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      Atherosclerotic plaque features relevant to rupture-risk detected by clinical photon-counting CT ex vivo: a proof-of-concept study

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          Abstract

          Background

          To identify subjects with rupture-prone atherosclerotic plaques before thrombotic events occur is an unmet clinical need. Thus, this proof-of-concept study aims to determine which rupture-prone plaque features can be detected using clinically available photon-counting computed tomography (PCCT).

          Methods

          In this retrospective study, advanced atherosclerotic plaques ( ex vivo, paraffin-embedded) from the Carotid Plaque Imaging Project were scanned by PCCT with reconstructed energy levels (45, 70, 120, 190 keV). Density in HU was measured in 97 regions of interest (ROIs) representing rupture-prone plaque features as demonstrated by histopathology (thrombus, lipid core, necrosis, fibrosis, intraplaque haemorrhage, calcium). The relationship between HU and energy was then assessed using a mixed-effects model for each plaque feature.

          Results

          Plaques from five men (age 79 ± 8 [mean ± standard deviation]) were included in the study. Comparing differences in coefficients ( b 1diff) of matched ROIs on plaque images obtained by PCCT and histology confirmed that calcium was distinguishable from all other analysed features. Of greater novelty, additional rupture-prone plaque features proved discernible from each other, particularly when comparing haemorrhage with fibrous cap ( p = 0.017), lipids ( p = 0.003) and necrosis ( p = 0.004) and thrombus compared to fibrosis ( p = 0.048), fibrous cap ( p = 0.028), lipids ( p = 0.015) and necrosis ( p = 0.017).

          Conclusions

          Clinically available PCCT detects not only calcification, but also other rupture-prone features of human carotid plaques ex vivo.

          Relevance statement

          Improved atherosclerotic plaque characterisation by photon-counting CT provides the ability to distinguish not only calcium, but also rupture-prone plaque features such as haemorrhage and thrombus. This may potentially improve monitoring and risk stratification of atherosclerotic patients in order to prevent strokes.

          Key points

          • CT of atherosclerotic plaques mainly detects calcium.

          • Many components, such as intra-plaque haemorrhage and lipids, determine increased plaque rupture risk.

          Ex vivo carotid plaque photon-counting CT distinguishes haemorrhage and thrombus.

          • Improved plaque photon-counting CT evaluation may refine risk stratification accuracy to prevent strokes.

          Graphical Abstract

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s41747-023-00410-4.

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          Most cited references30

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          2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes

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            From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.

            Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.
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              Multislice computed tomographic characteristics of coronary lesions in acute coronary syndromes.

              To evaluate the feasibility of noninvasive assessment of the characteristics of disrupted atherosclerotic plaques, the authors interrogated the culprit lesions in acute coronary syndromes (ACS) by multislice computed tomography (CT). Disrupted atherosclerotic plaques responsible for ACS histopathologically demonstrate large lipid cores and positive vascular remodeling. It is expected that plaques vulnerable to rupture should bear similar imaging signatures by CT. Either 0.5-mm x 16-slice or 64-slice CT was performed in 38 patients with ACS and compared with 33 patients with stable angina pectoris (SAP) before percutaneous coronary intervention. The coronary plaques in ACS and SAP were evaluated for the CT plaque characteristics, including vessel remodeling, consistency of noncalcified plaque (NCP <30 HU or 30 HU
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                Author and article information

                Contributors
                annelie.shami@med.lu.se
                Journal
                Eur Radiol Exp
                Eur Radiol Exp
                European Radiology Experimental
                Springer Vienna (Vienna )
                2509-9280
                30 January 2024
                30 January 2024
                December 2024
                : 8
                : 14
                Affiliations
                [1 ]Department of Clinical Sciences Malmö, Lund University, Clinical Research Center, ( https://ror.org/012a77v79) Jan Waldenströms Gata 35, CRC 91:12, 214 28 Malmö, Sweden
                [2 ]Department of Medical Imaging and Physiology, Skåne University Hospital, ( https://ror.org/02z31g829) Lund/Malmö, Sweden
                [3 ]GRID grid.411843.b, ISNI 0000 0004 0623 9987, Department of Cardiology, Malmö, , Skåne University Hospital, Lund University, ; Lund, Sweden
                [4 ]Wallenberg Centre for Molecular Medicine, Lund University, ( https://ror.org/012a77v79) Lund, Sweden
                [5 ]GRID grid.411843.b, ISNI 0000 0004 0623 9987, Department of Clinical Sciences Malmö, Medical Radiation Physics, , Skåne University Hospital, Lund University, ; 205 02 Malmö, Sweden
                [6 ]Department of Hematology, Oncology and Radiation Physics, Radiation Physics, Skåne University Hospital, ( https://ror.org/02z31g829) Lund, Sweden
                Author information
                http://orcid.org/0000-0002-6976-4397
                Article
                410
                10.1186/s41747-023-00410-4
                10825079
                38286959
                2cf87aa1-a8d1-4aac-9fcc-b0fdc7ab3b60
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 15 September 2023
                : 12 November 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100003793, Hjärt-Lungfonden;
                Award ID: 20200403
                Award ID: 20200183
                Award ID: 20220198
                Award ID: 20220044
                Award ID: 20220284
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004359, Vetenskapsrådet;
                Award ID: 2019-01260
                Award ID: 2019-01907
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100011077, Skånes universitetssjukhus;
                Funded by: Lund University Diabetes Centre, Swedish Foundation for Strategic Research
                Award ID: IRC15-0067
                Award ID: IRC15-0067
                Award ID: IRC15-0067
                Award ID: IRC15-0067
                Award ID: IRC15-0067
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100008590, STROKE-Riksförbundet;
                Funded by: FundRef http://dx.doi.org/10.13039/501100009802, Stiftelsen Söderström Königska Sjukhemmet;
                Award ID: SLS-969070
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100003748, Svenska Sällskapet för Medicinsk Forskning;
                Award ID: CG-22-0254
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004063, Knut och Alice Wallenbergs Stiftelse;
                Funded by: FundRef http://dx.doi.org/10.13039/501100006738, Medicinska Fakulteten, Lunds Universitet;
                Funded by: FundRef http://dx.doi.org/10.13039/501100009780, Region Skåne;
                Funded by: Lund University
                Categories
                Original Article
                Custom metadata
                © European Society of Radiology (ESR) 2024

                atherosclerosis,carotid arteries,carotid stenosis,plaque (atherosclerotic),tomography (x-ray computed)

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