Natural evolution of sleep apnoea syndrome: A five year longitudinal study

Abstract

We wanted to investigate the natural evolution of Obstructive Sleep Apnoea Syndrome (OSAS). We therefore followed 58 patients who refused any treatment at the time of diagnosis. Of the eligible patients 32 subjects enrolled in instrumental follow-up. The effects on daytime somnolence, daytime lung function and nocturnal respiratory disturbances were retrospectively evaluated by repeating Multiple Sleep Latency Test (MSLT), spirometry and polysomnography after a follow-up period of at least 5 years (5.7±0.2 SEM years). In the patient group as a whole the mean Apnoea+Hypopnoea Index (AFI), the mean low arterial oxygen saturation (SaO2 and the mean Body Mass Index (BMI) did not change over time. The only significant differences were the increase in mean duration of apnoeas (21.0 vs 23.5 s) and hypopneas (13.5 vs 16.3 s) and the decrease in AHI <80% (13.3 vs 7.9). No correlations were found between the changes in AHI or mean low SaO2, and age, BMI, AHI mean low SaO2 pulmonary function tests or arterial blood gases at baseline. No significant changes were observed in systemic blood pressure, pulmonary function tests, blood gases analysis or MSLT. 'Improved' (n=6) and 'worsened' (n=7) groups were defined by a reduction or increase in AHI over 35% of baseline value. At baseline the 'worsened' group tended to have lower AHI and higher mean low SaO2, compared with the 'improved' group. In the 'worsened' group the BMI rose significantly from 26.0 to 29.2, AHI rose significantly from 14.1 to 51.3 and mean low SaO2 decreased from 92 to 90 (Ns). In this subgroup the increase in AHI was not significantly correlated with the gain in BMI. Our results suggest that: 1) No significant changes in apnoea frequency or nocturnal hypoxaemia occur in the long-term evolution of untreated OSAS patients in the absence of changes in BMI and pulmonary function. 2) Severity of the syndrome and daytime parameters at baseline evaluation did not predict the evolution of the syndrome. 3) Weight gain does not contribute significantly to OSA syndrome exacerbation.