Evidence map›Paper›PMID 38257821›Full record

ReviewViruses2024

Myocardial Oedema as a Consequence of Viral Infection and Persistence-A Narrative Review with Focus on COVID-19 and Post COVID Sequelae.

Noel G Panagiotides, Michael Poledniczek, Martin Andreas, Martin Hülsmann, Alfred A Kocher, Christoph W Kopp, Aleksandra Piechota-Polanczyk, Annika Weidenhammer, Noemi Pavo, Patricia P Wadowski

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. New Insights into Cardiac Intensive Care.Reviews in cardiovascular medicine · 2026
    Review
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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

10 authors at 2 institutions in 2 countries.

Noel G PanagiotidesDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-5246-8241
Michael PoledniczekDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-6091-9823
Martin AndreasDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Martin HülsmannDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.
Alfred A KocherDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Christoph W KoppDivision of Angiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.
Aleksandra Piechota-PolanczykDepartment of Cell Cultures and Genomic Analysis, Medical University of Lodz, 90-752 Łódź, Poland.ORCID 0000-0001-8062-4435
Annika WeidenhammerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.
Noemi PavoDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.
Patricia P WadowskiDivision of Angiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-2462-4515
Medical University of Vienna · ATMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microvascular integrity is a critical factor in myocardial fluid homeostasis. The subtle equilibrium between capillary filtration and lymphatic fluid removal is disturbed during pathological processes leading to inflammation, but also in hypoxia or due to alterations in vascular perfusion and coagulability. The degradation of the glycocalyx as the main component of the endothelial filtration barrier as well as pericyte disintegration results in the accumulation of interstitial and intracellular water. Moreover, lymphatic dysfunction evokes an increase in metabolic waste products, cytokines and inflammatory cells in the interstitial space contributing to myocardial oedema formation. This leads to myocardial stiffness and impaired contractility, eventually resulting in cardiomyocyte apoptosis, myocardial remodelling and fibrosis. The following article reviews pathophysiological inflammatory processes leading to myocardial oedema including myocarditis, ischaemia-reperfusion injury and viral infections with a special focus on the pathomechanisms evoked by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In addition, clinical implications including potential long-term effects due to viral persistence (long COVID), as well as treatment options, are discussed.

Indexed as

COVID-19Virus DiseasesDisease ProgressionEdemaHumansPost-Acute COVID-19 SyndromeSARS-CoV-2coronavirus disease 2019glycocalyxmicrocirculationmyocardial oedemaplatelets

Identifiers

PMID38257821
PMCPMC10818479
OpenAlexW4390885257

What Socratic 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 Socratic graph.