Pub Date : 2024-01-30DOI: 10.1038/s41569-024-00990-7
Fernanda Rauber, Renata Bertazzi Levy
In this Comment, we critically examine the association between the increasing consumption of ultra-processed foods and their negative effect on cardiovascular health. We explore the historical evolution of food processing, the Nova food classification and the epidemiological evidence, and highlight the need for urgent public health interventions.
{"title":"Ultra-processed foods and cardiovascular disease","authors":"Fernanda Rauber, Renata Bertazzi Levy","doi":"10.1038/s41569-024-00990-7","DOIUrl":"10.1038/s41569-024-00990-7","url":null,"abstract":"In this Comment, we critically examine the association between the increasing consumption of ultra-processed foods and their negative effect on cardiovascular health. We explore the historical evolution of food processing, the Nova food classification and the epidemiological evidence, and highlight the need for urgent public health interventions.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 4","pages":"213-214"},"PeriodicalIF":49.6,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642639","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 : 2024-01-26DOI: 10.1038/s41569-024-00992-5
Femke Christina Ching-Chuan van Rhijn-Brouwer, Merel Hellemons, Michael Stingl, Kathryn Hoffmann, Joanne VanDerNagel, Todd E. Davenport, Eva Untersmayr, Carmen Scheibenbogen, David Putrino
{"title":"Graded exercise therapy should not be recommended for patients with post-exertional malaise","authors":"Femke Christina Ching-Chuan van Rhijn-Brouwer, Merel Hellemons, Michael Stingl, Kathryn Hoffmann, Joanne VanDerNagel, Todd E. Davenport, Eva Untersmayr, Carmen Scheibenbogen, David Putrino","doi":"10.1038/s41569-024-00992-5","DOIUrl":"10.1038/s41569-024-00992-5","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"430-431"},"PeriodicalIF":49.6,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-00992-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139567386","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 : 2024-01-26DOI: 10.1038/s41569-023-00986-9
Tamás G. Gergely, Zsófia D. Drobni, Marinos Kallikourdis, Han Zhu, Wouter C. Meijers, Tomas G. Neilan, Tienush Rassaf, Péter Ferdinandy, Zoltán V. Varga
Immune checkpoint molecules are physiological regulators of the adaptive immune response. Immune checkpoint inhibitors (ICIs), such as monoclonal antibodies targeting programmed cell death protein 1 or cytotoxic T lymphocyte-associated protein 4, have revolutionized cancer treatment and their clinical use is increasing. However, ICIs can cause various immune-related adverse events, including acute and chronic cardiotoxicity. Of these cardiovascular complications, ICI-induced acute fulminant myocarditis is the most studied, although emerging clinical and preclinical data are uncovering the importance of other ICI-related chronic cardiovascular complications, such as accelerated atherosclerosis and non-myocarditis-related heart failure. These complications could be more difficult to diagnose, given that they might only be present alongside other comorbidities. The occurrence of these complications suggests a potential role of immune checkpoint molecules in maintaining cardiovascular homeostasis, and disruption of physiological immune checkpoint signalling might thus lead to cardiac pathologies, including heart failure. Although inflammation is a long-known contributor to the development of heart failure, the therapeutic targeting of pro-inflammatory pathways has not been successful thus far. The increasingly recognized role of immune checkpoint molecules in the failing heart highlights their potential use as immunotherapeutic targets for heart failure. In this Review, we summarize the available data on ICI-induced cardiac dysfunction and heart failure, and discuss how immune checkpoint signalling is altered in the failing heart. Furthermore, we describe how pharmacological targeting of immune checkpoints could be used to treat heart failure. In this Review, Varga and colleagues provide an overview of the evidence on immune checkpoint inhibitor-induced heart failure and cardiac dysfunction that is unrelated to myocarditis, and discuss how pharmacological targeting of immune checkpoints might be a potential strategy to treat heart failure.
{"title":"Immune checkpoints in cardiac physiology and pathology: therapeutic targets for heart failure","authors":"Tamás G. Gergely, Zsófia D. Drobni, Marinos Kallikourdis, Han Zhu, Wouter C. Meijers, Tomas G. Neilan, Tienush Rassaf, Péter Ferdinandy, Zoltán V. Varga","doi":"10.1038/s41569-023-00986-9","DOIUrl":"10.1038/s41569-023-00986-9","url":null,"abstract":"Immune checkpoint molecules are physiological regulators of the adaptive immune response. Immune checkpoint inhibitors (ICIs), such as monoclonal antibodies targeting programmed cell death protein 1 or cytotoxic T lymphocyte-associated protein 4, have revolutionized cancer treatment and their clinical use is increasing. However, ICIs can cause various immune-related adverse events, including acute and chronic cardiotoxicity. Of these cardiovascular complications, ICI-induced acute fulminant myocarditis is the most studied, although emerging clinical and preclinical data are uncovering the importance of other ICI-related chronic cardiovascular complications, such as accelerated atherosclerosis and non-myocarditis-related heart failure. These complications could be more difficult to diagnose, given that they might only be present alongside other comorbidities. The occurrence of these complications suggests a potential role of immune checkpoint molecules in maintaining cardiovascular homeostasis, and disruption of physiological immune checkpoint signalling might thus lead to cardiac pathologies, including heart failure. Although inflammation is a long-known contributor to the development of heart failure, the therapeutic targeting of pro-inflammatory pathways has not been successful thus far. The increasingly recognized role of immune checkpoint molecules in the failing heart highlights their potential use as immunotherapeutic targets for heart failure. In this Review, we summarize the available data on ICI-induced cardiac dysfunction and heart failure, and discuss how immune checkpoint signalling is altered in the failing heart. Furthermore, we describe how pharmacological targeting of immune checkpoints could be used to treat heart failure. In this Review, Varga and colleagues provide an overview of the evidence on immune checkpoint inhibitor-induced heart failure and cardiac dysfunction that is unrelated to myocarditis, and discuss how pharmacological targeting of immune checkpoints might be a potential strategy to treat heart failure.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"443-462"},"PeriodicalIF":49.6,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139565772","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 : 2024-01-26DOI: 10.1038/s41569-024-00994-3
Artur Fedorowski, Alessandra Fanciulli, Satish R. Raj, Robert Sheldon, Cyndya A. Shibao, Richard Sutton
{"title":"Reply to ‘Graded exercise therapy should not be recommended for patients with post-exertional malaise’","authors":"Artur Fedorowski, Alessandra Fanciulli, Satish R. Raj, Robert Sheldon, Cyndya A. Shibao, Richard Sutton","doi":"10.1038/s41569-024-00994-3","DOIUrl":"10.1038/s41569-024-00994-3","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"432-432"},"PeriodicalIF":49.6,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-00994-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139567387","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 : 2024-01-23DOI: 10.1038/s41569-024-00991-6
Taufiek K. Rajab, Andrew D. Vogel, Joseph W. Turek
Heart valve replacement in newborn babies remains an unsolved problem because currently used heart valve implants do not grow. This lack of implant growth mandates serial re-operations until adult-size valve implants can be fitted. Partial heart transplantation is a new approach to solve this problem by transplanting only the part of the heart that contains the necessary valve.
{"title":"Partial heart transplantation: a new option for paediatric heart valve replacement","authors":"Taufiek K. Rajab, Andrew D. Vogel, Joseph W. Turek","doi":"10.1038/s41569-024-00991-6","DOIUrl":"10.1038/s41569-024-00991-6","url":null,"abstract":"Heart valve replacement in newborn babies remains an unsolved problem because currently used heart valve implants do not grow. This lack of implant growth mandates serial re-operations until adult-size valve implants can be fitted. Partial heart transplantation is a new approach to solve this problem by transplanting only the part of the heart that contains the necessary valve.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 5","pages":"277-278"},"PeriodicalIF":49.6,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139542505","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 : 2024-01-23DOI: 10.1038/s41569-024-00993-4
Gregory B. Lim
Anti-inflammatory therapy involving IL-1β inhibition might reduce the risk of cardiovascular events in individuals with clonal haematopoiesis by increasing the number of fibroblast-like cells in the fibrous cap region of atherosclerotic plaques, thereby stabilizing the plaque and reducing the likelihood of rupture.
{"title":"Fibroblast-like cells promote plaque stability in response to anti-IL-1β therapy","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-00993-4","DOIUrl":"10.1038/s41569-024-00993-4","url":null,"abstract":"Anti-inflammatory therapy involving IL-1β inhibition might reduce the risk of cardiovascular events in individuals with clonal haematopoiesis by increasing the number of fibroblast-like cells in the fibrous cap region of atherosclerotic plaques, thereby stabilizing the plaque and reducing the likelihood of rupture.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 3","pages":"155-155"},"PeriodicalIF":49.6,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139522632","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 : 2024-01-23DOI: 10.1038/s41569-024-00989-0
Julia C. Isbister, Christopher Semsarian
A molecular autopsy is undertaken in cases of sudden cardiac death with no definitive cause found after conventional autopsy, with the aim of identifying a pathological genetic variant that could account for the death. Greater awareness of malignant arrhythmias in the absence of structural changes in inherited cardiomyopathies has increased the applicability of molecular autopsies, and resulted in improved care of families but new challenges for clinicians.
{"title":"The role of the molecular autopsy in sudden cardiac death in young individuals","authors":"Julia C. Isbister, Christopher Semsarian","doi":"10.1038/s41569-024-00989-0","DOIUrl":"10.1038/s41569-024-00989-0","url":null,"abstract":"A molecular autopsy is undertaken in cases of sudden cardiac death with no definitive cause found after conventional autopsy, with the aim of identifying a pathological genetic variant that could account for the death. Greater awareness of malignant arrhythmias in the absence of structural changes in inherited cardiomyopathies has increased the applicability of molecular autopsies, and resulted in improved care of families but new challenges for clinicians.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 4","pages":"215-216"},"PeriodicalIF":49.6,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139542509","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 : 2024-01-12DOI: 10.1038/s41569-023-00984-x
Gabrielle Fredman, Charles N. Serhan
Timely resolution of the acute inflammatory response (or inflammation resolution) is an active, highly coordinated process that is essential to optimal health. Inflammation resolution is regulated by specific endogenous signalling molecules that function as ‘stop signals’ to terminate the inflammatory response when it is no longer needed; to actively promote healing, regeneration and tissue repair; and to limit pain. Specialized pro-resolving mediators are a superfamily of signalling molecules that initiate anti-inflammatory and pro-resolving actions. Without an effective and timely resolution response, inflammation can become chronic, a pathological state that is associated with many widely occurring human diseases, including atherosclerotic cardiovascular disease. Uncovering the mechanisms of inflammation resolution failure in cardiovascular diseases and identifying useful biomarkers for non-resolving inflammation are unmet needs. In this Review, we discuss the accumulating evidence that supports the role of non-resolving inflammation in atherosclerosis and the use of specialized pro-resolving mediators as therapeutic tools for the treatment of atherosclerotic cardiovascular disease. We highlight open questions about therapeutic strategies and mechanisms of disease to provide a framework for future studies on the prevention and treatment of atherosclerosis. In this Review, Fredman and Serhan discuss the role of specialized pro-resolving mediators, a superfamily of endogenous signalling lipids that mediate resolution of inflammation processes in atherosclerosis, and appraise the therapeutic potential of specialized pro-resolving mediators for the prevention and treatment of atherosclerosis, and the resolution of uncontrolled vascular inflammation.
{"title":"Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease","authors":"Gabrielle Fredman, Charles N. Serhan","doi":"10.1038/s41569-023-00984-x","DOIUrl":"10.1038/s41569-023-00984-x","url":null,"abstract":"Timely resolution of the acute inflammatory response (or inflammation resolution) is an active, highly coordinated process that is essential to optimal health. Inflammation resolution is regulated by specific endogenous signalling molecules that function as ‘stop signals’ to terminate the inflammatory response when it is no longer needed; to actively promote healing, regeneration and tissue repair; and to limit pain. Specialized pro-resolving mediators are a superfamily of signalling molecules that initiate anti-inflammatory and pro-resolving actions. Without an effective and timely resolution response, inflammation can become chronic, a pathological state that is associated with many widely occurring human diseases, including atherosclerotic cardiovascular disease. Uncovering the mechanisms of inflammation resolution failure in cardiovascular diseases and identifying useful biomarkers for non-resolving inflammation are unmet needs. In this Review, we discuss the accumulating evidence that supports the role of non-resolving inflammation in atherosclerosis and the use of specialized pro-resolving mediators as therapeutic tools for the treatment of atherosclerotic cardiovascular disease. We highlight open questions about therapeutic strategies and mechanisms of disease to provide a framework for future studies on the prevention and treatment of atherosclerosis. In this Review, Fredman and Serhan discuss the role of specialized pro-resolving mediators, a superfamily of endogenous signalling lipids that mediate resolution of inflammation processes in atherosclerosis, and appraise the therapeutic potential of specialized pro-resolving mediators for the prevention and treatment of atherosclerosis, and the resolution of uncontrolled vascular inflammation.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 11","pages":"808-823"},"PeriodicalIF":41.7,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-023-00984-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139431354","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 : 2024-01-04DOI: 10.1038/s41569-023-00979-8
Ashish Sarraju, Steven E. Nissen
Atherosclerotic plaque results from a complex interplay between lipid deposition, inflammatory changes, cell migration and arterial wall injury. Over the past two decades, clinical trials utilizing invasive arterial imaging modalities, such as intravascular ultrasonography, have shown that reducing levels of atherogenic lipoproteins, mainly serum LDL-cholesterol (LDL-C), to very low levels can safely reduce overall atherosclerotic plaque burden and favourably modify plaque composition. Classically, this outcome has been achieved with intensive statin therapy. Since 2016, newer and potent lipid-lowering strategies, such as proprotein convertase subtilisin–kexin type 9 inhibition, have shown incremental effects on plaque regression and risk of clinical events. Despite maximal reduction in plasma LDL-C levels, considerable residual cardiovascular risk remains in some patients. Therefore, there is a need to study therapeutic approaches that address residual risk beyond LDL-C reduction to promote plaque stabilization or regression. Contemporary imaging modalities, such as coronary computed tomography angiography, enable non-invasive assessment of the overall atherosclerotic plaque burden as well as of certain local plaque characteristics. This technology could allow further study of plaque stabilization and regression using novel therapeutic approaches. Non-invasive plaque assessment might also offer the potential to guide personalized management strategies if validated for this purpose. In this Review, Sarraju and Nissen summarize the clinical trial evidence for coronary atherosclerotic plaque stabilization and regression with plasma LDL-cholesterol-lowering therapy and other treatments. Invasive and non-invasive imaging modalities used to assess plaque burden and composition are discussed.
{"title":"Atherosclerotic plaque stabilization and regression: a review of clinical evidence","authors":"Ashish Sarraju, Steven E. Nissen","doi":"10.1038/s41569-023-00979-8","DOIUrl":"10.1038/s41569-023-00979-8","url":null,"abstract":"Atherosclerotic plaque results from a complex interplay between lipid deposition, inflammatory changes, cell migration and arterial wall injury. Over the past two decades, clinical trials utilizing invasive arterial imaging modalities, such as intravascular ultrasonography, have shown that reducing levels of atherogenic lipoproteins, mainly serum LDL-cholesterol (LDL-C), to very low levels can safely reduce overall atherosclerotic plaque burden and favourably modify plaque composition. Classically, this outcome has been achieved with intensive statin therapy. Since 2016, newer and potent lipid-lowering strategies, such as proprotein convertase subtilisin–kexin type 9 inhibition, have shown incremental effects on plaque regression and risk of clinical events. Despite maximal reduction in plasma LDL-C levels, considerable residual cardiovascular risk remains in some patients. Therefore, there is a need to study therapeutic approaches that address residual risk beyond LDL-C reduction to promote plaque stabilization or regression. Contemporary imaging modalities, such as coronary computed tomography angiography, enable non-invasive assessment of the overall atherosclerotic plaque burden as well as of certain local plaque characteristics. This technology could allow further study of plaque stabilization and regression using novel therapeutic approaches. Non-invasive plaque assessment might also offer the potential to guide personalized management strategies if validated for this purpose. In this Review, Sarraju and Nissen summarize the clinical trial evidence for coronary atherosclerotic plaque stabilization and regression with plasma LDL-cholesterol-lowering therapy and other treatments. Invasive and non-invasive imaging modalities used to assess plaque burden and composition are discussed.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"487-497"},"PeriodicalIF":49.6,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139090999","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 : 2024-01-03DOI: 10.1038/s41569-023-00972-1
Adam J. Nelson, Neha J. Pagidipati, Hayden B. Bosworth
Non-adherence to medication is a global health problem with far-reaching individual-level and population-level consequences but remains unappreciated and under-addressed in the clinical setting. With increasing comorbidity and polypharmacy as well as an ageing population, cardiovascular disease and medication non-adherence are likely to become increasingly prevalent. Multiple methods for detecting non-adherence exist but are imperfect, and, despite emerging technology, a gold standard remains elusive. Non-adherence to medication is dynamic and often has multiple causes, particularly in the context of cardiovascular disease, which tends to require lifelong medication to control symptoms and risk factors in order to prevent disease progression. In this Review, we identify the causes of medication non-adherence and summarize interventions that have been proven in randomized clinical trials to be effective in improving adherence. Practical solutions and areas for future research are also proposed. In this Review, Bosworth and colleagues describe the causes of medication non-adherence, discuss interventions that have been clinically shown to improve adherence and identify areas for future research.
{"title":"Improving medication adherence in cardiovascular disease","authors":"Adam J. Nelson, Neha J. Pagidipati, Hayden B. Bosworth","doi":"10.1038/s41569-023-00972-1","DOIUrl":"10.1038/s41569-023-00972-1","url":null,"abstract":"Non-adherence to medication is a global health problem with far-reaching individual-level and population-level consequences but remains unappreciated and under-addressed in the clinical setting. With increasing comorbidity and polypharmacy as well as an ageing population, cardiovascular disease and medication non-adherence are likely to become increasingly prevalent. Multiple methods for detecting non-adherence exist but are imperfect, and, despite emerging technology, a gold standard remains elusive. Non-adherence to medication is dynamic and often has multiple causes, particularly in the context of cardiovascular disease, which tends to require lifelong medication to control symptoms and risk factors in order to prevent disease progression. In this Review, we identify the causes of medication non-adherence and summarize interventions that have been proven in randomized clinical trials to be effective in improving adherence. Practical solutions and areas for future research are also proposed. In this Review, Bosworth and colleagues describe the causes of medication non-adherence, discuss interventions that have been clinically shown to improve adherence and identify areas for future research.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"417-429"},"PeriodicalIF":49.6,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087616","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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