João Pedro Ferreira, Pedro Marques, Stefan D. Anker, Javed Butler, Gerasimos Filippatos, Abhinav Sharma, Francisco Vasques‐Nóvoa, Luís Mendonça, João Sérgio Neves, Milton Packer, Faiez Zannad
Aims The efficacy of sodium–glucose co‐transporter 2 inhibitors (SGLT2i) among patients with cardiovascular‐kidney‐metabolic (CKM) conditions who experience severe estimated glomerular filtration rate (eGFR) deterioration during follow‐up is not well established. The aim of this study was to assess the risk of cardiovascular outcomes and mortality after eGFR deterioration to <25 ml/min/1.73 m 2 (and <20 ml/min/1.73 m 2 ), and whether such eGFR deterioration modified the effect of SGLT2i across CKM populations. Methods and results Pooled analysis of placebo‐controlled trials: EMPEROR‐Preserved, EMPEROR‐Reduced, EMPA‐REG OUTCOME, CANVAS‐R, and CREDENCE. Time‐updated models with stratification by study were used. The median follow‐up to eGFR deterioration was 17 months and total follow‐time was 29 months. Studied outcomes included heart failure hospitalization or cardiovascular mortality, the composite of cardiovascular mortality, stroke or myocardial infarction, and all‐cause mortality. Overall, 26 946 patients were included, of these 1392 (5.2%) experienced eGFR deterioration to <25 ml/min/1.73 m 2 (and 613 [2.3%] to <20 ml/min/1.73 m 2 ). Factors independently associated with a higher risk of eGFR deterioration were lower baseline eGFR and higher albuminuria, whereas allocation to SGLT2i was protective. eGFR deterioration was independently associated with a nearly twofold higher risk of subsequent cardiovascular outcomes and mortality. The beneficial impact of SGLT2i treatment on cardiovascular outcomes and mortality was maintained irrespective of patients experiencing eGFR deterioration (interaction‐ p >0.1 for all outcomes). Patients who experienced eGFR deterioration were more likely to permanently discontinue treatment, without significant differences in treatment discontinuation rates between the SGLT2i and placebo groups. Conclusions Severe eGFR deterioration during follow‐up was associated with an increased risk of subsequent cardiovascular events and mortality. SGLT2i reduced the probability and were beneficial irrespective of severe eGFR deterioration.
{"title":"Sodium–glucose co‐transporter 2 inhibitors in severe estimated glomerular filtration rate deterioration across cardiovascular‐kidney‐ metabolic conditions: A pooled analysis of randomized trials","authors":"João Pedro Ferreira, Pedro Marques, Stefan D. Anker, Javed Butler, Gerasimos Filippatos, Abhinav Sharma, Francisco Vasques‐Nóvoa, Luís Mendonça, João Sérgio Neves, Milton Packer, Faiez Zannad","doi":"10.1002/ejhf.70093","DOIUrl":"https://doi.org/10.1002/ejhf.70093","url":null,"abstract":"Aims The efficacy of sodium–glucose co‐transporter 2 inhibitors (SGLT2i) among patients with cardiovascular‐kidney‐metabolic (CKM) conditions who experience severe estimated glomerular filtration rate (eGFR) deterioration during follow‐up is not well established. The aim of this study was to assess the risk of cardiovascular outcomes and mortality after eGFR deterioration to <25 ml/min/1.73 m <jats:sup>2</jats:sup> (and <20 ml/min/1.73 m <jats:sup>2</jats:sup> ), and whether such eGFR deterioration modified the effect of SGLT2i across CKM populations. Methods and results Pooled analysis of placebo‐controlled trials: EMPEROR‐Preserved, EMPEROR‐Reduced, EMPA‐REG OUTCOME, CANVAS‐R, and CREDENCE. Time‐updated models with stratification by study were used. The median follow‐up to eGFR deterioration was 17 months and total follow‐time was 29 months. Studied outcomes included heart failure hospitalization or cardiovascular mortality, the composite of cardiovascular mortality, stroke or myocardial infarction, and all‐cause mortality. Overall, 26 946 patients were included, of these 1392 (5.2%) experienced eGFR deterioration to <25 ml/min/1.73 m <jats:sup>2</jats:sup> (and 613 [2.3%] to <20 ml/min/1.73 m <jats:sup>2</jats:sup> ). Factors independently associated with a higher risk of eGFR deterioration were lower baseline eGFR and higher albuminuria, whereas allocation to SGLT2i was protective. eGFR deterioration was independently associated with a nearly twofold higher risk of subsequent cardiovascular outcomes and mortality. The beneficial impact of SGLT2i treatment on cardiovascular outcomes and mortality was maintained irrespective of patients experiencing eGFR deterioration (interaction‐ <jats:italic>p</jats:italic> >0.1 for all outcomes). Patients who experienced eGFR deterioration were more likely to permanently discontinue treatment, without significant differences in treatment discontinuation rates between the SGLT2i and placebo groups. Conclusions Severe eGFR deterioration during follow‐up was associated with an increased risk of subsequent cardiovascular events and mortality. SGLT2i reduced the probability and were beneficial irrespective of severe eGFR deterioration.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"98 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145472789","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}
Unsupervised machine learning can improve the characterization and stratification of patients with cardiovascular diseases (CVDs). Clustering algorithms, which group patients based on patterns in clinical data, can reveal distinct subgroups that may differ in prognosis and treatment response. Despite increasing research in this area, the practical use of clustering methods in routine clinical care remains limited by the lack of accessible tools and rigorous external validation. This review presents a systematic framework for applying unsupervised machine learning techniques to CVD research. The framework outlines a stepwise process—from identifying patient clusters and establishing their associations with clinical outcomes to developing predictive models for assigning new patients to these clusters. This approach aims to generate robust, externally validated models that can be integrated into clinical practice to support improved risk stratification and personalized treatment strategies. This framework can enhance the usefulness of clustering in CVD research, by providing valuable resource for medical professionals, stakeholders, and researchers in exploring more effective strategies for managing CVDs.
{"title":"Unsupervised machine learning for cardiovascular disease: A framework for future studies","authors":"Emmanuel Bresso, Claire Lacomblez, Kévin Duarte, Luca Monzo, Guillaume Baudry, Jasper Tromp, Abhinav Sharma, Nicolas Girerd","doi":"10.1002/ejhf.70076","DOIUrl":"https://doi.org/10.1002/ejhf.70076","url":null,"abstract":"Unsupervised machine learning can improve the characterization and stratification of patients with cardiovascular diseases (CVDs). Clustering algorithms, which group patients based on patterns in clinical data, can reveal distinct subgroups that may differ in prognosis and treatment response. Despite increasing research in this area, the practical use of clustering methods in routine clinical care remains limited by the lack of accessible tools and rigorous external validation. This review presents a systematic framework for applying unsupervised machine learning techniques to CVD research. The framework outlines a stepwise process—from identifying patient clusters and establishing their associations with clinical outcomes to developing predictive models for assigning new patients to these clusters. This approach aims to generate robust, externally validated models that can be integrated into clinical practice to support improved risk stratification and personalized treatment strategies. This framework can enhance the usefulness of clustering in CVD research, by providing valuable resource for medical professionals, stakeholders, and researchers in exploring more effective strategies for managing CVDs.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"132 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145447377","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}
Venera Bytyqi,Dennis Kannenkeril,Julie Kolwelter,Peter Linz,Agnes Bosch,Kristina Striepe,Marina V Karg,Armin M Nagel,Michael Uder,Mario Schiffer,Stephan Achenbach,Roland E Schmieder
AIMSSodium-glucose co-transporter 2 inhibitors have become a cornerstone in managing chronic heart failure (CHF). While their acute impact on urinary glucose and sodium excretion is well-established, their mid- and long-term persistence of these effects remains uncertain. This study investigated fluid and sodium balance over 3 months in a randomized, placebo-controlled trial (NCT03128528).METHODS AND RESULTSOverall, 74 patients with New York Heart Association class II-III CHF and an ejection fraction (EF) ≤49% were randomized (2:1) to empagliflozin 10 mg (n = 48) or placebo (n = 26). Sodium, potassium, glucose, urea, and urine were determined from standardized 24-h urine collections. Free water clearance (FWC) and plasma/urine osmolality were calculated. Body weight was measured, and dedicated sodium magnetic resonance imaging (23Na-magnetic resonance imaging) was performed to quantify skin and muscle sodium levels at baseline, at 1 month, and at 3 months. Patients (mean age 66.4 years; 84% male; EF 40%; baseline N-terminal pro-B-type natriuretic peptide 707.9 pg/ml) were followed up at 1 and 3 months. Empagliflozin significantly increased natriuresis at 1 month (p = 0.040), while natriuresis returned to baseline by 3 months. Skin sodium content decreased at 1 month (p = 0.039) and remained reduced at 3 months (p = 0.013), while muscle sodium was unchanged. Persistent glucosuria (p < 0.001) increased urine osmolality at 3 months (p = 0.003). Urine volume increased transiently at 1 month (p = 0.046) but normalized by 3 months. Empagliflozin-treated patients showed a reduction in FWC at 1 and 3 months (p < 0.001), with a compensatory rise in copeptin levels, indicating increased vasopressin activity (1 month: p = 0.020; 3 months: p = 0.001).CONCLUSIONSMid-range effects of empagliflozin in heart failure with reduced EF include transient natriuresis and sustained glucosuria, with compensatory reductions in FWC. Reductions in skin sodium content were maintained, and volume homeostasis in CHF patients stabilized after 3 months.
{"title":"Short- and mid-term effects of empagliflozin on sodium balance and fluid regulation in chronic heart failure.","authors":"Venera Bytyqi,Dennis Kannenkeril,Julie Kolwelter,Peter Linz,Agnes Bosch,Kristina Striepe,Marina V Karg,Armin M Nagel,Michael Uder,Mario Schiffer,Stephan Achenbach,Roland E Schmieder","doi":"10.1002/ejhf.70078","DOIUrl":"https://doi.org/10.1002/ejhf.70078","url":null,"abstract":"AIMSSodium-glucose co-transporter 2 inhibitors have become a cornerstone in managing chronic heart failure (CHF). While their acute impact on urinary glucose and sodium excretion is well-established, their mid- and long-term persistence of these effects remains uncertain. This study investigated fluid and sodium balance over 3 months in a randomized, placebo-controlled trial (NCT03128528).METHODS AND RESULTSOverall, 74 patients with New York Heart Association class II-III CHF and an ejection fraction (EF) ≤49% were randomized (2:1) to empagliflozin 10 mg (n = 48) or placebo (n = 26). Sodium, potassium, glucose, urea, and urine were determined from standardized 24-h urine collections. Free water clearance (FWC) and plasma/urine osmolality were calculated. Body weight was measured, and dedicated sodium magnetic resonance imaging (23Na-magnetic resonance imaging) was performed to quantify skin and muscle sodium levels at baseline, at 1 month, and at 3 months. Patients (mean age 66.4 years; 84% male; EF 40%; baseline N-terminal pro-B-type natriuretic peptide 707.9 pg/ml) were followed up at 1 and 3 months. Empagliflozin significantly increased natriuresis at 1 month (p = 0.040), while natriuresis returned to baseline by 3 months. Skin sodium content decreased at 1 month (p = 0.039) and remained reduced at 3 months (p = 0.013), while muscle sodium was unchanged. Persistent glucosuria (p < 0.001) increased urine osmolality at 3 months (p = 0.003). Urine volume increased transiently at 1 month (p = 0.046) but normalized by 3 months. Empagliflozin-treated patients showed a reduction in FWC at 1 and 3 months (p < 0.001), with a compensatory rise in copeptin levels, indicating increased vasopressin activity (1 month: p = 0.020; 3 months: p = 0.001).CONCLUSIONSMid-range effects of empagliflozin in heart failure with reduced EF include transient natriuresis and sustained glucosuria, with compensatory reductions in FWC. Reductions in skin sodium content were maintained, and volume homeostasis in CHF patients stabilized after 3 months.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"36 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433928","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}
Riccardo M Inciardi,Henri Lu,Brian L Claggett,Akshay S Desai,Pardeep S Jhund,Alasdair D Henderson,Carolyn S P Lam,Bela Merkely,Michael Zi Miao,Michele Senni,Sanjiv J Shah,Kavita Sharma,Orly Vardeny,Mark C Petrie,Subodh Verma,Adriaan A Voors,Faiez Zannad,Bertram Pitt,Flaviana Amarante,James Lay-Flurrie,Andrea Glasauer,Andrea Scalise,John J V McMurray,Muthiah Vaduganathan,Scott D Solomon
AIMSWhile patients with severe heart failure (HF) were historically considered to have reduced left ventricular ejection fraction (LVEF), it is increasingly recognized that severe HF occurs across the full spectrum of LVEF. The aim of this study was to assess prevalence, cardiovascular (CV) outcome risk, and treatment response to the non-steroidal mineralocorticoid receptor antagonist finerenone among patients with severe HF in FINEARTS-HF.METHODS AND RESULTSTreatment effects of finerenone on the primary endpoint of total (first and recurrent) HF events and CV death were assessed by severe HF status, as defined by the adapted multiparametric ESC-HFA criteria including New York heart Association functional class III/IV, hospitalization for HF within the previous 12 months, and impairment of health status measured by Kansas City Cardiomyopathy Questionnaire total symptom score <75. Overall, 888 (14.8%) patients fulfilled the definition for severe HF. Patients with severe HF were older, with a higher comorbidity burden, and higher N-terminal pro-B-type natriuretic peptide levels. Over a median follow-up of 2.7 years, total HF events and CV death occurred at a higher rate among those with severe HF (31.6 per 100 patient-years [py]) as compared to those without severe HF (13.9 per 100py). Finerenone was beneficial in reducing the rate of the primary endpoint regardless of severe HF status (pinteraction = 0.98), with a greater absolute rate reduction in those with severe HF (5.9 per 100py) compared with those without severe HF (2.2 per 100py) in light of higher baseline risk. The proportion of patients who discontinued study treatment for any reason or experienced adverse events according to treatment assignment was similar regardless of severe HF status.CONCLUSIONSAmong patients with mildly reduced or preserved LVEF, severe HF was associated with a heightened risk of CV events. Treatment with finerenone appeared safe and effective, regardless of HF severity.
{"title":"Finerenone in patients with severe heart failure: The FINEARTS-HF trial.","authors":"Riccardo M Inciardi,Henri Lu,Brian L Claggett,Akshay S Desai,Pardeep S Jhund,Alasdair D Henderson,Carolyn S P Lam,Bela Merkely,Michael Zi Miao,Michele Senni,Sanjiv J Shah,Kavita Sharma,Orly Vardeny,Mark C Petrie,Subodh Verma,Adriaan A Voors,Faiez Zannad,Bertram Pitt,Flaviana Amarante,James Lay-Flurrie,Andrea Glasauer,Andrea Scalise,John J V McMurray,Muthiah Vaduganathan,Scott D Solomon","doi":"10.1002/ejhf.70083","DOIUrl":"https://doi.org/10.1002/ejhf.70083","url":null,"abstract":"AIMSWhile patients with severe heart failure (HF) were historically considered to have reduced left ventricular ejection fraction (LVEF), it is increasingly recognized that severe HF occurs across the full spectrum of LVEF. The aim of this study was to assess prevalence, cardiovascular (CV) outcome risk, and treatment response to the non-steroidal mineralocorticoid receptor antagonist finerenone among patients with severe HF in FINEARTS-HF.METHODS AND RESULTSTreatment effects of finerenone on the primary endpoint of total (first and recurrent) HF events and CV death were assessed by severe HF status, as defined by the adapted multiparametric ESC-HFA criteria including New York heart Association functional class III/IV, hospitalization for HF within the previous 12 months, and impairment of health status measured by Kansas City Cardiomyopathy Questionnaire total symptom score <75. Overall, 888 (14.8%) patients fulfilled the definition for severe HF. Patients with severe HF were older, with a higher comorbidity burden, and higher N-terminal pro-B-type natriuretic peptide levels. Over a median follow-up of 2.7 years, total HF events and CV death occurred at a higher rate among those with severe HF (31.6 per 100 patient-years [py]) as compared to those without severe HF (13.9 per 100py). Finerenone was beneficial in reducing the rate of the primary endpoint regardless of severe HF status (pinteraction = 0.98), with a greater absolute rate reduction in those with severe HF (5.9 per 100py) compared with those without severe HF (2.2 per 100py) in light of higher baseline risk. The proportion of patients who discontinued study treatment for any reason or experienced adverse events according to treatment assignment was similar regardless of severe HF status.CONCLUSIONSAmong patients with mildly reduced or preserved LVEF, severe HF was associated with a heightened risk of CV events. Treatment with finerenone appeared safe and effective, regardless of HF severity.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"69 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433894","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}
Filip Zemrak, Oscar Gonzalez Fernandez, William H. Marshall
{"title":"Letter regarding the article ‘Remote pulmonary artery pressure‐guided management of patients with heart failure: A clinical consensus statement of the Heart Failure Association ( HFA ) of the ESC ’","authors":"Filip Zemrak, Oscar Gonzalez Fernandez, William H. Marshall","doi":"10.1002/ejhf.70088","DOIUrl":"https://doi.org/10.1002/ejhf.70088","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"65 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427432","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}
{"title":"Reply to the letter regarding the article ‘Remote pulmonary artery pressure‐guided management of patients with heart failure: A clinical consensus statement of the Heart Failure Association ( HFA ) of the ESC’","authors":"Antoni Bayes‐Genis, Matteo Pagnesi, Marco Metra","doi":"10.1002/ejhf.70086","DOIUrl":"https://doi.org/10.1002/ejhf.70086","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"78 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427431","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}
Several urinary markers reflect disease severity and have the potential to support the management of heart failure (HF). Collecting urine samples is easy and inexpensive, and urine sample composition can be altered not only by underlying kidney impairments (i.e. filtration barrier damage and tubular injury) but also via neurohormonal and inflammatory activation, ageing, comorbidities, other medical conditions and pharmacological interventions. For instance, urinary sodium may help to predict the response to loop diuretic therapy in acute HF, while albuminuria is used as a risk marker and therapeutic target for the progression of cardiovascular and kidney diseases in chronic HF, especially when accompanied by kidney disease. However, these markers remain underutilized in clinical practice. This review paper underscores the role of urinary markers in HF, with a specific focus on: (i) the pathophysiologic mechanisms underlying urinary marker excretion, (ii) the prognostic values of urinary markers across diverse HF phenotypes and non-cardiovascular comorbidities (i.e. chronic kidney disease and diabetes), (iii) the impact of medical therapies on urinary markers, and (iv) existing knowledge gaps that challenge their implementation in clinical practice. The recommendations are aligned with current guidelines, evidence, and expert consensus.
{"title":"Urinary markers in heart failure - types, timing and thresholds. European Journal of Heart Failure expert consensus document.","authors":"Masatake Kobayashi,Biykem Bozkurt,Peder Langeland Myhre,Juan Carlos Lopez Azor,Mateusz Guzik,Gracjan Iwanek,Guillaume Baudry,Marta Cobo-Marcos,Òscar Miró,Jeroen Dauw,Piotr Ponikowski,Wilfried Mullens,Alberto Palazzuoli,Marco Metra,Jan Biegus","doi":"10.1002/ejhf.70079","DOIUrl":"https://doi.org/10.1002/ejhf.70079","url":null,"abstract":"Several urinary markers reflect disease severity and have the potential to support the management of heart failure (HF). Collecting urine samples is easy and inexpensive, and urine sample composition can be altered not only by underlying kidney impairments (i.e. filtration barrier damage and tubular injury) but also via neurohormonal and inflammatory activation, ageing, comorbidities, other medical conditions and pharmacological interventions. For instance, urinary sodium may help to predict the response to loop diuretic therapy in acute HF, while albuminuria is used as a risk marker and therapeutic target for the progression of cardiovascular and kidney diseases in chronic HF, especially when accompanied by kidney disease. However, these markers remain underutilized in clinical practice. This review paper underscores the role of urinary markers in HF, with a specific focus on: (i) the pathophysiologic mechanisms underlying urinary marker excretion, (ii) the prognostic values of urinary markers across diverse HF phenotypes and non-cardiovascular comorbidities (i.e. chronic kidney disease and diabetes), (iii) the impact of medical therapies on urinary markers, and (iv) existing knowledge gaps that challenge their implementation in clinical practice. The recommendations are aligned with current guidelines, evidence, and expert consensus.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"77 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427887","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}
Danielle H Robinson,Karlheinz Peter,James D McFadyen
Extracorporeal membrane oxygenation (ECMO) is increasingly being utilized in critical care globally to allow for adequate oxygenation in patients with cardiac and/or respiratory failure. Unfortunately, haemostatic complications - both thrombotic and haemorrhagic - are commonplace. Well established contributors to haemostatic dysfunction include patient-level characteristics, features of ECMO itself and the requirement of systemic anticoagulation to prevent circuit-related thrombosis. Research has focused on understanding how ECMO devices impact upon cellular components, particularly platelets, and plasma proteins involved in coagulation through assessment of phenotypic changes and activation profiles. A central feature of ECMO is the significant haemodynamic disturbances cells and circulating proteins experience within ECMO circuits. Given the body of evidence detailing the effects of haemodynamic shear on circulating cells critical for haemostasis, there is renewed focus on understanding the impact of shear on haemostatic dysfunction in ECMO. In this review, we describe the current landscape of ECMO-associated thrombosis and haemorrhage, provide insights into the impact of anticoagulation on haemostatic complications and highlight research evaluating the impact of shear on circulating cells and plasma proteins involved in haemostasis. Finally, we also discuss potential modifiers of haemostatic complications with a focus on development of personalized diagnostic and management approaches.
{"title":"Shear-induced dysregulation of haemostasis during extracorporeal membrane oxygenation: From cells to circuit.","authors":"Danielle H Robinson,Karlheinz Peter,James D McFadyen","doi":"10.1002/ejhf.70075","DOIUrl":"https://doi.org/10.1002/ejhf.70075","url":null,"abstract":"Extracorporeal membrane oxygenation (ECMO) is increasingly being utilized in critical care globally to allow for adequate oxygenation in patients with cardiac and/or respiratory failure. Unfortunately, haemostatic complications - both thrombotic and haemorrhagic - are commonplace. Well established contributors to haemostatic dysfunction include patient-level characteristics, features of ECMO itself and the requirement of systemic anticoagulation to prevent circuit-related thrombosis. Research has focused on understanding how ECMO devices impact upon cellular components, particularly platelets, and plasma proteins involved in coagulation through assessment of phenotypic changes and activation profiles. A central feature of ECMO is the significant haemodynamic disturbances cells and circulating proteins experience within ECMO circuits. Given the body of evidence detailing the effects of haemodynamic shear on circulating cells critical for haemostasis, there is renewed focus on understanding the impact of shear on haemostatic dysfunction in ECMO. In this review, we describe the current landscape of ECMO-associated thrombosis and haemorrhage, provide insights into the impact of anticoagulation on haemostatic complications and highlight research evaluating the impact of shear on circulating cells and plasma proteins involved in haemostasis. Finally, we also discuss potential modifiers of haemostatic complications with a focus on development of personalized diagnostic and management approaches.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"22 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427803","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 : 2025-11-01Epub Date: 2025-06-16DOI: 10.1002/ejhf.3730
Julio Nunez, Anna Mollar, Mayra Vera-Aviles, Syeeda Kabir, Akshay Shah, Paolo Polzella, Michael Desborough, Ingrid Cardells, Gema Miñana, Irene Del Canto, Vanessa Ferreira, Stefan Piechnik, Alicia Maceira, Samira Lakhal-Littleton
{"title":"Baseline serum ferritin predicts myocardial iron uptake following intravenous iron therapy - a hypothesis-generating study.","authors":"Julio Nunez, Anna Mollar, Mayra Vera-Aviles, Syeeda Kabir, Akshay Shah, Paolo Polzella, Michael Desborough, Ingrid Cardells, Gema Miñana, Irene Del Canto, Vanessa Ferreira, Stefan Piechnik, Alicia Maceira, Samira Lakhal-Littleton","doi":"10.1002/ejhf.3730","DOIUrl":"10.1002/ejhf.3730","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":" ","pages":"2352-2356"},"PeriodicalIF":10.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12765036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300818","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 : 2025-11-01Epub Date: 2025-08-15DOI: 10.1002/ejhf.3806
Yang Zhang, Fanwu Chi, Ren Zhu, Lian Hu
{"title":"Impact of misclassification bias on interpretation of finerenone efficacy in chronic obstructive pulmonary disease and heart failure with mildly reduced or preserved ejection fraction: A critical appraisal of the FINEARTS-HF subanalysis.","authors":"Yang Zhang, Fanwu Chi, Ren Zhu, Lian Hu","doi":"10.1002/ejhf.3806","DOIUrl":"https://doi.org/10.1002/ejhf.3806","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"27 11","pages":"2658"},"PeriodicalIF":10.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145898879","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：