Pub Date : 2026-02-06DOI: 10.1093/eurheartj/ehag008
Vincent Probst, Jean Baptiste Gourraud
{"title":"Inappropriate shocks in Brugada syndrome: a matter of data capture rather than programming?","authors":"Vincent Probst, Jean Baptiste Gourraud","doi":"10.1093/eurheartj/ehag008","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag008","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124236","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 : 2026-02-06DOI: 10.1093/eurheartj/ehag007
Federico Migliore, Luca Ottaviano, Silvia G Priori
{"title":"Programming optimization is crucial for minimizing inappropriate shocks in patients with Brugada syndrome with a subcutaneous implantable cardioverter-defibrillator.","authors":"Federico Migliore, Luca Ottaviano, Silvia G Priori","doi":"10.1093/eurheartj/ehag007","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag007","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124251","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 : 2026-02-06DOI: 10.1093/eurheartj/ehag106
{"title":"Correction to two articles.","authors":"","doi":"10.1093/eurheartj/ehag106","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag106","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131362","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 : 2026-02-06DOI: 10.1093/eurheartj/ehag001
Sadananda Bolar Naik
{"title":"The human side of a legendary cardiologist.","authors":"Sadananda Bolar Naik","doi":"10.1093/eurheartj/ehag001","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag001","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124192","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 : 2026-02-06DOI: 10.1093/eurheartj/ehaf1128
Haran Burri, Brenda R Kwak
{"title":"Left bundle branch pacing vs biventricular pacing: back to basics.","authors":"Haran Burri, Brenda R Kwak","doi":"10.1093/eurheartj/ehaf1128","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1128","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124225","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 : 2026-02-06DOI: 10.1093/eurheartj/ehaf1040
Havard Dalen, Andreas Østvik, Bjørnar Grenne
{"title":"Unveiling the future: deep learning redefines strain analysis in paediatric cardiology.","authors":"Havard Dalen, Andreas Østvik, Bjørnar Grenne","doi":"10.1093/eurheartj/ehaf1040","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf1040","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124266","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 : 2026-02-06DOI: 10.1093/eurheartj/ehag023
Stefano Ghio, Roberto Badagliacca, Michele D'Alto, Mauro Acquaro, Pietro Ameri, Paola Argiento, Natale Daniele Brunetti, Gavino Casu, Nadia Cedrone, Marco Confalonieri, Marco Corda, Michele Correale, Carlo D'Agostino, Elisabetta De Tommasi, Domenico Filomena, Giuseppe Galgano, Alessandra Greco, Massimo Grimaldi, Carlo Lombardi, Rosalinda Madonna, Giovanna Manzi, Valentina Mercurio, Massimiliano Mulè, Giuseppe Paciocco, Silvia Papa, Tommaso Recchioni, Antonella Romaniello, Emanuele Romeo, Laura Scelsi, Davide Stolfo, Marco Vatrano, Patrizio Vitulo, Carmine Dario Vizza
Background and aims: The aim of this study was to evaluate whether echocardiography-derived phenotypes describing different degrees of right ventricular (RV) remodelling and dysfunction add prognostic information to that of current risk stratification tools in patients with pulmonary arterial hypertension (PAH) at first follow-up.
Methods: In 11 centres of the Italian Pulmonary Hypertension NETwork (IPHNET), data were prospectively collected from patients with PAH who underwent re-evaluation between 6 and 12 months after diagnosis. Echocardiographic variables were combined a priori to define four phenotypes representing different degrees of RV dilatation and right ventricular-pulmonary arterial (RV-PA) coupling: a mildly dilated right ventricle with preserved RV-PA coupling defined phenotype-1; a mildly dilated right ventricle with poor RV-PA coupling defined phenotype-2; a severely dilated right ventricle with preserved RV-PA coupling defined phenotype-3; a severely dilated right ventricle with poor RV-PA coupling, either with or without tricuspid regurgitation of moderate degree or more, defined phenotype-4. Patients were followed up for all-cause death for a median of 3.7 years.
Results: These echocardiographic phenotypes were present in all European Society of Cardiology/European Respiratory Society or REVEAL 2.0 risk groups except for the high-risk groups, which included only phenotype-3 and phenotype-4. In each risk group, RV phenotype-4 identified patients with a poorer prognosis; RV phenotype-1 identified patients with better survival in intermediate risk groups.
Conclusions: Echocardiography-derived phenotypes describing different degrees of RV remodelling and dysfunction provide prognostic information which is independent of and additional to the clinically defined risk in PAH patients at first follow-up.
{"title":"Pulmonary arterial hypertension: right ventricular phenotyping to improve risk assessment at follow-up.","authors":"Stefano Ghio, Roberto Badagliacca, Michele D'Alto, Mauro Acquaro, Pietro Ameri, Paola Argiento, Natale Daniele Brunetti, Gavino Casu, Nadia Cedrone, Marco Confalonieri, Marco Corda, Michele Correale, Carlo D'Agostino, Elisabetta De Tommasi, Domenico Filomena, Giuseppe Galgano, Alessandra Greco, Massimo Grimaldi, Carlo Lombardi, Rosalinda Madonna, Giovanna Manzi, Valentina Mercurio, Massimiliano Mulè, Giuseppe Paciocco, Silvia Papa, Tommaso Recchioni, Antonella Romaniello, Emanuele Romeo, Laura Scelsi, Davide Stolfo, Marco Vatrano, Patrizio Vitulo, Carmine Dario Vizza","doi":"10.1093/eurheartj/ehag023","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag023","url":null,"abstract":"<p><strong>Background and aims: </strong>The aim of this study was to evaluate whether echocardiography-derived phenotypes describing different degrees of right ventricular (RV) remodelling and dysfunction add prognostic information to that of current risk stratification tools in patients with pulmonary arterial hypertension (PAH) at first follow-up.</p><p><strong>Methods: </strong>In 11 centres of the Italian Pulmonary Hypertension NETwork (IPHNET), data were prospectively collected from patients with PAH who underwent re-evaluation between 6 and 12 months after diagnosis. Echocardiographic variables were combined a priori to define four phenotypes representing different degrees of RV dilatation and right ventricular-pulmonary arterial (RV-PA) coupling: a mildly dilated right ventricle with preserved RV-PA coupling defined phenotype-1; a mildly dilated right ventricle with poor RV-PA coupling defined phenotype-2; a severely dilated right ventricle with preserved RV-PA coupling defined phenotype-3; a severely dilated right ventricle with poor RV-PA coupling, either with or without tricuspid regurgitation of moderate degree or more, defined phenotype-4. Patients were followed up for all-cause death for a median of 3.7 years.</p><p><strong>Results: </strong>These echocardiographic phenotypes were present in all European Society of Cardiology/European Respiratory Society or REVEAL 2.0 risk groups except for the high-risk groups, which included only phenotype-3 and phenotype-4. In each risk group, RV phenotype-4 identified patients with a poorer prognosis; RV phenotype-1 identified patients with better survival in intermediate risk groups.</p><p><strong>Conclusions: </strong>Echocardiography-derived phenotypes describing different degrees of RV remodelling and dysfunction provide prognostic information which is independent of and additional to the clinically defined risk in PAH patients at first follow-up.</p>","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":35.6,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131300","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 : 2026-02-05DOI: 10.1093/eurheartj/ehaf784.1736
T Mito, D Kinoshita, J Goto, T Shikama, Y Otaki, S Kato, T Watanabe, I K Jang, M Watanabe
Background The majority of plaque disruptions are silent, followed by healing, resulting in layered plaque formation. Some plaque disruptions result in occlusive thrombosis and acute myocardial infarction. Purpose This study aimed to test the hypothesis that the patients with layered plaque at culprit lesions would have robust endogenous anti-thrombotic defense mechanisms compared to those without layered plaque. Methods A total of 119 patients with chronic coronary syndrome were enrolled. Target lesions were imaged by optical coherence tomography (OCT). Factor analysis determined four groups of biomarkers, (1) anti-thrombotic factors: plasminogen, anti-thrombin 3, (2) atherogenic factors: low-density lipoprotein-cholesterol (LDL-C), malondialdehyde-modified low-density lipoprotein (MDA-LDL), (3) prothrombotic factors: D-dimer, fibrin degradation products (FDP), and (4) inflammatory factors: fibrinogen, and high-sensitive C reactive protein (hs-CRP). Patients were divided into three groups according to the tertiles of each of those four groups, and their association with a layered plaque was investigated. A layered plaque was defined as one or more layers of different optical densities and a clear demarcation from the underlying tissue. The arc of each layered plaque was assessed at 1-mm cross-section intervals. Layered plaque length is measured from a longitudinal view. The layer index, equivalent to layered plaque volume, is defined as mean layer arc × total layer length. Results The layered plaque was more prevalent in patients with higher levels of anti-thrombotic factor levels (p for trend=0.013) (Figure 1). Similarly, the layer index was higher in patients with higher anti-thrombotic factor levels (p for trend=0.006) (Figure 2). In contrast, other factors had no associations with layered plaque and layer index. In multivariable analysis, only the anti-thrombotic factor was associated with a higher layer index after adjusting for confounders. Conclusions The systemic anti-thrombotic factor levels might be more important determinants for layered plaque formation than atherogenic, prothrombotic, or inflammatory factors.Figure 1 Figure 2
{"title":"Healed plaque and systemic thrombogenicity in patients with chronic coronary syndrome","authors":"T Mito, D Kinoshita, J Goto, T Shikama, Y Otaki, S Kato, T Watanabe, I K Jang, M Watanabe","doi":"10.1093/eurheartj/ehaf784.1736","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf784.1736","url":null,"abstract":"Background The majority of plaque disruptions are silent, followed by healing, resulting in layered plaque formation. Some plaque disruptions result in occlusive thrombosis and acute myocardial infarction. Purpose This study aimed to test the hypothesis that the patients with layered plaque at culprit lesions would have robust endogenous anti-thrombotic defense mechanisms compared to those without layered plaque. Methods A total of 119 patients with chronic coronary syndrome were enrolled. Target lesions were imaged by optical coherence tomography (OCT). Factor analysis determined four groups of biomarkers, (1) anti-thrombotic factors: plasminogen, anti-thrombin 3, (2) atherogenic factors: low-density lipoprotein-cholesterol (LDL-C), malondialdehyde-modified low-density lipoprotein (MDA-LDL), (3) prothrombotic factors: D-dimer, fibrin degradation products (FDP), and (4) inflammatory factors: fibrinogen, and high-sensitive C reactive protein (hs-CRP). Patients were divided into three groups according to the tertiles of each of those four groups, and their association with a layered plaque was investigated. A layered plaque was defined as one or more layers of different optical densities and a clear demarcation from the underlying tissue. The arc of each layered plaque was assessed at 1-mm cross-section intervals. Layered plaque length is measured from a longitudinal view. The layer index, equivalent to layered plaque volume, is defined as mean layer arc × total layer length. Results The layered plaque was more prevalent in patients with higher levels of anti-thrombotic factor levels (p for trend=0.013) (Figure 1). Similarly, the layer index was higher in patients with higher anti-thrombotic factor levels (p for trend=0.006) (Figure 2). In contrast, other factors had no associations with layered plaque and layer index. In multivariable analysis, only the anti-thrombotic factor was associated with a higher layer index after adjusting for confounders. Conclusions The systemic anti-thrombotic factor levels might be more important determinants for layered plaque formation than atherogenic, prothrombotic, or inflammatory factors.Figure 1 Figure 2","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"223 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121864","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 : 2026-02-05DOI: 10.1093/eurheartj/ehaf784.2477
L Ordine, D Pacella, S Di Napoli, G Canciello, F Borrelli, R Lombardi, B Napolitano, R Martorano, L Moscano, R Polizzi, A Spinelli, G Esposito, M A Losi
Background Mitral annular disjunction (MAD) is a condition characterized by the abnormal attachment of the posterior mitral leaflet directly to the atrial wall. This condition is particularly prevalent in patients with mitral valve prolapse (MVP). The growing interest in MAD arises from various studies that have indicated its potential arrhythmic role. However, the findings are still controversial, and further research is needed to clarify its implications. Objective To better assess the arrhythmic risk linked to the presence of MAD in patients with MVP. Method We conducted a systematic search of the Medline, Cochrane, and Scopus electronic databases for studies published from their inception through December 2024. Our focus was on studies comparing arrhythmic MAD with non-arrhythmic MAD. Two investigators, L.O. and M.A.L., independently performed the searches using the following terms: mitral annular disjunction, mitral valve disjunction, ventricular arrhythmias, mitral valve prolapse, and sudden cardiac death. The prognostic performance of MAD in predicting major arrhythmias in the MVP population was summarized using pooled estimates for sensitivity, specificity, diagnostic odds ratio (DOR), negative predictive value (NPV), and positive predictive value (PPV). Confidence intervals were calculated using the DerSimonian and Laird method (1986, ref 1). Due to varying thresholds for identifying MAD, moderate heterogeneity was expected, assessed with I-squared and Kendall's Tau. A random-effects model was used when heterogeneity was not extremely low. The summary receiver operating characteristic (sROC) curve and area under the curve (AUC) were computed using a non-parametric summary ROC method, as described by Martinez-Camblor. Statistical analysis was performed with R version 4.4.0. Results After reviewing 66 articles, we identified a total of 7 studies enrolling 1977 patients with MVP. Of these 1171 MVP with MAD and 806 without MAD. MAD was defined as abnormal separation between the mitral valve junction and LV wall with a length of at least 1 mm (5 studies) or 2 mm (2 studies). MAD was assessed with echocardiography (4 studies) or cardiac magnetic resonance (CMR) (3 studies). In patients with MVP, MAD was associated with an increased arrhythmic risk with OR of 2.604 (95% CI: 2.012; 3.371) (Figure, upper panel). MAD resulted as an arrhythmic risk factor in patients with MVP with an AUC of 0.603 (Figure, lower panel). Conclusions While MVP is generally considered a benign condition, a subset of patients may face an elevated risk of life-threatening arrhythmias. Our findings suggest that MAD is a significant risk factor for arrhythmias in patients with MVP, reinforcing the need for careful evaluation and risk stratification in this population. Future studies should focus on refining MAD detection methods and establishing standardized diagnostic thresholds to improve risk prediction and clinical management.
{"title":"Mitral annular disjunction and its arrhythmic risk in mitral valve prolapse: a metanalysis","authors":"L Ordine, D Pacella, S Di Napoli, G Canciello, F Borrelli, R Lombardi, B Napolitano, R Martorano, L Moscano, R Polizzi, A Spinelli, G Esposito, M A Losi","doi":"10.1093/eurheartj/ehaf784.2477","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf784.2477","url":null,"abstract":"Background Mitral annular disjunction (MAD) is a condition characterized by the abnormal attachment of the posterior mitral leaflet directly to the atrial wall. This condition is particularly prevalent in patients with mitral valve prolapse (MVP). The growing interest in MAD arises from various studies that have indicated its potential arrhythmic role. However, the findings are still controversial, and further research is needed to clarify its implications. Objective To better assess the arrhythmic risk linked to the presence of MAD in patients with MVP. Method We conducted a systematic search of the Medline, Cochrane, and Scopus electronic databases for studies published from their inception through December 2024. Our focus was on studies comparing arrhythmic MAD with non-arrhythmic MAD. Two investigators, L.O. and M.A.L., independently performed the searches using the following terms: mitral annular disjunction, mitral valve disjunction, ventricular arrhythmias, mitral valve prolapse, and sudden cardiac death. The prognostic performance of MAD in predicting major arrhythmias in the MVP population was summarized using pooled estimates for sensitivity, specificity, diagnostic odds ratio (DOR), negative predictive value (NPV), and positive predictive value (PPV). Confidence intervals were calculated using the DerSimonian and Laird method (1986, ref 1). Due to varying thresholds for identifying MAD, moderate heterogeneity was expected, assessed with I-squared and Kendall's Tau. A random-effects model was used when heterogeneity was not extremely low. The summary receiver operating characteristic (sROC) curve and area under the curve (AUC) were computed using a non-parametric summary ROC method, as described by Martinez-Camblor. Statistical analysis was performed with R version 4.4.0. Results After reviewing 66 articles, we identified a total of 7 studies enrolling 1977 patients with MVP. Of these 1171 MVP with MAD and 806 without MAD. MAD was defined as abnormal separation between the mitral valve junction and LV wall with a length of at least 1 mm (5 studies) or 2 mm (2 studies). MAD was assessed with echocardiography (4 studies) or cardiac magnetic resonance (CMR) (3 studies). In patients with MVP, MAD was associated with an increased arrhythmic risk with OR of 2.604 (95% CI: 2.012; 3.371) (Figure, upper panel). MAD resulted as an arrhythmic risk factor in patients with MVP with an AUC of 0.603 (Figure, lower panel). Conclusions While MVP is generally considered a benign condition, a subset of patients may face an elevated risk of life-threatening arrhythmias. Our findings suggest that MAD is a significant risk factor for arrhythmias in patients with MVP, reinforcing the need for careful evaluation and risk stratification in this population. Future studies should focus on refining MAD detection methods and establishing standardized diagnostic thresholds to improve risk prediction and clinical management.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"89 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146122109","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}