In patients with COVID-19, it has been suggested that obstructive sleep apnea syndrome (OSAS) generates a pro-inflammatory condition that weakens blood vessel endothelium, including in the brain. Investigators of the current study sought to confirm whether OSAS, which is a common, underdiagnosed comorbidity in patients with COVID-19, might be a susceptibility factor for the development of COVID-19 encephalopathy. Results of the analysis were published in the journal CHEST.

In a cohort of patients experiencing COVID-19 encephalopathy who were hospitalized at Geneva University Hospitals in Geneva, Switzerland, an increased prevalence of gadolinium enhancement was detected in large arteries on brain magnetic resonance imaging (MRI; 90.6%), indicative of underlying endothelitis and an increased cerebrospinal fluid to plasma albumin ratio, which is suggestive of blood-brain barrier dysfunction. Pathologic findings in individuals with COVID-19 reported multisystemic endothelitis, including in the cerebral arteries.

It has been proposed that since individuals with OSAS share similar comorbidities (eg, older age, obesity, and cardiovascular disease, including hypertension) with patients with COVID-19 who experience a poor clinical outcome, chronic OSAS-related inflammation may expose the brain to systemic inflammation and thus pave the road for central nervous system injuries. It also has been suggested that the severity of OSAS, along with the treatment (type, adherence, and efficacy), may influence the association between OSAS and COVID-19 encephalopathy. Additionally, the association is likely underestimated, since OSAS is known to be underdiagnosed.


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In both OSAS and COVID-19, oxidative stress, metabolic changes, and a pro-inflammatory phenotype likely lead to endothelial dysfunction and injury. The challenge that remains is how to establish the link between OSAS and COVID-19 encephalopathy. The presence of OSAS has been associated with COVID-19 infection and severity, with a higher risk for the development of respiratory failure. A causal link, however, has not yet been established.

In individuals with severe COVID-19 infection, the “cytokine storm” provokes diffuse vascular damage and prevents the necessary immunologic balance for optimal SARS-CoV-2 neutralization. These inflammatory mechanisms result in diffuse endothelial injury that begins in the lungs and then spreads to multiple organs, which causes severe COVID-19.

Based on these findings, the investigators concluded that additional studies are warranted to confirm the relationship between OSAS and COVID-19 encephalopathy, as OSAS may be a possible actionable factor to target.

Reference

Breville G, Adler D, Uginet M, et al. Does endothelial vulnerability in obstructive sleep apnea syndrome promote COVID-19 encephalopathy? CHEST. Published online April 26, 2021. doi:10.1016/j.chest.2021.04.043