JACC. Heart failure最新文献

英文中文

Novel 4-Stage Classification to Estimate Right Atrial Pressure by Point-of-Care Ultrasound of Neck Vasculature 新的4期分型法估计右房压颈血管超声。

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102707

Diana de Oliveira-Gomes MD , Rachel M. Drazner MD, MPH , Michelle Dimza DO , Colby Ayers MS , Angela Duvalyan MD , Tiffany L. Brazile MD , Robert Morlend MD , Faris Araj MD , E. Ashley Hardin MD , Nicholas Hendren MD , Justin L. Grodin MD, MPH , Jennifer T. Thibodeau MD, MSCS , Mark H. Drazner MD, MSc

引用次数: 0

Serum Magnesium and the Effect of Empagliflozin in Heart Failure With Reduced Ejection Fraction 血清镁和恩格列净对心力衰竭伴射血分数降低的影响：来自emperr -Reduced的发现。

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102751

João Pedro Ferreira MD, PhD , Stefan D. Anker MD, PhD , Javed Butler MD, MPH, MBA , Francisco Vasques-Nóvoa MD , Pedro Marques MD , Stuart Pocock PhD , Gerasimos Filippatos MD, PhD , Faiez Zannad MD, PhD , Milton Packer MD

Background

Magnesium plays a central role in maintaining cellular homeostasis. Limited data exist on the clinical implications of magnesium derangements in heart failure with reduced ejection fraction (HFrEF) and on the influence of sodium-glucose cotransporter 2 (SGLT2) inhibitors on serum magnesium levels.

Objectives

Using the EMPEROR-Reduced (Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Reduced Ejection Fraction; NCT03057977) population, the authors studied the association of serum magnesium with outcomes, assessed the impact of empagliflozin on serum magnesium levels, and explored the influence of serum magnesium on the effect of empagliflozin on cardiovascular and renal outcomes.

Methods

Patients with HFrEF were randomized to receive placebo or 10 mg/day of empagliflozin. Laboratory results were available at baseline, week 4, weeks 12, 32, and 52, and every 24 weeks thereafter. The median follow-up time was 16 months. The primary outcome was a composite of cardiovascular death or heart failure (HF) hospitalization.

Results

A total of 3,730 patients were included. The mean serum magnesium levels at baseline were 0.83 ± 0.11 mmol/L. The corresponding magnesium quintiles were Q1 = 0.68 ± 0.07 mmol/L (n = 878); Q2 = 0.79 ± 0.02 (n = 724); Q3 = 0.84 ± 0.01 (n = 668); Q4 = 0.88 ± 0.02 (n = 733); and Q5 = 0.97 ± 0.05 (n = 727). The patients with higher magnesium levels were older and had a lower estimated glomerular filtration rate. Conversely, the patients with lower serum magnesium had diabetes more frequently. Lower magnesium levels were modestly associated with a higher risk of HF and kidney events; such associations were attenuated with full covariate adjustment. The effect of empagliflozin (vs placebo) on the study primary outcome was more pronounced at lower baseline serum magnesium levels (Q1 HR: 0.54 mmol/L [95% CI: 0.41-0.71 mmol/L]; Q2 HR: 0.69 mmol/L [95% CI: 0.50-0.96 mmol/L]; Q3 HR: 0.82 mmol/L [95% CI: 0.58-1.15 mmol/L]; Q4 HR: 0.99 mmol/L [95% CI: 0.72-1.37 mmol/L]; and Q5 HR: 0.87 mmol/L [95% CI: 0.65-1.17 mmol/L], P_interaction = 0.043). Empagliflozin rapidly increased magnesium levels by 0.05 mmol/L. The relative odds of experiencing lower magnesium levels were reduced with empagliflozin.

Conclusions

In EMPEROR-Reduced, low serum magnesium levels were modestly associated with poor HF and kidney outcomes. Empagliflozin increased serum magnesium levels and was associated with a more pronounced reduction of HF events among patients with low magnesium levels at baseline.

镁在维持细胞内稳态中起着核心作用。关于心力衰竭伴射血分数降低（HFrEF）患者镁紊乱的临床意义以及钠-葡萄糖共转运蛋白2 （SGLT2）抑制剂对血清镁水平的影响的数据有限。目的：采用EMPEROR-Reduced（恩帕列净在慢性心力衰竭伴射血分数降低患者中的结局试验；NCT03057977）人群，作者研究了血清镁与结局的关系，评估了恩帕列净对血清镁水平的影响，并探讨了血清镁对恩帕列净对心血管和肾脏结局的影响。方法HFrEF患者随机接受安慰剂或10mg /天的恩格列净治疗。在基线、第4周、第12周、第32周和第52周以及之后每24周提供实验室结果。中位随访时间为16个月。主要结局是心血管死亡或心力衰竭住院。结果共纳入3730例患者。基线时平均血清镁水平为0.83±0.11 mmol/L。相应的镁五分位数为Q1 = 0.68±0.07 mmol/L (n = 878)；Q2 = 0.79±0.02 (n = 724)；Q3 = 0.84±0.01 (n = 668)；Q4 = 0.88±0.02 (n = 733)；Q5 = 0.97±0.05 （n = 727）。镁水平较高的患者年龄较大，肾小球滤过率估计较低。相反，血清镁含量较低的患者患糖尿病的几率更高。较低的镁水平与较高的心衰和肾脏事件风险有中度相关性；这种关联在全协变量调整后减弱。依帕列净（与安慰剂相比）对研究主要结局的影响在基线血清镁水平较低时更为明显（Q1 HR: 0.54 mmol/L [95% CI: 0.41-0.71 mmol/L]; Q2 HR: 0.69 mmol/L [95% CI: 0.50-0.96 mmol/L]; Q3 HR: 0.82 mmol/L [95% CI: 0.58-1.15 mmol/L]; Q4 HR: 0.99 mmol/L [95% CI: 0.72-1.37 mmol/L]; Q5 HR: 0.87 mmol/L [95% CI: 0.65-1.17 mmol/L]， p相互作用= 0.043）。依帕列净使镁水平迅速升高0.05 mmol/L。恩格列净降低了镁水平较低的相对几率。结论：在EMPEROR-Reduced患者中，低血清镁水平与不良HF和肾脏预后有中度相关性。恩帕列净增加了血清镁水平，并且在基线时镁水平较低的患者中与HF事件的显著降低相关。

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引用次数: 0

Plasma Aldosterone Measurement to Guide Prevention and Treatment of Heart Failure in Black Adults With Hypertension 血浆醛固酮测定指导黑人高血压患者心力衰竭的预防和治疗

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102848

Bertram Pitt MD , Gian Paolo Rossi MD

引用次数: 0

HFmrEF and HFpEF HFmrEF和HFpEF

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102842

Virginia Anagnostopoulou MD , Abhinav Sharma MD, PhD , Pierpaolo Pellicori MD

引用次数: 0

How to Rescue the Field of Heart Failure 如何挽救心力衰竭领域

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102838

Eiran Z. Gorodeski MD, MPH , Shashank Shekhar MD , Robert A. Montgomery MD

引用次数: 0

Full issue PDF 完整版PDF

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/S2213-1779(26)00001-6

引用次数: 0

Clinical Implications of the P.V142I TTR Variant P.V142I TTR变异的临床意义：来自car的见解。

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102704

Isabel R. Wees MD , Colby Ayers MS , Frederick L. Ruberg MD , Mathew S. Maurer MD , Yevgeniy Brailovsky DO, MSc , Lily K. Stern MD , Jan M. Griffin MD , Michel G. Khouri MD , Lori R. Roth PA-C , Justin L. Grodin MD, MPH

引用次数: 0

Evolutionary History of the Comorbidity-Driven Coronary Microvascular Endothelial Inflammation Hypothesis and Its Metamorphosis to the Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction 由合并症驱动的冠状动脉微血管内皮炎症假说的进化史及其向脂肪因子假说的转变。

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102822

Milton Packer MD

For the past decade, the prevailing paradigm to explain heart failure with preserved ejection fraction (HFpEF) has assumed that multiple comorbidities act in concert to trigger a systemic inflammatory state that causes coronary microvascular dysfunction, nitric oxide/cyclic guanosine monophosphate (cGMP) deficiency–dependent titin abnormalities, and load-dependent cellular inflammation and fibrosis of the myocardium. By contrast, the recently proposed adipokine hypothesis elevates one comorbidity—visceral adiposity—to explain the coexistence of systemic inflammation, multiple comorbidities, and HFpEF and identifies a specific proximal causal mechanism (ie, the secretion of a proinflammatory suite of signaling molecules from dysfunctional fat). Excess visceral adiposity and adipokine imbalances have been shown not only to produce HFpEF experimentally but also to directly cause hypertension, insulin resistance and type 2 diabetes, and chronic kidney disease. Visceral adiposity and proinflammatory adipokines can also explain features of HFpEF that are not addressed by the coronary microvascular inflammation hypothesis (eg, atrial fibrillation, skeletal muscle and pulmonary abnormalities, and renal sodium retention and plasma volume expansion). Adipokine imbalances can also cause microvascular dysfunction and defects in cGMP signaling and in titin phosphorylation, and they can directly cause cardiac hypertrophy and fibrosis independently of an effect on the microvasculature. The comorbidity-driven microvascular inflammation hypothesis did not identify a blood-borne molecular mediator that selectively targets the heart, and phenomapping based on the clustering of comorbidities has not yielded reproducible groupings. By contrast, selective silencing of specific proinflammatory adipokines only in adipose tissue causes distant effects on the heart to modulate cardiac structure and the evolution of HFpEF. Clinical trials of drugs that enhance nitric oxide/cGMP signaling or have nonspecific anti-inflammatory effects have not produced favorable effects in clinical HFpEF whereas drugs that produce benefits in HFpEF (eg, glucagon-like peptide 1 receptor agonists, sodium-glucose cotransporter 2 inhibitors) act to normalize the adipokine secretory profile. Finally, whereas coronary microvascular dysfunction is present in 60% to 70% of patients with HFpEF (with endothelium-dependent dysfunction being seen in only 30%), central obesity (assessed by an increased waist-to-height ratio) or visceral adiposity (as by mesenteric or epicardial fat) is present in >85% to 95% of patients with the disorder. Therefore, when compared with the comorbidity-driven coronary microvascular endothelial inflammation hypothesis, the adipokine hypothesis provides an explanatory framework with a stronger evidentiary support and applicable to a broader range of patients with HFpEF. Further work is needed to support these observations.

在过去的十年中，解释具有保留射血分数（HFpEF）的心力衰竭的主流范式假设多种合并症协同作用，引发全身炎症状态，导致冠状动脉微血管功能障碍，一氧化氮/环鸟苷单磷酸（cGMP）缺乏依赖性的titin异常，以及负荷依赖性的细胞炎症和心肌纤维化。相比之下，最近提出的脂肪因子假说提出了一种合并症——内脏脂肪——来解释全身性炎症、多种合并症和HFpEF的共存，并确定了一种特定的近因机制（即，来自功能失调脂肪的促炎信号分子的分泌）。内脏过度肥胖和脂肪因子失衡不仅可以产生HFpEF，而且可以直接导致高血压、胰岛素抵抗和2型糖尿病以及慢性肾脏疾病。内脏脂肪和促炎脂肪因子也可以解释冠状动脉微血管炎症假说无法解释的HFpEF特征（如心房颤动、骨骼肌和肺部异常、肾钠潴存和血浆容量扩张）。脂肪因子失衡还可引起微血管功能障碍和cGMP信号通路和titin磷酸化缺陷，并可独立于对微血管的影响而直接引起心脏肥大和纤维化。合并症驱动的微血管炎症假说并没有确定一种选择性靶向心脏的血源性分子介质，基于合并症聚类的现象图谱也没有产生可重复的分组。相比之下，仅在脂肪组织中选择性沉默特异性促炎脂肪因子会对心脏产生遥远的影响，从而调节心脏结构和HFpEF的进化。增强一氧化氮/cGMP信号或具有非特异性抗炎作用的药物的临床试验并未对临床HFpEF产生有利作用，而对HFpEF产生有益作用的药物（如胰高血糖素样肽1受体激动剂、钠-葡萄糖共转运蛋白2抑制剂）可使脂肪因子分泌谱正常化。最后，尽管60% - 70%的HFpEF患者存在冠状动脉微血管功能障碍（内皮依赖性功能障碍仅见于30%），但85% - 95%的HFpEF患者存在中心性肥胖（通过腰高比增加来评估）或内脏脂肪（如肠系膜或心外膜脂肪）。因此，与合并症驱动的冠状动脉微血管内皮炎症假说相比，脂肪因子假说提供了一个证据支持更强的解释框架，适用于更广泛的HFpEF患者。需要进一步的工作来支持这些观察结果。

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引用次数: 0

Surveillance Patterns for Allograft Vasculopathy in Heart Transplant Recipients in PET Myocardial Perfusion Imaging Performing Centers in the United States 美国PET心肌灌注显像中心心脏移植受者同种异体移植血管病变的监测模式

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.102718

Attila Feher MD, PhD , Maria Alwan MD , Catherine X. Wright MD , Kevin J. Clerkin MD, MSc , Andrew J. Einstein MD, PhD , Edward J. Miller MD, PhD , Mouaz H. Al-Mallah MD, MSc

引用次数: 0

LV Structure and Function in HFrEF With and Without Peak-Flow-Triggered Adaptive Servo-Ventilation-Treated Sleep-Disordered Breathing 有和没有峰值流量触发的自适应伺服通气治疗睡眠呼吸障碍的HFrEF左室结构和功能。

IF 11.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC. Heart failure

Pub Date : 2026-02-01 DOI: 10.1016/j.jchf.2025.02.016

Shoichiro Yatsu MD, PhD , Anna Woo MD , Christian M. Horvath MD , Tomoyuki Tobushi MD , Alexander G. Logan MD , John S. Floras MD, DPhil , George Tomlinson PhD , T. Douglas Bradley MD

Background

Sleep-disordered breathing (SDB), comprising obstructive sleep apnea (OSA) and central sleep apnea (CSA), could promote left ventricular (LV) remodeling and systolic dysfunction.

Objectives

The authors tested the hypothesis, in the ADVENT-HF (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction) trial, that SDB is associated with reversible impairment of LV structure and function.

Methods

Participants underwent echocardiography (ejection fraction ≤45%) and polysomnography. They were classified as no-SDB (apnea-hypopnea index [AHI] <15/h); OSA (AHI ≥15/h with ≥50% of events obstructive), or CSA (AHI ≥15 with >50% of events central). Those with SDB were randomized to a control group or to peak-flow-triggered adaptive servo-ventilation (ASV_PF) to treat SDB and, in them, echocardiography was repeated 6 months later.

Results

Subjects with OSA (n = 543) had similar LV structure and function to those without SDB (n = 56). Subjects with CSA (n = 201) had greater LV mass index and lower LV ejection fraction than the other groups. LV volumes were higher in the CSA than in the OSA group (P < 0.05 for all). ASV_PF abolished SDB, but had no significant effect, whether evaluated by allocation or adherence, 6 months post-randomization on LV structure or function for the entire cohort (n = 549), or either subgroup.

Conclusions

Among patients with heart failure with reduced ejection fraction, those with OSA had similar LV structure and function to those without SDB. Patients with CSA had greater LV remodeling and systolic dysfunction than those with OSA or without SDB. Six months of SDB suppression of OSA and CSA by ASV_PF had no impact on LV structure or function. (Adaptive Servo-ventilation for Sleep-disordered Breathing in Patients with Heart Failure with Reduced Ejection Fraction [ADVENT-HF])

背景：睡眠呼吸障碍（SDB）包括阻塞性睡眠呼吸暂停（OSA）和中枢性睡眠呼吸暂停（CSA），可促进左心室（LV）重构和收缩功能障碍。目的：作者在adap - hf（自适应伺服通气治疗心力衰竭伴射血分数降低患者睡眠呼吸障碍）试验中验证了SDB与左室结构和功能可逆性损害相关的假设。方法：接受超声心动图（射血分数≤45%）和多导睡眠图检查。他们被分类为无sdb（呼吸暂停-低通气指数[AHI]占事件中心的50%）。SDB患者随机分为对照组或峰流量触发自适应伺服通气组（ASVPF）治疗SDB， 6个月后复查超声心动图。结果：OSA患者（n = 543）与非SDB患者（n = 56）的左室结构和功能相似。CSA组（n = 201）左室质量指数高于其他组，左室射血分数低于其他组。CSA组左室容积高于OSA组（P < 0.05）。ASVPF消除了SDB，但无论是通过分配还是依从性来评估，随机化后6个月对整个队列（n = 549）或两个亚组的LV结构或功能都没有显著影响。结论：在心力衰竭伴射血分数降低的患者中，OSA患者的左室结构和功能与无SDB患者相似。CSA患者的左室重构和收缩功能障碍高于OSA患者或无SDB患者。ASVPF对OSA和CSA的SDB抑制6个月对左室结构和功能没有影响。自适应伺服通气治疗心力衰竭伴射血分数降低患者睡眠呼吸障碍[ad - hf]。

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