Abstract:Purpose of review
The aim of this article is to summarize up-to-date research on the effects of obstructive sleep apnea (OSA) on retinal vascular conditions.
Recent findings
OSA is associated with the development of diabetic retinopathy, retinal vein occlusion, and central serous chorioretinopathy. The severity of OSA and biomarkers such as the apnea–hypopnea index (AHI) correlate with the severity of retinal disease. Dysregulation of circadian locomoto… Show more
“…As recently reviewed by D'Souza & Kappor [48], OSAS demonstrated a significant association with retinal vascular disorders. It is associated with the development of diabetic retinopathy, retinal vein occlusion, and central serous chorioretinopathy.…”
Retinal findings may change in patients with obstructive sleep apnea syndrome (OSAS). The present study aims to evaluate several retinal findings, such as macula layer thickness, the peripapillary retinal nerve fiber layer, and the optic nerve head in patients with OSAS, using optical coherence tomography (OCT); it also aims to monitor the result of several types of treatment of OSAS with OCT. A prospective comparative study was designed. Patients were recruited at a Sleep Unit of a University Hospital and underwent comprehensive ophthalmological examinations. Following exclusion criteria, fifty-two patients with OSAS were finally included. Patients were examined by OCT twice: once before treatment, and again after six months of treatment. In mild–moderate patients, where retinal swelling had been demonstrated, retinal thicknesses decreased [fovea (p = 0.026), as did inner ring macula (p = 0.007), outer ring macula (p = 0.015), and macular volume (p = 0.015)]. In severe patients, where retinal atrophy had been observed, retinal thickness increased [fovea (p < 0.001)]. No statistically significant differences in efficacy between treatments were demonstrated. In conclusion, OCT can evaluate the retina in patients with OSAS and help to monitor results after treatment. In severe OSAS, retinal thickness increased six months after treatment.
“…As recently reviewed by D'Souza & Kappor [48], OSAS demonstrated a significant association with retinal vascular disorders. It is associated with the development of diabetic retinopathy, retinal vein occlusion, and central serous chorioretinopathy.…”
Retinal findings may change in patients with obstructive sleep apnea syndrome (OSAS). The present study aims to evaluate several retinal findings, such as macula layer thickness, the peripapillary retinal nerve fiber layer, and the optic nerve head in patients with OSAS, using optical coherence tomography (OCT); it also aims to monitor the result of several types of treatment of OSAS with OCT. A prospective comparative study was designed. Patients were recruited at a Sleep Unit of a University Hospital and underwent comprehensive ophthalmological examinations. Following exclusion criteria, fifty-two patients with OSAS were finally included. Patients were examined by OCT twice: once before treatment, and again after six months of treatment. In mild–moderate patients, where retinal swelling had been demonstrated, retinal thicknesses decreased [fovea (p = 0.026), as did inner ring macula (p = 0.007), outer ring macula (p = 0.015), and macular volume (p = 0.015)]. In severe patients, where retinal atrophy had been observed, retinal thickness increased [fovea (p < 0.001)]. No statistically significant differences in efficacy between treatments were demonstrated. In conclusion, OCT can evaluate the retina in patients with OSAS and help to monitor results after treatment. In severe OSAS, retinal thickness increased six months after treatment.
“…While it is possible that OSA-induced nocturnal hypoxemia can cause sufficient retinal hypoxia to independently cause neovascularization, the more likely pathway is potentiation of other comorbid ischemic etiologies. 6 The combination of diabetic microvascular compromise and OSA-induced nocturnal hypoxemia may predispose to a higher incidence of diabetic retinopathy, and accordingly, a recent meta-analysis showed significantly increased risk of diabetic retinopathy with comorbid OSA. 7 Additionally, increased endothelial damage and vascular stasis associated with OSA may heighten the risk for retinal venous occlusion.…”
Section: Discussionmentioning
confidence: 99%
“… 7 Additionally, increased endothelial damage and vascular stasis associated with OSA may heighten the risk for retinal venous occlusion. 6 …”
“…Circadian clock disruption is also a potential mechanism of diabetes complications, such as diabetic retinopathy development. The excessive CLOCK-dependent expression of DEC2 and VEGF [ 80 ] leads to incorrect neovascularization and in consequence diabetic retinopathy. Moreover, VEGF translation is powered by HIF-1α [ 81 ] (see Figure 5 ).…”
Section: Clinical Implications Of Circadian Rhythm Gene Disruption In Osa Patientsmentioning
Obstructive sleep apnea (OSA) is a chronic condition characterized by recurrent pauses in breathing caused by the collapse of the upper airways, which results in intermittent hypoxia and arousals during the night. The disorder is associated with a vast number of comorbidities affecting different systems, including cardiovascular, metabolic, psychiatric, and neurological complications. Due to abnormal sleep architecture, OSA patients are at high risk of circadian clock disruption, as has been reported in several recent studies. The circadian clock affects almost all daily behavioral patterns, as well as a plethora of physiological processes, and might be one of the key factors contributing to OSA complications. An intricate interaction between the circadian clock and hypoxia may further affect these processes, which has a strong foundation on the molecular level. Recent studies revealed an interaction between hypoxia-inducible factor 1 (HIF-1), a key regulator of oxygen metabolism, and elements of circadian clocks. This relationship has a strong base in the structure of involved elements, as HIF-1 as well as PER, CLOCK, and BMAL, belong to the same Per-Arnt-Sim domain family. Therefore, this review summarizes the available knowledge on the molecular mechanism of circadian clock disruption and its influence on the development and progression of OSA comorbidities.
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