Hypertension and sleep health: a multidimensional puzzle

Blood pressure is a vital physiological characteristic, which is closely related to a multitude of body functions. Sleep patterns can be modified by lifestyle changes or therapeutic interventions, and good understanding of how they fit into blood pressure control can help prevent hypertension and its complications. Indeed, poorly sleep quality has been associated with hypertension and related comorbid states, such as obesity, metabolic syndrome, and mental health problems. These conditions are probably mutually related, although casualty is more difficult to establish. Insufficient or poor quality of sleep could lead to pathophysiological abnormalities linked to hypertension, such as increased sympathetic drive, which could it turn disturb healthy sleep patterns [1]. Nevertheless, sleep patterns vary geographically and historically. In areas with large seasonal fluctuations of daylight duration, a shortened sleep during summer has been linked to higher overall sympathetic drive and elevated blood pressure when compared with longer sleeps during winter. In modern times, this pattern has been modified by introduction of electricity, and multiple new lifestyle factors associated with disrupted sleep throughout the year. These factors include shift work, late time entertainment, television, the internet, and travel across time zones. In fact, over a half of participants in the National Sleep Foundation's 2013 International Bedroom Poll reported insufficient sleep on workdays. Admittedly, these lifestyle changes affect the sleep even in individuals who could afford enough bedtime. Insomnia is common and is associated with higher night-time SBP and blunted day-to-night SBP dipping [2]. The nocturnal awakenings could be compensated by daytime naps and these could be difficult to account for during sleep studies. Whilst there are many classifications of sleep disorder, they would usually manifest by sleep deprivation because of lack of the necessary amount or quality of sleep, disrupted sleep, and events occurring during sleep, such as sleep apnoea or restless legs syndrome. All of them could have detrimental effects on blood pressure. Also, different sleep phases can play specific roles in sustained blood pressure elevation. In this issue of the Journal of Hypertension, the analysis of the Wisconsin Sleep Cohort Study presented demonstrates that hypertension was linked to longitudinal increased decline in rapid eye movement (REM) sleep percentage, and a lesser decline in percentage of time spent in N3 sleep [3]. The findings are not easy to interpret. In fact, previously changes in sleep architecture, such as decreased percentage of time in slow-wave sleep and low non-REM sleep delta power are associated with increase in hypertension incidence in specific population [4]. The blood pressure dipping status is likely to play a role in these processes. N3 sleep (i.e. slow-wave sleep) is believed to be the most restorative type when heart rate, blood pressure, cerebral blood flow, and respiration decrease. During REM sleep, these processes are increased compared with non-REM sleep. The balance of the phases can drive the overall night-time blood pressure reduction. However, the ‘dipping’ status varies from day to day and the assignment of patients to dippers and nondippers is not reproducible over time, similarly to the variation in the sleep quality and duration [5,6]. Of note, nondipping status has been associated with sleep disturbance [7]. Unsurprisingly, nocturnal blood pressure is increasingly considered a better predictor of cardiovascular risk than daytime blood pressure [7,8]. Unfortunately, data on diurnal blood pressure variations were not available for in the Wisconsin Sleep Cohort Study [3]. Arguably the fact that office blood pressure was used for the study analysis could also lead to a misassignment of some people with white-coat hypertension as having essential hypertension. Perceived difficulties with initiation and maintenance of sleep are also important, and both medical and mental health problems play their roles. The Wisconsin Sleep Cohort Study reported that subjective insomnia, presented by difficulty falling asleep, was present in people with hypertension [3]. The clinical significance of this finding is difficult to establish as the overall sleep duration has not been affected and its relationship to clinical outcomes was beyond the scope of the study. Previously, self-reported sleep duration only moderately correlates with actual measured sleep [9]. This may well reflect the recognized phenomena of sleep state misperception when people report shorter than actual sleep duration. For example, anxiety and depression states are related to both sleep disturbance and increased risk of hypertension and its complications [10]. Assessment of mental health was beyond the scope of the Wisconsin Sleep Cohort Study and the choice of study population could also be of relevance as a meta-analysis of studies that assessed subjective sleep quality and blood pressure or hypertension showed that poor sleep quality was significantly associated with a greater likelihood of hypertension and patients with hypertension had significantly worse sleep quality scores with the opposite observed in blood pressure dippers [11]. There are also data indicating that hypertension could contribute towards shortening sleep duration, which, in turn, could further raise blood pressure [12]. Furthermore, the relationship between sleep duration and hypertension could be nonlinear. Whilst the role of sleep deprivation is more recognized, long sleep duration has been associated with hypertension prevalence in some cross-sectional studies but no published longitudinal studies have shown an association between long sleep duration and hypertension incidence [13]. Whilst there is little doubt that sleep health is implicated in pathophysiology of hypertension, the complexity of the relationship makes it difficult to identify specific sleep abnormalities implicated in blood pressure elevation at both epidemiological and individual patient level. This is largely because of lack of adequate tools for prolonged monitoring of sleep. Fortunately, the progress in affordable wearable technologies facilitating telemonitoring for both blood pressure and sleep parameters can provide the new insight in the relationship and help to model more effective interventions with personalized care, and timely feedback from healthcare professionals to direct the needed behavioural changes and treatments. Healthy sleep is vital for wellbeing and its value is not only increasingly appreciated by the public but also by employers and legislators. Future studies are awaited with interest. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.