Does Endothelial Vulnerability in OSA Syndrome Promote COVID-19 Encephalopathy?

Bréville, Gautier; Adler, Dan; Uginet, Marjolaine; Assal, Frédéric; Tamisier, Renaud; Lalive, Patrice H.; Pépin, Jean-Louis; Allali, Gilles

doi:10.1016/j.chest.2021.04.043

Cited by 6 publications

(10 citation statements)

References 5 publications

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“…7 This could result from either a direct (propagation of SARS-CoV-2 from the nose to the cortex, in particular the insula) or indirect insult (central nervous system [CNS] penetration of inflammatory cytokines in patients with preexisting vessel fragility), as supported by neuroimaging findings of patient 3 showing a bilateral vertebral artery gadolinium enhancement, suggestive of SARS-CoV-2mediated endotheliitis. 1,6 Indeed, the insula, in particular its mid and anterior areas, plays a pivotal role in interoception by linking awareness of body signals, such as breathing and pain, to the conscious experience of human emotions. 9,16,23 More specifically, insular lesions are associated with reduced sensitivity to the perception of unpleasantness stemming from both dyspnea and pain, and an altered insular activity has been demonstrated in chronic pain syndromes, eg, temporomandibular joint and fibromyalgia.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Decrease in pain perception during acute SARS-CoV-2 infection: a case series

Hentsch

Stancu

Allali

et al. 2021

PAIN

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Decrease in pain perception during acute SARS-CoV-2 infection: a case series

Hentsch

Stancu

Allali

et al. 2021

PAIN

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“…However, the impact of OSA over these symptoms is not well known. Previous studies suggest that both OSA and COVID-19 increase the expression of several inflammatory stress, including proinflammatory cytokines as IL-6, developing an endothelial vulnerability, and therefore, increasing the permeability of this markers to the brain ( 38 ). In fact, inflammation and endothelial dysfunction observed in OSA patients have been associated with a reduction of vascular elasticity and increase coagulation, promoting atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Impact of Obstructive Sleep Apnea (OSA) in COVID-19 Survivors, Symptoms Changes Between 4-Months and 1 Year After the COVID-19 Infection

et al. 2022

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ObjectiveTo determine the association between Obstructive Sleep Apnea (OSA) with long-term symptoms and inflammatory cytokines, exploring the changes between 4-months and 1-year after COVID-19 infection.MethodsWe conducted an observational, prospective cohort study, including patients ≥18 years old with confirmed diagnosis of COVID-19 between April to July 2020. All participants underwent two clinical follow-up visits, the first at 4-months (Visit 1) and the second at 1 year, after SARS-CoV-2 infection (Visit 2). Plasma glucose, total cholesterol, HDL, and triglycerides. Regarding pulmonary function, spirometry and lung diffusion capacity tests were assessed. For mental and neurocognitive evaluation, a short-form (SF-12), Beck depression and Hospital-Anxiety depression questionnaires were conducted at both time-points, whereas the Montreal Cognitive assessment was conducted during the second follow-up. Regarding to sleep evaluation, Epworth Sleepiness Scale, Insomnia Severity index and STOP-BANG questionnaire were conducted. Additionally, a home sleep apnea test and 7-day wrist actigraphy were performed in all participants. Inflammatory cytokines were measured using an inflammatory cytokine bead array kit. p-values < 0.05 were considered statistically significant and statistical analyses were performed using R software.ResultsA total of 60 patients were included in the first follow-up, from which 57 completed the second follow-up. The mean age was 46.4 years-old (SD ± 13.1) and 53.3% were male. 30% of cases reported mild COVID-19 infection, 28.3% with moderate illness, and 41.6% with severe illness. Moreover, 56.6% of them were admitted to the ICU. Regarding to metabolic values, the OSA group showed higher values of insulin resistance (IR) (27%), systolic blood pressure (SBP) 135.2 (±19.1), dyslipidemia (67.5%), total cholesterol 202.1 (±60.5), triglycerides 176.1 (±119.0) and HOMA-IR 9.0 (±18.8) in comparison with the non-OSA group. 1 year after COVID-19 infection, DLCO test remains abnormal in OSA patients (25% OSA vs. 3.6% non-OSA, p = 0.02). Finally, those participants with OSA who develop ARDS reported an adjusted OR 20.4 (95%-CI, 1.04–504) risk of neurocognitive impairment.DiscussionAmong patients with previous COVID-19, OSA impact the development of incident glycemic, neurocognitive impairment, and abnormal functional pulmonary changes that persist up to 1 year since acute phase.

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“…Some authors theorize that, in patients with SARS-CoV-2 and obstructive sleep apnea, a pro-inflammatory state is created that diminishes systemic blood vessel endothelium, including the brain. The mechanism of action for this injury is thought to be from oxidative stress, metabolic changes, and a pro-inflammatory phenotype that likely led to endothelial dysfunction and injury [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Causing Transient Central Sleep Apnea in Patients Treated for Obstructive Sleep Apnea with Continuous Positive Airway Pressure

Ghatak¹,

Saini

2022

Am J Case Rep

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Case series Patients: Female, 41-year-old • Male, 34-year-old Final Diagnosis: Central sleep apnea • obstructive sleep apnea Symptoms: Transient central sleep apnea Medication: — Clinical Procedure: — Specialty: Family Medicine Objective: Unusual clinical course Background: SARS-CoV-2 has globally affected humanity and devastated many families. Here, we attempt to identify which diseases are independent risk factors for severe SARS-CoV-2. There have been multiple studies that have evaluated the impact of obstructive sleep apnea (OSA) on SARS-CoV-2 outcomes, suggesting that OSA is an independent risk factor. SARS-CoV-2 has also been suggested to invade the central nervous system and be responsible for neurological signs and decreasing central respiratory drive. Central sleep apnea (CSA) is defined when apneas and hypopneas are associated with absent or reduced ventilatory effort, respectively, due to diminished central respiratory drive. Case Reports: Here, we describe 2 cases involving patients with OSA that developed transient central sleep apnea after being diagnosed with SARS-CoV-2 by polymerase chain reaction. They had similar past medical histories and presentation of illness. The differences included compliance of continuous positive airway pressure (CPAP), recovery, and severity of central sleep index. We review and address alternate causes for the development of CSA. We hypothesize that continuous and compliant use of CPAP machines may be beneficial in reducing recovery and severity of SARS-CoV-2. Conclusions: Our case report calls attention to the acquired central respiratory drive neurological complication associated with SARS-CoV-2. Our case report highlights the plausible existence of a relationship between development of central respiratory drive leading to CSA and SARS-CoV-2 infection. Further studies are needed to explore this relationship, including evaluating whether CSA occurs in SARS-CoV-2 patients with no history of OSA.

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Does Endothelial Vulnerability in OSA Syndrome Promote COVID-19 Encephalopathy?

Cited by 6 publications

References 5 publications

Decrease in pain perception during acute SARS-CoV-2 infection: a case series

Decrease in pain perception during acute SARS-CoV-2 infection: a case series

Impact of Obstructive Sleep Apnea (OSA) in COVID-19 Survivors, Symptoms Changes Between 4-Months and 1 Year After the COVID-19 Infection

SARS-CoV-2 Causing Transient Central Sleep Apnea in Patients Treated for Obstructive Sleep Apnea with Continuous Positive Airway Pressure

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