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Cardiac imaging is central to the diagnosis and risk stratification of coronary artery disease, beyond symptoms and clinical risk factors, by providing objective evidence of myocardial ischaemia and characterisation of coronary artery plaque. CT coronary angiography can detect coronary plaque with high resolution, estimate the degree of functional stenosis and characterise plaque features. However, coronary artery disease risk is also driven by biological processes, such as inflammation, that are not fully reflected by severity of stenosis, myocardial ischaemia or by coronary plaque features. New cardiac CT techniques can assess coronary artery inflammation by imaging perivascular fat, and this may represent an important step forward in identifying the ‘residual risk’ that is not detected by plaque or ischaemia imaging. Coronary artery disease risk assessment that incorporates clinical factors, plaque characteristics and perivascular inflammation offers a more comprehensive individualised approach to quantify and stratify coronary artery disease risk, with potential healthcare benefits for prevention, diagnosis and treatment recommendations. Furthermore, identifying new biomarkers of cardiovascular risk has the potential to refine early-life prevention strategies, before atherosclerosis becomes established.

Background and objective The impact of the COVID-19 pandemic on the quality of care for patients with acute myocardial infarction (AMI) is uncertain. We aimed to compare quality of AMI care in England and Wales during and before the COVID-19 pandemic using the 2020 European Society of Cardiology Association for Acute Cardiovascular Care quality indicators (QIs) for AMI. Methods Cohort study of linked data from the AMI and the percutaneous coronary intervention registries in England and Wales between 1 January 2017 and 27 May 2020 (representing 236 743 patients from 186 hospitals). At the patient level, the likelihood of attainment for each QI compared with pre COVID-19 was calculated using logistic regression. The date of the first national lockdown in England and Wales (23 March 2020) was chosen for time series comparisons. Results There were 10 749 admissions with AMI after 23 March 2020. Compared with before the lockdown, patients admitted with AMI during the first wave had similar age (mean 68.0 vs 69.0 years), with no major differences in baseline characteristics (history of diabetes (25% vs 26%), renal failure (6.4% vs 6.9%), heart failure (5.8% vs 6.4%) and previous myocardial infarction (22.9% vs 23.7%)), and less frequently had high Global Registry of Acute Coronary Events risk scores (43.6% vs 48.6%). There was an improvement in attainment for 10 (62.5%) of the 16 measured QIs including a composite QI (43.8% to 45.2%, OR 1.06, 95% CI 1.02 to 1.10) during, compared with before, the lockdown. Conclusion During the first wave of the COVID-19 pandemic in England and Wales, quality of care for AMI as measured against international standards did not worsen, but improved modestly.

Background Studies have reported significant reduction in acute myocardial infarction–related hospitalizations during the coronavirus disease 2019 (COVID‐19) pandemic. However, whether these trends are associated with increased incidence of out‐of‐hospital cardiac arrest (OHCA) in this population is unknown. Methods and Results Acute myocardial infarction hospitalizations with OHCA during the COVID‐19 period (February 1–May 14, 2020) from the Myocardial Ischaemia National Audit Project and British Cardiovascular Intervention Society data sets were analyzed. Temporal trends were assessed using Poisson models with equivalent pre–COVID‐19 period (February 1–May 14, 2019) as reference. Acute myocardial infarction hospitalizations during COVID‐19 period were reduced by >50% (n=20 310 versus n=9325). OHCA was more prevalent during the COVID‐19 period compared with the pre–COVID‐19 period (5.6% versus 3.6%), with a 56% increase in the incidence of OHCA (incidence rate ratio, 1.56; 95% CI, 1.39–1.74). Patients experiencing OHCA during COVID‐19 period were likely to be older, likely to be women, likely to be of Asian ethnicity, and more likely to present with ST‐segment–elevation myocardial infarction. The overall rates of invasive coronary angiography (58.4% versus 71.6%; P

Objectives: To examine short-term primary causes of death after percutaneous coronary intervention (PCI) in a national cohort before and during COVID-19. Background: Public reporting of PCI outcomes is a performance metric and a requirement in many healthcare systems. There are inconsistent data on the causes of death after PCI, and what proportion of these are attributable to cardiac causes. Methods: All patients undergoing PCI in England between 1st January 2017 and 10th May 2020 were retrospectively analysed (n=273,141), according to their outcome from the date of PCI; no death and in-hospital, post-discharge, and 30-day death. Results: The overall rates of in-hospital and 30-day death were 1.9% and 2.8%, respectively. The rate of 30-day death declined between 2017 (2.9%) and February 2020 (2.5%), mainly due to lower in-hospital death (2.1% vs. 1.5%), before rising again from 1st March 2020 (3.2%) due to higher rates of post-discharge mortality. Only 59.6% of 30-day deaths were due to cardiac causes, the most common being acute coronary syndrome, cardiogenic shock and heart failure, and this persisted throughout the study period. 10.4% of 30-day deaths after 1st March 2020 were due to confirmed COVID-19. Conclusions: In this nationwide study, we show that 40% of 30-day deaths are due to non-cardiac causes. Non-cardiac deaths have increased even more from the start of the COVID-19 pandemic, with one in ten deaths from March 2020 being COVID-19 related. These findings raise a question of whether public reporting of PCI outcomes should be cause-specific.

Targeting residual cardiovascular risk in primary and secondary prevention, would allow deployment of novel therapeutic agents, facilitating precision medicine. For example, lowering vascular inflammation is a promising strategy to reduce the residual inflammatory cardiovascular risk in patients already receiving optimal medical therapy, but prescribing novel anti-inflammatory treatments will be problematic due to the lack of specific companion diagnostic tests, to guide their targeted use in clinical practice. Currently available tests for the detection of coronary inflammation are either non-specific for the cardiovascular system (e.g. plasma biomarkers) or expensive and not readily available (e.g. hybrid positron emission tomography imaging). Recent technological advancements in coronary computed tomography angiography (CCTA) allow non-invasive detection of high-risk plaque features (positive remodelling, spotty calcification, low attenuation plaque, and napkin-ring sign) and help identify the vulnerable patient, but they provide only indirectly information about coronary inflammation. Perivascular fat attenuation index (FAI), a novel method for assessing coronary inflammation by analysing routine CCTA, captures changes in the perivascular adipose tissue composition driven by inflammatory signals coming from the inflamed coronary artery, by analysing the three-dimensional gradients of perivascular attenuation, followed by adjustments for technical, anatomical, and biological factors. By detecting vascular inflammation, perivascular FAI enhances cardiovascular risk discrimination which could aid more cost-effective deployment of novel therapeutic agents. In this article, we present the existing non-invasive modalities for the detection of coronary inflammation and provide a practical guide for their use in clinical practice.

BACKGROUND: Genetic variation at chromosome 9p21 is a recognized risk factor for coronary heart disease (CHD). However, its effect on disease progression and subsequent events is unclear, raising questions about its value for stratification of residual risk.METHODS: A variant at chromosome 9p21 (rs1333049) was tested for association with subsequent events during follow-up in 103 357 Europeans with established CHD at baseline from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) Consortium (73.1% male, mean age 62.9 years). The primary outcome, subsequent CHD death or myocardial infarction (CHD death/myocardial infarction), occurred in 13 040 of the 93 115 participants with available outcome data. Effect estimates were compared with case/control risk obtained from the CARDIoGRAMplusC4D consortium (Coronary Artery Disease Genome-wide Replication and Meta-analysis [CARDIoGRAM] plus The Coronary Artery Disease [C4D] Genetics) including 47 222 CHD cases and 122 264 controls free of CHD.RESULTS: Meta-analyses revealed no significant association between chromosome 9p21 and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline (GENIUSCHD odds ratio, 1.02; 95% CI, 0.99-1.05). This contrasted with a strong association in CARDIoGRAMPlusC4D odds ratio 1.20; 95% CI, 1.18-1.22; P for interaction < 0.001 compared with the GENIUS-CHD estimate. Similarly, no clear associations were identified for additional subsequent outcomes, including all-cause death, although we found a modest positive association between chromosome 9p21 and subsequent revascularization (odds ratio, 1.07; 95% CI, 1.04-1.09).CONCLUSIONS: In contrast to studies comparing individuals with CHD to disease-free controls, we found no clear association between genetic variation at chromosome 9p21 and risk of subsequent acute CHD events when all individuals had CHD at baseline. However, the association with subsequent revascularization may support the postulated mechanism of chromosome 9p21 for promoting atheroma development.

Genetic variation at chromosome 9p21 is a recognized risk factor for coronary heart disease (CHD). However, its effect on disease progression and subsequent events is unclear, raising questions about its value for stratification of residual risk.A variant at chromosome 9p21 (rs1333049) was tested for association with subsequent events during follow-up in 103 357 Europeans with established CHD at baseline from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) Consortium (73.1% male, mean age 62.9 years). The primary outcome, subsequent CHD death or myocardial infarction (CHD death/myocardial infarction), occurred in 13 040 of the 93 115 participants with available outcome data. Effect estimates were compared with case/control risk obtained from the CARDIoGRAMplusC4D consortium (Coronary Artery Disease Genome-wide Replication and Meta-analysis [CARDIoGRAM] plus The Coronary Artery Disease [C4D] Genetics) including 47 222 CHD cases and 122 264 controls free of CHD.Meta-analyses revealed no significant association between chromosome 9p21 and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline (GENIUS-CHD odds ratio, 1.02; 95% CI, 0.99-1.05). This contrasted with a strong association in CARDIoGRAMPlusC4D odds ratio 1.20; 95% CI, 1.18-1.22; P for interaction0.001 compared with the GENIUS-CHD estimate. Similarly, no clear associations were identified for additional subsequent outcomes, including all-cause death, although we found a modest positive association between chromosome 9p21 and subsequent revascularization (odds ratio, 1.07; 95% CI, 1.04-1.09).In contrast to studies comparing individuals with CHD to disease-free controls, we found no clear association between genetic variation at chromosome 9p21 and risk of subsequent acute CHD events when all individuals had CHD at baseline. However, the association with subsequent revascularization may support the postulated mechanism of chromosome 9p21 for promoting atheroma development.