부산대학교 도서관

Background: COVID-19 related myocarditis (MC) can manifest with no symptoms, chest pain, life-threatening arrhythmia with hemodynamic instability, or new heart failure. Evidence suggests that RAS inhibition may be beneficial for some patients during COVID-19 infection; however, the effect of these drugs on risk of developing COVID-19-induced MC is not well characterized.Methods: Using ICD-10 codes, a cohort of patients admitted between March-October 2020 with the primary diagnosis of COVID-19 was identified from the PearlDiver database (PearlDiver Technologies, Fort Wayne, IN). Use of RAS inhibitors over the past 6 months was used to split the cohort into two case-control matched groups based on age, gender, and Elixhauser Comorbidity Index. Using the same matching criteria, the RAS group was divided into ACEi and ARB groups. Records of all groups were reviewed to determine the incidence of MC, 60 days after admission. We used Pearsonʼs chi-squared test to compare the MC frequencies. Kaplan-Meier plot and log-rank test were used to compare time-to-event between groups. The strength of association was reported as Risk Ratios (RR) and 95% CI. A p-value <0.05 was deemed significant.Results: Patients using RAS inhibitors had a higher risk of 60-day MC than those who did not (RR = 3.71, 95% CI = 1.61-8.58, p = 0.0017). The p-value of the log-rank test for the 60-day Kaplan-Meier analysis was 0.0006. There was no significant risk difference between ACEi and ARB groups (RR = 0.4, 95% CI = 0.12-1.27, p = 0.18). (Figure 1)Discussion: Our study showed a significant increased risk of 60-day MC in COVID-19 patients taking RAS inhibitors, with no difference between ACEi and ARBs. A plausible explanation is that the RAS inhibition leads to cardiomyocyteʼs ACE2 overexpression, thereby permitting SARS-CoV-2ʼs cellular entry. This interpretation is limited due to the inherent bias associated with retrospective research and the paucity of additional evidence.