CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea
Obstructive sleep apnea is associated with an increased risk of cardiovascular events; whethertreatmentwithcontinuouspositiveairwaypressure(CPAP)preventsmajorcardio- vascular events is uncertain.
After a 1-week run-in period during which the participants used sham CPAP, we ran- domly assigned 2717 eligible adults between 45 and 75 years of age who had moderate-to- severe obstructive sleep apnea and coronary or cerebrovascular disease to receive CPAP treatment plus usual care (CPAP group) or usual care alone (usual-care group). The pri- mary composite end point was death from cardiovascular causes, myocardial infarction, stroke, or hospitalization for unstable angina, heart failure, or transient ischemic attack. Secondary end points included other cardiovascular outcomes, health-related quality of life, snoring symptoms, daytime sleepiness, and mood.
Most of the participants were men who had moderate-to-severe obstructive sleep apnea and minimal sleepiness. In the CPAP group, the mean duration of adherence to CPAP therapy was 3.3 hours per night, and the mean apnea–hypopnea index (the number of apnea or hypopnea events per hour of recording) decreased from 29.0 events per hour at baseline to 3.7 events per hour during follow-up. After a mean follow-up of 3.7 years, a primary end-point event had occurred in 229 participants in the CPAP group (17.0%) and in 207 participants in the usual-care group (15.4%) (hazard ratio with CPAP, 1.10; 95% confidence interval, 0.91 to 1.32; P=0.34). No significant effect on any individual or other composite cardiovascular end point was observed. CPAP significantly reduced snoring and daytime sleepiness and improved health-related quality of life and mood.
Therapy with CPAP plus usual care, as compared with usual care alone, did not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and es- tablished cardiovascular disease. (Funded by the National Health and Medical Research Council of Australia and others; SAVE ClinicalTrials.gov number, NCT00738179; Austra- lian New Zealand Clinical Trials Registry number, ACTRN12608000409370.)
R. Doug McEvoy, M.D., Nick A. Antic, M.D., Ph.D., Emma Heeley, Ph.D., Yuanming Luo, M.D., Qiong Ou, M.D., Xilong Zhang, M.D., Olga Mediano, M.D., Rui Chen, M.D., Luciano F. Drager, M.D., Ph.D., Zhihong Liu, M.D., Ph.D., Guofang Chen, M.D., Baoliang Du, M.D., Nigel McArdle, M.D., Sutapa Mukherjee, M.D., Ph.D., Manjari Tripathi, M.D., Laurent Billot, M.Sc., Qiang Li, M.Biostat., Geraldo Lorenzi‐Filho, M.D., Ferran Barbe, M.D., Susan Redline, M.D., M.P.H., Jiguang Wang, M.D., Ph.D., Hisatomi Arima, M.D., Ph.D., Bruce Neal, M.D., Ph.D., David P. White, M.D., Ron R. Grunstein, M.D., Ph.D., Nanshan Zhong, M.D., and Craig S. Anderson, M.D., Ph.D., for the SAVE Investigators and Coordinators*
The authors’ affiliations are listed in the Appendix. Address reprint requests to Dr. McEvoy at the Adelaide Institute for Sleep Health, Flinders University and Re‐ spiratory and Sleep Services, Southern Adelaide Local Health Network, Repatria‐ tion General Hospital, Daw Park, Adelaide SA 5041, Australia, or at doug.mcevoy@ flinders.edu.au; or to Dr. Luo at the First Affiliated Hospital of Guangzhou Medi‐ cal University, State Key Laboratory of Re‐ spiratory Disease, Guangzhou, China, or at email@example.com.
*A complete list of sites and trial investi‐ gators and coordinators in the Sleep Apnea Cardiovascular Endpoints (SAVE) study is provided in the Supplementary Appendix, available at NEJM.org.
This article was published on August 28, 2016, at NEJM.org.
N Engl J Med 2016;375:919-31. DOI: 10.1056/NEJMoa1606599