Evidence map›Paper›PMID 32295533›Full record

ArticleBMC cardiovascular disorders2020

Serum human epididymis protein 4 level as a predictor of clinical worsening in idiopathic pulmonary arterial hypertension: a pilot study.

Qi Jin, Yi Tang, Zhihong Liu, Wenlin Xie, Qin Luo, Zhihui Zhao, Qing Zhao, Zhiwei Huang, Xue Yu, Lu Yan and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Qi JinState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Yi TangState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Zhihong LiuState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China. zhihongliufuwai@163.com.
Wenlin XieDepartment of Pathology, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Qin LuoState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Zhihui ZhaoState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Qing ZhaoState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Zhiwei HuangState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Xue YuState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Lu YanState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Changming XiongState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Xinhai NiState Key Laboratory of Cardiovascular Disease, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, China.
Yinkun YanDepartment of Epidemiology, Capital institute of Pediatrics, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Institute of Pediatrics · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China 81370326National Natural Science Foundation of China 81641005National Natural Science Foundation of China 81800056National Precision Medical Research Program of China 2016YFC0905602
6 · The paper itself

Abstract

backgroundHuman epididymis protein 4 (HE4) was proved to be a novel biomarker for left heart failure. The purpose of this exploratory study was to evaluate the role of HE4 in patients with idiopathic pulmonary arterial hypertension (IPAH) who usually have concurrent right heart failure.

methods55 patients with newly diagnosed IPAH were continuously enrolled and serum HE4 levels were assessed at baseline. All patients were followed up from the date of blood sampling, and a composite endpoint of clinical worsening was detailedly recorded.

resultsSerum levels of HE4 were significantly higher in IPAH patients than healthy controls (6.9 ± 2.2 vs 4.4 ± 0.9 ng/ml, p < 0.05) and increased as cardiac function deteriorated. HE4 levels correlated with endothelin-1 (r = 0.331, p < 0.01) and right atrial pressure (r = 0.30, p < 0.03). After a mean follow-up of 20 ± 10 months, 13 patients experienced clinical worsening. Receiver operating characteristic analysis showed that HE4 levels > 6.5 ng/ml discriminated clinical worsening with a sensitivity of 92.31% and a specificity of 59.52% (area under the curve [AUC] = 0.81). Multivariate Cox regression analysis demonstrated that HE4 (χ

conclusionsSerum levels of HE4 were elevated in IPAH patients and correlated with disease severity. HE4 was an independent predictor of clinical worsening in IPAH patients.

Indexed as

AdultBiomarkersCase-Control StudiesDisease ProgressionFamilial Primary Pulmonary HypertensionFemaleHumansMalePilot ProjectsPredictive Value of TestsSeverity of Illness IndexUp-RegulationWAP Four-Disulfide Core Domain Protein 2Young AdultBiomarkersWAP Four-Disulfide Core Domain Protein 2WFDC2 protein, humanCardiac functionClinical worseningHuman epididymis protein 4Idiopathic pulmonary arterial hypertensionPredictor

Identifiers

PMID32295533
PMCPMC7160929
OpenAlexW3017213983

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.