Evidence map›Paper›PMID 32789839›Full record

ReviewCardiology journal2020

Cardiovascular disease during the COVID-19 pandemic: Think ahead, protect hearts, reduce mortality.

Guoliang Li, Ardan M Saguner, Jiaqi An, Yuye Ning, John D Day, Ligang Ding, Xavier Waintraub, Jie Wang

Abstract readReview
In one paragraph

Review in Cardiology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Measuring the QT interval on the go.Cardiology journal · 2021
    Article
  11. Review
  12. Article
  13. Post-COVID-19 heart syndrome.Cardiology journal · 2021
    Article
  14. Article
  15. Article
  16. Observational
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Guoliang LiDepartment of Cardiovascular Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. liguoliang_med@163.com.ORCID 0000-0002-2352-9404
Ardan M SagunerDepartment of Cardiology, University Heart Center Zurich, Switzerland.
Jiaqi AnAtrial Fibrillation Centre, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yuye NingDepartment of Cardiovascular Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0003-0727-1084
John D DayIntermountain Medical Center Heart Institute, United States.
Ligang DingDepartment of Cardiovascular Medicine, Clinical EP Lab & Arrhythmia Center, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xavier WaintraubCardiology Institute, Rhythmology Unit, Hôpital Universitaire La Pitié-Salpêtrière, Paris, France.
Jie WangDepartment of Cardiovascular Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is rapidly spreading globally. As of October 3, 2020, the number of confirmed cases has been nearly 34 million with more than 1 million fatalities. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is accountable for COVID-19. Newly diagnosed and worsening cardiovascular disease are common complications in COVID-19 patients, including acute cardiac injury, hypertension, arrhythmia, myocardial infarction, heart failure and sudden cardiac arrest. The mechanisms contributing to cardiac disease burden include hypoxemia, inflammatory factor storm, dysfunctional angiotensin converting enzyme 2 (ACE2), and drug-induced cardiac toxicity. Notably, the macrophages expressing ACE2 as direct host cells of SARS-CoV-2 secrete chemokine and inflammatory cytokines, as well as a decrease in cellular immune responses to SARS-CoV-2 infection due to elevated exhaustion levels and dysfunctional diversity of T cells, that may be accountable for the "hyperinflammation and cytokine storm syndrome" and subsequently acute cardiac injury and deteriorating cardiovascular disease in COVID-19 patients. However, no targeted medication or vaccines for COVID-19 are yet available. The management of cardiovascular disease in patients with COVID-19 include general supportive treatment, circulatory support, other symptomatic treatment, psychological assistance as well as online consultation. Further work should be concentrated on better understanding the pathogenesis of COVID-19 and accelerating the development of drugs and vaccines to reduce the cardiac disease burden and promote the management of COVID-19 patients, especially those with a severe disease course and cardiovascular complications.

Indexed as

BetacoronavirusCardiovascular DiseasesCoronavirus InfectionsCOVID-19HumansPandemicsPneumonia, ViralSARS-CoV-2Survival Rateangiotensin converting enzyme 2cardiovascular complicationsCOVID-19endotheliitisinflammatory factor stormonline consultation

Identifiers

PMID32789839
PMCPMC8078991

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.