Evidence map›Paper›PMID 32194638›Full record

ArticleFrontiers in genetics2020

A Novel Heterozygous Variant in F2 Gene in a Chinese Patient With Coronary Thrombosis and Acute Myocardial Infarction Leads to Antithrombin Resistance.

Yi Tang, Liyang Zhang, Wenlin Xie, Jieyuan Jin, Yujiao Luo, Mingyang Deng, Zhengyu Liu, Hong Wei Pan, Yi Zhang, Zhaofen Zheng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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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

11 authors at 4 institutions in 1 country.

Yi TangDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, China.
Liyang ZhangDepartment of Neurosurgery, The XiangYa Hospital, Central South University, Changsha, China.
Wenlin XieDepartment of Pathology, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Jieyuan JinDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, China.
Yujiao LuoDepartment of Hematopathology, The Second Xiangya Hospital, Central South University, Changsha, China.
Mingyang DengDepartment of Hematopathology, The Second Xiangya Hospital, Central South University, Changsha, China.
Zhengyu LiuDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, China.
Hong Wei PanDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, China.
Yi ZhangDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, China.
Zhaofen ZhengDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, China.
Liang-Liang FanDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, China.
Hunan Provincial People's Hospital · CNCentral South University · CNThe Seventh Affiliated Hospital of Sun Yat-sen University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombophilia refers to a group of conditions where the blood clots more easily than normal. These blood clots can cause problems such as deep vein thrombosis or pulmonary embolism. Most kinds of mutated coagulation factors II (F2) exhibit lower procoagulant activity, but in some cases, a higher coagulation rate has been observed. The underlying mechanism is that those variations can prevent F2s from being inhibited by antithrombin, leading to a contiguous activation of procoagulation, and causing recurrent thromboembolism. In this study, a patient was admitted to our hospital due to repeated chest pain for 2 days and aggravated for 4 h. A medical history investigation showed that he had three deep venous thromboses in the lower limbs and one portal vein thrombosis events during the past 10 years. The electrocardiogram showed Q wave elevation and slight ST segment elevation in lead V2, and coronary angiogram showed a total occlusion of the left anterior descending artery. Laboratory testing found that troponin I was obviously elevated. Family history also indicated that both his father (II-3) and grandfather (I-1) died from pulmonary thromboembolism. Whole-exome sequencing was performed to detect the genetic lesion of the patient, and a novel mutation (c.1621 C>T/p.R541W) of

Indexed as

acute myocardial infarctionantithrombin resistancecoronary thrombosisF2mutation

Identifiers

PMID32194638
PMCPMC7062912
OpenAlexW3010610740

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.