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Coronary artery disease (CAD) is a prevalent disease with high morbidity and mortality rates. Invasive coronary angiography is the reference standard for diagnosing CAD but is costly and associated with risks. Noninvasive imaging like cardiac magnetic resonance (CMR) facilitates CAD assessment and can serve as a gatekeeper to downstream invasive testing. Machine learning methods are increasingly applied for automated interpretation of imaging and other clinical results for medical diagnosis. In this study, we proposed a novel CAD detection method based on CMR images by utilizing the feature extraction ability of deep neural networks and combining the features with the aid of a random forest for the very first time. It is necessary to convert image data to numeric features so that they can be used in the nodes of the decision trees. To this end, the predictions of multiple stand-alone convolutional neural networks (CNNs) were considered as input features for the decision trees. The capability of CNNs in representing image data renders our method a generic classification approach applicable to any image dataset. We named our method RF-CNN-F, which stands for Random Forest with CNN Features. We conducted experiments on a large CMR dataset that we have collected and made publicly accessible. Our method achieved excellent accuracy (99.18%) using Adam optimizer compared to a stand-alone CNN trained using fivefold cross validation (93.92%) tested on the same dataset.

This study clinically implemented a ready-to-use quantitative perfusion (QP) cardiovascular magnetic resonance (QP CMR) workflow, encompassing a simplified dual-bolus gadolinium-based contrast agent (GBCA) administration scheme and fully automated QP image post-processing. Twenty-five patients with suspected obstructive coronary artery disease (CAD) underwent both adenosine stress perfusion CMR and an invasive coronary angiography or coronary computed tomography angiography. The dual-bolus protocol consisted of a pre-bolus (0.0075 mmol/kg GBCA at 0.5 mmol/ml concentration + 20 ml saline) and a main bolus (0.075 mmol/kg GBCA at 0.5 mmol/ml concentration + 20 ml saline) at an infusion rate of 3 ml/s. The arterial input function curves showed excellent quality. Stress MBF ≤ 1.84 ml/g/min accurately detected obstructive CAD (area under the curve 0.79; 95% Confidence Interval: 0.66 to 0.89). Combined visual assessment of color pixel QP maps and conventional perfusion images yielded a diagnostic accuracy of 84%, sensitivity of 70% and specificity of 93%. The proposed easy-to-use dual-bolus QP CMR workflow provides good image quality and holds promise for high accuracy in diagnosis of obstructive CAD. Implementation of this approach has the potential to serve as an alternative to current methods thus increasing the accessibility to offer high-quality QP CMR imaging by a wide range of CMR laboratories.

Key Points Depression is prevalent in the general population, and even more common among patients with coronary heart disease (CHD) Depression is a risk factor for incident CHD, and for cardiovascular morbidity and mortality in patients with established CHD Potential biological and behavioural mechanisms for this risk have been identified, but no single factor has been shown to account for more than a fraction of the total risk Very few clinical trials have been conducted to determine whether treating depression decreases the risk of cardiac events in patients with established CHD Each of the trials has substantial shortcomings, and more trials are needed Effective treatments for depression, identification of 'high-risk' depression subtypes, and an improved understanding of the biobehavioural pathways linking depression to cardiac morbidity and mortality are needed Depression is a highly prevalent risk factor for incident coronary heart disease (CHD) and for cardiovascular morbidity and mortality in patients with established CHD. In this Review, Carney and Freedland consider the evidence for depression as a cardiac risk factor, and summarize the biological and behavioural mechanisms that might link depression to CHD. They also consider whether treatment of depression can prevent cardiac morbidity and mortality in patients with CHD. Depression is a highly prevalent risk factor for incident coronary heart disease (CHD) and for cardiovascular morbidity and mortality in patients with established CHD. Several biological and behavioural mechanisms have been hypothesized to underlie the relationship between depression and CHD, but none has been shown to account for more than a small proportion of the risk. Only a few clinical trials have examined whether treating depression decreases the risk of cardiac events in patients with established CHD. None of these trials has shown that treatment results in improved cardiac outcomes, but the differences in depression outcomes between the intervention and control groups have been small and not clinically significant. Nevertheless, secondary analyses of these trials suggest that prognosis improves when depression improves. Concerted efforts to develop more potent interventions for depression, identification of high-risk subtypes of depression, and further research on the biobehavioural mechanisms linking depression to CHD are needed to pave the way for definitive clinical trials.

Key Points Extracellular vesicles are released in biological fluids both under basal conditions and in pathological settings Extracellular vesicles act as vectors of biological information by transferring their protein, lipid, and nucleic acid content to target cells Circulating levels of extracellular vesicles of different cellular origin are increased in cardiovascular diseases, including myocardial infarction; these extracellular vesicles could serve as diagnostic and prognostic biomarkers Extracellular vesicles might contribute to atherosclerosis development and progression by promoting initial lesion formation, intravascular calcifications, unstable plaque progression, and thrombus formation after rupture Extracellular vesicles released by stem cells (progenitor or mesenchymal stem cells) have potential therapeutic benefits on cardiac function after myocardial infarction Extracellular vesicles regulate the transfer of biological information, acting locally and remotely. Interest in extracellular vesicles, in particular exosomes, in the cardiovascular field emerged a decade ago, opening new research and therapeutic avenues. This Review summarizes current knowledge on the role of extracellular vesicles in coronary artery disease, and their emerging potential as biomarkers and therapeutic agents. Membrane vesicles released in the extracellular space are composed of a lipid bilayer enclosing soluble cytosolic material and nuclear components. Extracellular vesicles include apoptotic bodies, exosomes, and microvesicles (also known previously as microparticles). Originating from different subcellular compartments, the role of extracellular vesicles as regulators of transfer of biological information, acting locally and remotely, is now acknowledged. Circulating vesicles released from platelets, erythrocytes, leukocytes, and endothelial cells contain potential valuable biological information for biomarker discovery in primary and secondary prevention of coronary artery disease. Extracellular vesicles also accumulate in human atherosclerotic plaques, where they affect major biological pathways, including inflammation, proliferation, thrombosis, calcification, and vasoactive responses. Extracellular vesicles also recapitulate the beneficial effect of stem cells to treat cardiac consequences of acute myocardial infarction, and now emerge as an attractive alternative to cell therapy, opening new avenues to vectorize biological information to target tissues. Although interest in microvesicles in the cardiovascular field emerged about 2 decades ago, that for extracellular vesicles, in particular exosomes, started to unfold a decade ago, opening new research and therapeutic avenues. This Review summarizes current knowledge on the role of extracellular vesicles in coronary artery disease, and their emerging potential as biomarkers and therapeutic agents.

Key Points Inflammation and its failure to resolve are firmly established as central to the development and complications of several cardiovascular diseases Targeting of inflammatory processes in experimental models has been demonstrated to be beneficial in attenuating myocardial and arterial injury, reducing disease progression, and promoting healing, but clinical translation has been disappointing Current tools to measure 'inflammation' are nonspecific and represent downstream sequelae of biological processes, but provide little insight into disease state, site, or activation pathways Contemporary molecular techniques (such as proteomics and gene-expression analysis) improve our ability to characterize underlying biological processes, and identify activation pathways as biomarkers and as a basis to develop new therapeutics Noninvasive imaging tools enable the identification of activation of specific pathways and their sites, and can be used to monitor response to therapy Inflammatory processes are central to the development and complications of atherosclerosis and acute myocardial infarction. In this Review, Ruparelia et al . summarize the inflammatory pathways involved in these cardiovascular diseases, highlight contemporary techniques to characterize and quantify inflammation, and consider how they might be used to guide specific treatments. Inflammatory processes are firmly established as central to the development and complications of cardiovascular diseases. Elevated levels of inflammatory markers have been shown to be predictive of future cardiovascular events. The specific targeting of these processes in experimental models has been shown to attenuate myocardial and arterial injury, reduce disease progression, and promote healing. However, the translation of these observations and the demonstration of clear efficacy in clinical practice have been disappointing. A major limitation might be that tools currently used to measure 'inflammation' are insufficiently precise and do not provide information about disease site and activity, or discriminate between functionally important activation pathways. The challenge, therefore, is to make measures of inflammation that are more meaningful, and which can guide specific targeted therapies. In this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction, by providing an evaluation of the known and emerging inflammatory pathways. We highlight contemporary techniques to characterize and quantify inflammation, and consider how they might be used to guide specific treatments. Finally, we discuss emerging opportunities in the field, including their current limitations and challenges that are the focus of ongoing study.

Leisure sedentary behaviours are associated with increased risk of cardiovascular disease, but whether this relationship is causal is unknown. The aim of this study is to identify genetic determinants associated with leisure sedentary behaviours and to estimate the potential causal effect on coronary artery disease (CAD). Genome wide association analyses of leisure television watching, leisure computer use and driving behaviour in the UK Biobank identify 145, 36 and 4 genetic loci ( P  < 1×10 −8 ), respectively. High genetic correlations are observed between sedentary behaviours and neurological traits, including education and body mass index (BMI). Two-sample Mendelian randomization (MR) analysis estimates a causal effect between 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25–1.66, P  = 5.63 × 10 −07 ), that is partially independent of education and BMI in multivariable MR analyses. This study finds independent observational and genetic support for the hypothesis that increased sedentary behaviour by leisure television watching is a risk factor for CAD. Epidemiological studies have shown an association between sedentary behaviours and cardiovascular disease risk. Here, van de Vegte et al . perform GWAS for self-reported sedentary behaviours (TV watching, computer use, driving) and Mendelian randomization analyses to explore potential causal relationships with coronary artery disease.

Key Points The use of hormone-replacement therapy (HRT) has been vigorously debated Earlier observational data showed many benefits of HRT, which include reduced coronary heart disease (CHD) and mortality Randomized trials in older women (aged >60 years) have shown no benefit and increased harm Reassessment of clinical trials in women initiating treatment close to the onset of menopause and newer studies and meta-analyses now show benefit and rare risks More studies show benefit with oestrogen alone than with oestrogen plus progestogen The effects of reduced CHD and mortality in women initiating therapy around menopause suggest a possible role for HRT in primary prevention Clinical practice regarding the use of hormone-replacement therapy (HRT) has undergone many changes since its introduction in the 1940s. Here, Roger Lobo frames the current thinking on the use of HRT in postmenopausal women, beginning with a historical perspective and then discussing how the interpretation of HRT data has changed over time. For several decades, the role of hormone-replacement therapy (HRT) has been debated. Early observational data on HRT showed many benefits, including a reduction in coronary heart disease (CHD) and mortality. More recently, randomized trials, including the Women's Health Initiative (WHI), studying mostly women many years after the the onset of menopause, showed no such benefit and, indeed, an increased risk of CHD and breast cancer, which led to an abrupt decrease in the use of HRT. Subsequent reanalyzes of data from the WHI with age stratification, newer randomized and observational data and several meta-analyses now consistently show reductions in CHD and mortality when HRT is initiated soon after menopause. HRT also significantly decreases the incidence of various symptoms of menopause and the risk of osteoporotic fractures, and improves quality of life. In younger healthy women (aged 50–60 years), the risk–benefit balance is positive for using HRT, with risks considered rare. As no validated primary prevention strategies are available for younger women (<60 years of age), other than lifestyle management, some consideration might be given to HRT as a prevention strategy as treatment can reduce CHD and all-cause mortality. Although HRT should be primarily oestrogen-based, no particular HRT regimen can be advocated.

Antiretroviral therapy has largely transformed HIV infection into a chronic disease condition. As such, physicians and other providers caring for individuals living with HIV infection need to be aware of the potential cardiovascular complications of HIV infection and the nuances of how HIV infection increases the risk of cardiovascular diseases, including acute myocardial infarction, stroke, peripheral artery disease, heart failure and sudden cardiac death, as well as how to select available therapies to reduce this risk. In this Review, we discuss the epidemiology and clinical features of cardiovascular disease, with a focus on coronary heart disease, in the setting of HIV infection, which includes a substantially increased risk of myocardial infarction even when the HIV infection is well controlled. We also discuss the mechanisms underlying HIV-associated atherosclerotic cardiovascular disease, such as the high rates of traditional cardiovascular risk factors in patients with HIV infection and HIV-related factors, including the use of antiretroviral therapy and chronic inflammation in the setting of effectively treated HIV infection. Finally, we highlight available therapeutic strategies, as well as approaches under investigation, to reduce the risk of cardiovascular disease and lower inflammation in patients with HIV infection.Antiretroviral therapy has transformed HIV infection into a chronic disease, and cardiovascular diseases are an important health concern in this setting. This Review discusses the clinical features of cardiovascular disease in patients with HIV infection, including the mechanisms underlying HIV-associated atherosclerosis and approaches to reduce the cardiovascular risk.

Key Points The role of elevated blood triglycerides as an independent risk factor for cardiovascular disease (CVD) has been debated for more than half a century, but without resolution One of the reasons for this uncertainty is that hypertriglyceridaemia is often associated with decreased HDL-cholesterol levels and an increased number of atherogenic small dense LDL particles Large observational, epidemiological, genetic, and Mendelian randomization studies support the hypothesis that elevated blood triglyceride levels, either fasting or nonfasting, are independently associated with an increased risk of CVD Therapeutic targeting of hypertriglyceridaemia might provide further benefit in reducing CVD and events, in addition to that achieved with LDL-cholesterol lowering Hypertriglyceridaemia is currently treated with lifestyle interventions and with fibrates, which can be combined with high doses of omega-3 fatty acids, but CVD outcome studies have produced inconsistent results Some novel drugs, such as pemafibrate and volanesorsen, are being tested, but clinical data are preliminary The role of hypertriglyceridaemia as a risk factor for coronary artery disease (CAD) is debated. In this Review, Reiner summarizes the causes of hypertriglyceridaemia, and discusses whether elevated blood triglyceride levels are an important and independent risk factor for CAD. Finally, current and emerging management options for hypertriglyceridaemia are detailed. An elevated serum level of LDL cholesterol is a well-known risk factor for cardiovascular disease (CVD), but the role of elevated triglyceride levels is debated. Controversies regarding hypertriglyceridaemia as an independent risk factor for CVD have occurred partly because elevated triglyceride levels are often a component of atherogenic dyslipidaemia — they are associated with decreased levels of HDL cholesterol and increased levels of small dense LDL particles, which are highly atherogenic. Findings from several large studies indicate that elevated levels of triglycerides (either fasting or nonfasting) or, more specifically, triglyceride-rich lipoproteins and their remnants, are independently associated with increased risk of CVD. Possible mechanisms for this association include excessive free fatty acid release, production of proinflammatory cytokines, coagulation factors, and impairment of fibrinolysis. Therapeutic targeting of hypertriglyceridaemia could, therefore, reduce CVD and cardiovascular events, beyond the reduction achieved by LDL-cholesterol lowering. Elevated triglyceride levels are reduced with lifestyle interventions and fibrates, which can be combined with omega-3 fatty acids. Some new drugs are on the horizon, such as volanesorsen (which targets apolipoprotein C-III), pemafibrate, and others. However, CVD outcome studies with triglyceride-lowering agents have produced inconsistent results, meaning that no convincing evidence is available that lowering triglycerides by any approach can reduce mortality.

Cardiac imaging has a pivotal role in the prevention, diagnosis and treatment of ischaemic heart disease. SPECT is most commonly used for clinical myocardial perfusion imaging, whereas PET is the clinical reference standard for the quantification of myocardial perfusion. MRI does not involve exposure to ionizing radiation, similar to echocardiography, which can be performed at the bedside. CT perfusion imaging is not frequently used but CT offers coronary angiography data, and invasive catheter-based methods can measure coronary flow and pressure. Technical improvements to the quantification of pathophysiological parameters of myocardial ischaemia can be achieved. Clinical consensus recommendations on the appropriateness of each technique were derived following a European quantitative cardiac imaging meeting and using a real-time Delphi process. SPECT using new detectors allows the quantification of myocardial blood flow and is now also suited to patients with a high BMI. PET is well suited to patients with multivessel disease to confirm or exclude balanced ischaemia. MRI allows the evaluation of patients with complex disease who would benefit from imaging of function and fibrosis in addition to perfusion. Echocardiography remains the preferred technique for assessing ischaemia in bedside situations, whereas CT has the greatest value for combined quantification of stenosis and characterization of atherosclerosis in relation to myocardial ischaemia. In patients with a high probability of needing invasive treatment, invasive coronary flow and pressure measurement is well suited to guide treatment decisions. In this Consensus Statement, we summarize the strengths and weaknesses as well as the future technological potential of each imaging modality.Cardiac imaging has a pivotal role in the prevention, diagnosis and treatment of ischaemic heart disease. In this Consensus Statement, the authors summarize the use of SPECT, PET, MRI, echocardiography, CT and invasive coronary flow and pressure measurement, and describe the relative strengths and weaknesses of each modality.