TY - JOUR
T1 - Pulse Wave Amplitude Drops Index
T2 - A Biomarker of Cardiovascular Risk in Obstructive Sleep Apnea
AU - Solelhac, Geoffroy
AU - Sánchez-de-la-Torre, Manuel
AU - Blanchard, Margaux
AU - Berger, Mathieu
AU - Hirotsu, Camila
AU - Imler, Théo
AU - Sánchez-de-la-Torre, Alicia
AU - Haba-Rubio, Jose
AU - Marchi, Nicola Andrea
AU - Bayon, Virginie
AU - Bailly, Sébastien
AU - Goupil, François
AU - Waeber, Adrien
AU - Heiniger, Grégory
AU - Pigeanne, Thierry
AU - Gracia-Lavedan, Esther
AU - Zapater, Andrea
AU - Abad, Jorge
AU - Ordax, Estrella
AU - Masdeu, María José
AU - Cabriada-Nuño, Valentin
AU - Egea, Carlos
AU - Van Den Broecke, Sandra
AU - Vollenweider, Peter
AU - Marques-Vidal, Pedro
AU - Vaucher, Julien
AU - Bernardi, Giulio
AU - Betta, Monica
AU - Siclari, Francesca
AU - Barbé, Ferran
AU - Gagnadoux, Frédéric
AU - Heinzer, Raphael
PY - 2023/6/15
Y1 - 2023/6/15
N2 - Rationale: It is currently unclear which patients with obstructive sleep apnea (OSA) are at increased cardiovascular risk. Objective: To investigate the value of pulse wave amplitude drops (PWADs), reflecting sympathetic activations and vasoreactivity, as a biomarker of cardiovascular risk in OSA. Methods: PWADs were derived from pulse oximetry-based photoplethysmography signals in three prospective cohorts: HypnoLaus (N = 1,941), the Pays-de-la-Loire Sleep Cohort (PLSC; N = 6,367), and "Impact of Sleep Apnea syndrome in the evolution of Acute Coronary syndrome. Effect of intervention with CPAP" (ISAACC) (N = 692). The PWAD index was the number of PWADs (>30%) per hour during sleep. All participants were divided into subgroups according to the presence or absence of OSA (defined as ⩾15 or more events per hour or <15/h, respectively, on the apnea-hypopnea index) and the median PWAD index. Primary outcome was the incidence of composite cardiovascular events. Measurements and Main Results: Using Cox models adjusted for cardiovascular risk factors (hazard ratio; HR [95% confidence interval]), patients with a low PWAD index and OSA had a higher incidence of cardiovascular events compared with the high-PWAD and OSA group and those without OSA in the HypnoLaus cohort (HR, 2.16 [1.07-4.34], P = 0.031; and 2.35 [1.12-4.93], P = 0.024) and in the PLSC (1.36 [1.13-1.63], P = 0.001; and 1.44 [1.06-1.94], P = 0.019), respectively. In the ISAACC cohort, the low-PWAD and OSA untreated group had a higher cardiovascular event recurrence rate than that of the no-OSA group (2.03 [1.08-3.81], P = 0.028). In the PLSC and HypnoLaus cohorts, every increase of 10 events per hour in the continuous PWAD index was negatively associated with incident cardiovascular events exclusively in patients with OSA (HR, 0.85 [0.73-0.99], P = 0.031; and HR, 0.91 [0.86-0.96], P < 0.001, respectively). This association was not significant in the no-OSA group and the ISAACC cohort. Conclusions: In patients with OSA, a low PWAD index reflecting poor autonomic and vascular reactivity was independently associated with a higher cardiovascular risk.
AB - Rationale: It is currently unclear which patients with obstructive sleep apnea (OSA) are at increased cardiovascular risk. Objective: To investigate the value of pulse wave amplitude drops (PWADs), reflecting sympathetic activations and vasoreactivity, as a biomarker of cardiovascular risk in OSA. Methods: PWADs were derived from pulse oximetry-based photoplethysmography signals in three prospective cohorts: HypnoLaus (N = 1,941), the Pays-de-la-Loire Sleep Cohort (PLSC; N = 6,367), and "Impact of Sleep Apnea syndrome in the evolution of Acute Coronary syndrome. Effect of intervention with CPAP" (ISAACC) (N = 692). The PWAD index was the number of PWADs (>30%) per hour during sleep. All participants were divided into subgroups according to the presence or absence of OSA (defined as ⩾15 or more events per hour or <15/h, respectively, on the apnea-hypopnea index) and the median PWAD index. Primary outcome was the incidence of composite cardiovascular events. Measurements and Main Results: Using Cox models adjusted for cardiovascular risk factors (hazard ratio; HR [95% confidence interval]), patients with a low PWAD index and OSA had a higher incidence of cardiovascular events compared with the high-PWAD and OSA group and those without OSA in the HypnoLaus cohort (HR, 2.16 [1.07-4.34], P = 0.031; and 2.35 [1.12-4.93], P = 0.024) and in the PLSC (1.36 [1.13-1.63], P = 0.001; and 1.44 [1.06-1.94], P = 0.019), respectively. In the ISAACC cohort, the low-PWAD and OSA untreated group had a higher cardiovascular event recurrence rate than that of the no-OSA group (2.03 [1.08-3.81], P = 0.028). In the PLSC and HypnoLaus cohorts, every increase of 10 events per hour in the continuous PWAD index was negatively associated with incident cardiovascular events exclusively in patients with OSA (HR, 0.85 [0.73-0.99], P = 0.031; and HR, 0.91 [0.86-0.96], P < 0.001, respectively). This association was not significant in the no-OSA group and the ISAACC cohort. Conclusions: In patients with OSA, a low PWAD index reflecting poor autonomic and vascular reactivity was independently associated with a higher cardiovascular risk.
KW - Humans
KW - Cardiovascular Diseases/etiology
KW - Prospective Studies
KW - Risk Factors
KW - Sleep Apnea, Obstructive/complications
KW - Heart Disease Risk Factors
KW - Biomarkers
U2 - 10.1164/rccm.202206-1223OC
DO - 10.1164/rccm.202206-1223OC
M3 - Article
C2 - 37017487
SN - 1073-449X
VL - 207
SP - 1620
EP - 1632
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 12
ER -