Abstract
BackgroundAlthough sleep apnea-hypopnea syndrome (SAHS) is highly prevalent in patients with type 2 diabetes (T2D), it is unknown whether or not subjects with and without T2D share the same sleep breathing pattern.Methodology/Principal findingsA cross-sectional study in patients with SAHS according to the presence (n = 132) or not (n = 264) of T2D. Both groups were matched by age, gender, BMI, and waist and neck circumferences. A subgroup of 125 subjects was also matched by AHI. The exclusion criteria included chronic respiratory disease, alcohol abuse, use of sedatives, and heart failure. A higher apnea hypopnea index (AHI) was observed in T2D patients [32.2 (10.2–114.0) vs. 25.6 (10.2–123.4) events/hours; p = 0.002). When sleep events were evaluated separately, patients with T2D showed a significant increase in apnea events [8.4 (0.1–87.7) vs. 6.3 (0.0–105.6) e/h; p = 0.044), as well as a two-fold increase in the percentage of time spent with oxygen saturation <90% [15.7 (0.0–97.0) vs. 7.9 (0.0–95.6) %; <0.001)], higher rates of oxygen desaturation events, and also higher daily sleepiness [7.0 (0.0–21.0) vs. 5.0 (0.0–21.0); p = 0.006)] than subjects without T2D. Significant positive correlations between fasting plasma glucose and AHI, the apnea events, and CT90 were observed. Finally, multiple linear regression analyses showed that T2D was independently associated with AHI (R2 = 0.217), the apnea index (R2 = 0.194), CT90 (R2 = 0.222), and desaturation events.Conclusions/significanceT2D patients present a different pattern of sleep breathing than subject without diabetes. The most important differences are the severity of hypoxemia and the number of apneas whereas the incidence of hypopnea episodes is similar.
Highlights
Sleep apnea-hypopnea syndrome (SAHS) is well established as an independent risk factor for hypertension, myocardial infarction, and stroke [1]
Patients with type 2 diabetes mellitus (T2D) showed a higher apnea hypopnea index (AHI) than subjects without diabetes [32.2 (10.2–114.0) vs. 25.6 (10.2–123.4) events/hour; p = 0.002]
AHI: apnea-hypopnea index; SaO2: oxygen arterial saturation; CT90: cumulative percentage of time spent with oxygen saturation below 90%; ODI: oxygen desaturation index; EES: Epworth Sleepiness Scale score
Summary
Sleep apnea-hypopnea syndrome (SAHS) is well established as an independent risk factor for hypertension, myocardial infarction, and stroke [1]. The available data suggest that a long-term exposure to intermittent hypoxia and sleep fragmentation contribute to disorders of glucose metabolism [2]. In this regard, a high prevalence of fasting hyperglycemia, insulin resistance, and type 2 diabetes mellitus (T2D) has been found among SAHS patients in comparison with healthy subjects [3, 4]. We have contributed to demonstrating that T2D is an independent risk factor for severe nocturnal hypoxemia and the impairment of lung function parameters [8, 9]. Sleep apnea-hypopnea syndrome (SAHS) is highly prevalent in patients with type 2 diabetes (T2D), it is unknown whether or not subjects with and without T2D share the same sleep breathing pattern
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