Soluble neprilysin does not correlate with prognosis in pulmonary hypertension

Soluble neprilysin does not correlate with prognosis in pulmonary hypertension
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可溶性脑啡肽酶与肺动脉高压的预后无关

DOI:
10.1002/ehf2.12404
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发表时间:
2019
期刊:
影响因子:
3.8
通讯作者:
Takeishi Yasuchika
Takeishi Yasuchika
中科院分区:
医学3区
文献类型:
--
作者:
Yoshihisa Akiomi;Yokokawa Tetsuro;Misaka Tomofumi;Oikawa Masayoshi;Kobayashi Atsushi;Yamaki Takayoshi;Sugimoto Koichi;Kunii Hiroyuki;Nakazato Kazuhiko;Takeishi Yasuchika

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据报道,循环可溶性血钠溶素(sNEP)可以催化几种血管舒张肽(如利钠肽)的降解,预测射血分数降低的心力衰竭患者的预后。缺氧诱导肺内NEP表达降低已有报道。然而,sNEP与血流动力学参数之间的关系,以及sNEP对肺动脉高压(PH)的预后影响尚不清楚。我们的目的是阐明sNEP与PH患者的利钠肽、血流动力学(如超声心动图参数和右心导管参数)或预后之间的关系。方法和结果首先,我们研究了PH患者(右心导管的平均肺动脉压≥25 mmHg和肺动脉楔压≤15 mmHg,n= 79) sNEP水平与利钠肽、超声心动图或右心导管之间的关系。接下来,我们随访患者的全因死亡率。实验室数据显示sNEP与B型利钠肽(R= 0.022,P= 0.872)、N端proBNP (R= - 0.018,P= 0.872)和高敏感性肌钙蛋白I (R= 0.206,P= 0.107)无显著相关性。超声心动图及右心导管参数与左室射血分数(R= - 0.036,P= 0.764)、右室分数面积变化(R= - 0.259,P= 0.064)、三尖瓣压力梯度(R= - 0.037,P= 0.767)及右心导管参数均无显著相关性。Kaplan-Meier分析(平均随访1284天,log - rankP= 0.531)显示,NEP高组(sNEP≥中位数1.45 ng/mL,n= 39)和NEP低组(sNEP < 1.45 ng/mL,n= 40)的全因死亡率具有可同性。在Cox比例风险分析中,sNEP不是PH患者全因死亡率的预测因子(风险比0.902,95% CI 0.674-1.207,P= 0.487)。结论循环sNEP与PH患者的利钠肽、血流动力学参数及预后无关。
AimsIt has been reported that circulating soluble neprilysin (sNEP), which catalyses the degradation of several vasodilator peptides such as natriuretic peptides, predicts prognosis in heart failure patients with reduced ejection fraction. Hypoxia‐induced decrease in NEP expression in lungs has been reported. However, the associations between sNEP and haemodynamic parameters, as well as the prognostic impact of sNEP in pulmonary hypertension (PH), remain unclear. We aimed to clarify the relationships between sNEP and natriuretic peptide, haemodynamics (e.g. parameters of echocardiography and right heart catheter) or prognosis in PH patients.Methods and resultsFirst, we examined the associations between sNEP levels and natriuretic peptide, echocardiography, or right heart catheter in PH patients (mean pulmonary artery pressure ≥ 25 mmHg and pulmonary artery wedge pressure ≤ 15 mm Hg on the basis of right heart catheterization,n= 79). Next, we followed up the patients for all‐cause mortality. Laboratory data revealed no significant correlations between sNEP and B‐type natriuretic peptide (R= 0.022,P= 0.872), N‐terminal proBNP (R= −0.018,P= 0.872), and high‐sensitivity troponin I (R= 0.206,P= 0.107). Regarding the parameters of echocardiography and right heart catheter, there were no significant correlations between sNEP and left ventricular ejection fraction (R= −0.036,P= 0.764), right ventricular fractional area change (R= −0.259,P= 0.064), tricuspid valve pressure gradient (R= −0.037,P= 0.767), and any of the right heart catheter parameters. In the Kaplan–Meier analysis (mean follow‐up, 1284 days, log‐rankP= 0.531), all‐cause mortality rates were comparable between the higher NEP group (sNEP ≥ median levels of 1.45 ng/mL,n= 39) and the lower NEP group (sNEP < 1.45 ng/mL,n= 40). In the Cox proportional hazard analysis, sNEP was not a predictor of all‐cause mortality (hazard ratio 0.902, 95% CI 0.674–1.207,P= 0.487) in PH patients.ConclusionsCirculating sNEP does not correlate with natriuretic peptide, haemodynamic parameters, or prognosis in patients with PH.
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