Adequate Decongestion Is Still the Question in Heart Failure.

Adequate Decongestion Is Still the Question in Heart Failure.
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足够的解答仍然是心力衰竭的问题。

DOI:
10.1159/000511413
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发表时间:
2021
期刊:
影响因子:
1.9
通讯作者:
Zieroth S
Zieroth S
中科院分区:
医学4区
文献类型:
--
作者:
Reza N;Zieroth S

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当代急性心力衰竭(HF)治疗中最大的挑战之一是出院前肺充血的量化。出院时未能解决鼻塞症状会增加心力衰竭再住院和全因死亡率的风险[1]。使用临床评估按充血和灌注状态对患者进行分类可用于预测心力衰竭患者的临床结果[2]。然而,一些用于评估肺充血状态的传统病史和体格检查结果,如水肿、罗音和喘息,对失代偿性心力衰竭的诊断缺乏敏感性[3]。同样,肺静脉充血、间质水肿和胸腔积液等胸片检查结果可能无法可靠地识别和分类容量超负荷的患者[3]。此外,尽管胸部影像显示肺野清晰,心力衰竭患者仍可能出现血流动力学充血[4]。为了提高急性和慢性心力衰竭患者充血评估的诊断准确性,来自循环生物标志物(如利尿钠肽 [5])、成像技术(如肺超声检查 [6])和植入式监测器(如肺动脉压力传感器 [7])的附加数据正越来越多地纳入不同亚型心力衰竭患者的纵向护理中。尽管这些策略不断涌现,但心衰再住院率和心衰相关死亡率的持久降低尚未实现。仍然迫切需要确定一种具有成本效益、广泛适用、易于实施且准确的策略来识别和治疗因心力衰竭导致的血流动力学和临床充血患者。在本期《心脏病学》中,Kleiner Shochat 等人[8]尝试使用无创肺阻抗 (LI) 测量来满足这一需求,这是他们在 IMPEDANCE-HF 试验中引入的策略 [9]。在母试验中,研究人员使用了一种新型高灵敏度监测仪,该监测仪基于一种算法,通过从总经胸阻抗中减去计算出的胸壁阻抗来得出净 LI。通过这种推导方法,理论上,净 LI 最能代表肺充血。作者评估了 256 名慢性纽约心脏病协会 II-IV 级心力衰竭且左心室射血分数≤ 35% 的患者,这些患者在入组前一年内因急性心力衰竭入院,并将他们随机分为接受临床评估指导的常规治疗的对照组或治疗策略包括无创 LI 监测指导的干预组。值得注意的是,干预组中经历急性心衰住院主要疗效终点的患者较少,遭受全因死亡率和心衰相关死亡率的患者也较少。 IMPEDANCE-HF 试验的扩展旨在评估 LI 在 HF 住院期间测量的肺液含量变化与再入院之间的关联。不幸的是,数据采集的困难以及无法将肺充血的变化仅归因于主动减充血,使得这一发现无法作为合适的风险预测指标[10]。
One of the greatest challenges in the contemporary management of acute heart failure (HF) is the quantification of predischarge pulmonary congestion. Failure to resolve symptoms of congestion at hospital discharge is associated with increased risks for rehospitalization for HF and all-cause mortality [1]. Using clinical assessment to categorize patients by congestion and perfusion status can be used to predict clinical outcomes in patients with HF [2]. However, some traditional history and physical examination findings used to assess pulmonary congestion status, like edema, rales, and wheezing, lack sensitivity for the diagnosis of decompensated HF [3]. Similarly, chest radiography findings like pulmonary venous congestion, interstitial edema, and pleural effusions may not reliably identify and categorize patients with volume overload [3]. In addition, patients with HF can have hemodynamic congestion despite clear lung fields on chest imaging [4]. To augment the diagnostic accuracy of the assessment of congestion in patients with acute and chronic HF, additional data from circulating biomarkers like natriuretic peptides [5], imaging technologies such as lung ultrasonography [6], and implantable monitors such as pulmonary artery pressure sensors [7] are being increasingly incorporated into the longitudinal care of patients with diverse subtypes of HF. Despite the proliferation of these strategies, durable reductions in HF rehospitalizations and HF-related mortality have yet to be realized. There remains a substantial need to identify a cost-effective, widely applicable, easily implemented, and accurate strategy to identify and treat patients with hemodynamic and clinical congestion due to HF.In this issue of Cardiology, Kleiner Shochat et al.[8] attempt to address this need using the measurement of noninvasive lung impedance (LI), a strategy they introduced in the IMPEDANCE-HF trial [9]. In the parent trial, the investigators used a novel high-sensitivity monitor based on an algorithm that derived net LI by subtracting the calculated chest wall impedance from the total transthoracic impedance. With this derivation method, net LI would theoretically be most representative of pulmonary congestion. The authors evaluated 256 patients with chronic New York Heart Association Class II–IV HF and left ventricular ejection fraction≤ 35% who were admitted for acute HF within a year before recruitment and randomized them to a control group treated by clinical assessment-guided conventional therapy or an intervention group whose treatment strategy included guidance by noninvasive LI monitoring. Significantly, fewer patients in the intervention group experienced the primary efficacy endpoint of acute HF hospitalization, and fewer patients suffered all-cause and HF-related mortality. The IMPEDANCE-HF trial was extended to assess the association between change in pulmonary fluid content measured by LI during a HF hospitalization and hospital readmissions. Unfortunately, difficulties with data acquisition and inability to attribute the change in pulmonary congestion solely to active decongestion rendered this finding nonviable as a suitable risk predictor [10].
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