About: Investigational treatments for COVID-19 may increase ventricular arrhythmia risk through drug interactions

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About: Investigational treatments for COVID-19 may increase ventricular arrhythmia risk through drug interactions Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Investigational treatments for COVID-19 may increase ventricular arrhythmia risk through drug interactions
Creator	Campana, Chiara Dariolli, Rafael Gutierrez, Amy Irurzun-Arana, Itziar Pullinger, Taylor Sobie, Eric Varshneya, Meera
source	MedRxiv; Medline; PMC
abstract	Many drugs that have been proposed for treatment of COVID-19 are reported to cause cardiac adverse events, including ventricular arrhythmias. In order to properly weigh risks against potential benefits, particularly when decisions must be made quickly, mathematical modeling of both drug disposition and drug action can be useful for predicting patient response and making informed decisions. Here we explored the potential effects on cardiac electrophysiology of 4 drugs proposed to treat COVID-19: lopinavir, ritonavir, chloroquine, and azithromycin, as well as combination therapy involving these drugs. Our study combined simulations of pharmacokinetics (PK) with quantitative systems pharmacology (QSP) modeling of ventricular myocytes to predict potential cardiac adverse events caused by these treatments. Simulation results predicted that drug combinations can lead to greater cellular action potential prolongation, analogous to QT prolongation, compared with drugs given in isolation. The combination effect can result from both pharmacokinetic and pharmacodynamic drug interactions. Importantly, simulations of different patient groups predicted that females with pre-existing heart disease are especially susceptible to drug-induced arrhythmias, compared males with disease or healthy individuals of either sex. Overall, the results illustrate how PK and QSP modeling may be combined to more precisely predict cardiac risks of COVID-19 therapies.
has issue date	2020-05-26(xsd:dateTime)
bibo:doi	10.1101/2020.05.21.20109397
bibo:pmid	32511528
has license	cc-by-nc-nd
sha1sum (hex)	d7b8f065f19198ff6b1544ba835c0cd294a467d9
schema:url	https://doi.org/10.1101/2020.05.21.20109397
resource representing a document's title	Investigational treatments for COVID-19 may increase ventricular arrhythmia risk through drug interactions
has PubMed Central identifier	PMC7273296
has PubMed identifier	32511528
schema:publication	medRxiv
resource representing a document's body	covid:d7b8f065f19198ff6b1544ba835c0cd294a467d9#body_text
is schema:about of	named entity 'drugs' named entity 'therapies' named entity 'disease' named entity 'caused' named entity 'pharmacokinetics' named entity 'drugs' named entity 'predicted' named entity 'informed' named entity 'compared' named entity 'lead' named entity 'WEIGH' named entity 'PHARMACODYNAMIC DRUG INTERACTIONS' named entity 'OVERALL' named entity 'ventricular' named entity 'Many' named entity 'cellular' named entity 'drug-induced' named entity 'illustrate' named entity 'order' named entity 'mathematical modeling' named entity 'myocytes' named entity 'ventricular arrhythmias' named entity 'arrhythmias' named entity 'females' named entity 'simulations' named entity 'drug interactions' named entity 'drug action' named entity 'pharmacodynamic' named entity 'adverse events' named entity 'heart disease' named entity 'ventricular myocytes' named entity 'informed decisions' named entity 'action potential' named entity 'COVID-19' named entity 'drug interactions' named entity 'simulations' named entity 'heart failure' named entity 'pharmacometrics' named entity 'pharmacological' named entity 'drug-induced' named entity 'cardiac disease' named entity 'ordinary differential equations' named entity 'medRxiv' named entity 'IC50' named entity 'ventricular arrhythmias' named entity 'IC50' named entity 'chloroquine' named entity 'ritonavir' named entity 'decision making' named entity 'ionic currents' named entity 'heart disease' named entity 'drug combination' named entity 'IC50' named entity 'lopinavir' named entity 'cardiac electrophysiology' named entity 'pharmacodynamic' named entity 'lopinavir' named entity 'lopinavir' named entity 'medRxiv' named entity 'heart failure' named entity 'plasma' named entity 'Combination therapy' named entity 'action potentials' named entity 'azithromycin' named entity 'rectifier' named entity 'azithromycin' named entity 'physiological effects' named entity 'heart failure' named entity 'azithromycin' named entity 'IC50' named entity 'azithromycin' named entity 'prognosis' named entity 'plasma' named entity 'medRxiv' named entity 'lopinavir'

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