Effects of CPAP therapy on blood pressure variability (BPV) in people with comorbid obstructive sleep apnoea (OSA) and cardiovascular disease (CVD): SAVE Trial

Introduction: Higher BPV over an extended period is associated with adverse CVD outcomes including cardiac dysfunction and serious macro- and micro-CVD events. Two small, non-controlled, studies found decreased visit-to-visit BPV with continuous positive airways pressure (CPAP) use. We aimed to determine whether CPAP reduced BPV compared to usual care in people with comorbid OSA and coronary or cerebral CVD.Materials and methods: The SAVE study was an international, multi-centre, randomised, parallel group, open-label trial in which patients with moderate-severe OSA and established cardiac or cerebral CVD were randomised to CPAP or usual care. This sub-analysis included those participants with blood pressure (BP) measurements for ≥5 visits over the first two years (0 days, 1, 3, 6, 12 months and/or 24 months, post-randomization). BP measurements were taken in a resting, seated position in the clinic in duplicate (5 mins apart); the mean of BP duplicates was taken as the BP in each visit. BPV was defined as the standard deviation (SD) in BP across ≥5 (max. 6) clinic visits for each participant within the first 24 months post-randomization; both systolic and diastolic BPV were calculated. BPV was also calculated using the coefficient of variation (CV%), and the mean and maximum systolic and diastolic BP were ascertained for the CPAP and usual care groups. Data were assessed for normality and independent sample t-tests were used in this unadjusted analysis.Results: Of 2717 eligible adults (45-75 years), 2381 (88%) met the inclusion criteria (≥5 clinic visits with BP data available). A small increase in systolic BPV, as measured using SD, was observed in the CPAP therapy group compared with the usual care group (n=1178; SBP SD mean difference 0.42 mm Hg, 95% CI 0.02 to 0.82 mm Hg; p = 0.039). Systolic BPV, as measured using coefficient of variation (%) was similarly increased in the CPAP group (mean difference 0.35, 95% CI 0.05 to 0.64; p = 0.022). There was a similar, but non-significant trend towards increased diastolic BPV in the CPAP group according to SD (mean difference 0.23 mm Hg, 95% CI -0.00 to 0.46; p = 0.052). This increase in diastolic BPV was significant when measured using CV% (mean difference 0.36, 95% CI 0.06 to 0.67; p = 0.018). Mean diastolic BP was slightly reduced in the CPAP group (mean difference -0.78 mmHg, 95% CI -1.44 to -0.13; p = 0.020), but no other significant between-group BP differences were evident. Conclusions: CPAP produced a small increase in BPV, but this is unlikely to have had clinically relevant effects. These findings are in concordance with the main findings of the SAVE trial: neutral effects on cardiovascular and cerebrovascular endpoints.