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Artificial intelligence (AI) is likely to revolutionise the way medical images are analysed and has the potential to improve identification and analysis of vulnerable, or high-risk, coronary plaque and may thus lead to advances in treating coronary artery disease. However, coronary plaque analysis is challenging due to cardiac and respiratory motion as well as the small size of cardiovascular structures. Moreover, analysing coronary imaging data is currently time-consuming, requires high reader expertise with dedicated cardiovascular imaging training, and is subject to considerable inter- and intra-reader variability. AI has the potential to improve the imaging of vulnerable coronary plaque, but requires robust development, testing, and validation. Combining human reader expertise with AI may provide reliable and valid interpretation of images obtained using computed tomography, magnetic resonance imaging, positron emission tomography, intravascular ultrasound, or optical coherence tomography. In this Roadmap article, we review existing evidence for AI for vulnerable coronary plaque imaging and provide consensus recommendations developed by an interdisciplinary group of experts in AI and non-invasive and invasive coronary imaging. This Roadmap article also outlines future requirements for AI technology to address bias, uncertainty, explainability, and generalisability. This is essential for the clinical acceptance of AI and its use in handling the anticipated growing volume of coronary imaging procedures.

BACKGROUND: 18F-GP1 is a novel positron-emitting radiotracer that is highly specific for activated platelets and thrombus. In a proof-of-concept study, we aimed to determine its potential clinical application in establishing the role and origin of thrombus in ischemic stroke. METHODS: Eleven patients with recent ischemic stroke (n=9) or transient ischemic attack (n=2) underwent 18F-GP1 positron emission tomography and computed tomography angiography at a median of 11 (range, 2-21) days from symptom onset. 18F-GP1 uptake (maximum target-to-background ratio) was assessed in the carotid arteries and brain. RESULTS: 18F-GP1 uptake was identified in 10 of 11 patients: 4 in the carotid arteries only, 3 in the brain only, and 3 in both the brain and carotid arteries. In those with carotid uptake, 4 participants had >50% stenosis and 3 had nonstenotic disease. One case had bilateral stenotic disease (>70%), but only the culprit carotid artery demonstrated 18F-GP1 uptake. The average uptake was higher in the culprit (median maximum target-to-background ratio, 1.55 [interquartile range, 1.26-1.82]) compared with the contralateral nonculprit carotid artery (maximum target-to-background ratio, 1.22 [1.19-1.6]). In those with brain 18F-GP1 uptake (maximum target-to-background ratio, 6.45 [4.89-7.65]), areas of acute infarction on computed tomography correlated with brain 18F-GP1 uptake in 6 cases. Ex vivo autoradiography of postmortem infarcted brain tissue showed focal uptake corresponding to intraluminal thrombus within the culprit vessel and downstream microvasculature. There was also evidence of diffuse uptake within some of the infarcted brain tissue reflecting parenchymal petechial hemorrhage. CONCLUSIONS: 18F-GP1 positron emission tomography and computed tomography angiography is a novel noninvasive method of identifying in vivo cerebrovascular thrombosis, which holds major promise in understanding the role and origin of thrombosis in stroke. REGISTRATION: URL: https://www.CLINICALTRIALS: gov; Unique identifier: NCT03943966.

In this EACVI clinical scientific update, we will explore the current use of multi-modality imaging in the diagnosis, risk-stratification and follow-up of patients with aortic stenosis, with a particular focus on recent developments and future directions. Echocardiography is and will likely remain the key method of diagnosis and surveillance of aortic stenosis providing detailed assessments of valve haemodynamics and the cardiac remodelling response. CT is already widely used in the planning of transcutaneous aortic valve implantation. We anticipate its increased use as an anatomical adjudicator to clarify disease severity in patients with discordant echocardiographic measurements. CT calcium scoring is currently used for this purpose, however contrast computed tomography techniques are emerging that allow identification of both calcific and fibrotic valve thickening. Additionally, improved assessments of myocardial decompensation with echocardiography, cardiac magnetic resonance and computed tomography will become more commonplace in our routine assessment of aortic stenosis. Underpinning all of this will be widespread application of artificial intelligence. In combination we believe this new era of multi-modality imaging in aortic stenosis will improve the diagnosis, follow-up and timing of intervention in aortic stenosis as well as potentially accelerate the development of the novel pharmacological treatments required for this disease.

IMPORTANCE: Recurrent coronary events in patients with recent myocardial infarction remain a major clinical problem. Noninvasive measures of coronary atherosclerotic disease activity have the potential to identify individuals at greatest risk. OBJECTIVE: To assess whether coronary atherosclerotic plaque activity as assessed by noninvasive imaging is associated with recurrent coronary events in patients with myocardial infarction. DESIGN, SETTING, AND PARTICIPANTS: This prospective, longitudinal, international multicenter cohort study recruited participants aged 50 years or older with multivessel coronary artery disease and recent (within 21 days) myocardial infarction between September 2015 and February 2020, with a minimum 2 years' follow-up. INTERVENTION: Coronary 18F-sodium fluoride positron emission tomography and coronary computed tomography angiography. MAIN OUTCOMES AND MEASURES: Total coronary atherosclerotic plaque activity was assessed by 18F-sodium fluoride uptake. The primary end point was cardiac death or nonfatal myocardial infarction but was expanded during study conduct to include unscheduled coronary revascularization due to lower than anticipated primary event rates. RESULTS: Among 2684 patients screened, 995 were eligible, 712 attended for imaging, and 704 completed an interpretable scan and comprised the study population. The mean (SD) age of participants was 63.8 (8.2) years, and most were male (601 [85%]). Total coronary atherosclerotic plaque activity was identified in 421 participants (60%). After a median follow-up of 4 years (IQR, 3-5 years), 141 participants (20%) experienced the primary end point: 9 had cardiac death, 49 had nonfatal myocardial infarction, and 83 had unscheduled coronary revascularizations. Increased coronary plaque activity was not associated with the primary end point (hazard ratio [HR], 1.25; 95% CI, 0.89-1.76; P = .20) or unscheduled revascularization (HR, 0.98; 95% CI, 0.64-1.49; P = .91) but was associated with the secondary end point of cardiac death or nonfatal myocardial infarction (47 of 421 patients with high plaque activity [11.2%] vs 19 of 283 with low plaque activity [6.7%]; HR, 1.82; 95% CI, 1.07-3.10; P = .03) and all-cause mortality (30 of 421 patients with high plaque activity [7.1%] vs 9 of 283 with low plaque activity [3.2%]; HR, 2.43; 95% CI, 1.15-5.12; P = .02). After adjustment for differences in baseline clinical characteristics, coronary angiography findings, and Global Registry of Acute Coronary Events score, high coronary plaque activity was associated with cardiac death or nonfatal myocardial infarction (HR, 1.76; 95% CI, 1.00-3.10; P = .05) but not with all-cause mortality (HR, 2.01; 95% CI, 0.90-4.49; P = .09). CONCLUSIONS AND RELEVANCE: In this cohort study of patients with recent myocardial infarction, coronary atherosclerotic plaque activity was not associated with the primary composite end point. The findings suggest that risk of cardiovascular death or myocardial infarction in patients with elevated plaque activity warrants further research to explore its incremental prognostic implications.

AimsAortic stenosis is characterized by fibrosis and calcification of the valve, with a higher proportion of fibrosis observed in women. Stenotic bicuspid aortic valves progress more rapidly than tricuspid valves which may also influence the relative composition of the valve. We aimed to investigate the influence of cusp morphology on quantitative aortic valve composition quantified from contrast-enhanced computed tomography angiography in severe aortic stenosis. Methods and resultsPatients undergoing transcatheter aortic valve implantation with bicuspid and tricuspid valves were propensity matched 1:1 by age, sex, and comorbidities. Computed tomography angiograms were analyzed using semi-automated software to quantify fibrotic and calcific scores (volume/valve annular area) and the fibro-calcific ratio (fibrotic score/calcific score). The study population (n=140) was elderly (76±10 years, 62% male) and had a peak aortic jet velocity of 4.1±0.7 m/s. Compared to those with tricuspid valves (n=70), patients with bicuspid valves (n=70) had higher fibrotic scores (204 [interquartile range 118-267] versus 144[99-208] mm3/cm2, p=0.006) with similar calcific scores (p=0.614). Women had greater fibrotic scores than men in bicuspid (224[181-307] versus 169[109- 247] mm3/cm2; p=0.042) but not tricuspid valves (p=0.232). Men had greater calcific scores than women in both bicuspid (203[124-355] versus 130[70-182] mm3/cm2; p=0.008) and tricuspid (177[136-249] versus 100[62-150] mm3/cm2; p=0.004) valves. Among both valve types, women had greater fibro-calcific ratio compared to men (tricuspid 1.86[0.94-2.56] versus 0.86[0.54-1.24], p=0.001 and bicuspid 1.78[1.21-2.90] versus 0.74[0.44-1.53], p=0.001).ConclusionsIn severe aortic stenosis, bicuspid valves have proportionately more fibrosis than tricuspid valves, especially in women.

This 2022 European Atherosclerosis Society lipoprotein(a) [Lp(a)] consensus statement updates evidence for the role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and considers its inclusion in global risk estimation. Epidemiologic and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes in different ethnicities; elevated Lp(a) is a risk factor even at very low levels of low-density lipoprotein cholesterol. High Lp(a) is associated with both microcalcification and macrocalcification of the aortic valve. Current findings do not support Lp(a) as a risk factor for venous thrombotic events and impaired fibrinolysis. Very low Lp(a) levels may associate with increased risk of diabetes mellitus meriting further study. Lp(a) has pro-inflammatory and pro-atherosclerotic properties, which may partly relate to the oxidized phospholipids carried by Lp(a). This panel recommends testing Lp(a) concentration at least once in adults; cascade testing has potential value in familial hypercholesterolaemia, or with family or personal history of (very) high Lp(a) or premature ASCVD. Without specific Lp(a)-lowering therapies, early intensive risk factor management is recommended, targeted according to global cardiovascular risk and Lp(a) level. Lipoprotein apheresis is an option for very high Lp(a) with progressive cardiovascular disease despite optimal management of risk factors. In conclusion, this statement reinforces evidence for Lp(a) as a causal risk factor for cardiovascular outcomes. Trials of specific Lp(a)-lowering treatments are critical to confirm clinical benefit for cardiovascular disease and aortic valve stenosis.