Nighttime Blood Pressure in Normotensive Subjects With Chronic Insomnia: Implications for Cardiovascular Risk

Abstract

Objective:

To assess as whether insomniacs have higher nighttime blood pressure (BP) and a blunted day-to-night BP reduction, recognized markers of increased risk of cardiovascular morbidity and mortality.

Design:

Prospective case-control study.

Setting:

University hospital-based sleep research laboratory.

Participants:

Thirteen normotensive subjects with chronic primary insomnia (9 women, 42 ± 7 y) and 13 sex- and age-matched good sleepers.

Measurements and results:

Subjects underwent 2-week sleep diary and 3 sleep studies to provide subjective and objective sleep variables, and 24-h beat-to-beat BP recording to provide daytime, night-time and day-to-night BP changes ([nighttime-daytime]/daytime)*100) (BP dipping). Spectral analysis of the electroencephalogram (EEG) was also performed during sleep of night 3 to assess EEG activity in the β frequency (16-32 Hz), a measure of brain cortical activation. Nighttime SBP was higher (111 ± 15 vs 102 ± 12 mm Hg, P < 0.01) and day-to-night SBP dipping was lower (−8% ± 6% vs −15% ± 5%, P < 0.01) in insomniacs than good sleepers. Insomniacs also had higher activity in EEG β frequency (P < 0.05). Higher nighttime SBP and smaller SBP dipping were independently associated with increased EEG β activity (P < 0.05).

Conclusions:

Higher nighttime SBP and blunted day-to-night SBP dipping are present in normotensive subjects with chronic insomnia and are associated with a hyperactivity of the central nervous system during sleep. An altered BP profile in insomniacs could be one mechanism implicated in the link between insomnia and cardiovascular morbidity and mortality documented in epidemiological studies.

Citation:

Lanfranchi PA; Pennestri MH; Fradette L; Dumont M; Morin CM; Montplaisir J. Nighttime blood pressure in normotensive subjects with chronic insomnia: implications for cardiovascular risk. SLEEP 2009;32(6):760-766.

INSOMNIA REFERS TO THE SUBJECTIVE EXPERIENCE OF NON RESTORATIVE SLEEP DUE TO DIFFICULTY FALLING ASLEEP, DIFFICULTY MAINTAINING SLEEP or early awakening.^1,2 Insomnia is the most common sleep complaint in the general population, with a variable prevalence ranging from 2% to 48%, a broad range which reflects the variable definition of insomnia, different modalities of investigation, and the population under study.^2,3 Indeed, insomnia may appear in association with another medical or psychiatric disorder (comorbid insomnia), or as an independent condition as primary insomnia.³ Hallmarks of primary insomnia are the subjective experience of difficulty initiating and maintaining sleep, accompanied by distress or impairment in daytime function; the repetitive (as opposed to sporadic) recurrence of a poor sleep night;⁴ and duration of ≥ 1 month (according to DSM-IV definition)⁵, whereas ≥ 6 months duration is required to fulfill diagnostic criteria for chronic insomnia.^1–3

The pathophysiological mechanisms of primary insomnia remain elusive. Psychophysiological factors such as stress, anxiety, and autonomic hyperarousal are significant components of this condition⁶ and would appear to be implicated in its genesis and perpetuation. Polysomnography often fails to detect traditional criteria of poor sleep in insomniacs.² However, studies assessing quantitative electroencephalographic (EEG) spectral analysis have shown that, even in the presence of an apparently normal sleep architecture during polysomnography, these subjects have a decrease in EEG activity in the low frequencies (0.5-3.5 Hz) and an increased activity in high frequencies (14-45 Hz) during NREM sleep,^7–9 suggesting hyperactivity of the central nervous system during their sleep. Finally, studies using positron emission tomography assessing metabolic activity during NREM sleep have documented that insomniacs, compared to good sleepers, have higher metabolic activity in the ascending reticular activating system, along with areas pertaining to the emotion regulation and cognitive systems.¹⁰ These data suggest that the interaction of the systems regulating arousal, emotions, and cognitive function is part of the neurobiology of insomnia and support the concept that poor sleep is a symptom of a primary disorder of the arousal system. Indeed, as part of the arousal response, nocturnal plasma catecholamine concentration¹¹ and low frequency components of heart rate variability have been reported to be higher in insomniacs than good sleepers.¹²

Insomnia significantly impairs daytime function and predisposes to major depression.^1,3 There is also an emerging epidemiological evidence linking insomnia to higher cardiovascular morbidity and mortality.^13–17 However, at present, no studies have assessed the effects of insomnia on cardiovascular function, and to our knowledge, no data exist on nighttime BP, which has been shown to be relevant in assessing cardiovascular risk in recent large studies.^18,19 Blood pressure physiologically decreases during sleep,²⁰ a reduction commonly called dipping. Studies indicated that day-to-night and nighttime regulation of BP appear to be tightly coupled with autonomic changes occurring during the wake-sleep cycle.^21,22 This suggests that BP should be particularly sensitive to disturbances occurring during sleep, especially in the presence of hyperactivation of the sympathetic nervous system, such as that which may occur in insomniacs.

In the present study we investigated the 24-hour profile of arterial BP in subjects with chronic primary insomnia and tested the hypothesis that these subjects have higher nighttime BP and an attenuation of nocturnal BP dipping compared to good sleepers. We also assessed the relationship existing between nighttime BP and polysomnographic measures of poor sleep and EEG power spectra in the β frequencies.

METHODS

Study Population

This was a prospective case-control study, including 13 subjects with chronic primary insomnia (9 females, 30-60 years of age) and 13 age- and sex-matched good sleepers. The study was approved by the institutional ethics review board and subjects signed the approved consent form.

Subjects were diagnosed as having persistent primary insomnia based on DSM-IV-R criteria.⁵ To further operationalize the subjective insomnia complaint, they had to meet the following criteria: (a) self-reported difficulties initiating and/or maintaining sleep, defined as a sleep onset latency (time elapsed between light off and sleep onset) and/or wake after sleep onset > 30 min, with a corresponding total sleep time of < 6.5 h, and a sleep efficiency (ratio of sleep time/time spent in bed) of < 85% based on daily sleep diaries completed over 2 weeks²; (b) presence of insomnia ≥ 3 nights per week for ≥ 6 months; (c) Insomnia Severity Index score (which evaluates the severity of both sleep complaints and daytime function impairment) ≥ 15.²³ All subjects suffered from mixed insomnia: 12 subjects had maintenance insomnia and either initial or late insomnia, and 1 subject had initial and late insomnia. Good sleepers were defined by: (a) self-reported sleep latency and /or wake after sleep onset < 30 min with a corresponding sleep time ≥ 7 h and a sleep efficiency > 85%, for > 6 days per week, and (b) Insomnia Severity Index ≤ 7.²³

Exclusion criteria for all subjects included: hypertension (SBP ≥ 140 and DBP ≥ 90 mm Hg or use of antihypertensive drugs) and other cardiovascular diseases; current diagnosis of major depression, dysthymia, or anxiety disorders; neurological degenerative diseases (e.g., dementia, multiple sclerosis); other sleep disorders, including sleep apnea, restless legs syndrome, bruxism, and narcolepsy; diabetes; body mass index ≥ 32 kg/m²; smoking; alcohol or drug abuse; excessive use of caffeine (> 3 cups per day); unusual sleep schedule (bedtime after midnight and wake time after 09:00) and/or work shift; use of medications affecting the central and/or the autonomic nervous system.

Study Design and Procedures

Screening

The screening evaluation included: (a) a phone interview (b) 2-week sleep diaries in which insomniacs and good sleepers specified their sleep schedule (time in bed, time of sleep onset and offset, nighttime awakenings); (c) medical history and examination; (d) assessment of the severity of insomnia with the Insomnia Severity Index²³; (d) Beck Depression Inventory (BDI) to assess depressive symptoms (subjects with a score ≥ 23 for BDI were excluded)²⁴; and (e) full polysomnography recording in the sleep laboratory (night 1). Subjects with an apnea/hypopnea index ≥ 5 /h and those with ≥ 10 periodic leg movements/h were excluded.

Experimental Protocol (Figure 1)

Figure 1.

Screening and timetable of experimental procedures.

Subjects spent 40 hours in the sleep laboratory, which included 2 additional nights (night 2 served as adaptation night and night 3 was the experimental night) and the intervening day. Continuous recording of 3-lead ECG, respiration, and beat-to-beat BP, along with sleep recordings during the nights were performed during the 40-h period. During the daytime, subjects stayed in their rooms sitting in chairs reading, watching TV, and talking with study personnel. Only short monitored walks were allowed during the day. Lying in bed and naps were not allowed during the daytime. Caffeinated beverages were not allowed during the study.

Data Collection and Measurement

In the evening preceding sleep recordings, brachial cuff arterial BP was measured at rest in the sitting position in the nondominant arm to provide a baseline clinical value of systolic and diastolic BP (clinical SBP and DBP). The average over 2 measurements repeated at 2-min intervals was considered. Beat-to-beat noninvasive HR and BP were continuously recorded by using Portapres Model-2 (TNO Biomedical Instrumentation, Amsterdam, The Netherlands), which provides data through a continuous finger arterial pressure waveform.

BP and HR analyses were performed on the recording included between 08:00 following night 2 to 08:00 after night 3 (Figure 1). Average SBP, DBP, and HR of each hour of recording was calculated in each individual after removal of portions containing artifact. The hourly mean values were averaged to obtain daytime values (between 08:00 and 30 min before bedtime), and nighttime values (between light off in the evening and light on the following morning, which corresponded to the usual bed time and wake time of each subject). The percent of nocturnal BP change ([night-day]/day *100) was considered as the measure of day-to-night BP dipping.

Polysomnographic Recordings and Measures, EEG Digitalization, and Spectral Analyses.

Polysomnographic recordings included 10 EEG channels with a referential montage with linked ears, bilateral electrooculogram, chin electromyogram, bilateral tibialis electromyogram, pressure nasal cannula, thoracoabdominal strain gauges, finger pulse oximetry, and a 3-lead ECG (standard DI-DII and DIII). A Grass Model 15A94 amplifier system was used, and signals were digitized at a sampling rate of 256 Hz using commercial software (Harmonie, Stellate Systems, Montreal, Canada). Sleep stages were scored according to modified standard criteria on 20-sec epochs.²⁵ Periodic leg movements were scored according to Coleman's criteria.²⁶ Sleep latency was evaluated as the time elapsed between light off and sleep onset (defined as 3 consecutive epochs of stage 1 or 1 epoch of stages 2, 3, 4 or REM). Sleep efficiency was considered as the total sleep time/ total time in bed (between light off and light on in the following morning). Duration of time awake after sleep onset (defined as the amount of time awake between initial sleep onset and end of recording time) and the number of awakenings lasting ≥ 20 sec were also considered. Microarousals (abrupt shifts in EEG frequency lasting ≥ 3 sec, an expression of electrocortical activation) and sleep disordered breathing were scored according to American Sleep Disorders Association recommendations.^27,28

Power spectral analysis was performed on central (C3 and C4) and frontal (F3 ad F4) EEG derivations recorded during NREM sleep (sleep stages 2, 3, and 4) of the experimental night, using commercial software (Sensa, Stellate Systems, Montreal, Canada). Artifacts were detected automatically as well as by visual inspection. Spectral power was obtained by fast Fourier transforms performed on 4-sec artifact-free sections using a cosine window tapering, resulting in a 0.25-Hz spectral resolution.²⁹ Spectral power was averaged for β (16-32 Hz) frequency bands.

Statistical Analyses

Between-group comparison of demographic, clinical characteristics at entry, polysomnographic variables, and variables derived from 24-h BP recordings was performed by paired t-test or by Wilcoxon signed rank tests (for non-normally distributed variables). Assessment of normality was performed using the Shapiro-Wilk W test. Pearson correlation coefficients were calculated between nighttime BP and HR and age, body mass index, daytime BP and HR, and sleep variables including β activity in the EEG recording during NREM sleep. Partial correlation coefficients were also generated to examine the independent relationship between nighttime SBP and DBP (dependent variables) and polysomnographic and EEG measures, adjusting for potential confounders, in the overall population of 26 subjects. A 2-sided P-value ≤ 0.05 was considered statistically significant.

RESULTS

Table 1 shows clinical characteristics and subjective sleep variables from the 2-week home-based sleep diary. Subjects with insomnia, by definition, had shorter duration of sleep, longer sleep latency, and increased wake time after sleep onset compared to good sleepers. Subjects with insomnia also had slightly higher BDI scores than good sleepers and showed higher values of clinical diastolic blood pressure at screening, although in the normal range.

Table 1.

Demographic, Clinical, and Subjective Sleep Characteristics (from Sleep Diary) at Entry

(Paired t-test)	Good Sleepers	Insomniacs	P value
Sex, F/M	9/4	9/4
Age (years)	42 ± 9	42 ± 7	0.6
Body mass index (kg/m2)	24 ± 3	25 ± 4	0.6
Clinical SBP (mm Hg)	109 ± 11	115 ± 11	0.1
Clinical DBP (mm Hg)	62 ± 8	71 ± 7	0.01
Clinical HR (beats/min)	68 ± 9	71 ± 11	0.4
Insomnia Severity Index	2.8 ± 1.8	18.1 ± 2.1	<0.0001
Duration of insomnia (y)	-	23 ± 10
Beck Depression Inventory	2.4 ± 3.5	9.5 ± 2.1	<0.001
Sleep latency (min)	12 ± 12	46 ± 39	0.01
Total sleep time (min)	481 ± 69	345 ± 50	<0.0001
Wake time after sleep onset (min)	28 ± 28	147 ± 56	<0.0001
Sleep efficiency (%)	92 ± 7	65 ± 12	<0.0001

Data are presented as mean ± standard deviation.

SBP, systolic blood pressure;

DBP, diastolic blood pressure; HR, heart rate

Results from the polysomnographic recording of night 3 are reported in Tables 2 and 3. No significant differences were noted between good sleepers and insomniacs in objective measures of sleep latency, duration of wake after sleep onset, duration of sleep, and indices of sleep fragmentation such as microarousal index and number of awakenings. Controls had slightly more periodic leg movements during sleep. The percentage of NREM sleep stage was not significantly different, but a lower percentage of REM was found in insomniacs (Table 2). Quantitative EEG spectral analysis revealed insomnia subjects to have greater EEG activity in β frequencies across all-night NREM sleep in central and frontal derivations (Table 3). Morning questionnaires after night 3 assessing subjective evaluation of sleep quantity and quality of the night revealed that most of the insomnia subjects slept better in the lab than they usually did at home. However, subjective duration of wake time after sleep onset was longer (92 ± 52 min versus 45 ± 42 min, P = 0.01) and subjective sleep efficiency was lower (81% ± 13% versus 91% ± 9%, P < 0.05) in insomniacs than in good sleepers.

Table 2.

Polysomnographic Characteristics of Night 3 (Experimental) in Insomniacs and Good Sleepers

(Paired t-test)	Good Sleepers	Insomniacs	P value
Sleep latency (min)	14 ± 16	9 ± 4	0.3
Total sleep time (min)	415 ± 37	411 ± 31	0.8
Sleep efficiency (%)	86 ± 8	85 ±6	0.9
Wake time after sleep onset (min)	56 ± 30	60 ± 27	0.6
% Stage 1	7 ±2	8 ±3	0.4
% Stage 2	61 ±7	64 ± 7	0.1
% Stages 3-4	8 ± 8	8 ± 9	0.8
% REM sleep	25 ± 4	20 ± 5	0.005
Microarousal index (n/hour)	6.9 ± 2.8	8.6 ± 4.8	0.3
Periodic leg movement index (n/hour)	5.7 ± 5.8	2.4 ± 2.9	0.04
Apnea-hypopnea index (n/hour)	0.8 ± 1.2	0.6 ± 0.03	0.8

Data are presented as mean ± standard deviation

Table 3.

Electroencephalographic Activity in the β Frequencies (16–32 μV²/Hz) in Central (C3 and C4) and Frontal (F3 and F4) Leads during NREM Sleep

	Good Sleepers	Insomniacs	P
C3-A2	1.5 ± 0.7	1.9 ± 0.4	0.07*
C4-A1	1.5 ± 0.5	1.8 ± 0.5	0.05*
F3-A2	1.4 ± 0.5	1.8 ± 0.5	0.04*
F4-A1	1.5 ± 0.4	1.8 ± 0.6	0.09*

Data are presented as mean ± standard deviation.

*Wilcoxon Signed Rank Test

Hourly SBP and DBP (mean and standard error) across 24-h periods in the 2 groups are shown in Figure 2. Comparisons of average daytime and nighttime HR and BP measurements and day-to-night dipping are reported in Table 4. Daytime SBP was similar between groups. In contrast, nighttime SBP was higher (P = 0.01), and day-to-night SBP dipping was smaller (P = 0.01) in insomniacs than in good sleepers. Daytime (P = 0.02) and nighttime DBP (P = 0.01) were higher in insomniacs, whereas day-to-night DBP dipping did not differ between groups.

Figure 2.

Twenty-four hour SBP and DBP in insomniacs (circular symbols and continuous black lines) and controls (triangular symbols and dashed lines). Data at each hour represent the mean and standard error of hourly SBP and DBP calculated from beat-to-beat BP in each subject.

Table 4.

Daytime, Nighttime, and Day-to-Night Dipping in SBP, DBP, and HR Derived from 24-Hour Continuous Measurements

	Good Sleepers	Insomniacs	P value
Day SBP (mm Hg)	120 ± 12	120 ± 11	0.9
Day DBP (mm Hg)	66 ± 8	71 ± 7	0.02
Day HR (bpm)	68 ± 6	72 ± 8	0.2
Night SBP (mm Hg)	102 ± 12	111 ± 15	0.02
Night DBP (mm Hg)	56 ± 9	65 ± 10	0.01
Night HR (bpm)	59 ± 7	62 ± 7	0.3
SBP dipping (%)	−15 ± 5	−8 ± 6	0.01
DBP dipping (%)	−14 ± 7	−9 ± 8	0.1
HR dipping (%)	−13 ± 6	−13 ± 5	0.6

Data are presented as mean ± standard deviation.

Pearson correlation analysis showed nighttime SBP and DBP to be associated with body mass index (both, r = 0.6, P < 0.01) and daytime SBP (respectively r = 0.83 and 0.69, both P < 0.001) and DBP (respectively, r = 0.75 and 0.88, P < 0.001). No relationship was observed between cardiovascular variables and age, BDI score, and polysomnographic indices of sleep latency, sleep efficiency, wake time after sleep onset, microarousal index, and stage 3-4 NREM sleep. A borderline association was observed between nighttime SBP and EEG activity in β frequency in frontal leads at univariate analysis (r = 0.38, P = 0.08). However, this association was significant after adjusting for age, sex, body mass index, and daytime SBP (Table 5). No independent association was observed between EEG activity in the β frequencies and nighttime DBP (Table 5).

Table 5.

Partial Correlation Coefficients Between Nighttime Blood Pressure and EEG β Activity in the Frontal Lead, Age, Sex, Body Mass Index, and Daytime Blood Pressure

	Partial Correlation	P value
Nighttime SBP
EEG β activity F3-A2	0.48	0.04
Age	−0.27	0.3
Sex	−0.1	0.7
Body mass index	0.27	0.3
Daytime SBP	0.70	0.001
Nighttime DBP
EEG β activity F3-A2	0.39	0.1
Age	−0.12	0.6
Sex	−0.02	0.9
Body mass index	0.27	0.3
Daytime SBP	0.80	0.0001

Discussion

In this study we documented that normotensive subjects with chronic primary insomnia have an altered 24-h blood pressure profile with higher nighttime SBP and an attenuation of day-to-night SBP dipping as compared to good sleepers. The blunted SBP fall occurred in association with EEG indices of faster brain activity during NREM sleep. Subjects with insomnia had persistently higher values of DBP across the 24 hours and a nonsignificant attenuation of DBP dipping. Finally, no differences were observed in the HR profile between insomniacs and good sleepers.

Several extrinsic and intrinsic factors can influence the 24-h BP profile, including sleep. Experiments conducted using the constant routine paradigm (in which subjects stay supine and do not sleep for the entire 24-h period) have shown that the nighttime HR drop is maintained, while the nighttime BP drop is lost under sleep deprivation.³⁰ These observations suggest that, while HR is largely under the influence of the endogenous circadian pacemaker, BP is largely independent from this rhythm and is mainly linked to the sleep-wake cycle.

Loredo et al.³¹ observed that nocturnal BP dipping correlated with polysomnographic indices of poor sleep, including less slow wave sleep and longer wake time after sleep onset. Pedulla et al.³² reported that hypertensive non-dippers had less slow wave sleep and a higher microarousal rate than hypertensive dipper subjects. Indices of poor sleep have been also observed in non-dipper normotensive offspring of non-dipper hypertensive parents.³³ Little or no information regarding their sleep complaints were reported in these studies.

In our study higher nighttime SBP and blunted SBP dipping occurred in normotensive chronic insomnia sufferers even in the absence of polysomnographic criteria of poor sleep (Table 2), suggesting that blunted dipping can be a trait of insomnia, which persists even during a good night's sleep, such as occurred during the study. It is possible that even higher nocturnal BP and further attenuation of SBP dipping could occur during a typical poor sleep night at home, with short sleep duration and frequent awakenings. On the other hand, factors other than conventionally defined sleep disturbances may alter nocturnal BP in this condition. Indeed, we observed an association between nighttime SBP and EEG activity in the β frequency, a neurophysiological feature of insomnia^8,9: the higher the β activity, the higher the nighttime SBP. Increased EEG β activity, along with increased sigma and decreased delta activities, has been shown to be present in subjects with subjective insomnia, and to correlate with the relative subjective underestimation of sleep time compared to polysomnography observed in these subjects.³⁴ EEG activity in the β frequency has been shown to reflect the activation of the cortex (normally more pronounced during wakefulness and REM), in response to cognitive process and attention requirements³⁵ and is considered an index of the level of brain activation and alertness. Higher EEG β power has been shown to occur in association with relatively higher glucose metabolism in the ventromedial prefrontal cortex,³⁶ the neural substrate which integrates cognitive-affective information and regulates the hypothalamic-pituitary axis in response to emotional stress.³⁷ Therefore, our findings suggest that BP dysregulation is part of the complex interaction of systems regulating cognitive function, emotions, and autonomic arousal in this condition, whether or not conventionally defined polysomnographic indices of poor sleep are present.

Depression has been linked to increased risk for cardiovascular disease.³⁸ One study conducted in a non-psychiatric population found the presence of a weak but positive association between depression scores and nighttime SBP in men.³⁹ Our insomniacs, who did not have depression and anxiety disorders, had higher Beck Depression Inventory scores than controls. Although no relationship was observed between this score and nocturnal blood pressure, the potential effect of subclinical depression on blood pressure control in our insomniacs cannot totally be excluded.

Strengths of our study include the highly selected population of insomniacs and matched good sleepers, in accord to current standard research diagnostic criteria for insomnia,² and in the absence of potential confounding for sleep measures and cardiovascular profile. Secondly, beat-to-beat BP was recorded in standardized and controlled conditions in the laboratory, providing reliable and comparable measures of the day-to-night changes between subjects. Thirdly, assessment of cardiovascular measures and sleep measures was performed simultaneously, allowing us to underscore the important relationship between cardiovascular and EEG measures.

As a limitation, the case-control design of our study does not allow establishing causality between insomnia and BP dipping. Randomized controlled trials investigating the effect of insomnia treatment on nighttime blood pressure, and assessing the effect of nighttime blood pressure control on insomnia complaints could help clarify the nature of the association we observed.

Clinical Implications

Studies have demonstrated an independent link between insomnia and hypertension,^13,14 one of the leading risk factors for heart disease, stroke, and kidney disease.⁴⁰ More recent community-based large epidemiological studies have also underscored a significant association between symptoms of insomnia and long-term cardiovascular mortality independent of identified risk factors, including daytime hypertension.^16,17 For instance, difficulty falling asleep was found to predict mortality from coronary heart disease in a random sample of 1870 community-dwelling middle-aged males (adjusted OR 3.1)¹⁶ and in a large cohort involving more than 22,000 men and 10,000 women, (adjusted OR 1.71)¹⁷ over 12-17 years of follow-up. By contrast, one study with shorter follow-up periods failed to detect any significant association between insomnia and cardiovascular mortality.⁴¹ These data suggest that as with other cardiovascular risk factors, chronic insomnia may exert negative effects on the cardiovascular system over many years before the onset of overt disease in otherwise healthy individuals. The mechanisms involved in this association, and whether they can be reversed by treatment of insomnia, remain to be elucidated.

Higher nighttime SBP and lack of SBP dipping have been linked to cardiac and vascular damage⁴² and have been associated with biohumoral markers of endothelial dysfunction or activation,⁴³ a key factor implicated in the genesis and progression of atherosclerotic changes and its clinical manifestations.⁴⁴ Therefore, the presence of insomnia-related higher nighttime SBP and lack of SBP dipping could induce a persistently higher cardiovascular burden during the night in these subjects, leading to cardiovascular damage and increasing their long-term cardiovascular risk. Studies are warranted to examine whether insomniacs possess evidence of subclinical cardiovascular damage.

CONCLUSIONS

Nighttime SBP is higher and day-to-night SBP dipping is blunted in normotensive subjects with chronic insomnia and is associated with enhanced brain cortical activation during sleep. Insomnia-related altered BP profile might represent for otherwise healthy subjects, a condition of risk for cardiovascular morbidity and in subjects with overt cardiac disease, a potential for the progression of the disease, and an indicator of poor prognosis.

DISCLOSURE STATEMENT

This was not an industry supported study. Dr. Morin has participated in speaking engagements for Sanofi-Aventis, Sepracor, and Lundbeck and is on the advisory board of Sanofi-Aventis, Actelion, Pfizer, Eli Lilly, and Hoffman-LaRoche. Dr. Montplaisir has received research support from Boehringer-Ingelheim, Sanofi-Synthelabo, and GlaxoSmithKline and has consulted for Sanofi-Aventis, Boehringer-Ingelheim, Jazz, and Servier. The other authors have indicated no financial conflicts of interest.