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Background: A lesion-level risk prediction for acute coronary syndrome (ACS) needs better characterization., Objectives: This study sought to investigate the additive value of artificial intelligence-enabled quantitative coronary plaque and hemodynamic analysis (AI-QCPHA)., Methods: Among ACS patients who underwent coronary computed tomography angiography (CTA) from 1 month to 3 years before the ACS event, culprit and nonculprit lesions on coronary CTA were adjudicated based on invasive coronary angiography. The primary endpoint was the predictability of the risk models for ACS culprit lesions. The reference model included the Coronary Artery Disease Reporting and Data System, a standardized classification for stenosis severity, and high-risk plaque, defined as lesions with ≥2 adverse plaque characteristics. The new prediction model was the reference model plus AI-QCPHA features, selected by hierarchical clustering and information gain in the derivation cohort. The model performance was assessed in the validation cohort., Results: Among 351 patients (age: 65.9 ± 11.7 years) with 2,088 nonculprit and 363 culprit lesions, the median interval from coronary CTA to ACS event was 375 days (Q1-Q3: 95-645 days), and 223 patients (63.5%) presented with myocardial infarction. In the derivation cohort (n = 243), the best AI-QCPHA features were fractional flow reserve across the lesion, plaque burden, total plaque volume, low-attenuation plaque volume, and averaged percent total myocardial blood flow. The addition of AI-QCPHA features showed higher predictability than the reference model in the validation cohort (n = 108) (AUC: 0.84 vs 0.78; P < 0.001). The additive value of AI-QCPHA features was consistent across different timepoints from coronary CTA., Conclusions: AI-enabled plaque and hemodynamic quantification enhanced the predictability for ACS culprit lesions over the conventional coronary CTA analysis. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary Computed Tomography Angiography and Computational Fluid Dynamics II [EMERALD-II]; NCT03591328)., Competing Interests: Funding Support and Author Disclosures This study received funding from HeartFlow Inc. The company performed the computational fluid dynamics, and artificial intelligence quantitative coronary plaque analysis but was not involved in the study design, collection, analysis, and interpretation of data; the writing of this paper; or the decision to submit it for publication. Dr Koo has received institutional research grants from Abbott, Philips, and HeartFlow Inc. Dr Nam has received institutional research grants from Abbott and Genoss. Dr Merkely has received direct personal payments for speaker fees or studies from Abbott, AstraZeneca, Biotronik, Boehringer Ingelheim, CSL Behring, Daiichi Sankyo, DUKE Clinical Institute, Medtronic, and Novartis and institutional grants from Abbott, AstraZeneca, Biotronik, Boehringer Ingelheim, Boston Scientific, Bristol Myers Squibb, CSL Behring, Daiichi Sankyo, DUKE Clinical Institute, Eli Lilly, Medtronic, Novartis, Terumo, and VIFOR Pharma. Dr de Bruyne has received institutional unrestricted research grants from Abbott, Boston Scientific, and Biotronik; has received consulting fees from Abbott, Opsens, and Boston Scientific; and is a shareholder for Siemens, GE, Bayer, Philips, HeartFlow Inc, Edwards Life Sciences, Sanofi, and Omega Pharma. Dr Ko has equity in Artrya and has received honoraria from Medtronic, Abbott Vascular, and Canon Medical. Dr Leipsic is a consultant for and holds stock options in HeartFlow Inc and modest personal core lab fees from Arineta. Dr Shah has received honoraria as a speaker for HeartFlow Inc. Dr Bax has received unrestricted research grants from Abbott and Edwards Lifesciences to the Department of Cardiology, Leiden University Medical Center, the Netherlands. Dr Shaw has received honoraria from HeartFlow Inc and Elucid Imaging. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Coronary Computed Tomography Angiography (CCTA) has now become an established tool in the diagnostic process for patients suspected of coronary artery disease. In light of rapid technological development, CCTA has evolved into an imaging modality providing both anatomical and functional information to guide patient management. In this article, we describe the role of cardiac CT in assessing atherosclerotic plaque, chest pain evaluation, cardiovascular risk stratification, planning and guiding coronary intervention, as well as structural heart diseases., Competing Interests: Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article. O. Muller déclare des fonds de recherche/honoraria obtenus de la part de Edwards Lifescience et des honararia obtenu par Abbott Medical.

Background: Luminal stenosis, computed tomography-derived fractional-flow reserve (FFR CT ), and high-risk plaque features on coronary computed tomography angiography are all known to be associated with adverse clinical outcomes. The interactions between these variables, patient outcomes, and quantitative plaque volumes have not been previously described., Methods: Patients with coronary computed tomography angiography (n=4430) and one-year outcome data from the international ADVANCE (Assessing Diagnostic Value of Noninvasive FFR CT in Coronary Care) registry underwent artificial intelligence-enabled quantitative coronary plaque analysis. Optimal cutoffs for coronary total plaque volume and each plaque subtype were derived using receiver-operator characteristic curve analysis. The resulting plaque volumes were adjusted for age, sex, hypertension, smoking status, type 2 diabetes, hyperlipidemia, luminal stenosis, distal FFR CT , and translesional delta-FFR CT . Median plaque volumes and optimal cutoffs for these adjusted variables were compared with major adverse cardiac events, late revascularization, a composite of the two, and cardiovascular death and myocardial infarction., Results: At one year, 55 patients (1.2%) had experienced major adverse cardiac events, and 123 (2.8%) had undergone late revascularization (>90 days). Following adjustment for age, sex, risk factors, stenosis, and FFR CT , total plaque volume above the receiver-operator characteristic curve-derived optimal cutoff (total plaque volume >564 mm 3 ) was associated with the major adverse cardiac event/late revascularization composite (adjusted hazard ratio, 1.515 [95% CI, 1.093-2.099]; P =0.0126), and both components. Total percent atheroma volume greater than the optimal cutoff was associated with both major adverse cardiac event/late revascularization (total percent atheroma volume >24.4%; hazard ratio, 2.046 [95% CI, 1.474-2.839]; P <0.0001) and cardiovascular death/myocardial infarction (total percent atheroma volume >37.17%, hazard ratio, 4.53 [95% CI, 1.943-10.576]; P =0.0005). Calcified, noncalcified, and low-attenuation percentage atheroma volumes above the optimal cutoff were associated with all adverse outcomes, although this relationship was not maintained for cardiovascular death/myocardial infarction in analyses stratified by median plaque volumes., Conclusions: Analysis of the ADVANCE registry using artificial intelligence-enabled quantitative plaque analysis shows that total plaque volume is associated with one-year adverse clinical events, with incremental predictive value over luminal stenosis or abnormal physiology by FFR CT ., Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02499679., Competing Interests: Dr Patel has received research grants from HeartFlow, Bayer, Janssen, and the National Heart, Lung, and Blood Institute; and has served on the advisory board for HeartFlow, Bayer, and Janssen. Dr Nørgaard has received unrestricted institutional research grants from Siemens and HeartFlow. Dr Fairbairn has served on the Speakers Bureau for HeartFlow. Dr Nieman has received institutional research support from Siemens Healthineers, HeartFlow, GE Healthcare, and Bayer Healthcare. Dr Hurwitz Koweek has received research support and speaking fees from HeartFlow and Siemens. Dr Pontone has received institutional research grant and honorarium as consultant/speaker from GE Healthcare, Bracco, Medtronic, Bayer, and HeartFlow. Dr Rabbat has served as a consultant for HeartFlow. Ms Mullen is an employee of and owns equity in HeartFlow. Dr De Bruyne has an institutional consulting relationship with Boston Scientific, Abbott Vascular, CathWorks, Siemens, GE Healthcare, and Coroventis Research; has received institutional research grants from Abbott Vascular, Coroventis Research, CathWorks, and Boston Scientific; and holds equities in Philips, Siemens, GE Healthcare, Edwards Lifesciences, HeartFlow, Opsens, and Celiad. Dr Rogers is employee of and owns equity in HeartFlow. Dr Leipsic has received an unrestricted research grant from GE Healthcare, has stock options and received consulting fees from HeartFlow and Circle CVI, and speaking fees from GE and Philips. Dr Ng is an employee of HeartFlow. The other authors report no conflicts.

Ischemic heart disease is the most common cause of mortality worldwide. The pathophysiology of myocardial infarction relates to temporal changes of atherosclerotic plaque culminating in plaque rupture, erosion or hemorrhage and the subsequent thrombotic response. Coronary computed tomographic angiography (CCTA) provides the ability to visualize and quantify plaque, and plaque progression can be measured on a per-patient basis by comparing findings of serial CCTA. The Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography IMaging (PARADIGM) registry was established with the objective of identifying patterns of plaque progression in a large population. The registry comprises over 2000 patients with multiple CCTA scans performed at least two years apart. Unlike previous CCTA registries, a semi-automated plaque quantification technique permitting detailed analysis of plaque progression was performed on all patients with interpretable studies. Since the registry was established, 19 peer-reviewed publications were identified, and all are reviewed and summarized in this article., Competing Interests: Declaration of competing interest Dr. Kavitha Chinnaiyan is a non-compensated medical advisory board member of Heartflow Inc. The remaining authors have no relevant disclosures., (Copyright © 2021 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

In the absence of disease impacting the coronary arteries or myocardium, there exists a linear relationship between vessel volume and myocardial mass to ensure balanced distribution of blood supply. This balance may be disturbed in diseases of either the coronary artery tree, the myocardium, or both. However, in contemporary evaluation the coronary artery anatomy and myocardium are assessed separately. Recently the coronary lumen volume to myocardial mass ratio (V/M), measured noninvasively using coronary computed tomography angiography (CTCA), has emerged as an integrated measure of myocardial blood supply and demand in vivo. This has the potential to yield new insights into diseases where this balance is altered, thus impacting clinical diagnoses and management. In this review, we outline the scientific methodology underpinning CTCA-derived measurement of V/M. We describe recent studies describing alterations in V/M across a range of cardiovascular conditions, including coronary artery disease, cardiomyopathies and coronary microvascular dysfunction. Lastly, we highlight areas of unmet research need and future directions, where V/M may further enhance our understanding of the pathophysiology of cardiovascular disease., Competing Interests: Declaration of competing interest BLN has received institutional unrestricted research grants from Siemens and HeartFlow. JL is a consultant and holds stock options in Circle CVI and Heartflow, research grants from GE and modest speaker fees from GE and Philips. AI has received consulting fees from Canon, Artrya Medical and Boston Scientific. CT and AU are employees of HeartFlow Inc., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: This study sought to investigate the impact of low tube voltage scanning heterogeneity of coronary luminal attenuation on plaque quantification and characterization with coronary computed tomography angiography (CCTA)., Background: The impact of low tube voltage and coronary luminal attenuation on quantitative coronary plaque remains uncertain., Methods: A total of 1,236 consecutive patients (age: 60 ± 9 years; 41% female) who underwent serial CCTA at an interval of ≥2 years were included from an international registry. Patients with prior revascularization or nonanalyzable coronary CTAs were excluded. Total coronary plaque volume was assessed and subclassified based on specific Hounsfield unit (HU) threshold: necrotic core, fibrofatty plaque, and fibrous plaque and dense calcium. Luminal attenuation was measured in the aorta., Results: With increasing luminal HU (<350, 350-500, and >500 HU), percent calcified plaque was increased (16%, 27%, and 40% in the median; P < 0.001), and fibrofatty plaque (26%, 13%, and 4%; P < 0.001) and necrotic core (1.6%, 0.3%, and 0.0%; P < 0.001) were decreased. Higher tube voltage scanning (80, 100, and 120 kV) resulted in decreasing luminal attenuation (689 ± 135, 497 ± 89, and 391 ± 73 HU; P < 0.001) and calcified plaque volume (59%, 34%, and 23%; P < 0.001) and increased fibrofatty plaque (3%, 9%, and 18%; P < 0.001) and necrotic core (0.2%, 0.1%, and 0.6%; P < 0.001). Mediation analysis showed that the impact of 100 kV on plaque composition, compared with 120 kV, was primarily caused by an indirect effect through blood pool attenuation. Tube voltage scanning of 80 kV maintained a direct effect on fibrofatty plaque and necrotic core in addition to an indirect effect through the luminal attenuation., Conclusions: Low tube voltage usage affected plaque morphology, mainly through an increase in luminal HU with a resultant increase in calcified plaque and a reduction in fibrofatty and necrotic core. These findings should be considered as CCTA-based plaque measures are being used to guide medical management and, in particular, when being used as a measure of treatment response. (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411)., Competing Interests: Funding Support and Author Disclosures This work was supported by the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea funded by the Ministry of Science and ICT (MSIT) (grant number 2012027176). The study was also funded in part by a grant from the Dalio Foundation (New York, New York). Dr Leipsic receives institutional grants to provide core lab services to Edwards Life Sciences, Abbott, Boston Scientific, and Medtronic and is a consultant to and has stock options in Circle CVI and HeartFlow. Dr Andreini is on the Speakers Bureau for GE Healthcare and receives grant support from GE Healthcare and Bracco. Dr Budoff has received grant support from the National Institutes of Health and GE Healthcare. Dr Chun has received funding from a National Research Foundation grant funded by the South Korea government (MEST) (NRF- 2015R1D1A1A01059717). Dr Pontone has received institutional research grants from GE Healthcare, HeartFlow, Medtronic, Bracco, and Bayer. Dr Virmani has received institutional research support from 480 Biomedical, Abbott Vascular, ART, BioSensors International, Biotronik, Boston Scientific, CeloNova, Claret Medical, Cook Medical, Cordis, Edwards Lifesciences, Medtronic, MicroVention, OrbusNeich, ReCord, SINO Medical Technology, Spectranetics, Surmodics, Terumo Corporation, W.L. Gore, and Xeltis; has received honoraria from 480 Biomedical, Abbott Vascular, Boston Scientific, Cook Medical, Lutonix, Medtronic, Terumo Corporation, and W.L. Gore; and is a consultant for 480 Biomedical, Abbott Vascular, Medtronic, and W.L. Gore. Dr Samady has received grant support from Phillips/Volcano and St. Jude Abbott/Medtronic/Gilead. Dr Berman has received software royalties from Cedars-Sinai. Dr Bax has received unrestricted research grants from Biotronik, Medtronic, Boston Scientific, and Edwards Lifesciences. Dr Chang has received funding from the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT, and Future Planning (grant 2012027176). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

This article aims to clarify the value of cardiac CT as well as its new applications in the different areas of cardiology for both diagnosis and pretreatment evaluation, including stable coronary artery disease, acute coronary syndrome, valvular disease and the functional and morphological evaluation of the heart., Competing Interests: Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.