To The Editors:

Related to my earlier publications on central nervous system involvement in COVID-19,[1,2] I would like to stress the importance of diagnosing obstructive sleep apnea syndrome (OSAS) in infected patients, prompting early use of continuous positive air pressure (CPAP) to prevent hypoxemia.

OSAS is commonly related to obesity, which is considered an important risk factor for severe COVID-19. Nevertheless, publications about the possible association between OSAS and COVID-19 are relatively scarce.[3]

SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) receptor for host cell entry. In COVID-19 patients whose OSAS is untreated, augmented ACE2 expression and deregulation of the renin-angiotensin system occur. OSAS leads to repetitive airway collapse with apnea/hypopnea and hypoxia during sleep. Hypoxia/re-oxygenation during each apnea episode in OSAS patients worsens hypoxemia and can stimulate ACE2 synthesis in endothelial cells, inducing higher ACE activity and thus aggravating the cytokine storm typical of severe COVID-19. Thus, OSAS (particularly with concurrent obesity) could contribute to increased hypoxemia, further provoking the cytokine storm that can cause acute respiratory distress syndrome (ARDS), multiorgan failure and death in these patients.[1,2,4]

Non-invasive ventilation (NIV) plays a more significant and helpful role than first thought, mainly if used at early stages of COVID-19. CPAP is now the preferred form of NIV to manage hypoxemic COVID-19 patients. In fact, use of improved and enhanced CPAP equipment is providing growing evidence that this NIV method may benefit patients early in the disease’s progression, preventing ARDS and reducing the need for invasive ventilation.[3,5] Hence, I highly recommend beginning CPAP in COVID-19 patients as soon as the first respiratory symptoms appear—even during care outside of intensive care units—especially for those patients with OSAS.[4]