IJC Heart and Vasculature最新文献_第10页

Incidence of acute heart failure with and without concomitant pulmonary disease 急性心力衰竭伴或不伴肺部疾病的发生率

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-09 DOI: 10.1016/j.ijcha.2025.101837

Ida Arentz Taraldsen , Jasmin Dam Lukoschewitz , Aginsha Kandiah , Frederik Dencker Wisborg , Mohammed El-Sheikh , Nora Olsen El Caidi , Ove Andersen , Jens Dahlgaard Hove , Johannes Grand

Background

Acute heart failure (AHF) is the primary diagnosis in over one million emergency department (ED) hospitalizations each year in the United States (USA). The patients are often comorbid, with several competing causes for their symptoms, especially pulmonary diseases. The purpose of this study is to investigate the incidence and characteristics of patients admitted with AHF with and without concomitant pulmonary disease, compared to patients without AHF, in a large hospital in Denmark. Secondly, to investigate the mortality rate in AHF and how it is influenced by concomitant pulmonary disease.

Methods

We conducted a prospective cohort study at the medical ED at a large university hospital in Denmark in a two-year period during the Corona Virus Disease pandemic. Patient records were screened by trained cardiologists, to identify patients admitted with AHF. The cohort was stratified by AHF status and concomitant pulmonary disease.

Results

We included 7258 patients, of whom found 408 (5.6 %) patients had AHF. In the group with AHF, 106 patients (26 %) had a competing concomitant pulmonary cause of admission. The incidence rate for admission with AHF was 91/100.000 inhabitants/year. In a multivariable cox regression model, AHF was independently associated with mortality with an adjusted hazard ratio of 1.34 (1.13–1.58), p value <0.001. Pulmonary disease was associated with a worse prognosis in the group with AHF (HR_adj 1.74 (1.24–2.44), p-value < 0.001).

Conclusion

In this prospective observational cohort study, 5–7 % of all admissions to the medical ED was caused by AHF, and was associated with worse outcomes than patients without AHF. Concomitant pulmonary admission disease was associated with a worse prognosis among patients with AHF.

背景：急性心力衰竭（AHF）是美国每年超过100万急诊住院患者的主要诊断。这些患者通常是合并症，他们的症状有几个相互竞争的原因，尤其是肺部疾病。本研究的目的是调查丹麦一家大医院AHF合并和不合并肺部疾病患者与不合并AHF患者的发病率和特征。其次，探讨AHF的死亡率及其与合并肺部疾病的关系。方法在冠状病毒病大流行期间，我们在丹麦一家大型大学医院的内科急诊科进行了为期两年的前瞻性队列研究。患者记录由训练有素的心脏病专家筛选，以确定患有AHF的患者。该队列根据AHF状况和合并肺部疾病进行分层。结果共纳入7258例患者，其中408例（5.6%）为AHF。在AHF组中，106例患者（26%）有竞争合并肺部入院原因。住院AHF的发病率为91/10万居民/年。在多变量cox回归模型中，AHF与死亡率独立相关，校正风险比为1.34 (1.13-1.58)，p值<；0.001。肺部疾病与AHF组较差的预后相关（HRadj 1.74 (1.24-2.44)， p值<； 0.001）。结论：在这项前瞻性观察队列研究中，5 - 7%的内科急症是由AHF引起的，与无AHF的患者相比，这些患者的预后更差。合并肺部入院疾病与AHF患者较差的预后相关。

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引用次数: 0

Pericarditis at the crossroads: Unlocking the next wave of therapies 十字路口的心包炎：开启下一波治疗浪潮

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-08 DOI: 10.1016/j.ijcha.2025.101841

Massimo Imazio , Francesco Venturelli , Maria Cristina Tomat , Giulio Savonitto , Davide Stolfo , Valentino Collini

Pericarditis is an inflammation of the pericardial sac with different aetiologies. While often self-limited, up to 30 % of cases recur or become chronic, causing significant morbidity. Traditional treatments – nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids – have important limitations, including steroid dependence, high recurrence rates, and side effects. Accordingly, new targeted immunomodulatory therapies are under investigation to improve outcomes in refractory pericarditis. This review outlines the epidemiology and burden of pericarditis, current management and its shortcomings, and the rationale for novel therapies. We then discuss emerging therapeutic agents in development (biologics and small molecules), focusing on phase II/III candidates. The central role of interleukin-1 (IL-1) and related inflammasome pathways in pericardial inflammation provides a strong rationale for these targeted treatments. Key trials of IL-1 inhibitors (anakinra, rilonacept, canakinumab, goflikicept) have demonstrated dramatic reductions in recurrence rates, validating IL-1 as a therapeutic target. Other innovative approaches – such as NLRP3 inflammasome inhibitors and a cannabinoid-based agent – offer the prospect of oral, steroid-sparing therapy. We highlight the current challenges in developing these therapies, including heterogeneous disease causes, safety concerns, and trial design issues. Overall, the therapeutic pipeline for pericarditis is robust and poised to transform management. In the coming years, integration of targeted biologics and small molecules alongside conventional anti-inflammatories may significantly improve outcomes in recurrent pericarditis, moving towards more precise and effective treatment strategies.

心包炎是一种病因不同的心包囊炎症。虽然通常是自限性的，但高达30%的病例会复发或变成慢性疾病，造成严重的发病率。传统的治疗方法——非甾体抗炎药（NSAIDs）、秋水仙碱和皮质类固醇——有重要的局限性，包括类固醇依赖性、高复发率和副作用。因此，新的靶向免疫调节疗法正在研究中，以改善难治性心包炎的预后。这篇综述概述了心包炎的流行病学和负担，目前的管理和缺点，以及新疗法的基本原理。然后，我们讨论了正在开发的新兴治疗药物（生物制剂和小分子），重点是II/III期候选药物。白细胞介素-1 （IL-1）和相关炎性体通路在心包炎症中的核心作用为这些靶向治疗提供了强有力的理论依据。IL-1抑制剂（anakinra, rilonacept, canakinumab, goflikicept）的关键试验显示复发率显着降低，验证了IL-1作为治疗靶点。其他创新方法，如NLRP3炎性体抑制剂和一种基于大麻素的药物，提供了口服类固醇治疗的前景。我们强调了目前开发这些疗法的挑战，包括异质性疾病病因、安全性问题和试验设计问题。总的来说，心包炎的治疗途径是稳健的，并准备改变管理。在未来几年，靶向生物制剂和小分子药物与传统抗炎药的结合可能会显著改善复发性心包炎的预后，朝着更精确和有效的治疗策略发展。

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引用次数: 0

Prognostic impact of the number and Temporality of heart failure Hospitalisations: Analysis of a National healthcare database 心力衰竭住院人数和时间对预后的影响：对国家卫生保健数据库的分析

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-08 DOI: 10.1016/j.ijcha.2025.101833

Damien Logeart , François Roubille , Muriel Salvat , Christophe Tribouilloy , Fabrice Bauer , Jean-Christophe Eicher , François Picard , Jean-Jacques Von Hunolstein , Jean-Noël Trochu , Pascal de Groote , Emmanuelle Berthelot , Francis Fagnani , Leila Batel , Maxime Doublet , Thibaud Damy , Richard Isnard

Aims

To assess the prognostic impact of both the frequency and timing of prior heart failure (HF) hospitalisations on outcomes in patients with reduced left ventricular ejection fraction (LVEF).

Methods and results

This nationwide retrospective cohort study used the French national health insurance database to identify 730,052 adults with HF in 2017. A validated algorithm classified 226,747 as HF with reduced LVEF (<45 %), of whom 54,504 (24 %) had at least one HF-related hospitalisation >24 h within the preceding 24 months (worsening HF group). Patients were stratified by (1) time since the last HF hospitalisation (0–6, 6–24 months) and (2) number of hospitalisations (1, 2, ≥3). Mean age was 76 ± 15 years. Prior HF hospitalisation was the strongest predictor of mortality among all variables. After multivariable adjustment, prior hospitalisation was associated with increased risk of all-cause death (HR 1.61, 95 % CI 1.56–1.65), all-cause hospitalisation (HR 1.34, 95 % CI 1.32–1.37), and recurrent HF hospitalisation (HR 2.51, 95 % CI 2.43–2.59). Risks were greatest when the most recent hospitalisation occurred within 6 months and rose progressively with the number of prior events.

Conclusion

In patients with reduced LVEF, both recent and recurrent HF hospitalisations are strong predictors of mortality and rehospitalisation. These two simple markers identify highly vulnerable patients and should trigger intensified follow-up, optimisation of guideline-directed therapies, and implementation of transitional care and remote monitoring programs.

目的评估心力衰竭（HF）住院次数和时间对左室射血分数（LVEF）降低患者预后的影响。方法和结果：这项全国性的回顾性队列研究使用法国国家健康保险数据库，在2017年确定了730,052名HF成年人。经过验证的算法将226,747例患者归类为LVEF降低的HF(45%)，其中54,504例（24%）在过去24个月内至少有一次与HF相关的住院治疗（24小时）（恶化型HF组）。患者按(1)自上次HF住院时间（0-6个月、6-24个月）和(2)住院次数（1、2、≥3）进行分层。平均年龄76±15岁。在所有变量中，既往心力衰竭住院是死亡率最强的预测因子。多变量调整后，既往住院与全因死亡（HR 1.61, 95% CI 1.56-1.65）、全因住院（HR 1.34, 95% CI 1.32-1.37）和复发性心衰住院（HR 2.51, 95% CI 2.43-2.59）的风险增加相关。当最近一次住院发生在6个月内时，风险最大，并随着先前事件的次数逐渐增加。结论在LVEF降低的患者中，近期和复发心衰住院是死亡率和再住院的重要预测因素。这两种简单的标记物可识别高度脆弱的患者，并应加强随访，优化指导治疗，实施过渡护理和远程监测计划。

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引用次数: 0

Integrated proteomics and metabolomics analyses reveal potential molecular signatures of rabbit atherosclerotic plaques 综合蛋白质组学和代谢组学分析揭示了兔动脉粥样硬化斑块的潜在分子特征

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-08 DOI: 10.1016/j.ijcha.2025.101840

Chunfang Zan , Tianxiong Ji , Xinyu Zhang , Min-Fu Yang , Zhifang Wu , Sijin Li

Objective

This study aims to explore potential mechanisms associated with differentially abundant proteins and metabolites in rabbit plaques through integrated proteomics and untargeted metabolomics analyses.

Methods

Experimental rabbits were randomly divided into the model group and the sham group. Abdominal aortas were isolated, collected, and treated with proteinase K. Subsequently, a tandem mass tag (TMT)-labeled quantitative proteomics analysis and an untargeted metabolomics analysis via liquid chromatography-mass spectrometry (LC-MS) of abdominal aortas were performed to evaluate the possible protein and metabolite fingerprints in arterial plaques. Acquired data were analyzed using uni‐ and multivariate statistics. The correlation between differentially abundant proteins and metabolites was analyzed using the Pearson correlation coefficient strategy, and their possibly involved functional pathways were predicted by Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis.

Results

Advanced plaques develop in the model group. A total of 207 proteins are significantly altered in injured aortas compared to uninjured ones, with 133 upregulated and 74 downregulated proteins (fold changes > 1.2, P < 0.05). In plaques, 234 metabolites are significantly changed under the positive ion mode, and 187 under the negative ion mode. Notably, increases are observed in phosphatidylcholines (PCs) [PC 9:0] and lysophosphatidylcholines (LPCs) [LPC 20:2], two key lipid components. These metabolites are involved in some key metabolic pathways, including purine metabolism and vascular smooth muscle contraction.

Conclusions

The results confirm the potential of integrated proteomics and untargeted metabolomics in exploring the molecular characteristics of atherosclerosis. Identified proteins and metabolites may serve as promising biomarkers for plaque diagnosis.

目的本研究旨在通过综合蛋白质组学和非靶向代谢组学分析，探索兔斑块中差异丰富的蛋白质和代谢物的潜在机制。方法将实验兔随机分为模型组和假手术组。分离、收集腹主动脉并用蛋白酶k处理，随后对腹主动脉进行串联质量标签（TMT）标记的定量蛋白质组学分析和液相色谱-质谱（LC-MS）的非靶向代谢组学分析，以评估动脉斑块中可能的蛋白质和代谢物指纹图谱。使用单变量和多变量统计分析获得的数据。利用Pearson相关系数分析差异丰富蛋白与代谢物之间的相关性，并利用京都基因基因组百科全书（KEGG）富集分析预测其可能参与的功能通路。结果模型组出现晚期斑块。损伤主动脉与未损伤主动脉相比，共有207个蛋白发生显著改变，其中133个蛋白上调，74个蛋白下调（fold changes > 1.2, P < 0.05）。在斑块中，234种代谢物在正离子模式下发生显著变化，187种在负离子模式下发生显著变化。值得注意的是，两种关键的脂质成分磷脂酰胆碱（PCs） [pc9:0]和溶血磷脂酰胆碱（LPCs） [LPC 20:2]的含量均有所增加。这些代谢物参与一些关键的代谢途径，包括嘌呤代谢和血管平滑肌收缩。结论综合蛋白质组学和非靶向代谢组学在探索动脉粥样硬化分子特征方面具有一定的潜力。鉴定的蛋白质和代谢物可能作为斑块诊断的有希望的生物标志物。

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引用次数: 0

Thromboembolic risk of electrical cardioversion in patients with cardiogenic shock 心源性休克患者电转复的血栓栓塞风险

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-06 DOI: 10.1016/j.ijcha.2025.101835

Jonas Gmeiner , Lea Haag , Enzo Lüsebrink , Jan-Philipp Simon , Felix Michelson , Elina Oesterhaus , Wolf-Stephan Rudi , Ludwig Weckbach , Stefan Kääb , Michael Näbauer , Sven Peterß , Christopher Stremmel , Steffen Massberg , Martin Orban , Moritz F. Sinner , Clemens Scherer

Background

Cardiogenic shock patients with atrial fibrillation or flutter often require acute cardioversion despite absence of sufficient anticoagulation or the possibility to rule out left atrial appendage thrombus. Thromboembolic risk in these patients is unknown.

Methods

In this study, all cardiogenic shock patients from the LMUshock registry undergoing electrical cardioversion for atrial fibrillation or atrial flutter were included. The primary endpoint was new thromboembolic stroke or systemic embolism at 30 days. Secondary endpoints included performance of transesophageal echocardiography, all-cause mortality and bleeding according to BARC.

Results

Of 140 patients undergoing electrical cardioversion, 36 had preexisting and 104 experienced new onset of atrial fibrillation or flutter during ICU stay. Of these, 87.1 % had anticoagulation with unfractionated heparin and anticoagulation was adjudicated sufficient in 44.3 % at the time of cardioversion. Transesophageal echocardiography was performed in 37.9 % of patients before cardioversion. The primary endpoint was met in 3 patients (2.1 %), all of which had insufficient anticoagulation. All-cause mortality at 30 days was 37.9 % and bleeding ≥ BARC type 3a was found in 12.9 %.

Conclusions

Thromboembolic risk of electrical cardioversion was low despite the limited utilization of transesophageal echocardiography. This may be attributed to the routine administration of therapeutic anticoagulation in this study, but a high incidence of bleeding was observed.

背景：心源性休克合并心房颤动或扑动的患者，尽管没有足够的抗凝治疗或排除左心房附件血栓的可能性，但往往需要急性心律转复。这些患者的血栓栓塞风险尚不清楚。方法本研究纳入lmusshock登记的所有因心房颤动或心房扑动而接受电复律治疗的心源性休克患者。主要终点是30天内新的血栓栓塞性卒中或全身性栓塞。次要终点包括经食管超声心动图表现、全因死亡率和根据BARC的出血。结果140例电复律患者中，36例已存在心房颤动或扑动，104例在ICU住院期间新发。其中，87.1%的患者使用了未分级肝素抗凝治疗，44.3%的患者在复律时认为抗凝治疗是充分的。37.9%的患者在复律前进行了经食管超声心动图检查。3例（2.1%）患者达到了主要终点，所有患者抗凝治疗不足。30天全因死亡率为37.9%，出血≥BARC 3a型占12.9%。结论尽管经食管超声心动图的应用有限，但电转复的血栓栓塞风险较低。这可能是由于在本研究中常规给予治疗性抗凝，但观察到出血的发生率很高。

{"title":"Thromboembolic risk of electrical cardioversion in patients with cardiogenic shock","authors":"Jonas Gmeiner , Lea Haag , Enzo Lüsebrink , Jan-Philipp Simon , Felix Michelson , Elina Oesterhaus , Wolf-Stephan Rudi , Ludwig Weckbach , Stefan Kääb , Michael Näbauer , Sven Peterß , Christopher Stremmel , Steffen Massberg , Martin Orban , Moritz F. Sinner , Clemens Scherer","doi":"10.1016/j.ijcha.2025.101835","DOIUrl":"10.1016/j.ijcha.2025.101835","url":null,"abstract":"<div><h3>Background</h3><div>Cardiogenic shock patients with atrial fibrillation or flutter often require acute cardioversion despite absence of sufficient anticoagulation or the possibility to rule out left atrial appendage thrombus. Thromboembolic risk in these patients is unknown.</div></div><div><h3>Methods</h3><div>In this study, all cardiogenic shock patients from the LMUshock registry undergoing electrical cardioversion for atrial fibrillation or atrial flutter were included. The primary endpoint was new thromboembolic stroke or systemic embolism at 30 days. Secondary endpoints included performance of transesophageal echocardiography, all-cause mortality and bleeding according to BARC.</div></div><div><h3>Results</h3><div>Of 140 patients undergoing electrical cardioversion, 36 had preexisting and 104 experienced new onset of atrial fibrillation or flutter during ICU stay. Of these, 87.1 % had anticoagulation with unfractionated heparin and anticoagulation was adjudicated sufficient in 44.3 % at the time of cardioversion. Transesophageal echocardiography was performed in 37.9 % of patients before cardioversion. The primary endpoint was met in 3 patients (2.1 %), all of which had insufficient anticoagulation. All-cause mortality at 30 days was 37.9 % and bleeding ≥ BARC type 3a was found in 12.9 %.</div></div><div><h3>Conclusions</h3><div>Thromboembolic risk of electrical cardioversion was low despite the limited utilization of transesophageal echocardiography. This may be attributed to the routine administration of therapeutic anticoagulation in this study, but a high incidence of bleeding was observed.</div></div>","PeriodicalId":38026,"journal":{"name":"IJC Heart and Vasculature","volume":"61 ","pages":"Article 101835"},"PeriodicalIF":2.5,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High-sensitivity C-reactive protein is associated with altered cardiac structure and function in psoriasis: The PSOCADIA study 高敏c反应蛋白与银屑病患者心脏结构和功能改变有关：PSOCADIA研究

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-11-03 DOI: 10.1016/j.ijcha.2025.101832

Maria Dons , Morten Sengeløv , Kristoffer Grundtvig Skaarup , Niklas Dyrby Johansen , Mats C.H. Lassen , Sofie Bøgh-Sørensen , Julie I.H. Borchsenius , Filip Soeskov Davidovski , Nino E. Landler , Christoffer V. Nissen , Peter Riis Hansen , Brittany N. Weber , Claus Zachariae , Lone Skov , Tor Biering-Sørensen

Background

High sensitivity C-reactive protein (hsCRP) is a biomarker of systemic inflammation that may be associated with cardiovascular risk in psoriasis. We assessed the relationship between hsCRP levels and cardiac structure and function in a large cross-sectional cohort study of individuals with psoriasis.

Methods

Adults with psoriasis underwent hsCRP testing and transthoracic echocardiography. Myocardial dysfunction was defined as left ventricular ejection fraction < 50 % and/or global longitudinal strain (GLS) < 16 %. Diastolic dysfunction followed standard echocardiographic guidelines. Associations between hsCRP tertiles, cardiometabolic risk factors, and cardiac structure and function were evaluated. Logistic regression assessed odds of myocardial dysfunction with hsCRP > 2 mg/L.

Results

972 adults with psoriasis were prospectively included (median age 54 years, 44.9 % women, 75.2 % moderate-to-severe psoriasis). Median hsCRP was 1.14 mg/L. Lower hsCRP levels were linked to greater biologic therapy use. Higher hsCRP was associated with older age, female sex, increased body mass index, and greater cardiometabolic risk factor burden.

The highest hsCRP tertile had greater rates of myocardial dysfunction (28.8 %) and diastolic dysfunction (31.3 %) compared to the lowest tertile (17.6 % and 21.8 %, respectively, p < 0.05 for both). After multivariable adjustment, increasing hsCRP was associated with impaired GLS and LVEF, and an hsCRP > 2 mg/L was independently associated with a 45 % increased odds of myocardial dysfunction (OR 1.45, 95 % CI: 1.02 – 2.07, p = 0.042).

Conclusions

In psoriasis, elevated hsCRP was independently associated with impaired systolic function, reflected by reduced GLS and LVEF. These findings suggest systemic inflammation may be involved in early myocardial dysfunction in this population.

背景：高灵敏度c反应蛋白（hsCRP）是全身性炎症的生物标志物，可能与银屑病的心血管风险相关。我们在一项针对牛皮癣患者的大型横断面队列研究中评估了hsCRP水平与心脏结构和功能之间的关系。方法对成人银屑病患者行hsCRP检测和经胸超声心动图检查。心肌功能障碍定义为左心室射血分数（llt; 50%）和/或整体纵向应变（GLS）（llt; 16%）。舒张功能不全符合超声心动图标准。评估hsCRP类型、心脏代谢危险因素和心脏结构和功能之间的关系。Logistic回归评估2 mg/L hsCRP引起心肌功能障碍的几率。结果前瞻性纳入972例成人牛皮癣患者（中位年龄54岁，44.9%为女性，75.2%为中度至重度牛皮癣）。中位hsCRP为1.14 mg/L。较低的hsCRP水平与更多的生物治疗使用有关。较高的hsCRP与年龄较大、女性、体重指数增加和更大的心脏代谢危险因素负担相关。高hsCRP组的心肌功能障碍发生率（28.8%）和舒张功能障碍发生率（31.3%）高于低hsCRP组（分别为17.6%和21.8%,p < 0.05）。多变量调整后，hsCRP升高与GLS和LVEF受损相关，2 mg/L hsCRP与心肌功能障碍发生率增加45%独立相关（OR 1.45, 95% CI: 1.02 - 2.07, p = 0.042）。结论银屑病患者hsCRP升高与收缩功能受损独立相关，表现为GLS和LVEF降低。这些发现提示全身性炎症可能与该人群早期心肌功能障碍有关。

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引用次数: 0

Macrophage Phospholipase D3 promotes atherosclerosis via exacerbating foam cell formation and inducing inflammatory responses 巨噬细胞磷脂酶D3通过加剧泡沫细胞形成和诱导炎症反应来促进动脉粥样硬化

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-10-31 DOI: 10.1016/j.ijcha.2025.101834

Teng Li , Xiaobao Gu , Xiangyang Yin , Pengbo Zhai , Hongxu Yan , Zixun Wang , Yang Li , Bing Wang

Background

Atherosclerosis is a chronic inflammatory disease and a major cause of global morbidity and mortality. Phospholipase D3 (PLD3) has been reported to be elevated in atherosclerotic plaques, yet its functional role and molecular mechanisms remain unclear. This study investigated the role of PLD3 in atherosclerosis.

Methods

Single-cell RNA sequencing of human atherosclerotic tissues was analyzed to define PLD3 expression. Validation was performed in ApoE^-/- mice and THP-1-derived foam cells by qRT-PCR and western blotting. Lentiviral-mediated PLD3 knockdown was followed by oxidized LDL (ox-LDL) stimulation. Lipid accumulation and uptake were assessed by Oil Red O, BODIPY, and DiI-ox-LDL assays, while inflammatory cytokines were quantified by qRT-PCR. RNA sequencing was conducted to explore downstream mechanisms.

Results

PLD3 expression was markedly upregulated in atherosclerotic lesions and enriched in plaque macrophages, with diagnostic value confirmed by ROC analysis. In vitro, ox-LDL induced PLD3 upregulation in THP-1 macrophages. PLD3 silencing reduced lipid accumulation and uptake through downregulation of CD36, while concurrently decreasing IL-1β and TNF-α expression. Mechanistically, PLD3 deficiency suppressed NF-κB pathway activation.

Conclusion

PLD3 is highly expressed in plaque macrophages and promotes atherosclerosis by enhancing CD36-mediated lipid accumulation and activating NF-κB–driven inflammation. These findings identify PLD3 as a potential therapeutic target for atherosclerotic disease.

动脉粥样硬化是一种慢性炎症性疾病，是全球发病率和死亡率的主要原因。磷脂酶D3 （PLD3）在动脉粥样硬化斑块中升高，但其功能作用和分子机制尚不清楚。本研究探讨PLD3在动脉粥样硬化中的作用。方法分析人动脉粥样硬化组织的单细胞RNA测序，确定PLD3的表达。通过qRT-PCR和western blotting在ApoE^-/-小鼠和thp -1衍生泡沫细胞中进行验证。慢病毒介导的PLD3敲低之后是氧化LDL （ox-LDL）刺激。脂质积累和摄取通过Oil Red O、BODIPY和DiI-ox-LDL检测来评估，炎症细胞因子通过qRT-PCR来量化。通过RNA测序来探索其下游机制。结果spld3在动脉粥样硬化病变中表达明显上调，在斑块巨噬细胞中表达丰富，经ROC分析证实具有诊断价值。在体外，ox-LDL诱导THP-1巨噬细胞PLD3上调。PLD3沉默通过下调CD36减少脂质积累和摄取，同时降低IL-1β和TNF-α的表达。在机制上，PLD3缺乏抑制NF-κB通路的激活。结论pld3在斑块巨噬细胞中高表达，通过增强cd36介导的脂质积累和激活NF-κ b驱动的炎症来促进动脉粥样硬化。这些发现确定PLD3是动脉粥样硬化疾病的潜在治疗靶点。

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引用次数: 0

Impact of cardiovascular-kidney-metabolic syndrome staging on clinical outcomes and management of acute pulmonary embolism: A comprehensive analysis 心血管-肾-代谢综合征分期对急性肺栓塞临床结局和治疗的影响：一项综合分析

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-10-30 DOI: 10.1016/j.ijcha.2025.101831

Shay Zvi Cherevatsky , Marlon V. Gatuz , Adam Folman , Maguli S. Barel , Rami Abu-Fanne , Dmitry Abramov , Mamas A. Mamas , Ariel Roguin , Ofer Kobo

Background

Pulmonary embolism (PE) is a life-threatening condition with high morbidity and mortality rates. Cardiovascular-Kidney-Metabolic (CKM) syndrome, representing a complex interplay of cardiovascular disease, kidney dysfunction, and metabolic disorders, may significantly impact PE outcomes. This study investigates the influence of CKM syndrome staging on clinical outcomes and management strategies in acute PE patients.

Methods

This retrospective study analyzed 725,725 adult patients hospitalized with a primary diagnosis of PE between 2016 and 2019 using the National Inpatient Sample database. Patients were categorized into five CKM groups (0,1,2/3,4a, 4b) based on staging criteria. Multivariable logistic regression models were used to assess the relationship between in-hospital outcomes and CKM stages.

Results

As CKM stages advanced, patients exhibited distinct profiles characterized by older age, male predominance and a higher prevalence of comorbidities. Multivariate analysis revealed that advanced CKM stages were less likely to receive invasive treatments (systemic thrombolysis: aOR 0.86, 95 % CI 0.81–0.92, p < 0.001) but had higher odds of adverse outcomes, including MACCE (aOR 1.53, 95 % CI 1.45–1.60, p < 0.001), mortality (aOR 1.33, 95 % CI 1.25–1.41, p < 0.001), and major bleeding (aOR 1.15, 95 % CI 1.08–1.23, p < 0.001). All odds ratios were computed using CKM stage 0 as the reference group.

Conclusion

CKM syndrome staging significantly impacts clinical outcomes and management strategies in patients with PE. Advanced CKM stages are associated with higher risks of adverse events, including increased mortality and major bleeding complications. Paradoxically, these high-risk patients were less likely to receive invasive treatments, highlighting a critical gap in care.

肺栓塞（PE）是一种危及生命的疾病，具有很高的发病率和死亡率。心血管-肾-代谢（CKM）综合征是心血管疾病、肾功能障碍和代谢紊乱的复杂相互作用，可能会显著影响PE的预后。本研究探讨CKM综合征分期对急性PE患者临床结局和治疗策略的影响。方法：本回顾性研究使用全国住院患者样本数据库，分析了2016年至2019年期间725,725例原发性PE住院患者。根据分期标准将患者分为5组（0、1、2/3、4a、4b）。采用多变量logistic回归模型评估住院预后与CKM分期之间的关系。结果随着CKM分期的进展，患者表现出明显的特征，即年龄较大、男性居多、合并症发生率较高。多因素分析显示，CKM晚期患者接受侵入性治疗的可能性较小（全体性溶栓：aOR 0.86, 95% CI 0.81-0.92, p < 0.001），但不良结局的发生率较高，包括MACCE （aOR 1.53, 95% CI 1.45-1.60, p < 0.001）、死亡率（aOR 1.33, 95% CI 1.25-1.41, p < 0.001）和大出血（aOR 1.15, 95% CI 1.08-1.23, p < 0.001）。以CKM 0期为参照组计算所有比值比。结论ckm综合征分期对PE患者的临床结局和治疗策略有显著影响。CKM晚期与较高的不良事件风险相关，包括死亡率增加和主要出血并发症。矛盾的是，这些高风险患者不太可能接受侵入性治疗，这凸显了护理方面的严重差距。

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引用次数: 0

Middle to long-term outcomes and pathological changes of implanted expanded polytetrafluoroethylene valved conduits 植入膨胀聚四氟乙烯带瓣导管的中长期疗效及病理改变

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-10-30 DOI: 10.1016/j.ijcha.2025.101829

Yixuan Cai , Yaping Shan , Gang Chen, Yaping Mi, Hui Zhong, Ming Ye, Huifeng Zhang

Objectives

This study evaluated the mid to long-term outcomes of expanded polytetrafluoroethylene valved conduits and preliminarily explored the reasons for conduit failure.

Methods

The study included patients who received reconstruction with ePTFE valved conduits between June 2014 and March 2025. Echocardiography was used to evaluate the conduit function. Histopathological staining was applied to demonstrate the details of the failure conduits.

Results

104 patients had a median age of 90 months (interquartile range, 44.25–144 months) and a median follow-up of 48 months (IQR, 16–54.25 months). 4 early deaths (3.8 %) and 1 late death (1.0 %) occurred. 28 conduits (26.9 %) were detected with dysfunction, with 10 (9.6 %) progressing to failure. Infective endocarditis only occurred in 2 patients (1.9 %). 7 patients (6.7 %) received re-interventions, including 2 percutaneous interventions, 1 replacement after percutaneous intervention, and 4 direct replacements. Pathological staining showed no thrombus formation, but calcification on the valve junction. The valved conduit exhibited insufficient endothelialization, accompanied by the infiltration of inflammatory cells and remarkable neointimal hyperplasia.

Conclusions

The application of the ePTFE valved conduit presented low mortality rate and relatively appreciable conduit function. Conduit stenosis was the main cause of failure, characterized by calcification and neointimal hyperplasia, and might be related to inflammatory response and material damage.

目的评价膨胀式聚四氟乙烯带阀导管的中长期疗效，初步探讨导管失效的原因。方法本研究纳入2014年6月至2025年3月期间接受ePTFE带瓣导管再造术的患者。超声心动图评价导管功能。组织病理学染色显示了失败导管的细节。结果104例患者中位年龄为90个月（四分位间距44.25 ~ 144个月），中位随访时间为48个月（IQR 16 ~ 54.25个月）。4例早期死亡（3.8%）和1例晚期死亡（1.0%）。28条（26.9%）导管出现功能障碍，10条（9.6%）进展为衰竭。感染性心内膜炎仅发生2例（1.9%）。再介入7例（6.7%），经皮介入2例，经皮介入后置换术1例，直接置换术4例。病理染色未见血栓形成，但瓣膜连接处有钙化。瓣膜化导管内皮化不足，伴有炎症细胞浸润和明显的内膜增生。结论应用ePTFE带瓣导管死亡率低，导管功能较好。导管狭窄是失败的主要原因，以钙化和内膜增生为特征，可能与炎症反应和物质损伤有关。

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引用次数: 0

Multidimensional optimization of stent design for endothelial shear stress regulation: Geometric structuring, surface functionalization strategies to mitigate thrombosis and restenosis 内皮剪切应力调节支架设计的多维优化：几何结构、表面功能化策略以减轻血栓形成和再狭窄

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

IJC Heart and Vasculature

Pub Date : 2025-10-26 DOI: 10.1016/j.ijcha.2025.101830

Mengyuan Che , Liuliu Feng , Xinbing Liu , Liangfeng Zhao , Suying Zhou , Xinyu Zhong , Lingsen You , Yu Wang

The occurrence of in-stent restenosis (ISR) is closely associated with abnormal distribution of endothelial shear stress (ESS), and optimizing stent design is crucial for improving patient prognosis. This review aims to comprehensively explore how stent design parameters—including geometric structure and surface functionalization—influence neointimal hyperplasia and thrombosis by modulating ESS, while also summarizing the latest technological strategies. A detailed discussion is provided on the design evolution from traditional coronary stents to for non-coronary arteries (cerebral aneurysm) micro-woven stents, analyzing the mechanisms by which factors such as streamlined profiles, reduced strut thickness, and optimized spacing improve hemodynamics. Furthermore, the article critically evaluates the advantages and current limitations of cutting-edge technologies such as computational fluid dynamics (CFD)-based optimization and endothelialization-promoting functional coatings. We conclude that multidimensional stent design optimization represents a future trend in regulating ESS and suppressing restenosis. Future research should focus on integrating personalized design with highly biocompatible materials to advance the clinical translation of next-generation vascular stents.

支架内再狭窄（ISR）的发生与内皮剪切应力（ESS）分布异常密切相关，优化支架设计对改善患者预后至关重要。本文旨在全面探讨支架设计参数（包括几何结构和表面功能化）如何通过调节ESS影响内膜增生和血栓形成，同时总结最新的技术策略。详细讨论了从传统冠状动脉支架到非冠状动脉（脑动脉瘤）微编织支架的设计演变，分析了流线型轮廓、减少支架厚度和优化间距等因素改善血流动力学的机制。此外，本文还批判性地评估了基于计算流体动力学（CFD）的优化和促进内皮化的功能涂层等尖端技术的优势和当前的局限性。我们认为，多维支架设计优化是调节ESS和抑制再狭窄的未来趋势。未来的研究应着眼于将个性化设计与高生物相容性材料相结合，以推进下一代血管支架的临床转化。

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引用次数: 0