thin fibrous cap possessing adipophilin-positive macrophages and intraplaque hemorrhage with high clinical risk for carotid endarterectomy." Journal of Neurosurgery 114, no. 4 (April 2011): 1080–87. http://dx.doi.org/10.3171/2010.8.jns10423.
Full textAbstract:
Object Preoperative clinical risk classification of carotid artery (CA) stenosis anticipates the outcome of CA intervention. A higher incidence of neurological morbidity was noted after CA stenting (CAS) in patients with medical risks than in those without risks. However, little is known about the correlation between clinical risks and plaque composition. The purpose of this study was to characterize the CA plaque histology in 3 groups of patients who were classified based on clinical risks for carotid endarterectomy (CEA). Furthermore, the authors examined whether the plaque with high embolic potential after CA intervention, particularly CAS, could be predicted based on clinical risks for CEA. Methods Patients were divided into 4 groups, according to the CEA risk classification system, and 3 groups with more than 10 cases were enrolled in this study as follows: absence of all angiographic, medical, and neurological risks (Grade I, 27 cases); presence of medical risk, but no neurological risk (Grade III, 31 cases); and presence of neurological risk (Grade IV, 17 cases). Histopathological characteristics of CA plaques, including fibrous cap thickness, plaque disruption, thrombus formation, intraplaque hemorrhage (IPH), and adipophilin expression were examined without information regarding clinical status. Results Plaques in patients in Grades III and IV demonstrated a thin fibrous cap and enhanced IPH, compared with those in Grade I. Plaques in patients in Grade IV showed more adipophilin-expressing macrophages in the fibrous cap than in those of the other groups. Conclusions Plaques in Grades III and IV patients were characterized by thin fibrous cap atheroma with IPH. Adipophilin-positive macrophage infiltration in the fibrous cap might be correlated with instability in neurological status. The plaque morphology in patients with medical and neurological risks needs to be examined carefully with the aid of imaging modalities. In plaques demonstrating a thin fibrous cap and IPH, the CAS procedure should be avoided and CEA should be performed instead.
25
Boor, Paul J., Yonzhen Yang, and Bin Gong. "Role of the Media in Vascular Injury: Atherosclerosis and Dissection." Toxicologic Pathology 34, no. 1 (January 2006): 33–38. http://dx.doi.org/10.1080/01926230500369907.
Full textAbstract:
Although a metabolic role for endothelium in toxic injury has been well established, a similar role has not been as thoroughly explored for the vascular media. In this study two forms of vascular medial involvement in toxic injury are examined. Early atherosclerotic plaques are studied by immunohistochemistry for an α class glutathione- S-transferase (GST) isozyme known as hGSTA4-4, which has preferential metabolic activity for α, β-unsaturated aldehydes derived from lipid peroxidation, especially 4-hydroxy-2-nonenal. Findings in human plaque indicate that hGST A4-4 is highly upregulated in vascular smooth muscle cells (VSMCs) within the plaque and in the medial VSMCs underlying plaque. Endothelial cells, while not expressing hGST A4-4 distant from plaques, were found to express the isozyme in cytoplasm overlying plaque. In a series of second experiments, we illustrate a developmental model of dissecting aortic aneurysm (DAA) obtained by administering semicarbazide, an inhibitor of the little-studied VSMC enzyme semicarbazide-sensitive amine oxidase (SSAO), to pregnant rats during the last trimester of development. Newborn rats consistently developed DAA which is characterized by splitting of media of ascending thoracic aorta and extensive blood collections surrounding the vessel. These experimental examples emphasize the potential role of the media in toxic insults to blood vessels. Also, the potential importance of toxic injury to developing blood vessels by in utero exposure to xenobiotic substances is illustrated.
26
Zaragoza, Francisco J., Marion Eichmann, Dirk Flühs, Andrea Wittig, Wolfgang Sauerwein, and Lorenzo Brualla. "Monte Carlo Simulation of the Treatment of Uveal Melanoma Using Measured Heterogeneous 106Ru Plaques." Ocular Oncology and Pathology 5, no. 4 (October 15, 2018): 276–83. http://dx.doi.org/10.1159/000492599.
Full textAbstract:
Background/Aims: Ruthenium plaques are used for the treatment of ocular tumors. The aim of this work is the comparison between simulated absorbed dose distributions tallied in an anthropomorphic phantom, obtained from ideal homogeneous plaques, and real eye plaques in which the actual heterogeneous distribution of 106Ru was measured. The placement of the plaques with respect to the tumor location was taken into consideration to optimize the effectiveness of the treatment. Methods: The generic CCA and CCB, and the specific CCA1364 and CCB1256 106Ru eye plaques were modeled with the Monte Carlo code PENELOPE. To compare the suitability of each treatment for an anterior, equatorial and posterior tumor location, cumulative dose-volume histograms for the tumors and structures at risk were calculated. Results: Eccentric placements of the plaques, taking into account the inhomogeneities of the emitter map, can substantially reduce the dose delivered to structures at risk while maintaining the prescribed dose at the tumor apex. Conclusions: The emitter map distribution of the plaque and the computerized tomography of the patient used in a Monte Carlo simulation allow an accurate determination of the plaque position with respect to the tumor with the potential to reduce the dose to sensitive structures.
27
Cao, Xiao-qing, Xin-xin Liu, Meng-meng Li, Yu Zhang, Liang Chen, Lin Wang, Ming-xue Di, and Mei Zhang. "Overexpression of Prolyl-4-Hydroxylase-α1 Stabilizes but Increases Shear Stress-Induced Atherosclerotic Plaque in Apolipoprotein E-Deficient Mice." Disease Markers 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1701637.
Full textAbstract:
The rupture and erosion of atherosclerotic plaque can induce coronary thrombosis. Prolyl-4-hydroxylase (P4H) plays a central role in the synthesis of all known types of collagens, which are the most abundant constituent of the extracellular matrix in atherosclerotic plaque. The pathogenesis of atherosclerosis is thought to be in part caused by shear stress. In this study, we aimed to investigate a relationship between P4Hα1 and shear stress-induced atherosclerotic plaque. Carotid arteries of ApoE−/− mice were exposed to low and oscillatory shear stress conditions by the placement of a shear stress cast for 2 weeks; we divided 60 male ApoE−/− mice into three groups for treatments with saline (mock) (n=20), empty lentivirus (lenti-EGFP) (n=20), and lentivirus-P4Hα1 (lenti-P4Hα1) (n=20). Our results reveal that after 2 weeks of lenti-P4Hα1 treatment both low and oscillatory shear stress-induced plaques increased collagen and the thickness of fibrous cap and decreased macrophage accumulation but no change in lipid accumulation. We also observed that overexpression of P4Ha1 increased plaque size. Our study suggests that P4Hα1 overexpression might be a potential therapeutic target in stabilizing vulnerable plaques.
28
Pleskovič, Aleš, Sara Mankoč Ramuš, Zala Jenko Pražnikar, Marija Šantl Letonja, Andreja Cokan Vujkovac, Katarina Gazdikova, Martin Caprnda, Ludovit Gaspar, Peter Kruzliak, and Daniel Petrovič. "Polymorphism rs2073618 of the osteoprotegerin gene as a potential marker of subclinical carotid atherosclerosis in Caucasians with type 2 diabetes mellitus." Vasa 46, no. 5 (August 1, 2017): 355–62. http://dx.doi.org/10.1024/0301-1526/a000640.
Full textAbstract:
Abstract. Background: The OPG/RANKL/RANK (osteoprotegerin/receptor-activator of nuclear factor κB ligand/receptor-activator of nuclear factor κB) axis has been recently linked to the development of atherosclerosis and plaque destabilization. We have investigated whether polymorphism rs2073618 of the OPG gene is associated with subclinical markers of carotid atherosclerosis in subjects with type 2 diabetes mellitus (T2DM). Patients and methods: 595 subjects with T2DM were enrolled in the cross-sectional study. Subclinical markers of carotid atherosclerosis (carotid intima media thickness, plaque thickness, and plaques presence) were assessed with ultrasound at the time of recruitment. Genotyping for rs2073618 (a missense variant located in exon I of the OPG gene) was performed, and OPG serum levels were determined by ELISA. Results: Compared to the GG genotype, the CC genotype of the rs2073618 polymorphism had a significantly increased risk for the presence of carotid plaque (OR = 2.54, 95 % CI = 1.22–5.28, p = 0.01). No statistically significant difference could be detected (p = 0.68) upon comparing median values of serum OPG levels among studied genotype groups in subjects with T2DM. Multivariable linear regression analyses in T2DM subjects demonstrated that GC and CC genotypes (p = 0.03 and p = 0.003), together with statin therapy (p = 0.009), were independent predictors of the number of carotid segments with plaques. Conclusions: Despite the fact that OPG rs2073618 genotypes failed to predict the serum OPG levels as there was no statistical difference among compared genotypes, our results demonstrate that the rs2073618 polymorphism could be a possible genetic marker for the prediction of increased risk for carotid plaque burden as a measure of advanced subclinical atherosclerosis in T2DM subjects.
29
Steinkamp, Pieter J., Jasper Vonk, Lydian A. Huisman, Gert-Jan Meersma, Gilles F. H. Diercks, Jan-Luuk Hillebrands, Wouter B. Nagengast, et al. "VEGF-Targeted Multispectral Optoacoustic Tomography and Fluorescence Molecular Imaging in Human Carotid Atherosclerotic Plaques." Diagnostics 11, no. 7 (July 7, 2021): 1227. http://dx.doi.org/10.3390/diagnostics11071227.
Full textAbstract:
Vulnerable atherosclerotic carotid plaques are prone to rupture, resulting in ischemic strokes. In contrast to radiological imaging techniques, molecular imaging techniques have the potential to assess plaque vulnerability by visualizing diseases-specific biomarkers. A risk factor for rupture is intra-plaque neovascularization, which is characterized by overexpression of vascular endothelial growth factor-A (VEGF-A). Here, we study if administration of bevacizumab-800CW, a near-infrared tracer targeting VEGF-A, is safe and if molecular assessment of atherosclerotic carotid plaques in vivo is possible using multispectral optoacoustic tomography (MSOT). Healthy volunteers and patients with symptomatic carotid artery stenosis scheduled for carotid artery endarterectomy were imaged with MSOT. Secondly, patients were imaged two days after intravenous administration of 4.5 bevacizumab-800CW. Ex vivo fluorescence molecular imaging of the surgically removed plaque specimen was performed and correlated with histopathology. In this first-in-human MSOT and fluorescence molecular imaging study, we show that administration of 4.5 mg bevacizumab-800CW appeared to be safe in five patients and accumulated in the carotid atherosclerotic plaque. Although we could visualize the carotid bifurcation area in all subjects using MSOT, bevacizumab-800CW-resolved signal could not be detected with MSOT in the patients. Future studies should evaluate tracer safety, higher doses of bevacizumab-800CW or develop dedicated contrast agents for carotid atherosclerotic plaque assessment using MSOT.
30
Hellberg, Sanna, Heidi Liljenbäck, Olli Eskola, Veronique Morisson-Iveson, Matthew Morrison, William Trigg, Pekka Saukko, et al. "Positron Emission Tomography Imaging of Macrophages in Atherosclerosis with 18F-GE-180, a Radiotracer for Translocator Protein (TSPO)." Contrast Media & Molecular Imaging 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/9186902.
Full textAbstract:
Intraplaque inflammation plays an important role in the progression of atherosclerosis. The 18 kDa translocator protein (TSPO) expression is upregulated in activated macrophages, representing a potential target to identify inflamed atherosclerotic plaques. We preclinically evaluated 18F-GE-180, a novel third-generation TSPO radioligand, in a mouse model of atherosclerosis. Methods. Nine hypercholesterolemic mice deficient in low density lipoprotein receptor and apolipoprotein B48 (LDLR−/−ApoB100/100) and six healthy C57BL/6N mice were injected with 10 MBq of 18F-GE-180. Specificity of binding was demonstrated in three LDLR−/−ApoB100/100 mice by injection of nonradioactive reference compound of 18F-GE-180 before 18F-GE-180. Dynamic 30-minute PET was performed followed by contrast-enhanced CT, and the mice were sacrificed at 60 minutes after injection. Tissue samples were obtained for ex vivo biodistribution measurements, and aortas were cut into serial cryosections for digital autoradiography. The presence of macrophages and TSPO was studied by immunohistochemistry. The 18F-GE-180 retention in plaque areas with different macrophage densities and lesion-free vessel wall were compared. Results. The LDLR−/−ApoB100/100 mice showed large, inflamed plaques in the aorta. Autoradiography revealed significantly higher 18F-GE-180 retention in macrophage-rich plaque areas than in noninflamed areas (count densities 150 ± 45 PSL/mm2 versus 51 ± 12 PSL/mm2, p<0.001). Prominent retention in the vessel wall without plaque was also observed (220 ± 41 PSL/mm2). Blocking with nonradioactive GE-180 diminished the difference in count densities between macrophage-rich and noninflamed areas in atherosclerotic plaques and lowered the count density in vessel wall without plaque. Conclusion. 18F-GE-180 shows specific uptake in macrophage-rich areas of atherosclerotic plaques in mice. However, retention in atherosclerotic lesions does not exceed that in lesion-free vessel wall. The third-generation TSPO radioligand 18F-GE-180 did not show improved characteristics for imaging atherosclerotic plaque inflammation compared to previously studied TSPO-targeting tracers.
31
Hellberg, Sanna, Johanna Silvola, Heidi Liljenbäck, Max Kiugel, Olli Eskola, Harri Hakovirta, Sohvi Hörkkö, et al. "Amyloid-Targeting PET Tracer [18F]Flutemetamol Accumulates in Atherosclerotic Plaques." Molecules 24, no. 6 (March 19, 2019): 1072. http://dx.doi.org/10.3390/molecules24061072.
Full textAbstract:
Atherosclerosis is characterized by the accumulation of oxidized lipids in the artery wall, which triggers an inflammatory response. Oxidized low-density lipoprotein (ox-LDL) presents amyloid-like structural properties, and different amyloid species have recently been recognized in atherosclerotic plaques. Therefore, we studied the uptake of the amyloid imaging agent [18F]Flutemetamol in atherosclerotic plaques. The binding of [18F]Flutemetamol to human carotid artery plaque was studied in vitro. In vivo uptake of the tracer was studied in hypercholesterolemic IGF-II/LDLR−/−ApoB100/100 mice and C57BL/6N controls. Tracer biodistribution was studied in vivo with PET/CT, and ex vivo by gamma counter and digital ex vivo autoradiography. The presence of amyloid, ox-LDL, and macrophages in the plaques was examined by immunohistochemistry. [18F]Flutemetamol showed specific accumulation in human carotid plaque, especially in areas positive for amyloid beta. The aortas of IGF-II/LDLR−/−ApoB100/100 mice showed large thioflavin-S-positive atherosclerotic plaques containing ox-LDL and macrophages. Autoradiography revealed 1.7-fold higher uptake in the plaques than in a lesion-free vessel wall, but no difference in aortic tissue uptake between mouse strains were observed in the in vivo PET/CT. In conclusion, [18F]Flutemetamol binds to amyloid-positive areas in human atherosclerotic plaques. Further studies are warranted to clarify the uptake mechanisms, and the potential of the tracer for in vivo imaging of atherosclerosis in patients.
32
Seki, Nobuhiko, Takuhiro Yamaguchi, Kenji Eguchi, Masahiro Kaneko, and Masahiko Kusumoto. "Potential risk of asbestos exposure among Japanese general population: Japanese general screening study for asbestos-related diseases (JGSARD)." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 1530. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1530.
Full textAbstract:
1530 Background: The number of patients with pleural mesothelioma and lung cancer associated with asbestos exposure has recently been increasing in Japan. The aim of this study was to evaluate the results of screening for asbestos-related diseases in a group of Japanese general population. Methods: This prospective study was approved by the institutional review board. From 2006 to 2008, 9810 subjects (5283 men and 4527 women; mean age, 57 years) underwent chest radiography and low-dose CT examinations in 26 institutions in Japan. Among them, 6286 (64.1%) subjects underwent subsequent CT examinations after 2 years of interval. Clinical information such as histories of smoking and asbestos exposure was reviewed. Images were interpreted independently by 15 experienced pulmonologists or chest radiologists. Results: The history of asbestos exposure was definitely present in 1253 (12.8%) subjects, possibly present in 2058 (21.0%), and absent in 6499 (66.2%). On chest radiograph, pleural plaque and thickening were seen in 61 (0.6%) and 65 (0.6%) subjects, respectively. On low-dose CT, pleural plaque and thickening were identified in 264 (2.7%) and 245 (2.5%) subjects, respectively, and non-calcified pulmonary nodule/mass was seen in 1003 (10.2%). Furthermore, lung cancer was identified in 29 (0.3%) subjects. The history of asbestos exposure was not confirmed in 77 out of 264 subjects (29.2%) having pleural plaques on low-dose CT. Based on the logistic regression analysis, pleural plaque on low-dose CT was significantly correlated with male, age more than 60 years, smoking, and a history of asbestos exposure. Especially, total residential period in asbestos factory area as well as asbestos exposure work period showed significantly increased relative risk every 10 years. Similarly, lung cancer was significantly correlated with age more than 60 years, a history of asbestos exposure, and presence of pleural plaques. Conclusions: Our results indicate the presence of pleural plaques on low-dose CT among Japanese general population is closely associated with potential risk of asbestos exposure. However, about 30% of such subjects are not aware of a history of asbestos exposure.
33
Francis, Andrew A., Justin F. Deniset, Jose A. Austria, Renee K. LaValleé, Graham G. Maddaford, Thomas E. Hedley, Elena Dibrov, and Grant N. Pierce. "Effects of dietary flaxseed on atherosclerotic plaque regression." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 12 (June 15, 2013): H1743—H1751. http://dx.doi.org/10.1152/ajpheart.00606.2012.
Full textAbstract:
Dietary flaxseed can retard the progression of atherosclerotic plaques. However, it remains unclear whether these antiatherogenic effects extend to plaque regression. In the present study, the therapeutic potential of dietary flaxseed on atherosclerotic plaque regression and vascular contractile function was evaluated using a novel rabbit model. Rabbits were randomly assigned to receive either a regular diet for 12 wk ( group I) or a 1% cholesterol-supplemented diet for 4 wk followed by a regular diet for 8 wk ( group II). The remaining experimental animals were treated as in group II but were fed for an additional 14 wk with either a regular diet ( group III) or a 10% flaxseed-supplemented diet ( group IV). Animals in group II showed clear evidence of plaque growth stabilization. Their vessels also exhibited significantly lower norepinephrine-induced contraction and an impaired relaxation response to acetylcholine compared with animals in group I. Dietary flaxseed supplementation resulted in a significant ≈40% reduction in plaque formation ( P = 0.033). Animals in both groups II and III displayed improved contraction and endothelium-dependent vessel relaxation. Dietary flaxseed is a valuable strategy to accelerate the regression of atherosclerotic plaques; however, flaxseed intervention did not demonstrate a clear beneficial effect on the vessel contractile response and endothelium-dependent vasorelaxation.
34
Stankovic, Milos, Biljana Ljujic, Djordje Radak, Slobodanka Mitrovic, Srdjan Babic, Nebojsa Arsenijevic, Miodrag Lukic, and Nada Pejnovic. "Circulating IL-10 Levels in Carotid Artery Disease." Serbian Journal of Experimental and Clinical Research 20, no. 1 (March 1, 2019): 53–63. http://dx.doi.org/10.1515/sjecr-2017-0040.
Full textAbstract:
Abstract Carotid atherosclerosis may be associated with neurosymptoms including cerebral infarction. IL-10 exerts atheroprotective effects, but its role in carotid disease is not fully defined. We aimed to investigate serum IL-10 levels in patients undergoing endarterectomy and their relation to the degree of carotid stenosis, plaque types and neurosymptoms. Two hundred consecutive patients with atherosclerotic carotid stenosis and 29 healthy controls were enrolled in this study. Plaque types were classified according to AHA criteria. Serum IL-10 levels were determined by ELISA. Patients undergoing endarterectomy had significantly higher circulating IL-10 levels (18.7 ± 3.2 pg/ml) in comparison with healthy controls (7.2 ± 1.8pg/ml; P =0.0001) and IL- 10 has good discriminatory efficacy between these two groups (ROC curve, AUC = 0.723, P=0.0001). Patients with < 70% and those with > 70% of carotid stenosis did not differ in terms of age, sex, cardiovascular risk factors except hypertension, neurosymptoms and AHA plaque types. Circulating IL-10 levels differed significantly among patients with different carotid plaque types (P = 0.002). Patients with uncomplicated plaques had significantly higher serum levels of IL-10 (23.0 ± 6.1 pg/ml) compared to those with complicated plaques (13.0 ±1.4 pg/ml, P=0.035) and IL-10 can differentiate patients between these two groups (ROC curve, AUC = 0.413, P= 0.035). Our findings reveal an important role for IL-10 in carotid atherosclerosis. IL-10 might be a potential biomarker in discriminating patients with carotid disease from healthy controls. Decreased serum levels of IL-10 are related to complicated carotid plaques.
35
MacAskill, Mark G., David E. Newby, and Adriana A. S. Tavares. "Frontiers in positron emission tomography imaging of the vulnerable atherosclerotic plaque." Cardiovascular Research 115, no. 14 (June 24, 2019): 1952–62. http://dx.doi.org/10.1093/cvr/cvz162.
Full textAbstract:
AbstractRupture of vulnerable atherosclerotic plaques leading to an atherothrombotic event is the primary driver of myocardial infarction and stroke. The ability to detect non-invasively the presence and evolution of vulnerable plaques could have a huge impact on the future identification and management of atherosclerotic cardiovascular disease. Positron emission tomography (PET) imaging with an appropriate radiotracer has the potential to achieve this goal. This review will discuss the biological hallmarks of plaque vulnerability before going on to evaluate and to present PET imaging approaches which target these processes. The focus of this review will be on techniques beyond [18F]FDG imaging, some of which are clinically advanced, and others which are on the horizon. As inflammation is the primary driving force behind atherosclerotic plaque development, we will predominantly focus on approaches which either directly, or indirectly, target this process.
36
van den Bouwhuijsen, Quirijn J. A., Daniel Bos, M. Arfan Ikram, Albert Hofman, Gabriel P. Krestin, Oscar H. Franco, Aad van der Lugt, and Meike W. Vernooij. "Coexistence of Calcification, Intraplaque Hemorrhage and Lipid Core within the Asymptomatic Atherosclerotic Carotid Plaque: The Rotterdam Study." Cerebrovascular Diseases 39, no. 5-6 (2015): 319–24. http://dx.doi.org/10.1159/000381138.
Full textAbstract:
Background: There is a growing amount of evidence suggesting that the composition of carotid atherosclerotic plaques may be of clinical relevance. Yet, little is known on the coexistence of potentially vulnerable and stabilizing components within asymptomatic plaques. Therefore, in this study we set out to investigate the coexistence of intraplaque calcification, hemorrhage and lipid core within the carotid artery using a multi-modality imaging approach. Methods: In 329 subjects from the population-based Rotterdam Study, all with ultrasound-confirmed carotid wall thickening, we performed a multi-detector CT and a high-resolution MRI of the carotid artery bifurcation at both sides. On the CT examinations, we quantified the volume of intraplaque calcification, and using the MRI examinations we rated the presence of intraplaque hemorrhage and of lipid core. In total, we investigated 611 carotid arteries with plaques. With logistic regression models we investigated the relationship of calcification volume - as a potential stabilizing component - with the presence of potential vulnerable components (intraplaque hemorrhage and lipid core) within each carotid plaque. We adjusted all analyses for age, sex and maximal plaque thickness. Next, we stratified on degree of stenosis (≤ or >30%) to evaluate effect modification by atherosclerotic burden. Results: We found that a larger calcification volume was associated with a higher prevalence of intraplaque hemorrhage, and a lower prevalence of lipid core (fully-adjusted odds ratio (OR) per standard deviation (SD) increase in calcification volume: 2.04 (95% confidence intervals (CI): 1.49; 2.78) and 0.72 (95% CI: 0.58; 0.90), respectively). Stratification on the degree of stenosis showed no difference in the association between calcification volume and hemorrhage over strata, while the relationship between a larger calcification volume and a lower prevalence of lipid seemed more pronounced in persons with a high degree of stenosis. Conclusions: In this population-based setting, we found that there is a complex relationship between calcification, intraplaque hemorrhage and lipid core within the carotid atherosclerotic plaque. Plaques with a higher load of calcification contain more often hemorrhagic components, but less often lipid core. Our results suggest that both in small and large plaques, intraplaque calcification may not be a stabilizing factor per se. These findings create an urge for conducting prospective studies investigating the interrelation of these different plaque components with regard to future cerebrovascular events.
37
Naim, Cyrille, Maxime Douziech, Éric Therasse, Pierre Robillard, Marie-France Giroux, Frederic Arsenault, Guy Cloutier, and Gilles Soulez. "Vulnerable Atherosclerotic Carotid Plaque Evaluation by Ultrasound, Computed Tomography Angiography, and Magnetic Resonance Imaging: An Overview." Canadian Association of Radiologists Journal 65, no. 3 (August 2014): 275–86. http://dx.doi.org/10.1016/j.carj.2013.05.003.
Full textAbstract:
Ischemic syndromes associated with carotid atherosclerotic disease are often related to plaque rupture. The benefit of endarterectomy for high-grade carotid stenosis in symptomatic patients has been established. However, in asymptomatic patients, the benefit of endarterectomy remains equivocal. Current research seeks to risk stratify asymptomatic patients by characterizing vulnerable, rupture-prone atherosclerotic plaques. Plaque composition, biology, and biomechanics are studied by noninvasive imaging techniques such as magnetic resonance imaging, computed tomography, ultrasound, and ultrasound elastography. These techniques are at a developmental stage and have yet to be used in clinical practice. This review will describe noninvasive techniques in ultrasound, magnetic resonance imaging, and computed tomography imaging modalities used to characterize atherosclerotic plaque, and will discuss their potential clinical applications, benefits, and drawbacks.
38
Matthäus, Christian, Riccardo Cicchi, Tobias Meyer, Annika Lattermann, Michael Schmitt, Bernd F. M. Romeike, Christoph Krafft, et al. "Multimodal nonlinear imaging of atherosclerotic plaques differentiation of triglyceride and cholesterol deposits." Journal of Innovative Optical Health Sciences 07, no. 05 (September 2014): 1450027. http://dx.doi.org/10.1142/s1793545814500278.
Full textAbstract:
Cardiovascular diseases in general and atherothrombosis as the most common of its individual disease entities is the leading cause of death in the developed countries. Therefore, visualization and characterization of inner arterial plaque composition is of vital diagnostic interest, especially for the early recognition of vulnerable plaques. Established clinical techniques provide valuable morphological information but cannot deliver information about the chemical composition of individual plaques. Therefore, spectroscopic imaging techniques have recently drawn considerable attention. Based on the spectroscopic properties of the individual plaque components, as for instance different types of lipids, the composition of atherosclerotic plaques can be analyzed qualitatively as well as quantitatively. Here, we compare the feasibility of multimodal nonlinear imaging combining two-photon fluorescence (TPF), coherent anti-Stokes Raman scattering (CARS) and second-harmonic generation (SHG) microscopy to contrast composition and morphology of lipid deposits against the surrounding matrix of connective tissue with diffraction limited spatial resolution. In this contribution, the spatial distribution of major constituents of the arterial wall and atherosclerotic plaques like elastin, collagen, triglycerides and cholesterol can be simultaneously visualized by a combination of nonlinear imaging methods, providing a powerful label-free complement to standard histopathological methods with great potential for in vivo application.
39
Zhu, Ching, Ralph J. Barker, Andrew W. Hunter, Yuhua Zhang, Jane Jourdan, and Robert G. Gourdie. "Quantitative Analysis of ZO-1 Colocalization with Cx43 Gap Junction Plaques in Cultures of Rat Neonatal Cardiomyocytes." Microscopy and Microanalysis 11, no. 3 (May 12, 2005): 244–48. http://dx.doi.org/10.1017/s143192760505049x.
Full textAbstract:
The gap junction (GJ) is an aggregate of intercellular channels that facilitates cytoplasmic interchange of ions, second messengers, and other molecules of less than 1000 Da between cells. In excitable organs such as heart and brain, GJs configure extended intercellular pathways for stable and long-term propagation of action potential. In a previous study in adult rat heart, we have shown that the Drosophila disks-large related protein ZO-1 shows low to moderate colocalization at myocyte borders with the GJ protein Cx43. In the present study, we detail a protocol for characterizing the pattern and level of colocalization of ZO-1 with Cx43 in cultures of neonatal myocytes at the level of individual GJ plaques. The data indicate that ZO-1 shows on average a partial 26.6% overlap (SD = 11.3%) with Cx43 GJ plaques. There is a strong positive correlation between GJ plaque size and area of ZO-1 colocalization, indicating that the level of associated ZO-1 scales with the area of the GJ plaque. Qualitatively, the most prominent colocalization occurs at the plaque perimeter. These studies may provide insight into the presently unknown biological function of ZO-1 interaction with Cx43.
40
da Silva, Rafaela, Rodrigo Fraga-Silva, Sabine Steffens, Mathias Fabre, Inga Bauer, Irene Caffa, Mirko Magnone, et al. "Nicotinamide phosphoribosyltransferase inhibition reduces intraplaque CXCL1 production and associated neutrophil infiltration in atherosclerotic mice." Thrombosis and Haemostasis 111, no. 02 (2014): 308–22. http://dx.doi.org/10.1160/th13-07-0531.
Full textAbstract:
SummaryPharmacological treatments targeting CXC chemokines and the associated neutrophil activation and recruitment into atherosclerotic plaques hold promise for treating cardiovascular disorders. Therefore, we investigated whether FK866, a nicotinamide phosphoribosyltransferase (NAMPT) inhibitor with anti-inflammatory properties that we recently found to reduce neutrophil recruitment into the ischaemic myocardium, would exert beneficial effects in a mouse atherosclerosis model. Atherosclerotic plaque formation was induced by carotid cast implantation in ApoE-/- mice that were fed with a Western-type diet. FK866 or vehicle were administrated intraperitoneally from week 8 until week 11 of the diet. Treatment with FK866 reduced neutrophil infiltration and MMP-9 content and increased collagen levels in atherosclerotic plaques compared to vehicle. No effect on other histological parameters, including intraplaque lipids or macrophages, was observed. These findings were associated with a reduction in both systemic and intraplaque CXCL1 levels in FK866-treated mice. In vitro, FK866 did not affect MMP-9 release by neutrophils, but it strongly reduced CXCL1 production by endothelial cells which, in the in vivo model, were identified as a main CXCL1 source at the plaque level. CXCL1 synthesis inhibition by FK866 appears to reflect interference with nuclear factor-κB signalling as shown by reduced p65 nuclear levels in endothelial cells pre-treated with FK866. In conclusion, pharmacological inhibition of NAMPT activity mitigates inflammation in atherosclerotic plaques by reducing CXCL1-mediated activities on neutrophils. These results support further assessments of NAMPT inhibitors for the potential prevention of plaque vulnerability.
41
Andelovic, Kristina, Patrick Winter, Peter Michael Jakob, Wolfgang Rudolf Bauer, Volker Herold, and Alma Zernecke. "Evaluation of Plaque Characteristics and Inflammation Using Magnetic Resonance Imaging." Biomedicines 9, no. 2 (February 12, 2021): 185. http://dx.doi.org/10.3390/biomedicines9020185.
Full textAbstract:
Atherosclerosis is an inflammatory disease of large and medium-sized arteries, characterized by the growth of atherosclerotic lesions (plaques). These plaques often develop at inner curvatures of arteries, branchpoints, and bifurcations, where the endothelial wall shear stress is low and oscillatory. In conjunction with other processes such as lipid deposition, biomechanical factors lead to local vascular inflammation and plaque growth. There is also evidence that low and oscillatory shear stress contribute to arterial remodeling, entailing a loss in arterial elasticity and, therefore, an increased pulse-wave velocity. Although altered shear stress profiles, elasticity and inflammation are closely intertwined and critical for plaque growth, preclinical and clinical investigations for atherosclerosis mostly focus on the investigation of one of these parameters only due to the experimental limitations. However, cardiovascular magnetic resonance imaging (MRI) has been demonstrated to be a potent tool which can be used to provide insights into a large range of biological parameters in one experimental session. It enables the evaluation of the dynamic process of atherosclerotic lesion formation without the need for harmful radiation. Flow-sensitive MRI provides the assessment of hemodynamic parameters such as wall shear stress and pulse wave velocity which may replace invasive and radiation-based techniques for imaging of the vascular function and the characterization of early plaque development. In combination with inflammation imaging, the analyses and correlations of these parameters could not only significantly advance basic preclinical investigations of atherosclerotic lesion formation and progression, but also the diagnostic clinical evaluation for early identification of high-risk plaques, which are prone to rupture. In this review, we summarize the key applications of magnetic resonance imaging for the evaluation of plaque characteristics through flow sensitive and morphological measurements. The simultaneous measurements of functional and structural parameters will further preclinical research on atherosclerosis and has the potential to fundamentally improve the detection of inflammation and vulnerable plaques in patients.
42
Li, Ying, Wei Chen, Kaijun Liu, Yi Wu, Yonglin Chen, Chun Chu, Bingji Fang, Liwen Tan, and Shaoxiang Zhang. "A Voxel-Map Quantitative Analysis Approach for Atherosclerotic Noncalcified Plaques of the Coronary Artery Tree." Computational and Mathematical Methods in Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/957195.
Full textAbstract:
Noncalcified plaques (NCPs) are associated with the presence of lipid-core plaques that are prone to rupture. Thus, it is important to detect and monitor the development of NCPs. Contrast-enhanced coronary Computed Tomography Angiography (CTA) is a potential imaging technique to identify atherosclerotic plaques in the whole coronary tree, but it fails to provide information about vessel walls. In order to overcome the limitations of coronary CTA and provide more meaningful quantitative information for percutaneous coronary intervention (PCI), we proposed a Voxel-Map based on mathematical morphology to quantitatively analyze the noncalcified plaques on a three-dimensional coronary artery wall model (3D-CAWM). This approach is a combination of Voxel-Map analysis techniques, plaque locating, and anatomical location related labeling, which show more detailed and comprehensive coronary tree wall visualization.
43
Mintun, Mark A. "Utilizing Advanced Imaging and Surrogate Markers Across the Spectrum of Alzheimer's Disease." CNS Spectrums 10, S18 (November 2005): 13–16. http://dx.doi.org/10.1017/s1092852900014188.
Full textAbstract:
AbstractAlzheimer's disease is a degenerative neurological condition characterized by the presence of β-amyloid plaques and neurofibrillary tangles in the limbic and neocortical regions of the brain. Pittsburgh Compound-B (PIB), a benzothiazole analog, has recently been found to specifically label amyloid deposits in positron emission tomography (PET) studies of the brain, opening the door for a wide range of applications related to Alzheimer's disease. In this article, data demonstrating the specificity of PIB as a PET tracer for β-amyloid lesions are reviewed, and the potential clinical applications of PIB PET imaging is discussed. Because amyloid plaques are common even in elderly individuals who are not suffering from dementia, the primary diagnostic function of PIB PET imaging presumably would be to rule out, rather than definitively confirm, Alzheimer's diagnoses in elderly patients. Other possible uses include monitoring plaque loads in patients receiving anti-amyloid therapy for Alzheimer's disease, as well as assessing plaque formation in unaffected individuals as a means of evaluating future Alzheimer's disease.
44
Riuwpassa, Irene E., St Rafiah, and I. Wayan S.A. "Deteksi helicobacter pylori pada plak gigi dengan reverse transcriptionpolymerase chain reaction." Journal of Dentomaxillofacial Science 7, no. 1 (April 30, 2008): 38. http://dx.doi.org/10.15562/jdmfs.v7i1.192.
Full textAbstract:
Helicobacter pylori have been found associated with dental plaque. It was suggestedthat the oral environment may be one of the many potential pathways for theirtransmission. The aim of this study was to evaluate whether the oral cavity is apotential reservoir and possible sanctuary for Helicobacter pylori. Supragingival andsubgingival plaques were analyzed by a Helicobacter genus-specific reversetranscriptase-fragment was identified.
45
Sokeechand, B. Sumayyah H., and Bernardo L. Trigatti. "Un-JAMming atherosclerotic arteries: JAM-L as a target to attenuate plaque development." Clinical Science 133, no. 14 (July 2019): 1581–85. http://dx.doi.org/10.1042/cs20190541.
Full textAbstract:
Abstract Atherosclerosis is a chronic inflammatory disease and a major driver of heart attack and stroke. Atherosclerosis development is driven by the infiltration of leukocytes, including monocytes and neutrophils, among other inflammatory cells into the artery wall, monocyte differentiation to macrophages and uptake of oxidized low density lipoprotein. Macrophage activation and inflammatory cytokine production are major factors which drive ongoing inflammation and plaque development. Identification of novel pathways driving this on-going inflammatory process may provide new opportunities for therapeutic intervention. In their article published in Clinical Science (2019) (vol 133, 1215–1228), Sun and colleagues demonstrate a novel role for the junction adhesion molecule-like (JAML) protein in driving on-going atherosclerotic plaque inflammation and plaque development. They report that JAML is expressed in macrophages and other cells in atherosclerotic plaques in both humans and mice, and that silencing JAML expression attenuates atherosclerotic plaque progression in mouse models of early and late stage plaque development. They demonstrate that JAML is required for oxidized-low density lipoprotein (OxLDL)-induced up-regulation of inflammatory cytokine production by macrophages, pointing to it as a potential therapeutic target for reducing ongoing plaque inflammation.
46
Olejarz, Wioletta, Dominika Łacheta, and Grażyna Kubiak-Tomaszewska. "Matrix Metalloproteinases as Biomarkers of Atherosclerotic Plaque Instability." International Journal of Molecular Sciences 21, no. 11 (May 31, 2020): 3946. http://dx.doi.org/10.3390/ijms21113946.
Full textAbstract:
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.
47
Li, Meng, Yan Chen, Yan Zhang, Danna Li, and Jun Liu. "Correlation between monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 and coronary plaque characteristics." Experimental Biology and Medicine 245, no. 15 (July 8, 2020): 1335–43. http://dx.doi.org/10.1177/1535370220941424.
Full textAbstract:
In this work, our primary objective was to examine the interrelationship among the serum level of chemokine (C-C motif) ligand 2 (CCL2) and plaque characteristics in coronary culprit lesions. The clinical data of 116 coronary heart disease patients who were hospitalized in the Department of Cardiology of Henan Province People's Hospital from February 2015 to June 2017 were retrospectively analyzed. The study population was subdivided according to the concentration of CCL2 into low CCL2 group and high CCL2 group. The levels of blood lipid, creatinine, and uric acid were measured, and patients underwent coronary angiography. The characteristics of the culprit lesions were detected by intravascular ultrasound, and the correlation between the serum markers and the characteristics of coronary artery plaque was analyzed. Moreover, the coronary artery disease dataset from the Gene Expression Omnibus database was downloaded and the genes regulated were analyzed by CCL2 using gene set enrichment analysis (GSEA). Patients with high CCL2 group had higher LDL-C level and L/H ratio, and lower HDL-C level than the low CCL2 group. Compared with low-level CCL2 group, coronary plaque in the high CCL2 group had higher eccentric plaque and plaque rupture, and thin cap fibroatheromas, fibrofatty and necrotic core and lower fibrous tissue. CCL2 was positively correlated with the percentage of fibrofatty and necrotic core, and negatively correlated with the percentage of fibrous tissue. Furthermore, GSEA analysis showed that samples with high CCL2 expression were enriched for genes involved in different pathways, such as cell adhesion molecules and Nod-like receptor signaling pathway. The CCL2 level was correlated with vulnerable plaques of coronary artery and had certain value in detecting vulnerable plaques. These results indicated that CCL2 could be regarded as a clinical prognostic biomarker for coronary artery disease. Impact statement Vulnerable plaques are plaques which are susceptible to rupture or thrombosis and trigger a series of adverse events such as coronary disorders. CCL2 is a soluble basic protein belonging to the CC subfamily. Previous studies have been investigated on the correlation between inflammatory factors and clinical events, but there are few studies on the correlation between CCL2 and plaque characteristics. Our study found that the high expression of CCL2 is involved in multiple processes in the genesis and progression of coronary artery disease, and would be a potential clinical prognostic indicator. In addition, high expression of CCL2 may be related to gene pathways such as Nod-like receptor signaling pathway, suggesting that CCL2 is involved in the inflammatory response and immune process of coronary artery disease.
48
Shami, Annelie, Dorothee Atzler, Laura A. Bosmans, Holger Winkels, Svenja Meiler, Michael Lacy, Claudia van Tiel, et al. "Glucocorticoid-induced tumour necrosis factor receptor family-related protein (GITR) drives atherosclerosis in mice and is associated with an unstable plaque phenotype and cerebrovascular events in humans." European Heart Journal 41, no. 31 (July 30, 2020): 2938–48. http://dx.doi.org/10.1093/eurheartj/ehaa484.
Full textAbstract:
Abstract Aims GITR—a co-stimulatory immune checkpoint protein—is known for both its activating and regulating effects on T-cells. As atherosclerosis bears features of chronic inflammation and autoimmunity, we investigated the relevance of GITR in cardiovascular disease (CVD). Methods and results GITR expression was elevated in carotid endarterectomy specimens obtained from patients with cerebrovascular events (n = 100) compared to asymptomatic patients (n = 93) and correlated with parameters of plaque vulnerability, including plaque macrophage, lipid and glycophorin A content, and levels of interleukin (IL)-6, IL-12, and C-C-chemokine ligand 2. Soluble GITR levels were elevated in plasma from subjects with CVD compared to healthy controls. Plaque area in 28-week-old Gitr−/−Apoe−/− mice was reduced, and plaques had a favourable phenotype with less macrophages, a smaller necrotic core and a thicker fibrous cap. GITR deficiency did not affect the lymphoid population. RNA sequencing of Gitr−/−Apoe−/− and Apoe−/− monocytes and macrophages revealed altered pathways of cell migration, activation, and mitochondrial function. Indeed, Gitr−/−Apoe−/− monocytes displayed decreased integrin levels, reduced recruitment to endothelium, and produced less reactive oxygen species. Likewise, GITR-deficient macrophages produced less cytokines and had a reduced migratory capacity. Conclusion Our data reveal a novel role for the immune checkpoint GITR in driving myeloid cell recruitment and activation in atherosclerosis, thereby inducing plaque growth and vulnerability. In humans, elevated GITR expression in carotid plaques is associated with a vulnerable plaque phenotype and adverse cerebrovascular events. GITR has the potential to become a novel therapeutic target in atherosclerosis as it reduces myeloid cell recruitment to the arterial wall and impedes atherosclerosis progression.
49
Chai, Dayang, Xiangquan Kong, Shu Lu, and Junjie Zhang. "CD4+/CD8+ ratio positively correlates with coronary plaque instability in unstable angina pectoris patients but fails to predict major adverse cardiovascular events." Therapeutic Advances in Chronic Disease 11 (January 2020): 204062232092202. http://dx.doi.org/10.1177/2040622320922020.
Full textAbstract:
Background: The association between CD4+/CD8+ ratio and coronary plaque instability in patients with unstable angina pectoris (UAP) has not been investigated. We sought to elucidate the correlation between CD4+/CD8+ ratio and plaque instability in this patient population. Methods: We enrolled 266 UAP patients who underwent pre-intervention optical coherence tomography (OCT) examination and percutaneous coronary intervention in our center from January 2016 to January 2018. Features of coronary plaques in the culprit arteries were classified as unstable plaque and stable plaque. Primary endpoint was occurrence of a major adverse cardiovascular event (MACE). Receiver operating characteristic (ROC) analyses were used to determine the predictive efficacy of the CD4+/CD8+ ratio for a group of unstable plaque patients, and binary logistic regression analysis was performed to evaluate potential independent predictors of plaque instability. All-cause mortality and MACE between the two groups were analyzed. Results: UAP patients with unstable plaque had a higher CD4/CD8 ratio compared with stable plaque patients ( p < 0.05). Results of binary logistic regression analyses showed that CD4+/CD8+ ratio ⩾1.725 and prior stroke were predictors and risk factors of plaque instability ( p < 0.05). ROC analyses showed that CD4+/CD8+ ratio ⩾1.725 was predictive of plaque instability in UAP patients. However, the Kaplan–Meier estimate for MACE and all-cause mortality showed no statistical significance. Conclusions: Higher CD4+/CD8+ ratio is associated with higher risk of plaque instability in our cohort of UAP patients. However, CD4+/CD8+ ratio was not an independent predictor of 1-year MACE or all-cause mortality.
50
Pahk, Kisoo, Chanmin Joung, Hwa Young Song, Sungeun Kim, and Won-Ki Kim. "SP-8356, a Novel Inhibitor of CD147-Cyclophilin A Interactions, Reduces Plaque Progression and Stabilizes Vulnerable Plaques in apoE-Deficient Mice." International Journal of Molecular Sciences 21, no. 1 (December 21, 2019): 95. http://dx.doi.org/10.3390/ijms21010095.
Full textAbstract:
Interactions between CD147 and cyclophilin A (CypA) promote plaque rupture that causes atherosclerosis-related cardiovascular events, such as myocardial infarction and stroke. Here, we investigated whether SP-8356 ((1S,5R)-4-(3,4-dihydroxy-5-methoxystyryl)-6,6-dimethylbicyclo[3.1.1]hept-3-en-2-one), a novel drug, can exert therapeutic effects against plaque progression and instability through disruption of CD147-CypA interactions in apolipoprotein E-deficient (ApoE KO) mice. Immunocytochemistry and immunoprecipitation analyses were performed to assess the effects of SP-8356 on CD147-CypA interactions. Advanced plaques were induced in ApoE KO mice via partial ligation of the right carotid artery coupled with an atherogenic diet, and SP-8356 (50 mg/kg) orally administrated daily one day after carotid artery ligation for three weeks. The anti-atherosclerotic effect of SP-8356 was assessed using histological and molecular approaches. SP-8356 interfered with CD147-CypA interactions and attenuated matrix metalloproteinase-9 activation. Moreover, SP-8356 induced a decreased in atherosclerotic plaque size in ApoE KO mice and stabilized plaque vulnerability by reducing the necrotic lipid core, suppressing macrophage infiltration, and enhancing fibrous cap thickness through increasing the content of vascular smooth muscle cells. SP-8356 exerts remarkable anti-atherosclerotic effects by suppressing plaque development and improving plaque stability through inhibiting CD147-CypA interactions. Our novel findings support the potential utility of SP-8356 as a therapeutic agent for atherosclerotic plaque.