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Abstract Background The indications, complexity and capabilities of cardiovascular magnetic resonance (CMR) have rapidly expanded. Whether actual service provision and training have developed in parallel is unknown. Methods We undertook a systematic telephone and postal survey of all public hospitals on behalf of the British Society of Cardiovascular Magnetic Resonance to identify all CMR providers within the United Kingdom. Results Of the 60 CMR centres identified, 88% responded to a detailed questionnaire. Services are led by cardiologists and radiologists in equal proportion, though the majority of current trainees are cardiologists. The mean number of CMR scans performed annually per centre increased by 44% over two years. This trend was consistent across centres of different scanning volumes. The commonest indication for CMR was assessment of heart failure and cardiomyopathy (39%), followed by coronary artery disease and congenital heart disease. There was striking geographical variation in CMR availability, numbers of scans performed, and distribution of trainees. Centres without on site scanning capability refer very few patients for CMR. Just over half of centres had a formal training programme, and few performed regular audit. Conclusion The number of CMR scans performed in the UK has increased dramatically in just two years. Trainees are mainly located in large volume centres and enrolled in cardiology as opposed to radiology training programmes.

BACKGROUND: The indications, complexity and capabilities of cardiovascular magnetic resonance (CMR) have rapidly expanded. Whether actual service provision and training have developed in parallel is unknown. METHODS: We undertook a systematic telephone and postal survey of all public hospitals on behalf of the British Society of Cardiovascular Magnetic Resonance to identify all CMR providers within the United Kingdom. RESULTS: Of the 60 CMR centres identified, 88% responded to a detailed questionnaire. Services are led by cardiologists and radiologists in equal proportion, though the majority of current trainees are cardiologists. The mean number of CMR scans performed annually per centre increased by 44% over two years. This trend was consistent across centres of different scanning volumes. The commonest indication for CMR was assessment of heart failure and cardiomyopathy (39%), followed by coronary artery disease and congenital heart disease. There was striking geographical variation in CMR availability, numbers of scans performed, and distribution of trainees. Centres without on site scanning capability refer very few patients for CMR. Just over half of centres had a formal training programme, and few performed regular audit. CONCLUSION: The number of CMR scans performed in the UK has increased dramatically in just two years. Trainees are mainly located in large volume centres and enrolled in cardiology as opposed to radiology training programmes. [ABSTRACT FROM AUTHOR]

Background: Patients with osteoporosis demonstrate increased vascular calcification but the effect of osteoporosis treatments on vascular calcification remains unclear. The present study aimed to examine whether coronary or aortic calcification are influenced by denosumab and alendronic acid treatment., Methods and Results: In a double-blind randomized controlled SALTIRE2 (Study Investigating the Effect of Drugs Used to Treat Osteoporosis on the Progression of Calcific Aortic Stenosis) trial, patients with aortic stenosis were randomized 2:1:2:1 to denosumab, placebo injection, alendronic acid, or placebo capsule. Participants underwent serial imaging with computed tomography and 18F-sodium fluoride positron emission tomography for the assessment of vascular calcium burden and calcification activity, respectively. We report the prespecified secondary analyses of 24-month change in coronary calcium score, and 12-month changes in thoracic aorta calcium score, coronary and aortic 18F-sodium fluoride activity. One hundred fifty patients with aortic stenosis (72±8 years; 21% female) were randomized to denosumab (n=49), alendronic acid (n=51), and placebo (injection n=25, capsule n=25). There were no differences in change in coronary calcium scores between placebo (16 [-64 to 148] Agatston units) and either denosumab (94 [0-212] Agatston units, P =0.24) or alendronic acid (34 [-62 to 134], P =0.99). There were no differences in change in thoracic aorta calcium scores between placebo (132 [22-512] Agatston units) and either denosumab (118 [11-340], P =0.75) or alendronic acid (116 [26-498] Agatston units, P =0.62). There were no differences in changes in coronary or aortic 18F-sodium fluoride activity between treatment groups., Conclusions: Neither alendronic acid nor denosumab are associated with changes in the activity or progression of coronary or aortic calcification. Osteoporosis treatments do not appear to have major impact on vascular calcification of atherosclerosis., Registration: https://www.clinicaltrials.gov; Unique identifier: NCT02132026.

Coronary 18 F-sodium fluoride ( 18 F-fluoride) uptake is a marker of both atherosclerotic disease activity and disease progression. It is currently unknown whether there are rapid temporal changes in coronary 18 F-fluoride uptake and whether these are more marked in those with clinically unstable coronary artery disease. This study aimed to determine the natural history of coronary 18 F-fluoride uptake over 12 mo in patients with either advanced chronic coronary artery disease or a recent myocardial infarction. Methods: Patients with established multivessel coronary artery disease and either chronic disease or a recent acute myocardial infarction underwent coronary 18 F-fluoride PET and CT angiography, which was repeated at 3, 6, or 12 mo. Coronary 18 F-fluoride uptake was assessed in each vessel by measuring the coronary microcalcification activity (CMA). Coronary calcification was quantified by measuring calcium score, mass, and volume. Results: Fifty-nine patients had chronic coronary artery disease (median age, 68 y; 93% male), and 52 patients had a recent myocardial infarction (median age, 65 y; 83% male). Reflecting the greater burden of coronary artery disease, baseline CMA values were higher in those with chronic coronary artery disease. Coronary 18 F-fluoride uptake (CMA > 0) was associated with higher baseline calcium scores (294 Agatston units [AU] [interquartile range, 116-483 AU] vs. 72 AU [interquartile range, 8-222 AU]; P < 0.001) and more rapid progression of coronary calcification scores (39 AU [interquartile range, 10-82 AU] vs. 12 AU [interquartile range, 1-36 AU]; P < 0.001) than was the absence of uptake (CMA = 0). Coronary 18 F-fluoride uptake did not markedly alter over the course of 3, 6, or 12 mo in patients with either chronic coronary artery disease or a recent myocardial infarction. Conclusion: Coronary 18 F-fluoride uptake is associated with the severity and progression of coronary artery disease but does not undergo a rapid dynamic change in patients with chronic or unstable coronary artery disease. This finding suggests that coronary 18 F-fluoride uptake is a temporally stable marker of established and progressive disease., (© 2023 by the Society of Nuclear Medicine and Molecular Imaging.)

Post-infarction ventricular septal defect is a mechanical complication of acute MI. The incidence of this complication is low in the primary percutaneous coronary intervention era. However, the associated mortality is very high at 94% with medical management alone. Open surgical repair or percutaneous transcatheter closure still has an in-hospital mortality >40%. Retrospective comparisons between both closure methods are limited by observation and selection bias. This review addresses the assessment and optimisation of patients prior to repair, the optimal timing of repair, and the limitations in current data. The review considers techniques for percutaneous closure, and finally considers the path that future research should take to improve outcomes for patients., Competing Interests: Disclosures: LKW has received speaker fees from Medtronic Europe. PAC has acted as a proctor for Abbott Vascular. All other authors have no conflicts of interest to declare., (Copyright © 2023, Radcliffe Cardiology.)

Purpose: To determine whether quantitative plaque characterization by using CT coronary angiography (CTCA) can discriminate between type 1 and type 2 myocardial infarction., Materials and Methods: This was a secondary analysis of two prospective studies (ClinicalTrials.gov registration nos. NCT03338504 [2014-2019] and NCT02284191 [2018-2020]) that performed blinded quantitative plaque analysis on findings from CTCA in participants with type 1 myocardial infarction, type 2 myocardial infarction, and chest pain without myocardial infarction. Logistic regression analyses were performed to identify predictors of type 1 myocardial infarction., Results: Overall, 155 participants (mean age, 64 years ± 12 [SD]; 114 men) and 36 participants (mean age, 67 years ± 12; 19 men) had type 1 and type 2 myocardial infarction, respectively, and 136 participants (62 years ± 12; 78 men) had chest pain without myocardial infarction. Participants with type 1 myocardial infarction had greater total (median, 44% [IQR: 35%-50%] vs 35% [IQR: 29%-46%]), noncalcified (39% [IQR: 31%-46%] vs 34% [IQR: 29%-40%]), and low-attenuation (4.15% [IQR: 1.88%-5.79%] vs 1.64% [IQR: 0.89%-2.28%]) plaque burdens ( P < .05 for all) than those with type 2. Participants with type 2 myocardial infarction had similar low-attenuation plaque burden to those with chest pain without myocardial infarction (P = .4). Low-attenuation plaque was an independent predictor of type 1 myocardial infarction (adjusted odds ratio, 3.44 [95% CI: 1.84, 6.96]; P < .001), with better discrimination than noncalcified plaque burden and maximal area of coronary stenosis (C statistic, 0.75 [95% CI: 0.67, 0.83] vs 0.62 [95% CI: 0.53, 0.71] and 0.61 [95% CI: 0.51, 0.70] respectively; P ≤ .001 for both)., Conclusion: Higher low-attenuation coronary plaque burden in patients with type 1 myocardial infarction may help distinguish these patients from those with type 2 myocardial infarction. Keywords: Ischemia/Infarction, CT Angiography, Quantitative CTClinical trial registration nos. NCT03338504 and NCT02284191 Supplemental material is available for this article. © RSNA, 2022., Competing Interests: Disclosures of conflicts of interest: M.M. Author is a British Heart Foundation (BHF) clinical research fellow at the University of Edinburgh, a BHF grant (grant no. FS/19/46/34445) has supported author’s work since November 2019. A.B. Support for the present manuscript from the BHF (grant no. FS/16/75/32533). E.T. No relevant relationships. A.R.C. No relevant relationships. M.D. No relevant relationships. J.D.H. No relevant relationships. J.C. No relevant relationships. C.T. No relevant relationships. R.W. Clinical training research fellowship from the Medical Research Council UK (no. MR/V007017/1). A.G. Participation on advisory board for Abbott for brain and cardiac biomarkers, fees paid to author’s institution. M.R.D. No relevant relationships. C.R. No relevant relationships. N.C. Unrestricted research grants from Boston Scientific, Haemonetics, Beckmann Coulter, and HeartFlow; speakers fees from Abbott and Boston Scientific; travel sponsorship from Biosensors, Abbott, Edwards, and Medtronic. A.K. No relevant relationships. D.F. No relevant relationships. N.L.M. BHF grants (grant nos. CH/F/21/90010, RG/20/10/34966, and RE/18/5/34216) paid to author’s institution; payment or honoraria for lectures from Abbott Diagnostics and Siemens Healthineers; payment for participation on advisory boards for LumiraDX, Roche Diagnostics, and Siemens Healthineers; receipt of reagent from Siemens Healthineers to support research. P.J.S. Grants from Siemens Medical Systems and National Institutes of Health, paid to author’s institution; royalties or licenses from Cedars-Sinai Medical Systems, paid to author and author’s institution; consulting fees from IBA; several patents planned and pending, not related to this field of work, via Cedars-Sinai; vice-president of Society of Nuclear Medicine. D.E.N. Supported by the BHF (grant nos. CH/09/002, RG/16/10/32375, and RE/18/5/34216) and is the recipient of a Wellcome Trust Senior Investigator award (no. WT103782AIA); author is a co-applicant and co-author on the RAPID-CTA trial funded by the National Institute for Health (NIH) Research Health Technology Assessment Programme (no. 13/04/108) and the DEMAND-MI study funded by the BHF (FS/16/75/32533). D.D. NIH/National Heart, Lung, and Blood Institute grants (nos. 1R01HL148787-01A1 and 1R01HL151266); software royalties from Cedars-Sinai Medical Center, outside the current work. M.C.W. Supported by the BHF (grant no. FS/ICRF/20/26002); author has given talks for Canon Medical Systems and Siemens Healthineers; member of the board of directors of Society of Cardiovascular Computed Tomography; president-elect of the education committee of the British Society of Cardiovascular Imaging; president-elect of the European Society of Cardiovascular Radiology; Radiology: Cardiothoracic Imaging editorial board member., (© 2022 by the Radiological Society of North America, Inc.)

Background: Type 2 myocardial infarction is caused by myocardial oxygen supply-demand imbalance, and its diagnosis is increasingly common with the advent of high-sensitivity cardiac troponin assays. Although this diagnosis is associated with poor outcomes, widespread uncertainty and confusion remain among clinicians as to how to investigate and manage this heterogeneous group of patients with type 2 myocardial infarction., Methods: In a prospective cohort study, 8064 consecutive patients with increased cardiac troponin concentrations were screened to identify patients with type 2 myocardial infarction. We excluded patients with frailty or renal or hepatic failure. All study participants underwent coronary (invasive or computed tomography angiography) and cardiac (magnetic resonance or echocardiography) imaging, and the underlying causes of infarction were independently adjudicated. The primary outcome was the prevalence of coronary artery disease., Results: In 100 patients with a provisional diagnosis of type 2 myocardial infarction (median age, 65 years [interquartile range, 55-74 years]; 43% women), coronary and cardiac imaging reclassified the diagnosis in 7 patients: type 1 or 4b myocardial infarction in 5 and acute myocardial injury in 2 patients. In those with type 2 myocardial infarction, median cardiac troponin I concentrations were 195 ng/L (interquartile range, 62-760 ng/L) at presentation and 1165 ng/L (interquartile range, 277-3782 ng/L) on repeat testing. The prevalence of coronary artery disease was 68% (63 of 93), which was obstructive in 30% (28 of 93). Infarct-pattern late gadolinium enhancement or regional wall motion abnormalities were observed in 42% (39 of 93), and left ventricular systolic dysfunction was seen in 34% (32 of 93). Only 10 patients had both normal coronary and normal cardiac imaging. Coronary artery disease and left ventricular systolic dysfunction were previously unrecognized in 60% (38 of 63) and 84% (27 of 32), respectively, with only 33% (21 of 63) and 19% (6 of 32) on evidence-based treatments., Conclusions: Systematic coronary and cardiac imaging of patients with type 2 myocardial infarction identified coronary artery disease in two-thirds and left ventricular systolic dysfunction in one-third of patients. Unrecognized and untreated coronary or cardiac disease is seen in most patients with type 2 myocardial infarction, presenting opportunities for initiation of evidence-based treatments with major potential to improve clinical outcomes., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT03338504.

Background: Lipoprotein(a) [Lp(a)] is associated with increased risk of myocardial infarction, although the mechanism for this observation remains uncertain., Objectives: This study aims to investigate whether Lp(a) is associated with adverse plaque progression., Methods: Lp(a) was measured in patients with advanced stable coronary artery disease undergoing coronary computed tomography angiography at baseline and 12 months to assess progression of total, calcific, noncalcific, and low-attenuation plaque (necrotic core) in particular. High Lp(a) was defined as Lp(a) ≥ 70 mg/dL. The relationship of Lp(a) with plaque progression was assessed using linear regression analysis, adjusting for body mass index, segment involvement score, and ASSIGN score (a Scottish cardiovascular risk score comprised of age, sex, smoking, blood pressure, total and high-density lipoprotein [HDL]-cholesterol, diabetes, rheumatoid arthritis, and deprivation index)., Results: A total of 191 patients (65.9 ± 8.3 years of age; 152 [80%] male) were included in the analysis, with median Lp(a) values of 100 (range: 82 to 115) mg/dL and 10 (range: 5 to 24) mg/dL in the high and low Lp(a) groups, respectively. At baseline, there was no difference in coronary artery disease severity or plaque burden. Patients with high Lp(a) showed accelerated progression of low-attenuation plaque compared with low Lp(a) patients (26.2 ± 88.4 mm 3 vs -0.7 ± 50.1 mm 3 ; P = 0.020). Multivariable linear regression analysis confirmed the relation between Lp(a) and low-attenuation plaque volume progression (β = 10.5% increase for each 50 mg/dL Lp(a), 95% CI: 0.7%-20.3%). There was no difference in total, calcific, and noncalcific plaque volume progression., Conclusions: Among patients with advanced stable coronary artery disease, Lp(a) is associated with accelerated progression of coronary low-attenuation plaque (necrotic core). This may explain the association between Lp(a) and the high residual risk of myocardial infarction, providing support for Lp(a) as a treatment target in atherosclerosis., Competing Interests: Funding Support and Author Disclosures Drs Kaiser and Stroes were supported by the Netherlands Heart Foundation CVON 2017-20: generating the best evidence-based pharmaceutical targets for atherosclerosis [GENIUS II]). Dr Dey is supported by the National Institute of Health/National Heart, Lung, and Blood Institute grants (1R01HL148787-01A1 and 1R01HL151266). Dr Dweek is supported by the British Heart Foundation (FS/14/78/31020) and is the recipient of the Sir Jules Thorn Award for Biomedical Research 2015 (15/JTA); has received speaker fees from Pfizer and Novartis; and has received consultancy fees from Novartis, Jupiter Bioventures, and Silence therapeutics. Dr Stroes has received research grants/support to his institution from Amgen, Sanofi, Resverlogix, and Athera; and has served as a consultant for Amgen, Sanofi, Esperion, Novartis, and Ionis Pharmaceuticals. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Advances in imaging technology have driven the rapid expansion in the use of CT in the assessment of coronary atherosclerotic plaque. Based on a rapidly growing evidence base, current guidelines recommend coronary CT angiography as the first-line diagnostic test for patients presenting with stable chest pain. There is a growing need to refine current methods for diagnosis and risk stratification to improve the individualisation of preventative therapies. Imaging assessments of high-risk plaque with CT can be used to differentiate stable from unstable patterns of coronary atherosclerosis and potentially to improve patient risk stratification. This review will focus on coronary imaging with CT with a specific focus on the detection of coronary atherosclerosis, high-risk plaque features, and the implications for patient management., (© 2019 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)

Background Positron emission tomography (PET) using 18 F-sodium fluoride ( 18 F-fluoride) to detect microcalcification may provide insight into disease activity in coronary atherosclerosis. This study aimed to investigate the relationship between 18 F-fluoride uptake and progression of coronary calcification in patients with clinically stable coronary artery disease. Methods Patients with established multivessel coronary atherosclerosis underwent 18 F-fluoride PET-computed tomography angiography and computed tomography calcium scoring, with repeat computed tomography angiography and calcium scoring at one year. Coronary PET uptake was analyzed qualitatively and semiquantitatively in diseased vessels by measuring maximum tissue-to-background ratio. Coronary calcification was quantified by measuring calcium score, mass, and volume. Results In a total of 183 participants (median age 66 years, 80% male), 116 (63%) patients had increased 18 F-fluoride uptake in at least one vessel. Individuals with increased 18 F-fluoride uptake demonstrated more rapid progression of calcification compared with those without uptake (change in calcium score, 97 [39-166] versus 35 [7-93] AU; P <0.0001). Indeed, the calcium score only increased in coronary segments with 18 F-fluoride uptake (from 95 [30-209] to 148 [61-289] AU; P <0.001) and remained unchanged in segments without 18 F-fluoride uptake (from 46 [16-113] to 49 [20-115] AU; P =0.329). Baseline coronary 18 F-fluoride maximum tissue-to-background ratio correlated with 1-year change in calcium score, calcium volume, and calcium mass (Spearman ρ=0.37, 0.38, and 0.46, respectively; P <0.0001 for all). At the segmental level, baseline 18 F-fluoride activity was an independent predictor of calcium score at 12 months ( P <0.001). However, at the patient level, this was not independent of age, sex, and baseline calcium score ( P =0.50). Conclusions Coronary 18 F-fluoride uptake identifies both patients and individual coronary segments with more rapid progression of coronary calcification, providing important insights into disease activity within the coronary circulation. At the individual patient level, total calcium score remains an important marker of disease burden and progression. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02110303.

Objectives: The goal of this study was to determine whether ticagrelor reduces high-sensitivity troponin I concentrations in patients with established coronary artery disease and high-risk coronary plaque., Background: High-risk coronary atherosclerotic plaque is associated with higher plasma troponin concentrations suggesting ongoing myocardial injury that may be a target for dual antiplatelet therapy., Methods: In a randomized, double-blind, placebo-controlled trial, patients with multivessel coronary artery disease underwent coronary 18 F-fluoride positron emission tomography/coronary computed tomography scanning and measurement of high-sensitivity cardiac troponin I. Patients were randomized (1:1) to receive ticagrelor 90 mg twice daily or matched placebo. The primary endpoint was troponin I concentration at 30 days in patients with increased coronary 18 F-fluoride uptake., Results: In total, 202 patients were randomized to treatment, and 191 met the pre-specified criteria for inclusion in the primary analysis. In patients with increased coronary 18 F-fluoride uptake (120 of 191), there was no evidence that ticagrelor had an effect on plasma troponin concentrations at 30 days (ratio of geometric means for ticagrelor vs. placebo: 1.11; 95% confidence interval: 0.90 to 1.36; p = 0.32). Over 1 year, ticagrelor had no effect on troponin concentrations in patients with increased coronary 18 F-fluoride uptake (ratio of geometric means: 0.86; 95% confidence interval: 0.63 to 1.17; p = 0.33)., Conclusions: Dual antiplatelet therapy with ticagrelor did not reduce plasma troponin concentrations in patients with high-risk coronary plaque, suggesting that subclinical plaque thrombosis does not contribute to ongoing myocardial injury in this setting. (Dual Antiplatelet Therapy to Reduce Myocardial Injury [DIAMOND]; NCT02110303)., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Cardiovascular disease is one of the leading causes of mortality and morbidity worldwide. Atherosclerosis imaging has traditionally focused on detection of obstructive luminal stenoses or measurements of plaque burden. However, with advances in imaging technology it has now become possible to noninvasively interrogate plaque composition and disease activity, thereby differentiating stable from unstable patterns of disease and potentially improving risk stratification. This manuscript reviews multimodality imaging in this field, focusing on carotid and coronary atherosclerosis and how these novel techniques have the potential to complement current imaging assessments and improve clinical decision making., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Within the SCOT-HEART (Scottish COmputed Tomography of the HEART Trial) trial of patients with stable chest pain, the use of coronary computed tomography angiography (CTA) reduced the rate of death from coronary heart disease or nonfatal myocardial infarction (primary endpoint)., Objectives: This study sought to assess the consistency and mechanisms of the 5-year reduction in this endpoint., Methods: In this open-label trial, 4,146 participants were randomized to standard care alone or standard care plus coronary CTA. This study explored the primary endpoint by symptoms, diagnosis, coronary revascularizations, and preventative therapies., Results: Event reductions were consistent across symptom and risk categories (p = NS for interactions). In patients who were not diagnosed with angina due to coronary heart disease, coronary CTA was associated with a lower primary endpoint incidence rate (0.23; 95% confidence interval [CI]: 0.13 to 0.35 vs. 0.59; 95% CI: 0.42 to 0.80 per 100 patient-years; p < 0.001). In those who had undergone coronary CTA, rates of coronary revascularization were higher in the first year (hazard ratio [HR]: 1.21; 95% CI: 1.01 to 1.46; p = 0.042) but lower beyond 1 year (HR: 0.59; 95% CI: 0.38 to 0.90; p = 0.015). Patients assigned to coronary CTA had higher rates of preventative therapies throughout follow-up (p < 0.001 for all), with rates highest in those with CT-defined coronary artery disease. Modeling studies demonstrated the plausibility of the observed effect size., Conclusions: The beneficial effect of coronary CTA on outcomes is consistent across subgroups with plausible underlying mechanisms. Coronary CTA improves coronary heart disease outcomes by enabling better targeting of preventative treatments to those with coronary artery disease. (Scottish COmputed Tomography of the HEART Trial [SCOT-HEART]; NCT01149590)., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Coronary 18 F-fluoride positron emission tomography identifies ruptured and high-risk atherosclerotic plaque. The optimal method to identify, to quantify, and to categorize increased coronary 18 F-fluoride uptake and determine its reproducibility has yet to be established. This study aimed to optimize the identification, quantification, categorization, and scan-rescan reproducibility of increased 18 F-fluoride activity in coronary atherosclerotic plaque., Methods: In a prospective observational study, patients with multi-vessel coronary artery disease underwent serial 18 F-fluoride positron emission tomography. Coronary 18 F-fluoride activity was visually assessed, quantified, and categorized with reference to maximal tissue to background ratios. Levels of agreement for both visual and quantitative methods were determined between scans and observers., Results: Thirty patients (90% male, 20 patients with stable coronary artery disease, and 10 with recent type 1 myocardial infarction) underwent paired serial positron emission tomography-coronary computed tomography angiography imaging within an interval of 12±5 days. A mean of 3.7±1.8 18 F-fluoride positive plaques per patient was identified after recent acute coronary syndrome, compared with 2.4±2.3 positive plaques per patient in stable coronary artery disease. The bias in agreement in maximum tissue to background ratio measurements in visually positive plaques was low between observers (mean difference, -0.01; 95% limits of agreement, -0.32 to 0.30) or between scans (mean difference, 0.06; 95% limits of agreement, -0.49 to 0.61). Good agreement in the categorization of focal 18 F-fluoride uptake was achieved using visual assessment alone (κ=0.66) and further improved at higher maximum tissue to background ratio values., Conclusions: Coronary 18 F-fluoride activity is a precise and reproducible metric in the coronary vasculature. The analytical performance of 18 F-fluoride is sufficient to assess the prognostic utility of this radiotracer as a noninvasive imaging biomarker of plaque vulnerability., Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifiers: NCT02110303 and NCT02278211.