Background: OSA is associated with high cardiovascular morbidity and mortality. Randomised controlled trials have shown that on average CPAP treatment of OSA reduces blood pressure by about 3 to 5mmHg, although with considerable inter-individual variation. No predictors of BP change with CPAP have been convincingly identified. This prospective study aimed to determine predictors of BP change, which might provide insight into the aetiology of the raised blood pressure seen in untreated OSA.
Methods: Eighty-six patients with daytime hypersomnolence, warranting treatment with CPAP, were recruited. 24h mean BP (24hMBP), subjective sleepiness, fasting venous blood samples, and anthropometric measurements, were assessed at baseline and after 6 months CPAP treatment.
Results: The 24hMBP fell at 6 months from 101.0 (SD10.3) to 96.1 (9.1) mmHg (change = -4.92 (95%CI -2.8 to -7.1) mmHg). The Epworth sleepiness score (ESS) fell from a median of 16 (IQR 12 to 18) to 4 (2 to 7), with a mean fall of 9.7 (95% CI 8.6 to 10.8). Several factors correlated with the fall in 24hMBP but, after allowing for the baseline 24hMBP, only the fall in ESS and the BMI remained significant independent predictors (P= 0.006 and 0.007 respectively). There was also a correlation between the fall in 24hMBP and the fall in pulse rate (r= 0.44, p< 0.0001). There were no other independent predictors of 24hMBP fall, such as baseline OSA severity, overnight hypoxia, caffeine intake, or being on anti-hypertensive drugs.
Conclusion: Improvement in hypersomnolence and the BMI are independent correlates of the fall in 24hMBP following CPAP therapy. Markers of initial OSA severity did not predict 24hMBP fall. This suggests that sleep fragmentation and its effects may be more important than hypoxia in the pathogenesis of the hypertension associated with human sleep apnoea.