Non-dipping nocturnal blood pressure correlates with obstructive sleep apnoea severity in normotensive subjects and may reverse with therapy

Sophie J Crinion; Jana Kleinerova; Brian Kent; Geraldine Nolan; Cormac T Taylor; Silke Ryan; Walter T McNicholas

doi:10.1183/23120541.00338-2021

Non-dipping nocturnal blood pressure correlates with obstructive sleep apnoea severity in normotensive subjects and may reverse with therapy

ERJ Open Res. 2021 Aug 16;7(3):00338-2021. doi: 10.1183/23120541.00338-2021. eCollection 2021 Jul.

Authors

Sophie J Crinion^{1

2}, Jana Kleinerova³, Brian Kent⁴, Geraldine Nolan⁵, Cormac T Taylor⁶, Silke Ryan^{5

6

7}, Walter T McNicholas^{5

6

7}

Affiliations

¹ Respirology and Sleep Medicine, Kingston Health Sciences Centre, Kingston, Canada.
² Dept of Medicine, Queen's University, Kingston, Canada.
³ Dept of Respiratory Medicine, Mater Misericordiae University Hospital, Dublin, Ireland.
⁴ Dept of Respiratory Medicine, St James' Hospital, Dublin, Ireland.
⁵ Dept of Respiratory and Sleep Medicine, St Vincent's University Hospital, Dublin, Ireland.
⁶ School of Medicine, University College Dublin, Dublin, Ireland.
⁷ These authors contributed equally.

Abstract

Background: Obstructive sleep apnoea (OSA) is strongly associated with systemic hypertension, but there are limited data on the relationship with blood pressure (BP) in normotensive subjects. Here, we examined the relationship of OSA with nocturnal BP in a documented diurnal normotensive cohort, explored potential intermediate pathways and assessed the effects on BP of continuous positive airways pressure (CPAP) therapy.

Methods: 65 males referred for assessment of possible OSA and normotensive on 24-hour BP monitoring underwent overnight inpatient polysomnography (age 41±7 years, body mass index (BMI) 34±6 kg·m^-2, apnoea-hypopnoea index (AHI) 14 (interquartile range 5-26)). Urine and serum were assessed for markers of sympathetic activation, renin-angiotensin-aldosterone system activity, oxidative stress, endothelial function and systemic inflammation. In a subset of patients, 24-hour BP monitoring was repeated after CPAP therapy.

Results: Within this normotensive cohort, night-time systolic and diastolic BP and nocturnal BP dip were highest in the fourth OSA severity quartile (p<0.05). Nocturnal BP dip correlated with AHI (r=-0.327, p<0.05) and oxygen desaturation index (ODI) (r=-0.371, p<0.05), but only ODI was an independent predictor of BP dip (B=-0.351, p<0.01) and non-dipping status (B=0.046, p<0.05). Overnight urinary norepinephrine correlated with nocturnal systolic BP (r=0.387, p<0.01) with a trend towards correlation with systolic dipping (p=0.087). In 20 CPAP-treated patients, night-time systolic BP decreased (p<0.05) and mean nocturnal BP dip increased (p≤0.05).

Conclusion: In this normotensive cohort, OSA severity was associated with higher nocturnal BP, which improved following CPAP therapy, and intermittent hypoxia was the most important OSA-related variable in this relationship.