ATS 2021 will feature presentations of original research from accepted abstracts. Mini Symposia and Thematic Poster Sessions are abstract based sessions.
Please use the form below to browse scientific abstracts and case reports accepted for ATS 2021. Abstracts presented at the ATS 2021 will be published in the Online Abstract Issue of the American Journal of Respiratory and Critical Care Medicine, Volume 203, May 3, 2021.
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Cardiovascular Benefit of CPAP Is Modified by the Sleep Apnea Related Pulse Rate Response in Coronary Artery Disease Patients with Nonsleepy OSA: Findings from the RICCADSA Randomized Controlled Trial
Session Title
B14 - B014 PATHOPHYSIOLOGY, CARDIOVASCULAR DISEASE, AND COVID- WHAT'S HAPPENING IN SLEEP RESEARCH RIGHT NOW
Abstract
A1103 - Cardiovascular Benefit of CPAP Is Modified by the Sleep Apnea Related Pulse Rate Response in Coronary Artery Disease Patients with Nonsleepy OSA: Findings from the RICCADSA Randomized Controlled Trial
Author Block: A. Azarbarzin1, A. Zinchuk2, D. Wellman1, L. Taranto Montemurro1, D. Vena1, L. Gell1, L. Messineo1, D. White1, D. J. Gottlieb1, S. S. Redline1, Y. Peker3, S. A. Sands1; 1Medicine, Brigham and Women's Hospital/ Harvard Medical School, Boston, MA, United States, 2Internal Medicine, Yale University, New Haven, CT, United States, 3Pulmonary Medicine, Koc University School of Medicine, Istanbul, Turkey.
Rationale: Randomized controlled trials in patients with coronary artery disease and nonsleepy obstructive sleep apnea (OSA) have not demonstrated a protective effect of continuous positive airway pressure (CPAP) on adverse cardiovascular outcomes in intention-to-treat analyses. Recently, analysis of large cohort studies revealed that a subgroup of patients with nonsleepy OSA who demonstrated a greater respiratory-event-related pulse rate response (ΔHR) were at increased risk of cardiovascular morbidity and mortality. Here we test the hypothesis that a larger pre-treatment ΔHR was associated with greater CPAP-related reduction in adverse cardiovascular outcomes in patients with coronary artery disease and nonsleepy OSA (apnea-hypopnea index ≥15 events/hr and Epworth Sleepiness Scale score <10).
Methods: ∆HR was measured from the oximetry pulse rate signals collected during baseline polysomnography of the RICCADSA randomized controlled trial (NCPAP:Ncontrol=112:113; male=86%; age=66±8 [mean±SD] yr; 87% on beta-blockers). The primary outcome was a composite of repeat revascularization, myocardial infarction, stroke, and cardiovascular mortality. Multivariable Cox regression assessed whether the effect of auto-titrating CPAP treatment on the primary outcome was moderated by ∆HR per significant interaction. Primary models included covariates (age, sex, BMI, and revascularization type) to maximize model precision. Secondary analysis examined ∆HR responsiveness by normalizing against event severity measures (desaturation area, arousal intensity, event duration). Sensitivity analysis excluded individuals not using beta-blockers.
Results: ∆HR measures were obtained in 92% of patients (mean±SD: 7.1±3.7 BPM). 48 composite events over a 57-month median follow-up were recorded. A significant interaction between treatment and ∆HR was observed (interaction hazard ratio [95%CI]: 0.51 [0.26-0.98], p=0.043); at elevated ∆HR (10.8 BPM, +1SD) treatment hazard ratio was 0.39 [0.15-0.98] in contrast to no significant effect at normal ∆HR (7.1 BPM; hazard ratio 0.76 [0.42-1.37], p=0.4). Normalized ∆HR measures were stronger determinants of treatment-related risk reduction (interaction hazard ratios: desaturation area 0.45 [0.23-0.87], arousal intensity 0.30 [0.12-0.75], event duration 0.45 [0.23-0.87]); i.e. treatment benefit is associated with greater normalized ∆HR (responsiveness) rather than just event severity. Exclusion of patients not using beta-blockers yielded similar findings.
Conclusions: A distinct protective effect of CPAP on adverse cardiovascular outcomes was shown in the coronary artery disease patients with nonsleepy OSA who exhibit greater HR responses to OSA events. Our study provides novel evidence that a greater heart rate responsiveness to obstructive events is an identifiable, deleterious, and potentially-reversible risk factor, that could be used to select patients most likely to exhibit long-term cardiovascular benefit from CPAP therapy.
Author Block: A. Azarbarzin1, A. Zinchuk2, D. Wellman1, L. Taranto Montemurro1, D. Vena1, L. Gell1, L. Messineo1, D. White1, D. J. Gottlieb1, S. S. Redline1, Y. Peker3, S. A. Sands1; 1Medicine, Brigham and Women's Hospital/ Harvard Medical School, Boston, MA, United States, 2Internal Medicine, Yale University, New Haven, CT, United States, 3Pulmonary Medicine, Koc University School of Medicine, Istanbul, Turkey.
Rationale: Randomized controlled trials in patients with coronary artery disease and nonsleepy obstructive sleep apnea (OSA) have not demonstrated a protective effect of continuous positive airway pressure (CPAP) on adverse cardiovascular outcomes in intention-to-treat analyses. Recently, analysis of large cohort studies revealed that a subgroup of patients with nonsleepy OSA who demonstrated a greater respiratory-event-related pulse rate response (ΔHR) were at increased risk of cardiovascular morbidity and mortality. Here we test the hypothesis that a larger pre-treatment ΔHR was associated with greater CPAP-related reduction in adverse cardiovascular outcomes in patients with coronary artery disease and nonsleepy OSA (apnea-hypopnea index ≥15 events/hr and Epworth Sleepiness Scale score <10).
Methods: ∆HR was measured from the oximetry pulse rate signals collected during baseline polysomnography of the RICCADSA randomized controlled trial (NCPAP:Ncontrol=112:113; male=86%; age=66±8 [mean±SD] yr; 87% on beta-blockers). The primary outcome was a composite of repeat revascularization, myocardial infarction, stroke, and cardiovascular mortality. Multivariable Cox regression assessed whether the effect of auto-titrating CPAP treatment on the primary outcome was moderated by ∆HR per significant interaction. Primary models included covariates (age, sex, BMI, and revascularization type) to maximize model precision. Secondary analysis examined ∆HR responsiveness by normalizing against event severity measures (desaturation area, arousal intensity, event duration). Sensitivity analysis excluded individuals not using beta-blockers.
Results: ∆HR measures were obtained in 92% of patients (mean±SD: 7.1±3.7 BPM). 48 composite events over a 57-month median follow-up were recorded. A significant interaction between treatment and ∆HR was observed (interaction hazard ratio [95%CI]: 0.51 [0.26-0.98], p=0.043); at elevated ∆HR (10.8 BPM, +1SD) treatment hazard ratio was 0.39 [0.15-0.98] in contrast to no significant effect at normal ∆HR (7.1 BPM; hazard ratio 0.76 [0.42-1.37], p=0.4). Normalized ∆HR measures were stronger determinants of treatment-related risk reduction (interaction hazard ratios: desaturation area 0.45 [0.23-0.87], arousal intensity 0.30 [0.12-0.75], event duration 0.45 [0.23-0.87]); i.e. treatment benefit is associated with greater normalized ∆HR (responsiveness) rather than just event severity. Exclusion of patients not using beta-blockers yielded similar findings.
Conclusions: A distinct protective effect of CPAP on adverse cardiovascular outcomes was shown in the coronary artery disease patients with nonsleepy OSA who exhibit greater HR responses to OSA events. Our study provides novel evidence that a greater heart rate responsiveness to obstructive events is an identifiable, deleterious, and potentially-reversible risk factor, that could be used to select patients most likely to exhibit long-term cardiovascular benefit from CPAP therapy.
