Evidence map›Paper›PMID 34013612›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)2021

Coronary microvascular dysfunction pathophysiology in COVID-19.

Jie Yin, Shaoshen Wang, Yang Liu, Junhong Chen, Dongye Li, Tongda Xu

Open access · bronzeAbstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Article
  8. Myocardial ischaemia following COVID-19: a cardiovascular magnetic resonance study.The international journal of cardiovascular imaging · 2025
    Observational
  9. Coronary Implications of COVID-19.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Review
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  11. Article
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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

6 authors at 1 institution in 1 country.

Jie YinInstitute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, China.
Shaoshen WangDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Yang LiuInstitute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, China.
Junhong ChenDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Dongye LiInstitute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0003-4875-0209
Tongda XuDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, accumulating evidence has highlighted the role of endothelial dysfunction in COVID-19 progression. Coronary microvascular dysfunction (CMD) plays a pivotal role in cardiovascular disease (CVD) and CVD-related risk factors (eg, age, gender, hypertension, diabetes mellitus, and obesity). Equally, these are also risk factors for COVID-19. The purpose of this review was to explore CMD pathophysiology in COVID-19, based on recent evidence. COVID-19 mechanisms were reviewed in terms of imbalanced renin-angiotensin-aldosterone-systems (RAAS), systemic inflammation and immune responses, endothelial dysfunction, and coagulatory disorders. Based on these mechanisms, we addressed CMD pathophysiology within the context of COVID-19, from five perspectives. The first was the disarrangement of local RAAS and Kallikrein-kinin-systems attributable to SARS-Cov-2 entry, and the concomitant decrease in coronary microvascular endothelial angiotensin I converting enzyme 2 (ACE2) levels. The second was related to coronary microvascular obstruction, induced by COVID-19-associated systemic hyper-inflammation and pro-thrombotic state. The third was focused on how pneumonia/acute respiratory distress syndrome (ARDS)-related systemic hypoxia elicited oxidative stress in coronary microvessels and cardiac sympathetic nerve activation. Fourthly, we discussed how autonomic nerve dysfunction mediated by COVID-19-associated mental, physical, or physiological factors could elicit changes in coronary blood flow, resulting in CMD in COVID-19 patients. Finally, we analyzed reciprocity between the coronary microvascular endothelium and perivascular cellular structures due to viremia, SARS-CoV-2 dissemination, and systemic inflammation. These mechanisms may function either consecutively or intermittently, finally culminating in CMD-mediated cardiovascular symptoms in COVID-19 patients. However, the underlying molecular pathogenesis remains to be clarified.

Indexed as

SARS-CoV-2Cardiovascular DiseasesCoronary VesselsCOVID-19Disease ProgressionEndothelium, VascularFemaleHumansInflammationMaleMicrocirculationModels, CardiovascularRenin-Angiotensin SystemRisk FactorsThrombosiscoronary microvascular dysfunctionCOVID-19SARS-CoV-2

Identifiers

PMID34013612
PMCPMC8236988
OpenAlexW3161622711

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.