tetano
Editor, Senior Moderator
Life Sci
. 2022 Sep 29;121018.
doi: 10.1016/j.lfs.2022.121018. Online ahead of print.
Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality
Aneta Aleksova[SUP] 1 [/SUP], Alessandra Lucia Fluca[SUP] 2 [/SUP], Giulia Gagno[SUP] 2 [/SUP], Alessandro Pierri[SUP] 2 [/SUP], Laura Padoan[SUP] 3 [/SUP], Agnese Derin[SUP] 4 [/SUP], Rita Moretti[SUP] 5 [/SUP], Elena Aleksova Noveska[SUP] 6 [/SUP], Eros Azzalini[SUP] 7 [/SUP], Stefano D'Errico[SUP] 8 [/SUP], Antonio Paolo Beltrami[SUP] 9 [/SUP], Alimuddin Zumla[SUP] 10 [/SUP], Giuseppe Ippolito[SUP] 11 [/SUP], Gianfranco Sinagra[SUP] 2 [/SUP], Milijana Janjusevic[SUP] 2 [/SUP]
Affiliations
Abstract
Since the very beginning of the coronavirus disease 2019 (COVID-19) pandemic in early 2020, it was evident that patients with cardiovascular disease (CVD) were at an increased risk of developing severe illness, and complications spanning cerebrovascular disorders, dysrhythmias, acute coronary syndrome, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure, thromboembolic disease, stroke, and death. Underlying these was excessive systemic inflammation and coagulopathy due to SARS-COV-2 infection, the effects of which also continued long-term as evidenced by post-COVID-19 CVS complications. The acute and chronic CVS effects of COVID-19 occurred even among those who were not hospitalized and had no previous CVD or those with mild symptoms. This comprehensive review summarizes the current understanding of molecular mechanisms triggered by the SARS-CoV-2 virus on various cells that express the angiotensin-converting enzyme 2, leading to endothelial dysfunction, inflammation, myocarditis, impaired coagulation, myocardial infarction, arrhythmia and a multisystem inflammatory syndrome in children or Kawasaki-like disease.
Keywords: COVID-19; Endothelial dysfunction; Inflammation; Myocardial injury; Oxidative stress; Thrombosis.
. 2022 Sep 29;121018.
doi: 10.1016/j.lfs.2022.121018. Online ahead of print.
Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality
Aneta Aleksova[SUP] 1 [/SUP], Alessandra Lucia Fluca[SUP] 2 [/SUP], Giulia Gagno[SUP] 2 [/SUP], Alessandro Pierri[SUP] 2 [/SUP], Laura Padoan[SUP] 3 [/SUP], Agnese Derin[SUP] 4 [/SUP], Rita Moretti[SUP] 5 [/SUP], Elena Aleksova Noveska[SUP] 6 [/SUP], Eros Azzalini[SUP] 7 [/SUP], Stefano D'Errico[SUP] 8 [/SUP], Antonio Paolo Beltrami[SUP] 9 [/SUP], Alimuddin Zumla[SUP] 10 [/SUP], Giuseppe Ippolito[SUP] 11 [/SUP], Gianfranco Sinagra[SUP] 2 [/SUP], Milijana Janjusevic[SUP] 2 [/SUP]
Affiliations
- PMID: 36183780
- DOI: 10.1016/j.lfs.2022.121018
Abstract
Since the very beginning of the coronavirus disease 2019 (COVID-19) pandemic in early 2020, it was evident that patients with cardiovascular disease (CVD) were at an increased risk of developing severe illness, and complications spanning cerebrovascular disorders, dysrhythmias, acute coronary syndrome, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure, thromboembolic disease, stroke, and death. Underlying these was excessive systemic inflammation and coagulopathy due to SARS-COV-2 infection, the effects of which also continued long-term as evidenced by post-COVID-19 CVS complications. The acute and chronic CVS effects of COVID-19 occurred even among those who were not hospitalized and had no previous CVD or those with mild symptoms. This comprehensive review summarizes the current understanding of molecular mechanisms triggered by the SARS-CoV-2 virus on various cells that express the angiotensin-converting enzyme 2, leading to endothelial dysfunction, inflammation, myocarditis, impaired coagulation, myocardial infarction, arrhythmia and a multisystem inflammatory syndrome in children or Kawasaki-like disease.
Keywords: COVID-19; Endothelial dysfunction; Inflammation; Myocardial injury; Oxidative stress; Thrombosis.