Heart failure with preserved ejection fraction: a forest of a variety of trees.

Heart failure with preserved ejection fraction: a forest of a variety of trees.
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射血分数保留的心力衰竭:各种树木的森林。

DOI:
10.1093/eurheartj/ehu212
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发表时间:
2014
影响因子:
39.3
通讯作者:
Pfeffer,MarcA
Pfeffer,MarcA
中科院分区:
医学1区
文献类型:
--
作者:
Shah,AmilM;Pfeffer,MarcA

文献摘要

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在射血分数(HFrEF)降低的心力衰竭(HF)中,左心室(LV)收缩功能障碍的严重程度已被证明是一个重要的预后指标和有效的治疗靶点。右室收缩的测量通常不是量化的,但当它们被量化时,它们提供了额外的预后信息。现在公认的是,多达一半的心衰患者的左心室射血分数(HFpEF)测量的收缩功能得到了更好的保存,1表现出与HFrEF相似的HF再住院率和功能下降,2与年龄匹配的对照组相比,死亡风险更高。3虽然心功能异常提示心衰的诊断,但HFpEF的机制显然是多因素的,其中包括年龄、动脉硬化、肾功能障碍、心房颤动和肥胖等(图1)。即使在心脏内,虽然左室舒张功能障碍是一个重要的潜在心脏扰动,但额外的心功能异常也可能导致,包括微小的左室收缩和/或收缩和/或松弛异常,左房(LA)功能受损,肺血管功能障碍,变时性功能不全,以及外周氧摄取受损。4除了病原学的异质性外,表型的异质性和合并症的显著贡献使理解这种综合征特别具有挑战性。Melenovsky等人。现在适当地呼吁我们注意RV功能障碍作为一种促成机制的重要性。5右室与左室平行运行,右室也通过室间隔和心包与左室紧密相连。右室通常射入低阻抗、高度扩张的肺血管床,并且相对于左室表现出较高的后负荷敏感性。因此,右室功能障碍可能是由于后负荷不匹配所致,就像在肺动脉高压(PAH)中常见的那样,和/或由于内在的心肌病过程。Melenovsky等人。在一项单中心回顾性研究中,对96例临床心衰、左心室射血分数≥为50%、肺动脉楔压升高的患者进行了单中心回顾性研究,探讨右室功能障碍的患病率、相关性和预后相关性,所有患者都在48小时内接受了右心导管术和超声心动图检查。右室功能障碍,定义为右室面积改变分数(FAC),35%,在他们的队列中有31%存在。这项研究的主要发现是,右室功能障碍是一个强大的单变量死亡率预测因子,平均随访时间为1.4年。通过结合有创血流动力学数据和ECHO的功能数据,作者还询问了HFpEF中介导RV功能障碍的复杂机制。虽然与肺动脉(PA)压力有关,但经PA压力调整后,RV功能障碍仍与死亡率显著相关。此外,与对照组相比,HFpEF组更高的PA压和更低的RV FAC之间的关系更陡峭,这表明HFpEF对后负荷的敏感性更高。这项研究的发现对HFpEF中RV功能障碍的预后价值的预测是理解右室对这一综合征的贡献的重要的额外一步。事实上,RV功能障碍在HFpEF中的重要性并不令人惊讶,因为RV功能障碍先前已在HFpEF 7中描述,并且是心肌梗死后EF(HFrEF)8降低和(LV)收缩功能障碍的心衰患者不良结局的公认危险因素。9不幸的是,…
In heart failure (HF) with reduced ejection fraction (HFrEF), the magnitude of left ventricular (LV) contractile dysfunction which defines this group has proven an important prognostic marker and effective target for therapy. Measures of right ventricular (RV) contraction are not commonly quantified, but when they are they provide additional prognostic information. It is now well recognized that up to half of HF patients have more preserved contractile function as measured by LVEF (HFpEF), 1 demonstrate rates of HF re-hospitalization and functional decline similar to HFrEF, 2 and have a higher risk of death compared with age-matched controls. 3 While abnormal cardiac performance is implied in the HF diagnosis, the mechanisms underlying HFpEF are clearly multifactorial, with contributions of age, arterial stiffening, renal dysfunction, atrial fibrillation, and obesity, among others (Figure 1). Even within the heart, while LV diastolic dysfunction is an important underlying cardiac perturbation, additional abnormalities of cardiac function may contribute, including subtle abnormalities of LV systolic function, dyssynchronous ventricular contraction and/or relaxation, impaired left atrial (LA) function, pulmonary vascular dysfunction, chronotropic incompetence, and impaired peripheral oxygen extraction. 4 In addition to aetiological heterogeneity, phenotypic heterogeneity and the prominent contribution of comorbidities make understanding this syndrome particularly challenging. Melenovsky et al. now appropriately call our attention to the importance of RV dysfunction as a contributing mechanism. 5 Operating in parallel with the left ventricle, the right ventricle is also intimately coupled to the left ventricle via the interventricular septum and pericardium. The right ventricle normally ejects into the low impedance, highly distensible pulmonary vascular bed, and demonstrates heightened afterload sensitivity relative to the left ventricle. 6 RV dysfunction may therefore result from afterload mismatch, as commonly seen in pulmonary arterial hypertension (PAH), and/or as a result of an intrinsic cardiomyopathic process. Melenovsky et al. explore the prevalence, correlates, and prognostic relevance of RV dysfunction in a single-centre retrospective study of 96 selected patients with clinical HF, LVEF≥ 50%, and an elevated pulmonary artery wedge pressure, all of whom underwent right heart catheterization and echocardiography within 48 h of each other. RV dysfunction, defined as an RV fractional area change (FAC), 35%, was present in 31% of their cohort. The major finding of this study was that RV dysfunction was a powerful univariate predictor of mortality over a median follow-up of 1.4 years. By combining invasive haemodynamic data with functional data from echo, the authors also interrogated the complex mechanisms mediating RV dysfunction in HFpEF. While associated with pulmonary artery (PA) pressure, RV dysfunction remained significantly associated with mortality after adjusting for PA pressure. In addition, the relationship between higher PA pressure and lower RV FAC was steeper in HFpEF compared with a sample of ‘controls’, suggesting greater afterload sensitivity in HFpEF.This study’s finding of the prognostic value of RV dysfunction in HFpEF is an important, additional step in understanding the contribution of the right ventricle to this syndrome. Indeed, the importance of RV dysfunction in HFpEF is not surprising, as RV dysfunction has previously been described in HFpEF 7 and is a recognized risk factor for adverse outcomes in patients with HF with reduced EF (HFrEF) 8 and (LV) systolic dysfunction following myocardial infarction. 9 It is unfortunate that the …