Abstract
BACKGROUND: Obesity is one of the most prominent risk factors for obstructive sleep apnea (OSA). Weight loss decreases the number of shorter respiratory events (<40 s), whereas the number of longer events remains almost unchanged. However, it is unknown how body mass index (BMI) affects individual obstruction event severity within OSA severity categories when age, sex, smoking, daytime sleepiness, snoring, hypertension, heart failure, and sleeping posture are considered. Therefore, we investigated whether individual obstruction event severity varies with BMI within the OSA severity categories when considering the most important confounding factors.
METHODS: Polygraphic recordings of 723 subjects without CPAP treatment and with an apnea-hypopnea index (AHI) of ≥5 events/hour were reanalyzed retrospectively. The effect of BMI on the severities of OSA and individual obstruction events was evaluated in general, within OSA severity categories, and between different BMI groups (ie, BMI < 25; 25 ≤ BMI < 30; 30 ≤ BMI < 35; 35 ≤ BMI < 40; and BMI ≥ 40 kg/m2).
RESULTS: AHI increased in mild and severe (β ≥ 0.10, P < .001) OSA categories, with increasing BMI. However, the proportion of apneas from all respiratory events decreased (β = −0.55, P = .068) with increasing BMI in all the OSA categories. An increase in BMI led to a decrease in the median duration of individual apneas, hypopneas, and desaturations in all OSA categories, whereas desaturation depth increased statistically significantly in the severe category (β = 0.20, P < .001).
CONCLUSIONS: Because BMI is related to the duration of individual obstruction events, its effect on OSA severity is more complex than its effect on AHI would implicate. Therefore, overall severity of OSA may not be the same for non-obese patient and obese patient who have similar AHI. Thus, these patient-specific characteristics of individual breathing cessations should be considered when estimating the severity of disease and risk of related adverse health effects.
Footnotes
- Correspondence: Timo Leppänen, Department of Clinical Neurophysiology, Diagnostic Imaging Center, Kuopio University Hospital, P.O. Box 100, FI-70029 Kuopio, Finland. E-mail: leppanen_timo{at}outlook.com.
Financial support was provided by the Academy of Finland (decision 313697); the Department of Applied Physics, University of Eastern Finland; Kuopio University Hospital, the Research Committee of the Kuopio University Hospital Catchment Area for the State Research Funding (projects 5041754, 5041755, 5041767, and 5041768); Instrumentarium Science Foundation; the Research Foundation of the Pulmonary Diseases; the Respiratory Foundation of Kuopio Region; Seinäjoki Central Hospital (grants 6020 and 6047); the Competitive State Research Financing of Expert Responsibility Area of Tampere University Hospital (grants VTR3221, VTR3228, and EVO2089).
The study was performed at the Department of Clinical Neurophysiology, Diagnostic Imaging Center, Kuopio University Hospital, Kuopio, Finland.
Dr Leppänen presented the research data at the Nordic Congress of Clinical Neurophysiology and Kuopio Epilepsy Symposium at the Kuopio Music Centre, held March 15-17, 2017, in Kuopio, Finland.
The authors have disclosed no conflicts of interest.
Supplementary material related to this paper is available at http://www.rcjournal.com.
- Copyright © 2019 by Daedalus Enterprises