Jakob Versnjak,Titus Kuehne,Pauline Fahjen,Nina Jovanovic,Ulrike Löber,Gabriele G Schiattarella,Nicola Wilck,Holger Gerhardt,Dominik N Müller,Frank Edelmann,Philipp Mertins,Roland Eils,Michael Gotthardt,Sofia K Forslund,Benjamin Wild,Marcus Kelm
AIMSHeart failure with preserved ejection fraction (HFpEF) has become the predominant form of heart failure and a leading cause of global cardiovascular morbidity and mortality. Due to its heterogeneous nature, HFpEF presents substantial challenges in diagnosis and management. Given the limited treatment options and lifestyle-associated comorbidities, early identification is crucial for establishing effective preventive strategies. Here, we introduce and validate a machine learning-based multi-omics approach that integrates clinical and molecular data to detect and characterize HFpEF.METHODS AND RESULTSA supervised classifier was trained on a stratified subset of UK Biobank participants (n = 401 917) to identify phenotypic profiles associated with subsequent symptom-defined HFpEF during longitudinal follow-up. Model performance was validated in a non-overlapping hold-out subset from all 22 UK Biobank assessment centres (n = 100 446; 6726 HFpEF cases; 7394 with multi-omics data). The classifier demonstrated robust discriminatory performance, with a receiver operating characteristic area under the curve (ROC AUC) of 0.931 (95% confidence interval [CI] 0.930-0.931), a sensitivity of 0.857 (95% CI 0.855-0.860) and a specificity of 0.847 (95% CI 0.846-0.847). It identified individuals who subsequently developed HFpEF an average of 6.3 ± 3.9 years before symptom onset in asymptomatic individuals. Similarity network fusion (SNF) identified distinct subgroups, including a high-risk cluster characterized by elevated mortality and dysregulated inflammatory pathways, which was distinguishable with high accuracy (ROC AUC 0.988; 95% CI 0.985-0.990).CONCLUSIONSWe identified HFpEF phenotypes at an early stage, often several years before the onset of clinical symptoms, when the disease trajectory may still be amenable to modification. The molecular characterization provides novel insights into the underlying disease complexity and enables more refined risk stratification.
保留射血分数的心力衰竭（HFpEF）已成为心力衰竭的主要形式，也是全球心血管疾病发病率和死亡率的主要原因。由于其异质性，HFpEF在诊断和管理方面提出了重大挑战。鉴于有限的治疗选择和与生活方式相关的合并症，早期识别对于制定有效的预防策略至关重要。在这里，我们介绍并验证了一种基于机器学习的多组学方法，该方法整合了临床和分子数据来检测和表征HFpEF。方法和结果在英国生物银行参与者的分层子集（n = 401 917）上训练sa监督分类器，以在纵向随访期间识别与随后症状定义的HFpEF相关的表型谱。在来自所有22个UK Biobank评估中心的非重叠保留子集中验证了模型的性能（n = 100 446； 6726例HFpEF病例；7394例多组学数据）。分类器表现出稳健的判别性能，受试者曲线下工作特征面积（ROC AUC）为0.931(95%置信区间[CI] 0.930-0.931)，灵敏度为0.857 (95% CI 0.855-0.860)，特异性为0.847 （95% CI 0.846-0.847）。该研究确定了在无症状个体出现症状前平均6.3±3.9年出现HFpEF的个体。相似网络融合（SNF）识别出不同的亚群，包括以死亡率升高和炎症通路失调为特征的高风险聚类，其区分准确率很高（ROC AUC 0.988; 95% CI 0.985-0.990）。结论：我们在早期阶段就发现了HFpEF的表型，通常在临床症状出现前几年，此时疾病轨迹可能仍然可以改变。分子表征提供了对潜在疾病复杂性的新见解，并使更精细的风险分层成为可能。
{"title":"Deep phenotyping of heart failure with preserved ejection fraction through multi-omics integration.","authors":"Jakob Versnjak,Titus Kuehne,Pauline Fahjen,Nina Jovanovic,Ulrike Löber,Gabriele G Schiattarella,Nicola Wilck,Holger Gerhardt,Dominik N Müller,Frank Edelmann,Philipp Mertins,Roland Eils,Michael Gotthardt,Sofia K Forslund,Benjamin Wild,Marcus Kelm","doi":"10.1002/ejhf.70041","DOIUrl":"https://doi.org/10.1002/ejhf.70041","url":null,"abstract":"AIMSHeart failure with preserved ejection fraction (HFpEF) has become the predominant form of heart failure and a leading cause of global cardiovascular morbidity and mortality. Due to its heterogeneous nature, HFpEF presents substantial challenges in diagnosis and management. Given the limited treatment options and lifestyle-associated comorbidities, early identification is crucial for establishing effective preventive strategies. Here, we introduce and validate a machine learning-based multi-omics approach that integrates clinical and molecular data to detect and characterize HFpEF.METHODS AND RESULTSA supervised classifier was trained on a stratified subset of UK Biobank participants (n = 401 917) to identify phenotypic profiles associated with subsequent symptom-defined HFpEF during longitudinal follow-up. Model performance was validated in a non-overlapping hold-out subset from all 22 UK Biobank assessment centres (n = 100 446; 6726 HFpEF cases; 7394 with multi-omics data). The classifier demonstrated robust discriminatory performance, with a receiver operating characteristic area under the curve (ROC AUC) of 0.931 (95% confidence interval [CI] 0.930-0.931), a sensitivity of 0.857 (95% CI 0.855-0.860) and a specificity of 0.847 (95% CI 0.846-0.847). It identified individuals who subsequently developed HFpEF an average of 6.3 ± 3.9 years before symptom onset in asymptomatic individuals. Similarity network fusion (SNF) identified distinct subgroups, including a high-risk cluster characterized by elevated mortality and dysregulated inflammatory pathways, which was distinguishable with high accuracy (ROC AUC 0.988; 95% CI 0.985-0.990).CONCLUSIONSWe identified HFpEF phenotypes at an early stage, often several years before the onset of clinical symptoms, when the disease trajectory may still be amenable to modification. The molecular characterization provides novel insights into the underlying disease complexity and enables more refined risk stratification.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"1 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103418","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}
Tariq Jamal Siddiqi,Muhammad Shahzeb Khan,Saad Ahmed Waqas,Harriette G C Van Spall,Michael D Shapiro,Gregg C Fonarow,James L Januzzi,Aasim M Afzal,Ambarish Pandey,Javed Butler,Stephen J Greene
AIMSEffects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on heart failure hospitalization (HFH) and cardiovascular (CV) death among patients with varying overlap of cardiovascular-kidney-metabolic (CKM) comorbidity are not well characterized. This study aimed to assess effects GLP-1RAs on HFH and CV death across populations with varying type and number of CKM comorbidity.METHODS AND RESULTSOnline databases were queried through November 2024 for primary and secondary analyses of clinical outcome trials of GLP-1RAs in patients with heart failure (HF), type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), obesity, and combinations of these diseases. Primary outcome was a composite HFH or CV death. Secondary outcomes were first HFH and CV death. Hazard ratios (HRs), risk ratios (RRs), and their 95% confidence intervals (CI) were derived using random-effects models. Fifteen trials (n = 87 549) were included. Compared with placebo, GLP-1RAs reduced the relative risk of composite HFH/CV death in HF (HR 0.81, 95% CI 0.69-0.96), T2DM (HR 0.85, 95% CI 0.78-0.93), and obesity (HR 0.70, 95% CI 0.58-0.86), with a non-significant risk reduction in CKD (HR 0.79, 95% CI 0.61-1.01). GLP-1RAs reduced the risk of HFH in T2DM (HR 0.89, 95% CI 0.80-0.99) and obesity (HR 0.63, 95% CI 0.45-0.87), with a non-significant risk reduction among patients with HF (HR 0.85, 95% CI 0.69-1.04) and CKD (HR 0.82, 95% CI 0.64-1.06). GLP-1RAs also significantly reduced CV death in HF (HR 0.88, 95% CI 0.77-0.99), T2DM (HR 0.85, 95% CI 0.78-0.93), and in obesity (HR 0.83, 95% CI 0.73-0.93), with a non-significant risk reduction in CKD (HR 0.80, 95% CI 0.60-1.08). Effects were consistent across subgroups, except for HF with reduced ejection fraction (HFrEF), where GLP-1RAs showed a non-significant risk increase in HFH (HR 1.17, 95% CI 0.93-1.47) but significantly reduced CV death (HR 0.67, 95% CI 0.50-0.90). GLP-1RAs were not associated with increased risk for serious adverse events (RR 0.94, 95% CI 0.89-1.00).CONCLUSIONSGlucagon-like peptide-1 receptor agonists reduce HFH and CV death across CKM conditions, with generally consistent effects in varying combinations of these diseases. The potential exception is among patients with HFrEF, where a reduction in risk of CV death, but a numeric increase in HFH, was observed. Definitive CV outcome trials are needed to definitively determine effects of GLP-1RAs in patients with established HFrEF.
胰高血糖素样肽-1受体激动剂（GLP-1RAs）对不同重叠心血管-肾-代谢（CKM）合并症患者心力衰竭住院（HFH）和心血管（CV）死亡的影响尚不清楚。本研究旨在评估GLP-1RAs在不同类型和数量CKM合并症人群中对HFH和CV死亡的影响。方法和结果通过在线数据库查询到2024年11月，对GLP-1RAs在心力衰竭（HF）、2型糖尿病（T2DM）、慢性肾脏疾病（CKD）、肥胖和这些疾病合并患者的临床结局试验进行主要和次要分析。主要终点为HFH或CV复合死亡。次要结局为首次HFH和CV死亡。使用随机效应模型推导出风险比（hr）、风险比（rr）及其95%置信区间（CI）。纳入15项试验（n = 87 549）。与安慰剂相比，GLP-1RAs降低了HF （HR 0.81, 95% CI 0.69-0.96）、T2DM （HR 0.85, 95% CI 0.78-0.93）和肥胖（HR 0.70, 95% CI 0.58-0.86）中HFH/CV复合死亡的相对风险，而CKD （HR 0.79, 95% CI 0.61-1.01）的风险降低不显著（HR 0.79, 95% CI 0.61-1.01）。GLP-1RAs降低了T2DM （HR 0.89, 95% CI 0.80-0.99）和肥胖（HR 0.63, 95% CI 0.45-0.87）患者HFH的风险，而HF （HR 0.85, 95% CI 0.69-1.04）和CKD （HR 0.82, 95% CI 0.64-1.06）患者的风险降低不显著。GLP-1RAs还显著降低HF （HR 0.88, 95% CI 0.77-0.99）、T2DM （HR 0.85, 95% CI 0.78-0.93）和肥胖（HR 0.83, 95% CI 0.73-0.93）的CV死亡，而CKD （HR 0.80, 95% CI 0.60-1.08）的CV死亡风险无显著降低（HR 0.80, 95% CI 0.60-1.08）。除伴有射血分数降低的HF （HFrEF）外，其他亚组的效果一致，其中GLP-1RAs显示HFH的风险无显著增加（HR 1.17, 95% CI 0.93-1.47），但显著降低CV死亡（HR 0.67, 95% CI 0.50-0.90）。GLP-1RAs与严重不良事件风险增加无关（RR 0.94, 95% CI 0.89-1.00）。结论胰高血糖素样肽-1受体激动剂可降低慢性肾病患者HFH和CV的死亡率，在这些疾病的不同组合中具有普遍一致的效果。潜在的例外是HFrEF患者，他们观察到CV死亡风险降低，但HFH的数量增加。需要明确的CV结局试验来明确确定GLP-1RAs对HFrEF患者的影响。
{"title":"Effect of glucagon-like peptide-1 receptor agonists on heart failure outcomes and cardiovascular death across varying cardiovascular-kidney-metabolic comorbidity.","authors":"Tariq Jamal Siddiqi,Muhammad Shahzeb Khan,Saad Ahmed Waqas,Harriette G C Van Spall,Michael D Shapiro,Gregg C Fonarow,James L Januzzi,Aasim M Afzal,Ambarish Pandey,Javed Butler,Stephen J Greene","doi":"10.1002/ejhf.70048","DOIUrl":"https://doi.org/10.1002/ejhf.70048","url":null,"abstract":"AIMSEffects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on heart failure hospitalization (HFH) and cardiovascular (CV) death among patients with varying overlap of cardiovascular-kidney-metabolic (CKM) comorbidity are not well characterized. This study aimed to assess effects GLP-1RAs on HFH and CV death across populations with varying type and number of CKM comorbidity.METHODS AND RESULTSOnline databases were queried through November 2024 for primary and secondary analyses of clinical outcome trials of GLP-1RAs in patients with heart failure (HF), type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), obesity, and combinations of these diseases. Primary outcome was a composite HFH or CV death. Secondary outcomes were first HFH and CV death. Hazard ratios (HRs), risk ratios (RRs), and their 95% confidence intervals (CI) were derived using random-effects models. Fifteen trials (n = 87 549) were included. Compared with placebo, GLP-1RAs reduced the relative risk of composite HFH/CV death in HF (HR 0.81, 95% CI 0.69-0.96), T2DM (HR 0.85, 95% CI 0.78-0.93), and obesity (HR 0.70, 95% CI 0.58-0.86), with a non-significant risk reduction in CKD (HR 0.79, 95% CI 0.61-1.01). GLP-1RAs reduced the risk of HFH in T2DM (HR 0.89, 95% CI 0.80-0.99) and obesity (HR 0.63, 95% CI 0.45-0.87), with a non-significant risk reduction among patients with HF (HR 0.85, 95% CI 0.69-1.04) and CKD (HR 0.82, 95% CI 0.64-1.06). GLP-1RAs also significantly reduced CV death in HF (HR 0.88, 95% CI 0.77-0.99), T2DM (HR 0.85, 95% CI 0.78-0.93), and in obesity (HR 0.83, 95% CI 0.73-0.93), with a non-significant risk reduction in CKD (HR 0.80, 95% CI 0.60-1.08). Effects were consistent across subgroups, except for HF with reduced ejection fraction (HFrEF), where GLP-1RAs showed a non-significant risk increase in HFH (HR 1.17, 95% CI 0.93-1.47) but significantly reduced CV death (HR 0.67, 95% CI 0.50-0.90). GLP-1RAs were not associated with increased risk for serious adverse events (RR 0.94, 95% CI 0.89-1.00).CONCLUSIONSGlucagon-like peptide-1 receptor agonists reduce HFH and CV death across CKM conditions, with generally consistent effects in varying combinations of these diseases. The potential exception is among patients with HFrEF, where a reduction in risk of CV death, but a numeric increase in HFH, was observed. Definitive CV outcome trials are needed to definitively determine effects of GLP-1RAs in patients with established HFrEF.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"22 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103417","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}
AIMSImplementing optimal guideline-directed medical therapy is still challenging in patients with heart failure (HF). This prospective study assessed the benefits of large-scale, nationwide, multi-annual implementation of HF therapies in China.METHODS AND RESULTSThis longitudinal, pre-post comparison design included patients in hospitals accredited by the National Heart Failure Center Accreditation Program (HF-CAP). Patients were divided into four groups: 6-12 months before accreditation (Pre); >0 -≤12 months after accreditation (Y1); >12-≤24 months after accreditation (Y2), and >24 months after accreditation (Y2+). The primary endpoint was 1-year composite HF readmission and/or cardiovascular death. Secondary endpoints included 1-year HF readmission alone, 1-year cardiovascular death alone, and association between phone calls and/or visits and outcomes. Overall, 408 073 patients with HF from 646 centres were included. After HF-CAP accreditation, more patients with HF were treated following discharge. Compared with the Pre group, risk of meeting the primary endpoint decreased in Y1 and was incrementally lower in Y2 and Y2+: fully adjusted odds ratios (OR) and 95% confidence intervals (CIs) were 0.893 (0.871-0.916), 0.855 (0.830-0.880) and 0.720 (0.695-0.745), respectively (all p < 0.0001). Risk of HF readmission alone reduced from Y1 onwards (OR 0.865 [95% CI 0.841-0.891]). Risk of cardiovascular death reduced from Y2 onwards (OR 0.942 [95% CI 0.904-0.983]). Phone calls had little association with patient outcomes; however, face-to-face visits reduced risk of cardiovascular death (OR 0.624 [95% CI 0.597-0.651]).CONCLUSIONSGuideline-directed medical therapy implementation and follow-up after HF hospitalization was achievable in ~400 000 patients and was associated with cardiovascular benefits 1-year post-initiation.
在心力衰竭（HF）患者中实施最佳的指导药物治疗仍然具有挑战性。这项前瞻性研究评估了在中国大规模、全国性、每年多次实施心衰治疗的益处。方法和结果这项纵向、前后比较设计纳入了国家心力衰竭中心认证计划（HF-CAP）认可的医院的患者。患者分为四组：前6-12个月（Pre）；>0 -认证后≤12个月（Y1）；>认证后12-≤24个月（Y2）， >认证后24个月（Y2+）。主要终点是1年合并心衰再入院和/或心血管死亡。次要终点包括1年心力衰竭再入院，1年心血管死亡，以及电话和/或就诊与预后的关系。总共纳入了来自646个中心的408073例心衰患者。在HF- cap认证后，更多的HF患者在出院后接受治疗。与Pre组相比，Y1组达到主要终点的风险降低，Y2组和Y2+组达到主要终点的风险逐渐降低：完全调整的优势比（OR）和95%置信区间（ci）分别为0.893（0.871-0.916）、0.855（0.830-0.880）和0.720(0.695-0.745)（均p < 0.0001）。仅HF再入院的风险从1岁开始降低（OR 0.865 [95% CI 0.841-0.891]）。心血管死亡风险从Y2开始降低（OR 0.942 [95% CI 0.904-0.983]）。打电话与病人的预后关系不大；然而，面对面访问降低了心血管死亡风险（OR 0.624 [95% CI 0.597-0.651]）。结论：约40万例心衰患者住院后可实现指南指导的药物治疗实施和随访，并在开始治疗后1年心血管获益。
{"title":"Nationwide implementation of heart failure therapies: National Heart Failure Center Accreditation Program (HF-CAP) in China.","authors":"Jingmin Zhou,Xuejuan Jin,Yamei Xu,Zhonglei Xie,Xiaotong Cui,Yanyan Wang,Hua Wang,Xinli Li,Yugang Dong,Yuhua Liao,Weimin Li,Alexandre Mebazaa,Jiefu Yang,Junbo Ge, ","doi":"10.1002/ejhf.70035","DOIUrl":"https://doi.org/10.1002/ejhf.70035","url":null,"abstract":"AIMSImplementing optimal guideline-directed medical therapy is still challenging in patients with heart failure (HF). This prospective study assessed the benefits of large-scale, nationwide, multi-annual implementation of HF therapies in China.METHODS AND RESULTSThis longitudinal, pre-post comparison design included patients in hospitals accredited by the National Heart Failure Center Accreditation Program (HF-CAP). Patients were divided into four groups: 6-12 months before accreditation (Pre); >0 -≤12 months after accreditation (Y1); >12-≤24 months after accreditation (Y2), and >24 months after accreditation (Y2+). The primary endpoint was 1-year composite HF readmission and/or cardiovascular death. Secondary endpoints included 1-year HF readmission alone, 1-year cardiovascular death alone, and association between phone calls and/or visits and outcomes. Overall, 408 073 patients with HF from 646 centres were included. After HF-CAP accreditation, more patients with HF were treated following discharge. Compared with the Pre group, risk of meeting the primary endpoint decreased in Y1 and was incrementally lower in Y2 and Y2+: fully adjusted odds ratios (OR) and 95% confidence intervals (CIs) were 0.893 (0.871-0.916), 0.855 (0.830-0.880) and 0.720 (0.695-0.745), respectively (all p < 0.0001). Risk of HF readmission alone reduced from Y1 onwards (OR 0.865 [95% CI 0.841-0.891]). Risk of cardiovascular death reduced from Y2 onwards (OR 0.942 [95% CI 0.904-0.983]). Phone calls had little association with patient outcomes; however, face-to-face visits reduced risk of cardiovascular death (OR 0.624 [95% CI 0.597-0.651]).CONCLUSIONSGuideline-directed medical therapy implementation and follow-up after HF hospitalization was achievable in ~400 000 patients and was associated with cardiovascular benefits 1-year post-initiation.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"1 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103511","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}
Tomonari Harada,Yogesh N V Reddy,Hidemi Sorimachi,Masaru Obokata,Jwan A Naser,Atsushi Tada,Shunichi Doi,Tatsuro Ibe,Mackram F Eleid,Sorin V Pislaru,Rebecca T Hahn,Barry A Borlaug
AIMSThe pathophysiology of tricuspid regurgitation (TR) during exercise in heart failure with preserved ejection fraction (HFpEF) is not well understood.METHODS AND RESULTSWe investigated dynamic changes in TR severity during exercise in patients with HFpEF and associated relationships with haemodynamics, cardiopulmonary reserve, and prognosis using invasive haemodynamic exercise testing with simultaneous echocardiography and expired gas analysis. Among 169 patients with HFpEF (91 no TR, 44 mild TR, 34 ≥ moderate TR), older age and atrial fibrillation were more common in patients with greater TR severity. Right heart remodelling and dysfunction were more frequently observed with greater TR severity, particularly in the right atrium, along with stepwise increases in right atrial (RA) pressure and interventricular septal flattening, and decreases in cardiac output (CO). During exercise, TR severity frequently worsened, and over half of the patients with moderate TR at rest displayed severe TR during exercise, accompanied by profound RA dilatation, reduced RA reservoir strain, increased septal flattening, and more severely impaired CO reserve. Abnormalities in tricuspid annular motion and ventricular interaction were amplified by exercise with greater TR, but exercise pulmonary vascular pressures did not differ across groups. Patients with ≥ moderate TR during exercise displayed higher event rates (hazard ratio 2.85, 95% confidence interval 1.18-6.85), but patients with mild TR had similar prognosis as those without TR in adjusted models.CONCLUSIONSTricuspid regurgitation in HFpEF is related to advanced RA myopathy and often worsens during exercise leading to dynamic right-sided heart failure, exaggerated ventricular interaction, impaired CO reserve, and increased risk for adverse outcomes. These data emphasize the clinical importance of exercise evaluation and call for further study of novel treatments in those with significant resting and provocable TR.
{"title":"Dynamic tricuspid regurgitation in heart failure with preserved ejection fraction.","authors":"Tomonari Harada,Yogesh N V Reddy,Hidemi Sorimachi,Masaru Obokata,Jwan A Naser,Atsushi Tada,Shunichi Doi,Tatsuro Ibe,Mackram F Eleid,Sorin V Pislaru,Rebecca T Hahn,Barry A Borlaug","doi":"10.1002/ejhf.70050","DOIUrl":"https://doi.org/10.1002/ejhf.70050","url":null,"abstract":"AIMSThe pathophysiology of tricuspid regurgitation (TR) during exercise in heart failure with preserved ejection fraction (HFpEF) is not well understood.METHODS AND RESULTSWe investigated dynamic changes in TR severity during exercise in patients with HFpEF and associated relationships with haemodynamics, cardiopulmonary reserve, and prognosis using invasive haemodynamic exercise testing with simultaneous echocardiography and expired gas analysis. Among 169 patients with HFpEF (91 no TR, 44 mild TR, 34 ≥ moderate TR), older age and atrial fibrillation were more common in patients with greater TR severity. Right heart remodelling and dysfunction were more frequently observed with greater TR severity, particularly in the right atrium, along with stepwise increases in right atrial (RA) pressure and interventricular septal flattening, and decreases in cardiac output (CO). During exercise, TR severity frequently worsened, and over half of the patients with moderate TR at rest displayed severe TR during exercise, accompanied by profound RA dilatation, reduced RA reservoir strain, increased septal flattening, and more severely impaired CO reserve. Abnormalities in tricuspid annular motion and ventricular interaction were amplified by exercise with greater TR, but exercise pulmonary vascular pressures did not differ across groups. Patients with ≥ moderate TR during exercise displayed higher event rates (hazard ratio 2.85, 95% confidence interval 1.18-6.85), but patients with mild TR had similar prognosis as those without TR in adjusted models.CONCLUSIONSTricuspid regurgitation in HFpEF is related to advanced RA myopathy and often worsens during exercise leading to dynamic right-sided heart failure, exaggerated ventricular interaction, impaired CO reserve, and increased risk for adverse outcomes. These data emphasize the clinical importance of exercise evaluation and call for further study of novel treatments in those with significant resting and provocable TR.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"18 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103416","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}
AIMSThe need to perform endomyocardial biopsy (EMB) in patients with non-ischaemic dilated cardiomyopathies (DCM) is debated. Here we sought to determine the extent of left ventricular collagen volume fraction (LV-CVF) in DCM patients and to evaluate it as a prognostic marker.METHODS AND RESULTSIn this retrospective longitudinal study, we included 524 patients with suspected DCM who underwent left ventricular EMB (LV-EMB) as a part of their clinical work-up. LV-CVF was quantified using automated image processing of high-resolution scans of LV-EMB. Deep phenotyping was performed including assessment of late gadolinium enhancement on cardiac magnetic resonance imaging. Endpoints were (i) composite endpoint of heart failure-related death, sudden cardiac death, aborted sudden cardiac death (appropriate implantable cardioverter-defibrillator shock, reported sustained ventricular tachycardia, or cardiopulmonary resuscitation), or cardiac transplantation, and (ii) all-cause mortality. LV-EMB was associated with 0.76% major and 2.1% minor complications. No death occurred due to EMB. LV-CVF could be reliably quantified using Bayesian classification. During a median follow-up of 43.2 months (2084 patient-years), 48 patients with LV-CVF >32% and 14 patients with LV-CVF ≤32% reached the composite endpoint (log-rank p < 0.0001). A total of 62 patients reached the endpoint all-cause mortality, from which 38 presented with LV-CVF >32% and 17 with LV-CVF ≤32% (log-rank p = 0.009). In multivariable analyses, LV-CVF and N-terminal pro-B-type natriuretic peptide (NT-proBNP) (hazard ratio 2.03, 95% confidence interval 1.32-3.11) were independent predictors of unfavourable outcome.CONCLUSIONSLeft ventricular EMB is a safe diagnostic procedure. The extent of CVF in LV-EMB provides prognostic information in patients with DCM in addition to existing measures of left ventricular ejection fraction or NT-proBNP.
目的：对非缺血性扩张型心肌病（DCM）患者进行心肌内膜活检（EMB）的必要性存在争议。在这里，我们试图确定DCM患者左心室胶原体积分数（LV-CVF）的范围，并将其作为预后指标进行评估。方法和结果在这项回顾性纵向研究中，我们纳入了524例疑似DCM的患者，他们接受了左心室EMB （LV-EMB）作为临床检查的一部分。LV-CVF采用LV-EMB高分辨率扫描的自动图像处理进行量化。进行深度表型分析，包括评估心脏磁共振成像的晚期钆增强。终点为(i)心力衰竭相关死亡、心源性猝死、流产性心源性猝死（适当的植入式心律转复除颤器休克、报告的持续性室性心动过速或心肺复苏）或心脏移植的复合终点，以及（ii）全因死亡率。LV-EMB有0.76%的严重并发症和2.1%的轻微并发症。无EMB死亡病例。使用贝叶斯分类可以可靠地量化LV-CVF。在中位43.2个月（2084患者年）的随访期间，48例LV-CVF≤32%的患者和14例LV-CVF≤32%的患者达到了复合终点（log-rank p = 32%）， 17例LV-CVF≤32% （log-rank p = 0.009）。在多变量分析中，LV-CVF和n端前b型利钠肽（NT-proBNP）（风险比2.03,95%可信区间1.32-3.11）是不良结局的独立预测因子。结论左心室EMB是一种安全的诊断方法。除了现有的左室射血分数或NT-proBNP测量外，LV-EMB中CVF的程度提供了DCM患者的预后信息。
{"title":"Safety and prognostic value of left ventricular endomyocardial biopsy in dilated cardiomyopathy.","authors":"Elham Kayvanpour,Farbod Sedaghat-Hamedani,Daniel Tian Li,Ebe Amr,Ali Amr,Bernd Lahrmann,Alan Lai,Chriswh Reich,Chenyang Wang,Esther Herpel,Derliz Mereles,Lutz Frankenstein,Niels Grabe,Hugo A Katus,Norbert Frey,Benjamin Meder","doi":"10.1002/ejhf.70019","DOIUrl":"https://doi.org/10.1002/ejhf.70019","url":null,"abstract":"AIMSThe need to perform endomyocardial biopsy (EMB) in patients with non-ischaemic dilated cardiomyopathies (DCM) is debated. Here we sought to determine the extent of left ventricular collagen volume fraction (LV-CVF) in DCM patients and to evaluate it as a prognostic marker.METHODS AND RESULTSIn this retrospective longitudinal study, we included 524 patients with suspected DCM who underwent left ventricular EMB (LV-EMB) as a part of their clinical work-up. LV-CVF was quantified using automated image processing of high-resolution scans of LV-EMB. Deep phenotyping was performed including assessment of late gadolinium enhancement on cardiac magnetic resonance imaging. Endpoints were (i) composite endpoint of heart failure-related death, sudden cardiac death, aborted sudden cardiac death (appropriate implantable cardioverter-defibrillator shock, reported sustained ventricular tachycardia, or cardiopulmonary resuscitation), or cardiac transplantation, and (ii) all-cause mortality. LV-EMB was associated with 0.76% major and 2.1% minor complications. No death occurred due to EMB. LV-CVF could be reliably quantified using Bayesian classification. During a median follow-up of 43.2 months (2084 patient-years), 48 patients with LV-CVF >32% and 14 patients with LV-CVF ≤32% reached the composite endpoint (log-rank p < 0.0001). A total of 62 patients reached the endpoint all-cause mortality, from which 38 presented with LV-CVF >32% and 17 with LV-CVF ≤32% (log-rank p = 0.009). In multivariable analyses, LV-CVF and N-terminal pro-B-type natriuretic peptide (NT-proBNP) (hazard ratio 2.03, 95% confidence interval 1.32-3.11) were independent predictors of unfavourable outcome.CONCLUSIONSLeft ventricular EMB is a safe diagnostic procedure. The extent of CVF in LV-EMB provides prognostic information in patients with DCM in addition to existing measures of left ventricular ejection fraction or NT-proBNP.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"78 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145083493","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}
Maria Knierim, Nico Hartmann, Wiebke Maurer, Steffen Pabel, Simon Sedej, Dirk von Lewinski, Jan Gummert, Christian Sohns, Katrin Streckfuss‐Bömeke, Samuel Sossalla
{"title":"Atrial fibrillation in end‐stage heart failure: Cellular mechanisms behind CASTLE‐HTx","authors":"Maria Knierim, Nico Hartmann, Wiebke Maurer, Steffen Pabel, Simon Sedej, Dirk von Lewinski, Jan Gummert, Christian Sohns, Katrin Streckfuss‐Bömeke, Samuel Sossalla","doi":"10.1002/ejhf.70051","DOIUrl":"https://doi.org/10.1002/ejhf.70051","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"68 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077361","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}
Gasnat Shaboodien, Charle Viljoen, Polycarp Ndibangwi, Julian Hoevelmann, Lameez Pearce, Susanna Haidari, Margherita Torchio, Federica Dagradi, Carla Spazzolini, Sarah Kraus, Ntobeko A.B. Ntusi, Peter J. Schwartz, Karen Sliwa
{"title":"Initial investigations into single nucleotide polymorphisms and their association with QTc and left ventricular function in peripartum cardiomyopathy","authors":"Gasnat Shaboodien, Charle Viljoen, Polycarp Ndibangwi, Julian Hoevelmann, Lameez Pearce, Susanna Haidari, Margherita Torchio, Federica Dagradi, Carla Spazzolini, Sarah Kraus, Ntobeko A.B. Ntusi, Peter J. Schwartz, Karen Sliwa","doi":"10.1002/ejhf.70036","DOIUrl":"https://doi.org/10.1002/ejhf.70036","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"51 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077352","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}
João Pedro Ferreira, Pedro Marques, Bernhard Haring, João Sérgio Neves
{"title":"Glucagon‐like peptide‐1 receptor agonists across the cardiovascular‐kidney‐metabolic spectrum: One size does not fit all","authors":"João Pedro Ferreira, Pedro Marques, Bernhard Haring, João Sérgio Neves","doi":"10.1002/ejhf.70055","DOIUrl":"https://doi.org/10.1002/ejhf.70055","url":null,"abstract":"","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"10 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077354","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}
Masatake Kobayashi,Kevin Duarte,João Pedro Ferreira,Guillaume Baudry,Luca Monzo,John J V McMurray,Dirk J Van Veldhuisen,Bertram Pitt,Faiez Zannad,Nicolas Girerd
AIMSMineralocorticoid receptor antagonists (MRAs) are often underused in patients with heart failure (HF) and reduced ejection fraction (HFrEF). Individual treatment effect (ITE) may assist physicians in making timely decisions about which patients are the best suited for personalized therapy. We aimed at developing and validating a model to estimate ITE of MRAs in patients with HFrEF.METHODS AND RESULTSRALES and EMPHASIS-HF trials were the derivation trials used to estimate ITE of MRAs versus placebo on cardiovascular death or HF hospitalization in HFrEF over a 2-year period using counterfactual random forest method. ITE prediction models were built using linear regression and applied to the EPHESUS trial in patients with left ventricular systolic dysfunction and/or HF after myocardial infarction. In the RALES and EMPHASIS-HF trials (n = 3887), age, body weight, blood pressure, heart rate, hypertension and diabetes prevalence, stroke history, left ventricular ejection fraction, renal function, and serum sodium and potassium concentrations were identified to determine ITE scores (adjusted R2 = 0.25). As ITE scores increased, hazard ratio for treatment effect decreased from 0.82 (95% confidence interval [CI] 0.67-1.02) at ITE score 5 to 0.47 (95% CI 0.35-0.63) at ITE score 20 (p for interaction = 0.014). In the EPHESUS trial (n = 6472), a similar pattern was observed, with greater treatment effects in patients with higher ITE scores (p for interaction = 0.007).CONCLUSIONSIn HFrEF across various clinical settings, our simple ITE model predicted individual responses to MRA therapy. Although treatment effects may be attenuated at lower ITE scores, point estimates with wide CIs still generally favour benefit, suggesting that these patients still benefit.
{"title":"An individual treatment effect approach to predict response to mineralocorticoid receptor antagonists in patients with heart failure and reduced ejection fraction.","authors":"Masatake Kobayashi,Kevin Duarte,João Pedro Ferreira,Guillaume Baudry,Luca Monzo,John J V McMurray,Dirk J Van Veldhuisen,Bertram Pitt,Faiez Zannad,Nicolas Girerd","doi":"10.1002/ejhf.70047","DOIUrl":"https://doi.org/10.1002/ejhf.70047","url":null,"abstract":"AIMSMineralocorticoid receptor antagonists (MRAs) are often underused in patients with heart failure (HF) and reduced ejection fraction (HFrEF). Individual treatment effect (ITE) may assist physicians in making timely decisions about which patients are the best suited for personalized therapy. We aimed at developing and validating a model to estimate ITE of MRAs in patients with HFrEF.METHODS AND RESULTSRALES and EMPHASIS-HF trials were the derivation trials used to estimate ITE of MRAs versus placebo on cardiovascular death or HF hospitalization in HFrEF over a 2-year period using counterfactual random forest method. ITE prediction models were built using linear regression and applied to the EPHESUS trial in patients with left ventricular systolic dysfunction and/or HF after myocardial infarction. In the RALES and EMPHASIS-HF trials (n = 3887), age, body weight, blood pressure, heart rate, hypertension and diabetes prevalence, stroke history, left ventricular ejection fraction, renal function, and serum sodium and potassium concentrations were identified to determine ITE scores (adjusted R2 = 0.25). As ITE scores increased, hazard ratio for treatment effect decreased from 0.82 (95% confidence interval [CI] 0.67-1.02) at ITE score 5 to 0.47 (95% CI 0.35-0.63) at ITE score 20 (p for interaction = 0.014). In the EPHESUS trial (n = 6472), a similar pattern was observed, with greater treatment effects in patients with higher ITE scores (p for interaction = 0.007).CONCLUSIONSIn HFrEF across various clinical settings, our simple ITE model predicted individual responses to MRA therapy. Although treatment effects may be attenuated at lower ITE scores, point estimates with wide CIs still generally favour benefit, suggesting that these patients still benefit.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"171 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068360","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}
Jonas Sundermeyer,Song Li,Van-Khue Ton,Rachna Kataria,Elric Zweck,Kevin John,Manreet K Kanwar,Jaime Hernandez-Montfort,Shashank S Sinha,A Reshad Garan,Jacob Abraham,Vanessa Blumer,Ajar Kochar,Karthikeyan Ranganathan,Gavin W Hickey,Mohit Pahuja,Scott Lundgren,Sandeep Nathan,Esther Vorovich,Shelley Hall,Wissam Khalife,Andrew Schwartzman,Ju Kim,Oleg Alec Vishnevsky,Justin Fried,Maryjane Farr,Joseph Mishkin,I-Hui Chang,Onyedika Ilonze,Alexandra Arias,Jun Nakata,Jeffrey Marbach,Hiram Bezerra,Ann Gage,Joyce Wald,Sunu Thomas,Faisal Rahman,Amirali Masoumi,Aasim Afsal,Salman Gohar,Rachel Goodman,Karol D Walec,Peter Natov,Borui Li,Paavni Sangal,Qiuyue Kong,Peter Zazzali,Neil M Harwani,Saraschandra Vallabhajosyula,Arvind Bhimaraj,Claudius Mahr,Daniel Burkhoff,Navin K Kapur
AIMSComorbidity burden is a major determinant of outcomes. Its prognostic impact on cardiogenic shock (CS) across CS subtypes remains insufficiently characterized. We aimed to characterize the prevalence and distribution of comorbidities in CS, assess their impacts on outcomes, and identify high-risk comorbidity patterns in all-cause, acute myocardial infarction-related (AMI-CS) and heart failure-related CS (HF-CS).METHODS AND RESULTSCardiogenic shock patients from the multicentre Cardiogenic Shock Working Group (CSWG) registry (2020-2024) were analysed. We used adjusted logistic regression models to assess the impact of comorbidities individually, in combination, and as a cumulative burden on in-hospital mortality. We developed the Comorbidity Risk Index for Cardiogenic Shock (COMRI-CS) to capture the association between comorbidities and CS mortality. Among 6815 patients (26.5% AMI-CS, 53.6% HF-CS), 6087 (89.3%) presented with ≥1 comorbidity, and 4390 (64.4%) with ≥3 comorbidities. In-hospital mortality increased with comorbidity burden (AMI-CS: 35.4%, 39.6%, 47.1% with 1-3, 4-6, ≥7 comorbidities, respectively; HF-CS: 19.6%, 24.9%, 27.5%, respectively). A high comorbidity burden was independently associated with a 51% higher relative mortality risk in AMI-CS (odds ratio [OR] 1.51, 95% confidence interval [CI] 1.02-2.23, p = 0.037), and a more pronounced increase of 122% in HF-CS (OR 2.22, 95% CI 1.49-3.37, p < 0.001). Distinct high-risk comorbidities and combinations were identified, varying across CS subtypes. With each COMRI-CS point, in-hospital mortality increased by ~5.5%.CONCLUSIONSIn this large real-world CS cohort, comorbidity burden was highly prevalent, varied across subtypes, and was independently associated with mortality. Integrating chronic conditions into early CS risk stratification may enhance clinical decision-making in CS management.
目的：合并症负担是结果的主要决定因素。其对心源性休克（CS）的预后影响在CS亚型中仍未充分表征。我们的目的是描述CS中合并症的患病率和分布，评估其对结果的影响，并确定全因急性心肌梗死相关（AMI-CS）和心力衰竭相关CS （HF-CS）的高风险合并症模式。方法和结果对2020-2024年多中心心源性休克工作组（CSWG）登记的心源性休克患者进行分析。我们使用调整后的逻辑回归模型来评估合并症单独、联合以及作为累积负担对住院死亡率的影响。我们开发了心源性休克共病风险指数（COMRI-CS），以捕捉共病与心源性休克死亡率之间的关系。6815例患者（AMI-CS占26.5%，HF-CS占53.6%）中，6087例（89.3%）存在≥1种合并症，4390例（64.4%）存在≥3种合并症。住院死亡率随合并症负担增加而增加（AMI-CS分别为1-3、4-6、≥7个合并症，分别为35.4%、39.6%、47.1%；HF-CS分别为19.6%、24.9%、27.5%）。AMI-CS患者较高的共病负担与相对死亡风险增加51%独立相关（比值比[OR] 1.51, 95%可信区间[CI] 1.02-2.23, p = 0.037），而HF-CS患者的相对死亡风险增加更为显著，为122%（比值比[OR] 2.22, 95% CI 1.49-3.37, p < 0.001）。确定了不同的高危合并症和组合，不同的CS亚型不同。每增加一个COMRI-CS点，住院死亡率增加约5.5%。结论：在这个庞大的现实世界CS队列中，合并症负担非常普遍，在不同亚型之间存在差异，并且与死亡率独立相关。将慢性疾病纳入早期CS风险分层可以提高CS管理的临床决策。
{"title":"Impact of comorbidity burden on outcome in patients with cardiogenic shock: A Cardiogenic Shock Working Group analysis.","authors":"Jonas Sundermeyer,Song Li,Van-Khue Ton,Rachna Kataria,Elric Zweck,Kevin John,Manreet K Kanwar,Jaime Hernandez-Montfort,Shashank S Sinha,A Reshad Garan,Jacob Abraham,Vanessa Blumer,Ajar Kochar,Karthikeyan Ranganathan,Gavin W Hickey,Mohit Pahuja,Scott Lundgren,Sandeep Nathan,Esther Vorovich,Shelley Hall,Wissam Khalife,Andrew Schwartzman,Ju Kim,Oleg Alec Vishnevsky,Justin Fried,Maryjane Farr,Joseph Mishkin,I-Hui Chang,Onyedika Ilonze,Alexandra Arias,Jun Nakata,Jeffrey Marbach,Hiram Bezerra,Ann Gage,Joyce Wald,Sunu Thomas,Faisal Rahman,Amirali Masoumi,Aasim Afsal,Salman Gohar,Rachel Goodman,Karol D Walec,Peter Natov,Borui Li,Paavni Sangal,Qiuyue Kong,Peter Zazzali,Neil M Harwani,Saraschandra Vallabhajosyula,Arvind Bhimaraj,Claudius Mahr,Daniel Burkhoff,Navin K Kapur","doi":"10.1002/ejhf.70017","DOIUrl":"https://doi.org/10.1002/ejhf.70017","url":null,"abstract":"AIMSComorbidity burden is a major determinant of outcomes. Its prognostic impact on cardiogenic shock (CS) across CS subtypes remains insufficiently characterized. We aimed to characterize the prevalence and distribution of comorbidities in CS, assess their impacts on outcomes, and identify high-risk comorbidity patterns in all-cause, acute myocardial infarction-related (AMI-CS) and heart failure-related CS (HF-CS).METHODS AND RESULTSCardiogenic shock patients from the multicentre Cardiogenic Shock Working Group (CSWG) registry (2020-2024) were analysed. We used adjusted logistic regression models to assess the impact of comorbidities individually, in combination, and as a cumulative burden on in-hospital mortality. We developed the Comorbidity Risk Index for Cardiogenic Shock (COMRI-CS) to capture the association between comorbidities and CS mortality. Among 6815 patients (26.5% AMI-CS, 53.6% HF-CS), 6087 (89.3%) presented with ≥1 comorbidity, and 4390 (64.4%) with ≥3 comorbidities. In-hospital mortality increased with comorbidity burden (AMI-CS: 35.4%, 39.6%, 47.1% with 1-3, 4-6, ≥7 comorbidities, respectively; HF-CS: 19.6%, 24.9%, 27.5%, respectively). A high comorbidity burden was independently associated with a 51% higher relative mortality risk in AMI-CS (odds ratio [OR] 1.51, 95% confidence interval [CI] 1.02-2.23, p = 0.037), and a more pronounced increase of 122% in HF-CS (OR 2.22, 95% CI 1.49-3.37, p < 0.001). Distinct high-risk comorbidities and combinations were identified, varying across CS subtypes. With each COMRI-CS point, in-hospital mortality increased by ~5.5%.CONCLUSIONSIn this large real-world CS cohort, comorbidity burden was highly prevalent, varied across subtypes, and was independently associated with mortality. Integrating chronic conditions into early CS risk stratification may enhance clinical decision-making in CS management.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"24 1","pages":""},"PeriodicalIF":18.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068359","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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