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Wang J, Yu F, Zhang M, Lu J, Qian Z. A 3D framework for segmentation of carotid artery vessel wall and identification of plaque compositions in multi-sequence MR images. Comput Med Imaging Graph 2024; 116:102402. [PMID: 38810486 DOI: 10.1016/j.compmedimag.2024.102402] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/24/2023] [Revised: 04/30/2024] [Accepted: 05/14/2024] [Indexed: 05/31/2024]
Abstract
Accurately assessing carotid artery wall thickening and identifying risky plaque components are critical for early diagnosis and risk management of carotid atherosclerosis. In this paper, we present a 3D framework for automated segmentation of the carotid artery vessel wall and identification of the compositions of carotid plaque in multi-sequence magnetic resonance (MR) images under the challenge of imperfect manual labeling. Manual labeling is commonly done in 2D slices of these multi-sequence MR images and often lacks perfect alignment across 2D slices and the multiple MR sequences, leading to labeling inaccuracies. To address such challenges, our framework is split into two parts: a segmentation subnetwork and a plaque component identification subnetwork. Initially, a 2D localization network pinpoints the carotid artery's position, extracting the region of interest (ROI) from the input images. Following that, a signed-distance-map-enabled 3D U-net (Çiçek etal, 2016)an adaptation of the nnU-net (Ronneberger and Fischer, 2015) segments the carotid artery vessel wall. This method allows for the concurrent segmentation of the vessel wall area using the signed distance map (SDM) loss (Xue et al., 2020) which regularizes the segmentation surfaces in 3D and reduces erroneous segmentation caused by imperfect manual labels. Subsequently, the ROI of the input images and the obtained vessel wall masks are extracted and combined to obtain the identification results of plaque components in the identification subnetwork. Tailored data augmentation operations are introduced into the framework to reduce the false positive rate of calcification and hemorrhage identification. We trained and tested our proposed method on a dataset consisting of 115 patients, and it achieves an accurate segmentation result of carotid artery wall (0.8459 Dice), which is superior to the best result in published studies (0.7885 Dice). Our approach yielded accuracies of 0.82, 0.73 and 0.88 for the identification of calcification, lipid-rich core and hemorrhage components. Our proposed framework can be potentially used in clinical and research settings to help radiologists perform cumbersome reading tasks and evaluate the risk of carotid plaques.
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Affiliation(s)
- Jian Wang
- Institute of Intelligent Diagnostics, Beijing United-Imaging Research Institute of Intelligent Imaging, Building 3-4F, 9 Yongteng N. Road, Beijing 100080, China.
| | - Fan Yu
- Department of Radiology and Nuclear medicine, Xuanwu Hospital, Capital Medical University, Changchun Street, No. 45, Beijing 100053, China; Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Beijing 100053, China.
| | - Mengze Zhang
- Institute of Intelligent Diagnostics, Beijing United-Imaging Research Institute of Intelligent Imaging, Building 3-4F, 9 Yongteng N. Road, Beijing 100080, China.
| | - Jie Lu
- Department of Radiology and Nuclear medicine, Xuanwu Hospital, Capital Medical University, Changchun Street, No. 45, Beijing 100053, China; Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Beijing 100053, China.
| | - Zhen Qian
- Institute of Intelligent Diagnostics, Beijing United-Imaging Research Institute of Intelligent Imaging, Building 3-4F, 9 Yongteng N. Road, Beijing 100080, China.
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Miceli G, Basso MG, Pintus C, Pennacchio AR, Cocciola E, Cuffaro M, Profita M, Rizzo G, Tuttolomondo A. Molecular Pathways of Vulnerable Carotid Plaques at Risk of Ischemic Stroke: A Narrative Review. Int J Mol Sci 2024; 25:4351. [PMID: 38673936 PMCID: PMC11050267 DOI: 10.3390/ijms25084351] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/26/2024] [Revised: 04/05/2024] [Accepted: 04/12/2024] [Indexed: 04/28/2024] Open
Abstract
The concept of vulnerable carotid plaques is pivotal in understanding the pathophysiology of ischemic stroke secondary to large-artery atherosclerosis. In macroscopic evaluation, vulnerable plaques are characterized by one or more of the following features: microcalcification; neovascularization; lipid-rich necrotic cores (LRNCs); intraplaque hemorrhage (IPH); thin fibrous caps; plaque surface ulceration; huge dimensions, suggesting stenosis; and plaque rupture. Recognizing these macroscopic characteristics is crucial for estimating the risk of cerebrovascular events, also in the case of non-significant (less than 50%) stenosis. Inflammatory biomarkers, such as cytokines and adhesion molecules, lipid-related markers like oxidized low-density lipoprotein (LDL), and proteolytic enzymes capable of degrading extracellular matrix components are among the key molecules that are scrutinized for their associative roles in plaque instability. Through their quantification and evaluation, these biomarkers reveal intricate molecular cross-talk governing plaque inflammation, rupture potential, and thrombogenicity. The current evidence demonstrates that plaque vulnerability phenotypes are multiple and heterogeneous and are associated with many highly complex molecular pathways that determine the activation of an immune-mediated cascade that culminates in thromboinflammation. This narrative review provides a comprehensive analysis of the current knowledge on molecular biomarkers expressed by symptomatic carotid plaques. It explores the association of these biomarkers with the structural and compositional attributes that characterize vulnerable plaques.
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Affiliation(s)
- Giuseppe Miceli
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Maria Grazia Basso
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Chiara Pintus
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Andrea Roberta Pennacchio
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Elena Cocciola
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Mariagiovanna Cuffaro
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Martina Profita
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Giuliana Rizzo
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
| | - Antonino Tuttolomondo
- Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy; (G.M.); (M.G.B.); (C.P.); (A.R.P.); (E.C.); (M.C.); (M.P.); (G.R.)
- Internal Medicine and Stroke Care Ward, University Hospital, Policlinico “P. Giaccone”, 90127 Palermo, Italy
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Kang JH, Kawano T, Murata M, Toita R. Vascular calcification and cellular signaling pathways as potential therapeutic targets. Life Sci 2024; 336:122309. [PMID: 38042282 DOI: 10.1016/j.lfs.2023.122309] [Citation(s) in RCA: 11] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/05/2023] [Revised: 11/21/2023] [Accepted: 11/24/2023] [Indexed: 12/04/2023]
Abstract
Increased vascular calcification (VC) is observed in patients with cardiovascular diseases such as atherosclerosis, diabetes, and chronic kidney disease. VC is divided into three types according to its location: intimal, medial, and valvular. Various cellular signaling pathways are associated with VC, including the Wnt, mitogen-activated protein kinase, phosphatidylinositol-3 kinase/Akt, cyclic nucleotide-dependent protein kinase, protein kinase C, calcium/calmodulin-dependent kinase II, adenosine monophosphate-activated protein kinase/mammalian target of rapamycin, Ras homologous GTPase, apoptosis, Notch, and cytokine signaling pathways. In this review, we discuss the literature concerning the key cellular signaling pathways associated with VC and their role as potential therapeutic targets. Inhibitors to these pathways represent good candidates for use as potential therapeutic agents for the prevention and treatment of VC.
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Affiliation(s)
- Jeong-Hun Kang
- National Cerebral and Cardiovascular Center Research Institute, 6-1 Shinmachi, Kishibe, Suita, Osaka 564-8565, Japan.
| | - Takahito Kawano
- Center for Advanced Medical Innovation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
| | - Masaharu Murata
- Center for Advanced Medical Innovation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
| | - Riki Toita
- Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 1-8-31 Midorigaoka, Ikeda, Osaka, 563-8577, Japan; AIST-Osaka University Advanced Photonics and Biosensing Open Innovation Laboratory, AIST, 2-1 Yamadaoka, Suita, Osaka 565-0871, Japan
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Lin RA, Hsieh JT, Huang CC, Yang CY, Lin YP, Tarng DC. Circulating Osteocalcin Fractions are Associated with Vascular Calcification and Mortality in Chronic Hemodialysis Patients. Calcif Tissue Int 2023; 113:416-425. [PMID: 37665403 DOI: 10.1007/s00223-023-01122-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/02/2023] [Accepted: 07/31/2023] [Indexed: 09/05/2023]
Abstract
BACKGROUND Vascular calcification, a component of chronic kidney disease-mineral and bone disorder (CKD-MBD), is prevalent in patients with end-stage kidney disease (ESKD) and contributes to high mortality. However, the association between the blood level of total osteocalcin (OC) and vascular calcification and mortality remains inconclusive. We, therefore, investigated whether different OC fractions can serve as biomarkers of vascular calcification and mortality in the ESKD population. METHODS This observational cohort study enrolled patients on maintenance hemodialysis. Plasma carboxylated OC (cOC), uncarboxylated OC (ucOC), and intact parathyroid hormone (PTH) were measured. The percentage of carboxylated OC (%cOC) was calculated as dividing cOC by total OC. The vascular calcification severity was defined by an aortic calcification grade. The patients were followed for three years and one month. RESULTS A total of 184 patients were enrolled. In the multivariable logistic regression, plasma %cOC, but not cOC or ucOC, was independently associated with the severity of vascular calcification (OR 1.019, p = 0.036). A significant U-shaped correlation was found between plasma %cOC and PTH (p = 0.002). In the multivariable Cox regression, patients with higher plasma %cOC had a higher risk of mortality (quartiles Q4 versus Q1-Q3, HR 1.991 [95% CI: 1.036-3.824], p = 0.039). CONCLUSIONS In patients undergoing chronic hemodialysis, plasma %cOC positively correlated with vascular calcification and exhibited a U-shaped correlation with PTH. Furthermore, a higher plasma %cOC was associated with increased mortality. These findings suggest that plasma %cOC may serve as a biomarker for CKD-MBD and a predictor of clinical outcomes in chronic hemodialysis patients.
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Affiliation(s)
- Ruei-An Lin
- Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Department of Medical Education, National Taiwan University Hospital, Taipei, Taiwan
| | - Jyh-Tong Hsieh
- Institute of Clinical Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang Ming Chiao Tung University, 201, Sec. 2, Shih-Pai Rd., Beitou Dist, Taipei, 11217, Taiwan
| | - Chin-Chou Huang
- Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
| | - Chih-Yu Yang
- Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.
- Institute of Clinical Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.
- Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
- National Yang Ming Chiao Tung University, Hsinchu, Taiwan.
- Stem Cell Research Center, National Yang Ming Chiao Tung University, Taipei, Taiwan.
| | - Yao-Ping Lin
- Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
| | - Der-Cherng Tarng
- Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Institute of Clinical Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- National Yang Ming Chiao Tung University, Hsinchu, Taiwan
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Fote GM, Raefsky S, Mock K, Chaudhari A, Shafie M, Yu W. Intracranial Arterial Calcifications: Potential Biomarkers of Stroke Risk and Outcome. Front Neurol 2022; 13:900579. [PMID: 36119671 PMCID: PMC9475140 DOI: 10.3389/fneur.2022.900579] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2022] [Accepted: 06/24/2022] [Indexed: 11/30/2022] Open
Abstract
Intracranial artery calcifications (IAC), a common and easily identifiable finding on computed tomorgraphy angiography (CTA), has gained recognition as a possible risk factor for ischemic stroke. While atherosclerosis of intracranial arteries is believed to be a mechanism that commonly contributes to ischemic stroke, and coronary artery calcification is well-established as a predictor of both myocardial infarction (MI) and ischemic stroke risk, IAC is not currently used as a prognostic tool for stroke risk or recurrence. This review examines the pathophysiology and prevalence of IAC, and current evidence suggesting that IAC may be a useful tool for prediction of stroke incidence, recurrence, and response to acute ischemic stroke therapy.
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Affiliation(s)
- Gianna M. Fote
- School of Medicine, University of California, Irvine, Irvine, CA, United States
| | - Sophia Raefsky
- Department of Neurosciences, University of California, San Diego, La Jolla, CA, United States
| | - Kelton Mock
- School of Medicine, University of California, Irvine, Irvine, CA, United States
| | - Amit Chaudhari
- Department of Neurology, University of California, Irvine, Irvine, CA, United States
- *Correspondence: Amit Chaudhari
| | - Mohammad Shafie
- Department of Neurology, University of California, Irvine, Irvine, CA, United States
| | - Wengui Yu
- Department of Neurology, University of California, Irvine, Irvine, CA, United States
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Automated Classification of Atherosclerotic Radiomics Features in Coronary Computed Tomography Angiography (CCTA). Diagnostics (Basel) 2022; 12:diagnostics12071660. [PMID: 35885564 PMCID: PMC9318450 DOI: 10.3390/diagnostics12071660] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/10/2022] [Revised: 06/23/2022] [Accepted: 07/01/2022] [Indexed: 12/24/2022] Open
Abstract
Radiomics is the process of extracting useful quantitative features of high-dimensional data that allows for automated disease classification, including atherosclerotic disease. Hence, this study aimed to quantify and extract the radiomic features from Coronary Computed Tomography Angiography (CCTA) images and to evaluate the performance of automated machine learning (AutoML) model in classifying the atherosclerotic plaques. In total, 202 patients who underwent CCTA examination at Institut Jantung Negara (IJN) between September 2020 and May 2021 were selected as they met the inclusion criteria. Three primary coronary arteries were segmented on axial sectional images, yielding a total of 606 volume of interest (VOI). Subsequently, the first order, second order, and shape order of radiomic characteristics were extracted for each VOI. Model 1, Model 2, Model 3, and Model 4 were constructed using AutoML-based Tree-Pipeline Optimization Tools (TPOT). The heatmap confusion matrix, recall (sensitivity), precision (PPV), F1 score, accuracy, receiver operating characteristic (ROC), and area under the curve (AUC) were analysed. Notably, Model 1 with the first-order features showed superior performance in classifying the normal coronary arteries (F1 score: 0.88; Inverse F1 score: 0.94), as well as in classifying the calcified (F1 score: 0.78; Inverse F1 score: 0.91) and mixed plaques (F1 score: 0.76; Inverse F1 score: 0.86). Moreover, Model 2 consisting of second-order features was proved useful, specifically in classifying the non-calcified plaques (F1 score: 0.63; Inverse F1 score: 0.92) which are a key point for prediction of cardiac events. Nevertheless, Model 3 comprising the shape-based features did not contribute to the classification of atherosclerotic plaques. Overall, TPOT shown promising capabilities in terms of finding the best pipeline and tailoring the model using CCTA-based radiomic datasets.
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Clinical risk scores for stroke correlate with molecular signatures of vulnerability in symptomatic carotid patients. iScience 2022; 25:104219. [PMID: 35494231 PMCID: PMC9046225 DOI: 10.1016/j.isci.2022.104219] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/27/2021] [Revised: 02/22/2022] [Accepted: 04/05/2022] [Indexed: 11/20/2022] Open
Abstract
Unstable carotid stenosis is an important cause of ischemic stroke, yet the basis of disease pathophysiology remains largely unknown. We hypothesized that integrated analyses of symptomatic carotid stenosis patients at increased stroke risk stratified by clinical scores, CAR and ABCD2, with transcriptomic and clinical data could improve identification of molecular pathways and targets for instability. We show that high CAR score reflects plaque instability processes related to intra-plaque hemorrhage, angiogenesis, inflammation, and foam cell differentiation, whereas ABCD2 associates with neutrophil-mediated immunity, foam cell differentiation, cholesterol transport, and coagulation. Repressed processes in plaques from high-risk patients were ossification, chondrocyte differentiation, SMC migration, and ECM organization. ABCB5 gene was found as the top upregulated in high-risk patient’s plaques, localized to macrophages in areas with neovascularization and intra-plaque hemorrhage. The link between ABCB5 and intra-plaque hemorrhage suggests its key role for plaque instability that warrants further exploration.
We integrated stroke risk in carotid stenosis patients with plaque transcriptomics High CAR and ABCD2 scores reflect plaque instability processes and hemorrhage ABCB5 is upregulated in high-risk plaques, macrophages, and around neovessels CAR and ABCD2 capture vulnerable plaque features and improve risk stratification
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Miralles M, Arrébola M, Lago A, Brugger S, Lara R, Medina P, Clará A, Plana E. Intra-plaque calcium and its relation with the progression of carotid atheromatous disease. INT ANGIOL 2022; 41:312-321. [PMID: 35583455 DOI: 10.23736/s0392-9590.22.04872-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
Abstract
BACKGROUND Calcification and progression of atheromatous disease (AD) both have been independently related with the risk of stroke. However, the link between the two phenomena is still unclear. The main objective of this study was to analyze the temporal evolution of Ca content of carotid atheromatous plaques and its relation with the progression of carotid AD using quantitative CT Angiography (CTA). METHODS Forty-three asymptomatic patients with stenosis of the internal carotid artery (ICA)>50% completed the study. Contrast mold volume and calcium (Ca) content by quantitative CTA and Modified Agatston Score (Ca volume x radiological density) were assessed at baseline and after 12±2 months. Biochemical parameters, including main markers of Ca/Phosphorus (P) metabolism, were determined. RESULTS CTA measurement showed an increase of volumetric stenosis (volume decrease of the contrast mold), compared to baseline (475.45 (155.6) mm3 x U.H vs 501.3 (171.9) mm3 x U.H; p=0.04) as well as an increase of intra-plaque Ca (64.58 (57.8) mm3x U.H. vs 56.8 (52.3) p=0.002). An inverse correlation between baseline Ca content and volumetric stenosis progression (r= - 0.481; p<0.001), as well as between the increase of carotid Ca and plasma levels of vitamin D (r= 0.4; p=0.025) were also found. Multiple regression analysis found a model with baseline intra-plaque Ca, adjusted by body mass index (BMI) as most predictive of carotid AD progression. CONCLUSIONS These results suggest that a higher content of Ca confers greater stability against the progression of carotid AD and, eventually, its ability to generate symptomatology.
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Affiliation(s)
- Manuel Miralles
- Department Angiology and Vascular Surgery, La Fe University and Polytechnic Hospital, Valencia, Spain - .,Department of Surgery, University of Valencia, Valencia, Spain - .,Haemostasis, Thrombosis, Arteriosclerosis and Vascular Biology Research Group, Medical Research Institute, Hospital La Fe, Valencia, Spain -
| | - Manel Arrébola
- Department Angiology and Vascular Surgery, La Fe University and Polytechnic Hospital, Valencia, Spain
| | - Aida Lago
- Department of Neurology, La Fe University and Polytechnic Hospital, Valencia, Spain
| | - Sara Brugger
- Department of Radiology, La Fe University and Polytechnic Hospital, Valencia, Spain
| | - Raúl Lara
- Department Angiology and Vascular Surgery, La Fe University and Polytechnic Hospital, Valencia, Spain
| | - Pilar Medina
- Haemostasis, Thrombosis, Arteriosclerosis and Vascular Biology Research Group, Medical Research Institute, Hospital La Fe, Valencia, Spain
| | - Albert Clará
- Department of Angiology and Vascular Surgery, Del Mar University Hospital, Barcelona, Spain
| | - Emma Plana
- Haemostasis, Thrombosis, Arteriosclerosis and Vascular Biology Research Group, Medical Research Institute, Hospital La Fe, Valencia, Spain
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Silva H, Tassone C, Ross EG, Lee JT, Zhou W, Nelson D. Collagen Fibril Orientation in Tissue Specimens From Atherosclerotic Plaque Explored Using Small Angle X-Ray Scattering. J Biomech Eng 2022; 144:024505. [PMID: 34529040 PMCID: PMC10782870 DOI: 10.1115/1.4052432] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/24/2021] [Revised: 08/22/2021] [Indexed: 01/12/2023]
Abstract
Atherosclerotic plaques can gradually develop in certain arteries. Disruption of fibrous tissue in plaques can result in plaque rupture and thromboembolism, leading to heart attacks and strokes. Collagen fibrils are important tissue building blocks and tissue strength depends on how fibrils are oriented. Fibril orientation in plaque tissue may potentially influence vulnerability to disruption. While X-ray scattering has previously been used to characterize fibril orientations in soft tissues and bones, it has never been used for characterization of human atherosclerotic plaque tissue. This study served to explore fibril orientation in specimens from human plaques using small angle X-ray scattering (SAXS). Plaque tissue was extracted from human femoral and carotid arteries, and each tissue specimen contained a region of calcified material. Three-dimensional (3D) collagen fibril orientation was determined along scan lines that started away from and then extended toward a given calcification. Fibrils were found to be oriented mainly in the circumferential direction of the plaque tissue at the majority of locations away from calcifications. However, in a number of cases, the dominant fibril direction differed near a calcification, changing from circumferential to longitudinal or thickness (radial) directions. Further study is needed to elucidate how these fibril orientations may influence plaque tissue stress-strain behavior and vulnerability to rupture.
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Affiliation(s)
- Herbert Silva
- NASA, 2101 NASA Parkway Building 13 R 208, Houston, TX 77058
| | - Christopher Tassone
- Stanford Synchrotron Radiation Lightsource, 2575 Sand Hill Road, Menlo Park, CA 94025
| | - Elsie Gyang Ross
- Division of Vascular Surgery, Stanford Medical Center, 300 Pasteur Drive, Stanford, CA 94305
| | - Jason T. Lee
- Division of Vascular Surgery, Stanford Medical Center, 300 Pasteur Drive, Stanford, CA 94305
| | - Wei Zhou
- Vascular Surgery Division, College of Medicine, University of Arizona, Tucson, AZ 85724
| | - Drew Nelson
- Mechanical Engineering Department, Stanford University, Stanford, CA 94305
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10
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Kelley R, Bir S. Carotid atherosclerotic disease: A systematic review of pathogenesis and management. Brain Circ 2022; 8:127-136. [PMID: 36267431 PMCID: PMC9578307 DOI: 10.4103/bc.bc_36_22] [Citation(s) in RCA: 24] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/16/2022] [Revised: 08/02/2022] [Accepted: 08/03/2022] [Indexed: 11/12/2022] Open
Abstract
Carotid stenosis is an important contributor to ischemic stroke risk with resultant significant impact on neurological disability and death in adults and with worldwide implications. Management of carotid stenosis is impacted by whether there are associated symptoms along with the degree of stenosis. Understanding of the pathogenesis of carotid atherosclerosis or stenosis is important in management of carotid stenosis. Atherosclerotic plaque formation is a chronic insidious process with a number of potential contributors to the formation of such a plaque. The definition of atherosclerosis is not simply limited to abnormal deposition of lipid but also includes a chronic, complex, inflammatory process. Molecularly, in atherosclerosis, there is decreasing nitric oxide (NO) bioavailability, activity and/or expression of endothelial NO synthase, or increasing degradation of NO secondary to enhanced superoxide production. These above changes cause endothelial dysfunction leading to formation of foam cell followed by formation on lipid plaque. After lipid plaque formation, stable or unstable atherosclerotic plaque is formed depending on the calcium deposition over the lipid plaque. It continues to be clearly established that carotid intervention for symptomatic high-grade carotid stenosis is best managed with intervention either by carotid endarterectomy or carotid stenting. However, asymptomatic carotid stenosis is the subject of considerable controversy in terms of optimal management. This review of carotid atherosclerosis is an attempt to incorporate the information provided by more recent studies on pathogenesis and management which may help in the decision-making process for optimal management for protection against stroke.
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11
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Saba L, Nardi V, Cau R, Gupta A, Kamel H, Suri JS, Balestrieri A, Congiu T, Butler APH, Gieseg S, Fanni D, Cerrone G, Sanfilippo R, Puig J, Yang Q, Mannelli L, Faa G, Lanzino G. Carotid Artery Plaque Calcifications: Lessons From Histopathology to Diagnostic Imaging. Stroke 2022; 53:290-297. [PMID: 34753301 DOI: 10.1161/strokeaha.121.035692] [Citation(s) in RCA: 33] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The role of calcium in atherosclerosis is controversial and the relationship between vascular calcification and plaque vulnerability is not fully understood. Although calcifications are present in ≈50% to 60% of carotid plaques, their association with cerebrovascular ischemic events remains unclear. In this review, we summarize current understanding of carotid plaque calcification. We outline the role of calcium in atherosclerotic carotid disease by analyzing laboratory studies and histopathologic studies, as well as imaging findings to understand clinical implications of carotid artery calcifications. Differences in mechanism of calcium deposition express themselves into a wide range of calcification phenotypes in carotid plaques. Some patterns, such as rim calcification, are suggestive of plaques with inflammatory activity with leakage of the vasa vasourm and intraplaque hemorrhage. Other patterns such as dense, nodular calcifications may confer greater mechanical stability to the plaque and reduce the risk of embolization for a given degree of plaque size and luminal stenosis. Various distributions and patterns of carotid plaque calcification, often influenced by the underlying systemic pathological condition, have a different role in affecting plaque stability. Modern imaging techniques afford multiple approaches to assess geometry, pattern of distribution, size, and composition of carotid artery calcifications. Future investigations with these novel technologies will further improve our understanding of carotid artery calcification and will play an important role in understanding and minimizing stroke risk in patients with carotid plaques.
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Affiliation(s)
- Luca Saba
- Department of Radiology (L.S., R.C., A.B.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Valentina Nardi
- Azienda Ospedaliero Universitaria (A.O.U.), Department of Cardiovascular Medicine (V.N.), Mayo Clinic, Rochester, MN
| | - Riccardo Cau
- Department of Radiology (L.S., R.C., A.B.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Ajay Gupta
- Department of Radiology (A.G.), Weill Cornell Medicine, New York, New York
| | - Hooman Kamel
- Department of Neurology (H.K.), Weill Cornell Medicine, New York, New York
| | - Jasjit S Suri
- Stroke Diagnosis and Monitoring Division, AtheroPoint LLC, Roseville, CA (J.S.S.)
| | - Antonella Balestrieri
- Department of Radiology (L.S., R.C., A.B.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Terenzio Congiu
- Department of Pathology (T.C., D.F., G.C., G.F.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Anthony P H Butler
- Department of Radiology, University of Otago, Christchurch, New Zealand (A.P.H.B., S.G.)
| | - Steven Gieseg
- Department of Radiology, University of Otago, Christchurch, New Zealand (A.P.H.B., S.G.)
| | - Daniela Fanni
- Department of Pathology (T.C., D.F., G.C., G.F.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Giulia Cerrone
- Department of Pathology (T.C., D.F., G.C., G.F.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Roberto Sanfilippo
- Department of Vascular Surgery (R.S.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Josep Puig
- Department of Radiology (IDI), Hospital Universitari de Girona, Spain (J.P.)
| | - Qi Yang
- Xuanwu Hospital, Capital Medical University, Xicheng District, Beijing, China (Q.Y.)
| | | | - Gavino Faa
- Department of Pathology (T.C., D.F., G.C., G.F.), di Cagliari - Polo di Monserrato s.s, Cagliari, Italy
| | - Giuseppe Lanzino
- Department of Neurologic Surgery (G.L.), Mayo Clinic, Rochester, MN
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12
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Xu X, Hua Y, Liu B, Zhou F, Wang L, Hou W. Correlation Between Calcification Characteristics of Carotid Atherosclerotic Plaque and Plaque Vulnerability. Ther Clin Risk Manag 2021; 17:679-690. [PMID: 34234444 PMCID: PMC8257076 DOI: 10.2147/tcrm.s303485] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/04/2021] [Accepted: 05/17/2021] [Indexed: 11/25/2022] Open
Abstract
Purpose To investigate the relationship between calcification characteristics of carotid atherosclerotic plaque and lipid rich necrotic core (LRNC) and intraplaque hemorrhage (IPH). Methods Patients with severe carotid stenosis undergoing carotid endarterectomy (CEA) were selected. Ultrasound and CT angiography (CTA) were performed to evaluate the calcification characteristics of the plaque before the surgery. Results A total of 142 patients were included and 142 pathological specimens of postoperative plaque were obtained accordingly. There were 78 plaques (54.9%) with LRNC and 41 (28.9%) with IPH. The plaque with LRNC had higher calcification rate (93.6%) compared with the plaque with IPH (87.8%). LRNC was often found in multiple calcification (P = 0.003) and mixed type calcification (P = 0.001). Multiple calcification was more likely to combine with IPH (P = 0.008), while simple basal calcification was not likely to combine IPH (P = 0.002). Smaller granular calcification was more likely to be associated with IPH (P < 0.05). In multivariate regression analysis of IPH and calcification characteristics, simple basal calcification was still a protective factor for IPH (OR, 0.25; 95% CI, 0.09–0.66; P = 0.005), while multiple calcification was closely related to the occurrence of IPH (OR, 3.58; 95% CI, 1.49–8.61; P = 0.004). Conclusion Calcification characteristics of carotid atherosclerotic plaques are closely related to the vulnerability of plaques, especially multiple calcification and mixed type calcification.
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Affiliation(s)
- Xiangli Xu
- Department of Ultrasound, the Second Hospital of Harbin, Harbin, People's Republic of China
| | - Yang Hua
- Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Beibei Liu
- Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Fubo Zhou
- Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Lili Wang
- Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Weihong Hou
- Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
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13
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Ignatyev IM, Gafurov MR, Krivosheeva NV. Criteria for Carotid Atherosclerotic Plaque Instability. Ann Vasc Surg 2020; 72:340-349. [PMID: 32927044 DOI: 10.1016/j.avsg.2020.08.145] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/21/2020] [Revised: 08/14/2020] [Accepted: 08/16/2020] [Indexed: 11/18/2022]
Abstract
BACKGROUND The study aim is to determine the criteria for carotid atherosclerotic plaque instability with the use of an advanced ultrasound technology, immunohistochemical analysis, and electron paramagnetic resonance (EPR) and assess their correlations with histologic results. METHODS A total of 92 patients were included in the study and were examined by ultrasound duplex scanning and ultrasound elastography. Plaques harvested during carotid endarterectomy were obtained for histologic analysis, immunofluorescent assay, and EPR spectroscopic measurements. RESULTS Multivariate logistic regression analysis showed that plaques with an area >90 mm2 (odds ratio [OR], 4.05; 95% confidence interval [CI], 1.32-13.2; P = 0.006), plaque volume index > 0.6 cm3 (OR, 2.72; 95% CI, 1.05-9.58; P = 0.04), and juxtaluminal black area ≥8 mm2 (OR, 2.82; 95% CI, 1.22-6. 23; P = 0.02) were statistically significant independent predictors of histologically verified unstable plaques. Unstable plaques occurred in 94% of the patients with these indicators. Significant increases in the number of CD68+ and CD36+ cells (inflammatory markers) and CD31+ cells (neovasculogenesis markers) were revealed in unstable plaques by the immunohistochemical assay. EPR data analysis showed that divalent manganese could serve as a marker of plaque instability. CONCLUSIONS Additional ultrasound criteria, verified by histologic studies, significantly increased the information content for identifying patients with unstable plaques, which can be of great importance in stratifying the risk of ischemic stroke, especially in asymptomatic patients. The degree of calcification is not a mandatory criterion for plaque stabilization.
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Affiliation(s)
- Igor M Ignatyev
- Interregional Clinical and Diagnostic Centre, Kazan, Russia; Department of Cardiovascular and Endovascular Surgery, Kazan State Medical University, Kazan, Russia.
| | - Marat R Gafurov
- Institute of Physics of the Kazan (Volga Region) Federal University, Kazan, Russia
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14
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Extracellular vesicle signalling in atherosclerosis. Cell Signal 2020; 75:109751. [PMID: 32860954 PMCID: PMC7534042 DOI: 10.1016/j.cellsig.2020.109751] [Citation(s) in RCA: 24] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/16/2020] [Revised: 08/20/2020] [Accepted: 08/21/2020] [Indexed: 12/12/2022]
Abstract
Atherosclerosis is a major cardiovascular disease and in 2016, the World Health Organisation (WHO) estimated 17.5 million global deaths, corresponding to 31% of all global deaths, were driven by inflammation and deposition of lipids into the arterial wall. This leads to the development of plaques which narrow the vessel lumen, particularly in the coronary and carotid arteries. Atherosclerotic plaques can become unstable and rupture, leading to myocardial infarction or stroke. Extracellular vesicles (EVs) are a heterogeneous population of vesicles secreted from cells with a wide range of biological functions. EVs participate in cell-cell communication and signalling via transport of cargo including enzymes, DNA, RNA and microRNA in both physiological and patholophysiological settings. EVs are present in atherosclerotic plaques and have been implicated in cellular signalling processes in atherosclerosis development, including immune responses, inflammation, cell proliferation and migration, cell death and vascular remodeling during progression of the disease. In this review, we summarise the current knowledge regarding EV signalling in atherosclerosis progression and the potential of utilising EV signatures as biomarkers of disease.
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15
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Otomo S, Maekawa K, Baba T, Goto T, Yamamoto T. Evaluation of the risk factors for neurological and neurocognitive impairment after selective cerebral perfusion in thoracic aortic surgery. J Anesth 2020; 34:527-536. [PMID: 32361889 DOI: 10.1007/s00540-020-02783-x] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/01/2019] [Accepted: 04/18/2020] [Indexed: 12/18/2022]
Abstract
PURPOSE Neurologic complications are seen often after the surgery of the thoracic aorta that uses selective antegrade cerebral perfusion. The objective of this study was to evaluate the impact of atherosclerotic risk factors on neurologic complications in patients who underwent surgery to the thoracic aorta using SCP. METHODS Data were collected retrospectively on 94 patients who underwent elective ascending aorta/aortic arch replacement. Concomitant procedures were performed as needed. All patients had magnetic resonance imaging (MRI), angiography (MRA) and carotid ultrasound before surgery. Individual cognitive status was measured using four neuropsychological tests before surgery and 7 days after extubation. We compared perioperative factors for risk factors associated with postoperative stroke and postoperative cognitive decline (POCD). RESULTS 11 patients had strokes after surgery. Operation and extracorporeal circulation times were significantly longer in patients with stroke than those without stroke. Coronary artery disease and SCP time > 150 min were independently associated with postoperative stroke. Of the 83 patients without postoperative stroke, 20 suffered POCD. POCD patients had a significantly higher rate of heterogeneous carotid plaque, and operation time was significant longer in patients with POCD than those without POCD. Independent predictors of POCD were concomitant CABG, heterogeneous carotid plaque, history of cerebrovascular disease and operation time > 450 min. CONCLUSIONS We found that prolonged SCP time and coronary artery disease increased the risk of postoperative stroke. Heterogeneous carotid plaque, history of cerebrovascular disease, concomitant CABG and prolonged operation time were further significant predictors of POCD.
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Affiliation(s)
- Sumi Otomo
- Department of Anesthesiology, National Hospital Organization Kumamoto Saishun Medical Center, 2659 Suya, Koushi, Kumamoto, 861-1196, Japan. .,Department of Anesthesiology, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan.
| | - Kengo Maekawa
- Department of Anesthesiology, Kumamoto Chuo Hospital, Kumamoto, Japan
| | - Tomoko Baba
- Department of Anesthesiology, Minamata City Hospital and Medical Center, Kumamoto, Japan
| | - Tomoko Goto
- Department of Anesthesiology, Itoh Dento-Maxillofacial Hospital, Kumamoto, Japan
| | - Tatsuo Yamamoto
- Department of Anesthesiology, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
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16
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Caparosa EM, Sedgewick AJ, Zenonos G, Zhao Y, Carlisle DL, Stefaneanu L, Jankowitz BT, Gardner P, Chang YF, Lariviere WR, LaFramboise WA, Benos PV, Friedlander RM. Regional Molecular Signature of the Symptomatic Atherosclerotic Carotid Plaque. Neurosurgery 2020; 85:E284-E293. [PMID: 30335165 DOI: 10.1093/neuros/nyy470] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/23/2018] [Accepted: 09/06/2018] [Indexed: 12/11/2022] Open
Abstract
BACKGROUND Many studies have explored molecular markers of carotid plaque development and vulnerability to rupture, usually having examined whole carotid plaques. However, there are regional differences in plaque morphology and known shear-related mechanisms in areas surrounding the lipid core. OBJECTIVE To determine whether there are regional differences in protein expression along the long axis of the carotid plaque and how that might produce gaps in our understanding of the carotid plaque molecular signature. METHODS Levels of 7 inflammatory cytokines (IL-1β, IL-6, IL-8, IL-10, IL-12 p70, IFN-γ, and TNF-α) and caspase-3 were analyzed in prebifurcation, bifurcation, and postbifurcation segments of internal carotid plaques surgically removed from symptomatic and asymptomatic patients. Expression profiles of miRNAs and mRNAs were determined with microarrays for the rupture-prone postbifurcation segment for comparison with published whole plaque results. RESULTS Expression levels of all proteins examined, except IL-10, were lowest in the prebifurcation segment and significantly higher in the postbifurcation segment. Patient group differences in protein expression were observed for the prebifurcation segment; however, no significant differences were observed in the postbifurcation segment between symptomatic and asymptomatic patients. Expression profiles from postbifurcation carotid plaques identified 4 novel high priority miRNAs differentially expressed between patient groups (miR-214, miR-484, miR-942, and miR-1287) and 3 high-confidence miRNA:mRNA targets, including miR-214:APOD, miR-484:DACH1, and miR-942:GPR56. CONCLUSION The results demonstrate regional differences in protein expression for the first time and show that focus on the rupture-prone postbifurcation region leads to prioritization for further study of novel miRNA gene regulation mechanisms.
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Affiliation(s)
- Ellen M Caparosa
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Andrew J Sedgewick
- Joint Carnegie-Mellon -University of Pittsburgh PhD Program in Computational Biology, Pittsburgh, Pennsylvania.,Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Georgios Zenonos
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Yin Zhao
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Diane L Carlisle
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Lucia Stefaneanu
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Brian T Jankowitz
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Paul Gardner
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - Yue-Fang Chang
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | - William R Lariviere
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
| | | | - Panayiotis V Benos
- Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, Pennsylvania.,Joint Carnegie-Mellon -University of Pittsburgh PhD Program in Computational Biology, Pittsburgh, Pennsylvania
| | - Robert M Friedlander
- Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
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17
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Fourman LT, Saylor CF, Cheru L, Fitch K, Looby S, Keller K, Robinson JA, Hoffmann U, Lu MT, Burdo T, Lo J. Anti-Inflammatory Interleukin 10 Inversely Relates to Coronary Atherosclerosis in Persons With Human Immunodeficiency Virus. J Infect Dis 2020; 221:510-515. [PMID: 31077265 PMCID: PMC7325621 DOI: 10.1093/infdis/jiz254] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/15/2019] [Accepted: 05/10/2019] [Indexed: 12/31/2022] Open
Abstract
Interleukin 10 (IL-10) is an anti-inflammatory cytokine that may be protective against coronary atherosclerosis. In an observational study of persons with human immunodeficiency virus (PWH) and uninfected controls, IL-10 was measured in serum samples by means of enzyme-linked immunosorbent assay, and coronary atherosclerosis was assessed using computed tomographic angiography. Among PWH, a 10-fold decrease in IL-10 was associated with a 2.6-fold increase in the odds of coronary plaque (P = .01), after controlling for traditional and nontraditional cardiovascular risk factors. IL-10 was also inversely associated with total coronary plaque (ρ = -0.19; P = .02) and noncalcified coronary plaque (ρ = -0.24; P = .004). Our findings suggest a role for IL-10 in mitigating atherosclerosis in PWH. Clinical Trials Registration. NCT00455793.
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Affiliation(s)
- Lindsay T Fourman
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
| | - Charles F Saylor
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
| | - Lediya Cheru
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
| | - Kathleen Fitch
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
| | - Sara Looby
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
- The Yvonne L. Munn Center for Nursing Research, Massachusetts General Hospital, Boston
| | - Kiana Keller
- Department of Neurology, Massachusetts General Hospital and Harvard Medical School
| | - Jake A Robinson
- Department of Neuroscience, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania
| | - Udo Hoffmann
- Department of Radiology, Massachusetts General Hospital and Harvard Medical School
| | - Michael T Lu
- Department of Radiology, Massachusetts General Hospital and Harvard Medical School
| | - Tricia Burdo
- Department of Neuroscience, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania
| | - Janet Lo
- Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School
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18
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Calcification associates with transcriptomic signatures related to plaque stability in carotid arteries. Atherosclerosis 2019; 288:156-157. [DOI: 10.1016/j.atherosclerosis.2019.06.906] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/04/2019] [Revised: 06/13/2019] [Accepted: 06/19/2019] [Indexed: 11/22/2022]
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19
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Ikebe Y, Ishimaru H, Imai H, Abe K, Izumo T, Morofuji Y, Ideguchi R, Morikawa M, Uetani M. Quantitative Susceptibility Mapping for Carotid Atherosclerotic Plaques: A Pilot Study. Magn Reson Med Sci 2019; 19:135-140. [PMID: 31155568 PMCID: PMC7232036 DOI: 10.2463/mrms.mp.2018-0077] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022] Open
Abstract
Purpose: Identifying plaque components such as intraplaque hemorrhage, lipid rich necrosis, and calcification is important to evaluate vulnerability of carotid atherosclerotic plaque; however, conventional vessel wall MR imaging may fail to discriminate plaque components. We aimed to evaluate the components of plaques using quantitative susceptibility mapping (QSM), a newly developed post-processing technique to provide voxel-based quantitative susceptibilities. Methods: Seven patients scheduled for carotid endarterectomy were enrolled. Magnitude and phase images of five-echo 3D fast low angle shot (FLASH) were obtained using a 3T MRI, and QSM was calculated from the phase images. Conventional carotid vessel wall images (black-blood T1-weighted images [T1WI], T2-weighted images [T2WI], proton-density weighted images [PDWI], and time-of-flight images [TOF]) were also obtained. Pathological findings including intraplaque hemorrhage, calcification, and lipid rich necrosis at the thickest plaque section were correlated with relative susceptibility values with respect to the sternocleidomastoid muscle on QSM. On conventional vessel wall images, the contrast–noise ratio (CNR) between the three components and sternocleidomastoid muscle was measured respectively. Wilcoxon signed-rank test analyses were performed to assess the relative susceptibility values and CNR. Results: Pathologically, lipid rich necrosis was proved in all of seven cases, and intraplaque hemorrhage in five of seven cases. Mean relative susceptibility value of hemorrhage was higher than lipid rich necrosis unexceptionally (P = 0.0313). There were no significant differences between CNR of hemorrhage and lipid rich necrosis on all sequences. In all six cases with plaque calcification, susceptibility value of calcification was significantly lower than lipid rich necrosis unexceptionally (P = 0.0156). There were significant differences between CNRs of lipid rich necrosis and calcification on T1WI, PDWI, TOF (P < 0.05). Conclusion: QSM of carotid plaque would provide a novel quantitative MRI contrast that enables reliable differentiation among intraplaque hemorrhage, lipid rich necrosis, and calcification, and be useful to identify vulnerable plaques.
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Affiliation(s)
- Yohei Ikebe
- Department of Radiological Sciences, Nagasaki University Graduate School of Biomedical Sciences
| | - Hideki Ishimaru
- Department of Radiological Sciences, Nagasaki University Graduate School of Biomedical Sciences
| | | | - Kuniko Abe
- Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences
| | - Tsuyoshi Izumo
- Department of Neurosurgery, Nagasaki University Graduate School of Biomedical Sciences
| | - Yoichi Morofuji
- Department of Neurosurgery, Nagasaki University Graduate School of Biomedical Sciences
| | - Reiko Ideguchi
- Department of Radiological Sciences, Nagasaki University Graduate School of Biomedical Sciences
| | - Minoru Morikawa
- Department of Radiological Sciences, Nagasaki University Graduate School of Biomedical Sciences
| | - Masataka Uetani
- Department of Radiological Sciences, Nagasaki University Graduate School of Biomedical Sciences
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20
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Plaque components segmentation in carotid artery on simultaneous non-contrast angiography and intraplaque hemorrhage imaging using machine learning. Magn Reson Imaging 2019; 60:93-100. [PMID: 30959178 DOI: 10.1016/j.mri.2019.04.001] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2018] [Revised: 02/27/2019] [Accepted: 04/02/2019] [Indexed: 01/09/2023]
Abstract
PURPOSE This study sought to determine the feasibility of using Simultaneous Non-contrast Angiography and intraPlaque Hemorrhage (SNAP) to detect the lipid-rich/necrotic core (LRNC), and develop a machine learning based algorithm to segment plaque components on SNAP images. METHODS Sixty-eight patients (age: 58±9 years, 24 males) with carotid artery atherosclerotic plaque were imaged on a 3 T MR scanner with both traditional multi-contrast vessel wall MR sequences (TOF, T1W, and T2W) and 3D SNAP sequence. The manual segmentations of carotid plaque components including LRNC, intraplaque hemorrhage (IPH), calcification (CA) and fibrous tissue (FT) on traditional multi-contrast images were used as reference. By utilizing the intensity and morphological information from SNAP, a machine learning based two steps algorithm was developed to firstly identify LRNC (with or without IPH), CA and FT, and then segmented IPH from LRNC. Ten-fold cross-validation was used to evaluate the performance of proposed method. The overall pixel-wise accuracy, the slice-wise sensitivity & specificity & Youden's index, and the Pearson's correlation coefficient of the component area between the proposed method and the manual segmentation were reported. RESULTS In the first step, all tested classifiers (Naive Bayes (NB), Support Vector Machine (SVM), Random Forest (RF), Gradient Boosting Decision Tree (GBDT) and Artificial Neural Network (ANN)) had overall pixel-wise accuracy higher than 0.88. For RF, GBDT and ANN classifiers, the correlation coefficients of areas were all higher than 0.82 (p < 0.001) for LRNC and 0.79 for CA (p < 0.001), and the Youden's indexes were all higher than 0.79 for LRNC and 0.76 for CA, which were better than that of NB and SVM. In the second step, the overall pixel-wise accuracy was higher than 0.78 for the five classifiers, and RF achieved the highest Youden's index (0.69) with the correlation coefficients as 0.63 (p < 0.001). CONCLUSIONS The RF is the overall best classifier for our proposed method, and the feasibility of using SNAP to identify plaque components, including LRNC, IPH, CA, and FT has been validated. The proposed segmentation method using a single SNAP sequence might be a promising tool for atherosclerotic plaque components assessment.
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21
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Cardellini M, Rovella V, Scimeca M, Anemona L, Bischetti S, Casella S, Saggini A, Bonanno E, Ballanti M, Davato F, Menghini R, Ippoliti A, Santeusanio G, Di Daniele N, Federici M, Mauriello A. Chronic Kidney Disease Is Linked to Carotid Nodular Calcification, An Unstable Plaque Not Correlated to Inflammation. Aging Dis 2019; 10:71-81. [PMID: 30705769 PMCID: PMC6345328 DOI: 10.14336/ad.2018.0117] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2017] [Accepted: 01/17/2018] [Indexed: 12/11/2022] Open
Abstract
The incidence and the different type of carotid calcifications, nodular and non-nodular, and their role in the acute cerebrovascular disease has not yet been defined. Various studies have correlated the presence of specific risk factors, in particular the chronic kidney disease, with the presence of calcification, but not with the type of calcification. Since it is likely that carotid nodular calcifications rather than those with non-nodular aspect may represent a plaque at high risk of rupture, the purpose of our study was to evaluate the role of nodular calcification in the pathogenesis of cerebrovascular syndromes and their possible correlation with specific risk factors. A total of 168 carotid plaques from symptomatic and asymptomatic patients submitted to endarterectomy, whom complete clinical and laboratory assessment of major cardiovascular risk factors was available, were studied. In 21 endarterectomies (5 from symptomatic and 16 from asymptomatic patients) an eruptive calcified nodule, consisting of calcified plates associated to a small amount of fibrous tissue without extracellular lipids and inflammatory cells, was found protruding into the lumen. Nodular calcifications were significantly observed in patients affected by chronic kidney disease (with GFR<60 ml / min / 1.73 m2), with a normal lipidic and glycemic profile. On the contrary, non-nodular calcification, mainly correlated to diabetes, were stable lesions. Results of our study suggest that the mechanisms and the clinical significance of carotid atherosclerotic calcification may be different. The nodular calcification could represent a type of unstable plaque, significantly related to chronic kidney disease, without inflammation, morphologically different from the classical vulnerable plaques.
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Affiliation(s)
- Marina Cardellini
- 1Center for Atherosclerosis, Department of Medicine, Policlinico Tor Vergata, Rome, and Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Valentina Rovella
- 2Hypertension and Nephrology Unit, Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Manuel Scimeca
- 3Department of Biomedicine and Prevention, University of Rome Tor Vergata, Italy.,4OrchideaLab S.r.l., via del Grecale 6, Morlupo, Roma, Italy
| | - Lucia Anemona
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
| | | | - Sara Casella
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
| | - Andrea Saggini
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
| | - Elena Bonanno
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
| | - Marta Ballanti
- 1Center for Atherosclerosis, Department of Medicine, Policlinico Tor Vergata, Rome, and Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Francesca Davato
- 1Center for Atherosclerosis, Department of Medicine, Policlinico Tor Vergata, Rome, and Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Rossella Menghini
- 1Center for Atherosclerosis, Department of Medicine, Policlinico Tor Vergata, Rome, and Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Arnaldo Ippoliti
- 6Vascular Surgery, Department of Biomedicine and Prevention, University of Rome Tor Vergata, Italy
| | - Giuseppe Santeusanio
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
| | - Nicola Di Daniele
- 2Hypertension and Nephrology Unit, Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Massimo Federici
- 1Center for Atherosclerosis, Department of Medicine, Policlinico Tor Vergata, Rome, and Department of Systems Medicine, University of Rome Tor Vergata, Italy
| | - Alessandro Mauriello
- 5Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Italy
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22
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Holden RM, Hétu MF, Li TY, Ward E, Couture LE, Herr JE, Christilaw E, Adams MA, Johri AM. The Heart and Kidney: Abnormal Phosphate Homeostasis Is Associated With Atherosclerosis. J Endocr Soc 2018; 3:159-170. [PMID: 30620003 PMCID: PMC6316987 DOI: 10.1210/js.2018-00311] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/24/2018] [Accepted: 11/20/2018] [Indexed: 11/19/2022] Open
Abstract
Context Phosphate has gained recognition as a risk factor for adverse cardiovascular outcomes, potentially due to accelerated vascular calcification. Fibroblast growth factor-23 (FGF-23) is a counter-regulatory hormone that increases renal phosphate excretion to maintain normal levels. Objective The purpose of the study was to determine the association of phosphate and FGF-23 to atherosclerosis. Design and Setting A prospective cohort study (n = 204) of outpatients referred for coronary angiography over of a 1-year recruitment period at the Kingston General Hospital. Intervention Blood was collected, and a focused carotid ultrasound was performed. Main Outcome Measure Degree of angiographic coronary artery disease was scored. Carotid maximum plaque height, total area, grayscale median, and tissue pixel distribution were measured. Plasma phosphate was assessed by mineral assay and FGF-23 by ELISA. Results Carotid plaque burden [total plaque area (TPA)] was associated with higher levels of phosphate (TPA, r = 0.20, P < 0.01) and FGF-23 (r = 0.19, P < 0.01). FGF-23 was associated with increased plaque % calcium-like tissue. Participants with no coronary artery disease had significantly lower phosphate levels. Phosphate was associated with higher grayscale median (GSM) in male subjects but with lower GSM in female subjects. FGF-23 was associated with increased plaque % fat in male subjects but increased plaque % calcium in female subjects. Conclusions Phosphate was independently associated with the severity of atherosclerosis in terms of plaque burden and composition. FGF-23 was associated with plaque calcification. These findings suggest that abnormal phosphate homeostasis may play an under-recognized but potentially modifiable role in cardiovascular disease.
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Affiliation(s)
- Rachel M Holden
- Department of Medicine, Queen's University, Kingston, Ontario, Canada.,Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada
| | - Marie-France Hétu
- Department of Medicine, Division of Cardiology, Cardiovascular Imaging Network at Queen's University, Kingston, Ontario, Canada
| | - Terry Y Li
- Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada
| | - Emilie Ward
- Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada
| | - Laura E Couture
- Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada
| | - Julia E Herr
- Department of Medicine, Division of Cardiology, Cardiovascular Imaging Network at Queen's University, Kingston, Ontario, Canada
| | - Erin Christilaw
- Department of Medicine, Queen's University, Kingston, Ontario, Canada
| | - Michael A Adams
- Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada
| | - Amer M Johri
- Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada.,Department of Medicine, Division of Cardiology, Cardiovascular Imaging Network at Queen's University, Kingston, Ontario, Canada
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23
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Guo ZY, Zhang B, Yan YH, Gao SS, Liu JJ, Xu L, Hui PJ. Specific matrix metalloproteinases and calcification factors are associated with the vulnerability of human carotid plaque. Exp Ther Med 2018; 16:2071-2079. [PMID: 30186442 DOI: 10.3892/etm.2018.6424] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/25/2017] [Accepted: 04/13/2018] [Indexed: 12/20/2022] Open
Abstract
The rupture of atherosclerotic plaque provokes the majority of acute cerebrovascular events. Studies have demonstrated that various matrix metalloproteinases (MMPs) may promote atherosclerotic plaque progression and rupture. However, results have been incongruous and the mechanisms of this remain obscured. Therefore, in the current study, carotid plaques were characterized by assessing the levels of MMPs and calcification factors, and evaluating their association with plaque vulnerability. Human carotid plaques were obtained from carotid endarterectomies, and classified into stable and vulnerable groups by ultrasonography and histological analyses. The mRNA and protein levels of MMPs, vascular endothelial growth factor (VEGF), bone sialoprotein 2 (BSP) and osteopontin were investigated by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. Immunohistochemistry was used to localize MMP-2 and MMP-14 in stable and vulnerable plaques. The activation of various associated signaling pathways was also investigated using western blotting. The mRNA levels of MMP-2, -7, -9 and -14 were elevated in vulnerable plaques, among which expression of MMP-2 and -14 were the highest. Consistent with the mRNA levels, the protein levels of MMP-2 and -14 were also elevated. Immunohistochemistry also demonstrated positive staining of MMP-2 and MMP-14 in vulnerable plaques. Factors that indicate neovascularization and calcification, including VEGF and BSP, were concurrently elevated in vulnerable plaques. In addition, the protein levels of extracellular regulated kinase (ERK) and protein kinase C (PKC) were upregulated in vulnerable plaques. The current study provides novel insights into the MMP profiles of vulnerability plaques, and may assist in the development of novel methods for the diagnosis of plaque vulnerability and the prevention of plaque rupture.
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Affiliation(s)
- Zhou-Ying Guo
- Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.,Department of Ultrasound, The First Hospital of Lianyungang, Lianyungang, Jiangsu 222000, P.R. China
| | - Bai Zhang
- Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China
| | - Yan-Hong Yan
- Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China
| | - Shang-Shang Gao
- Department of Biochemical and Molecular of Medical College, Soochow University, Suzhou, Jiangsu 215123, P.R. China
| | - Jing-Jing Liu
- Department of Biochemical and Molecular of Medical College, Soochow University, Suzhou, Jiangsu 215123, P.R. China
| | - Lan Xu
- Department of Biochemical and Molecular of Medical College, Soochow University, Suzhou, Jiangsu 215123, P.R. China
| | - Pin-Jing Hui
- Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China
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24
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Superficial and multiple calcifications and ulceration associate with intraplaque hemorrhage in the carotid atherosclerotic plaque. Eur Radiol 2018; 28:4968-4977. [PMID: 29876705 PMCID: PMC6223859 DOI: 10.1007/s00330-018-5535-7] [Citation(s) in RCA: 37] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2018] [Revised: 04/18/2018] [Accepted: 05/11/2018] [Indexed: 01/09/2023]
Abstract
Objective Intraplaque hemorrhage (IPH) and ulceration of carotid atherosclerotic plaques have been associated with vulnerability while calcification has been conventionally thought protective. However, studies suggested calcification size and location may increase plaque vulnerability. This study explored the association between calcium configurations and ulceration with IPH. Methods One hundred thirty-seven consecutive symptomatic patients scheduled for carotid endarterectomy were recruited. CTA and CTP were performed prior to surgery. Plaque samples were collected for histology. According to the location, calcifications were categorized into superficial, deep and mixed types; according to the size and number, calcifications were classified as thick and thin, multiple and single. Results Seventy-one plaques had IPH (51.8%) and 83 had ulceration (60.6%). The appearance of IPH and ulceration was correlated (r = 0.49; p < 0.001). The incidence of multiple, superficial and thin calcifications was significantly higher in lesions with IPH and ulceration compared with those without. After adjusting factors including age, stenosis and ulceration, the presence of calcification [OR (95% CI), 3.0 (1.1-8.2), p = 0.035], multiple calcification [3.9 (1.4-10.9), p = 0.009] and superficial calcification [3.4 (1.1-10.8), p = 0.001] were all associated with IPH. ROC analysis showed that the AUC of superficial and multiple calcifications in detecting IPH was 0.63 and 0.66, respectively (p < 0.05). When the ulceration was combined, AUC increased significantly to 0.82 and 0.83, respectively. Results also showed that patients with lesions of both ulceration and IPH have significantly reduced brain perfusion in the area ipsilateral to the infarction. Conclusions Superficial and multiple calcifications and ulceration were associated with carotid IPH, and they may be a surrogate for higher risk lesions. Key Points • CTA-defined superficial and multiple calcifications in carotid atherosclerotic plaques are independently associated with the presence of intraplaque hemorrhage. • The combination of superficial and multiple calcifications and ulceration is highly predictive of carotid intraplaque hemorrhage. • Patients with lesions of both ulceration and intraplaque hemorrhage have significantly reduced brain perfusion in the area ipsilateral to the infarction.
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25
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Saba L, Yuan C, Hatsukami TS, Balu N, Qiao Y, DeMarco JK, Saam T, Moody AR, Li D, Matouk CC, Johnson MH, Jäger HR, Mossa-Basha M, Kooi ME, Fan Z, Saloner D, Wintermark M, Mikulis DJ, Wasserman BA. Carotid Artery Wall Imaging: Perspective and Guidelines from the ASNR Vessel Wall Imaging Study Group and Expert Consensus Recommendations of the American Society of Neuroradiology. AJNR Am J Neuroradiol 2018; 39:E9-E31. [PMID: 29326139 DOI: 10.3174/ajnr.a5488] [Citation(s) in RCA: 198] [Impact Index Per Article: 28.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Identification of carotid artery atherosclerosis is conventionally based on measurements of luminal stenosis and surface irregularities using in vivo imaging techniques including sonography, CT and MR angiography, and digital subtraction angiography. However, histopathologic studies demonstrate considerable differences between plaques with identical degrees of stenosis and indicate that certain plaque features are associated with increased risk for ischemic events. The ability to look beyond the lumen using highly developed vessel wall imaging methods to identify plaque vulnerable to disruption has prompted an active debate as to whether a paradigm shift is needed to move away from relying on measurements of luminal stenosis for gauging the risk of ischemic injury. Further evaluation in randomized clinical trials will help to better define the exact role of plaque imaging in clinical decision-making. However, current carotid vessel wall imaging techniques can be informative. The goal of this article is to present the perspective of the ASNR Vessel Wall Imaging Study Group as it relates to the current status of arterial wall imaging in carotid artery disease.
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Affiliation(s)
- L Saba
- From the Department of Medical Imaging (L.S.), University of Cagliari, Cagliari, Italy
| | - C Yuan
- Departments of Radiology (C.Y., N.B., M.M.-B.)
| | - T S Hatsukami
- Surgery (T.S.H.), University of Washington, Seattle, Washington
| | - N Balu
- Departments of Radiology (C.Y., N.B., M.M.-B.)
| | - Y Qiao
- The Russell H. Morgan Department of Radiology and Radiological Sciences (Y.Q., B.A.W.), Johns Hopkins Hospital, Baltimore, Maryland
| | - J K DeMarco
- Department of Radiology (J.K.D.), Walter Reed National Military Medical Center, Bethesda, Maryland
| | - T Saam
- Department of Radiology (T.S.), Ludwig-Maximilian University Hospital, Munich, Germany
| | - A R Moody
- Department of Medical Imaging (A.R.M.), Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada
| | - D Li
- Biomedical Imaging Research Institute (D.L., Z.F.), Cedars-Sinai Medical Center, Los Angeles, California
| | - C C Matouk
- Departments of Neurosurgery, Neurovascular and Stroke Programs (C.C.M., M.H.J.).,Radiology and Biomedical Imaging (C.C.M., M.H.J.)
| | - M H Johnson
- Departments of Neurosurgery, Neurovascular and Stroke Programs (C.C.M., M.H.J.).,Radiology and Biomedical Imaging (C.C.M., M.H.J.).,Surgery (M.H.J.), Yale University School of Medicine, New Haven, Connecticut
| | - H R Jäger
- Neuroradiological Academic Unit (H.R.J.), Department of Brain Repair and Rehabilitation, University College London Institute of Neurology, London, UK
| | | | - M E Kooi
- Department of Radiology (M.E.K.), CARIM School for Cardiovascular Diseases, Maastricht University Medical Center, Maastricht, the Netherlands
| | - Z Fan
- Biomedical Imaging Research Institute (D.L., Z.F.), Cedars-Sinai Medical Center, Los Angeles, California
| | - D Saloner
- Department of Radiology and Biomedical Imaging (D.S.), University of California, San Francisco, California
| | - M Wintermark
- Department of Radiology (M.W.), Neuroradiology Division, Stanford University, Stanford, California
| | - D J Mikulis
- Division of Neuroradiology (D.J.M.), Department of Medical Imaging, University Health Network
| | - B A Wasserman
- The Russell H. Morgan Department of Radiology and Radiological Sciences (Y.Q., B.A.W.), Johns Hopkins Hospital, Baltimore, Maryland
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26
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Al Sultan AYA, Alsubhi AMA. Anesthetic Considerations for Carotid Endarterectomy: A Postgraduate Educational Review. Anesth Essays Res 2018; 12:1-6. [PMID: 29628544 PMCID: PMC5872842 DOI: 10.4103/aer.aer_217_17] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023] Open
Abstract
Carotid endarterectomy (CEA) has shown a significant benefit in preventing ipsilateral stroke when it is compared to conservative management. Surgical morbidity and mortality must be kept to a minimum to achieve this benefit. Neurological status of the CEA patients can be monitored easily during regional anesthesia depending on the awake testing (neurocognitive assessment) method of the CEA patients. In addition, specific parameters can help us to monitor and to predict the neurological status of the CEA patients during the procedures such as regional cerebral oxygen saturation (rSO2) and middle cerebral artery velocity (MCAv) changes. We conducted a computerized literature search involving humans, published in English until December 2017, and indexed through Medical Databases; MEDLINE/PubMed, EMBASE, and Web of Science. We reviewed articles performed for prospective and other types of studies related to CEA procedures and techniques which can predict patient's status during the procedure. Searching relevant articles and discussing the results to allow meaningful rate comparison, and to conclude a result view which benefits the CEA patients and the medical staff during the CEA procedures. In total, studies observed cerebral rSO2 and MCAv have significant value during CEA procedures. Patients with neurological symptoms during the procedures showed changes of cerebral rSO2 and MCAv more than the patients without neurological symptoms. Mentioned parameters (cerebral rSO2 and MCAv) showed significant increasing right after the procedure. Mostly, CEA surgeries under local anesthesia were observed, for monitoring patients' consciousness status and comparing it to patients who undergo general anesthesia, to view the reliability of these techniques during CEA procedures, and to predict and avoid intraoperative neurological symptoms.
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27
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Baek JH, Yoo J, Song D, Kim YD, Nam HS, Heo JH. The Protective Effect of Middle Cerebral Artery Calcification on Symptomatic Middle Cerebral Artery Infarction. Stroke 2017; 48:3138-3141. [PMID: 28939676 DOI: 10.1161/strokeaha.117.017821] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2017] [Revised: 08/25/2017] [Accepted: 08/30/2017] [Indexed: 01/29/2023]
Abstract
BACKGROUND AND PURPOSE The presence of intracranial artery calcification is associated with an increased risk for stroke. However, calcified atherosclerotic plaques are also known to be less vulnerable to rupture. Given this discrepancy, we investigated whether the vulnerability of intracranial arterial atherosclerosis differed based on the presence or absence of calcification. METHODS We considered consecutive patients with acute stroke in the unilateral middle cerebral artery (MCA) territory. Patients with any stenotic MCAs were included in this study. Symptomatic MCA was defined as the occurrence of infarctions relevant to the stenotic MCA. The presence of calcification in the MCA was evaluated on noncontrast thin-section computed tomography images using a 3dimensional software package. Generalized estimating equations were used to compare the frequency of calcification between symptomatic and asymptomatic stenosis. RESULTS Of the 1066 MCAs examined in 533 patients, 645 MCAs were stenotic and were included in the study. Among the 645 stenotic MCAs, 406 MCAs (62.9%) were symptomatic. Calcification was observed in 36 MCAs (5.6%). Calcification in the MCA was more frequently observed in the asymptomatic group (7.9% versus 4.2%; P=0.032). On multivariable analysis, the presence of calcification in MCA atherosclerosis was less frequent in the symptomatic group (odds ratio, 0.46; 95% confidence interval, 0.23-0.92; P=0.027). CONCLUSIONS This study showed that calcified atherosclerosis in the MCA was less frequently symptomatic.
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Affiliation(s)
- Jang-Hyun Baek
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea
| | - Joonsang Yoo
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea
| | - Dongbeom Song
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea
| | - Young Dae Kim
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea
| | - Hyo Suk Nam
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea
| | - Ji Hoe Heo
- From the Department of Neurology, Yonsei University College of Medicine (J.-H.B., J.Y., D.S., Y.D.K., H.S.N., J.H.H.) and Department of Neurology, National Medical Center (J.-H.B.), Seoul, Republic of Korea.
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28
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Kim GH, Youn HJ. Is Carotid Artery Ultrasound Still Useful Method for Evaluation of Atherosclerosis? Korean Circ J 2016; 47:1-8. [PMID: 28154582 PMCID: PMC5287171 DOI: 10.4070/kcj.2016.0232] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/13/2016] [Accepted: 06/30/2016] [Indexed: 01/12/2023] Open
Abstract
Carotid ultrasound is an imaging modality that allows non-invasive assessment of vascular anatomy and function. Carotid intima-media thickness (IMT) has been shown to predict cardiovascular (CV) risk in multiple large studies. However, in 2013, American College of Cardiology/American Heart Association guidelines designated that the carotid IMT as class III evidence level was not recommended for use in clinical practice as a routine measurement of risk assessment for a first atherosclerotic CV event. Following the announcement of this guideline, combined common carotid IMT and plaque, including plaque tissue characterization and plaque burden, using 3D ultrasound was reported to be better than either measurement alone in a variety of studies. Moreover, changes in the intima thickness were related to aging and early atherosclerosis, and remodeling of the media thickness was associated with hypertension. Separate measurement is useful for evaluating the effects of different atherosclerotic risk factors on the arterial wall; however, a more detailed and elaborate technique needs to be developed. If so, separate measurement will play an important role in the assessment of atherosclerosis and arterial wall change according to a variety of risk factors, such as metabolic syndrome. In addition, although carotid blood flow velocity is a useful tool for risk classification and prediction in clinical practice, further clinical research is needed. The value of carotid IMT by ultrasound examination for risk stratification remains controversial, and groups developing future guidelines should consider the roles of plaque presence and burden and hemodynamic parameters in additional risk stratification beyond carotid IMT in clinical practice.
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Affiliation(s)
- Gee-Hee Kim
- Division of Cardiology, Department of Internal Medicine, St. Vincent's Hospital, Suwon, Korea
| | - Ho-Joong Youn
- Division of Cardiology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea
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29
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Bover J, Górriz JL, Ureña-Torres P, Lloret MJ, Ruiz-García C, daSilva I, Chang P, Rodríguez M, Ballarín J. Detección de las calcificaciones cardiovasculares: ¿una herramienta útil para el nefrólogo? Nefrologia 2016; 36:587-596. [DOI: 10.1016/j.nefro.2016.05.021] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2016] [Accepted: 05/19/2016] [Indexed: 12/12/2022] Open
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30
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Eisenmenger LB, Aldred BW, Kim SE, Stoddard GJ, de Havenon A, Treiman GS, Parker DL, McNally JS. Prediction of Carotid Intraplaque Hemorrhage Using Adventitial Calcification and Plaque Thickness on CTA. AJNR Am J Neuroradiol 2016; 37:1496-503. [PMID: 27102316 DOI: 10.3174/ajnr.a4765] [Citation(s) in RCA: 47] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/20/2015] [Accepted: 01/28/2016] [Indexed: 12/21/2022]
Abstract
BACKGROUND AND PURPOSE Carotid intraplaque hemorrhage is associated with stroke, plaque thickness, stenosis, ulceration, and adventitial inflammation. Conflicting data exist on whether calcification is a marker of plaque instability, and no data exist on adventitial calcification. Our goal was to determine whether adventitial calcification and soft plaque (a rim sign) help predict carotid intraplaque hemorrhage. MATERIALS AND METHODS This was a retrospective cohort study of 96 patients who underwent carotid MRA and CTA within 1 month, from 2009 to 2016. We excluded occlusions (n = 4) and near occlusions (n = 0), leaving 188 carotid arteries. Intraplaque hemorrhage was detected by using MPRAGE. Calcification, adventitial pattern, stenosis, maximum plaque thickness (total, soft, and hard), ulceration, and intraluminal thrombus on CTA were recorded. Atherosclerosis risk factors and medications were recorded. We used mixed-effects multivariable Poisson regression, accounting for 2 vessels per patient. For the final model, backward elimination was used with a threshold of P < .10. Receiver operating characteristic analysis determined intraplaque hemorrhage by using the area under the curve. RESULTS Our final model included the rim sign (prevalence ratio = 11.9, P < .001) and maximum soft-plaque thickness (prevalence ratio = 1.2, P = .06). This model had excellent intraplaque hemorrhage prediction (area under the curve = 0.94), outperforming the rim sign, maximum soft-plaque thickness, NASCET stenosis, and ulceration (area under the curve = 0.88, 0.86, 0.77, and 0.63, respectively; P < .001). Addition of the rim sign performed better than each marker alone, including maximum soft-plaque thickness (area under the curve = 0.94 versus 0.86, P < .001), NASCET stenosis (area under the curve = 0.90 versus 0.77, P < .001), and ulceration (area under the curve = 0.90 versus 0.63, P < .001). CONCLUSIONS The CTA rim sign of adventitial calcification with internal soft plaque is highly predictive of carotid intraplaque hemorrhage.
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Affiliation(s)
- L B Eisenmenger
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research
| | - B W Aldred
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research
| | - S-E Kim
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research
| | - G J Stoddard
- Department of Orthopedics (G.J.S.), Design and Biostatistics Center
| | | | - G S Treiman
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research Department of Surgery (G.S.T.), University of Utah, Salt Lake City, Utah Department of Surgery (G.S.T.), VA Salt Lake City Health Care System, Salt Lake City, Utah
| | - D L Parker
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research
| | - J S McNally
- From the Department of Radiology (L.B.E., B.W.A., S.-E.K., G.S.T., D.L.P., J.S.M.), Utah Center for Advanced Imaging Research
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31
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Calcified carotid artery plaques predict cardiovascular outcomes in the elderly. J Hypertens 2016; 33:810-7; discussion 817. [PMID: 25915886 DOI: 10.1097/hjh.0000000000000488] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
BACKGROUND Identifying plaque composition using ultrasound may aid in stratifying patients at high risk for cardiovascular disease (CVD). Calcification is an integral part of plaque progression and may contribute to plaque vulnerability. We investigated the ability of calcified carotid plaques identified using carotid ultrasound to predict cardiovascular outcomes in older adults. METHODS Participants included 187 hypertensive and 187 normotensive adults undergoing a duplex scan to identify the presence of calcified carotid plaques. Hypertensive participants received either blood pressure treatment or placebo, and all participants were followed for incident cardiovascular events and death for a maximum of 11 years. RESULTS The untreated hypertensive group was significantly associated with a higher time-to-any CVD event [relative risk (RR) 2.97, 95% confidence interval (CI) 2.03-4.35, P < 0.0001] and mortality (RR 3.11, 95% CI 1.92-5.04, P < 0.0001) when compared to the normotensive group. Participants with calcified carotid plaques had higher cardiovascular event rates (RR 6.22, 95% CI 1.97-19.6, P = 0.0018) and mortality (RR 6.30, 95% CI 1.55-25.7, P = 0.010) when compared to those without plaque. After controlling for age, male sex, blood pressure status, glucose, and IMT, the presence of calcified carotid plaques remained predictive of CVD events (RR 2.35, 95% CI 1.5-3.8, P = 0.0005) and mortality (RR 2.72, 95% CI 1.4-5.2, P = 0.0021). CONCLUSION Calcified carotid plaques may predict mortality and cardiovascular outcomes independent of traditional CVD risk factors and may serve as an additional CVD risk assessment in the elderly.
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Mohebali J, Patel VI, Romero JM, Hannon KM, Jaff MR, Cambria RP, LaMuraglia GM. Acoustic shadowing impairs accurate characterization of stenosis in carotid ultrasound examinations. J Vasc Surg 2016; 62:1236-44. [PMID: 26506272 DOI: 10.1016/j.jvs.2015.06.137] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2015] [Accepted: 06/04/2015] [Indexed: 12/24/2022]
Abstract
OBJECTIVE Duplex ultrasonography (DUS) has been the mainstay for diagnosing carotid artery stenosis and is often the sole diagnostic modality used prior to intervention. Highly calcified plaque, however, results in an acoustic shadow (AcS) that obscures the vessel lumen and inhibits the sonographer's ability to obtain Doppler velocity measurements. It is unknown whether DUS can accurately determine the degree of carotid stenosis in these settings. METHODS From July 2012 to December 2013, all patients with AcS on DUS measuring ≥5 mm in the longitudinal axis were cross-referenced with multidetector computed tomographic angiography (MD-CTA) images of the neck to define the study population. After standardizing the MD-CTA windows, percent stenosis was determined by cross-sectional area reduction using two separate previously described methods based on North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST) criteria. DUS waveform parameters in the internal carotid artery near the AcS were then compared with these MD-CTA measurements to determine the accuracy of DUS in characterizing the severity of carotid stenosis. RESULTS During this period, 8517 DUS studies were performed at the Massachusetts General Hospital, 550 of which had AcS, for an incidence of 6.45%. There were 92 lesions with a concomitant MD-CTA; however, seven were excluded because of poor study quality, because ≥6 months had elapsed between DUS and MD-CTA, or because the patient had undergone carotid reconstruction between studies. Of the 85 remaining lesions, DUS characterized 17 as severe (peak systolic velocity [PSV] >250 cm/s), 31 as moderate (PSV = 151-250 cm/s), and 37 as mild (PSV ≤150 cm/s) stenoses using PSV criteria. PSV weakly correlated with CTA-NASCET (r = 0.361; P = .004) and CTA-ECST (r = 0.306; P = .004) percent stenosis. Using PSV >250 cm/s as the predictor of >70% stenosis, and a ≥70% cutoff by both CTA-ECST and CTA-NASCET methods as the reference measure, DUS sensitivity ranged from 22.7% to 32.5%, specificity from 89.4% to 91.1%, positive predictive value from 88.2% to 76.4%, and negative predictive value from 25% to 60.2%. A subgroup analysis of lesions identified as non-severe by DUS revealed that waveforms with lower deceleration were associated with severe stenosis on CTA. CONCLUSIONS In the presence of AcS, DUS alone is inadequate to accurately determine the degree of carotid stenosis with sensitivity, specificity, and negative predictive values far below that needed for clinical decision-making. MD-CTA may be necessary for improved characterization of plaque in these AcS lesions. Further studies are needed to determine DUS parameters that may identify patients who should undergo further evaluation with MD-CTA to characterize the true severity of the stenosis.
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Affiliation(s)
- Jahan Mohebali
- Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass
| | - Virendra I Patel
- Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass; Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass
| | - Javier M Romero
- Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass
| | - Kathleen M Hannon
- Section of Vascular Medicine, Division of Cardiovascular Medicine, Massachusetts General Hospital Vascular Center and Harvard Medical School, Boston, Mass
| | - Michael R Jaff
- Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass; Section of Vascular Medicine, Division of Cardiovascular Medicine, Massachusetts General Hospital Vascular Center and Harvard Medical School, Boston, Mass
| | - Richard P Cambria
- Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass; Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass
| | - Glenn M LaMuraglia
- Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass; Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Mass.
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Han RI, Wheeler TM, Lumsden AB, Reardon MJ, Lawrie GM, Grande-Allen KJ, Morrisett JD, Brunner G. Morphometric analysis of calcification and fibrous layer thickness in carotid endarterectomy tissues. Comput Biol Med 2016; 70:210-219. [PMID: 26851729 DOI: 10.1016/j.compbiomed.2016.01.019] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/11/2015] [Revised: 12/20/2015] [Accepted: 01/14/2016] [Indexed: 12/22/2022]
Abstract
BACKGROUND Advanced atherosclerotic lesions are commonly characterized by the presence of calcification. Several studies indicate that extensive calcification is associated with plaque stability, yet recent studies suggest that calcification morphology and location may adversely affect the mechanical stability of atherosclerotic plaques. The underlying cause of atherosclerotic calcification and the importance of intra-plaque calcium distribution remains poorly understood. METHOD The goal of this study was the characterization of calcification morphology based on histological features in 20 human carotid endarterectomy (CEA) specimens. Representative frozen sections (10μm thick) were cut from the common, bulb, internal and external segments of CEA tissues and stained with von Kossa׳s reagent for calcium phosphate. The morphology of calcification (calcified patches) and fibrous layer thickness were quantified in 135 histological sections. RESULTS Intra-plaque calcification was distributed heterogeneously (calcification %-area: bulb segment: 14.2±2.1%; internal segment: 12.9±2.8%; common segment: 4.6±1.1%; p=0.001). Calcified patches were found in 20 CEAs (patch size: <0.1mm(2) to >1.0mm(2)). Calcified patches were most abundant in the bulb and least in the common segment (bulb n=7.30±1.08; internal n=4.81±1.17; common n=2.56±0.56; p=0.0007). Calcified patch circularity decreased with increasing size (<0.1mm(2): 0.77±0.01, 0.1-1mm(2): 0.62±0.01, >1.0mm(2): 0.51±0.02; p=0.0001). A reduced fibrous layer thickness was associated with increased calcium patch size (p<0.0001). CONCLUSIONS In advanced carotid atherosclerosis, calcification appears to be a heterogeneous and dynamic atherosclerotic plaque component, as indicated by the simultaneous presence of few large stabilizing calcified patches and numerous small calcific patches. Future studies are needed to elucidate the associations of intra-plaque calcification size and distribution with atherothrombotic events.
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Affiliation(s)
- Richard I Han
- Division of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX, United States; Department of Bioengineering, Rice University, Houston, TX, United States
| | - Thomas M Wheeler
- Department of Pathology & Immunology, Baylor College of Medicine, Houston, TX, United States
| | - Alan B Lumsden
- Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, TX, United States
| | - Michael J Reardon
- Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, TX, United States
| | - Gerald M Lawrie
- Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, TX, United States
| | | | - Joel D Morrisett
- Division of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX, United States
| | - Gerd Brunner
- Division of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX, United States; Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, TX, United States.
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Abstract
Although still in its infancy, coronary atherosclerosis imaging with PET holds promise in improving understanding of the pathophysiologic processes that underlie plaque progression and adverse cardiovascular events. Fludeoxyglucose F 18 offers the potential to measure inflammatory activity within the plaque itself whereas fluoride F 18 allows detection of microcalcification, both of which are key characteristics of plaques at risk of rupture. Further work is required to improve these imaging techniques and to assess their ability to predict cardiac events prospectively.
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Prasad K. Pathophysiology and Medical Treatment of Carotid Artery Stenosis. Int J Angiol 2015; 24:158-72. [PMID: 26417183 DOI: 10.1055/s-0035-1554911] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022] Open
Abstract
Stroke is the third leading cause of mortality. Approximately 80 to 85% strokes are ischemic due to carotid artery stenosis (CAS). The prevalence of significant CAS is 7% in women and 9% in men. Severe asymptomatic CAS varies from 0 to 3.1%. Prevalence of symptomatic CAS is high in patients with peripheral arterial disease. CAS is due to atherosclerosis, the major risk factors for which include dyslipidemia, hypertension, diabetes, obesity, cigarette smoking, advanced glycation end products (AGEs) and its receptors (RAGE, soluble RAGE [sRAGE]), lack of exercise and C-reactive protein (CRP). This article discusses the basic mechanism of atherosclerosis and the mechanisms by which these risk factors induce atherosclerosis. The role of AGEs and its receptors in the development and progression of CAS has been discussed in detail. Lifestyle changes and medical treatment of CAS such as lifestyle changes, lipid-lowering agents, antihypertensive agents, antidiabetic drugs, anti-AGE therapy, measures to elevate soluble receptors of AGE (sRAGE, esRAGE). CRP-lowering agents have been discussed in detail. The drugs especially lipid-lowering agents, and antihypertensive and antidiabetic drugs suppress, regress, and slow the progression of CAS. The possible role of lowering the levels of AGEs and raising the levels of sRAGE in the treatment of CAS has been proposed. Lifestyle changes besides medical treatment have been stressed. Lifestyle changes and medical treatment not only would slow the progression of CAS but would also regress the CAS.
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Affiliation(s)
- Kailash Prasad
- Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
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Katano H, Mase M, Nishikawa Y, Yamada K. Calcified Carotid Plaques Show Double Symptomatic Peaks According to Agatston Calcium Score. J Stroke Cerebrovasc Dis 2015; 24:1341-50. [DOI: 10.1016/j.jstrokecerebrovasdis.2015.02.010] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/02/2015] [Accepted: 02/10/2015] [Indexed: 11/24/2022] Open
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Effect of Calcification Modulus and Geometry on Stress in Models of Calcified Atherosclerotic Plaque. Cardiovasc Eng Technol 2014. [DOI: 10.1007/s13239-014-0186-6] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
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Vuilleumier N, Montecucco F, Hartley O. Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity. World J Cardiol 2014; 6:314-326. [PMID: 24944761 PMCID: PMC4062126 DOI: 10.4330/wjc.v6.i5.314] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/23/2013] [Accepted: 03/18/2014] [Indexed: 02/06/2023] Open
Abstract
Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies against apolipoprotein A-1 (anti-apoA-1 IgG), the major proteic fraction of high density lipoprotein. Current clinical studies indicate that high levels of anti-apoA-1 IgG are associated with a worse cardiovascular prognosis. In addition, in vitro and animal studies indicate a pro-inflammatory and pro-atherogenic role, supporting the hypothesis that these autoantibodies may play a direct causal role in CVD, and furthermore that they could potentially represent a therapeutic target for CVD in the future.
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Abstract
The extracellular matrix (ECM) is an essential component of the human body that is responsible for the proper function of various organs. Changes in the ECM have been implicated in the pathogenesis of several cardiovascular conditions including atherosclerosis, restenosis, and heart failure. Matrix components, such as collagens and noncollagenous proteins, influence the function and activity of vascular cells, particularly vascular smooth muscle cells and macrophages. Matrix proteins have been shown to be implicated in the development of atherosclerotic complications, such as plaque rupture, aneurysm formation, and calcification. ECM proteins control ECM remodeling through feedback signaling to matrix metalloproteinases (MMPs), which are the key players of ECM remodeling in both normal and pathological conditions. The production of MMPs is closely related to the development of an inflammatory response and is subjected to significant changes at different stages of atherosclerosis. Indeed, blood levels of circulating MMPs may be useful for the assessment of the inflammatory activity in atherosclerosis and the prediction of cardiovascular risk. The availability of a wide variety of low-molecular MMP inhibitors that can be conjugated with various labels provides a good perspective for specific targeting of MMPs and implementation of imaging techniques to visualize MMP activity in atherosclerotic plaques and, most interestingly, to monitor responses to antiatheroslerosis therapies. Finally, because of the crucial role of ECM in cardiovascular repair, the regenerative potential of ECM could be successfully used in constructing engineered scaffolds and vessels that mimic properties of the natural ECM and consist of the native ECM components or composite biomaterials. These scaffolds possess a great promise in vascular tissue engineering.
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How does calcification influence plaque vulnerability? Insights from fatigue analysis. ScientificWorldJournal 2014; 2014:417324. [PMID: 24955401 PMCID: PMC3997847 DOI: 10.1155/2014/417324] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/20/2013] [Accepted: 01/18/2014] [Indexed: 12/18/2022] Open
Abstract
Background. Calcification is commonly believed to be associated with cardiovascular disease burden. But whether or not the calcifications have a negative effect on plaque vulnerability is still under debate. Methods and Results. Fatigue rupture analysis and the fatigue life were used to evaluate the rupture risk. An idealized baseline model containing no calcification was first built. Based on the baseline model, we investigated the influence of calcification on rupture path and fatigue life by adding a circular calcification and changing its location within the fibrous cap area. Results show that 84.0% of calcified cases increase the fatigue life up to 11.4%. For rupture paths 10D far from the calcification, the life change is negligible. Calcifications close to lumen increase more fatigue life than those close to the lipid pool. Also, calcifications in the middle area of fibrous cap increase more fatigue life than those in the shoulder area. Conclusion. Calcifications may play a positive role in the plaque stability. The influence of the calcification only exists in a local area. Calcifications close to lumen may be influenced more than those close to lipid pool. And calcifications in the middle area of fibrous cap are seemly influenced more than those in the shoulder area.
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Yamada S, Oshima M, Watanabe Y, Ogata H, Hashimoto K, Miyake H. Intramural location and size of arterial calcification are associated with stenosis at carotid bifurcation. Eur J Radiol 2014; 83:957-963. [PMID: 24637069 DOI: 10.1016/j.ejrad.2014.02.009] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/05/2013] [Accepted: 02/08/2014] [Indexed: 11/17/2022]
Abstract
PURPOSE The purpose of this study was to investigate the association between internal carotid artery (ICA) stenosis and intramural location and size of calcification at the ICA origins and the origins of the cervical arteries proximal to the ICA. METHOD A total of 1139 ICAs were evaluated stenosis and calcification on the multi-detector row CT angiography. The intramural location was categorized into none, outside and inside location. The calcification size was evaluated on the 4-point grading scale. The multivariate analyses were adjusted for age, serum creatinine level, hypertension, hyperlipidemia, diabetes mellitus, smoking and alcohol habits. RESULTS Outside calcification at the ICA origins showed the highest multivariate odds ratio (OR) for the presence of ICA stenosis (30.0) and severe calcification (a semicircle or more of calcification at the arterial cross-sectional surfaces) did the second (14.3). In the subgroups of >70% ICA stenosis, the multivariate OR of outside location increased to 44.8 and that of severe calcification also increased to 32.7. Four of 5 calcified carotid plaque specimens extracted by carotid endarterectomy were histologically confirmed to be calcified burdens located outside the internal elastic lamia which were defined as arterial medial calcification. CONCLUSIONS ICA stenosis was strongly associated with severe calcification located mainly outside the carotid plaque. Outside calcification at the ICA origins should be evaluated separately from inside calcification, as a marker for the ICA stenosis. Additionally, we found that calcification at the origins of the cervical arteries proximal to the ICA was significantly associated with the ICA stenosis.
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Affiliation(s)
- Shigeki Yamada
- Department of Neurosurgery & Stroke Center, Rakuwakai Otowa Hospital, Otowachinji-cho 2, Yamashina-ku, Kyoto 607-8602, Japan; Department of Neurosurgery, Hamamatsu Rosai Hospital, 25 Shogen-cho, Higashi-ku, Hamamatsu city, Shizuoka 430-8525, Japan; Interfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan.
| | - Marie Oshima
- Interfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan.
| | - Yoshihiko Watanabe
- Department of Neurosurgery, Hamamatsu Rosai Hospital, 25 Shogen-cho, Higashi-ku, Hamamatsu city, Shizuoka 430-8525, Japan.
| | - Hideki Ogata
- Department of Neurosurgery, Hamamatsu Rosai Hospital, 25 Shogen-cho, Higashi-ku, Hamamatsu city, Shizuoka 430-8525, Japan.
| | - Kenji Hashimoto
- Department of Neurosurgery, Kishiwada Municipal Hospital, 1001 Gakuhara-cho, Kishiwada city, Osaka 596-8501, Japan.
| | - Hidenori Miyake
- Department of Neurosurgery, Hamamatsu Rosai Hospital, 25 Shogen-cho, Higashi-ku, Hamamatsu city, Shizuoka 430-8525, Japan.
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Zhongzhao Teng, Jing He, Sadat U, Mercer JR, Xiaoyan Wang, Bahaei NS, Thomas OM, Gillard JH. How Does Juxtaluminal Calcium Affect Critical Mechanical Conditions in Carotid Atherosclerotic Plaque? An Exploratory Study. IEEE Trans Biomed Eng 2014; 61:35-40. [DOI: 10.1109/tbme.2013.2275078] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
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Strauss HW, Fox JJ. Additional applications of approved radiopharmaceuticals for nuclear cardiology. Clin Transl Imaging 2013. [DOI: 10.1007/s40336-013-0038-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022]
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Katano H, Yamada K. Upregulation of ANGPTL4 messenger RNA and protein in severely calcified carotid plaques. J Stroke Cerebrovasc Dis 2013; 23:933-47. [PMID: 24075588 DOI: 10.1016/j.jstrokecerebrovasdis.2013.07.046] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/03/2013] [Revised: 07/27/2013] [Accepted: 07/31/2013] [Indexed: 01/04/2023] Open
Abstract
BACKGROUND In carotid atherosclerotic lesions, calcified plaques are thought to be stable and to evoke very few symptoms. However, the molecular activity in calcified plaques and their clinical significance have not been fully clarified yet. METHODS Carotid plaques from 18 endarterectomy patients were classified into high- and low-calcified plaques on the basis of Agatston calcium score. Twelve plaques were investigated for the alteration of gene expression by microarray analysis and real-time polymerase chain reaction (PCR) and 6 other plaques underwent protein assessment to elucidate the difference in molecular biological activity between the groups. RESULTS Microarray analysis demonstrated 93 angiogenesis or growth factor-related transcripts that are reliably expressed (175 probe sets). Among them, angiopoietin-like protein 4 (ANGPTL4) expression was significantly elevated, whereas fibroblast growth factor receptor 2 (FGFR2) expression was significantly suppressed. Quantitative messenger RNA analysis was performed with real-time PCR. Augmented or decreased protein expression of each gene was confirmed by Western blotting analysis and immunohistochemistry. CONCLUSIONS In high-calcified plaques, ANGPTL4 might be upregulated for antiangiogenic modulating function together with the downregulation of FGFR2, contributing to the stability of the plaques.
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Affiliation(s)
- Hiroyuki Katano
- Department of Neurosurgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Department of Medical informatics and Integrative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
| | - Kazuo Yamada
- Department of Neurosurgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
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HAKIMI M, HYHLIK-DÜRR A, VON AU A, BETZ M, DEMIREL S, DIHLMANN S, BÖCKLER D, GROSS-WEISSMANN M. The expression of glycophorin A and osteoprotegerin is locally increased in carotid atherosclerotic lesions of symptomatic compared to asymptomatic patients. Int J Mol Med 2013; 32:331-8. [DOI: 10.3892/ijmm.2013.1401] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/23/2013] [Accepted: 04/19/2013] [Indexed: 11/06/2022] Open
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Klinghammer L, Urschel K, Cicha I, Lewczuk P, Raaz-Schrauder D, Achenbach S, Garlichs CD. Impact of telmisartan on the inflammatory state in patients with coronary atherosclerosis – Influence on IP-10, TNF-α and MCP-1. Cytokine 2013; 62:290-6. [DOI: 10.1016/j.cyto.2013.02.001] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2012] [Revised: 12/20/2012] [Accepted: 02/01/2013] [Indexed: 01/06/2023]
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Association between carotid plaque enhancement shown by multidetector CT angiography and histologically validated microvessel density. Eur Radiol 2012; 22:2237-45. [PMID: 22572988 DOI: 10.1007/s00330-012-2467-5] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/14/2011] [Revised: 02/21/2012] [Accepted: 02/24/2012] [Indexed: 10/28/2022]
Abstract
PURPOSE Carotid plaques analysed by MDCTA can show contrast enhancement. The purpose of this study was to explore the association between carotid plaque enhancement (CPE) and microvessel density. MATERIALS AND METHODS We obtained IRB approval. Twenty-nine consecutive (male, 20; median age, 63) symptomatic patients studied with 16-detector CT were prospectively analysed. Examinations were performed before and after intravenous contrast medium administration, and analysis of plaque enhancement was performed. Patients underwent "en bloc" carotid endarterectomy; histological sections were prepared and the presence of microvessels quantified. Logistic regression analysis as well as ROC curve and area under the curve was calculated. RESULTS A statistically significant association between the degree of CPE and microvessel density (P = 0.009; rho = 0.553) was observed. The ROC curve analysis confirmed this association with an area under the curve of 0.906, 0.735, 0.644 and 0.546 for CPE of 10 HU, 15 HU, 20 HU and 25 HU respectively. There was a statistically significant difference between the CPE and the degree of neovascularisation (P = 0.0003). CONCLUSION Results of this preliminary study suggest that CPE might be associated with the microvessel density. Histological analysis seems to demonstrate that the degree of intra-plaque neo-vascularisation is statistically associated with CPE. KEY POINTS Carotid artery plaque enhancement at CT is associated with microvessel density. The degree of intra-plaque neo-vascularisation is statistically associated with carotid plaque enhancement. Plaque enhancement at CT should be considered when assessing vulnerable plaques.
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Evaluation of serum biomarkers for patients at increased risk of stroke. Int J Vasc Med 2012; 2012:906954. [PMID: 22506118 PMCID: PMC3312268 DOI: 10.1155/2012/906954] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/30/2011] [Revised: 01/06/2012] [Accepted: 01/06/2012] [Indexed: 11/29/2022] Open
Abstract
Early recognition of vulnerable patients is an important issue for stroke prevention. In our study, a multiscore analysis of various biomarkers was performed to evaluate its superiority over the analysis of single factors. Study subjects (n = 110) were divided into four groups: asymptomatic patients with stable (n = 25) and unstable (n = 36) plaques and symptomatic patients with stable (n = 13) and unstable (n = 36) plaques. Serum levels of MMP-1, -2, -3, -7, -8, -9, TIMP-1, -2, TNF-α, IL-1b, and IL-6, -8, -10, -12 were measured. Multi-score analysis was performed using multiple receiver operating characteristics (ROC) and determination of appropriate cutoff values. Significant differences between the groups were observed for MMP-1, -7, -9 and TIMP-1 in serum of the study subjects (P < 0.05). Multiple biomarker analysis led to a significant increase in the AUC (area under curve). In case of plaque instability, positive predictive value (PPV) for up to 86.4% could be correctly associated with vulnerable plaques. Thus, multiscore analysis might be preferable than the use of single biomarkers.
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Graf IM, Kim S, Wang B, Smalling R, Emelianov S. Noninvasive detection of intimal xanthoma using combined ultrasound, strain rate and photoacoustic imaging. ULTRASONICS 2012; 52:435-41. [PMID: 22078093 DOI: 10.1016/j.ultras.2011.10.005] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 03/30/2011] [Revised: 09/29/2011] [Accepted: 10/10/2011] [Indexed: 05/07/2023]
Abstract
BACKGROUND AND MOTIVATION The structure, composition and mechanics of carotid artery are good indicators of early progressive atherosclerotic lesions. The combination of three imaging modalities (ultrasound, strain rate and photoacoustic imaging) which could provide corroborative information about the named arterial properties could enhance the characterization of intimal xanthoma. METHODS The experiments were performed using a New Zealand white rabbit model of atherosclerosis. The aorta excised from an atherosclerotic rabbit was scanned ex vivo using the three imaging techniques: (1) ultrasound imaging of the longitudinal section: standard ultrasound B-mode (74Hz frame rate); (2) strain rate imaging: the artery was flushed with blood and a 1.5Hz physiologic pulsation was induced, while the ultrasound data were recorded at higher frame rate (296Hz); (3) photoacoustic imaging: the artery was irradiated with nanosecond pulsed laser light of low fluence in the 1210-1230nm wavelength range and the photoacoustic data was recorded at 10Hz frame rate. Post processing algorithms based on cross-correlation and optical absorption variation were implemented to derive strain rate and spectroscopic photoacoustic images, respectively. RESULTS Based on the spatio-temporal variation in displacement of different regions within the arterial wall, strain rate imaging reveals differences in tissue mechanical properties. Additionally, spectroscopic photoacoustic imaging can spatially resolve the optical absorption properties of arterial tissue and identify the location of lipid pools. CONCLUSIONS The study demonstrates that ultrasound, strain rate and photoacoustic imaging can be used to simultaneously evaluate the structure, the mechanics and the composition of atherosclerotic lesions to improve the assessment of plaque vulnerability.
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Affiliation(s)
- Iulia M Graf
- Department of Biomedical Engineering, University of Texas at Austin, Austin, TX 78712, USA
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FDG-PET-CT as a Biomarker for Aortic Valve Inflammation. CURRENT CARDIOVASCULAR IMAGING REPORTS 2012. [DOI: 10.1007/s12410-011-9117-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/14/2022]
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