Circulation最新文献_第2页

Letter by Ran et al Regarding Article, "Targeting uPARAP Modifies Lymphatic Vessel Architecture and Attenuates Lymphedema". Ran等人关于文章“靶向uPARAP修饰淋巴管结构并减轻淋巴水肿”的信。

IF 38.6 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-27 Epub Date: 2026-01-26 DOI: 10.1161/CIRCULATIONAHA.125.074549

Qingzhi Ran, Yongkang Zhang, Hengwen Chen

引用次数: 0

Highlights From the Circulation Family of Journals. 从循环家族期刊的亮点。

IF 38.6 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-27 Epub Date: 2026-01-26 DOI: 10.1161/CIRCULATIONAHA.125.079074

引用次数: 0

Association of Statin Discontinuation in Pregnancy With Maternal Cardiovascular Health and Birth Outcomes: A Nationwide Cohort Study. 妊娠期停用他汀类药物与产妇心血管健康和出生结局的关系：一项全国性队列研究

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-23 DOI: 10.1161/circulationaha.125.078919

Yongtai Cho,Danbee Kang,HyunJoo Lim,Hyesung Lee,Eun-Young Choi,Ju-Young Shin,Ki Hong Choi

BACKGROUNDDiscontinuing statin therapy before pregnancy remains challenging, especially in high-risk women. We evaluated the risks of maternal cardiovascular, gestational, and fetal outcomes associated with continuing versus discontinuing statin therapy before the last menstrual period (LMP).METHODSWe conducted a nationwide cohort study using data from the National Health Insurance Database of South Korea collected between 2009 and 2023. Women who used statins for 12 to 24 weeks before their LMP between 2010 and 2022 were stratified by whether they discontinued statins before their LMP. Maternal cardiovascular outcomes were major adverse cardiovascular and cerebrovascular events (MACCE), a composite of myocardial infarction, stroke, coronary revascularization, and cardiovascular death. Gestational and fetal outcomes included preterm delivery, pre-eclampsia/eclampsia, other hypertensive disorders of pregnancy, gestational diabetes, nonlive birth, major congenital malformations, and low birth weight. Propensity scores were estimated from potential confounders, and overlap weighting was applied to control for confounding factors. The weighted hazard ratio for MACCE was estimated using a Cox proportional hazards model. Weighted risk ratios for gestational outcomes were estimated using generalized linear models with 95% CIs.RESULTSAmong 13 374 women with preconception statin use, 7493 (56.0%) continued statin therapy beyond their LMP, and 5881 (44.0%) discontinued statin therapy before their LMP. Compared with continued statin, discontinued statin before the LMP was not associated with an increased risk of maternal MACCE (hazard ratio, 1.00 [95% CI, 0.72-1.37]). Even among women with established familial hypercholesterolemia (n=2435; hazard ratio, 0.92 [95% CI, 0.46-1.85]) or atherosclerotic cardiovascular disease (n=1879; hazard ratio, 0.83 [95% CI, 0.46-1.49]), there was no significant difference in the risk of MACCE between the 2 groups. Statin discontinuation was associated with a lower risk of nonlive birth (risk ratio, 0.89 [95% CI, 0.82-0.95]) and low birth weight (risk ratio, 0.88 [95% CI, 0.78-0.99]).CONCLUSIONSIn this nationwide cohort, discontinuation of statins at pregnancy was not associated with increased maternal cardiovascular risk, including among high-risk women. Secondary analyses suggested differences in fetal outcomes between groups; however, these findings should be interpreted cautiously given the observational design.

怀孕前停用他汀类药物仍然具有挑战性，特别是在高危妇女中。我们评估了在末次月经（LMP）前继续或停止他汀类药物治疗与母体心血管、妊娠和胎儿结局相关的风险。方法：我们使用2009年至2023年间收集的韩国国家健康保险数据库的数据进行了一项全国性队列研究。2010年至2022年间，在LMP前使用他汀类药物12至24周的女性根据是否在LMP前停用他汀类药物进行分层。产妇心血管结局为主要心脑血管不良事件（MACCE），包括心肌梗死、卒中、冠状动脉血运重建术和心血管性死亡。妊娠和胎儿结局包括早产、先兆子痫/子痫、妊娠期其他高血压疾病、妊娠期糖尿病、非活产、重大先天性畸形和低出生体重。从潜在的混杂因素中估计倾向得分，并应用重叠加权来控制混杂因素。使用Cox比例风险模型估计MACCE的加权风险比。使用95% ci的广义线性模型估计妊娠结局的加权风险比。结果在13374名孕前使用他汀类药物的女性中，7493名（56.0%）在LMP后继续他汀类药物治疗，5881名（44.0%）在LMP前停止他汀类药物治疗。与继续服用他汀类药物相比，LMP前停用他汀类药物与母体MACCE风险增加无关（风险比为1.00 [95% CI, 0.72-1.37]）。即使在有家族性高胆固醇血症（n=2435，风险比0.92 [95% CI, 0.46-1.85]）或动脉粥样硬化性心血管疾病（n=1879，风险比0.83 [95% CI, 0.46-1.49]）的女性中，两组间MACCE的风险也没有显著差异。停用他汀类药物与较低的非活产风险（风险比0.89 [95% CI, 0.82-0.95]）和低出生体重（风险比0.88 [95% CI, 0.78-0.99]）相关。结论：在这项全国性队列研究中，妊娠期停用他汀类药物与产妇心血管风险增加无关，包括高危妇女。二次分析提示两组胎儿结局存在差异；然而，考虑到观察设计，这些发现应谨慎解释。

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引用次数: 0

Polycystic Ovarian Syndrome and the Long-term Risk of Arrhythmias. 多囊卵巢综合征和心律失常的长期风险。

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-22 DOI: 10.1161/circulationaha.125.078039

Marie Sofie Reinert,Helene Vistisen Ryde,Louise Marqvard Sørensen,Sofie Engstrøm Johansen,Pernille Fog Svendsen,Lars Køber,Emil L Fosbøl,Eva Havers-Borgersen

BACKGROUNDPolycystic ovarian syndrome (PCOS) is associated with increased cardiovascular morbidity and a higher risk of atherosclerotic cardiovascular disease. PCOS has been associated with electrocardiographic alterations. However, the potential long-term risk of cardiac arrhythmias in women with PCOS remains insufficiently investigated.METHODSWomen diagnosed with PCOS in Denmark (1977-2024) were matched on age and year of index with female controls from the background population (ratio 1:4). The primary outcome was incident arrhythmia, with subtype of arrhythmia and cardiac implantable electronic device (CIED, ie, pacemaker and cardioverter defibrillator implantation) as secondary outcomes. Patients were followed from date of PCOS diagnosis until date of event, emigration, death, or end of study (January 31, 2024).RESULTSThe study included 26 728 women with PCOS (median age, 27.8 years [interquartile range, 23.7-32.1]) and 106 912 controls. Women with PCOS had a higher comorbidity burden and pharmacotherapy use compared with controls. The 25-year associated risk of arrhythmias was higher among women with PCOS (6.3% [95% CI, 5.6-6.9]) compared with controls (4.2% [95% CI, 3.9-4.5]), equivalent to incidence rates of 23.8 (95% CI, 22.1-25.6) and 15.7 (95% CI, 15.0-16.4) per 10 000 person-years, respectively, an unadjusted hazard ratio (HR) of 1.56 (95% CI, 1.43-1.71), and an adjusted HR of 1.48 (95% CI, 1.35-1.63). Across subtypes of arrhythmias, women with PCOS were associated with a higher risk of advanced atrioventricular block (adjusted HR, 1.76 [95% CI, 1.05-2.93]), cardiac arrest (adjusted HR, 1.44 [95% CI, 1.03-2.08]), and atrial fibrillation or flutter (adjusted HR, 1.44 [95% CI, 1.20-1.73]) compared with controls. Women with PCOS were more likely to receive a CIED compared with controls (incidence rates of 1.9 [95% CI, 1.5-2.5] and 1.1 [95% CI, 0.9-1.3] per 10 000 person-years, respectively; adjusted HR, 1.85 [95% CI, 1.30-2.63]). The higher associated risk of arrhythmias and likelihood of receiving a CIED among women with PCOS was independent of use of metformin, oral contraception, spironolactone, antiandrogens, and glucagon-like peptide receptor analogs.CONCLUSIONSWomen with PCOS had a higher associated long-term risk of developing arrhythmias and a higher incidence of receiving a CIED compared with female controls from the background population. Despite low absolute event rates, these findings emphasize the clinical relevance of early cardiovascular risk assessment and preventive strategies for patients diagnosed with PCOS.

背景：多囊卵巢综合征（PCOS）与心血管发病率增加和动脉粥样硬化性心血管疾病的高风险相关。多囊卵巢综合征与心电图改变有关。然而，多囊卵巢综合征女性发生心律失常的潜在长期风险仍未得到充分研究。方法将1977-2024年丹麦诊断为多囊卵巢综合征（PCOS）的女性与背景人群中的女性对照进行年龄和年份匹配（比例为1:4）。主要终点为偶发性心律失常，次要终点为心律失常亚型和心脏植入式电子装置（CIED，即起搏器和心律转复除颤器植入术）。患者从PCOS诊断之日起随访至事件、移民、死亡或研究结束之日（2024年1月31日）。结果纳入26 728例PCOS患者（中位年龄27.8岁[四分位数间距23.7-32.1岁]）和106 912例对照组。与对照组相比，多囊卵巢综合征的女性有更高的合并症负担和药物治疗使用。与对照组（4.2% [95% CI, 3.9-4.5]）相比，PCOS女性患者25年的心律失常相关风险更高（6.3% [95% CI, 5.6-6.9]），相当于每10000人年的发病率分别为23.8 （95% CI, 22.1-25.6）和15.7 (95% CI, 15.0-16.4)，未经调整的风险比（HR）为1.56 (95% CI, 1.43-1.71)，调整后的风险比（HR）为1.48 （95% CI, 1.35-1.63）。在心律失常亚型中，与对照组相比，PCOS女性发生晚期房室传导阻滞（校正后的HR， 1.76 [95% CI, 1.05-2.93]）、心脏骤停（校正后的HR， 1.44 [95% CI, 1.03-2.08]）、心房颤动或扑动（校正后的HR， 1.44 [95% CI, 1.20-1.73]）的风险更高。与对照组相比，多囊卵巢综合征（PCOS）女性更有可能接受CIED（发病率分别为1.9 [95% CI, 1.5-2.5]和1.1 [95% CI, 0.9-1.3] / 10000人年；调整后HR为1.85 [95% CI, 1.30-2.63]）。多囊卵巢综合征（PCOS）女性发生心律失常和CIED的相关风险较高，与二甲双胍、口服避孕药、螺内酯、抗雄激素和胰高血糖素样肽受体类似物的使用无关。结论：与背景人群中的女性对照组相比，PCOS女性发生心律失常的长期相关风险更高，接受CIED的发生率更高。尽管绝对事件发生率较低，但这些发现强调了PCOS患者早期心血管风险评估和预防策略的临床相关性。

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引用次数: 0

Association of Pre-Fontan Hemodynamics With Long-Term Outcomes After Fontan Palliation: A Study From the Pediatric Cardiac Care Consortium. Fontan前血流动力学与Fontan姑息后长期预后的关系：一项来自儿科心脏护理协会的研究。

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-22 DOI: 10.1161/circulationaha.125.076880

Divya Suthar,Yanxu Yang,Asaad G Beshish,Jessica Knight,Xiao Song,Amanda Thomas,Hua Hao,Fawwaz R Shaw,Kathy Jenkins,Jeffrey P Jacobs,Matthew E Oster,Alvaro Alonso,Yijian Huang,Geetha Raghuveer,Gurumurthy Hiremath,Bradley Marino,Lydia Wright,Shriprasad R Deshpande,Anitha S John,Mansi M Gaitonde,Bahaaldin Alsoufi,David M Overman,Charles Canter,James St Louis,Rajiv Devanagondi,Kimberly E McHugh,Lazaros Kochilas

BACKGROUNDLong-term outcomes after Fontan vary widely. Although pre-Fontan hemodynamics predict early failure, their association with long-term outcomes remains unclear. We hypothesized that pre-Fontan hemodynamics predict long-term risk of death or transplantation.METHODSWe analyzed data from the Pediatric Cardiac Care Consortium, a US-based multicenter registry including patients undergoing first-time Fontan with pre-Fontan catheterization and long-term follow-up. Patients undergoing a Fontan procedure before 18 years of age at any time between 1982 and 2011 were included in the study. Outcomes of interest were in-hospital Fontan failure (death or takedown) and postdischarge death or transplantation, identified through matching with the National Death Index and the Organ Procurement and Transplantation Network through 2022. Associations between pre-Fontan hemodynamics and long-term risk for death or transplantation were assessed with Kaplan-Meier survival curves and extended Cox regression.RESULTSAmong 1175 patients (736 [62.6%] male, 626 [53.3%] with systemic left ventricle), 1111 were discharged with Fontan physiology. Over a median postdischarge follow-up of 20.6 years (interquartile range, 18.2-24.4 years), 85 deaths and 49 transplantations occurred. Pre-Fontan mean pulmonary arterial pressure was the strongest hemodynamic predictor of postdischarge outcomes with a continuous association and no clear inflection point; 25-year transplantation-free survival declined from 83.7% (95% CI, 77.6-88.3) in the low mean pulmonary arterial pressure tertile to 73.7% (95% CI, 65.5-80.3) in the highest tertile (log-rank P=0.02). Each 1-SD increase in mean pulmonary arterial pressure was associated with 1.33-fold higher odds of in-hospital failure (adjusted odds ratio, 1.33 [95% CI, 1.00-1.77]; P=0.05) and a 2.2-fold higher hazard of death or transplantation (adjusted hazard ratio, 2.20 [95% CI, 1.62-3.00]; P<0.01) estimated at discharge. This hazard declined 3% per year after discharge (adjusted hazard ratio per year, 0.97 [95% CI, 0.95-0.99]; P<0.01) and resolved by 17 years in patients with systemic right ventricle and by 23 years in those with systemic left ventricle. Additional independent risk factors included systemic right ventricle versus systemic left ventricle (adjusted hazard ratio, 2.39 [95% CI, 1.65-3.46]; P<0.01) and delayed Fontan completion (>4 years of age versus 2 to 4 years of age; adjusted hazard ratio, 1.80 [95% CI, 1.25-2.60]; P=0.02).CONCLUSIONSElevated pre-Fontan mean pulmonary arterial pressure is a strong predictor of in-hospital and long-term post-Fontan risk of death or transplantation. Systemic right ventricle and delayed Fontan completion (>4 years of age) further increased risk. These findings support early Fontan consideration and ongoing hemodynamic surveillance to optimize long-term outcomes.

方丹治疗后的长期结果差异很大。尽管fontan前的血流动力学可以预测早期衰竭，但其与长期预后的关系尚不清楚。我们假设fontan前的血流动力学可以预测死亡或移植的长期风险。方法：我们分析了来自儿科心脏护理联盟的数据，该联盟是一个美国多中心注册中心，包括首次接受Fontan术前导管置入和长期随访的患者。在1982年至2011年期间，18岁之前接受Fontan手术的患者被纳入研究。通过与国家死亡指数（National death Index）和器官获取和移植网络（Organ Procurement and transplantation Network）匹配到2022年，研究的结果是医院内Fontan衰竭（死亡或移除）和出院后死亡或移植。采用Kaplan-Meier生存曲线和扩展Cox回归评估fontan前血流动力学与长期死亡或移植风险之间的关系。结果1175例患者（男性736例（62.6%），系统性左心室626例（53.3%））中，1111例患者出院。出院后随访中位数为20.6年（四分位数范围为18.2-24.4年），发生85例死亡和49例移植。fontan前平均肺动脉压是出院后预后的最强血流动力学预测因子，具有持续的相关性，没有明确的拐点；25年无移植生存率从低平均肺动脉压组的83.7% （95% CI, 77.6-88.3）下降到高平均肺动脉压组的73.7% (95% CI, 65.5-80.3) （log-rank P=0.02）。平均肺动脉压每升高1-SD，住院失败的几率增加1.33倍（校正风险比1.33 [95% CI, 1.00-1.77]； P=0.05），死亡或移植的风险增加2.2倍（校正风险比2.20 [95% CI, 1.62-3.00]； P4岁对2- 4岁；校正风险比1.80 [95% CI, 1.25-2.60]； P=0.02）。结论fontan术前平均肺动脉压升高是fontan术后住院和远期死亡或移植风险的重要预测因子。全身性右心室和Fontan完成延迟（4岁）进一步增加了风险。这些发现支持早期考虑Fontan和持续的血流动力学监测，以优化长期结果。

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引用次数: 0

2026 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association. 2026心脏病和中风统计：来自美国心脏协会的美国和全球数据报告

IF 38.6 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-21 DOI: 10.1161/CIR.0000000000001412

Latha P Palaniappan, Norrina B Allen, Zaid I Almarzooq, Cheryl A M Anderson, Pankaj Arora, Christy L Avery, Carissa M Baker-Smith, Nisha Bansal, Maria E Currie, Rebecca S Earlie, Wenjun Fan, Jessica L Fetterman, Bethany Barone Gibbs, Debra G Heard, Swapnil Hiremath, Haoyun Hong, Hyacinth I Hyacinth, Chinwe Ibeh, Tian Jiang, Michelle C Johansen, Dhruv S Kazi, Darae Ko, Tak W Kwan, Michelle H Leppert, Yilun Li, Jared W Magnani, Karlyn A Martin, Seth S Martin, Erin D Michos, Michael E Mussolino, Oluwabunmi Ogungbe, Nisha I Parikh, Marco V Perez, Sarah M Perman, Ashish Sarraju, Nilay S Shah, Mellanie V Springer, Marie-Pierre St-Onge, Evan L Thacker, Seda Tierney, Sarah M Urbut, Harriette G C Van Spall, Jenifer H Voeks, Seamus P Whelton, Sally S Wong, Juan Zhao, Sadiya S Khan

Background: The American Heart Association annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and cardiovascular-kidney-metabolic syndrome) that contribute to cardiovascular health. The 2026 Heart Disease and Stroke Statistics Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).

Methods: The American Heart Association, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistics Update with review of published literature through the year before writing. The 2026 Statistics Update is the product of a full year's worth of effort in 2025 by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year's edition includes a new chapter on cardiovascular-kidney-metabolic syndrome, as well as an expanded chapter on tobacco and nicotine use and exposure.

Results: Each of the chapters in the Statistics Update focuses on a different topic related to heart disease and stroke statistics.

Conclusions: The Statistics Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

背景：美国心脏协会每年报告与心脏病、中风和心血管危险因素相关的最新统计数据，包括核心健康行为（吸烟、体育活动、营养、睡眠和肥胖）和健康因素（胆固醇、血压、血糖控制和心血管-肾-代谢综合征），这些因素有助于心血管健康。《2026年心脏病和中风统计更新》提供了一系列主要临床心脏和循环系统疾病的最新数据（包括中风、脑部健康、妊娠并发症、肾脏疾病、先天性心脏病、心律失常、心脏骤停、亚临床动脉粥样硬化、冠心病、心肌病、心力衰竭、瓣膜疾病、静脉血栓栓塞、心血管疾病和心血管疾病）。（以及外周动脉疾病）和相关结果（包括护理质量、程序和经济成本）。方法：美国心脏协会通过其流行病学和预防统计委员会持续监测和评估美国和全球心脏病和中风的数据来源，在年度统计更新中提供最新信息，并在撰写前一年审查已发表的文献。《2026年统计更新》是2025年由敬业的志愿临床医生和科学家、忠诚的政府专业人员和美国心脏协会工作人员一整年努力的结果。今年的版本包括一个关于心血管肾脏代谢综合征的新章节，以及一个关于烟草和尼古丁使用和暴露的扩展章节。结果：统计更新中的每一章都侧重于与心脏病和中风统计相关的不同主题。结论：《最新统计数据》为普通公众、政策制定者、媒体专业人员、临床医生、卫生保健管理人员、研究人员、卫生倡导者和其他寻求有关这些因素和条件的最佳可用数据的人员提供了重要资源。

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引用次数: 0

ALDH2/eIF3E Interaction Modulates Protein Translation Critical for Cardiomyocyte Ferroptosis in Acute Myocardial Ischemia Injury. ALDH2/eIF3E相互作用调节急性心肌缺血损伤中心肌细胞铁下沉的关键蛋白翻译。

IF 38.6 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-20 Epub Date: 2025-10-20 DOI: 10.1161/CIRCULATIONAHA.125.075220

Xin Chen, Xiujian Yu, Shanshan Zhong, Ping Sha, Rui Li, Xiaodong Xu, Ningning Liang, Lili Zhang, Luxiao Li, Jingyu Zhang, Mingyao Zhou, Tongwei Lv, Haoran Ma, Yongqiang Wang, Yanwen Ye, Chunzhao Yin, Shiting Chen, Jinwei Tian, Aijun Sun, Weiyuan Wang, Dewen Yan, Huang-Tian Yang, Hui Huang, Pan Li, Huiyong Yin

Background: As an iron-dependent form of regulated cell death caused by lipid peroxidation, ferroptosis has been implicated in ischemic injury, but the underlying mechanisms in acute myocardial infarction (AMI) remain poorly defined. ALDH2 (acetaldehyde dehydrogenase 2) catalyzes detoxification of lipid aldehydes derived from lipid peroxidation and acetaldehydes from alcohol consumption. The Glu504Lys polymorphism of ALDH2 (rs671, ALDH2*2), affecting ≈40% of East Asians, is associated with increased risk of myocardial infarction (MI). This study aims to investigate the role of ALDH2*2 and ferroptosis in AMI.

Methods: A Chinese cohort of 177 patients with acute heart failure with ALDH2 wild type and ALDH2*2 was enrolled. The MI mouse model of left anterior descending coronary artery ligation was conducted on wild-type and ALDH2*2 mice and mice with cardiomyocyte-specific knockdown of eIF3E (eukaryotic translation initiation factor 3 subunit E) by adeno-associated virus. The lipid peroxidation products were measured by mass spectrometry-based lipidomics and metabolomics in human plasma, mouse serum samples, mouse heart tissues, and primary cardiac myocytes.

Results: Human ALDH2*2 carriers exhibit more severe heart failure after AMI with features of ferroptosis in plasma, as seen through lipidomic analysis, characterized by increased bioactive lipids and decreased antioxidants, such as coenzyme Q10 and BH4 (tetrahydrobiopterin). Similar features were observed in MI mouse models of ALDH2*2, whereas ferroptosis inhibition by Fer-1 significantly improved heart function and reversed ferroptosis markers. Importantly, ALDH2*2 significantly decreased ALDH2 protein levels, whereas ferroptosis-related markers, including TFRC (transferrin receptor) and ACSL4 (acyl-coenzyme A synthetase long-chain family member 4) were notably upregulated in the infarct heart tissues. Mechanistically, ALDH2 physically interacts with the eIF3 complex via the eIF3E factor, which prevents eIF3E-eIF4G1 (eukaryotic initiation factor 4G)-mRNA assembly. The ALDH2*2 variant causes ALDH2 deficiency, disrupting its interaction with the eIF3 complex by releasing the bound eIF3E to assemble an eIF3E-eIF4G1-mRNA ternary complex, thereby driving selective translation of mRNAs (eg, TFRC, ACSL4, and UAP1) containing the GAGGACR (R represents A/G) motif to promote ferroptosis. Consistently, cardiomyocyte-specific eIF3E knockdown restored ALDH2*2 cardiac function by attenuating ferroptosis in MI.

Conclusions: ALDH2*2 aggravates acute heart failure after MI by promoting the selective translation of mRNAs containing the GAGGACR motif, thereby driving cardiomyocyte ferroptosis. Targeting ferroptosis represents a potential therapeutic option for mitigating MI injury, especially for ALDH2*2 carriers.

背景：作为一种由脂质过氧化引起的铁依赖性细胞死亡形式，铁下沉与缺血性损伤有关，但其在急性心肌梗死（AMI）中的潜在机制仍不明确。ALDH2（乙醛脱氢酶2）催化脂质过氧化产生的脂质醛和酒精消耗产生的乙醛解毒。ALDH2 （rs671, ALDH2*2）的Glu504Lys多态性影响约40%的东亚人，与心肌梗死（MI）风险增加相关。本研究旨在探讨ALDH2*2和铁下垂在AMI中的作用。方法：选取177例ALDH2野生型和ALDH2*2型急性心力衰竭患者为研究对象。以野生型、ALDH2*2小鼠和心肌细胞特异性敲低eIF3E（真核翻译起始因子3亚单位E）小鼠为实验对象，采用腺相关病毒建立左冠状动脉前降支结扎心肌梗死小鼠模型。脂质过氧化产物通过基于质谱的脂质组学和代谢组学在人血浆、小鼠血清样本、小鼠心脏组织和原代心肌细胞中进行测量。结果：人类ALDH2*2携带者AMI后心力衰竭更为严重，血浆呈铁上吊特征，脂质组学分析显示其生物活性脂质升高，辅酶Q10和BH4（四氢生物蝶呤）等抗氧化剂降低。在心肌梗死小鼠ALDH2*2模型中也观察到类似的特征，而fer1抑制铁下垂可显著改善心功能并逆转铁下垂标志物。重要的是，ALDH2*2显著降低了ALDH2蛋白水平，而心肌梗死组织中与铁中毒相关的标志物，包括TFRC（转铁蛋白受体）和ACSL4（酰基辅酶A合成酶长链家族成员4）显著上调。从机制上讲，ALDH2通过eIF3E因子与eIF3复合物相互作用，从而阻止eIF3E- eif4g1（真核起始因子4G）-mRNA组装。ALDH2*2变异体导致ALDH2缺陷，通过释放结合的eIF3E组装eIF3E- eif4g1 - mrna三重复合物，破坏其与eIF3复合物的相互作用，从而驱动含有GAGGACR （R代表A/G）基序的mrna（如TFRC， ACSL4和UAP1）的选择性翻译，促进铁死亡。与此一致的是，心肌细胞特异性eIF3E敲低ALDH2*2通过减轻心肌梗死患者的铁凋亡而恢复心功能。结论：ALDH2*2通过促进含有GAGGACR基序的mrna的选择性翻译，从而加剧心肌梗死后的急性心力衰竭，从而推动心肌细胞铁凋亡。靶向铁下垂是减轻心肌梗死损伤的潜在治疗选择，特别是对于ALDH2*2携带者。

{"title":"ALDH2/eIF3E Interaction Modulates Protein Translation Critical for Cardiomyocyte Ferroptosis in Acute Myocardial Ischemia Injury.","authors":"Xin Chen, Xiujian Yu, Shanshan Zhong, Ping Sha, Rui Li, Xiaodong Xu, Ningning Liang, Lili Zhang, Luxiao Li, Jingyu Zhang, Mingyao Zhou, Tongwei Lv, Haoran Ma, Yongqiang Wang, Yanwen Ye, Chunzhao Yin, Shiting Chen, Jinwei Tian, Aijun Sun, Weiyuan Wang, Dewen Yan, Huang-Tian Yang, Hui Huang, Pan Li, Huiyong Yin","doi":"10.1161/CIRCULATIONAHA.125.075220","DOIUrl":"10.1161/CIRCULATIONAHA.125.075220","url":null,"abstract":"Background: As an iron-dependent form of regulated cell death caused by lipid peroxidation, ferroptosis has been implicated in ischemic injury, but the underlying mechanisms in acute myocardial infarction (AMI) remain poorly defined. ALDH2 (acetaldehyde dehydrogenase 2) catalyzes detoxification of lipid aldehydes derived from lipid peroxidation and acetaldehydes from alcohol consumption. The Glu504Lys polymorphism of ALDH2 (rs671, ALDH2*2), affecting ≈40% of East Asians, is associated with increased risk of myocardial infarction (MI). This study aims to investigate the role of ALDH2*2 and ferroptosis in AMI.Methods: A Chinese cohort of 177 patients with acute heart failure with ALDH2 wild type and ALDH2*2 was enrolled. The MI mouse model of left anterior descending coronary artery ligation was conducted on wild-type and ALDH2*2 mice and mice with cardiomyocyte-specific knockdown of eIF3E (eukaryotic translation initiation factor 3 subunit E) by adeno-associated virus. The lipid peroxidation products were measured by mass spectrometry-based lipidomics and metabolomics in human plasma, mouse serum samples, mouse heart tissues, and primary cardiac myocytes.Results: Human ALDH2*2 carriers exhibit more severe heart failure after AMI with features of ferroptosis in plasma, as seen through lipidomic analysis, characterized by increased bioactive lipids and decreased antioxidants, such as coenzyme Q10 and BH4 (tetrahydrobiopterin). Similar features were observed in MI mouse models of ALDH2*2, whereas ferroptosis inhibition by Fer-1 significantly improved heart function and reversed ferroptosis markers. Importantly, ALDH2*2 significantly decreased ALDH2 protein levels, whereas ferroptosis-related markers, including TFRC (transferrin receptor) and ACSL4 (acyl-coenzyme A synthetase long-chain family member 4) were notably upregulated in the infarct heart tissues. Mechanistically, ALDH2 physically interacts with the eIF3 complex via the eIF3E factor, which prevents eIF3E-eIF4G1 (eukaryotic initiation factor 4G)-mRNA assembly. The ALDH2*2 variant causes ALDH2 deficiency, disrupting its interaction with the eIF3 complex by releasing the bound eIF3E to assemble an eIF3E-eIF4G1-mRNA ternary complex, thereby driving selective translation of mRNAs (eg, TFRC, ACSL4, and UAP1) containing the GAGGACR (R represents A/G) motif to promote ferroptosis. Consistently, cardiomyocyte-specific eIF3E knockdown restored ALDH2*2 cardiac function by attenuating ferroptosis in MI.Conclusions: ALDH2*2 aggravates acute heart failure after MI by promoting the selective translation of mRNAs containing the GAGGACR motif, thereby driving cardiomyocyte ferroptosis. Targeting ferroptosis represents a potential therapeutic option for mitigating MI injury, especially for ALDH2*2 carriers.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"164-184"},"PeriodicalIF":38.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145328177","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}

引用次数: 0

Letter by Pyrpyris et al Regarding Article, "Nonculprit Vulnerable Plaques and Prognosis in Myocardial Infarction With Versus Without ST-Segment Elevation: A PROSPECT II Substudy". Pyrpyris等人关于文章“非罪魁祸首易损斑块与st段抬高与非st段抬高心肌梗死预后：PROSPECT II亚研究”的信。

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-20 DOI: 10.1161/circulationaha.125.076284

Nikolaos Pyrpyris,Kyriakos Dimitriadis,Konstantinos Tsioufis

引用次数: 0

Response by Maeng et al to Letters Regarding Article, "Nonculprit Vulnerable Plaques and Prognosis in Myocardial Infarction With Versus Without ST-Segment Elevation: A PROSPECT II Substudy". Maeng等人对文章《非罪魁祸首易损斑块与st段抬高与非st段抬高心肌梗死预后：PROSPECT II亚研究》的回应。

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-20 DOI: 10.1161/circulationaha.125.077511

Michael Maeng,Pernille G Thrane,David Erlinge,Akiko Maehara,Gregg W Stone

引用次数: 0

Environmental Stressors and Cardiovascular Health: Acting Locally for Global Impact in a Changing World: A Statement of the European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the World Heart Federation. 环境压力源和心血管健康：在不断变化的世界中为全球影响采取局部行动：欧洲心脏病学会、美国心脏病学会、美国心脏协会和世界心脏联合会的声明。

IF 37.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation

Pub Date : 2026-01-20 DOI: 10.1161/circulationaha.125.079034

Thomas Münzel,Thomas Lüscher,Christopher M Kramer,Keith Churchwell,Amam Mbakwem,Sanjay Rajagopalan

Non-communicable diseases (NCDs) account for 70% of global mortality and are responsible for over 38 million deaths annually, with cardiovascular disease (CVD) constituting most of these fatalities. While traditional risk factors for CVD have long been recognized, there is growing evidence that a rising prevalence of ubiquitous environmental risk factors (ERFs) may play an increasingly significant role in the genesis and rising prevalence of NCDs. ERFs include many interconnected anthropogenic exposures with cumulative compound health impacts, including air pollution, noise exposure, artificial light at night, plastic pollution, chemical pollution and the various effects of climate change, such as heat extremes, desert storms, floods and wildfires. Urbanization has intensified the impact of many ERFs and created intense exposure environments, highlighting the urgency and the opportunity to address these for maximum public health benefit. Impactful intervention often requires regulatory and policy-driven efforts addressing the genesis of exposures and minimizes their health impact, particularly in vulnerable populations who may contribute the least but may be impacted the most. Solutions must involve the development of resiliency and adaptation measures to a changing world, where the probability of sudden catastrophic and cascading events is much more likely. Political will and international cooperation are essential in establishing and enforcing regulations that promote cleaner air and water, quieter and natural biodiverse environments, and sustainable infrastructure in urban, and rural medical facilities. Integration of planetary and environmental health into cardiovascular care will be vital in reducing the burden of NCDs globally. By addressing the root causes of environmental stressors, it is possible to reduce the incidence of CVDs and promote healthier, just and sustainable societies.

非传染性疾病（NCDs）占全球死亡率的70%，每年造成3800多万人死亡，其中心血管疾病（CVD）占大多数。虽然心血管疾病的传统风险因素早已被认识到，但越来越多的证据表明，无处不在的环境风险因素（ERFs）的患病率上升可能在非传染性疾病的发生和患病率上升中起着越来越重要的作用。环境影响因子包括许多相互关联的、具有累积复合健康影响的人为暴露，包括空气污染、噪音暴露、夜间人造光、塑料污染、化学污染以及极端高温、沙漠风暴、洪水和野火等气候变化的各种影响。城市化加剧了许多环境影响因子的影响，造成了高度暴露的环境，突出了解决这些问题的紧迫性和机会，以最大限度地造福公众健康。有效的干预措施往往需要监管和政策驱动的努力，解决接触的根源，并尽量减少其对健康的影响，特别是对危害最小但可能受影响最大的弱势群体。解决方案必须包括制定弹性和适应措施，以适应不断变化的世界，在这个世界中，突然发生灾难性和连锁事件的可能性要大得多。政治意愿和国际合作对于制定和执行促进更清洁的空气和水、更安静和自然的生物多样性环境以及城市和农村医疗设施的可持续基础设施的法规至关重要。将地球和环境卫生纳入心血管保健对于减轻全球非传染性疾病负担至关重要。通过解决环境压力源的根本原因，就有可能减少心血管疾病的发病率，并促进更健康、公正和可持续的社会。

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引用次数: 0