About: Possible Mechanisms Responsible for Acute Coronary Events in COVID-19

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Possible Mechanisms Responsible for Acute Coronary Events in COVID-19
Creator	Bawa, Bawa, D Bawa, Danish Gaddam, Danish Gaddam, J Gaddam, Jashwanth Garikipati, Jashwanth Garikipati, S Garikipati, Subhash Grewal, S Grewal, Udhayvir Patel, H Patel, Harsh Patel, Samarthkumar Sheth, Aakash Thakkar, S Thakkar, Subhash
Source	Elsevier; Medline; PMC
abstract	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.
has issue date	2020-07-21(xsd:dateTime)
bibo:doi	10.1016/j.mehy.2020.110125
bibo:pmid	32763657
has license	no-cc
sha1sum (hex)	ad5aa8ec8f16fe6c7762bb31d8ee07ed217b9a2d
schema:url	https://doi.org/10.1016/j.mehy.2020.110125
resource representing a document's title	Possible Mechanisms Responsible for Acute Coronary Events in COVID-19
has PubMed Central identifier	PMC7371587
has PubMed identifier	32763657
schema:publication	Med Hypotheses
resource representing a document's body	covid:ad5aa8ec8f16fe6c7762bb31d8ee07ed217b9a2d#body_text
is schema:about of	named entity 'chemokines' named entity 'Direct' named entity 'formation' named entity 'hypercoagulable' named entity 'heart' named entity 'myocardial' named entity 'infection' named entity 'coronavirus' named entity 'Possible' named entity 'Coronary' named entity 'Mechanisms' named entity 'severe' named entity 'COVID-19' named entity 'causing' named entity 'response' named entity 'COVID-19' named entity 'initiation' named entity 'mechanism' named entity 'generate' named entity 'COVID-19' named entity 'recognized' named entity 'Mechanisms' named entity 'vasoconstriction' named entity 'smooth muscle cells' named entity 'oxygen radicals' named entity 'coronavirus' named entity 'proteases' named entity 'COVID' named entity 'immune response' named entity 'collagen' named entity 'pathogen' named entity 'human body' named entity 'Systemic viral' named entity 'intima' named entity 'tissue factor' named entity 'coagulation factors' named entity 'secretion' named entity 'COVID' named entity 'chemokines' named entity 'vasoactive' named entity 'fatty streaks' named entity 'COVID-19' named entity 'COVID-19' named entity 'SARS-CoV2' named entity 'myocardial injury' named entity 'cytokine storm' named entity 'protein' named entity 'organ damage' named entity 'Platelets' named entity 'arterial pressure' named entity 'myocardial ischemia' named entity 'COVID-19' named entity 'infection' named entity 'cardiovascular complications' named entity 'cardiovascular' named entity 'shear stress' named entity 'viscosity' named entity 'COVID-19 infection' named entity 'plasma' named entity 'respiratory viral infections' named entity 'endothelial' named entity 'acute coronary syndromes' named entity 'coronary vasoconstriction' named entity 'viral infections' named entity 'endothelial'

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