Pub Date : 2026-02-09DOI: 10.1038/s41569-026-01264-0
Rafael Zubiran, Alan T Remaley
{"title":"Calculation methods for LDL cholesterol are evolving tools for accuracy in lipidology.","authors":"Rafael Zubiran, Alan T Remaley","doi":"10.1038/s41569-026-01264-0","DOIUrl":"https://doi.org/10.1038/s41569-026-01264-0","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":" ","pages":""},"PeriodicalIF":44.2,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150135","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 : 2026-01-26DOI: 10.1038/s41569-026-01247-1
Omar Hahad,Sojin Wass,Sanjay Rajagopalan,Shady Abohashem,Hua Hao,Ana Navas-Acien,Lavanya Bellumkonda,Kai Chen,Robert D Brook,Khurram Nasir,Philipp Lurz,David E Lanfear,Arvind Bhimaraj,Sadeer Al-Kindi
Environmental exposures have a crucial role in the incidence and progression of heart failure (HF) by exacerbating genetic predisposition and other pathophysiological mechanisms. The exposome - encompassing pollution, climate and the urban environment - and the biological responses to these factors shape cardiovascular health in complex ways. Air, noise and light pollution, exposure to toxic metals, and extremes of temperature adversely affect HF outcomes. Social determinants of health, including socioeconomic status, amplify these environmental risks, disproportionately affecting vulnerable populations. Conversely, green spaces and walkable neighbourhoods are linked to a reduced risk of HF, improved vascular health and medication adherence. Emerging evidence suggests that environmental stressors influence HF outcomes from early life by altering gene expression through epigenetic mechanisms. Despite these insights, research gaps remain. Future studies must integrate environmental, genetic and multiomics data to refine risk prediction and guide targeted public health interventions. A comprehensive understanding of the exposome in the aetiology of HF is essential for developing prevention strategies that address both biological and social determinants of cardiovascular health.
{"title":"The environmental exposome in heart failure risk and progression.","authors":"Omar Hahad,Sojin Wass,Sanjay Rajagopalan,Shady Abohashem,Hua Hao,Ana Navas-Acien,Lavanya Bellumkonda,Kai Chen,Robert D Brook,Khurram Nasir,Philipp Lurz,David E Lanfear,Arvind Bhimaraj,Sadeer Al-Kindi","doi":"10.1038/s41569-026-01247-1","DOIUrl":"https://doi.org/10.1038/s41569-026-01247-1","url":null,"abstract":"Environmental exposures have a crucial role in the incidence and progression of heart failure (HF) by exacerbating genetic predisposition and other pathophysiological mechanisms. The exposome - encompassing pollution, climate and the urban environment - and the biological responses to these factors shape cardiovascular health in complex ways. Air, noise and light pollution, exposure to toxic metals, and extremes of temperature adversely affect HF outcomes. Social determinants of health, including socioeconomic status, amplify these environmental risks, disproportionately affecting vulnerable populations. Conversely, green spaces and walkable neighbourhoods are linked to a reduced risk of HF, improved vascular health and medication adherence. Emerging evidence suggests that environmental stressors influence HF outcomes from early life by altering gene expression through epigenetic mechanisms. Despite these insights, research gaps remain. Future studies must integrate environmental, genetic and multiomics data to refine risk prediction and guide targeted public health interventions. A comprehensive understanding of the exposome in the aetiology of HF is essential for developing prevention strategies that address both biological and social determinants of cardiovascular health.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"40 1","pages":""},"PeriodicalIF":49.6,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044599","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 : 2026-01-23DOI: 10.1038/s41569-026-01249-z
Mattia Galli, Antonio Abbate, Marc P. Bonaca, Filippo Crea, Maurizio Forte, Giacomo Frati, Mario Gaudino, C. Michael Gibson, Diana A. Gorog, Roxana Mehran, Rocco A. Montone, Michelle L. O’Donoghue, P. Gabriel Steg, Sebastiano Sciarretta, Dominick J. Angiolillo
{"title":"Residual cardiovascular risk in coronary artery disease: from pathophysiology to established and novel therapies","authors":"Mattia Galli, Antonio Abbate, Marc P. Bonaca, Filippo Crea, Maurizio Forte, Giacomo Frati, Mario Gaudino, C. Michael Gibson, Diana A. Gorog, Roxana Mehran, Rocco A. Montone, Michelle L. O’Donoghue, P. Gabriel Steg, Sebastiano Sciarretta, Dominick J. Angiolillo","doi":"10.1038/s41569-026-01249-z","DOIUrl":"https://doi.org/10.1038/s41569-026-01249-z","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"68 1","pages":""},"PeriodicalIF":49.6,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146032821","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 : 2026-01-22DOI: 10.1038/s41569-026-01256-0
Irene Fernández-Ruiz
Treatment with low-dose IL-2 increases regulatory T cell numbers and reduces arterial inflammation in patients with an acute coronary syndrome and residual systemic inflammation compared with placebo, according to findings from the IVORY trial.
{"title":"Low-dose IL-2 therapy reduces arterial inflammation in acute coronary syndromes","authors":"Irene Fernández-Ruiz","doi":"10.1038/s41569-026-01256-0","DOIUrl":"10.1038/s41569-026-01256-0","url":null,"abstract":"Treatment with low-dose IL-2 increases regulatory T cell numbers and reduces arterial inflammation in patients with an acute coronary syndrome and residual systemic inflammation compared with placebo, according to findings from the IVORY trial.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 3","pages":"146-146"},"PeriodicalIF":44.2,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021438","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 : 2026-01-22DOI: 10.1038/s41569-026-01253-3
Allison B Herman,Julián Candia,David M Wilson,Stefano Donega,Martin Picard,Luigi Ferrucci
Chronic inflammation has long been recognized as a major risk factor for and a causal contributor to cardiovascular disease (CVD). However, advances in omics technologies and deepening insights into CVD pathogenesis have expanded our understanding of the underlying mechanisms. Inflammation is now seen not as an isolated cause, but as one of several biological responses to cumulative tissue damage over time. In this Review, we propose that inflammation initially functions as a resilience mechanism, acting to resolve molecular and cellular damage driven by environmental stressors and intrinsic age-related entropy. With ageing, however, this protective response can become dysregulated and maladaptive, promoting collateral pathological changes. We illustrate this theory through two examples, atherosclerosis and age-related impairment of tissue perfusion, and support these conceptual models using proteomic data from large population studies with cardiovascular outcomes. Our findings reaffirm the central role of inflammation in CVD pathophysiology, but also indicate that the upstream biological driver of inflammation is molecular damage that is either not readily prevented or repaired by inadequate resilience mechanisms. Understanding the coordination of these responses offers new opportunities for targeted prevention and treatment of CVD.
{"title":"Molecular damage associated with ageing drives inflammation in cardiovascular disease.","authors":"Allison B Herman,Julián Candia,David M Wilson,Stefano Donega,Martin Picard,Luigi Ferrucci","doi":"10.1038/s41569-026-01253-3","DOIUrl":"https://doi.org/10.1038/s41569-026-01253-3","url":null,"abstract":"Chronic inflammation has long been recognized as a major risk factor for and a causal contributor to cardiovascular disease (CVD). However, advances in omics technologies and deepening insights into CVD pathogenesis have expanded our understanding of the underlying mechanisms. Inflammation is now seen not as an isolated cause, but as one of several biological responses to cumulative tissue damage over time. In this Review, we propose that inflammation initially functions as a resilience mechanism, acting to resolve molecular and cellular damage driven by environmental stressors and intrinsic age-related entropy. With ageing, however, this protective response can become dysregulated and maladaptive, promoting collateral pathological changes. We illustrate this theory through two examples, atherosclerosis and age-related impairment of tissue perfusion, and support these conceptual models using proteomic data from large population studies with cardiovascular outcomes. Our findings reaffirm the central role of inflammation in CVD pathophysiology, but also indicate that the upstream biological driver of inflammation is molecular damage that is either not readily prevented or repaired by inadequate resilience mechanisms. Understanding the coordination of these responses offers new opportunities for targeted prevention and treatment of CVD.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"263 1","pages":""},"PeriodicalIF":49.6,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021675","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 : 2026-01-19DOI: 10.1038/s41569-026-01251-5
John G. F. Cleland
{"title":"Reply to: ‘The use of β-blockers after myocardial infarction: no doubts remain’","authors":"John G. F. Cleland","doi":"10.1038/s41569-026-01251-5","DOIUrl":"10.1038/s41569-026-01251-5","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 3","pages":"209-209"},"PeriodicalIF":44.2,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003812","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 : 2026-01-14DOI: 10.1038/s41569-026-01250-6
Rainer Kaiser,Leo Nicolai
Platelets are the key cell types in haemostasis after vascular injury and crucially contribute to thrombus formation. In addition to their aggregation and clot contraction functions after stimulation by soluble agonists or extracellular matrix proteins, platelets can adopt a highly activated state known as procoagulant activation. Procoagulant platelets influence the pathophysiology underlying various cardiovascular diseases, including myocardial infarction, stroke and deep vein thrombosis. Findings described in the past decade position procoagulant platelets at the dynamic intersection between thrombosis and inflammation. In this Review, we discuss the expanding research on procoagulant platelets, describing how this platelet activation state contributes to macrovascular and microvascular clot formation in cardiovascular diseases. We summarize the key receptors and signalling pathways that control platelet procoagulant activation and that distinguish the procoagulant phenotype from other platelet activation states. Finally, we highlight the clinical significance of platelet procoagulant activation and discuss how the individual pathways involved in this activation can be targeted with the use of both readily available and novel therapeutic approaches, providing a framework for future research that might lead to new diagnostic and therapeutic applications in cardiovascular disease, septic inflammation and immune complex-mediated diseases.
{"title":"Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.","authors":"Rainer Kaiser,Leo Nicolai","doi":"10.1038/s41569-026-01250-6","DOIUrl":"https://doi.org/10.1038/s41569-026-01250-6","url":null,"abstract":"Platelets are the key cell types in haemostasis after vascular injury and crucially contribute to thrombus formation. In addition to their aggregation and clot contraction functions after stimulation by soluble agonists or extracellular matrix proteins, platelets can adopt a highly activated state known as procoagulant activation. Procoagulant platelets influence the pathophysiology underlying various cardiovascular diseases, including myocardial infarction, stroke and deep vein thrombosis. Findings described in the past decade position procoagulant platelets at the dynamic intersection between thrombosis and inflammation. In this Review, we discuss the expanding research on procoagulant platelets, describing how this platelet activation state contributes to macrovascular and microvascular clot formation in cardiovascular diseases. We summarize the key receptors and signalling pathways that control platelet procoagulant activation and that distinguish the procoagulant phenotype from other platelet activation states. Finally, we highlight the clinical significance of platelet procoagulant activation and discuss how the individual pathways involved in this activation can be targeted with the use of both readily available and novel therapeutic approaches, providing a framework for future research that might lead to new diagnostic and therapeutic applications in cardiovascular disease, septic inflammation and immune complex-mediated diseases.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"3 1","pages":""},"PeriodicalIF":49.6,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968384","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 : 2026-01-12DOI: 10.1038/s41569-026-01248-0
Giulio Francesco Romiti, Marco Proietti
Oral anticoagulants are the cornerstone of stroke risk prevention in patients with atrial fibrillation, regardless of whether sinus rhythm is restored. Evidence from two new randomized trials questions the need for long-term treatment with oral anticoagulants after successful ablation of atrial fibrillation and promises to change clinical practice.
{"title":"Oral anticoagulant therapy after ablation for atrial fibrillation","authors":"Giulio Francesco Romiti, Marco Proietti","doi":"10.1038/s41569-026-01248-0","DOIUrl":"10.1038/s41569-026-01248-0","url":null,"abstract":"Oral anticoagulants are the cornerstone of stroke risk prevention in patients with atrial fibrillation, regardless of whether sinus rhythm is restored. Evidence from two new randomized trials questions the need for long-term treatment with oral anticoagulants after successful ablation of atrial fibrillation and promises to change clinical practice.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 3","pages":"143-144"},"PeriodicalIF":44.2,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956032","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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