Discussion
In this study, we have shown that patients with COVID-19 who use ACEIs
as antihypertensive have less multilobar involvement compared to
patients who use drugs other than ACEIs as antihypertensive treatment
and have a diagnosis of COVID-19. That multilobar involvement was less
common in patients using ACEIs in our study suggests that viral
replication is limited and viral load decreases in these patients. The
significance of multilobar involvement and ACEIs in predicting mortality
in the univariate regression analysis supports these results.
ACEIs treatment has been shown to reduce viral load and inhibit viral
replication in previous studies 13, 14. The
renin-angiotensin system (RAAS) is critical in maintaining electrolyte
balance and regulating blood pressure 8. Therefore,
blockade of the RAAS pathway with ACEIs is considered among the leading
treatment options in the treatment of hypertension 8.
When the literature is examined, there are different views about the
results of ACEIs use in COVID 19 cases. It has been reported that ACE2
receptors act as binding sites for virions of betacoronaviruses1, and the RAAS pathway is considered to play a
critical role in acute lung injury caused by viruses besides blood
pressure regulation 1, 14, 15. Therefore, a view has
been proposed that patients using ACEIs may be at higher risk for
SARS-CoV-2 infections, given that the number of ACE2 receptors will
increase 1. However, sufficient evidence was not
obtained to support or reject this view. The reason for this uncertainty
is that there are not enough studies showing the ACE2 receptor levels in
patients using ACEIs 16. When the previous studies
were examined, it is seen that no significant difference was found
concerning ACE2 activity between the patient groups who were using ACEIs
and were not using ACEIs for the treatment of heart failure, atrial
fibrillation, and coronary artery disease 16-19.
Angiotensin 2 has been shown to have pro-inflammatory properties, cause
endothelial and microvascular dysfunctions, and play a role in
maintaining vascular tone 14, 20, 21 . Therefore, the
RAAS blockade will also likely to decrease inflammatory cytokine release14. Through this mechanism, the RAAS blockade can
contribute to hemodynamic stabilization in the case of inflammation and
will play a critical role in preventing sepsis-related adverse clinical
outcomes 14, 22. However, it is still unclear whether
angiotensin II blockade that arises from ACEIs is associated with an
improved clinical outcome in patients with COVID-19. In previous
studies, it was reported that mostly bilateral or multilobar lung
involvement was detected during the admission of COVID-19 cases23. In a study conducted with 102 patients with a
confirmed diagnosis of COVID-19, the findings showed that the number of
lung lobes affected by COVID-19 was associated with mortality24. Lung injury has been shown to correlate with viral
load in patients infected with COVID-19 13, 14.
In previous studies, it was reported that mortality rates in patients
using ACEIs were lower than the patients who did not. In a cohort study
in which 52 727 patients with a diagnosis of sepsis were included, it
was shown that mortality rates were lower in patients using ACEIs or
ARBs compared to the patients who did not use them regardless of the
infectious agent and underlying comorbid diseases 22.
Consistent with this study, other studies have also found an association
between ACEIs use and reduced mortality rates in patients hospitalized
with a diagnosis of community-acquired pneumonia 22,
25, 26.
In our study, the mortality rate was statistically different between the
two groups. This difference may arise from the decreased viral load and
multilobar involvement in patients using ACEIs. The small sample size
and being single-centred are the major limitations of our study.
Prospective studies that would be conducted with a higher number of
patients may reflect the effects of ACEIs use on the mortality more
accurately.