Pub Date : 2025-12-23DOI: 10.1093/eurheartj/ehaf1033
Anna Kamdar,Kenneth Mangion,Jonathan R Dalzell
{"title":"Transcriptomics in cardiac allograft rejection: refining a diagnosis or redefining an enigma?","authors":"Anna Kamdar,Kenneth Mangion,Jonathan R Dalzell","doi":"10.1093/eurheartj/ehaf1033","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1033","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"123 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807598","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf1032
Carol Ann Remme,Jolanda van der Velden
{"title":"Reducing the variant of uncertain significance burden in inherited cardiac disorders: from variant to function to action?","authors":"Carol Ann Remme,Jolanda van der Velden","doi":"10.1093/eurheartj/ehaf1032","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1032","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"12 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807599","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf940
Annemien E van den Bosch,Jop W Schneijdenberg,Jolien W Roos-Hesselink
{"title":"Pulmonary vascular resistance in Fontan circulation: what are the prognostic implications?","authors":"Annemien E van den Bosch,Jop W Schneijdenberg,Jolien W Roos-Hesselink","doi":"10.1093/eurheartj/ehaf940","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf940","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"24 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807597","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf979
Simon Kraler,Luca Liberale,Amedeo Tirandi,Margherita Moriero,Yifan Wang,Mohamed Farag,Federico Carbone,Maria B Bertolotto,Valentina Pusterla,Davide Ramoni,Stefano Ministrini,Yustina M Puspitasari,Francesco Bruno,Lorenz Räber,Davide Di Vece,Christian Templin,Olivier Muller,François Mach,Filippo Crea,Giovanni G Camici,Tetiana Lapikova-Bryhinska,Alexander Akhmedov,Arnold von Eckardstein,Diana A Gorog,Fabrizio Montecucco,Thomas F Lüscher
BACKGROUND AND AIMSPatients with acute coronary syndromes (ACS) are at high ischaemic risk to which cholesterol, inflammation, and yet-to-be-identified pathways jointly contribute. The junctional protein associated with coronary artery disease (JCAD) drives incident cardiovascular events by acting on coagulation and fibrinolysis. This study aimed to assess whether JCAD serves as a novel marker of or target to address residual risk.METHODSIn the discovery cohort (SPUM-ACS; n = 4787), ACS patients at residual lipid risk [RLR; on-statin LDL cholesterol (LDL-c) ≥70 mg/dL or ≥1.8 mmol/L], residual inflammatory risk [RIR; on-statin high-sensitivity C-reactive protein (hs-CRP) ≥2.0 mg/L], or both (RILR; on-statin LDL-c ≥70 mg/dL and hs-CRP ≥2.0 mg/L) were identified and compared with propensity-score matched controls. Contributions of hs-CRP, LDL-c and JCAD to recurrent major adverse cardiovascular events (MACE) were analysed. In an independent cohort (RISK-PPCI study; n = 496), effects of JCAD on endogenous coagulation and fibrinolysis were gauged, and JCAD-MACE associations were externally validated.RESULTSAt 1 year, patients at RLR, RIR, or RILR were at higher MACE risk as compared to controls [hazard ratio (HR), 1.55, 95% confidence interval (CI) 1.08-2.23; HR 1.80, 95% CI 1.24-2.61; and HR 1.75, 95% CI 1.12-2.75, respectively]. In those at RLR, MACE risk rose with increasing hs-CRP and JCAD, respectively, in uni- (HR per log2 increase, 1.17, 95% CI 1.06-1.30; HR 1.29, 95% CI 1.03-1.62) and multivariable-adjusted models [adjusted (a)HR 1.16, 95% CI 1.03-1.30; aHR 1.27, 95% CI 1.01-1.60]. In those at RIR, MACE risk increased 1.28-fold per log2 increase in JCAD (HR 1.28, 95% CI 1.03-1.59), which prevailed in multivariable-adjusted models (aHR 1.31, 95% CI 1.04-1.65). Similarly, in patients at RILR, MACE risk increased almost linearly with increasing JCAD (HR 1.45, 95% CI 1.09-1.92), independently of potential confounders (aHR 1.47, 95% CI 1.11-1.97). Plasma levels of JCAD correlated positively with proxies of impaired endogenous fibrinolysis, with the JCAD-MACE association being similarly observed in the external validation cohort.CONCLUSIONSAcute coronary syndrome patients at RLR, RIR, or both are at high ischaemic risk. By modulating coagulation and endogenous fibrinolysis, JCAD represents a promising candidate to address the high residual risk that persists in ACS patients receiving guideline-recommended care.CLINICALTRIALS.GOV IDENTIFIERSNCT01000701, NCT02562690.
背景和目的急性冠脉综合征（ACS）患者具有高的缺血风险，胆固醇、炎症和尚未确定的途径共同促成了这一风险。与冠状动脉疾病（JCAD）相关的连接蛋白通过作用于凝血和纤溶来驱动心血管事件。本研究旨在评估JCAD是否可以作为解决剩余风险的新标记或目标。方法在发现队列（SPUM-ACS; n = 4787）中，ACS患者存在残留脂质风险[RLR；他汀类药物低密度脂蛋白胆固醇(LDL-c)≥70 mg/dL或≥1.8 mmol/L，残余炎症风险[RIR；他汀类药物高敏c反应蛋白(hs-CRP)≥2.0 mg/L]，或两者都有（RILR；他汀类药物LDL-c≥70 mg/dL和hs-CRP≥2.0 mg/L），并与倾向评分匹配的对照组进行比较。分析hs-CRP、LDL-c和JCAD对复发性主要不良心血管事件（MACE）的影响。在一项独立队列研究（RISK-PPCI研究；n = 496）中，测量了JCAD对内源性凝血和纤溶的影响，并对JCAD与mace的关联进行了外部验证。结果1年后，与对照组相比，RLR、RIR或RILR组患者的MACE风险更高[危险比（HR）， 1.55, 95%可信区间（CI） 1.08-2.23；Hr 1.80, 95% ci 1.24-2.61；HR 1.75, 95% CI 1.12-2.75]。在RLR组中，MACE风险分别随着hs-CRP和JCAD的升高而升高，单变量（HR / log2升高，1.17,95% CI 1.06-1.30; HR 1.29, 95% CI 1.03-1.62）和多变量调整模型[调整(a)HR 1.16, 95% CI 1.03-1.30；aHR 1.27, 95% CI 1.01-1.60]。在RIR组中，JCAD每增加log2， MACE风险增加1.28倍（HR 1.28, 95% CI 1.03-1.59），这在多变量调整模型中普遍存在（aHR 1.31, 95% CI 1.04-1.65）。同样，在RILR的患者中，MACE风险几乎随JCAD的增加而线性增加（HR 1.45, 95% CI 1.09-1.92），独立于潜在的混杂因素（aHR 1.47, 95% CI 1.11-1.97）。血浆中JCAD水平与内源性纤维蛋白溶解受损的指标呈正相关，在外部验证队列中也观察到JCAD- mace关联。结论急性冠脉综合征RLR、RIR或两者均有较高的缺血性风险。通过调节凝血和内源性纤维蛋白溶解，JCAD有望解决ACS患者接受指南推荐治疗时持续存在的高残留风险。
{"title":"The junctional protein associated with coronary artery disease predicts adverse cardiovascular events in patients with acute coronary syndromes at high residual risk.","authors":"Simon Kraler,Luca Liberale,Amedeo Tirandi,Margherita Moriero,Yifan Wang,Mohamed Farag,Federico Carbone,Maria B Bertolotto,Valentina Pusterla,Davide Ramoni,Stefano Ministrini,Yustina M Puspitasari,Francesco Bruno,Lorenz Räber,Davide Di Vece,Christian Templin,Olivier Muller,François Mach,Filippo Crea,Giovanni G Camici,Tetiana Lapikova-Bryhinska,Alexander Akhmedov,Arnold von Eckardstein,Diana A Gorog,Fabrizio Montecucco,Thomas F Lüscher","doi":"10.1093/eurheartj/ehaf979","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf979","url":null,"abstract":"BACKGROUND AND AIMSPatients with acute coronary syndromes (ACS) are at high ischaemic risk to which cholesterol, inflammation, and yet-to-be-identified pathways jointly contribute. The junctional protein associated with coronary artery disease (JCAD) drives incident cardiovascular events by acting on coagulation and fibrinolysis. This study aimed to assess whether JCAD serves as a novel marker of or target to address residual risk.METHODSIn the discovery cohort (SPUM-ACS; n = 4787), ACS patients at residual lipid risk [RLR; on-statin LDL cholesterol (LDL-c) ≥70 mg/dL or ≥1.8 mmol/L], residual inflammatory risk [RIR; on-statin high-sensitivity C-reactive protein (hs-CRP) ≥2.0 mg/L], or both (RILR; on-statin LDL-c ≥70 mg/dL and hs-CRP ≥2.0 mg/L) were identified and compared with propensity-score matched controls. Contributions of hs-CRP, LDL-c and JCAD to recurrent major adverse cardiovascular events (MACE) were analysed. In an independent cohort (RISK-PPCI study; n = 496), effects of JCAD on endogenous coagulation and fibrinolysis were gauged, and JCAD-MACE associations were externally validated.RESULTSAt 1 year, patients at RLR, RIR, or RILR were at higher MACE risk as compared to controls [hazard ratio (HR), 1.55, 95% confidence interval (CI) 1.08-2.23; HR 1.80, 95% CI 1.24-2.61; and HR 1.75, 95% CI 1.12-2.75, respectively]. In those at RLR, MACE risk rose with increasing hs-CRP and JCAD, respectively, in uni- (HR per log2 increase, 1.17, 95% CI 1.06-1.30; HR 1.29, 95% CI 1.03-1.62) and multivariable-adjusted models [adjusted (a)HR 1.16, 95% CI 1.03-1.30; aHR 1.27, 95% CI 1.01-1.60]. In those at RIR, MACE risk increased 1.28-fold per log2 increase in JCAD (HR 1.28, 95% CI 1.03-1.59), which prevailed in multivariable-adjusted models (aHR 1.31, 95% CI 1.04-1.65). Similarly, in patients at RILR, MACE risk increased almost linearly with increasing JCAD (HR 1.45, 95% CI 1.09-1.92), independently of potential confounders (aHR 1.47, 95% CI 1.11-1.97). Plasma levels of JCAD correlated positively with proxies of impaired endogenous fibrinolysis, with the JCAD-MACE association being similarly observed in the external validation cohort.CONCLUSIONSAcute coronary syndrome patients at RLR, RIR, or both are at high ischaemic risk. By modulating coagulation and endogenous fibrinolysis, JCAD represents a promising candidate to address the high residual risk that persists in ACS patients receiving guideline-recommended care.CLINICALTRIALS.GOV IDENTIFIERSNCT01000701, NCT02562690.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"85 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807602","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf990
Eliot G Peyster,David Smith,Therese Bittermann,Paco E Bravo,Kenneth B Margulies
BACKGROUND AND AIMSCardiac sarcoidosis (CS) is poorly understood, challenging to diagnose, and portends a poor prognosis. A lack of animal models necessitates the use of residual human samples to study sarcoidosis, which in turn necessitates the use of analytical tools compatible with archival, fixed tissue. This study employed high-plex spatial protein analysis to characterize the immunologic, fibrotic, and metabolic landscape of CS.METHODSCardiac tissues from 64 patients-39 with CS and 25 without CS (Controls)-were analysed using the GeoMx Digital Spatial Profiler. Regions of interest (ROIs) with and without granulomatous inflammation were selected to examine protein abundance. ROIs were further divided into areas of illumination to separately analyse distinct protein profiles in myocytes, stroma, and vessels. A 79-protein panel was used to characterize immune and parenchymal cell populations. Differential protein abundance was evaluated using mixed-effects modeling. A predictive model was developed using a subset of seven proteins to distinguish inflammation-free CS ROIs from control ROIs.RESULTSSpatial profiling demonstrated marked heterogeneity within and between sarcoidosis granulomas. Inflammation-free ROIs from CS hearts exhibited a 'distance gradient', with protein abundance varying by proximity to granulomatous inflammation. The seven-protein predictive model achieved 95.9% accuracy and an area under the receiver operating characteristic curve of 0.993 in differentiating inflammation-free CS ROIs from Controls.CONCLUSIONSSpatial proteomics revealed novel features of the CS microenvironment and identified a distinct immune signature in tissue lacking overt inflammation. These findings may improve diagnostic accuracy in clinical biopsies from patients with suspected CS.
{"title":"Cardiac sarcoidosis: new insights beyond the granuloma using spatial proteomics.","authors":"Eliot G Peyster,David Smith,Therese Bittermann,Paco E Bravo,Kenneth B Margulies","doi":"10.1093/eurheartj/ehaf990","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf990","url":null,"abstract":"BACKGROUND AND AIMSCardiac sarcoidosis (CS) is poorly understood, challenging to diagnose, and portends a poor prognosis. A lack of animal models necessitates the use of residual human samples to study sarcoidosis, which in turn necessitates the use of analytical tools compatible with archival, fixed tissue. This study employed high-plex spatial protein analysis to characterize the immunologic, fibrotic, and metabolic landscape of CS.METHODSCardiac tissues from 64 patients-39 with CS and 25 without CS (Controls)-were analysed using the GeoMx Digital Spatial Profiler. Regions of interest (ROIs) with and without granulomatous inflammation were selected to examine protein abundance. ROIs were further divided into areas of illumination to separately analyse distinct protein profiles in myocytes, stroma, and vessels. A 79-protein panel was used to characterize immune and parenchymal cell populations. Differential protein abundance was evaluated using mixed-effects modeling. A predictive model was developed using a subset of seven proteins to distinguish inflammation-free CS ROIs from control ROIs.RESULTSSpatial profiling demonstrated marked heterogeneity within and between sarcoidosis granulomas. Inflammation-free ROIs from CS hearts exhibited a 'distance gradient', with protein abundance varying by proximity to granulomatous inflammation. The seven-protein predictive model achieved 95.9% accuracy and an area under the receiver operating characteristic curve of 0.993 in differentiating inflammation-free CS ROIs from Controls.CONCLUSIONSSpatial proteomics revealed novel features of the CS microenvironment and identified a distinct immune signature in tissue lacking overt inflammation. These findings may improve diagnostic accuracy in clinical biopsies from patients with suspected CS.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"22 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807595","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf941
Jacob Y Cao,Alexander C Egbe,Nick Olsen,C Charles Jain,Barry A Borlaug,Yogesh N V Reddy,Heidi C Connolly,David Celermajer,Rachael Cordina,William R Miranda
BACKGROUND AND AIMSDecrease in pulmonary vascular resistance (PVR) during exercise confers favourable prognosis in biventricular physiology, but its role in Fontan circulation remains unknown. This study aimed to evaluate the prognostic value of PVR index (PVRI) response to exercise in adults post-Fontan palliation.METHODSRetrospective cohort of 88 adults (age ≥18 years) post-Fontan undergoing exercise (supine cycling) cardiac catheterization. Patients were categorized into absence (n = 23) or presence (n = 65) of exercise-induced reduction in PVRI. The clinical endpoint was a composite of death or transplantation.RESULTSAge at catheterization was 32.2 ± 8.8 years, and 45.5% were female. Resting and exercise PVRI were 1.9 ± 0.9 and 1.2 (interquartile range [IQR] 0.8-2.1) WU·m2, respectively. Clinical, biochemical and echocardiographic parameters were not associated with PVRI response to exercise. During a follow-up of 2.2 ± 1.4 (IQR 1.2-2.6) years, resting PVRI was not associated with the clinical endpoint (hazard ratio [HR] 0.95 per WU·m2, 95% confidence interval [CI] 0.52-1.74; P = 0.86), whereas exercise PVRI was (HR 2.15 per WU·m2, 95% CI 1.24-3.73; P = .007). Exercise PVRI remained predictive of outcomes after adjusting for exercise pulmonary artery wedge pressure (HR 2.08 per WU·m2, 95% CI 1.19-3.62; P = .01) or clinical risk factors individually. Two-year event-free survival was lower in the no PVRI reduction than in the reduction group (67% vs 95%; P < .001).CONCLUSIONSIn adults post-Fontan, PVRI response to exercise is a robust predictor of clinical outcomes and offers additive prognostic information beyond resting invasive haemodynamic data and clinical risk factors, underscoring the importance of invasive exercise testing in this population.
背景和目的运动期间肺血管阻力（PVR）的降低在双心室生理学中具有良好的预后，但其在Fontan循环中的作用尚不清楚。本研究旨在评估成人fontan姑息治疗后PVR指数（PVRI）对运动反应的预后价值。方法回顾性队列研究88例（年龄≥18岁）fontan术后行运动（仰卧循环）心导管置入术的成年人。患者被分为无（n = 23）或有（n = 65）运动引起的PVRI减少。临床终点为死亡或移植的复合终点。结果置管年龄为32.2±8.8岁，女性占45.5%。静息和运动PVRI分别为1.9±0.9和1.2（四分位间距[IQR] 0.8 ~ 2.1） WU·m2。临床、生化和超声心动图参数与运动后PVRI反应无关。在2.2±1.4 （IQR 1.2-2.6）年的随访期间，静息PVRI与临床终点无关（风险比[HR] 0.95 / WU·m2, 95%可信区间[CI] 0.52-1.74; P = 0.86），而运动PVRI为（风险比[HR] 2.15 / WU·m2, 95% CI 1.24-3.73; P = 0.007）。在单独调整运动肺动脉楔压（HR 2.08 / WU·m2, 95% CI 1.19-3.62; P = 0.01）或临床危险因素后，运动PVRI仍可预测结果。PVRI未减少组的两年无事件生存率低于减少组（67% vs 95%; P < 0.001）。结论：在fontan后的成年人中，PVRI对运动的反应是临床结果的一个强有力的预测因素，除了静息侵袭性血流动力学数据和临床危险因素外，还提供了附加的预后信息，强调了有创性运动测试在这一人群中的重要性。
{"title":"Adults with Fontan circulation: prognostic value of exercise pulmonary vascular resistance index.","authors":"Jacob Y Cao,Alexander C Egbe,Nick Olsen,C Charles Jain,Barry A Borlaug,Yogesh N V Reddy,Heidi C Connolly,David Celermajer,Rachael Cordina,William R Miranda","doi":"10.1093/eurheartj/ehaf941","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf941","url":null,"abstract":"BACKGROUND AND AIMSDecrease in pulmonary vascular resistance (PVR) during exercise confers favourable prognosis in biventricular physiology, but its role in Fontan circulation remains unknown. This study aimed to evaluate the prognostic value of PVR index (PVRI) response to exercise in adults post-Fontan palliation.METHODSRetrospective cohort of 88 adults (age ≥18 years) post-Fontan undergoing exercise (supine cycling) cardiac catheterization. Patients were categorized into absence (n = 23) or presence (n = 65) of exercise-induced reduction in PVRI. The clinical endpoint was a composite of death or transplantation.RESULTSAge at catheterization was 32.2 ± 8.8 years, and 45.5% were female. Resting and exercise PVRI were 1.9 ± 0.9 and 1.2 (interquartile range [IQR] 0.8-2.1) WU·m2, respectively. Clinical, biochemical and echocardiographic parameters were not associated with PVRI response to exercise. During a follow-up of 2.2 ± 1.4 (IQR 1.2-2.6) years, resting PVRI was not associated with the clinical endpoint (hazard ratio [HR] 0.95 per WU·m2, 95% confidence interval [CI] 0.52-1.74; P = 0.86), whereas exercise PVRI was (HR 2.15 per WU·m2, 95% CI 1.24-3.73; P = .007). Exercise PVRI remained predictive of outcomes after adjusting for exercise pulmonary artery wedge pressure (HR 2.08 per WU·m2, 95% CI 1.19-3.62; P = .01) or clinical risk factors individually. Two-year event-free survival was lower in the no PVRI reduction than in the reduction group (67% vs 95%; P < .001).CONCLUSIONSIn adults post-Fontan, PVRI response to exercise is a robust predictor of clinical outcomes and offers additive prognostic information beyond resting invasive haemodynamic data and clinical risk factors, underscoring the importance of invasive exercise testing in this population.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"32 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807593","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 : 2025-12-23DOI: 10.1093/eurheartj/ehaf1031
Steven M Hollenberg,Mervyn Singer
{"title":"Septic cardiomyopathy: a form of myocardial hibernation?","authors":"Steven M Hollenberg,Mervyn Singer","doi":"10.1093/eurheartj/ehaf1031","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1031","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"6 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807596","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 : 2025-12-22DOI: 10.1093/eurheartj/ehaf637
Rohit Jhawar,Luca Cristin,Francesca N Delling
{"title":"Is it all about mitral annular disjunction?","authors":"Rohit Jhawar,Luca Cristin,Francesca N Delling","doi":"10.1093/eurheartj/ehaf637","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf637","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"11 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145801324","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 : 2025-12-22DOI: 10.1093/eurheartj/ehaf1011
{"title":"Correction to: 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy: Developed by the task force on the management of cardiovascular disease and pregnancy of the European Society of Cardiology (ESC) Endorsed by the European Society of Gynecology (ESG).","authors":"","doi":"10.1093/eurheartj/ehaf1011","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1011","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"20 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145801295","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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