Abstract P2189: Role Of Innate Immune Response And Mitochondrial Ros In The Cardiac And Pulmonary Sequelae Of Covid-19

Abstract only Intro: Cardiac risk rises during acute SARS-CoV-2 infection and in long COVID syndrome, but the mechanisms behind COVID-19-linked arrhythmias are unknown. Here, we test the hypothesis that innate immune activation and mitochondrial ROS contribute to cardiac conduction abnormalities and...

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Bibliographic Details
Published in:Circulation research 2023-08, Vol.133 (Suppl_1)
Main Authors: Liu, Ting, Ashok, Deepthi, Craney, Morgan, Wong, Amanda, Foster, D B, Pekosz, Andrew, Villano, Jason, O'Rourke, Brian
Format: Article
Language:English
Online Access:Get full text
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Summary:Abstract only Intro: Cardiac risk rises during acute SARS-CoV-2 infection and in long COVID syndrome, but the mechanisms behind COVID-19-linked arrhythmias are unknown. Here, we test the hypothesis that innate immune activation and mitochondrial ROS contribute to cardiac conduction abnormalities and pulmonary dysfunction in a COVID-19 hamster model. Results: ECGs and subpleural pressures were recorded by radiotelemetry over a 4-week timespan after SARS-CoV-2 infection. Multiple cardiac arrhythmias were observed, including bradycardia, sinus pauses, and atrioventricular block (AVB). RR intervals and sinus arrhythmia (RR> mean+100ms, RR100) increased transiently 3-5 days after SARS-CoV-2 infection (baseline/peak: RR, 167±3ms/241±7ms; RR100, 5.5±0.4min -1 /22.7±3.0min -1 ) and returned to levels ≤ baseline by 7 dpi. After the acute phase, these measures increased above baseline over 3 weeks (at 28dpi: RR, 190±2ms, p
ISSN:0009-7330
1524-4571
DOI:10.1161/res.133.suppl_1.P2189