Evidence map›Paper›PMID 33228225›Full record

ReviewCells2020

Cardiovascular Manifestations of COVID-19 Infection.

Ajit Magadum, Raj Kishore

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 4% 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

115 citing papers in PubMed, 2 syntheses or guidelines pooled it, 241 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
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  12. Cause of Death Analysis in a 9½-Year-Old with COVID-19 and Dravet Syndrome.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  13. Article
  14. Article
  15. Navigating Cardiovascular Challenges of Obesity: Exploring Preventive Approaches.Endocrine, metabolic & immune disorders drug targets · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

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

2 authors at 1 institution in 1 country.

Ajit MagadumCenter for Translational Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0001-7298-8255
Raj KishoreCenter for Translational Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0002-8168-3004
Temple University · US

Funding

Small and large animal surgery, physiology and histologyP01HL134608 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI Raj Kishore · 2017 to 2026
$21.0M
TNF mRNA stability and restenosisR01HL091983 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KISHORE, RAJ · 2009 to 2022
$5.3M
Restoration of myocardial reparative function of diabetic progenitor cells by epigenetic modulationR01HL143892 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KISHORE, RAJ · 2020 to 2023
$2.2M
NHLBI NIH HHS P01 HL134608NHLBI NIH HHS R01 HL091983NHLBI NIH HHS R01 HL143892NIH HHS HL091983, HL143892, and HL134608
6 · The paper itself

Abstract

SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus's pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.

Indexed as

PandemicsAngiotensin-Converting Enzyme 2AnimalsBlood PlateletsCardiovascular DiseasesComorbidityCOVID-19CytokinesDisease Models, AnimalEndothelial CellsHumansReactive Oxygen SpeciesRisk FactorsSARS-CoV-2Virus InternalizationACE2 protein, humanAngiotensin-Converting Enzyme 2CytokinesReactive Oxygen Speciesangiotensin converting enzyme-2cardiovascular diseaseCOVID-19cytokine storm and inflammationmyocardial injurySARS-CoV-2

Identifiers

PMID33228225
PMCPMC7699571
OpenAlexW3101625880

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.