Pub Date : 2024-11-05DOI: 10.1038/s41569-024-01094-y
Zhuoming Zhou, Wei Chen, Yihai Cao, Reza Abdi, Wei Tao
Autologous saphenous veins are the most frequently used conduits for coronary and peripheral artery bypass grafting. However, vein graft failure rates of 40–50% within 10 years of the implantation lead to poor long-term outcomes after bypass surgery. Currently, only a few therapeutic approaches for vein graft disease have been successfully translated into clinical practice. Building on the past two decades of advanced understanding of vein graft biology and the pathophysiological mechanisms underlying vein graft disease, nanomedicine-based strategies offer promising opportunities to address this important unmet clinical need. In this Review, we provide deep insight into the latest developments in the rational design and applications of nanoparticles that have the potential to target specific cells during various pathophysiological stages of vein graft disease, including early endothelial dysfunction, intermediate intimal hyperplasia and late-stage accelerated atherosclerosis. Additionally, we underscore the convergence of nanofabricated biomaterials, with a particular focus on hydrogels, external graft support devices and cell-based therapies, alongside bypass surgery to improve local delivery efficiency and therapeutic efficacy. Finally, we provide a specific discussion on the considerations, challenges and novel perspectives for the future clinical translation of nanomedicine for the treatment of vein graft disease. In this Review, Tao and colleagues discuss the design and applications of nanoparticles and nanofabricated biomaterials, such as hydrogels, external graft support devices and cell-based therapies, for the treatment of vein graft disease and highlight the potential of using these nanofabricated biomaterials alongside bypass surgery to improve local delivery efficiency and therapeutic efficacy.
{"title":"Nanomedicine-based strategies for the treatment of vein graft disease","authors":"Zhuoming Zhou, Wei Chen, Yihai Cao, Reza Abdi, Wei Tao","doi":"10.1038/s41569-024-01094-y","DOIUrl":"10.1038/s41569-024-01094-y","url":null,"abstract":"Autologous saphenous veins are the most frequently used conduits for coronary and peripheral artery bypass grafting. However, vein graft failure rates of 40–50% within 10 years of the implantation lead to poor long-term outcomes after bypass surgery. Currently, only a few therapeutic approaches for vein graft disease have been successfully translated into clinical practice. Building on the past two decades of advanced understanding of vein graft biology and the pathophysiological mechanisms underlying vein graft disease, nanomedicine-based strategies offer promising opportunities to address this important unmet clinical need. In this Review, we provide deep insight into the latest developments in the rational design and applications of nanoparticles that have the potential to target specific cells during various pathophysiological stages of vein graft disease, including early endothelial dysfunction, intermediate intimal hyperplasia and late-stage accelerated atherosclerosis. Additionally, we underscore the convergence of nanofabricated biomaterials, with a particular focus on hydrogels, external graft support devices and cell-based therapies, alongside bypass surgery to improve local delivery efficiency and therapeutic efficacy. Finally, we provide a specific discussion on the considerations, challenges and novel perspectives for the future clinical translation of nanomedicine for the treatment of vein graft disease. In this Review, Tao and colleagues discuss the design and applications of nanoparticles and nanofabricated biomaterials, such as hydrogels, external graft support devices and cell-based therapies, for the treatment of vein graft disease and highlight the potential of using these nanofabricated biomaterials alongside bypass surgery to improve local delivery efficiency and therapeutic efficacy.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 4","pages":"255-272"},"PeriodicalIF":41.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142580063","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 : 2024-10-25DOI: 10.1038/s41569-024-01077-z
Sanjay Rajagopalan, Scott McAlister, Jason Jay, Richard D. Pham, Robert D. Brook, Khurram Nasir, Mark. J. Nieuwenhuijsen, Philip Landrigan, Allegra Wiesler, Christina Vernon Sanborn, Justin R. Carron, Kara Hammond Brooks, Aruni Bhatnagar, Sadeer Al-Kindi
Cardiovascular disease is the leading cause of morbidity and mortality worldwide, with a substantial amount of health-care resources targeted towards its diagnosis and management. Environmental sustainability in cardiovascular care can have an important role in reducing greenhouse gas emissions and pollution and could be beneficial for improving health metrics and societal well-being and minimizing the cost of health care. In this Review, we discuss the motivations and frameworks for sustainable cardiovascular care with an emphasis on the reduction of the climate-related and environmental effects of cardiovascular care. We also provide an overview of greenhouse gas emissions related to the provision of health care, including their measurement and quantification, carbon accounting, carbon disclosures and climate effects. The principles of life-cycle assessment, waste prevention and circular economics in health care are discussed, and the emissions associated with various sectors of cardiovascular care as well as the rationale for prevention as a powerful approach to reduce these emissions are presented. Finally, we highlight the challenges in environmental sustainability and future directions as applicable to cardiovascular practice. In this Review, Rajagopalan and colleagues summarize the sources of greenhouse gas emissions related to the provision of cardiovascular health care and suggest strategies to reduce carbon emissions and costs, including the use of renewable energy, waste reduction and disease prevention.
{"title":"Environmental sustainability in cardiovascular practice: current challenges and future directions","authors":"Sanjay Rajagopalan, Scott McAlister, Jason Jay, Richard D. Pham, Robert D. Brook, Khurram Nasir, Mark. J. Nieuwenhuijsen, Philip Landrigan, Allegra Wiesler, Christina Vernon Sanborn, Justin R. Carron, Kara Hammond Brooks, Aruni Bhatnagar, Sadeer Al-Kindi","doi":"10.1038/s41569-024-01077-z","DOIUrl":"10.1038/s41569-024-01077-z","url":null,"abstract":"Cardiovascular disease is the leading cause of morbidity and mortality worldwide, with a substantial amount of health-care resources targeted towards its diagnosis and management. Environmental sustainability in cardiovascular care can have an important role in reducing greenhouse gas emissions and pollution and could be beneficial for improving health metrics and societal well-being and minimizing the cost of health care. In this Review, we discuss the motivations and frameworks for sustainable cardiovascular care with an emphasis on the reduction of the climate-related and environmental effects of cardiovascular care. We also provide an overview of greenhouse gas emissions related to the provision of health care, including their measurement and quantification, carbon accounting, carbon disclosures and climate effects. The principles of life-cycle assessment, waste prevention and circular economics in health care are discussed, and the emissions associated with various sectors of cardiovascular care as well as the rationale for prevention as a powerful approach to reduce these emissions are presented. Finally, we highlight the challenges in environmental sustainability and future directions as applicable to cardiovascular practice. In this Review, Rajagopalan and colleagues summarize the sources of greenhouse gas emissions related to the provision of cardiovascular health care and suggest strategies to reduce carbon emissions and costs, including the use of renewable energy, waste reduction and disease prevention.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 4","pages":"241-254"},"PeriodicalIF":41.7,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142489618","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 : 2024-10-23DOI: 10.1038/s41569-024-01092-0
Neil Bodagh, Steven E. Williams
In this Tools of the Trade article, Bodagh and Williams highlight the utility of OpenEP, an open-source platform that offers standardized solutions for storage and analysis of electroanatomic mapping data.
在这篇 "贸易工具 "文章中，Bodagh 和 Williams 重点介绍了 OpenEP 的实用性，这是一个开源平台，可为电解剖图数据的存储和分析提供标准化解决方案。
{"title":"OpenEP and EP Workbench for electrophysiology data analysis","authors":"Neil Bodagh, Steven E. Williams","doi":"10.1038/s41569-024-01092-0","DOIUrl":"10.1038/s41569-024-01092-0","url":null,"abstract":"In this Tools of the Trade article, Bodagh and Williams highlight the utility of OpenEP, an open-source platform that offers standardized solutions for storage and analysis of electroanatomic mapping data.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 1","pages":"3-3"},"PeriodicalIF":41.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487243","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 : 2024-10-23DOI: 10.1038/s41569-024-01088-w
Ulrich Schotten, Andreas Goette, Sander Verheule
Atrial fibrosis is one of the main manifestations of atrial cardiomyopathy, an array of electrical, mechanical and structural alterations associated with atrial fibrillation (AF), stroke and heart failure. Atrial fibrosis can be both a cause and a consequence of AF and, once present, it accelerates the progression of AF. The pathophysiological mechanisms leading to atrial fibrosis are diverse and include stretch-induced activation of fibroblasts, systemic inflammatory processes, activation of coagulation factors and fibrofatty infiltrations. Importantly, atrial fibrosis can occur in different forms, such as reactive and replacement fibrosis. The diversity of atrial fibrosis mechanisms and patterns depends on sex, age and comorbidity profile, hampering the development of therapeutic strategies. In addition, the presence and severity of comorbidities often change over time, potentially causing temporal changes in the mechanisms underlying atrial fibrosis development. This Review summarizes the latest knowledge on the molecular and cellular mechanisms of atrial fibrosis, its association with comorbidities and the sex-related differences. We describe how the various patterns of atrial fibrosis translate into electrophysiological mechanisms that promote AF, and critically appraise the clinical applicability and limitations of diagnostic tools to quantify atrial fibrosis. Finally, we provide an overview of the newest therapeutic interventions under development and discuss relevant knowledge gaps related to the association between clinical manifestations and pathological mechanisms of atrial fibrosis and to the translation of this knowledge to a clinical setting. In this Review, Schotten and colleagues summarize the latest knowledge on the molecular and cellular mechanisms of atrial fibrosis, describe the electrophysiological manifestations of atrial fibrosis, critically appraise the diagnostic tools to quantify atrial fibrosis, discuss emerging therapeutic interventions, and highlight knowledge gaps and future research directions.
{"title":"Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches","authors":"Ulrich Schotten, Andreas Goette, Sander Verheule","doi":"10.1038/s41569-024-01088-w","DOIUrl":"10.1038/s41569-024-01088-w","url":null,"abstract":"Atrial fibrosis is one of the main manifestations of atrial cardiomyopathy, an array of electrical, mechanical and structural alterations associated with atrial fibrillation (AF), stroke and heart failure. Atrial fibrosis can be both a cause and a consequence of AF and, once present, it accelerates the progression of AF. The pathophysiological mechanisms leading to atrial fibrosis are diverse and include stretch-induced activation of fibroblasts, systemic inflammatory processes, activation of coagulation factors and fibrofatty infiltrations. Importantly, atrial fibrosis can occur in different forms, such as reactive and replacement fibrosis. The diversity of atrial fibrosis mechanisms and patterns depends on sex, age and comorbidity profile, hampering the development of therapeutic strategies. In addition, the presence and severity of comorbidities often change over time, potentially causing temporal changes in the mechanisms underlying atrial fibrosis development. This Review summarizes the latest knowledge on the molecular and cellular mechanisms of atrial fibrosis, its association with comorbidities and the sex-related differences. We describe how the various patterns of atrial fibrosis translate into electrophysiological mechanisms that promote AF, and critically appraise the clinical applicability and limitations of diagnostic tools to quantify atrial fibrosis. Finally, we provide an overview of the newest therapeutic interventions under development and discuss relevant knowledge gaps related to the association between clinical manifestations and pathological mechanisms of atrial fibrosis and to the translation of this knowledge to a clinical setting. In this Review, Schotten and colleagues summarize the latest knowledge on the molecular and cellular mechanisms of atrial fibrosis, describe the electrophysiological manifestations of atrial fibrosis, critically appraise the diagnostic tools to quantify atrial fibrosis, discuss emerging therapeutic interventions, and highlight knowledge gaps and future research directions.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 4","pages":"225-240"},"PeriodicalIF":41.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487832","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 : 2024-10-18DOI: 10.1038/s41569-024-01095-x
Filip K. Swirski, Christoph J. Binder
Consumption of a high-fat diet leads to the progressive growth of atherosclerotic lesions. Two new studies document that, despite similar overall exposure to high-fat diet over a lifetime, an intermittent consumption of high-fat diet early in life accelerates atherosclerosis compared with continuous consumption of a high-fat diet. The mechanisms for accelerated atherosclerosis include reprogramming of macrophages and neutrophils.
{"title":"Lower your cholesterol early, and stick with it!","authors":"Filip K. Swirski, Christoph J. Binder","doi":"10.1038/s41569-024-01095-x","DOIUrl":"10.1038/s41569-024-01095-x","url":null,"abstract":"Consumption of a high-fat diet leads to the progressive growth of atherosclerotic lesions. Two new studies document that, despite similar overall exposure to high-fat diet over a lifetime, an intermittent consumption of high-fat diet early in life accelerates atherosclerosis compared with continuous consumption of a high-fat diet. The mechanisms for accelerated atherosclerosis include reprogramming of macrophages and neutrophils.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 2","pages":"69-70"},"PeriodicalIF":41.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142448210","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 : 2024-10-11DOI: 10.1038/s41569-024-01076-0
Radosław Lenarczyk, Marco Proietti, Jan F. Scheitz, Dipen Shah, Eberhard Siebert, Diana A. Gorog, Jacek Kowalczyk, Nikolaos Bonaros, George Ntaios, Wolfram Doehner, Nicolas M. Van Mieghem, Sandor Nardai, Jan Kovac, Roland Fiszer, Roberto Lorusso, Eliano Navarese, Sergio Castrejón, Andrea Rubboli, José Miguel Rivera-Caravaca, Alaide Chieffo, Gregory Y. H. Lip
Over the past 50 years, the number and invasiveness of percutaneous cardiovascular procedures globally have increased substantially. However, cardiovascular interventions are inherently associated with a risk of acute brain injury, both periprocedurally and postprocedurally, which impairs medical outcomes and increases health-care costs. Current international clinical guidelines generally do not cover the area of acute brain injury related to cardiovascular invasive procedures. In this international Consensus Statement, we compile the available knowledge (including data on prevalence, pathophysiology, risk factors, clinical presentation and management) to formulate consensus recommendations on the prevention, diagnosis and treatment of acute brain injury caused by cardiovascular interventions. We also identify knowledge gaps and possible future directions in clinical research into acute brain injury related to cardiovascular interventions. Invasive cardiovascular procedures are inherently associated with a risk of acute brain injury, both during and after the intervention. In this international Consensus Statement, the authors provide consensus recommendations on the prevention, diagnosis and treatment of acute brain injury caused by cardiovascular interventions.
{"title":"Clinical and subclinical acute brain injury caused by invasive cardiovascular procedures","authors":"Radosław Lenarczyk, Marco Proietti, Jan F. Scheitz, Dipen Shah, Eberhard Siebert, Diana A. Gorog, Jacek Kowalczyk, Nikolaos Bonaros, George Ntaios, Wolfram Doehner, Nicolas M. Van Mieghem, Sandor Nardai, Jan Kovac, Roland Fiszer, Roberto Lorusso, Eliano Navarese, Sergio Castrejón, Andrea Rubboli, José Miguel Rivera-Caravaca, Alaide Chieffo, Gregory Y. H. Lip","doi":"10.1038/s41569-024-01076-0","DOIUrl":"10.1038/s41569-024-01076-0","url":null,"abstract":"Over the past 50 years, the number and invasiveness of percutaneous cardiovascular procedures globally have increased substantially. However, cardiovascular interventions are inherently associated with a risk of acute brain injury, both periprocedurally and postprocedurally, which impairs medical outcomes and increases health-care costs. Current international clinical guidelines generally do not cover the area of acute brain injury related to cardiovascular invasive procedures. In this international Consensus Statement, we compile the available knowledge (including data on prevalence, pathophysiology, risk factors, clinical presentation and management) to formulate consensus recommendations on the prevention, diagnosis and treatment of acute brain injury caused by cardiovascular interventions. We also identify knowledge gaps and possible future directions in clinical research into acute brain injury related to cardiovascular interventions. Invasive cardiovascular procedures are inherently associated with a risk of acute brain injury, both during and after the intervention. In this international Consensus Statement, the authors provide consensus recommendations on the prevention, diagnosis and treatment of acute brain injury caused by cardiovascular interventions.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 4","pages":"273-303"},"PeriodicalIF":41.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-01076-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404905","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 : 2024-10-11DOI: 10.1038/s41569-024-01074-2
Marta Gigli, Davide Stolfo, Marco Merlo, Gianfranco Sinagra, Matthew R. G. Taylor, Luisa Mestroni
Dilated cardiomyopathy (DCM) is a complex disease with multiple causes and various pathogenic mechanisms. Despite improvements in the prognosis of patients with DCM in the past decade, this condition remains a leading cause of heart failure and premature death. Conventional treatment for DCM is based on the foundational therapies for heart failure with reduced ejection fraction. However, increasingly, attention is being directed towards individualized treatments and precision medicine. The ability to confirm genetic causality is gradually being complemented by an increased understanding of genotype–phenotype correlations. Non-genetic factors also influence the onset of DCM, and growing evidence links genetic background with concomitant non-genetic triggers or precipitating factors, increasing the extreme complexity of the pathophysiology of DCM. This Review covers the spectrum of pathophysiological mechanisms in DCM, from monogenic causes to the coexistence of genetic abnormalities and triggering environmental factors (the ‘two-hit’ hypothesis). The roles of common genetic variants in the general population and of gene modifiers in disease onset and progression are also discussed. Finally, areas for future research are highlighted, particularly novel therapies, such as small molecules, RNA and gene therapy, and measures for the prevention of arrhythmic death. In this Review, Mestroni and colleagues provide an overview of the pathophysiological mechanisms underlying dilated cardiomyopathy, including both genetic and non-genetic causes, and discuss the development of novel therapies, such as small molecules and gene therapy.
{"title":"Pathophysiology of dilated cardiomyopathy: from mechanisms to precision medicine","authors":"Marta Gigli, Davide Stolfo, Marco Merlo, Gianfranco Sinagra, Matthew R. G. Taylor, Luisa Mestroni","doi":"10.1038/s41569-024-01074-2","DOIUrl":"10.1038/s41569-024-01074-2","url":null,"abstract":"Dilated cardiomyopathy (DCM) is a complex disease with multiple causes and various pathogenic mechanisms. Despite improvements in the prognosis of patients with DCM in the past decade, this condition remains a leading cause of heart failure and premature death. Conventional treatment for DCM is based on the foundational therapies for heart failure with reduced ejection fraction. However, increasingly, attention is being directed towards individualized treatments and precision medicine. The ability to confirm genetic causality is gradually being complemented by an increased understanding of genotype–phenotype correlations. Non-genetic factors also influence the onset of DCM, and growing evidence links genetic background with concomitant non-genetic triggers or precipitating factors, increasing the extreme complexity of the pathophysiology of DCM. This Review covers the spectrum of pathophysiological mechanisms in DCM, from monogenic causes to the coexistence of genetic abnormalities and triggering environmental factors (the ‘two-hit’ hypothesis). The roles of common genetic variants in the general population and of gene modifiers in disease onset and progression are also discussed. Finally, areas for future research are highlighted, particularly novel therapies, such as small molecules, RNA and gene therapy, and measures for the prevention of arrhythmic death. In this Review, Mestroni and colleagues provide an overview of the pathophysiological mechanisms underlying dilated cardiomyopathy, including both genetic and non-genetic causes, and discuss the development of novel therapies, such as small molecules and gene therapy.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 3","pages":"183-198"},"PeriodicalIF":41.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404906","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 : 2024-10-09DOI: 10.1038/s41569-024-01093-z
Robin Hofmann, Stefan James
In contrast to the ABYSS investigators’ interpretation of the primary results of their trial, we believe that β-blockers can be safely discontinued in the majority of patients after an uncomplicated myocardial infarction. However, in individuals developing symptoms of angina or heart failure, β-blocker treatment remains one of several guideline-recommended therapies.
{"title":"β-blockers after MI: does ABYSS confirm REDUCEd use after all?","authors":"Robin Hofmann, Stefan James","doi":"10.1038/s41569-024-01093-z","DOIUrl":"10.1038/s41569-024-01093-z","url":null,"abstract":"In contrast to the ABYSS investigators’ interpretation of the primary results of their trial, we believe that β-blockers can be safely discontinued in the majority of patients after an uncomplicated myocardial infarction. However, in individuals developing symptoms of angina or heart failure, β-blocker treatment remains one of several guideline-recommended therapies.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 1","pages":"7-8"},"PeriodicalIF":41.7,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385077","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 : 2024-09-25DOI: 10.1038/s41569-024-01091-1
Christopher X. Wong, Hung Fat Tse, Eue-Kuen Choi, Tze-Fan Chao, Koichi Inoue, Katrina Poppe, Eugene Tan, Yoga Yuniadi, Erdie Fadreguilan, Sofian Johar, Ngai Yin Chan, Narayan Namboodiri, S. Mokaddas Hossain, Huang He, Thoranis Chantrarat, Abdul Raqib Bin Abd Ghani, Narantuya Davaakhuu, Nwe Nwe, Ghazala Irfan, Minh That Ton, Rohan Gunawardena, Prashanthan Sanders
The burden of atrial fibrillation (AF) is increasing worldwide; however, most existing data on AF epidemiology are from Western regions. According to our analyses, the estimated absolute prevalence of AF in the Asia–Pacific region in 2023 was approximately 80 million, which is much higher than has been calculated for other global regions.
{"title":"The burden of atrial fibrillation in the Asia–Pacific region","authors":"Christopher X. Wong, Hung Fat Tse, Eue-Kuen Choi, Tze-Fan Chao, Koichi Inoue, Katrina Poppe, Eugene Tan, Yoga Yuniadi, Erdie Fadreguilan, Sofian Johar, Ngai Yin Chan, Narayan Namboodiri, S. Mokaddas Hossain, Huang He, Thoranis Chantrarat, Abdul Raqib Bin Abd Ghani, Narantuya Davaakhuu, Nwe Nwe, Ghazala Irfan, Minh That Ton, Rohan Gunawardena, Prashanthan Sanders","doi":"10.1038/s41569-024-01091-1","DOIUrl":"10.1038/s41569-024-01091-1","url":null,"abstract":"The burden of atrial fibrillation (AF) is increasing worldwide; however, most existing data on AF epidemiology are from Western regions. According to our analyses, the estimated absolute prevalence of AF in the Asia–Pacific region in 2023 was approximately 80 million, which is much higher than has been calculated for other global regions.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 12","pages":"841-843"},"PeriodicalIF":41.7,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142317016","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 : 2024-09-25DOI: 10.1038/s41569-024-01068-0
Thomas Münzel, Omar Hahad, Jos Lelieveld, Michael Aschner, Mark J. Nieuwenhuijsen, Philip J. Landrigan, Andreas Daiber
Healthy, uncontaminated soils and clean water support all life on Earth and are essential for human health. Chemical pollution of soil, water, air and food is a major environmental threat, leading to an estimated 9 million premature deaths worldwide. The Global Burden of Disease study estimated that pollution was responsible for 5.5 million deaths related to cardiovascular disease (CVD) in 2019. Robust evidence has linked multiple pollutants, including heavy metals, pesticides, dioxins and toxic synthetic chemicals, with increased risk of CVD, and some reports suggest an association between microplastic and nanoplastic particles and CVD. Pollutants in soil diminish its capacity to produce food, leading to crop impurities, malnutrition and disease, and they can seep into rivers, worsening water pollution. Deforestation, wildfires and climate change exacerbate pollution by triggering soil erosion and releasing sequestered pollutants into the air and water. Despite their varied chemical makeup, pollutants induce CVD through common pathophysiological mechanisms involving oxidative stress and inflammation. In this Review, we provide an overview of the relationship between soil and water pollution and human health and pathology, and discuss the prevalence of soil and water pollutants and how they contribute to adverse health effects, focusing on CVD. In this Review, Münzel and colleagues describe the adverse effects of soil and water pollution, including heavy metal, pesticide, and microplastic and nanoplastic pollution, on cardiovascular health and provide an overview of the eco-disruptive causes of this pollution.
{"title":"Soil and water pollution and cardiovascular disease","authors":"Thomas Münzel, Omar Hahad, Jos Lelieveld, Michael Aschner, Mark J. Nieuwenhuijsen, Philip J. Landrigan, Andreas Daiber","doi":"10.1038/s41569-024-01068-0","DOIUrl":"10.1038/s41569-024-01068-0","url":null,"abstract":"Healthy, uncontaminated soils and clean water support all life on Earth and are essential for human health. Chemical pollution of soil, water, air and food is a major environmental threat, leading to an estimated 9 million premature deaths worldwide. The Global Burden of Disease study estimated that pollution was responsible for 5.5 million deaths related to cardiovascular disease (CVD) in 2019. Robust evidence has linked multiple pollutants, including heavy metals, pesticides, dioxins and toxic synthetic chemicals, with increased risk of CVD, and some reports suggest an association between microplastic and nanoplastic particles and CVD. Pollutants in soil diminish its capacity to produce food, leading to crop impurities, malnutrition and disease, and they can seep into rivers, worsening water pollution. Deforestation, wildfires and climate change exacerbate pollution by triggering soil erosion and releasing sequestered pollutants into the air and water. Despite their varied chemical makeup, pollutants induce CVD through common pathophysiological mechanisms involving oxidative stress and inflammation. In this Review, we provide an overview of the relationship between soil and water pollution and human health and pathology, and discuss the prevalence of soil and water pollutants and how they contribute to adverse health effects, focusing on CVD. In this Review, Münzel and colleagues describe the adverse effects of soil and water pollution, including heavy metal, pesticide, and microplastic and nanoplastic pollution, on cardiovascular health and provide an overview of the eco-disruptive causes of this pollution.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"22 2","pages":"71-89"},"PeriodicalIF":41.7,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314070","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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