Evidence map›Paper›PMID 36946389›Full record

ArticleClinical cardiology2023

Synergistic role of circulating CD14++CD16+ monocytes and fibrinogen in predicting the cardiovascular events after myocardial infarction.

Chong Zhang, Shan Zeng, Wenjie Ji, Zhi Li, Haonan Sun, Tianming Teng, Ying Yu, Xin Zhou, Qing Yang

Open access · goldAbstract read
In one paragraph

Article in Clinical cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 5 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

9 authors at 3 institutions in 1 country.

Chong ZhangDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Shan ZengTianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Heart Center, Pingjin Hospital, Tianjin, China.
Wenjie JiTianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Heart Center, Pingjin Hospital, Tianjin, China.
Zhi LiDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Haonan SunDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Tianming TengDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Ying YuDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Center for Cardiovascular Diseases, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xin ZhouDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.ORCID http://orcid.org/0000-0003-1395-7103
Qing YangDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Tianjin Medical University General Hospital · CNPingjin Hospital · CNTianjin Medical University · CN

Funding

National Natural Science Foundation of China 81970304Tianjin Municipal Science and Technology Commission 18ZXZNSY00290Tianjin Municipal Science and Technology Commission 19JCQNJC11500
6 · The paper itself

Abstract

backgroundMonocytes and fibrinogen (FIB) play important roles in driving acute and reparative inflammatory pathways after myocardial infarction (MI). In humans, there are three subsets of monocytes, namely, CD14++CD16- (Mon1), CD14++CD16+ (Mon2), and CD14+CD16++ (Mon3). During the inflammatory response, monocyte subsets express high levels of integrin α HYPOTHESIS: However, whether there is a synergistic role of FIB combined with Mon2 counts in prioritizing patients at high risk of future major adverse cardiovascular events (MACEs) after MI remains unknown.

methodsThe MI patients who treated with primary percutaneous coronary intervention were enrolled. MI patients were categorized into four groups, that is, low FIB/low Mon2, low FIB/high Mon2, high FIB/low Mon2, and high FIB/high Mon2, according to cutoff values of 3.28 g/L for FIB and 32.20 cells/μL for Mon2. Kaplan-Meier survival analysis and Cox proportional hazards models were used to estimate the risk of MACEs of MI patients during a median follow-up of 2.7 years. Mediating effects of high FIB levels and MACEs associated with high monocyte subsets were calculated by mediation analysis.

resultsHigh FIB/high Mon2 group had the highest risk of MACEs during a median follow-up of 2.7 years. Moreover, mediation analysis showed that a high FIB level could explain 24.9% (p < .05) of the increased risk of MACEs associated with Mon2.

conclusionThis work provides evidence indicating the translational potential of a synergistic role of FIB combined with Mon2 in prioritizing patients at high risk of future MACEs after MI.

Indexed as

MonocytesMyocardial InfarctionFibrinogenFlow CytometryHumansFibrinogenfibrinogenmajor adverse cardiovascular eventsmonocyte subsetsmyocardial infarction

Identifiers

PMID36946389
PMCPMC10189084
OpenAlexW4353016859

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.