Produção Nacional
Does obstructive sleep apnea lead to increased risk of COVID-19 infection and severity?
2020; American Academy of Sleep Medicine; Volume: 16; Issue: 8 Linguagem: Inglês
10.5664/jcsm.8596
ISSN1550-9397
AutoresSérgio Tufik, David Gozal, Isabela A. Ishikura, Gabriel Natan Pires, Mônica L. Andersen,
Tópico(s)Sleep and related disorders
ResumoFree AccessLetters to the EditorDoes obstructive sleep apnea lead to increased risk of COVID-19 infection and severity? Sergio Tufik, MD, PhD, David Gozal, MD, PhD, Isabela Antunes Ishikura, MSc, Gabriel Natan Pires, PhD, Monica Levy Andersen, PhD Sergio Tufik, MD, PhD Departamento de Psicobiologia Universidade Federal de São Paulo, São Paulo, Brazil *Contributed equally , David Gozal, MD, PhD Department of Child Health and the Child Health Research Institute, The University of Missouri School of Medicine, Columbia, Missouri *Contributed equally , Isabela Antunes Ishikura, MSc Departamento de Psicobiologia Universidade Federal de São Paulo, São Paulo, Brazil , Gabriel Natan Pires, PhD Departamento de Psicobiologia Universidade Federal de São Paulo, São Paulo, Brazil Department of Physiological Sciences, Santa Casa de São Paulo School of Medical Sciences, São Paulo, Brazil , Monica Levy Andersen, PhD Departamento de Psicobiologia Universidade Federal de São Paulo, São Paulo, Brazil Published Online:August 15, 2020https://doi.org/10.5664/jcsm.8596Cited by:42SectionsAbstractEpubPDF ShareShare onFacebookXLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTCitation:Tufik S, Gozal D, Ishikura IA, Pires GN, Andersen ML. Does obstructive sleep apnea lead to increased risk of COVID-19 infection and severity? J Clin Sleep Med. 2020;16(8):1425–1426.INTRODUCTIONCOVID-19 usually manifests as respiratory compromise, particularly in the severe presentations of the disease, being particularly likely among people aged >60 years, men, and those with obesity and cardiometabolic dysfunction. 1,2Severe COVID-19 is associated with a variety of proinflammatory mediators playing a role in the pathophysiology of the disease and with recruitment of the coagulation cascade with its attendant consequences.3,4Although most confirmed COVID-19 cases are associated with a common clinical presentation of respiratory failure, considerable concern has emerged in light of the serious cardiovascular manifestations observed in patients with COVID-19.5 The putative mechanisms involved in cardiovascular outcomes in COVID-19 may include6 direct myocardial injury (involving the angiotensin-converting enzyme 2 signaling pathway), systemic inflammation, altered myocardial demand-supply balance (leading to acute myocardial ischemia), and electrolyte imbalance (increasing the vulnerability to various tachyarrhythmias). Indeed, evidence of cardiac injury, shock, and arrhythmias is present in 7.2%, 8.7%, and 16.7% of patients, respectively—that is, higher than the prevalence among patients in intensive care units who are not infected with SARS-CoV-2.7 Therefore, it is possible that an arrhythmogenic effect of COVID-19 potentially contributes to adverse disease outcomes. The cardiac outcomes of COVID-19 seem to be multifactorial, in light of other concurrent symptoms, all of which may exert proarrhythmic potential such as fever and tachycardia, high inflammatory status, catecholamine adrenergic response, and possible myocardial damage directly influenced by the virus.3,8Individuals with pre-existing cardiovascular disease may be predisposed to COVID-19 infection and be at elevated risk of adverse outcomes.2,9 This association is remarkably similar to the many observational studies showing an association between sleep apnea and heart rhythm disorders.10 Accordingly, we believe that the underlying presence of OSA may not only facilitate susceptibility to SARS-CoV-2 infection but also be an inherent risk factor for severe COVID-19 and increase the overall mortality of the disease.OSA is the most common sleep-related breathing disorder and is highly prevalent, possibly affecting up to 1 billion people around the world.11,12 It is characterized by transient increases in upper airway resistance, causing reductions or interruption of the airflow accompanied by increased respiratory effort.10 During OSA episodes, higher sympathetic outflow promotes the release of catecholamines and their effect on myocardial tissue in addition to elevated systemic blood pressure and tachycardia.10 These responses to both hypoxemia and arousal lead to increased oxygen demand and tissue hypoxia, resulting in myocardial ischemia and thereby facilitating the triggering of both atrial and ventricular arrhythmias.10 Thus, we call attention to the potential contribution of the intermittent hypoxia that characterizes patients with OSA, which can further interfere with lung ventilation. This severity of hypoxia may further interact with pulmonary parenchymal involvement along with pulmonary vascular endothelial dysfunction resulting from the infectious response to SARS-CoV-213 and could be a potential reason for the enhanced severity and adverse outcomes of OSA, as exemplified by a functional cardiac overload in this context. In addition, older age facilitates the occurrence of OSA, obesity is a major risk factor for OSA, and male sex is clearly overrepresented in patients with OSA when compared to premenopausal women. These factors are essentially identical to the risk factors associated with increased severity and mortality of COVID-19.Another factor that merits attention is the relationship between OSA and arrhythmias. Nocturnal cardiac arrhythmias are present in 40% of all patients with OSA and in 92.3% of patients with severe OSA.14,15 Although OSA has been shown to promote the onset of atrial fibrillation, it has also been associated with atrial fibrillation recurrence after antiarrhythmic drug treatment, electrical cardioversion, and ablation therapy,16–18 thereby posing an obstacle to the successful treatment of arrhythmic episodes.Thus, as COVID-19 impacts the cardiovascular system, pre-existing cardiovascular disease associated with coexisting morbidities, such as OSA, may exacerbate the clinical course evolution of COVID-19, leading to increased probability of intensive care unit requirements. However, although there is not an established therapeutic regimen for COVID-19 to date, several drugs are being tentatively used based on their anti-SARS-CoV-2 in vitro properties, such as chloroquine, hydroxychloroquine, and some antiretrovirals. Note that these drugs could also contribute to adverse outcomes, particularly arrhythmias, especially in the presence of long QT syndrome or other conduction defects.19As researchers have observed, among the prominent risk factors for COVID-19 are cardiovascular and respiratory diseases, age >60 years, obesity, and male sex, yet little attention has been given to OSA, a condition whose prevalence and severity are remarkably affected by similar risk factors. Aggravating this scenario, many patients with OSA are currently undiagnosed and/or untreated because of the high costs of polysomnography and limited access to specialized sleep clinics.Given these considerations, we highlight the presence of OSA as a potential comorbidity that merits inclusion as a risk for negative outcomes (such as intensive care unit admission, assisted ventilation, or death) in patients with COVID-19. OSA could act as a facilitator of SARS-CoV-2 infection, and once infection has occurred it could trigger a higher incidence of cardiovascular outcomes, such as arrhythmias, cardiac ischemia, and hypercoagulability states, leading to an unfavorable clinical progression.COVID-19 remains a serious public health concern worldwide even after 5 months since the first case of the disease and has already affected millions of people. The current uncertainties regarding COVID-19 prevention, diagnosis, prognosis, and treatment should encourage researchers to intensify clinical and epidemiological studies. As such, we strongly recommend screening for OSA using currently available simple tools20 to enable the better delineation of risk factors and thereby formulate more accurate prevention strategies and therapeutic approaches.DISCLOSURE STATEMENTS.T., I.A.I., G.N.P. and M.L.A. works are supported by grants from Associação Fundo de Incentivo à Pesquisa (AFIP) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). S.T. and M.L.A. received fellowships from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq). D.G. is supported by National Institutes of Health grants HL130984 and HL140548. The authors have no further conflicts of interest to declare.REFERENCES1. Lu R, Zhao X, Li J, et al.. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395(10224):565–574. https://doi.org/10.1016/S0140-6736(20)30251-8 CrossrefGoogle Scholar2. Zhou F, Yu T, Du R, et al.. 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Volume 16 • Issue 8 • August 15, 2020ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationMay 12, 2020Submitted in final revised formMay 18, 2020Accepted for publicationMay 19, 2020Published onlineAugust 15, 2020 Information© 2020 American Academy of Sleep MedicinePDF download
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