Evidence map›Paper›PMID 32984892›Full record

Trial reportEuropean heart journal2020

Angiotensin-converting enzyme 2 (ACE2) levels in relation to risk factors for COVID-19 in two large cohorts of patients with atrial fibrillation.

Lars Wallentin, Johan Lindbäck, Niclas Eriksson, Ziad Hijazi, John W Eikelboom, Michael D Ezekowitz, Christopher B Granger, Renato D Lopes, Salim Yusuf, Jonas Oldgren and 1 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 4 pooled it
19.5field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 4 syntheses or guidelines pooled it, 123 citations in OpenAlex.

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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 3 countries.

Lars WallentinDepartment of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Johan LindbäckUppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
Niclas ErikssonUppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
Ziad HijaziDepartment of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
John W EikelboomPopulation Health Research Institute, McMaster University and Hamilton Health Sciences, Hamilton, Canada.
Michael D EzekowitzThomas Jefferson Medical College and the Heart Center, Wynnewood, PA, USA.
Christopher B GrangerDuke Clinical Research Institute, Duke University Medical Center, Duke Health, Durham, NC, USA.
Renato D LopesDuke Clinical Research Institute, Duke University Medical Center, Duke Health, Durham, NC, USA.
Salim YusufPopulation Health Research Institute, McMaster University and Hamilton Health Sciences, Hamilton, Canada.
Jonas OldgrenDepartment of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Agneta SiegbahnUppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
Uppsala University · SEClinical Research Institute · USPopulation Health Research Institute · CAJefferson College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe global COVID-19 pandemic is caused by the SARS-CoV-2 virus entering human cells using angiotensin-converting enzyme 2 (ACE2) as a cell surface receptor. ACE2 is shed to the circulation, and a higher plasma level of soluble ACE2 (sACE2) might reflect a higher cellular expression of ACE2. The present study explored the associations between sACE2 and clinical factors, cardiovascular biomarkers, and genetic variability. METHODS AND

resultsPlasma and DNA samples were obtained from two international cohorts of elderly patients with atrial fibrillation (n = 3999 and n = 1088). The sACE2 protein level was measured by the Olink Proteomics® Multiplex CVD II96 × 96 panel. Levels of the biomarkers high-sensitive cardiac troponin T (hs-cTnT), N-terminal probrain natriuretic peptide (NT-proBNP), growth differentiation factor 15 (GDF-15), C-reactive protein, interleukin-6, D-dimer, and cystatin-C were determined by immunoassays. Genome-wide association studies were performed by Illumina chips. Higher levels of sACE2 were statistically significantly associated with male sex, cardiovascular disease, diabetes, and older age. The sACE2 level was most strongly associated with the levels of GDF-15, NT-proBNP, and hs-cTnT. When adjusting for these biomarkers, only male sex remained associated with sACE2. We found no statistically significant genetic regulation of the sACE2 level.

conclusionsMale sex and clinical or biomarker indicators of biological ageing, cardiovascular disease, and diabetes are associated with higher sACE2 levels. The levels of GDF-15 and NT-proBNP, which are associated both with the sACE2 level and a higher risk for mortality and cardiovascular disease, might contribute to better identification of risk for severe COVID-19 infection.

Indexed as

BetacoronavirusAgedAngiotensin-Converting Enzyme 2AntithrombinsAtrial FibrillationBiomarkersCohort StudiesCoronavirus InfectionsCOVID-19DabigatranFemaleHumansMaleMiddle AgedPandemicsPeptidyl-Dipeptidase AACE2 protein, humanAngiotensin-Converting Enzyme 2AntithrombinsapixabanBiomarkersDabigatranPeptidyl-Dipeptidase APyrazolesPyridonesWarfarinACE2AgeAtrial fibrillationBiomarkerCardiovascular diseaseCOVID-19

Identifiers

PMID32984892
PMCPMC7543499
OpenAlexW3088385564

What OpenQuestion holds

Textmetadata
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.