4. DISCUSSION:
Our comprehensive meta-analysis reported NOAF to be a major occurrence
in patients with COVID-19. Across 30 studies encompassing a total of
81,929 COVID-19 patients, we found the overall pooled random effects
estimate of NOAF prevalence to be 7.8% (95% CI: 6.54% to 9.32%).
Published literature shows that the prevalence of NOAF in COVID-19
patients ranges from 1% to 19%. , This finding
underscores the importance of monitoring cardiac rhythm in COVID-19
patients. In literature, the incidence of NOAF in surgical and medical
mixed intensive care units ranged from 1.7% to 29.5%. However, little
information is available regarding the occurrence of NOAF in critically
ill COVID-19 patients.
One of the key findings of our analysis was the significant association
between NOAF and disease severity in COVID-19 patients. Compared with
COVID-19 patients without any history of atrial fibrillation, those who
developed NOAF during their illness had a substantially increased risk
of severe disease Our analysis also demonstrated that NOAF in COVID-19
patients posed a greater risk of severe disease when compared with
patients who had a pre-existing history of atrial fibrillation.
Furthermore, a correlation between NOAF and elevated mortality risk in
COVID-19 patients was reported in our meta-analysis. NOAF significantly
increased the risk of death compared with COVID-19 patients without
atrial fibrillation. In addition, our analysis reported that COVID-19
patients with NOAF had a higher mortality risk than those with
pre-existing atrial fibrillation. This result suggests that NOAF, a
COVID-19 complication, may have unique implications for disease severity
beyond what is typically associated with pre-existing atrial
fibrillation. This finding emphasizes the need for more focused
investigations and further studies to better comprehend the underlying
mechanisms causing severe disease among COVID-19 patients with NOAF,
potentially guiding customized clinical management strategies for these
patients.
Effective clinical management and intervention depend on understanding
the pathophysiologic mechanisms underlying NOAF in COVID-19 patients.
Even though numerous theories have been put forth, the precise
mechanisms causing NOAF in COVID-19 patients are unknown. An extremely
inflammatory response brought on by the SARS-CoV-2 virus defines
COVID-19. This cytokine storm can result in myocardial injury and
disruption of the heart’s typical electrical conduction system. Atrial
fibrillation pathogenesis has been linked to inflammatory mediators like
interleukin-6 (IL-6) and tumor necrosis factor-alpha. Elevated levels of
these cytokines in COVID-19 patients may contribute to the development
of NOAF by promoting atrial remodeling and electrical instability. Aside
from this, the autonomic nervous system is crucial in controlling heart
rhythm. Critically ill COVID-19 patients frequently exhibit
dysregulation of sympathetic and parasympathetic activity, which can
foster the development of NOAF. Hypoxia, stress response, and drugs used
for the management of COVID-19 (such as catecholamines) may all cause
autonomic dysfunction, leading to NOAF. Further according to recent
reports, COVID-19 can cause myocardial injury and ischemia due to
various factors, including direct viral damage, micro thrombosis, and
hypoxia. These circumstances can affect the atria’s electrical
stability, creating the perfect environment for atrial fibrillation to
start and continue. Myocardial injury may also affect the atrial
refractory period and promote reentry circuits, facilitating atrial
fibrillation. Viral entry into myocardial cells can disrupt the heart’s
typical electrical properties, predisposing to atrial
fibrillation., A comprehensive understanding of these
mechanisms is essential for developing targeted preventive and
therapeutic strategies for NOAF in COVID-19 patients, ultimately
improving their clinical outcomes.
It is critical to acknowledge some of the limitations of this
meta-analysis. First, we found significant heterogeneity associated with
the pooled estimates; as the included studies differed in design,
patient characteristics, and location, which may have introduced some
variation. The method used for atrial fibrillation surveillance varied
across included studies. Strains of SARS-CoV-2 virus, co-morbidities of
included patients, vaccination status were not accounted for in the
present analysis. The present study didn’t account for type of atrial
fibrillation based on the duration. Finally this is a study level
meta-analysis and hence is limited in its ability to account for
heterogeneity observed among the pooled estimate.
In conclusion, our meta-analysis provides valuable insights into the
prevalence and clinical implications of NOAF in COVID-19 patients. The
results indicate a strong correlation between NOAF and a higher risk of
severe illness and mortality among COVID-19. These findings highlight
the value of careful surveillance, early detection, and tailored NOAF
management strategies among COVID-19 patients to enhance clinical
outcomes. Further research is warranted to elucidate the mechanisms
underlying this association and guide clinical practice.