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心力衰竭患者血浆中内源性血管生成素和BOC水平升高,心脏移植后随着血流动力学改善而降低。

Elevated plasma endocan and BOC in heart failure patients decrease after heart transplantation in association with improved hemodynamics.

作者信息

Ahmed Salaheldin, Ahmed Abdulla, Bouzina Habib, Lundgren Jakob, Rådegran Göran

机构信息

Department of Clinical Sciences Lund, Cardiology, Lund University, Lund, Sweden.

The Hemodynamic Lab, The Section for Heart Failure and Valvular Disease, VO. Heart and Lung Medicine, Skåne University Hospital, Lund, Sweden.

出版信息

Heart Vessels. 2020 Nov;35(11):1614-1628. doi: 10.1007/s00380-020-01656-3. Epub 2020 Jul 10.

DOI:10.1007/s00380-020-01656-3
PMID:32651845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7502449/
Abstract

BACKGROUND

The prevalence of heart failure (HF) is rising with ageing population and constitutes a major health problem globally. A common complication of HF is pulmonary hypertension (PH) which negatively impacts survival. A pathophysiological association between HF and PH with tumorigenic processes has been suggested. We aimed to identify the plasma levels of, and the association between tumour-related proteins and hemodynamic improvements in patients with HF and PH due to left heart disease (LHD) before and 1-year after heart transplantation (HT).

METHODS

Forty-eight tumour-related proteins were measured with proximity extension assay in plasma from 20 controls and 26 HF patients before and 1-year after HT. Patients' hemodynamics were measured with right heart catheterization.

RESULTS

Out of 48 proteins, specifically, plasma levels of endocan and brother of CDO (BOC) were elevated in end-stage HF patients compared to controls (p < 0.001), but decreased after HT (p < 0.01), towards controls' levels. The decrease of endocan levels after HT correlated with improved mean pulmonary arterial pressure (r = 0.80, p < 0.0001), pulmonary arterial wedge pressure (r = 0.63, p = 0.0012), and pulmonary vascular resistance (r = 0.70, p < 0.001). The decrease and normalization of BOC after HT correlated with decreased mean right atrial pressure (r = 0.61 p = 0.0015) and NT-proBNP (r = 0.57, p = 0.0022), as well as increased cardiac index (r = - 0.51, p = 0.0086) and left-ventricular stroke work index (r = - 0.57, p = 0.0039).

CONCLUSION

Our results suggest that (i) plasma endocan in HF may reflect the state of pulmonary vascular congestion and PH-LHD, whereas (ii) plasma BOC may reflect the cardiac function and the hemodynamic overload in HF. The exact role of these proteins and their clinical applicability as biomarkers in HF and PH-LHD ought to be investigated in larger cohorts.

摘要

背景

随着人口老龄化,心力衰竭(HF)的患病率不断上升,已成为全球主要的健康问题。HF的常见并发症是肺动脉高压(PH),它对生存率有负面影响。有人提出HF和PH与致瘤过程之间存在病理生理联系。我们旨在确定因左心疾病(LHD)导致HF和PH的患者在心脏移植(HT)前及HT后1年时血浆中肿瘤相关蛋白的水平,以及这些蛋白与血流动力学改善之间的关联。

方法

采用邻近延伸分析方法检测20名对照者和26名HF患者在HT前及HT后1年血浆中的48种肿瘤相关蛋白。通过右心导管检查测量患者的血流动力学。

结果

在48种蛋白中,具体而言,与对照者相比,终末期HF患者血浆中的内皮糖蛋白(endocan)和CDO兄弟蛋白(BOC)水平升高(p<0.001),但HT后降低(p<0.01),接近对照者水平。HT后内皮糖蛋白水平的降低与平均肺动脉压改善相关(r = 0.80,p<0.0001)、肺动脉楔压改善相关(r = 0.63,p = 0.0012)以及肺血管阻力改善相关(r = 0.70,p<0.001)。HT后BOC水平的降低及恢复正常与平均右心房压降低相关(r = 0.61,p = 0.0015)和N末端脑钠肽原(NT-proBNP)降低相关(r = 0.57,p = 0.0022),以及与心脏指数升高相关(r = -0.51,p = 0.0086)和左心室每搏功指数升高相关(r = -0.57,p = 0.0039)。

结论

我们 的结果表明,(i)HF患者血浆中的内皮糖蛋白可能反映肺血管充血状态和PH-LHD,而(ii)血浆中的BOC可能反映HF患者的心脏功能和血流动力学负荷。这些蛋白的确切作用及其作为HF和PH-LHD生物标志物的临床适用性应在更大的队列中进行研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/aad012c1bfcf/380_2020_1656_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/ce2126533a67/380_2020_1656_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/3cf09ec49b35/380_2020_1656_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/943699a1033f/380_2020_1656_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/aad012c1bfcf/380_2020_1656_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/ce2126533a67/380_2020_1656_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/3cf09ec49b35/380_2020_1656_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/943699a1033f/380_2020_1656_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51ba/7502449/aad012c1bfcf/380_2020_1656_Fig4_HTML.jpg

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