Abstract
Introduction: Obstructive sleep apnoea (OSA) is associated with future major adverse cardiovascular events (MACE). Early CPAP use predicts long-term use, however, it is unknown if early use predicts reduced MACE risk. We assessed whether early and long-term CPAP use measurements predicted MACE and investigated potential dose–response relationships.
Method: Participants: 2717 adults with moderate–severe OSA (laboratory-based polysomnography, apnoea/hypopnoea index ≥15/h) attending a tertiary sleep clinic 2006–2010 completed baseline assessments and were followed-up for a median of 7.1 years.
CPAP treatment: Month-long supervised CPAP trial and periodic review during post-trial follow-up.
Outcomes: Time to cardiac death or non-fatal hospitalisations due to MACE (a composite of coronary heart disease (CHD), cerebrovascular disease, revascularisation procedures for CHD or cerebrovascular disease, peripheral vascular disease, heart failure, and atrial fibrillation), or end of follow-up/non-cardiac death, using Cox proportional hazards models.
Predictors: Average nightly CPAP use from device downloads during week 1 of CPAP trial and available data for entire follow-up period (All).
Covariates: Known baseline risk factors for MACE (age, sex, BMI, smoking, hypertension, diabetes, dyslipidaemia, socio-economic measures, physical activity).
Results: MACE occurred in 18% participants (n = 490). Week 1 CPAP downloads: Each additional hour of CPAP use predicted a 4.4% reduction in MACE risk (HR 0.956, 95% CI 0.926–0.987, p = 0.005). Compared to zero use, each tertile of increasing use predicted a comparable reduction in MACE risk (tertile 0: ref, tertile I: HR 0.746, 95% CI 0.582–0.958, p = 0.022, tertile II: HR 0.708, 95% CI 0.546–0.918, p = 0.009, tertile III: HR 0.767, 95% CI 0.598–0.984, p = 0.037).All CPAP downloads: Each additional hour of CPAP use predicted a 5.5% reduction in MACE risk (HR 0.945, 95% CI 0.915–0.977, p < 0.001). Compared to zero use, each tertile of increasing use predicted a comparable reduction in MACE risk (tertile 0: ref, tertile I: HR 0.613, 95% CI 0.473–0.795, p = <0.001, tertile II: HR 0.716, 95% CI 0.558–0.920, p = 0.009, tertile III: HR 0.647, 95% CI 0.502–0.834, p < 0.001).
Conclusion: In sleep clinic patients with moderate/severe OSA, both early and ongoing CPAP use is similarly associated with reduced MACE risk compared to CPAP non-users. Any CPAP use reduced risk with no evident dose–response relationship between CPAP use and MACE.
Conflict of Interest: Yes- Funding provided by the National Health and Medical Research Council grant [APP1145970].