Artificial intelligence (AI) is transforming echocardiography, ushering in an era of improved diagnostic precision, efficiency and patient care. In this Review, we present an in-depth exploration of AI applications in ec...Artificial intelligence (AI) is transforming echocardiography, ushering in an era of improved diagnostic precision, efficiency and patient care. In this Review, we present an in-depth exploration of AI applications in echocardiography, highlighting the latest advances, practical implementations and future directions. We discuss the integration of AI throughout the echocardiographic workflow, from image acquisition and analysis to interpretation. We outline the potential of AI to automate routine measurements and calculations, enable task shifting, recognize disease-specific patterns and uncover new phenogroups that might surpass current diagnostic classifications. Moreover, we address the aspects needed to create trustworthy AI systems, through careful validation, navigating regulatory requirements and upholding ethical standards, thereby presenting a balanced perspective on the advantages and limitations of this rapidly evolving technology. Through an examination of current AI applications, clinical studies and technological breakthroughs, we offer a comprehensive understanding of the evolving role of AI in the future of echocardiography and its capacity to advance cardiovascular care, while also acknowledging the current limitations of the widespread clinical implementation of AI-supported echocardiography.
Coronary CT angiography is widely implemented, with an estimated 2.2 million procedures in patients with stable chest pain every year in Europe alone. In parallel, artificial intelligence and machine learning are poised...Coronary CT angiography is widely implemented, with an estimated 2.2 million procedures in patients with stable chest pain every year in Europe alone. In parallel, artificial intelligence and machine learning are poised to transform coronary atherosclerotic plaque evaluation by improving reliability and speed. However, little is known about how to use coronary atherosclerosis imaging biomarkers to individualize recommendations for medical treatment. This Consensus Statement from the Quantitative Cardiovascular Imaging (QCI) Study Group outlines key recommendations derived from a three-step Delphi process that took place after the third international QCI Study Group meeting in September 2024. Experts from various fields of cardiovascular imaging agreed on the use of age-adjusted and gender-adjusted percentile curves, based on coronary plaque data from the DISCHARGE and SCOT-HEART trials. Two key issues were addressed: the need to harness the reliability and precision of artificial intelligence and machine learning tools and to tailor treatment on the basis of individualized plaque analysis. The QCI Study Group recommends that the presence of any atherosclerotic plaque should lead to a recommendation of pharmacological treatment, whereas the 70th percentile of total plaque volume warrants high-intensity treatment. The aim of these recommendations is to lay the groundwork for future trials and to unlock the potential of coronary CT angiography to improve patient outcomes globally.
Heart failure (HF) and obesity place a substantial burden on health-care systems worldwide. Obesity is associated with an estimated 5-7% increase in the incidence of new-onset HF for each unit increase in body mass index...Heart failure (HF) and obesity place a substantial burden on health-care systems worldwide. Obesity is associated with an estimated 5-7% increase in the incidence of new-onset HF for each unit increase in body mass index. This obesity-associated risk is more pronounced for HF with preserved ejection fraction than for HF with reduced ejection fraction. The relationship between HF and obesity has historically been underrecognized. However, because of the development of weight-loss drugs with beneficial effects on outcomes in patients with HF with preserved ejection fraction, this link is now clear. In this Review, we provide a summary of the effects of obesity on the development of HF, exploring the epidemiology and potential pathophysiological mechanisms linking these two conditions. We also discuss management strategies, including lifestyle interventions and novel pharmaceutical approaches. This Review adds an impetus to all practitioners of cardiovascular medicine, especially specialists in HF, to become well-versed in obesity management and underscores the need for further research on the effects of intentional weight loss in various cardiovascular conditions.
Hypertension is the most prevalent modifiable risk factor for cardiovascular disease and for cardiovascular and all-cause mortality globally. Suboptimal control of elevated blood pressure places a substantial burden on h...Hypertension is the most prevalent modifiable risk factor for cardiovascular disease and for cardiovascular and all-cause mortality globally. Suboptimal control of elevated blood pressure places a substantial burden on health-care systems worldwide. Several factors contribute to this suboptimal control, such as limited awareness of hypertension, lack of appropriate diagnosis and poor control of blood pressure among those with a diagnosis. These factors can be due to patient non-adherence to treatment, inertia among health-care professionals and low uptake and implementation of clinical guideline recommendations. From 2003 to 2018, the European Society of Hypertension and the European Society of Cardiology jointly published four sets of guidelines on hypertension. However, the two societies released separate guidelines on hypertension in 2023 and 2024, respectively. These two sets of European guidelines agree on most recommendations, but some differences have been identified. In this Expert Recommendation, we highlight the key consensus recommendations from the two guidelines; compare differing approaches to the definition, classification, diagnosis and treatment of hypertension; and aim to help health-care professionals in their decision-making to improve the management of hypertension and to reduce the burden of hypertension-associated outcomes and premature deaths.
A misconception persisting among the scientific and clinical communities relates to the correlation between arterial stenosis and acute ischaemic events, including myocardial infarction and cerebral stroke. This Perspect...A misconception persisting among the scientific and clinical communities relates to the correlation between arterial stenosis and acute ischaemic events, including myocardial infarction and cerebral stroke. This Perspective article challenges the approach that most of the current guidelines codify, which is based on the concept that occlusive arterial stenosis generally provokes ischaemic events. We highlight the mechanistic differences between chronic or inducible ischaemia caused by flow-limiting stenoses and acute thrombotic events and question the traditional reliance on stenosis grading as a biomarker for therapeutic decision-making that many guidelines enshrine. Furthermore, we review the latest evidence highlighting the lack of a correlation between stenosis severity and the occurrence of acute thrombotic complications of atherosclerosis, in the light of a major clinical trial that included a large contemporary population and showed that only one-third of major adverse cardiovascular events occur in individuals with obstructive coronary artery disease. These considerations aim to foster a shift, grounded in contemporary evidence, towards treatment approaches that address modifying plaque biology rather than stenoses per se, using pharmacological treatment as a fundamental factor in risk mitigation and moving away from sole reliance on stenosis grading as a primary determinant of therapeutic decisions.
Narayan SM, Chung MK, Adedinsewo D
… +17 more, Brant LCC, Davis LL, Duncker D, Hall JL, Han JK, Lam CSP, Lewis E, Loscalzo J, Márquez MF, Rahimzadeh V, Rodriguez F, Sanders P, Svennberg E, Stein K, Turakhia M, Yancy C, Armoundas AA
Nat Rev Cardiol
· 2026 Jan · PMID 40670723
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The emergence and rapid adoption of digital health technologies (DHT) present unprecedented opportunities to democratize and reduce disparities in health care by monitoring health and disease at the point of care in all...The emergence and rapid adoption of digital health technologies (DHT) present unprecedented opportunities to democratize and reduce disparities in health care by monitoring health and disease at the point of care in all patients. However, limited access to DHT is becoming a major obstacle to realizing these goals. Access to DHT is influenced not only by well-recognized social determinants of health, but also by digital determinants of health, such as digital literacy and the need for broad access to digital infrastructure, as well as commercial and economic factors. Addressing these challenges and designing unbiased systems of care are essential to enable broad access to DHT and to benefit diverse and under-represented communities. Doing so will fill gaps in the clinical evidence base and avoid perpetuating historical biases. In this Review, we propose a personalized framework to improve access to DHT, addressing determinants of access at the individual, interpersonal, community, society, government and industry levels. We frame these issues globally, highlighting how the challenges to DHT access and potential solutions might differ between continents while also emphasizing common themes. We provide perspectives from partners across the spectrum of health care, including clinicians, clinical trialists, and experts from digital health and industry.
The term cardiomyopathy is used to describe a large family of complex heart muscle disorders of diverse aetiology and pathophysiology. For decades, the management of individual cardiomyopathy subtypes has focused primari...The term cardiomyopathy is used to describe a large family of complex heart muscle disorders of diverse aetiology and pathophysiology. For decades, the management of individual cardiomyopathy subtypes has focused primarily on the management of symptoms and the prevention of disease-related complications, such as heart failure and sudden cardiac death. Treatment of progressive myocardial dysfunction has relied on conventional evidence-based heart failure therapies, with variable success. In contrast to other areas of medicine, cardiology is characterized by few aetiology-targeted therapies, but cardiomyopathies offer an ideal model for innovation because, in many individuals, the disorder has a monogenic cause, the expression of which is modified by complex genetic mechanisms, comorbidities and lifestyle. Elucidation of the complex cellular and molecular pathways that result in downstream tissue phenotypes has led to the investigation of new or repurposed pharmacological agents and, in parallel, therapies that modify or mitigate the effects of causative genetic variants, offering the prospect of targeting the disease at its source. In this Review, we describe some of the most promising therapeutic approaches in cardiomyopathy and discuss their potential effect on the lives of patients and relatives.
Given its crucial role in determining patient symptoms and outcomes in various cardiopulmonary diseases, the thorough and accurate assessment of right ventricular function is essential for both diagnosis and ongoing pati...Given its crucial role in determining patient symptoms and outcomes in various cardiopulmonary diseases, the thorough and accurate assessment of right ventricular function is essential for both diagnosis and ongoing patient monitoring. In the era of precision medicine, a more detailed characterization of patients with cardiopulmonary diseases is needed, especially with the emergence of novel pharmacological and device-based therapies, such as transcatheter tricuspid valve intervention, gene therapy in patients with cardiomyopathy and anti-obesity interventions for patients with heart failure. Precise and reproducible quantification of right ventricular morphology and function are crucial for risk stratification, the selection of different therapies for the appropriate patients and the evaluation of treatment outcomes. As our understanding of right ventricular pathophysiology expands, the need for sensitive markers of functional deterioration, reliable prognostic indicators and more precise surrogates for clinical trials becomes increasingly important. In this Roadmap, we address current challenges in the standardization of image acquisition, analysis and interpretation across different modalities. We explore the factors limiting the clinical adoption of more advanced approaches and provide expert recommendations to overcome these barriers. Additionally, we outline potential next steps for incorporating parameters of right ventricular function as surrogate end points in multicentre clinical trials of new drugs or devices, and highlight new research opportunities, including the integration of artificial intelligence technologies. Finally, we issue a call for international collaboration on selected priority areas.
The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial...The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial infarction. Heart failure is classified into two main types: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). These forms fundamentally differ, especially in how metabolism is regulated, but they also have shared features such as mitochondrial dysfunction. HFrEF is typically driven by neuroendocrine activation and mechanical strain, which demands a higher ATP production to sustain cardiac contraction. However, the primary energy source in a healthy heart (fatty acid β-oxidation) is often suppressed in HFrEF. Although glucose uptake increases in HFrEF, mitochondrial dysfunction disrupts glucose oxidation, and glycolysis and ketone oxidation only partially compensate for this imbalance. Conversely, HFpEF, particularly in individuals with metabolic diseases, such as obesity or type 2 diabetes mellitus, results from both mechanical and metabolic overload. Elevated glucose and lipid levels overwhelm normal metabolic pathways, leading to an accumulation of harmful metabolic byproducts that impair mitochondrial and cellular function. In this Review, we explore how disruptions in cardiac metabolism are not only markers of heart failure but also key drivers of disease progression. We also examine how metabolic intermediates influence signalling pathways that modify proteins and regulate gene expression in the heart. The growing recognition of the role of metabolic alterations in heart failure has led to groundbreaking treatments that target these metabolic disruptions, offering new hope for these patients.
Heart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced e...Heart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced ejection fraction. Furthermore, HF compromises vascular function, creating and sustaining a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac function. In HF, systemic arterial dysfunction, characterized by increased arterial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function. Reduced coronary blood flow impairs myocardial oxygen delivery and consequently cardiomyocyte metabolism and function. Coronary microvascular dysfunction is heterogeneous in its pathogenesis and manifestations, complicating the diagnosis and management across different HF phenotypes. Understanding the alterations in function in different segments of the vasculature, from the aorta to the capillary level, offers mechanistic insights into disease drivers and therapeutic interventions. Interventional approaches can improve vascular haemodynamics, whereas established and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression, inflammation, and oxidative stress, thereby improving vascular function and HF-related outcomes. In this Review, we provide a mechanistic framework of vascular dysfunction in the pathogenesis of HF with or without reduced ejection fraction, pointing towards integrated therapies that consider the vascular implications of contemporary HF management across HF phenotypes.
The interaction between inflammation and metabolism (immunometabolism) is a crucial factor in the pathophysiology of heart failure, whether the cardiac failure originates from ischaemic injury or systemic metabolic disor...The interaction between inflammation and metabolism (immunometabolism) is a crucial factor in the pathophysiology of heart failure, whether the cardiac failure originates from ischaemic injury or systemic metabolic disorders, and whether it is associated with reduced or preserved ejection fraction. Ischaemia, metabolic stress and comorbidity-driven systemic inflammation attract innate and adaptive immune cells to the myocardium and induce their polarization towards pro-inflammatory or anti-inflammatory phenotypes through cell-intrinsic metabolic shifts involving oxidative phosphorylation and anaerobic glycolysis. These infiltrating immune cells modulate cardiac and systemic metabolism. The bidirectional metabolic crosstalk between immune cells and parenchymal and stromal cardiac cells contributes to adverse cardiac remodelling. In turn, ischaemic injury and deregulated metabolism stimulate bone marrow and extramedullary myelopoiesis, which increases immune cell recruitment and perpetuates a non-resolving chronic inflammatory state. Pharmacological interventions targeting metabolism have shown promise for improving outcomes in patients with heart failure, but immunomodulatory approaches face multiple challenges. Understanding the complex metabolic pathways and cell-cell interactions that regulate immunometabolism in heart failure is essential to identify new therapies that shift the balance from maladaptive to cardioprotective immune responses. In this Review, we provide a comprehensive overview of the intricate cellular and molecular mechanisms that govern immunometabolism in heart failure and discuss potential approaches to non-invasively monitor and treat patients with heart failure.