Possible mechanisms responsible for acute coronary events in COVID-19

Published by Elsevier Ltd..

The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.

Media Type:

Electronic Article

Year of Publication:

2020

Contained In:

Medical hypotheses - Vol. 143 (2020), p. 110125

Language:

English

Contributors:

Sheth, Aakash R
Grewal, Udhayvir S
Patel, Harsh P
Thakkar, Samarthkumar
Garikipati, Subhash
Gaddam, Jashwanth
Bawa, Danish

Links:

Volltext

Keywords:

*Betacoronavirus
*Models, Cardiovascular
*Pandemics
Acute Coronary Syndrome
CD4-Positive T-Lymphocytes
Chemokines
Coronary Artery Disease
Coronary Vessels
Coronavirus Infections
Cytokine Release Syndrome
Cytokines
Humans
Immunity, Innate
Journal Article
Plaque, Atherosclerotic
Platelet Activation
Pneumonia, Viral
Vasoconstriction
Virus Diseases

Notes:

Date Completed 13.10.2020

Date Revised 13.10.2020

published: Print-Electronic

Citation Status MEDLINE

Copyright: From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Physical Description:

Online-Ressource

doi:

10.1016/j.mehy.2020.110125

PMID:

32763657

PPN (Catalogue-ID):

NLM314317694