Publication date: Jul 22, 2024

Angiotensin-converting enzyme 2 (ACE2) of the renin-angiotensin-aldosterone system (RAAS) serves as a functional receptor to gain entry into the cells for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19). The interaction between SARS-CoV-2 and ACE2 is a potential virulent factor in infectivity. Our study aims to ascertain the association of RAAS inhibitors with adverse cardiovascular and other outcomes in hospitalized COVID-19 patients. This is a retrospective study of medical records of ≥ 18-year-old patients hospitalized for COVID-19 from March 2020 to October 2020. Primary outcomes were acute cardiovascular events (ST-elevation myocardial infarction, non-ST elevation myocardial infarction type 1, acute congestive heart failure, acute stroke) and mortality. Secondary outcomes were respiratory failure, need for and duration of mechanical ventilation, acute deep vein thrombosis or pulmonary embolism (DVT/PE), and readmission rate. Among 376 hospitalized COVID-19 patients, 149 were on RAAS inhibitors. No statistically significant differences were found between RAAS inhibitor and non-RAAS inhibitor groups with respect to acute cardiovascular events (6% vs. 6. 2%, p=0. 94), acute DVT/PE (4. 7% vs. 4. 8%, p=0. 97), hypoxia (62. 4% vs. 58. 6%, p=0. 46), need for mechanical ventilation (18. 1% vs. 16. 7%, p=0. 72), mortality (19. 5% vs. 22%, p=0. 56), and readmission rate (11. 4% vs. 14. 1%, p=0. 45). Some nuances discovered were a higher rate of hospitalizations among Native Americans receiving RAAS inhibitors (30. 2% vs 19. 8%) and significantly lower levels of procalcitonin in patients on RAAS inhibitors. Among hospitalized patients with COVID-19, those on RAAS inhibitors showed no significant differences in acute cardiovascular events, acute DVT/PE, hypoxia, need for mechanical ventilation, readmission, or mortality rate compared to those not on them. However, further large-scale studies are needed to validate these findings.

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