Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624065
Title: Mechanisms of obstructive sleep apnoea in congestive heart failure
Author: Carlisle, Thomas
Awarding Body: Imperial College London
Current Institution: Imperial College London
Date of Award: 2013
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Abstract:
Approximately 50% of chronic heart failure (CHF) patients have obstructive sleep apnoea (OSA); however the mechanisms associated with OSA in CHF patients are incompletely understood. The overall aim of this thesis was to characterise upper airway phenotypes that may contribute to OSA in patients with CHF. Specifically, I sought to test the hypothesis that CHF patients with OSA have overnight rostral fluid shift. Pharyngeal phenotypes were measured non-invasively; pharyngeal calibre was measured using acoustic reflection, pharyngeal collapsibility using the passive critical closing pressure (Pcrit) technique, and changes in pharyngeal compliance during sleep using oesophageal pressure manometry combined with direct visualisation of the pharynx using bronchoscopy. Chapter 5 investigated differences in pharyngeal anatomy and morphology in healthy younger and older male volunteers using acoustic reflection, testing the hypothesis that older healthy males have similar pharyngeal dimensions to younger healthy males. The findings of this thesis showed that CHF patients with OSA have similar pharyngeal cross-sectional areas to CHF patients without OSA and healthy controls (Chapter 3). Pharyngeal collapsibility was also similar between groups (Chapter 4). CHF patients may be predisposed to pharyngeal collapse due to overnight attenuation of normal pharyngeal dilation during inspiration (Chapter 6). Finally, it was demonstrated that there may be differences in pharyngeal dimensions and morphology in older males compared to younger males (Chapter 5). The implications of the studies presented in this thesis are that fluid shift may be a contributing factor to OSA in CHF but the findings in this thesis suggest that its role is not likely to be dominant over more established mechanisms of OSA. Moreover, there may be no special features of CHF that explain the high prevalence of OSA in CHF.
Supervisor: Morrell, Mary ; Simonds, Anita ; Cowie, Martin Sponsor: National Heart & Lung Institute Foundation
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.624065  DOI: Not available
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