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1.
Curr Cardiol Rep ; 22(5): 36, 2020 05 13.
Article in English | MEDLINE | ID: covidwho-309604

ABSTRACT

It has been pointed out that the second paragraph of the section "Treatments for SARS-CoV-2 Infection" contains an error. The original article has been corrected.

2.
Curr Cardiol Rep ; 22(5): 32, 2020 04 21.
Article in English | MEDLINE | ID: covidwho-100111

ABSTRACT

PURPOSE OF REVIEW: Coronavirus disease of 2019 (COVID-19) is a cause of significant morbidity and mortality worldwide. While cardiac injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury remains unclear. Here, we review our current knowledge of the biology of SARS-CoV-2 and the potential mechanisms of myocardial injury due to viral toxicities and host immune responses. RECENT FINDINGS: A number of studies have reported an epidemiological association between history of cardiac disease and worsened outcome during COVID infection. Development of new onset myocardial injury during COVID-19 also increases mortality. While limited data exist, potential mechanisms of cardiac injury include direct viral entry through the angiotensin-converting enzyme 2 (ACE2) receptor and toxicity in host cells, hypoxia-related myocyte injury, and immune-mediated cytokine release syndrome. Potential treatments for reducing viral infection and excessive immune responses are also discussed. COVID patients with cardiac disease history or acquire new cardiac injury are at an increased risk for in-hospital morbidity and mortality. More studies are needed to address the mechanism of cardiotoxicity and the treatments that can minimize permanent damage to the cardiovascular system.


Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/immunology , Heart Diseases/complications , Heart Diseases/immunology , Heart Diseases/virology , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus , COVID-19 , Coronavirus Infections/therapy , Cytokines/immunology , Humans , Hypoxia/pathology , Myocytes, Cardiac/pathology , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/therapy , SARS-CoV-2
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