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}
Pub Date : 2024-05-02DOI: 10.1038/s41569-024-01028-8
Jonatan Wärme, Martin O. Sundqvist, Stefan James, Robin Hofmann
{"title":"Screening for Helicobacter pylori infection in patients with cardiovascular and gastrointestinal disease","authors":"Jonatan Wärme, Martin O. Sundqvist, Stefan James, Robin Hofmann","doi":"10.1038/s41569-024-01028-8","DOIUrl":"10.1038/s41569-024-01028-8","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 8","pages":"593-593"},"PeriodicalIF":41.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-01028-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855126","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 : 2024-05-02DOI: 10.1038/s41569-024-01029-7
Azita H. Talasaz, Behnood Bikdeli
{"title":"Reply to ‘Screening for Helicobacter pylori infection in patients with cardiovascular and gastrointestinal disease’","authors":"Azita H. Talasaz, Behnood Bikdeli","doi":"10.1038/s41569-024-01029-7","DOIUrl":"10.1038/s41569-024-01029-7","url":null,"abstract":"","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 8","pages":"594-595"},"PeriodicalIF":41.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-01029-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140859331","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 : 2024-04-25DOI: 10.1038/s41569-024-01036-8
Gregory B. Lim
Treatment for periodontal disease might reduce the recurrence of atrial fibrillation (AF) in patients undergoing ablation, suggesting that periodontitis is a modifiable risk factor for AF.
牙周病治疗可减少接受消融术的患者心房颤动（房颤）的复发，这表明牙周炎是房颤的一个可改变的风险因素。
{"title":"Periodontal treatment reduces AF recurrence","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-01036-8","DOIUrl":"10.1038/s41569-024-01036-8","url":null,"abstract":"Treatment for periodontal disease might reduce the recurrence of atrial fibrillation (AF) in patients undergoing ablation, suggesting that periodontitis is a modifiable risk factor for AF.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"355-355"},"PeriodicalIF":49.6,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140648671","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 : 2024-04-25DOI: 10.1038/s41569-024-01023-z
Yvonne Döring, Emiel P. C. van der Vorst, Christian Weber
Atherosclerosis is the primary underlying cause of myocardial infarction and stroke. Atherosclerotic cardiovascular disease is characterized by a chronic inflammatory reaction in medium-to-large-sized arteries, with its onset and perpetuation driven by leukocytes infiltrating the subendothelial space. Activation of endothelial cells triggered by hyperlipidaemia and lipoprotein retention in the arterial intima initiates the accumulation of pro-inflammatory leukocytes in the arterial wall, fostering the progression of atherosclerosis. This inflammatory response is coordinated by an array of soluble mediators, namely cytokines and chemokines, that amplify inflammation both locally and systemically and are complemented by tissue-specific molecules that regulate the homing, adhesion and transmigration of leukocytes. Despite abundant evidence from mouse models, only a few therapies targeting leukocytes in atherosclerosis have been assessed in humans. The major challenges for the clinical translation of these therapies include the lack of tissue specificity and insufficient selectivity of inhibition strategies. In this Review, we discuss the latest research on receptor–ligand pairs and interactors that regulate leukocyte influx into the inflamed artery wall, primarily focusing on studies that used pharmacological interventions. We also discuss mechanisms that promote the resolution of inflammation and highlight how major findings from these research areas hold promise as potential therapeutic strategies for atherosclerotic cardiovascular disease. In this Review, the authors discuss the receptors, ligands and interactors that regulate immune cell recruitment in atherosclerosis, describe mechanisms that promote the resolution of inflammation in atherosclerotic lesions, and highlight potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.
{"title":"Targeting immune cell recruitment in atherosclerosis","authors":"Yvonne Döring, Emiel P. C. van der Vorst, Christian Weber","doi":"10.1038/s41569-024-01023-z","DOIUrl":"10.1038/s41569-024-01023-z","url":null,"abstract":"Atherosclerosis is the primary underlying cause of myocardial infarction and stroke. Atherosclerotic cardiovascular disease is characterized by a chronic inflammatory reaction in medium-to-large-sized arteries, with its onset and perpetuation driven by leukocytes infiltrating the subendothelial space. Activation of endothelial cells triggered by hyperlipidaemia and lipoprotein retention in the arterial intima initiates the accumulation of pro-inflammatory leukocytes in the arterial wall, fostering the progression of atherosclerosis. This inflammatory response is coordinated by an array of soluble mediators, namely cytokines and chemokines, that amplify inflammation both locally and systemically and are complemented by tissue-specific molecules that regulate the homing, adhesion and transmigration of leukocytes. Despite abundant evidence from mouse models, only a few therapies targeting leukocytes in atherosclerosis have been assessed in humans. The major challenges for the clinical translation of these therapies include the lack of tissue specificity and insufficient selectivity of inhibition strategies. In this Review, we discuss the latest research on receptor–ligand pairs and interactors that regulate leukocyte influx into the inflamed artery wall, primarily focusing on studies that used pharmacological interventions. We also discuss mechanisms that promote the resolution of inflammation and highlight how major findings from these research areas hold promise as potential therapeutic strategies for atherosclerotic cardiovascular disease. In this Review, the authors discuss the receptors, ligands and interactors that regulate immune cell recruitment in atherosclerosis, describe mechanisms that promote the resolution of inflammation in atherosclerotic lesions, and highlight potential strategies to target these pathways for the treatment of atherosclerotic cardiovascular disease.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 11","pages":"824-840"},"PeriodicalIF":41.7,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41569-024-01023-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140648752","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 : 2024-04-25DOI: 10.1038/s41569-024-01033-x
Karina Huynh
Findings from the ORBITA-COSMIC trial show that treatment of patients with stable coronary artery disease using a coronary sinus reducer improves angina symptoms but does not increase transmural myocardial perfusion.
{"title":"The coronary sinus reducer improves angina symptoms in patients with stable CAD","authors":"Karina Huynh","doi":"10.1038/s41569-024-01033-x","DOIUrl":"10.1038/s41569-024-01033-x","url":null,"abstract":"Findings from the ORBITA-COSMIC trial show that treatment of patients with stable coronary artery disease using a coronary sinus reducer improves angina symptoms but does not increase transmural myocardial perfusion.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"356-356"},"PeriodicalIF":49.6,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140648792","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 : 2024-04-23DOI: 10.1038/s41569-024-01034-w
Karina Huynh
Three randomized clinical trials presented at ACC.24 demonstrate that olezarsen and plozasiran, RNA-based therapies that target APOC3, can robustly reduce plasma triglyceride levels in patients with moderate to severe hypertriglyceridaemia.
{"title":"RNA-based therapies targeting APOC3 lower triglyceride levels in patients with hypertriglyceridaemia","authors":"Karina Huynh","doi":"10.1038/s41569-024-01034-w","DOIUrl":"10.1038/s41569-024-01034-w","url":null,"abstract":"Three randomized clinical trials presented at ACC.24 demonstrate that olezarsen and plozasiran, RNA-based therapies that target APOC3, can robustly reduce plasma triglyceride levels in patients with moderate to severe hypertriglyceridaemia.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"353-353"},"PeriodicalIF":49.6,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639759","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 : 2024-04-23DOI: 10.1038/s41569-024-01032-y
Gregory B. Lim
According to data from the IMPROVE-HCM trial, ninerafaxstat is well tolerated by patients with symptomatic non-obstructive hypertrophic cardiomyopathy and improves exercise performance among those who are most symptomatically limited.
{"title":"Benefits of ninerafaxstat in non-obstructive hypertrophic cardiomyopathy","authors":"Gregory B. Lim","doi":"10.1038/s41569-024-01032-y","DOIUrl":"10.1038/s41569-024-01032-y","url":null,"abstract":"According to data from the IMPROVE-HCM trial, ninerafaxstat is well tolerated by patients with symptomatic non-obstructive hypertrophic cardiomyopathy and improves exercise performance among those who are most symptomatically limited.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"357-357"},"PeriodicalIF":49.6,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140637549","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 : 2024-04-23DOI: 10.1038/s41569-024-01025-x
Julie Sanders, Tim Clayton, Stacey Matthews, Sarah Murray, Lynn Laidlaw, Richard Evans, Rochelle Wynne
The under-representation of women in cardiovascular clinical trials persists across participant, clinician and research roles. This gap perpetuates health inequity and hampers the generation, translation and implementation of optimal evidence-based care. Urgent action is needed to address barriers, promote diversity, and ensure inclusive trial design and health-care delivery and dissemination, for more equitable cardiovascular health.
{"title":"Strategies for the delivery of sex-based equity in cardiovascular clinical trials","authors":"Julie Sanders, Tim Clayton, Stacey Matthews, Sarah Murray, Lynn Laidlaw, Richard Evans, Rochelle Wynne","doi":"10.1038/s41569-024-01025-x","DOIUrl":"10.1038/s41569-024-01025-x","url":null,"abstract":"The under-representation of women in cardiovascular clinical trials persists across participant, clinician and research roles. This gap perpetuates health inequity and hampers the generation, translation and implementation of optimal evidence-based care. Urgent action is needed to address barriers, promote diversity, and ensure inclusive trial design and health-care delivery and dissemination, for more equitable cardiovascular health.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 7","pages":"433-434"},"PeriodicalIF":49.6,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140637645","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 : 2024-04-23DOI: 10.1038/s41569-024-01035-9
Jennifer Harman
Data from the DanGer Shock trial demonstrate that implantation of a microaxial flow pump in patients with ST-segment elevation myocardial infarction complicated by cardiogenic shock increases the survival rate compared with standard care alone.
DanGer 休克试验的数据表明，与单纯标准治疗相比，为 ST 段抬高型心肌梗死并发心源性休克患者植入微轴流泵可提高存活率。
{"title":"Heart pump increases survival in STEMI-related cardiogenic shock","authors":"Jennifer Harman","doi":"10.1038/s41569-024-01035-9","DOIUrl":"10.1038/s41569-024-01035-9","url":null,"abstract":"Data from the DanGer Shock trial demonstrate that implantation of a microaxial flow pump in patients with ST-segment elevation myocardial infarction complicated by cardiogenic shock increases the survival rate compared with standard care alone.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"21 6","pages":"355-355"},"PeriodicalIF":49.6,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639903","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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