Evidence map›Paper›PMID 34484561›Full record

ReviewOxidative medicine and cellular longevity2021

COVID-19 and Acute Coronary Syndromes: From Pathophysiology to Clinical Perspectives.

Luca Esposito, Francesco Paolo Cancro, Angelo Silverio, Marco Di Maio, Patrizia Iannece, Antonio Damato, Carmine Alfano, Giuseppe De Luca, Carmine Vecchione, Gennaro Galasso

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  6. Coronary Implications of COVID-19.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
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  17. COVID-19 and the heart.World journal of clinical cases · 2022
    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 3 institutions in 1 country.

Luca EspositoDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.ORCID https://orcid.org/0000-0003-0515-639X
Francesco Paolo CancroDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.ORCID https://orcid.org/0000-0001-7189-8469
Angelo SilverioDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.ORCID https://orcid.org/0000-0001-9749-8092
Marco Di MaioDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.
Patrizia IanneceDepartment of Chemistry and Biology, University of Salerno, Fisciano, Italy.
Antonio DamatoVascular Pathophysiology Unit, IRCCS Neuromed, Pozzilli, Isernia, Italy.
Carmine AlfanoDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.
Giuseppe De LucaDivision of Cardiology, Azienda Ospedaliera-Universitaria "Maggiore della Carità, " Eastern Piedmont University, Novara, Italy.
Carmine VecchioneDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.
Gennaro GalassoDepartment of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy.ORCID https://orcid.org/0000-0002-7265-7613
University of Salerno · ITIstituto Neurologico Mediterraneo · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute coronary syndromes (ACS) are frequently reported in patients with coronavirus disease 2019 (COVID-19) and may impact patient clinical course and mortality. Although the underlying pathogenesis remains unclear, several potential mechanisms have been hypothesized, including oxygen supply/demand imbalance, direct viral cellular damage, systemic inflammatory response with cytokine-mediated injury, microvascular thrombosis, and endothelial dysfunction. The severe hypoxic state, combined with other conditions frequently reported in COVID-19, namely sepsis, tachyarrhythmias, anemia, hypotension, and shock, can induce a myocardial damage due to the mismatch between oxygen supply and demand and results in type 2 myocardial infarction (MI). In addition, COVID-19 promotes atherosclerotic plaque instability and thrombus formation and may precipitate type 1 MI. Patients with severe disease often show decrease in platelets count, higher levels of d-dimer, ultralarge von Willebrand factor multimers, tissue factor, and prolongation of prothrombin time, which reflects a prothrombotic state. An endothelial dysfunction has been described as a consequence of the direct viral effects and of the hyperinflammatory environment. The expression of tissue factor, von Willebrand factor, thromboxane, and plasminogen activator inhibitor-1 promotes the prothrombotic status. In addition, endothelial cells generate superoxide anions, with enhanced local oxidative stress, and endothelin-1, which affects the vasodilator/vasoconstrictor balance and platelet aggregation. The optimal management of COVID-19 patients is a challenge both for logistic and clinical reasons. A deeper understanding of ACS pathophysiology may yield novel research insights and therapeutic perspectives in higher cardiovascular risk subjects with COVID-19.

Indexed as

Acute Coronary SyndromeCOVID-19HumansSARS-CoV-2

Identifiers

PMID34484561
PMCPMC8410438
OpenAlexW3197790205

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.