ESC Heart Failure最新文献_第3页

Adaptation of right ventricular function following tricuspid transcatheter edge-to-edge repair 三尖瓣经导管边缘到边缘修复后右心室功能的适应性。

IF 3.7 2区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

ESC Heart Failure

Pub Date : 2025-10-28 DOI: 10.1002/ehf2.70001

Sara Bombace, Sebastian Rosch, Anne R. Schöber, Maximilian von Roeder, Florian Schlotter, Karl-Philip Rommel, Recha Blessing, Christian Lücke, Matthias Gutberlet, Anna Sannino, Holger Thiele, Philipp Lurz, Karl-Patrik Kresoja

Background

The impact of tricuspid transcatheter edge-to-edge repair (T-TEER) on right ventricular (RV) remodelling remains unclear.

Objectives

This study focused on characterizing changes in RV ejection fraction (RVEF) following T-TEER and their prognostic implications.

Methods

Patients with significant tricuspid regurgitation (TR) who underwent T-TEER and cardiac magnetic resonance (CMR) imaging were included. Follow-up CMR was performed within 1 to 3 months after the procedure. Patients were classified by postprocedural RVEF change: decreased (≤−5%), stable (−4% to 4%) or increased (≥5%). The primary outcome was a composite of all-cause mortality or heart failure hospitalization.

Results

The study included 69 patients (median age 78 years; 54% female). RVEF decreased in 32 (46%), was stable in 27 (39%), and increased in 10 (15%). Compared with patients with decreased and stable RVEF, those with increased RVEF had lower baseline RVEF (43% vs. 52% and 50%, respectively, P = 0.007) and lower baseline RV to pulmonary artery coupling (0.78 vs. 1.00 and 1.18, P = 0.045). Pulmonary artery systolic pressure was lower in patients with stable RVEF (42 mmHg vs. 52 mmHg in decreased and 49 mmHg in increased RVEF group, P = 0.048). TR severity was significantly reduced in the decreased and stable RVEF groups (P < 0.001 for both) while it worsened in the increased RVEF group (P = 0.037). After T-TEER, effective RVEF rose significantly in decreased (30% to 35%) and stable (31% to 39%) groups (both P < 0.001) but tended to decline in the increased group (30% to 20%; P = 0.17). During a median follow-up of 1016 days, 16 patients died, and 15 were hospitalized for heart failure. Event rates were lowest in the stable RVEF group and highest in the increased RVEF group (log-rank P = 0.004).

Conclusions

RV response to T-TEER is heterogeneous, mostly influenced by baseline RV function, RV-PA coupling and TR progression. Only a minority of patients exhibited an increase in RVEF post T-TEER, and these patients showed worsening TR and a poorer prognosis.

背景：三尖瓣经导管边缘到边缘修复（T-TEER）对右心室（RV）重塑的影响尚不清楚。目的：本研究的重点是表征T-TEER后右室射血分数（RVEF）的变化及其预后意义。方法：对有明显三尖瓣反流（TR）的患者进行T-TEER和心脏磁共振（CMR）成像。术后1 ~ 3个月随访CMR。根据术后RVEF变化将患者分为降低（≤-5%）、稳定（-4% ~ 4%）或升高（≥5%）。主要结局是全因死亡率或心力衰竭住院的综合结果。结果：研究纳入69例患者（中位年龄78岁，女性54%）。RVEF下降32例（46%），稳定27例（39%），升高10例（15%）。与RVEF降低和稳定的患者相比，RVEF升高的患者基线RVEF较低（分别为43%比52%和50%，P = 0.007），基线RV -肺动脉耦合较低（0.78比1.00和1.18,P = 0.045）。稳定RVEF患者肺动脉收缩压较低（42 mmHg， RVEF降低组为52 mmHg， RVEF升高组为49 mmHg， P = 0.048）。结论：RV对T-TEER的反应是不均匀的，主要受基线RV功能、RV- pa耦合和TR进展的影响。只有少数患者在T-TEER后RVEF增加，这些患者TR恶化，预后较差。

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引用次数: 0

Reply to the letter ‘Methodological issues in outpatient worsening heart failure research’ 回复“门诊加重心力衰竭研究的方法学问题”信函。

IF 3.7 2区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

ESC Heart Failure

Pub Date : 2025-10-28 DOI: 10.1002/ehf2.70010

Joseph McCambridge, Kenneth McDonald

<p>My co-authors and I would like to thank Dr. Hnid for his response to our recently published article, ‘A prospective analysis of management and outcomes of worsening heart failure (WHF) in the outpatient setting’.<span><sup>1</sup></span> He raised several interesting points we would like to address.</p><p>Firstly, a concern was raised about the use of two diagnostic definitions of WHF in the study, which allowed for the inclusion of patients who did not meet the objective criteria for WHF requiring at least one symptom, one physical sign, and a third feature of WHF. As stated in the paper, this was done to provide insight into the prevalence and risk of subclinical or ‘silent’ heart failure (HF) deterioration. It is being increasingly recognised that the inability to detect asymptomatic but clinically meaningful worsening is a limitation of the current standard definition for WHF.<span><sup>2</sup></span> While we acknowledge that diagnosis based on physician discretion can lead to misclassification, all patients in our study were defined as having WHF by cardiologists working in a specialist HF clinic. Indeed, patients who were treated for WHF in the emergency department without admission were actually excluded from the study to minimise misclassification, as these patients would often have been diagnosed and treated by non-specialists.</p><p>Secondly, we acknowledge, as mentioned in the article, that the small cohort sample size from a single centre is an inherent limitation of the study. The well-resourced nature of our HF unit is relatively unique and may also limit the applicability of these findings. However, this may also suggest that our study potentially underestimates the prognostic risk associated with outpatient WHF, particularly in areas without a comparable ambulatory care service.</p><p>Thirdly, it was highlighted that approximately half of the patients in our cohort with HF and reduced ejection fraction of less than 40% (HFrEF) were on optimal guideline-directed medical therapy (GDMT) at the time of WHF diagnosis, which could have contributed to a higher rate of adverse outcomes. The absolute number of HFrEF patients not on GDMT (<i>n</i> = 45 out of 87) was small, and it was noted that the rate of initial stabilisation after WHF (75.6%, 34/45) was similar to the overall study cohort (78.6%, 184/234) and those with HFrEF on optimal GDMT (78.6%, 33/42). Anecdotally, many of the patients not on optimal GDMT had either a recent HF diagnosis and presented with WHF during uptitration or were last seen in clinic before the use of sodium-glucose cotransporter 2 (SGLT2) inhibitors became widespread. Difficulties in achieving optimal GDMT are also an ongoing challenge worldwide<span><sup>3</sup></span> with a recent study showing that only 50% of patients with chronic HFrEF were on optimal medical therapy.<span><sup>4</sup></span> This ubiquitous challenge in HFrEF care may even argue for the ‘real world’ applicability of our findings.<

我和我的合著者感谢Hnid博士对我们最近发表的文章《门诊加重心力衰竭（WHF）的管理和结果的前瞻性分析》的回应他提出了几个有趣的观点，我们想谈谈。首先，研究中对WHF的两种诊断定义的使用引起了关注，这允许将不符合WHF客观标准的患者包括在内，这些患者需要至少一种症状、一种体征和WHF的第三个特征。如文中所述，这样做是为了深入了解亚临床或“沉默”心力衰竭（HF）恶化的患病率和风险。越来越多的人认识到，无法发现无症状但临床上有意义的恶化是目前WHF标准定义的局限性。2虽然我们承认，基于医生判断的诊断可能导致错误分类，但我们研究中的所有患者都被心衰专科诊所的心脏病专家定义为患有WHF。事实上，在急诊科接受WHF治疗而未入院的患者实际上被排除在研究之外，以尽量减少错误分类，因为这些患者通常是由非专科医生诊断和治疗的。其次，我们承认，正如文章中提到的，来自单一中心的小队列样本量是该研究的固有局限性。我们的心衰单位资源丰富的性质是相对独特的，也可能限制了这些发现的适用性。然而，这也可能表明我们的研究可能低估了与门诊WHF相关的预后风险，特别是在没有类似门诊护理服务的地区。第三，值得强调的是，在我们的队列中，大约有一半的心衰患者和射血分数降低低于40% （HFrEF）的患者在诊断为心衰时正在接受最佳指导药物治疗（GDMT），这可能导致更高的不良结局发生率。未接受GDMT治疗的HFrEF患者的绝对数量很少（n = 45 / 87），值得注意的是，WHF后的初始稳定率（75.6%,34/45）与总体研究队列（78.6%,184/234）和接受最佳GDMT治疗的HFrEF患者（78.6%,33/42）相似。有趣的是，许多未接受最佳GDMT治疗的患者要么最近被诊断为心衰，并在升级期间出现WHF，要么是在广泛使用钠-葡萄糖共转运蛋白2 （SGLT2）抑制剂之前最后一次出现在临床。在全球范围内，实现最佳GDMT的困难也是一个持续的挑战，最近的一项研究表明，只有50%的慢性HFrEF患者接受了最佳药物治疗这一在HFrEF治疗中普遍存在的挑战甚至可能会为我们的研究结果在“现实世界”中的适用性争论。最后，Hnid博士强调，正如我们在文章中详细讨论的那样，仅根据临床症状和体格检查来定义心衰的临床稳定性存在局限性。我们强烈同意临床稳定性需要一个更客观的生物学定义，并认为我们的研究结果说明了这一点的必要性。没有宣布。

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引用次数: 0

Letter to the editor: Soluble urokinase plasminogen activator receptor and outcomes in HFpEF: A TOPCAT ancillary study 致编辑：可溶性尿激酶纤溶酶原激活剂受体和HFpEF的结局：一项TOPCAT辅助研究。

IF 3.7 2区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

ESC Heart Failure

Pub Date : 2025-10-28 DOI: 10.1002/ehf2.70012

Ahmed Raza, Shahzadi Gulfishan

<p>The recently published study by Hutten et al.<span><sup>1</sup></span> provides valuable insights into the prognostic role of Soluble urokinase plasminogen activator receptor (suPAR) as a biomarker in patients with heart failure with preserved ejection fraction (HFpEF). The authors are to be commended for addressing this timely and clinically significant topic, as it sheds light on the complex interplay between inflammation and cardiovascular outcomes, while also exploring the relationship between suPAR and mineralocorticoid receptor antagonist therapy. Their work adds depth to the ongoing search for biomarkers that can improve risk stratification in HFpEF and potentially guide therapeutic decision-making. However, it has the following limitations.</p><p>First, there is a lack of a healthy control or external comparator group. Without a non-HFpEF comparator, it is difficult to determine whether elevated suPAR is uniquely predictive in HFpEF or simply reflects chronic inflammation seen across many comorbid states (CKD, diabetes, obesity). This reduces the specificity of suPAR as a HFpEF biomarker. A study by Fujisaka et al.<span><sup>2</sup></span> on suPAR and cardiac diastolic dysfunction reported similar concerns, noting that the absence of control groups limits the interpretation of suPAR as a disease-specific marker. Second, suPAR is a nonspecific inflammatory biomarker. suPAR reflects systemic immune activation and is elevated in diverse conditions (e.g., infections, CKD and diabetes). This non-specificity may inflate associations with outcomes in HFpEF, as comorbidities rather than HFpEF itself could drive elevated risk. Dupuy et al.<span><sup>3</sup></span> reported that suPAR had prognostic value in chronic HF broadly but lacked discriminatory ability in specific phenotypes like HFpEF, raising concerns about the overestimation of disease specificity. Third, there is a limited temporal biomarker assessment. Only baseline and 1-year suPAR levels were measured. This snapshot view misses dynamic changes in suPAR that may better predict clinical outcomes. A pilot study by Ohnewein et al.<span><sup>4</sup></span> tracking novel biomarkers in HF patients showed that dynamic monitoring (sST2, suPAR and GDF-15) improved prognostic insights compared to single measurements. Finally, there is geographic and ethnic homogeneity of the cohort. The study used only the North American TOPCAT cohort, predominantly White participants (91.6%). This limits generalizability to more diverse HFpEF populations, especially since HFpEF prevalence and inflammatory burden vary across ethnic groups. A study done by Pfeffer et al.<span><sup>5</sup></span> shows that regional variation in the TOPCAT trial itself significantly altered observed outcomes, underlining the risk of overgeneralization.</p><p>Future HFpEF biomarker studies should not only include healthy controls and non-HFpEF heart failure populations to clarify whether suPAR elevations are disease-specific

Hutten等人最近发表的研究1为可溶性尿激酶纤溶酶原激活物受体（suPAR）作为生物标志物在保留射血分数（HFpEF）心力衰竭患者的预后作用提供了有价值的见解。作者应对这一及时且具有临床意义的主题表示赞赏，因为它揭示了炎症和心血管结局之间复杂的相互作用，同时也探索了suPAR和矿皮质激素受体拮抗剂治疗之间的关系。他们的工作为正在进行的生物标志物研究增加了深度，这些生物标志物可以改善HFpEF的风险分层，并可能指导治疗决策。然而，它有以下限制。首先，缺乏健康的对照或外部比较组。如果没有非HFpEF比较物，很难确定suPAR升高是HFpEF的唯一预测指标，还是仅仅反映了许多共病状态（CKD、糖尿病、肥胖）的慢性炎症。这降低了suPAR作为HFpEF生物标志物的特异性。Fujisaka等人的一项关于suPAR和心脏舒张功能障碍的研究报告了类似的担忧，并指出缺乏对照组限制了suPAR作为疾病特异性标志物的解释。其次，suPAR是一种非特异性炎症生物标志物。suPAR反映了全身免疫激活，并在多种情况下（如感染、慢性肾病和糖尿病）升高。这种非特异性可能会夸大与HFpEF结果的关联，因为合并症而不是HFpEF本身可能导致风险升高。Dupuy等人3报道，suPAR在慢性心衰中具有广泛的预后价值，但在HFpEF等特定表型中缺乏区分能力，这引起了对疾病特异性高估的担忧。第三，有一个有限的时间生物标志物评估。仅测量基线和1年suPAR水平。这种快照视图忽略了suPAR的动态变化，而这些变化可能更好地预测临床结果。Ohnewein等人进行的一项试点研究显示，与单一测量相比，动态监测（sST2、suPAR和GDF-15）可改善预后。最后，研究对象在地理和种族上存在同质性。该研究仅使用了北美TOPCAT队列，主要是白人参与者（91.6%）。这限制了对更多样化的HFpEF人群的推广，特别是因为HFpEF的患病率和炎症负担因种族而异。Pfeffer等人的一项研究表明，TOPCAT试验本身的区域差异显著地改变了观察到的结果，强调了过度概括的风险。未来的HFpEF生物标志物研究不仅应该包括健康对照和非HFpEF心力衰竭人群，以明确suPAR升高是疾病特异性的还是仅仅反映合合症驱动的炎症，还应该整合多标志物面板，将suPAR与hf特异性生物标志物（如n端前b型利钠肽、ST2和半凝集素-3）结合起来，以提高诊断精度。此外，定期（6-12个月）的连续生物标志物采样将为预后轨迹和治疗反应性提供有价值的见解。为了确保全球适用性，未来的试验还必须优先考虑种族和地域多样化的患者招募，解决当前同质队列的局限性。总之，虽然Hutten等人通过强调suPAR在HFpEF中的预后潜力做出了重要贡献，但其非特异性、有限的时间评估和缺乏多样化的比较物限制了其临床适用性。未来的研究应通过纳入适当的对照组、纵向生物标志物监测、整合多标志物小组和招募不同人群来解决这些差距，以更准确地定义suPAR在HFpEF管理中的作用。所有作者都阅读并认可了稿件的最终版本。他们对数据的完整性和数据分析的准确性承担全部责任。作者声明无利益冲突。作者确认，本手稿是对所报道研究的诚实、准确和透明的描述，没有遗漏研究的任何重要方面，并且已经解释了计划研究中的任何差异（如果相关，已登记）。数据共享不适用于本文，因为在当前研究中没有生成数据集；所有数据均来源于已发表的文献。

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引用次数: 0

Role of NPPB for recovery post ventricular assist device in paediatric dilated cardiomyopathy: Single-cell multiomics NPPB在小儿扩张型心肌病心室辅助装置后恢复中的作用：单细胞多组学。

IF 3.7 2区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

ESC Heart Failure

Pub Date : 2025-10-20 DOI: 10.1002/ehf2.15430

Yosuke Kugo, Takuji Kawamura, Akima Harada, Yuji Tominaga, Kenji Miki, Hidekazu Ishida, Takayoshi Ueno, Shigeru Miyagawa

Aims

Paediatric heart transplantation requires lifelong immunosuppression, highlighting the need for recovery-oriented strategies. A subset of children with dilated cardiomyopathy (DCM) recovers left ventricular (LV) function after LV assist device (LVAD) implantation, allowing for device explantation. We aimed to identify factors associated with LV functional recovery using single-nucleus multiomics analysis of LV tissue collected at LVAD implantation.