Evidence is available that the frequency and severity of arterial hypertension, and, in general, of cardiovascular diseases, bear a relationship with sleep disorders and, more specifically, with sleep duration [1,2]. Indeed, on the one side patients with cardiovascular diseases often complain of a number of sleep disturbances, including sleep fragmentation, insomnia, and breathing disorders during sleep.
On the other side, patients with sleep complaints seem to be more frequently affected by cardiovascular problems. Given such a complex bidirectional relationship between these phenomena, it is therefore often difficult to determine which is the cause and which is the effect between cardiovascular problems and sleep disorders.
Sleep-related breathing disorders, and, in particular, obstructive sleep apnea (OSA) syndrome, formerly named Pickwickian syndrome , are among the most common problems occurring during sleep in the general population, with at least 4% of middle-aged men and 2% of middle-aged women being affected in the developed world, its prevalence is increasing in parallel with the increasing prevalence of obesity [4–6].
A number of studies have shown OSA to be strictly related to the presence of hypertension and to represent an independent risk factor for the development of a high blood pressure (BP) condition [5,6]. Evidence of a relationship between arterial hypertension and excessive daytime somnolence has also been provided [7,8], whereas sleep fragmentation and a reduction in nocturnal sleep duration have been identified as factors majorly responsible for the increased sympathetic activity and the occurrence of elevated BP levels extending during daytime [9,10].
Given the large number of papers demonstrating the complex and multiple links relating sleep disorders and sleep duration with the occurrence of high BP levels, it is somehow surprising that only limited evidence has been up to now provided on the clinical relevance of multimodal sleep patterns over 24 h. In particular, the actual impact of mid-day naps on cardiovascular outcome still remains a debated issue.
Observational data collected so far on this issue, largely based on either case–control or prospective cohort studies, have indeed yielded conflicting results. On the one side, a consistent number of articles have suggested a positive association between occurrence of daytime sleep and cardiovascular disease [11,12], with the observation that the BP changes associated with daytime ‘siesta’, and, in particular, the BP increase following awakening after a mid-day nap, may be related to early evening onset of stroke . On the other side, a protective effect of ‘siesta’ against fatal cardiovascular outcome has been suggested by studies showing a stress-releasing effect of daytime naps .
The inconsistency in the evidence collected on this issue so far may depend on several factors, including differences in study design and/or in the geographical location of individuals being investigated; sex-related and age-related mechanisms; and the bidirectional relationship reported to characterize the link between daytime sleep patterns and cardiovascular disorders, with data showing that mid-day naps may favor cardiovascular complications, but, at the same time, that preexisting cardiovascular diseases may increase the incidence of multimodal sleep over 24 h [15,16].
Finally, there is a general consensus on the fact that all observations on the clinical impact of daytime nap habits should be weighted for the possible concomitant occurrence of alterations in duration and quality of night-time sleep. An increased frequency and duration of mid-day naps could, in fact, represent an indirect marker of nighttime sleep disordered breathing, and more specifically of sleep apnea. Such an association might thus importantly contribute to explain the observed link between mid-day ‘siesta’ and increased rate of cardiovascular disease and/or of BP elevation over 24 h.
The interpretation of these findings is further complicated by the evidence that a number of cardiovascular diseases are associated with disrupted sleep patterns over 24 h, including not only poor night-time sleep quality but also night-time sleep deprivation and, as a consequence, an increased frequency of mid-day naps and/or hypersomnia. For example, symptomatic heart failure patients with nocturnal paroxysmal dyspnea and nocturia demonstrate decreased nocturnal sleep duration and, because of a compensating increase in daytime resting periods, are also characterized by an increased frequency of ‘siesta’ as compared with healthy individuals.
The possibility of an increased risk of cardiovascular morbidity and mortality associated with mid-day napping is thus an important reason for concern, from a public health viewpoint, and a strong stimulus for further studies in this area.
The article by Cao et al.  published in this issue of the Journal of Hypertension provides additional novel and stimulating information on the relationship between the duration of habitual mid-day naps and the BP levels or risk of hypertension in a large population of middle-aged and old adult population.
This article reports on the results of an observational study conducted on more than 27 000 participants. Patients were examined according to a cross-sectional study design, with information on sleep obtained through a structured questionnaire administered by a trained interviewer, and with information on BP being derived from a hospital visit during which BP was measured using a mercury manometer, while the occurrence of hypertension was explored based on the self-reported history of physician's diagnosis of elevated BP levels and/or of the current use of antihypertensive drugs. Patients were categorized into five groups according to the self-reported nap duration, namely no napping, and mid-day napping with duration <30, =30, =60, and >90 min, respectively. The conclusion of the study by Cao et al.  is that people habitually taking longer mid-day naps display elevated BP levels and an increased risk of hypertension more frequently, compared with people not taking mid-day naps or taking naps for short duration (<30 min). Even after adjusting for possible confounders, longer afternoon naps duration (≥30 min) remained associated with an increased risk of hypertension.
This study has the merit of offering novel and interesting data on the relation of mid-day naps occurrence and duration with BP levels in a very large number of middle-aged and elderly individuals. However, a few important limitations of this work have to be acknowledged, in the perspective of the need of further studies addressing this interesting issue. Admittedly, some of these limitations are inherent in any study including a huge number of individuals, wherein the advantage of studying large numbers is counterbalanced by less precision in measuring relevant variables. First, the main variables on which this study focuses, that is, the occurrence and duration of mid-day naps in people who take siesta regularly, were not directly measured but were only self-reported through a questionnaire. Admittedly, such an approach only allows generating hypotheses that require to be further tested, and therefore cannot provide evidence of any causal link between mid-day nap features and BP elevations. In fact, the use of quantitative diagnostic tools, such as actigraphy, polisomnography, or other objective measures of nap duration, would have been necessary to adequately support the study results. Second, the identification of a high BP condition was based either on office BP values obtained during one single hospital visit with the auscultatory method or on self-reported diagnosis of hypertension previously made by a physician or of current use of hypertensive drugs. A more precise assessment of the BP condition in the individuals participating in this study would have required repeated clinic measurements of BP coupled with out-of-office BP monitoring, the latter aimed at confirming the occurrence of high BP levels in their daily life conditions . Third, there were large differences in the baseline characteristics between individuals found to be hypertensive and those who were not hypertensive. The hypertensive group was older, with higher prevalence of men, higher BMI, higher frequency of diabetes, coronary artery disease, stroke, and hyperlipidemia. Moreover, metabolic syndrome, which includes higher BP levels in its definition was more prevalent among hypertensive than among normotensive individuals. Thus, the finding that individuals who reported to nap more frequently and for longer periods had higher BP levels cannot per se be taken as an unequivocal demonstration that napping is a risk marker of hypertension. In fact, we cannot exclude that the link between longer naps and hypertension could be due to other concomitant factors, such as the presence of comorbidities or of metabolic syndrome. Fourth, this study does not provide any information on participants’ sleep quality and, in particular, on the occurrence of sleep apnea. This is indeed an important limitation, as OSA could be a potentially important confounder in determining the mechanisms responsible for the link between longer mid-day naps and high BP levels. In fact, nocturnal OSA was repeatedly shown in previous studies to be associated with both elevated BP levels and disrupted sleep at night, and to be accompanied by daytime somnolence, which might favor a more frequent occurrence of naps.
In conclusion, in spite of the novel and interesting observation of a link between longer mid-day naps and higher BP levels, based on the analysis of a very large database, the study by Cao et al.  has to face the limitations coming from its cross-sectional design and the indirect assessment of a number of important variables. As a consequence of these methodological problems, this study cannot provide a definitive demonstration of the occurrence of a causal link between longer daytime siesta and risk of hypertension, also on the background of many potential confounders of this relationship, and of the possible bidirectional nature of the link between mid-day naps and high BP, which could make reverse causality a likely possibility in this setting, at least in some cases. The demonstration of the occurrence of a cause–effect relation between features of daytime siesta and elevated BP levels thus remains to be provided by future longitudinal studies, which should be based on objective quantification of daytime sleep parameters and should include a more precise assessment of the presence of hypertension, also based on out-of-office BP monitoring.
Until these studies are available, whether afternoon naps are causally associated with increased risk of hypertension or should be considered as innocent bystanders, being themselves the consequence of other factors affecting such an association, this is likely to remain an unanswered question.
Conflicts of interest
There are no conflicts of interest to disclose in relation to this paper.
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