Discussion
Our result showed that blood pressure (SBP and/or DBP and/or MAP) was lower in the pregnant women with better sleep quality: shorter sleep latency, longer duration of sleep, better efficiency and lower PSQI scores. UA PI was similarly lower in women with better sleep quality. The correlation between sleep and BP was the most significant in the first trimester as demonstrated by liner regression analysis.
Sleep latency, duration and efficiency were important aspects of sleep with significant correlation to BP. A previous cohort study by William et al. found that mean 1st and 2ndtrimester SBP and DBP values were similar among women reporting to be short sleepers (≤ 6 hours) versus women reporting to sleep >9 hours. However, both short and long sleep duration in early pregnancy were associated with increased mean 3rd trimester SBP and DBP compared to women who sleep for 9 hours in their study15.Their study findings were in line with some previous studies done in the non-pregnant population1-4. The analysis in our study differed from these previous studies. Sleep duration, sleep efficiency, latency and PSQI were considered as continuous variables in mixed model and linear regression analysis instead of categorical variables as in those studies. We believe that correlation analysis using continuous variables offers a more comprehensive comparison. The sleep duration for our study subjects fell between 4.7 and 8.7 hours. There was no subject with > 9 hours of sleep. This may also explain the different findings as William et al’s study showed higher BP in women who slept > 9 hours.
The mechanism linking sleep and blood pressure is very complex. One possible mechanism is increased oxidative stress and reduced nitric oxide (NO) in poor sleepers. NO is an important mediator in vascular function causing dilatation of the vessels and thus resulting in lower BP. In the case of obstructive sleep apnoea, nocturnal hypoxemia induces oxidative stress which triggers an inflammatory response and reduction in NO20-21. Another possible mechanism is through the sympathetic pathway and the hypothalamic-pituitary-adrenal axis. In some experimental studies, increased secretion of catecholamines, altered sympathovagal balance and disruption in cortisol levels were postulated to link poor sleep with elevated blood pressure22-25. A few interesting studies showed that increase in pro-inflammatory cytokines such as Interleukin-1 and Tumour necrosis factor-alpha alter sleep pattern and may potentially cause elevated blood pressure26-28. However, the exact underlying mechanism remains to be elucidated.
UA PI and RI were significantly lower in women with better sleep as shown in our study. The association between sleep quality and uterine artery blood flow was reported in literature. One postulation is that poor sleep may lead to suboptimal trophoblastic invasion of myometrium and consequently higher blood flow resistance. In other words, higher blood pressure in people with poorer sleep can potentially be contributed by placental dysfunction. Another possible explanation is that sleep is associated with worse uterine artery doppler and higher blood pressure via a common mechanism such as reduced NO which leads to vasoconstriction.