Decreases in hepatokine Fetuin-A levels are associated with hepatic hypoperfusion and predict cardiac outcomes in patients with heart failure. (In press)
Decreases in hepatokine Fetuin-A levels are associated with hepatic hypoperfusion and predict cardiac outcomes in patients with heart failure. (In press)
复制标题
肝因子胎球蛋白-A 水平的降低与肝脏灌注不足相关，可预测心力衰竭患者的心脏结局。
DOI：
10.1007/s00392-022-02023-0
复制
发表时间：
2022
影响因子：
5
通讯作者：
Takeishi Yasuchi
中科院分区：
文献类型：
--
作者：
Tomita Yusuke;Misaka Tomofumi;Yoshihisa Akiomi;Ichijo Yasuhiro;Ishibashi Shinji;Matsuda Mitsuko;Yamadera Yukio;Ohara Himika;Sugawara Yukiko;Hotsuki Yu;Watanabe Koichiro;Anzai Fumiya;Sato Yu;Sato Takamasa;Oikawa Masayoshi;Kobayashi Atsushi;Takeishi Yasuchi
背景在心力衰竭（HF）的病理生理学中，心脏和肝脏的相互作用仍有待充分了解。肝细胞因子是由肝脏合成和分泌的蛋白质，调节外周组织的全身代谢。本研究旨在澄清hepatokine Fetuin-A在HF.Methods和resultsWe患者的临床相关性招募了217名参与者，其中包括187名住院的HF患者和30名对照受试者，他们被要求具有可比的年龄和性别特征，谁从来没有HF或结构性心脏异常。首先，我们检测了胎球蛋白-A的水平，发现HF患者的水平显著低于对照组。接下来，根据腹部超声检查评估的肝脏血流动力学将HF患者分为四组，腹部超声检查通过腹腔动脉的峰值收缩期速度（PSV）和剪切波弹性成像（SWE）确定肝脏灌注不足。肝灌注不足的HF患者的胎球蛋白-A水平显著降低，但肝硬度升高的HF患者和无肝硬度升高的HF患者之间无差异。相关性分析表明，循环胎球蛋白A与腹腔动脉的PSV呈正相关，但与肝脏的SWE无关。Kaplan-Meier分析表明，HF患者胎球蛋白-A水平较低与心源性死亡和失代偿性HF.ConclusionsLiver-derived hepatokine Fetuin-A可能是一个新的靶点，参与心-肝相互作用，以及一个有用的生物标志物，用于预测HF患者的预后。
BackgroundInteractions of the heart and the liver remain to be fully understood in the pathophysiology of heart failure (HF). Hepatokines are proteins synthesized and secreted from the liver and regulate systemic metabolisms of peripheral tissues. This study sought to clarify the clinical relevance of hepatokine Fetuin-A in patients with HF.Methods and resultsWe enrolled 217 participants including 187 hospitalized patients with HF and 30 control subjects who were sought with a comparable age- and sex profile and who had never had HF or structural cardiac abnormalities. First, we examined the levels of Fetuin-A and found that its levels were significantly lower in patients with HF than in the controls. Next, HF patients were categorized into four groups based on hepatic hemodynamics assessed by abdominal ultrasonography which determines liver hypoperfusion by peak systolic velocity (PSV) of the celiac artery and liver stiffness by shear wave elastography (SWE). Fetuin-A levels were significantly decreased in HF patients with liver hypoperfusion compared to those without, but were not different between HF patients with and without elevated liver stiffness. Correlation analysis revealed that circulating Fetuin-A was positively correlated with PSV of the celiac artery but not with SWE of the liver. Kaplan–Meier analysis demonstrated that HF patients with lower Fetuin-A levels were significantly associated with increased adverse outcomes including cardiac deaths and decompensated HF.ConclusionsLiver-derived hepatokine Fetuin-A may be a novel target involved in the cardio-hepatic interactions, as well as a useful biomarker for predicting the prognosis in patients with HF.Graphical abstract