Evidence map›Paper›PMID 38451350›Full record

ArticleIntensive care medicine experimental2024

The association between coronary artery calcification and vectorcardiography in mechanically ventilated COVID-19 patients: the Maastricht Intensive Care COVID cohort.

Eda Aydeniz, Frank van Rosmalen, Jip de Kok, Bibi Martens, Alma M A Mingels, Mustafa Emin Canakci, Casper Mihl, Kevin Vernooy, Frits W Prinzen, Joachim E Wildberger and 3 more

Open access · goldAbstract read
In one paragraph

Article in Intensive care medicine experimental, 2024. 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
1.6field-weighted citation impact, top 19% 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, 4 citations in OpenAlex.

  1. Article
  2. Article
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 2 institutions in 2 countries.

Eda AydenizDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands. eda.aydeniz@mumc.nl.ORCID http://orcid.org/0009-0007-4950-9026
Frank van RosmalenDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-9522-3711
Jip de KokDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-5495-0285
Bibi MartensCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0003-3105-6640
Alma M A MingelsCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-4648-5053
Mustafa Emin CanakciDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-9015-1782
Casper MihlCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0003-1348-6970
Kevin VernooyCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-8818-5964
Frits W PrinzenCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-8917-9032
Joachim E WildbergerCardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-4810-6854
Iwan C C van der HorstDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0003-3891-8522
Bas C T van BusselDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0003-1621-7848
Rob G H DriessenDepartment of Intensive Care Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-8287-6166
Maastricht University · NLMaastricht University Medical Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary artery calcification (CAC) is associated with poor outcome in critically ill patients. A deterioration in cardiac conduction and loss of myocardial tissue could be an underlying cause. Vectorcardiography (VCG) and cardiac biomarkers provide insight into these underlying causes. The aim of this study was to investigate whether a high degree of CAC is associated with VCG-derived variables and biomarkers, including high-sensitivity troponin-T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP).

methodsMechanically ventilated coronavirus-19 (COVID-19) patients with an available chest computed tomography (CT) and 12-lead electrocardiogram (ECG) were studied. CAC scores were determined using chest CT scans. Patients were categorized into 3 sex-specific tertiles: low, intermediate, and high CAC. Daily 12 leads-ECGs were converted to VCGs. Daily hs-cTnT and NT-proBNP levels were determined. Linear mixed-effects regression models examined the associations between CAC tertiles and VCG variables, and between CAC tertiles and hs-cTnT or NT-proBNP levels.

resultsIn this study, 205 patients (73.2% men, median age 65 years [IQR 57.0; 71.0]) were included. Compared to the lowest CAC tertile, the highest CAC tertile had a larger QRS area at baseline (6.65 µVs larger [1.50; 11.81], p = 0.012), which decreased during admission (- 0.27 µVs per day [- 0.43; - 0.11], p = 0.001). Patients with the highest CAC tertile also had a longer QRS duration (12.02 ms longer [4.74; 19.30], p = 0.001), higher levels of log hs-cTnT (0.79 ng/L higher [0.40; 1.19], p < 0.001) and log NT-proBNP (0.83 pmol/L higher [0.30; 1.37], p = 0.002).

conclusionPatients with a high degree of CAC had the largest QRS area and higher QRS amplitude, which decreased more over time when compared to patients with a low degree of CAC. These results suggest that CAC might contribute to loss of myocardial tissue during critical illness. These insights could improve risk stratification and prognostication of patients with critical illness.

Indexed as

COVID-19Intensive care unitVascular calcificationVectorcardiography

Identifiers

PMID38451350
PMCPMC10920503
OpenAlexW4392548487

What OpenQuestion holds

Textmetadata
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.