Abstract
Blood pressure variability (BPV) is recognized as a prognostic marker of cardiovascular disease (CVD), the leading cause of death in the United States (U.S.). BPV can be classified based on the time scale as very short-term (beat-to-beat), short-term (within 24 hours), and long-term (day-to-day and visit-to-visit). Psychological distress, which includes symptoms of depression, anxiety, and perceived stress, and behavioral risk factors, such as poor sleep quality or sleep behaviors, are known to be associated with increased BPV. Yet, the interrelationships among psychological distress, sleep, and BPV remain still unclear. In this dissertation, we systematically reviewed the current literature on the associations between sleep and BPV. In order to address the research gaps identified from the review, we investigated the impact of sleep behaviors on short-term BPV (specifically in the form of morning blood pressure surge [MBPS]) while considering psychological risk factors.
First, a systematic review of 22 studies was conducted to describe the current evidence in the literature on the association between sleep and BPV (manuscript 1). The overall findings suggested that individuals with poor sleep quality or longer sleep duration are more likely to have an increased short-term (24-hour BPV, morning blood pressure (BP) surge, and nocturnal BP non-dipping pattern) and visit-to-visit BPV. In addition, shorter sleep duration was significantly associated with a nocturnal BP non-dipping pattern. Lastly, during the non-rapid eye movement (non-REM) sleep stage, a statistically significantly lower beat-to-beat BPV was observed in the deep sleep stage. The findings of this systematic review suggest that further research is needed to better understand the intricate interplay between sleep and BPV, as well as explore how various aspects of sleep impact distinct features of BPV and how they are implicated in CVD risk.
Next, a cross-sectional pilot study was performed to assess psychological distress, sleep quality, forced awakening, and MBPS (manuscripts 2 and 3). Thirty-two healthy adults aged 30 years and above participated in this pilot study, which included one night of natural awakening and one night of forced awakening. In manuscript 2, we examined the impact of forced awakening on MBPS using a paired t-test and investigated whether the forced awakening is associated with MBPS, independent of sleep quality using a linear mixed model. The findings of manuscript 2 demonstrated that (1) MBPS was 74% greater during forced awakening compared to natural awakening, and (2) forced awakening was significantly associated with increased MBPS after controlling for covariates (age, sex, mean arterial pressure) and sleep quality. In manuscript 3, we investigated the potential impact of psychological distress (symptoms of depression, anxiety, and perceived stress) on the MBPS difference between natural and forced awakenings, independent of sleep quality, using multiple linear regression. The results of manuscript 3 showed that individuals with higher anxiety levels were more likely to have a greater MBPS difference after controlling for covariates and sleep quality. Findings from this cross-sectional study suggest that forced awakening may play a significant role in increasing MBPS, leading to an elevated risk of cardiovascular events.
To alleviate the impact of forced awakening on MBPS and potential cardiovascular events, future research may be warranted to examine the influence of using the snooze function on MBPS and to investigate the potential impact of the noise of alarm clocks and alarm anxiety on MBPS in a larger sample of individuals at known risk for CVD. Such research may yield valuable insights to develop targeted interventions to mitigate the risk of cardiovascular events associated with elevated MBPS.
