Obstructive Sleep Apnea (OSA) is the most common sleep-related breathing disorder
being highly prevalent worldwide. It characterizes by transient increases in upper
airway resistance, reducing and interrupting the airflow, with elevated respiratory
effort. In response to these events, the body becomes hypoxemic and lead to increased
oxygen demand, affecting cardiac tissue which can trigger both atrial and ventricular
arrhythmias. In addition to hypoxia, OSA induces awakenings during sleep, resulting
in sleep deprivation and poor sleep quality. The sleep deprivation is associated with
alterations in immune response, in brain neurotransmitter function and in metabolic
process of our body[1].
Covid-19 manifests as respiratory compromise in some patients infected by the disease.
It has been observed that this new pathology resulted from SARS-CoV-2 involves respiratory
failure, myocardial injury, systemic inflammation, altered myocardial demand-supply
balance and electrolyte imbalance[2]. All these events have potential and negative effects in patients who have diabetes,
heart diseases and obesity. Studies have confirmed that aged and male patients are
also in a greater risk to develop the severe Covid-19. The pathophysiology of Covid-19
has not been well understood. Many studies have been performed to investigate the
course of the disease and how SARS-CoV-2 acts in lungs, heart, kidneys, brain and
in immune responses. The alterations in body after Covid-19 infection predispose patients
to develop severe systemic symptoms, and sometimes death.
It is important to point out the similarities between Covid-19 and OSA in respect
to population risk and outcomes[3]. Both diseases are more prevalent in males, aged, obese, diabetics and patients
with cardiac injuries. All these comorbidities lead to physiological changes in body
function, which may intensify the symptoms and the severity of OSA and Covid-19. The
hypoxia presented in OSA may interact with pulmonary parenchymal involvement along
with pulmonary vascular endothelial dysfunction from the infectious response to SARS-CoV-2
and can be a potential factor to aggravate the severity and infection in patients
with Covid-19. In respect to cardiac outcomes, we should emphasize that OSA is strongly
associated with hypertension[4] and arrhythmias, inducing onset atrial fibrillation and recurrence after different
types of antiarrhythmic treatments. Nocturnal cardiac arrhythmias are prevalent in
92.3% of patients with severe OSA and 40% of all patients with OSA[5],[6]. Patients with severe Covid-19 infection present cardiac myocyte injury that is
suspected to be related to ventricular tachycardia/fibrillation; however, the mechanisms
are still under investigation. 44% of patients hospitalized with Covid-19 admitted
to intensive care unit presented arrhythmias as demonstrated by a study with 138 patients[2]. In respect to hypertension, 23.7% of patients who developed severe Covid-19 outcomes
have hypertension as comorbidity and 16.2% have diabetes[7].
At this moment, OSA has not been stablished as a risk factor for patients with Covid-19.
However, the comorbidities of this sleep disorder, such as diabetes, hypertension,
obesity and arrhythmias have been strongly associated with severe Covid-19. Most of
patients with OSA have one or more of these comorbidities or will develop if no intervention
were required. A factor that has been neglected by researches is the damage in body
function caused by sleep deprivation experienced by patients with OSA. It has been
demonstrated that sleep deprivation induces immune suppression, which can facilitate
susceptibility to SARS-CoV-2 infection. The mechanism involved in the immune response
is related with sustained activation of the inflammatory response in persistent sleep
disturbances, resulting in chronic inflammation that is recognized to predispose major
diseases, such as depression, cancers, cardiovascular diseases, among others[6]. Covid-19 has been attributed to increased inflammatory indicators and the presence
of a cytokine storm[2], as well as sleep disturbances are associated with higher levels of C-reactive protein
and interleukin-6[8]. The role of sleep deprivation of OSA becomes significant in respect to infection
risk, predicting pneumonia risk and susceptibility to the common cold[9],[10].
Up to this moment, we can conclude that OSA and Covid-19 have similarities and have
effects on inflammatory and cardiovascular outcomes[3]. Although OSA has been a common sleep-related breathing disorder[11], many patients are still underdiagnosed, which can complicate their body response
to SARS-Cov-2 infection. Patients with OSA that are in treatment with CPAP should
maintain the treatment to avoid/reduce progression of Covid-19 symptoms. In this new
scenario of pandemic caused by SARS-CoV-2, we should pay attention to patients with
OSA, since they may be more prone to develop the severe degree of Covid-19.
