Protocol and rationale of the Australian multicentre registry for serial cardiac computed tomography angiography (ARISTOCRAT): a prospective observational study of the natural history of pericoronary adipose tissue attenuation and radiomics.

Cardiac computed tomography angiography atherosclerosis inflammation pericoronary adipose tissue (PCAT) radiomics

Journal

Cardiovascular diagnosis and therapy
ISSN: 2223-3652
Titre abrégé: Cardiovasc Diagn Ther
Pays: China
ID NLM: 101601613

Informations de publication

Date de publication:
30 Jun 2024
Historique:
received: 11 10 2023
accepted: 11 05 2024
medline: 8 7 2024
pubmed: 8 7 2024
entrez: 8 7 2024
Statut: ppublish

Résumé

Vascular inflammation plays a crucial role in the development of atherosclerosis and atherosclerotic plaque rupture resulting in acute coronary syndrome (ACS). Pericoronary adipose tissue (PCAT) attenuation quantified from routine coronary computed tomography angiography (CCTA) has emerged as a promising non-invasive imaging biomarker of coronary inflammation. However, a detailed understanding of the natural history of PCAT attenuation is required before it can be used as a surrogate endpoint in trials of novel therapies targeting coronary inflammation. This article aims to explore the natural history of PCAT attenuation and its association with changes in plaque characteristics. The Australian natuRal hISTOry of periCoronary adipose tissue attenuation, RAdiomics and plaque by computed Tomographic angiography (ARISTOCRAT) registry is a multi-centre observational registry enrolling patients undergoing clinically indicated serial CCTA in 9 centres across Australia. CCTA scan parameters will be matched across serial scans. Quantitative analysis of plaque and PCAT will be performed using semiautomated software. The primary endpoint is to explore temporal changes in patient-level and lesion-level PCAT attenuation by CCTA and their associations with changes in plaque characteristics. Secondary endpoints include evaluating: (I) impact of statin therapy on PCAT attenuation and plaque characteristics; and (II) changes in PCAT attenuation and plaque characteristics in specific subgroups according to sex and risk factors. ARISTOCRAT will further our understanding of the natural history of PCAT attenuation and its association with changes in plaque characteristics. This study has been prospectively registered with the Australia and New Zealand Clinical Trials Registry (ACTRN12621001018808).

Sections du résumé

Background UNASSIGNED
Vascular inflammation plays a crucial role in the development of atherosclerosis and atherosclerotic plaque rupture resulting in acute coronary syndrome (ACS). Pericoronary adipose tissue (PCAT) attenuation quantified from routine coronary computed tomography angiography (CCTA) has emerged as a promising non-invasive imaging biomarker of coronary inflammation. However, a detailed understanding of the natural history of PCAT attenuation is required before it can be used as a surrogate endpoint in trials of novel therapies targeting coronary inflammation. This article aims to explore the natural history of PCAT attenuation and its association with changes in plaque characteristics.
Methods UNASSIGNED
The Australian natuRal hISTOry of periCoronary adipose tissue attenuation, RAdiomics and plaque by computed Tomographic angiography (ARISTOCRAT) registry is a multi-centre observational registry enrolling patients undergoing clinically indicated serial CCTA in 9 centres across Australia. CCTA scan parameters will be matched across serial scans. Quantitative analysis of plaque and PCAT will be performed using semiautomated software.
Discussion UNASSIGNED
The primary endpoint is to explore temporal changes in patient-level and lesion-level PCAT attenuation by CCTA and their associations with changes in plaque characteristics. Secondary endpoints include evaluating: (I) impact of statin therapy on PCAT attenuation and plaque characteristics; and (II) changes in PCAT attenuation and plaque characteristics in specific subgroups according to sex and risk factors. ARISTOCRAT will further our understanding of the natural history of PCAT attenuation and its association with changes in plaque characteristics.
Trial Registration UNASSIGNED
This study has been prospectively registered with the Australia and New Zealand Clinical Trials Registry (ACTRN12621001018808).

Identifiants

pubmed: 38975008
doi: 10.21037/cdt-23-392
pii: cdt-14-03-447
pmc: PMC11223934
doi:

Types de publication

Journal Article

Langues

eng

Pagination

447-458

Informations de copyright

2024 Cardiovascular Diagnosis and Therapy. All rights reserved.

Déclaration de conflit d'intérêts

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-23-392/coif). P.J.P. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from July 2022 to June 2024. S.J.N. as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from September 2023 to August 2025. D.T.L.W. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from February 2021 to January 2023. K.C. was supported by the National Health and Medical Research Council postgraduate scholarship (No. APP2002573), which covers a portion of the research-related expenses and stipend to help with living expenses, research-related travel costs and other expenses associated with research project. S.J.N. received consulting fees from Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi- Regeneron, Vaxxinity, CSL Sequiris, and Novo Nordisk; received grants from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Cyclarity, Eli Lilly, Esperion, Resverlogix, New Amsterdam Pharma, Novartis, InfraReDx and Sanofi-Regeneron. D.T.L.W. received honoraria for lectures from Eli-Lilly, Pfizer and Boehringer. The other authors have no conflicts of interest to declare.

Auteurs

Kevin Cheng (K)

Monash Cardiovascular Research Centre, Victorian Heart Institute, Monash Health, Monash University, Clayton, VIC, Australia.

Andrew Lin (A)

Monash Cardiovascular Research Centre, Victorian Heart Institute, Monash Health, Monash University, Clayton, VIC, Australia.
Cedars-Sinai Medical Center, Biomedical Imaging Research Institute, Los Angeles, CA, USA.

Peter J Psaltis (PJ)

Vascular Research Centre, Heart and Vascular Program, Lifelong Health Theme, SAHMRI, Adelaide, SA, Australia.
Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
Department of Cardiology, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, SA, Australia.

Adil Rajwani (A)

Department of Cardiology, Royal Perth Hospital, Perth, WA, Australia.

Angus Baumann (A)

Alice Springs Hospital, Alice Springs, NT, Australia.

Nicholas Brett (N)

Department of Radiology, Royal Hobart Hospital, Hobart, TAS, Australia.

Nadarajah Kangaharan (N)

Department of Cardiology, Royal Darwin Hospital, Tiwi, NT, Australia.

James Otton (J)

Department of Cardiology, Liverpool Hospital, Liverpool, NSW, Australia.

Stephen J Nicholls (SJ)

Monash Cardiovascular Research Centre, Victorian Heart Institute, Monash Health, Monash University, Clayton, VIC, Australia.

Damini Dey (D)

Cedars-Sinai Medical Center, Biomedical Imaging Research Institute, Los Angeles, CA, USA.

Dennis T L Wong (DTL)

Monash Cardiovascular Research Centre, Victorian Heart Institute, Monash Health, Monash University, Clayton, VIC, Australia.

Classifications MeSH