Guazzi Marco, Novello Gabriele, Bursi Francesca, Caretti Anna, Furlotti Noemi, Arena Ross, Argiento Paola, Núñez Julio, Bayes-Genis Antoni, Metra Marco
Department of Health Science, University of Milano School of Medicine, Milan, Italy.
Division of Cardiology, San Paolo Hospital, Milan, Italy.
ESC Heart Fail. 2025 Apr;12(2):781-789. doi: 10.1002/ehf2.14982. Epub 2024 Aug 8.
Acute heart failure (AHF) classification and management are primarily based on lung congestion and/or hypoperfusion. The quantification of the vascular and tissue lung damage is not standard practice though biomarkers of lung injury may play a relevant role in this context. Haemodynamic stress promotes alveolar and vascular derangement with loss of functional units, impaired lung capillary permeability and fluid swelling. This culminates in a remodelling process with activation of inflammatory and cytokines pathways. Four families of lung surfactant proteins (i.e., SP-A, SP-B, SP-C, and SP-D), essential for the membrane biology and integrity are released by alveolar type II pneumocites. With deregulation of fluid handling and gas exchange pathways, SPs become sensitive markers of lung injury. We report the pathobiology of lung damage; the pathophysiological and clinical implications of alveolar SPs along with the newest evidence for some classical HF biomarkers that have also shown to reflect a vascular and/or a tissue lung-related activity.
急性心力衰竭(AHF)的分类与管理主要基于肺充血和/或灌注不足。虽然肺损伤生物标志物在这方面可能发挥相关作用,但对肺血管和组织损伤的量化并非标准做法。血流动力学应激会促进肺泡和血管紊乱,导致功能单位丧失、肺毛细血管通透性受损和液体渗出。这最终会引发一个炎症和细胞因子途径激活的重塑过程。肺泡Ⅱ型上皮细胞会释放对膜生物学和完整性至关重要的四类肺表面活性物质蛋白(即SP-A、SP-B、SP-C和SP-D)。随着液体处理和气体交换途径失调,肺表面活性物质蛋白成为肺损伤的敏感标志物。我们报告了肺损伤的病理生物学;肺泡表面活性物质蛋白的病理生理和临床意义,以及一些经典心力衰竭生物标志物的最新证据,这些证据也显示出反映血管和/或与肺组织相关的活性。