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  • br Method br Results br Discussion br


    Conflict of interest
    Funding This work was supported by the APA Science Directorate.
    Introduction Obstructive sleep apnoea (OSA) is a common disease, with a prevalence of 3–5% symptomatic and 24–26% asymptomatic patients [1–3]. OSA is caused by episodic upper airway obstruction which occurs during sleep. Obstruction can be total (apnoea) or partial (hypopnea), and can occur several times during sleep [4]. The Apnoea–Hypopnea Index (AHI) is used to classify the severity of the illness: mild AHI 5 to <15; moderate 15 to <30; and severe 30 or more [5]. It is well known that patients with severe OSA have higher morbidity and mortality rates compared to those with mild or moderate levels [6,7]. This is relevant mainly in patients with arterial hypertension, coronary disease and stroke [8,9], ventricular dysfunction [10]. For this reason, severe cases require more immediate treatment [11,12]. However, severe OSA includes a very broad spectrum in a group of patients with an AHI≥30, and morbid-mortality outcomes could be different in patients with different degrees of severe disease. In a preliminary study, Jurcevic et al. postulated that patients with AHI≥60 had increased mortality and more severe clinical parameters [13]. The study compared them to patients with AHI<60. Thus, the cut-off point included the conventional severity category. In this scenario, it is very complicated to differentiate the added effect of the proposed new category. Our goal was to identify the clinical and polysomnographic association between moderate to severe OSA with an arbitrary category known as Extreme OSA, defined as an AHI>100. We hypothesised that patients with Extreme OSA (AHI>100) is associated with an increased comorbidities and/or risk factors in comparison with moderate to severe levels.
    Results The average age was 48.9±13.7 years. Forty-eight (51%) had arterial naloxone hydrochloride under treatment. Seven (7%) patients had normal weight, 39 (41%) were overweight, and 10 (11%) suffered from morbid obesity. Forty-three (46%) patients exhibited sleepiness. Only the greater than 10% in T90 variable was more frequent in the severe OSA control group (24%) vs. moderate OSA control group (5%), this difference was significant (p<0.01); there were no other differences between control groups. The case group had significant differences with the control group in age, weight, BMI, neck circumference, ESS score, saturation time ≤90%, and nadir saturation. These variables had a higher average value in the Extreme-OSA group. Furthermore, the average age was lower in the Extreme-OSA group as compared to the control group. Arterial hypertension, sleepiness, and obesity were higher in the Extreme-OSA group (Table 1). In the bivariate analysis, T90>10% was the variable with the closest association with Extreme-OSA (crude OR: 19.68, p<0.001), followed by obesity (crude OR: 9.29, p=0.005), arterial hypertension (crude OR: 6.31, p=0.006), and, to a lesser degree, sleepiness, neck circumference, BMI, and weight. Age and nadir saturation during sleep had an inverse association with the probability of having Extreme-OSA in the crude regression models (Table 2).
    Discussion Our results for the bivariate analysis are consistent with the associations found in the study conducted by Jurcevic et al. [13], who included the category of AHI≥60. In the adjusted analysis, we found that the group with Extreme-OSA has an increased and consistent association with arterial hypertension, more time with saturation ≤90%, and higher neck circumference. We also found differences in the magnitude of these associations depending on whether the Extreme OSA cases were compared with moderate or severe OSA controls, suggesting that the differences are more notable when compared with patients with moderate OSA. The association between arterial hypertension and Extreme OSA is very high when compared to patients with severe OSA, and increases even more when compared to patients with moderate OSA, consistent with the findings of the study conducted by Nieto et al. [24], which established that the probability of arterial hypertension increased depending on the severity of the OSA. This suggests that the principal clinical characteristic of patients with Extreme OSA is that of having a greater probability of arterial hypertension, which is in keeping with other studies that found a close association between OSA and resistant hypertension [25], which increased analogously depending on the severity of the OSA.