Is sleep a mechanistic factor in the blood pressure lowering effects of low-dose aspirin taken at bedtime? A pilot study.

INTRODUCTION

This was a pilot study designed to test the hypothesis that bedtime administration of acetylsalicylic acid (ASA) lowers BP through sleep improvements that impact the inflammatory, and renin-angiotensin-aldosterone system (RAAS). We predicted that ASA would enhance sleep consolidation and lower sympathetic activation, protecting against the physiological stress of fragmented sleep.

METHODS

Seven participants (5F, 2M, mean age 25.71 ± 4.03 years, body mass index (BMI) 22.40 ± 1.91 kg/m2) completed this within-subject, double-blind, balanced study involving 2 × 5 in-patient days. Participants were randomized to daily intake of ASA (81 mg/day) or placebo at bedtime for 2 weeks before each hospital research stay that included 1 baseline (BL) night, 2 nights of an experimental sleep disturbance (ESD) protocol and finally, 1 night of recovery sleep. The ESD protocol included 1-h delayed sleep onset, fragmentation of sleep with 5 × 20-min awakenings, and a 1-h earlier lights on time.

RESULTS

ASA did not decrease BP following the 2-week at-home ASA administration, nor during ESD. Evening renin was significantly reduced (p = .048), compared to placebo after 2 weeks of ASA. Mood and well-being improved after 2 weeks of ASA. There were statistical trends toward decreased 24-h average heart rate (p = .053), and increased heart rate variability (p = .080). When challenged with the ESD protocol, ASA was associated with a longer duration of individual slow waves (p = .013), lower 24-h average HR (p < .001) and a trend to greater non-rapid eye movement delta power (p = .061).

CONCLUSIONS

This pilot study is the first investigation exploring effects of ASA on renal & hemodynamic parameters at night, implicating sleep as an important mechanistic factor.