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ObjectiveThe study evaluates the relationship of coronary stenosis, atherosclerotic plaque characteristics (APCs) and age using artificial intelligence enabled quantitative coronary computed tomographic angiography (AI-QCT).MethodsThis is a post-hoc analysis of data from 303 subjects enrolled in the CREDENCE (Computed TomogRaphic Evaluation of Atherosclerotic Determinants of Myocardial IsChEmia) trial who were referred for invasive coronary angiography and subsequently underwent coronary computed tomographic angiography (CCTA). In this study, a blinded core laboratory analysing quantitative coronary angiography images classified lesions as obstructive (≥50%) or non-obstructive (<50%) while AI software quantified APCs including plaque volume (PV), low-density non-calcified plaque (LD-NCP), non-calcified plaque (NCP), calcified plaque (CP), lesion length on a per-patient and per-lesion basis based on CCTA imaging. Plaque measurements were normalised for vessel volume and reported as % percent atheroma volume (%PAV) for all relevant plaque components. Data were subsequently stratified by age <65 and ≥65 years.ResultsThe cohort was 64.4±10.2 years and 29% women. Overall, patients >65 had more PV and CP than patients <65. On a lesion level, patients >65 had more CP than younger patients in both obstructive (29.2 mm3 vs 48.2 mm3; p<0.04) and non-obstructive lesions (22.1 mm3 vs 49.4 mm3; p<0.004) while younger patients had more %PAV (LD-NCP) (1.5% vs 0.7%; p<0.038). Younger patients had more PV, LD-NCP, NCP and lesion lengths in obstructive compared with non-obstructive lesions. There were no differences observed between lesion types in older patients.ConclusionAI-QCT identifies a unique APC signature that differs by age and degree of stenosis and provides a foundation for AI-guided age-based approaches to atherosclerosis identification, prevention and treatment.

Question Which of the following is the next best step in management? calcium channel blocker therapy for coronary spasm coronary stenting for revascularisation of plaque rupture cardiac surgery for myocardial bridging (MB) systemic anticoagulation for coronary embolism For the answer see page 656 From the question on page 636 Answer: C Intravascular ultrasound (IVUS) showed an extravascular 'half-moon' structure (arrow), representing an overlying muscle band with corresponding atherosclerotic plaque (figure 1C).

Near-infrared spectroscopy (NIRS) intravascular ultrasound imaging can detect lipid-rich plaques (LRPs). LRPs are associated with acute coronary syndromes or myocardial infarction, which can result in revascularisation or cardiac death. In this study, we aimed to establish the relationship between LRPs detected by NIRS-intravascular ultrasound imaging at unstented sites and subsequent coronary events from new culprit lesions. In this prospective, cohort study (LRP), patients from 44 medical centres were enrolled in Italy, Latvia, Netherlands, Slovakia, UK, and the USA. Patients with suspected coronary artery disease who underwent cardiac catheterisation with possible ad hoc percutaneous coronary intervention were eligible to be enrolled. Enrolled patients underwent scanning of non-culprit segments using NIRS-intravascular ultrasound imaging. The study had two hierarchal primary hypotheses, patient and plaque, each testing the association between maximum 4 mm Lipid Core Burden Index (maxLCBI4mm) and non-culprit major adverse cardiovascular events (NC-MACE). Enrolled patients with large LRPs (≥250 maxLCBI4mm) and a randomly selected half of patients with small LRPs (<250 maxLCBI4mm) were followed up for 24 months. This study is registered with ClinicalTrials.gov, NCT02033694. Between Feb 21, 2014, and March 30, 2016, 1563 patients were enrolled. NIRS-intravascular ultrasound device-related events were seen in six (0·4%) patients. 1271 patients (mean age 64 years, SD 10, 883 [69%] men, 388 [31%]women) with analysable maxLCBI4mm were allocated to follow-up. The 2-year cumulative incidence of NC-MACE was 9% (n=103). Both hierarchical primary hypotheses were met. On a patient level, the unadjusted hazard ratio (HR) for NC-MACE was 1·21 (95% CI 1·09–1·35; p=0·0004) for each 100-unit increase maxLCBI4mm) and adjusted HR 1·18 (1·05–1·32; p=0·0043). In patients with a maxLCBI4mm more than 400, the unadjusted HR for NC-MACE was 2·18 (1·48–3·22; p<0·0001) and adjusted HR was 1·89 (1·26–2·83; p=0·0021). At the plaque level, the unadjusted HR was 1·45 (1·30–1·60; p<0·0001) for each 100-unit increase in maxLCBI4mm. For segments with a maxLCBI4mm more than 400, the unadjusted HR for NC-MACE was 4·22 (2·39–7·45; p<0·0001) and adjusted HR was 3·39 (1·85–6·20; p<0·0001). NIRS imaging of non-obstructive territories in patients undergoing cardiac catheterisation and possible percutaneous coronary intervention was safe and can aid in identifying patients and segments at higher risk for subsequent NC-MACE. NIRS-intravascular ultrasound imaging adds to the armamentarium as the first diagnostic tool able to detect vulnerable patients and plaques in clinical practice. Infraredx.

The notion that heart attacks develop from coronary-artery stenosis is an oversimplification of a process involving lipid metabolism, inflammation, macrophage activation, collagen breakdown, and plaque rupture. These insights are leading to new ideas for treatment and prevention. Atherosclerotic lesions in humans typically form over the course of years to decades, one of the longest incubation periods among human diseases. Despite the chronicity of atherosclerosis, thrombotic complications — the most dreaded clinical consequences of this disease — occur suddenly, and often without warning. Our familiarity with the disease has generally led us to accept this apparent paradox without wonder. What mechanisms explain the abrupt transition from stable ischemic heart disease or asymptomatic atherosclerosis to acute coronary syndromes? This review examines our current understanding of the mechanisms underlying these syndromes. According to the traditional view, progressive stenosis narrows the . . .

Key Points Most acute coronary events result from sudden luminal thrombosis due to rupture of an atherosclerotic plaque Modern computed tomography (CT) scanners enable robust coronary plaque characterization and quantification Large plaque volume, low CT attenuation, napkin-ring sign, positive remodelling, and spotty calcification are all associated with plaques vulnerable to rupture Computational fluid dynamic simulation enables plaque-specific endothelial shear stress and fractional flow reserve assessment, and thus permits functional characterization of plaques Coupling individual plaque morphology with plaque-specific functional data will enable new noninvasive detection of vulnerable plaques with CT Catastrophic acute coronary events are often the result of ruptured atherosclerotic plaques and subsequent luminal thrombosis. Preventing such an event seems to be the only effective strategy to reduce mortality and morbidity of coronary artery disease. This Review highlights how computed tomography angiography might be combined with fluid dynamic assessment to identify rupture-prone plaques in patients with coronary artery disease. Most acute coronary syndromes are caused by sudden luminal thrombosis due to atherosclerotic plaque rupture or erosion. Preventing such an event seems to be the only effective strategy to reduce mortality and morbidity of coronary heart disease. Coronary lesions prone to rupture have a distinct morphology compared with stable plaques, and provide a unique opportunity for noninvasive imaging to identify vulnerable plaques before they lead to clinical events. The submillimeter spatial resolution and excellent image quality of modern computed tomography (CT) scanners allow coronary atherosclerotic lesions to be detected, characterized, and quantified. Large plaque volume, low CT attenuation, napkin-ring sign, positive remodelling, and spotty calcification are all associated with a high risk of acute cardiovascular events in patients. Computation fluid dynamics allow the calculation of lesion-specific endothelial shear stress and fractional flow reserve, which add functional information to plaque assessment using CT. The combination of morphologic and functional characteristics of coronary plaques might enable noninvasive detection of vulnerable plaques in the future.

Background. Little is known about coronary plaque in human immunodeficiency virus (HIV)-infected women. Methods. Sixty HIV-infected and 30 non-HIV-infected women without symptoms or history of cardiovascular disease were recruited to assess coronary plaque with coronary computed tomographic angiography and immune activation. Data from 102 HIV-infected men and 41 non-HIV-infected male controls were compared. Results. HIV-infected women demonstrated significantly higher percentages of segments with noncalcified plaque (mean ± SD, 74% ± 28% vs 23% ± 39% compared to female control subjects; median [interquartile range], 75% [63%-100%] vs 0% [0%-56%]; P = .007) and more segments with noncalcified plaque (mean ± SD, 0.92 ± 1.48 vs 0.40 ± 1.44; median [interquartile range], 0 [0-2] vs 0 [0-0]; P= .04). Immune activation parameters, including soluble CD163 (sCD163; P = .006), CXCL10 (P = .002), and percentages of CD14⁺CD16⁺ monocytes (P = .008), were higher in HIV-infected women than in female control subjects, but no differences were seen in general inflammatory markers. Among HIV-infected women with noncalcified coronary plaque, sCD163 levels were significantly higher than in HIV-infected women without noncalcified plaque (P = .04). In multivariate modeling for sCD163 levels among male and female subjects, significant effects of HIV (P < .0001), age (P = .002), and sex (P = .0002) were seen. Conclusions. Young, asymptomatic, HIV-infected women, demonstrate increased noncalcified coronary plaque and increased immune activation, particularly monocyte activation. Independent effects of sex, HIV status, and aging on immune activation may contribute to cardiovascular disease in this population. Clinical Trials Registration. NCT00455793.

Background The TyG index is an indicator of insulin resistance (IR), which is associated with the development and prognosis of cardiovascular disease. This study aimed to summarize the relationship between the TyG index and the risk, severity, and prognosis of coronary artery disease (CAD) by performing a systematic review and meta-analysis. Methods The PubMed, EMBASE, The Cochrane Library, and Web of Science databases were searched for articles published from inception until May 1, 2023. Cross-sectional studies, retrospective or prospective cohort studies recruiting patients with CAD were included. For the analysis of CAD severity, the outcomes were coronary artery calcification, coronary artery stenosis, coronary plaque progression, multi-vessel CAD, and in-stent re-stenosis. For the analysis of CAD prognosis, the primary outcome was major adverse cardiovascular events (MACE). Results Forty-one studies were included in this study. Compared to patients with the lowest TyG index, those with the highest TyG index had a higher CAD risk [odds ratio (OR): 1.94, 95% confidence interval (CI) 1.20–3.14, I 2  = 91%, P  = 0.007]. Additionally, these patients were more likely to have stenotic coronary arteries (OR: 3.49, 95% CI 1.71–7.12, I 2  = 0%, P  = 0.0006), progressed plaques (OR: 1.67, 95% CI 1.28–2.19, I 2  = 0%, P  = 0.002), and with more vessels involved (OR: 2.33, 95% CI 1.59–3.42, I 2  = 0%, P  < 0.0001). When calculated as a categorized variable, it appears that acute coronary syndrome (ACS) patients with higher TyG index levels may have a higher incidence rate of MACE [hazard ratio (HR): 2.09, 95% CI 1.68–2.62, I 2  = 87%, P < 0.00001], whereas chronic coronary syndrome (CCS) or stable CAD patients with higher TyG index levels showed a trend towards an increased incidence rate of MACE (HR: 1.24, 95% CI 0.96–1.60, I 2  = 85%, P = 0.09). When calculated as a continuous variable, ACS patients had an HR of 2.28 per 1-unit/1-standard deviation increment of the TyG index (95% CI 1.44–3.63, I 2  = 95%, P = 0.0005). Similarly, CCS or stable CAD patients had an HR of 1.49 per 1-unit/1-standard deviation increment of the TyG index (95% CI 1.21–1.83, I 2  = 75%, P = 0.0001). Myocardial infarction with non-obstructive coronary arteries patients had an HR of 1.85 per 1-unit increment of the TyG index (95% CI 1.17–2.93, P = 0.008). Conclusions The TyG index is a simple new synthetic index that has been proven to be a valuable tool in the whole-course management of CAD patients. Patients with higher TyG index levels are at a higher risk of CAD, more severe coronary artery lesions, and worse prognosis compared to those with lower TyG index levels.

Debulking techniques are often necessary for successful lesion preparation in percutaneous coronary intervention. The aim of this study was to compare plaque modification of severely calcified lesions by coronary intravascular lithotripsy (IVL) with that of rotational atherectomy (RA) using optical coherence tomography (OCT). ROTA.shock was a 1:1 randomized, prospective, double-arm, multicenter noninferiority trial designed to compare final minimal stent area after IVL with RA for lesion preparation in percutaneous coronary interventional treatment of severely calcified lesions. On the basis of OCT acquired before and immediately after IVL or RA in 21 of the 70 patients included, we performed a detailed analysis of the modification of the calcified plaque. After RA and IVL, calcified plaque fractures were present in 14 of the patients (67%), with a significantly greater number of fractures after IVL (3.23 ± 0.49) than after RA (1.67 ± 0.52; p < 0.001). Plaque fractures after IVL were longer than after RA (IVL: 1.67 ± 0.43 mm vs RA: 0.57 ± 0.55 mm; p = 0.01), resulting in a greater total volume of the fractures (IVL: 1.47 ± 0.40 mm3 vs RA: 0.48 ± 0.27 mm3; p = 0.003). Use of RA was associated with a greater acute lumen gain than was use of IVL (RA: 0.46 ± 0.16 mm2 vs IVL: 0.17 ± 0.14 mm2; p = 0.03). In conclusion, we were able to show differences in plaque modification of calcified coronary lesions by OCT: although RA leads to a greater acute lumen gain, IVL induces more and longer fractures of the calcified plaque.

The formation of blood clots—thrombosis—at sites of atherosclerotic plaque rupture is a major clinical problem despite ongoing improvements in antithrombotic therapy. Progress in identifying the pathogenic mechanisms regulating arterial thrombosis has led to the development of newer therapeutics, and there is general anticipation that these treatments will have greater efficacy and improved safety. However, major advances in this field require the identification of specific risk factors for arterial thrombosis in affected individuals and a rethink of the 'one size fits all' approach to antithrombotic therapy.

The future of imaging is the integration of function and anatomy. Hongki Yoo et al . have successfully done just that by combining two existing intravascular imaging techniques into a single catheter-based system. Their dual-modality intra-arterial catheter uses a combination of optical frequency domain imaging and near-infrared fluorescence imaging to simultaneously provide molecular information in the context of the surrounding three-dimensional microanatomy of the artery wall. Advancing understanding of human coronary artery disease requires new methods that can be used in patients for studying atherosclerotic plaque microstructure in relation to the molecular mechanisms that underlie its initiation, progression and clinical complications, including myocardial infarction and sudden cardiac death. Here we report a dual-modality intra-arterial catheter for simultaneous microstructural and molecular imaging in vivo using a combination of optical frequency domain imaging (OFDI) and near-infrared fluorescence (NIRF) imaging. By providing simultaneous molecular information in the context of the surrounding tissue microstructure, this new catheter could provide new opportunities for investigating coronary atherosclerosis and stent healing and for identifying high-risk biological and structural coronary arterial plaques in vivo .