TY - JOUR
T1 - Low Prognostic Value of Novel Nocturnal Metrics in Patients With OSA and High Cardiovascular Event Risk
T2 - Post Hoc Analyses of the SAVE Study
AU - Linz, Dominik
AU - Loffler, Kelly A.
AU - Sanders, Prashanthan
AU - Catcheside, Peter
AU - Anderson, Craig S.
AU - Zheng, Danni
AU - Quan, Wei Wei
AU - Barnes, Mary
AU - Redline, Susan
AU - McEvoy, R. Doug
AU - Baumert, Mathias
N1 - Funding Information:
FUNDING/SUPPORT: The SAVE (Sleep Apnea Cardiovascular Endpoints) trial was funded by project grants 1006501 and 1060078 from the National Health and Medical Research Council (NHMRC) of Australia and by the Respironics Sleep and Respiratory Research Foundation and Philips Respironics. Supplementary trial funding was provided by Fisher & Paykel Healthcare and the Australasian Sleep Trials Network (enabling grant 343020 from the NHMRC). In-kind donations were provided by Philips Respironics for CPAP equipment and by ResMed for sleep apnea diagnostic devices. S. R. was supported in part by NIH R35HL135818. P. S. and R. D. M. were supported by Practitioner Fellowships from the National Health and Medical Research Council of Australia.Author contributions: C. S. A. and R. D. M. were the primary investigators. D. L. K. A. L. P. C. R. D. M. and M. Baumert planned the analyses. K. A. L. and M. Baumert had access to raw data. M. Baumert completed all custom quantification of the oximetry data; K. A. L. carried out statistical analyses. D. Z. and M. Barnes provided advice on statistical methods. D. L. P. C. P. S. C. S. A. W. Q. S. R. and R. D. M. provided insight into the interpretation of the results. D. L. K. A. L. R. D. M. and M. Baumert drafted the manuscript. All of the authors read and approved the manuscript for submission. Financial/nonfinancial disclosures: The authors have reported to CHEST the following: D. L. reports having served on the advisory board of LivaNova and Medtronic, having received lecture and/or consulting fees from Bayer, LivaNova, Medtronic, and ResMed, and having received research funding from Sanofi, ResMed and Medtronic. P. S. reports having served on the advisory board of Biosense-Webster, Medtronic, Abbott, Boston Scientific, and CathRx; he also reports that the University of Adelaide has received, on his behalf, lecture and/or consulting fees from Biosense-Webster, Medtronic, Abbott, and Boston Scientific and that the University of Adelaide has received, on his behalf, research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik, and LivaNova. R. D. M. reports receiving research funding from Philips Respironics, ResMed, and Fisher & Paykel. None declared (C. S. A. S. R. P. C. K. A. L. D. Z. W. Q. M. Barnes, and M. Baumert). ∗SAVE (Sleep Apnea Cardiovascular Endpoints) Investigators: For list of investigators, see e-Appendix 1. Other Contributions: The authors thank David Tickner for exporting ApneaLink data and all SAVE investigators, collaborators, and participants. Additional Information: The e-Appendix, e-Figures and e-Tables can be found in the Supplemental Materials section of the online article.
Funding Information:
Financial/nonfinancial disclosures: The authors have reported to CHEST the following: D. L. reports having served on the advisory board of LivaNova and Medtronic, having received lecture and/or consulting fees from Bayer, LivaNova, Medtronic, and ResMed, and having received research funding from Sanofi , ResMed and Medtronic. P. S. reports having served on the advisory board of Biosense-Webster, Medtronic, Abbott, Boston Scientific, and CathRx; he also reports that the University of Adelaide has received, on his behalf, lecture and/or consulting fees from Biosense-Webster, Medtronic, Abbott, and Boston Scientific and that the University of Adelaide has received, on his behalf, research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik, and LivaNova. R. D. M. reports receiving research funding from Philips Respironics, ResMed, and Fisher & Paykel. None declared (C. S. A., S. R., P. C., K. A. L., D. Z., W. Q., M. Barnes, and M. Baumert).
Funding Information:
FUNDING/SUPPORT: The SAVE (Sleep Apnea Cardiovascular Endpoints) trial was funded by project grants 1006501 and 1060078 from the National Health and Medical Research Council (NHMRC) of Australia and by the Respironics Sleep and Respiratory Research Foundation and Philips Respironics. Supplementary trial funding was provided by Fisher & Paykel Healthcare and the Australasian Sleep Trials Network (enabling grant 343020 from the NHMRC). In-kind donations were provided by Philips Respironics for CPAP equipment and by ResMed for sleep apnea diagnostic devices. S. R. was supported in part by NIH R35HL135818. P. S. and R. D. M. were supported by Practitioner Fellowships from the National Health and Medical Research Council of Australia.
Publisher Copyright:
© 2020
PY - 2020/7/13
Y1 - 2020/7/13
N2 - Background: Traditional methods for the quantification of OSA severity may not encapsulate potential relationships between hypoxemia in OSA and cardiovascular risk. Research Question: Do novel nocturnal oxygen saturation (SpO2) metrics have prognostic value in patients with OSA and high cardiovascular event risk? Study Design and Methods: We conducted post hoc analyses of the Sleep Apnea Cardiovascular Endpoints (SAVE) trial. In 2687 individuals, Cox proportional hazards models that were stratified for treatment allocation were used to determine the associations between clinical characteristics, pulse oximetry-derived metrics that were designed to quantify sustained and episodic features of hypoxemia, and cardiovascular outcomes. Metrics included oxygen desaturation index, time <90% SpO2, average SpO2 for the entire recording (mean SpO2), average SpO2 during desaturation events (desaturation SpO2), average baseline SpO2 interpolated across episodic desaturation events (baseline SpO2), episodic desaturation event duration and desaturation/resaturation-time ratio, and mean and SD of pulse rate. Results: Neither apnea-hypopnea index, oxygen desaturation index, nor any of the novel SpO2 metrics were associated with the primary SAVE composite cardiovascular outcome. Mean and baseline SpO2 were associated with heart failure (hazard ratio [HR], 0.81; 95% CI, 0.69-0.95; P = .009; and HR, 0.78; 95% CI, 0.67-0.90; P = .001, respectively) and myocardial infarction (HR, 0.86; 95% CI, 0.77-0.95; P = .003; and HR, 0.81; 95% CI, 0.73-0.90; P < .001, respectively). Desaturation duration and desaturation/resaturation time ratio, with established risk factors, predicted future heart failure (area under the curve, 0.86; 95% CI, 0.79-0.93). Interpretation: Apnea-hypopnea index and oxygen desaturation index were not associated with cardiovascular outcomes. In contrast, the pattern of oxygen desaturation was associated with heart failure and myocardial infarction. However, concomitant risk factors remained the predominant determinants for secondary cardiovascular events and thus deserve the most intensive management.
AB - Background: Traditional methods for the quantification of OSA severity may not encapsulate potential relationships between hypoxemia in OSA and cardiovascular risk. Research Question: Do novel nocturnal oxygen saturation (SpO2) metrics have prognostic value in patients with OSA and high cardiovascular event risk? Study Design and Methods: We conducted post hoc analyses of the Sleep Apnea Cardiovascular Endpoints (SAVE) trial. In 2687 individuals, Cox proportional hazards models that were stratified for treatment allocation were used to determine the associations between clinical characteristics, pulse oximetry-derived metrics that were designed to quantify sustained and episodic features of hypoxemia, and cardiovascular outcomes. Metrics included oxygen desaturation index, time <90% SpO2, average SpO2 for the entire recording (mean SpO2), average SpO2 during desaturation events (desaturation SpO2), average baseline SpO2 interpolated across episodic desaturation events (baseline SpO2), episodic desaturation event duration and desaturation/resaturation-time ratio, and mean and SD of pulse rate. Results: Neither apnea-hypopnea index, oxygen desaturation index, nor any of the novel SpO2 metrics were associated with the primary SAVE composite cardiovascular outcome. Mean and baseline SpO2 were associated with heart failure (hazard ratio [HR], 0.81; 95% CI, 0.69-0.95; P = .009; and HR, 0.78; 95% CI, 0.67-0.90; P = .001, respectively) and myocardial infarction (HR, 0.86; 95% CI, 0.77-0.95; P = .003; and HR, 0.81; 95% CI, 0.73-0.90; P < .001, respectively). Desaturation duration and desaturation/resaturation time ratio, with established risk factors, predicted future heart failure (area under the curve, 0.86; 95% CI, 0.79-0.93). Interpretation: Apnea-hypopnea index and oxygen desaturation index were not associated with cardiovascular outcomes. In contrast, the pattern of oxygen desaturation was associated with heart failure and myocardial infarction. However, concomitant risk factors remained the predominant determinants for secondary cardiovascular events and thus deserve the most intensive management.
KW - SAVE
KW - cardiovascular risk
KW - heart failure
KW - hypoxemia
KW - sleep apnea
UR - http://www.scopus.com/inward/record.url?scp=85096633731&partnerID=8YFLogxK
U2 - 10.1016/j.chest.2020.06.072
DO - 10.1016/j.chest.2020.06.072
M3 - Article
C2 - 32679239
AN - SCOPUS:85096633731
VL - 158
SP - 2621
EP - 2631
JO - Chest
JF - Chest
SN - 0012-3692
IS - 6
ER -