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Insights into Friedman stage II and III OSA patients through drug-induced sleep endoscopy.

ABSTRACT: Background:The Friedman staging is a classic system to predict outcomes of obstructive sleep apnea (OSA) surgery. Increasing stage indicates more severe upper airway (UA) obstruction and worse surgical successful rate. In previous studies, the UA obstruction between stages were usually assessed based on awake examination. Drug-induced sleep endoscopy (DISE) is a new method that can evaluate airway collapse characteristics during sleep. Therefore, we planned to compare Friedman staging and DISE findings and fulfill the knowledge gap on the correlation between awake and sedated UA examination. Methods:Retrospective case series study that assessed patients with OSA who underwent DISE. Subjects were classified to stage II and stage III groups based on Friedman staging system. UA collapse characteristics based on velum, oropharynx, tongue base, epiglottis (VOTE) classification, including single/multiple obstruction sites, single/combined upper and lower obstruction levels, collapse degree and patterns in different sites, and surgical results among the groups were analyzed. Results:A total of 175 cases were analyzed. No significant differences were found in baseline measurements between groups. Stage III patients (n=102) had a higher proportion (74.5%) with 3 or 4 obstruction sites than stage II (57.5%, n=73). Velum (V) + oropharynx (O) + tongue base (T) was the most common multi-sites combined obstruction pattern with 33% in stage II and 37% in stage III, isolated lower level obstruction was the least with 6% and 4%, respectively. No significant differences were found in obstruction sites and levels. 106 patients underwent surgeries and 33 had post-surgical sleep study, 73.7% and 63.6% response rate were found in stage II and III with no significant difference. Conclusions:Upper and lower combined obstruction was the main pattern of collapse in both, Friedman stage II and III patients. Patients with OSA and Friedman stage III had more than 2 sites of obstruction than stage II patients.

SUBMITTER: Zhao C

PROVIDER: S-EPMC7399404 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Insights into Friedman stage II and III OSA patients through drug-induced sleep endoscopy.

Zhao Chen C Viana Alonço A Ma Yifei Y Capasso Robson R

Journal of thoracic disease 20200701 7

<h4>Background</h4>The Friedman staging is a classic system to predict outcomes of obstructive sleep apnea (OSA) surgery. Increasing stage indicates more severe upper airway (UA) obstruction and worse surgical successful rate. In previous studies, the UA obstruction between stages were usually assessed based on awake examination. Drug-induced sleep endoscopy (DISE) is a new method that can evaluate airway collapse characteristics during sleep. Therefore, we planned to compare Friedman staging an ...[more]

PMID: 32802445

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Project description:Study Objectives: Obstructive sleep apnea (OSA) is increasingly recognized as a complex and heterogenous disorder. As a result, a "one-size-fits-all" management approach should be avoided. Therefore, evaluation of pathophysiological endotyping in OSA patients is emphasized, with upper airway collapse during sleep as one of the main features. To assess the site(s) and pattern(s) of upper airway collapse, natural sleep endoscopy (NSE) is defined as the gold standard. As NSE is labor-intensive and time-consuming, it is not feasible in routine practice. Instead, drug-induced sleep endoscopy (DISE) is the most frequently used technique and can be considered as the clinical standard. Flow shape and snoring analysis are non-invasive measurement techniques, yet are still evolving. Although DISE is used as the clinical alternative to assess upper airway collapse, associations between DISE and NSE observations, and associated flow and snoring signals, have not been quantified satisfactorily. In the current project we aim to compare upper airway collapse identified in patients with OSA using endoscopic techniques as well as flow shape analysis and analysis of tracheal snoring sounds between natural and drug-induced sleep. Methods: This study is a blinded prospective comparative multicenter cohort study. The study population will consist of adult patients with a recent diagnosis of OSA. Eligible patients will undergo a polysomnography (PSG) with NSE overnight and a DISE within 3 months. During DISE the upper airway is assessed under sedation by an experienced ear, nose, throat (ENT) surgeon using a flexible fiberoptic endoscope in the operating theater. In contrast to DISE, NSE is performed during natural sleep using a pediatric bronchoscope. During research DISE and NSE, the standard set-up is expanded with additional PSG measurements, including gold standard flow and analysis of tracheal snoring sounds. Conclusions: This project will be one of the first studies to formally compare collapse patterns during natural and drug-induced sleep. Moreover, this will be, to the authors' best knowledge, the first comparative research in airflow shape and tracheal snoring sounds analysis between DISE and NSE. These novel and non-invasive diagnostic methods studying upper airway mechanics during sleep will be simultaneously validated against DISE and NSE. Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT04729478.

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Project description:A surge of data has reproducibly identified strong associations of OSA with cardiac arrhythmias. As an extension of epidemiologic and clinic-based findings, experimental investigations have made strides in advancing our understanding of the putative OSA and cardiac arrhythmogenesis mechanistic underpinnings. Although most studies have focused on the links between OSA and atrial fibrillation (AF), relationships with ventricular arrhythmias have also been characterized. Key findings implicate OSA-related autonomic nervous system fluctuations typified by enhanced parasympathetic activation during respiratory events and sympathetic surges subsequent to respiratory events, which contribute to augmented arrhythmic propensity. Other more immediate pathophysiologic influences of OSA-enhancing arrhythmogenesis include intermittent hypoxia, intrathoracic pressure swings leading to atrial stretch, and hypercapnia. Intermediate pathways by which OSA may trigger arrhythmia include increased systemic inflammation, oxidative stress, enhanced prothrombotic state, and vascular dysfunction. Long-term OSA-associated sequelae such as hypertension, atrial enlargement and fibrosis, ventricular hypertrophy, and coronary artery disease also predispose to cardiac arrhythmia. These factors can lead to a reduction in atrial effective refractory period, triggered and abnormal automaticity, and promote slowed and heterogeneous conduction; all of these mechanisms increase the persistence of reentrant arrhythmias and prolong the QT interval. Cardiac electrical and structural remodeling observed in OSA animal models can progress the arrhythmogenic substrate to further enhance arrhythmia generation. Future investigations clarifying the contribution of specific OSA-related mechanistic pathways to arrhythmia generation may allow targeted preventative therapies to mitigate OSA-induced arrhythmogenicity. Furthermore, interventional studies are needed to clarify the impact of OSA pathophysiology reversal on cardiac arrhythmogenesis and related adverse outcomes.

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Insights into Friedman stage II and III OSA patients through drug-induced sleep endoscopy.

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Insights into Friedman stage II and III OSA patients through drug-induced sleep endoscopy.

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