2022
DOI: 10.1016/j.ccep.2021.10.004
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COVID-19, Acute Myocardial Injury, and Infarction

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Cited by 47 publications
(77 citation statements)
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“…The COVID-19 cohort exhibited a median aCCI of 3 points vs. 1 point in the non-COVID-19 cohort. A detailed analysis highlighted an increase observed in cardiovascular pathology (congestive heart failure and myocardial infarction) and dementia in the COVID-19 cohort, with data in line with similar studies (25)(26)(27), since those conditions are associated with common exacerbations, hospitalinpatient, and ultimately poor long-term outcomes. Other pulmonary diseases, such as chronic obstructive pulmonary disease, were not related to a significant increase in 1-year mortality with similar results in both cohorts (28).…”
Section: Discussionsupporting
confidence: 74%
“…The COVID-19 cohort exhibited a median aCCI of 3 points vs. 1 point in the non-COVID-19 cohort. A detailed analysis highlighted an increase observed in cardiovascular pathology (congestive heart failure and myocardial infarction) and dementia in the COVID-19 cohort, with data in line with similar studies (25)(26)(27), since those conditions are associated with common exacerbations, hospitalinpatient, and ultimately poor long-term outcomes. Other pulmonary diseases, such as chronic obstructive pulmonary disease, were not related to a significant increase in 1-year mortality with similar results in both cohorts (28).…”
Section: Discussionsupporting
confidence: 74%
“…The ACE2 receptor serves as a master regulator of RAS. Beyond causing direct cellular damage through viral infiltration, SARS-CoV-2 downregulates ACE2 expression following unfavorable effects, including vasoconstriction, dysfunction of the endothelium, inflammatory responses (hyper-inflammation), activation of coagulation, and ultimately increased vascular permeability [ 34 ].…”
Section: Direct Cellular Injurymentioning
confidence: 99%
“…17,18,21 Following entry of SARS-CoV-2 into the host cell, ACE2 is subsequently downregulated, resulting in increased circulation of deleterious angiotensin II, which has been shown to result in cardiac dysfunction (Figure). 17,18,[22][23][24][25][26] Given this mechanism of cell entry, great concern arose surrounding the safety of continued use of chronic renin angiotensin system inhibitors, such as angiotensinconverting enzyme inhibitors and angiotensin receptor blockers, as use of these agents has been shown to increase ACE2 expression and presumably increase opportunity for viral cell entry. 6,27,28 Meanwhile, others proposed the use of these agents as possible COVID-19 therapeutics to combat the resultant downregulation of ACE2.…”
Section: Coronaviruses and The Cardiovascular System-overviewmentioning
confidence: 99%