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.