tetano
Editor, Senior Moderator
JACC Clin Electrophysiol
. 2020 Sep;6(9):1193-1204.
doi: 10.1016/j.jacep.2020.08.002. Epub 2020 Aug 10.
Arrhythmias and COVID-19: A Review
Parinita Dherange[SUP] 1 [/SUP], Joshua Lang[SUP] 1 [/SUP], Pierre Qian[SUP] 1 [/SUP], Blake Oberfeld[SUP] 2 [/SUP], William H Sauer[SUP] 1 [/SUP], Bruce Koplan[SUP] 1 [/SUP], Usha Tedrow[SUP] 3 [/SUP]
Affiliations
Abstract
Current understanding of the impact of coronavirus disease-2019 (COVID-19) on arrhythmias continues to evolve as new data emerge. Cardiac arrhythmias are more common in critically ill COVID-19 patients. The potential mechanisms that could result in arrhythmogenesis among COVID-19 patients include hypoxia caused by direct viral tissue involvement of lungs, myocarditis, abnormal host immune response, myocardial ischemia, myocardial strain, electrolyte derangements, intravascular volume imbalances, and drug sides effects. To manage these arrhythmias, it is imperative to increase the awareness of potential drug-drug interactions, to monitor QTc prolongation while receiving COVID therapy and provide special considerations for patients with inherited arrhythmia syndromes. It is also crucial to minimize exposure to COVID-19 infection by stratifying the need for intervention and using telemedicine. As COVID-19 infection continues to prevail with a potential for future surges, more data are required to better understand pathophysiology and to validate management strategies.
Keywords: COVID-19; QT prolongation; SARS-CoV-2; arrhythmias; channelopathies; myocarditis; torsades de pointes.
. 2020 Sep;6(9):1193-1204.
doi: 10.1016/j.jacep.2020.08.002. Epub 2020 Aug 10.
Arrhythmias and COVID-19: A Review
Parinita Dherange[SUP] 1 [/SUP], Joshua Lang[SUP] 1 [/SUP], Pierre Qian[SUP] 1 [/SUP], Blake Oberfeld[SUP] 2 [/SUP], William H Sauer[SUP] 1 [/SUP], Bruce Koplan[SUP] 1 [/SUP], Usha Tedrow[SUP] 3 [/SUP]
Affiliations
- PMID: 32972561
- DOI: 10.1016/j.jacep.2020.08.002
Abstract
Current understanding of the impact of coronavirus disease-2019 (COVID-19) on arrhythmias continues to evolve as new data emerge. Cardiac arrhythmias are more common in critically ill COVID-19 patients. The potential mechanisms that could result in arrhythmogenesis among COVID-19 patients include hypoxia caused by direct viral tissue involvement of lungs, myocarditis, abnormal host immune response, myocardial ischemia, myocardial strain, electrolyte derangements, intravascular volume imbalances, and drug sides effects. To manage these arrhythmias, it is imperative to increase the awareness of potential drug-drug interactions, to monitor QTc prolongation while receiving COVID therapy and provide special considerations for patients with inherited arrhythmia syndromes. It is also crucial to minimize exposure to COVID-19 infection by stratifying the need for intervention and using telemedicine. As COVID-19 infection continues to prevail with a potential for future surges, more data are required to better understand pathophysiology and to validate management strategies.
Keywords: COVID-19; QT prolongation; SARS-CoV-2; arrhythmias; channelopathies; myocarditis; torsades de pointes.