Pub Date : 2024-05-30DOI: 10.1038/s41569-024-01038-6
David Bode, Julius Ryan D. Pronto, Gabriele G. Schiattarella, Niels Voigt
Atrial fibrillation (AF) is a continually growing health-care burden that often presents together with metabolic disorders, including diabetes mellitus and obesity. Current treatments often fall short of preventing AF and its adverse outcomes. Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individual’s metabolic profile. AF itself can induce changes in glucose, lipid and ketone metabolism, mitochondrial function and myofibrillar energetics (as part of a process referred to as ‘metabolic remodelling’), which can all contribute to atrial dysfunction. In this Review, we discuss our current understanding of AF in the setting of metabolic disorders, as well as changes in atrial metabolism that are relevant to the development of AF. We also describe the potential of available and emerging treatment strategies to target metabolic remodelling in the setting of AF and highlight key questions and challenges that need to be addressed to improve outcomes in these patients. In this Review, the authors describe the changes in metabolism that predispose individuals to developing atrial fibrillation (AF) and highlight the potential of available and emerging therapeutic strategies that target metabolic remodelling to treat AF.
{"title":"Metabolic remodelling in atrial fibrillation: manifestations, mechanisms and clinical implications","authors":"David Bode, Julius Ryan D. Pronto, Gabriele G. Schiattarella, Niels Voigt","doi":"10.1038/s41569-024-01038-6","DOIUrl":"10.1038/s41569-024-01038-6","url":null,"abstract":"Atrial fibrillation (AF) is a continually growing health-care burden that often presents together with metabolic disorders, including diabetes mellitus and obesity. Current treatments often fall short of preventing AF and its adverse outcomes. Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individual’s metabolic profile. AF itself can induce changes in glucose, lipid and ketone metabolism, mitochondrial function and myofibrillar energetics (as part of a process referred to as ‘metabolic remodelling’), which can all contribute to atrial dysfunction. In this Review, we discuss our current understanding of AF in the setting of metabolic disorders, as well as changes in atrial metabolism that are relevant to the development of AF. We also describe the potential of available and emerging treatment strategies to target metabolic remodelling in the setting of AF and highlight key questions and challenges that need to be addressed to improve outcomes in these patients. In this Review, the authors describe the changes in metabolism that predispose individuals to developing atrial fibrillation (AF) and highlight the potential of available and emerging therapeutic strategies that target metabolic remodelling to treat AF.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 10","pages":"682-700"},"PeriodicalIF":41.7,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-29DOI: 10.1038/s41569-024-01043-9
Karina Huynh
Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.
{"title":"A distinct platelet differentiation pathway is involved in age-related thrombocytosis","authors":"Karina Huynh","doi":"10.1038/s41569-024-01043-9","DOIUrl":"10.1038/s41569-024-01043-9","url":null,"abstract":"Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"438-438"},"PeriodicalIF":49.6,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141176159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-28DOI: 10.1038/s41569-024-01042-w
Irene Fernández-Ruiz
In patients with type 2 diabetes mellitus and obesity, bariatric metabolic surgery is associated with a lower risk of the incidence of first-ever congestive heart failure than treatment with glucagon-like peptide 1 receptor agonists, according to a new study.
{"title":"Bariatric metabolic surgery more effective than GLP1R agonists in preventing congestive HF","authors":"Irene Fernández-Ruiz","doi":"10.1038/s41569-024-01042-w","DOIUrl":"10.1038/s41569-024-01042-w","url":null,"abstract":"In patients with type 2 diabetes mellitus and obesity, bariatric metabolic surgery is associated with a lower risk of the incidence of first-ever congestive heart failure than treatment with glucagon-like peptide 1 receptor agonists, according to a new study.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"438-438"},"PeriodicalIF":49.6,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-28DOI: 10.1038/s41569-024-01044-8
Gregory B. Lim
Data from the SEQUOIA-HCM trial show that aficamten, a cardiac myosin inhibitor, increases exercise capacity and improves quality of life in patients with symptomatic obstructive hypertrophic cardiomyopathy.
{"title":"Aficamten reduces symptoms in obstructive hypertrophic cardiomyopathy","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-01044-8","DOIUrl":"10.1038/s41569-024-01044-8","url":null,"abstract":"Data from the SEQUOIA-HCM trial show that aficamten, a cardiac myosin inhibitor, increases exercise capacity and improves quality of life in patients with symptomatic obstructive hypertrophic cardiomyopathy.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"437-437"},"PeriodicalIF":49.6,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-21DOI: 10.1038/s41569-024-01041-x
Karina Huynh
A study in Nature describes a single-cell-type strategy for vascular cell therapies that involves the artificial transplantation of mitochondria to endothelial cells, which promotes mitophagy and facilitates the formation of functional vessels in ischaemic tissue without the need for mesenchymal stromal cell support.
{"title":"Artificially transplanted mitochondria in endothelial cells promote mitophagy","authors":"Karina Huynh","doi":"10.1038/s41569-024-01041-x","DOIUrl":"10.1038/s41569-024-01041-x","url":null,"abstract":"A study in Nature describes a single-cell-type strategy for vascular cell therapies that involves the artificial transplantation of mitochondria to endothelial cells, which promotes mitophagy and facilitates the formation of functional vessels in ischaemic tissue without the need for mesenchymal stromal cell support.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"439-439"},"PeriodicalIF":49.6,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141076268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-20DOI: 10.1038/s41569-024-01040-y
Irene Fernández-Ruiz
Activation of the bile acid receptor TGR5 inhibits CD36-mediated fatty acid uptake in cardiomyocytes and protects against cardiac lipotoxicity and the development of diabetic cardiomyopathy in mice, according to a new study.
{"title":"Bile acid receptor protects against diabetic cardiomyopathy","authors":"Irene Fernández-Ruiz","doi":"10.1038/s41569-024-01040-y","DOIUrl":"10.1038/s41569-024-01040-y","url":null,"abstract":"Activation of the bile acid receptor TGR5 inhibits CD36-mediated fatty acid uptake in cardiomyocytes and protects against cardiac lipotoxicity and the development of diabetic cardiomyopathy in mice, according to a new study.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"440-440"},"PeriodicalIF":49.6,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141069495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15DOI: 10.1038/s41569-024-01037-7
Shaunak S. Adkar, Nicholas J. Leeper
Cardiovascular disease is the leading cause of death worldwide, and it commonly results from atherosclerotic plaque progression. One of the increasingly recognized drivers of atherosclerosis is dysfunctional efferocytosis, a homeostatic mechanism responsible for the clearance of dead cells and the resolution of inflammation. In atherosclerosis, the capacity of phagocytes to participate in efferocytosis is hampered, leading to the accumulation of apoptotic and necrotic tissue within the plaque, which results in enlargement of the necrotic core, increased luminal stenosis and plaque inflammation, and predisposition to plaque rupture or erosion. In this Review, we describe the different forms of programmed cell death that can occur in the atherosclerotic plaque and highlight the efferocytic machinery that is normally implicated in cardiovascular physiology. We then discuss the mechanisms by which efferocytosis fails in atherosclerosis and other cardiovascular and cardiometabolic diseases, including myocardial infarction and diabetes mellitus, and discuss therapeutic approaches that might reverse this pathological process. In this Review, Adkar and Leeper describe the mechanisms of programmed cell death and efferocytosis, discuss how efferocytosis becomes impaired in atherosclerosis and other cardiometabolic diseases, and suggest potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.
{"title":"Efferocytosis in atherosclerosis","authors":"Shaunak S. Adkar, Nicholas J. Leeper","doi":"10.1038/s41569-024-01037-7","DOIUrl":"10.1038/s41569-024-01037-7","url":null,"abstract":"Cardiovascular disease is the leading cause of death worldwide, and it commonly results from atherosclerotic plaque progression. One of the increasingly recognized drivers of atherosclerosis is dysfunctional efferocytosis, a homeostatic mechanism responsible for the clearance of dead cells and the resolution of inflammation. In atherosclerosis, the capacity of phagocytes to participate in efferocytosis is hampered, leading to the accumulation of apoptotic and necrotic tissue within the plaque, which results in enlargement of the necrotic core, increased luminal stenosis and plaque inflammation, and predisposition to plaque rupture or erosion. In this Review, we describe the different forms of programmed cell death that can occur in the atherosclerotic plaque and highlight the efferocytic machinery that is normally implicated in cardiovascular physiology. We then discuss the mechanisms by which efferocytosis fails in atherosclerosis and other cardiovascular and cardiometabolic diseases, including myocardial infarction and diabetes mellitus, and discuss therapeutic approaches that might reverse this pathological process. In this Review, Adkar and Leeper describe the mechanisms of programmed cell death and efferocytosis, discuss how efferocytosis becomes impaired in atherosclerosis and other cardiometabolic diseases, and suggest potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 11","pages":"762-779"},"PeriodicalIF":41.7,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-01037-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140925028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-07DOI: 10.1038/s41569-024-01014-0
Simone Fezzi, Daixin Ding, Felix Mahfoud, Jiayue Huang, Alexandra J. Lansky, Shengxian Tu, William Wijns
This Perspective article is a form of ‘pastiche’, inspired by the 1993 review by Lincoff and Topol entitled ‘Illusion of reperfusion’, and explores how their concept continues to apply to percutaneous revascularization in patients with coronary artery disease and ischaemia. Just as Lincoff and Topol argued that reperfusion of acute myocardial infarction was facing unresolved obstacles that hampered clinical success in 1993, we propose that challenging issues are similarly jeopardizing the potential benefits of stent-based angioplasty today. By analysing the appropriateness and efficacy of percutaneous coronary intervention (PCI), we emphasize the limitations of relying solely on visual angiographic guidance, which frequently leads to inappropriate stenting and overtreatment in up to one-third of patients and the associated increased risk of periprocedural myocardial infarction. The lack of optimal revascularization observed in half of patients undergoing PCI confers risks such as suboptimal physiology after PCI, residual angina and long-term stent-related events, leaving an estimated 76% of patients with an ‘illusion of revascularization’. These outcomes highlight the need to refine our diagnostic tools by integrating physiological assessments with targeted intracoronary imaging and emerging strategies, such as co-registration systems and angiography-based computational methods enhanced by artificial intelligence, to achieve optimal revascularization outcomes. In 1993, Lincoff and Topol claimed that the thrombolytic treatment of ST-segment elevation myocardial infarction was suboptimal in many patients and gave an ‘illusion of reperfusion’. In this Perspective article, the authors propose that a similar illusion of revascularization exists for contemporary percutaneous revascularization in patients with coronary artery disease and ischaemia, and identify how outcomes might be improved.
{"title":"Illusion of revascularization: does anyone achieve optimal revascularization during percutaneous coronary intervention?","authors":"Simone Fezzi, Daixin Ding, Felix Mahfoud, Jiayue Huang, Alexandra J. Lansky, Shengxian Tu, William Wijns","doi":"10.1038/s41569-024-01014-0","DOIUrl":"10.1038/s41569-024-01014-0","url":null,"abstract":"This Perspective article is a form of ‘pastiche’, inspired by the 1993 review by Lincoff and Topol entitled ‘Illusion of reperfusion’, and explores how their concept continues to apply to percutaneous revascularization in patients with coronary artery disease and ischaemia. Just as Lincoff and Topol argued that reperfusion of acute myocardial infarction was facing unresolved obstacles that hampered clinical success in 1993, we propose that challenging issues are similarly jeopardizing the potential benefits of stent-based angioplasty today. By analysing the appropriateness and efficacy of percutaneous coronary intervention (PCI), we emphasize the limitations of relying solely on visual angiographic guidance, which frequently leads to inappropriate stenting and overtreatment in up to one-third of patients and the associated increased risk of periprocedural myocardial infarction. The lack of optimal revascularization observed in half of patients undergoing PCI confers risks such as suboptimal physiology after PCI, residual angina and long-term stent-related events, leaving an estimated 76% of patients with an ‘illusion of revascularization’. These outcomes highlight the need to refine our diagnostic tools by integrating physiological assessments with targeted intracoronary imaging and emerging strategies, such as co-registration systems and angiography-based computational methods enhanced by artificial intelligence, to achieve optimal revascularization outcomes. In 1993, Lincoff and Topol claimed that the thrombolytic treatment of ST-segment elevation myocardial infarction was suboptimal in many patients and gave an ‘illusion of reperfusion’. In this Perspective article, the authors propose that a similar illusion of revascularization exists for contemporary percutaneous revascularization in patients with coronary artery disease and ischaemia, and identify how outcomes might be improved.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 9","pages":"652-662"},"PeriodicalIF":41.7,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140845335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-03DOI: 10.1038/s41569-024-01031-z
Gregory B. Lim
In the AEGIS-II trial, infusion of apolipoprotein A-I to increase cholesterol efflux capacity did not improve outcomes in patients with acute myocardial infarction.
{"title":"No benefit of apoA-I infusion after myocardial infarction","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-01031-z","DOIUrl":"10.1038/s41569-024-01031-z","url":null,"abstract":"In the AEGIS-II trial, infusion of apolipoprotein A-I to increase cholesterol efflux capacity did not improve outcomes in patients with acute myocardial infarction.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"354-354"},"PeriodicalIF":49.6,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140821303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-02DOI: 10.1038/s41569-024-01024-y
Viola Vaccarino, J. Douglas Bremner
Psychological stress is generally accepted to be associated with an increased risk of cardiovascular disease (CVD), but results have varied in terms of how stress is measured and the strength of the association. Additionally, the mechanisms and potential causal links have remained speculative despite decades of research. The physiological responses to stress are well characterized, but their contribution to the development and progression of CVD has received little attention in empirical studies. Evidence suggests that physiological responses to stress have a fundamental role in the risk of CVD and that haemodynamic, vascular and immune perturbations triggered by stress are especially implicated. Stress response physiology is regulated by the corticolimbic regions of the brain, which have outputs to the autonomic nervous system. Variation in these regulatory pathways might explain interindividual differences in vulnerability to stress. Dynamic perturbations in autonomic, immune and vascular functions are probably also implicated as CVD risk mechanisms of chronic, recurring and cumulative stressful exposures, but more data are needed from prospective studies and from assessments in real-life situations. Psychological assessment remains insufficiently recognized in clinical care and prevention. Although stress-reduction interventions might mitigate perceived stress levels and potentially reduce cardiovascular risk, more data from randomized trials are needed. Physiological responses to stress are thought to increase the risk of cardiovascular disease via haemodynamic, vascular and immune perturbations. In this Review, Vaccarino and Bremner focus on issues with the measurement of psychological stress and the underlying pathobiology connecting stress to the risk of cardiovascular disease.
{"title":"Stress and cardiovascular disease: an update","authors":"Viola Vaccarino, J. Douglas Bremner","doi":"10.1038/s41569-024-01024-y","DOIUrl":"10.1038/s41569-024-01024-y","url":null,"abstract":"Psychological stress is generally accepted to be associated with an increased risk of cardiovascular disease (CVD), but results have varied in terms of how stress is measured and the strength of the association. Additionally, the mechanisms and potential causal links have remained speculative despite decades of research. The physiological responses to stress are well characterized, but their contribution to the development and progression of CVD has received little attention in empirical studies. Evidence suggests that physiological responses to stress have a fundamental role in the risk of CVD and that haemodynamic, vascular and immune perturbations triggered by stress are especially implicated. Stress response physiology is regulated by the corticolimbic regions of the brain, which have outputs to the autonomic nervous system. Variation in these regulatory pathways might explain interindividual differences in vulnerability to stress. Dynamic perturbations in autonomic, immune and vascular functions are probably also implicated as CVD risk mechanisms of chronic, recurring and cumulative stressful exposures, but more data are needed from prospective studies and from assessments in real-life situations. Psychological assessment remains insufficiently recognized in clinical care and prevention. Although stress-reduction interventions might mitigate perceived stress levels and potentially reduce cardiovascular risk, more data from randomized trials are needed. Physiological responses to stress are thought to increase the risk of cardiovascular disease via haemodynamic, vascular and immune perturbations. In this Review, Vaccarino and Bremner focus on issues with the measurement of psychological stress and the underlying pathobiology connecting stress to the risk of cardiovascular disease.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 9","pages":"603-616"},"PeriodicalIF":41.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140819523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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