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(Hypertension. 1996;28:937-943.)
© 1996 American Heart Association, Inc.
Articles |
Short-term Variability of Blood Pressure During Sleep in Snorers With or Without Apnea
Service d'Exploration Fonctionnelle Multidisciplinaire, Hopital Ambroise Pare, Universite Rene Descartes, Boulogne, France.
Correspondence to Dr Michel Leroy, Service d'Exploration Fonctionnelle, Hopital Ambroise Pare, 92100 Boulogne, France.
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Abstract |
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In normal subjects, the level and variability of blood pressure decrease during non–rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (
15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P<.05) correlated with apnea plus hypopnea (P<.0001) and transient electroencephalographic arousal number per hour of sleep (P<.0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P<.001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with ß-blockers or calcium antagonists may be a risk factor for acute coronary events.
Key Words: blood pressure • sleep • sleep apnea syndromes
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Introduction |
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Several studies have addressed the cardiovascular effects of sleep in normal humans and animals.1 2 3 It has been shown that non–rapid eye movement (non-REM) sleep, which corresponds to about 80% of total sleep, is associated with bradycardia and a decrease in the level and variability of blood pressure (BP). These changes become more pronounced as non-REM sleep progresses from stage 1 to stage 4. Moreover, spectral analysis of BP and interbeat intervals as well as measurement of sympathetic nerve traffic to skeletal muscles by microneurographic techniques suggest a decrease in sympathetic activity during slow-wave sleep.2 3 Only during REM sleep, which is associated with dreaming and occurs for several minutes at variable intervals, do BP and sympathetic tone return to the levels observed during wakefulness. The night may therefore have a relative protective effect for the cardiovascular system.
In contrast, obstructive sleep apnea syndrome, a disorder characterized by recurrent episodes of upper-airway obstruction during sleep, is associated with large swings in nocturnal arterial BP. At the beginning of apnea, BP falls in time with inspiratory efforts against obstruction, whereas it rises abruptly at the end of apnea, coincident with an electroencephalographic (EEG) arousal. Several studies suggest that sleep apnea is associated with increased cardiovascular morbidity such as hypertension,4 5 6 coronary disease,7 and stroke.8 9 If the repetitive hemodynamic oscillations related to apnea play a role in the development of cardiovascular disease, it may be important for prognosis to measure their amplitudes and repetition during sleep.
In this study, we evaluated prospectively a computer-derived index of BP variability from beat-to-beat BP traces during sleep. Our purpose was to determine how this index differs among subjects with or without sleep apnea who snore and whether it correlates with the number of respiratory events per hour of sleep. Several studies have found that apneic individuals are more likely to have systemic hypertension than nonapneic individuals.4 5 6 To examine whether respiratory disturbances during sleep contribute to increased BP variability independently of elevated mean BP level, we excluded individuals with diurnal systemic hypertension. We also evaluated this index as well as systolic and diastolic BPs during the various sleep stages. To examine whether this index is influenced by coexistent cardiovascular disease and its treatment, we studied subjects without any known cardiovascular disease and subjects treated for ischemic heart disease.
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Methods |
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Subjects
We initially recruited 75 individuals (73 men and 2 women) reporting habitual snoring without systemic hypertension (defined as systolic BP
160 mm Hg and/or diastolic BP 95 on three different occasions) who were consecutively referred to the sleep laboratory for overnight polysomnography. To study the effect of sleep stage on the index of BP variability, we estimated that each subject had to spend at least 20 minutes of cumulative time in each sleep stage. Fifteen subjects had to be excluded after polysomnography because total cumulative time spent in stages 3 and 4 or REM was of insufficient duration. Thirty-two of the 60 remaining subjects had a history of ischemic heart disease documented by coronary angiography and were treated with either ß-blockers (n=21), calcium antagonists (n=6), or both (n=5). The other 28 subjects had no ischemic heart disease, peripheral vascular disease, transient ischemic attacks, or strokes that could be documented by history and physical examination and were not treated with any cardiovascular drug. In addition, 6 control subjects (5 men, 1 woman) without any sleep complaint, habitual snoring, or cardiovascular disease were recruited from the staff at our institution. Every subject underwent pulmonary function tests, including measurements of pulmonary volumes and flow-volume curves and determination of arterial blood gas. The study was approved by the Ethics Committee of our hospital. All subjects gave informed consent.
Polysomnography
The all-night sleep study began at the subject's usual bed time, around 10 to 11 PM, and was terminated after the subject awakened or around 7 AM. The polysomnographic data were recorded with a 16-channel polygraph (Reega 2000, Alvar) at a paper speed of 15 mm/s. Sleep was assessed with four EEGs, horizontal and vertical electrooculograms, and submental electromyogram. Respiration was monitored with thoracic and abdominal piezo sensors (Nihon Kohden), a diaphragmatic electromyogram, and oronasal thermocouples. An electrocardiogram was also recorded with three skin electrodes.
Polysomnography data were analyzed manually. Sleep staging was established according to the standard criteria of Rechtschaffen and Kales.10 Apnea was defined as cessation of oronasal airflow for more than 10 seconds. Hypopnea was defined as a reduction of oronasal airflow to at least 50% of the value prevailing during preceding normal breathing for at least 10 seconds followed by transient EEG arousal. An arousal was defined as an episode lasting 3 seconds or longer in which there was a return of alpha or theta activity associated with increased electromyogram activity. Desaturations by 4% or more were counted, but desaturation was not a criteria for scoring either apnea or hypopnea. Apnea-hypopnea index was defined as the number of apnea plus hypopnea episodes per hour of sleep. Arousal index was defined as the number of arousals per hour of sleep. A cutoff point of greater than or equal to 15 in apnea-hypopnea index was used for categorization of subjects with or without sleep apnea. This cutoff point has been used to describe sleep apnea, but it is important to note that the clinical importance of any particular cutoff point has not been adequately determined. Hence, subjects were categorized into four groups: subjects without cardiovascular disease with or without sleep apnea, and subjects with treated ischemic heart disease with or without sleep apnea.
BP Measurements
Beat-to-beat photoplethysmographic BP (Finapres, Ohmeda, Inc) was continuously monitored during sleep. The cuff wrapped around the finger was deflated and the Finapres system switched off for 10 minutes every 2 hours for the subject's comfort. The position of the recording arm, which was not fixed, was monitored by video recording. All systolic and diastolic BP values were sent to a personal computer (PC Intel 386 SX) and analyzed with software we developed. Automatic calibration was not recognized as a BP signal; therefore, time intervals corresponding to calibration were excluded from computation. However, the analysis considered that systolic and diastolic BPs had remained constant during automatic reset of the signal lasting less than 3 seconds. BP recording was synchronized with polysomnography.
Beat-to-beat systolic or diastolic BP varies with successive increases and decreases; therefore, we considered that each decrease or increase ended as soon as pressure started to vary in the opposite direction. A frequency distribution histogram of all these increases and decreases according to their amplitudes was drawn (Fig 1
). The histogram approximated a gaussian curve, the mean of the distribution being zero. The SD of the distribution, which is in proportion to the number of large variations of pressure, was used as an estimate of variability. For each subject, analysis of the stored data during the total sleep time provided the mean±SD of all arterial BP values (systolic and diastolic) as well as the SD of the distribution of BP variations (systolic and diastolic). The total sleep time was defined as the interval of time separating sleep onset (beginning of first stage 2) from morning awakening but excluding nocturnal awakenings occurring during the sleep period. This allowed exclusion of the movements causing artifacts because they are usually observed during periods of sustained wakefulness.
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A second step consisted of analyzing BP according to sleep stage. All periods of continuous recording in a sleep stage lasting more than 180 seconds were considered. For each subject, data were analyzed for the cumulative time of the night spent in a given sleep stage.
Statistical Analysis
Data were analyzed with the SAS statistical package.11 Results are expressed as mean±SE. Within-individual SD values of BP (systolic and diastolic) during sleep were calculated as the square root of the pooled within-individual variances in each group, and individual coefficients of variation (SD/mean) of systolic or diastolic BP were also compared between groups with a Kruskal-Wallis test. Comparisons between two groups were performed with a nonparametric Mann-Whitney test. A one-way ANOVA was used for comparisons between groups. When a significant difference was observed, multiple pairwise comparisons were performed with Fisher's protected least significant difference test. Comparison of percentages of total sleep time spent in the different sleep stages was performed with a 
2 test. Comparisons of systolic and diastolic BPs and SD values of the distribution of systolic and diastolic BP variations between different sleep stages and between groups were carried out by two-way multiple ANOVA with one repeated measurement and one grouping factor. When a statistically significant effect of sleep stage was observed, multiple comparisons between sleep stages were performed with the contrast method. Relationships between SD values of the distribution of systolic and diastolic BP variations and age, body mass index (weight in kilograms divided by the square of height in meters), number of desaturations, apnea-hypopnea index, and arousal index were evaluated with a nonparametric test (Spearman rank correlation analysis). A value of P<.05 was considered statistically significant.
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Results |
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Clinical characteristics and results of polysomnography in the control group and the four experimental groups of subjects are shown in Table 1
. None of the subjects had PaO2 less than 65 mm Hg or PaCO2 greater than 45 mm Hg when awake. Seven subjects from the ischemic heart disease group had significant obstructive pulmonary disease with the ratio of forced expiratory volume in 1 second to vital capacity less than or equal to 70% of the predicted value. Age, body mass index, and total sleep time were not different between the control group and the four experimental groups. In subjects with sleep apnea, the degree of severity of sleep disturbance as assessed by apnea-hypopnea index was similar in those with ischemic heart disease and those without cardiovascular disease. However, the group of apneic subjects without cardiovascular disease had significantly more 4% desaturations than the group with coexistent sleep apnea and ischemic heart disease (P<.05). Arousal index was higher in groups with sleep apnea than in those without (P<.05).
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BP values during the total sleep time are shown in Table 2. Neither individual average values of systolic or diastolic arterial BPs nor individual coefficients of variation of systolic or diastolic BPs differed between the control group and the four experimental groups. However, the SD values of the distribution of systolic or diastolic BP variations during total sleep time were significantly higher in groups with sleep apnea than in those without (P<.05). In subjects with sleep apnea, they did not differ among subjects without cardiovascular disease and those with treated ischemic heart disease. In subjects without sleep apnea, they were similar in both groups and did not differ from the control group. When the 60 subjects were considered, the SD values of the distribution of systolic and diastolic BP variations during total sleep time were both correlated with apnea-hypopnea index (
=.55, P<.0001 and =.50, P<.0001, respectively) and arousal index (=.58, P<.0001 and =.59, P<.0001, respectively) but not with age or body mass index. Only the SD of systolic BP variations was correlated with the number of desaturations (=.27, P<.05).
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The percentages of total sleep time spent in the different sleep stages did not differ among the four experimental groups and the control group (Fig 2) and were similar to normal values for adults.12 In subjects with or without sleep apnea, there was an effect of sleep stage on apnea-hypopnea index (P<.0001), with no interaction. Apnea-hypopnea index was lower in deep (stages 3 and 4) than in light (stages 1 and 2) non-REM sleep (P<.01) and REM sleep (P<.001) (Fig 3). Although systolic BP did not differ among groups, it differed according to sleep stage (P<.0001), with a significant interaction among groups and sleep stages (P<.05) (Fig 4). Diastolic BP did not differ among groups but was significantly higher in REM sleep than in stages 1 and 2 (P<.001) and stages 3 and 4 of non-REM sleep (P<.001), with no interaction among groups and sleep stages. In the control group and the four experimental groups, variability of BP as assessed by the SD of the distributions of systolic and diastolic BP variations decreased as non-REM sleep progressed from stages 1 and 2 to stages 3 and 4 (P<.0001) (Fig 5). During REM sleep, the SD of systolic BP variations returned to values similar to those of stages 1 and 2, whereas the SD of diastolic BP variations increased to values higher than those of stages 1 and 2 (P<.01).
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Discussion |
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This study shows that in snorers without diurnal systemic hypertension, the SD of the distribution of all-night BP variations, a parameter that can be easily computed during sleep studies as an index of short-term BP variability, correlates with the severity of sleep apnea and sleep fragmentation. Although individual average values of nocturnal systolic and diastolic BPs were similar in the four groups of snorers, this index of variability was greater among apneic than nonapneic snorers. Moreover, in apneic snorers with coexistent ischemic heart disease, nocturnal BP variability was also increased compared with nonapneic snorers despite treatment with ß-blockers, calcium antagonists, or both. In subjects with sleep apnea, as in those without, BP variability depended on sleep stage, decreasing during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep.
In subjects with sleep apnea, a progressive increase in sympathetic tone is observed during apneic episodes, and a large increase in BP occurs with the resumption of breathing.13 14 Some reports also suggest that the normal decline in BP observed during sleep is blunted.14 15 Increased cardiovascular morbidity of sleep apnea syndrome may be related to this increase in the level and variability of nocturnal BP. Indeed, in subjects with untreated essential hypertension, target-organ damage has been shown to be related not only to the level of 24-hour mean intra-arterial BP but also to BP variability.16 If short-lasting oscillations of BP in sleep apnea subjects adversely affect the function and structure of the cardiovascular system, it may be important to measure nocturnal BP level and its short-term variability during polysomnography.
With this aim, we recorded beat-to-beat BP with a Finapres system. BP measured with this device may differ from intrabrachial BP. Indeed, arterial BP changes normally along the vascular tree. Moreover, to avoid discomfort to the subject, we did not fix the hand bearing the Finapres. Thus, variations in hydrostatic level caused by change in hand position introduced some uncertainty in the BP measurement. However, in a sleeping subject, the degree of hand excursion above and below the heart is limited. If we assume 15 cm as the greatest possible distance between midthorax and bed levels in a supine subject, maximal changes in BP related to the hydrostatic level of the hand should be at most ±11 mm Hg.
The algorithm we used to estimate BP variability did depend on computing BP changes and not on absolute pressures. The small amount of noise introduced by occasional movements was insufficient to obscure the results of the overall analysis of the BP changes. In a few subjects, we monitored hand movements with an actigraph. Examining the BP tracing concomitantly with the other parameters recorded during polysomnography, we observed that the amplitude of most of the occasional movements associated with transient EEG arousals during sleep was not large enough to generate BP artifacts. Thus, the number of artifacts was small compared with the total number of BP variations (>500 per hour) and could not significantly affect the SD of their distribution. The Finapres device has been shown to be an accurate method for monitoring of fast BP changes, such as those induced by handgrip exercise, the Valsalva maneuver, and diving tests.17 18 This noninvasive technique, which makes prolonged beat-to-beat recordings possible, may therefore be reliable for the measurement of the short-term variability of BP during sleep.
Other methods have been used previously for estimation of BP variability. SD values and variation coefficients of beat-to-beat systolic and diastolic BPs have been separately computed for each half hour as well as SD values and variation coefficients obtained by averaging the mean values of the 48 half hours during a 24-hour period.1 Since the duration of a continuous sleep stage may be highly variable, this method, which is based on computation during time intervals of constant duration, does not allow the study of the effect of sleep stage on BP variability. In our study, individual coefficients of variation of beat-to-beat systolic or diastolic BPs computed during the total sleep time did not differ among the four experimental groups. This apparent discrepancy with the results obtained with the SD of the distribution of BP variations may be explained by the fact that the latter reflects only short-term variability, whereas within-individual SD values of absolute pressures reflect both short- and long-term variabilities. Indeed, all the BP changes we computed lasted less than 20 seconds. Spectral analysis of BP and interbeat interval has also been used in healthy subjects for estimation of the short-term variability of BP and concomitant variations of sympathetic and vagal tones to the heart according to sleep stages.3 This method limits BP recording to short stationary periods with regard to breathing and EEG data. Thus, it cannot be used in subjects with sleep-disordered breathing, in whom respiratory events and transient arousals are to a considerable extent nonstationary.
Compared with our control group of age-matched nonsnorers, the short-term variability of BP was not increased in both groups of nonapneic snorers. However, it is well known that some subjects with snoring and airflow limitation but no hypopnea or apnea, the so-called upper-airway resistance syndrome, may have BP rises concomitant with recurrent brief EEG arousals.15 19 In some nonapneic snorers of our study (2 of the 12 without cardiovascular disease and 6 of the 15 with ischemic heart disease), the number of transient arousals punctuating sleep ranged between 20 and 30 per hour, values that are above normal.20 In normal subjects, arousal caused by auditory stimuli elicit K complexes during non-REM sleep that are accompanied by bursts of sympathetic nerve activity and transient increases in BP.2 Elevations of arterial BP concomitant with arousals caused by periodic leg movements have also been reported.21 It is therefore likely that a wide distribution of BP variations may be observed in subjects suffering not only from sleep apnea syndrome but also from other sleep disruption disorders, such as periodic leg movements or upper-airway resistance syndrome.
In previous studies focusing on the hemodynamic influence of EEG arousals, BP changes were measured only during randomly selected periods a few minutes long. Identification of falls and rises in systolic BP with a computer algorithm has been proposed as a screening tool for sleep disruption syndrome of various causes.22 However, to our knowledge, the present study is the first to propose a method for evaluation of short-term variability during total sleep time as well as various sleep stages in sleep apnea subjects. We found that the frequency of large-amplitude BP oscillations was increased in snorers with or without respiratory disturbances during stages 1 and 2 of non-REM and REM sleep compared with stages 3 and 4 of slow-wave sleep. Since the SD of the distribution of BP variations was correlated with the apnea-hypopnea index, its decrease during stages 3 and 4 of slow-wave sleep may be related to the decrease in the number of respiratory events in these sleep stages. Indeed, in all four groups of snorers, abnormal breathing occurred more frequently in stages 1 and 2 of non-REM and REM sleep than in stages 3 and 4 of slow-wave sleep. This is consistent with previous data23 24 and has been related to increased upper-airway collapsibility during stages 1 and 2 of non-REM and REM sleep compared with stages 3 and 4 of non-REM sleep.25 However, although the apnea-hypopnea index in sleep apnea subjects decreased significantly in stages 3 and 4 of non-REM sleep, it remained much higher than values in nonapneic snorers during stages 1 and 2 of non-REM or REM sleep. Nevertheless, BP variability in stages 3 and 4 of non-REM sleep was at the same level or even lower than values in nonapneic snorers and control subjects during stages 1 and 2 of non-REM and REM sleep. Therefore, the decrease in BP variability during stages 3 and 4 of non-REM sleep is unlikely to be totally related to the decrease in respiratory events during these stages. The fact that a decrease in BP variability during stages 3 and 4 of slow-wave sleep compared with stages 1 and 2 of non-REM and REM sleep has also been reported recently in normal subjects gives further support to the influence of sleep stage independent of ventilation.3 A decrease of sleep time spent in REM as well as in stages 3 and 4 of slow-wave sleep is usually observed in severe sleep apnea syndrome. The fact that these subjects spend most of the night in stages 1 and 2 may also contribute to an increase in nocturnal BP variability. In our study, we found that the percentages of total sleep time in the different sleep stages were similar in the four groups of subjects. Since the participants in our study had to spend at least 20 minutes of total cumulative time in stages 3 and 4 and REM sleep, we eliminated some severe sleep apnea subjects with disturbed sleep architecture.
In subjects with an apnea-hypopnea index of 15 or higher, the SD of the distribution of BP variations did not differ significantly between those without cardiovascular disease and those with ischemic heart disease. Both groups had a similar severity of sleep respiratory disturbance according to apnea-hypopnea and arousal indexes. However, the number of desaturations was higher in the group without cardiovascular disease. Reports that oxygen supplementation hardly alters postapneic BP elevations do not support the idea that hypoxemia plays an important role in the increased variability of nocturnal BP.26 The weak correlation of BP variability with the number of desaturations when the 60 subjects were considered may be related to the fact that both desaturation and the degree of arousal are related to apnea duration and that the magnitude of BP rise is also related to the degree of arousal.27
In nonapneic snorers with ischemic heart disease, the index of BP variability did not differ from values in nonapneic subjects without cardiovascular disease. Therefore, it is likely that in nonhypertensive, nonapneic individuals, this index is not influenced by coexistent ischemic heart disease and its treatment. However, since we did not study hypertensive subjects, we cannot rule out the possibility that this index depends on mean BP level. For clarification of this issue, BP variability should be examined in hypertensive subjects with and without sleep apnea.
A high prevalence of undiagnosed sleep-disordered breathing in the middle-aged population has been recently recognized.28 If increased nocturnal BP variability has a role in the occurrence of cardiovascular complications, its assessment in individuals with sleep respiratory disturbances may have some prognostic importance. Our data showing increased BP variability in subjects with ischemic heart disease and sleep apnea also suggest that treatment with ß-blockers or calcium antagonists does not attenuate nocturnal BP oscillations associated with sleep respiratory disturbance. Acute changes in pressure have been suspected to favor the rupture of atherosclerotic plaques and repetitive sympathetic activation to favor platelet aggregation.29 This suggests that coexistent sleep apnea in individuals with ischemic heart disease may increase the risk of acute coronary events.
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Acknowledgments |
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This work was supported by grants from Baxter, Interventional Cardiology France, Federation Francaise de Cardiologie, and Fond Special des Comites Departementaux Contre les Maladies Respiratoires et la Tuberculose (grant 91MR7). The authors thank Christine Le Bonniec and Sabine Stefanidi for technical assistance.
Received August 9, 1995;
first decision November 30, 1995; first decision July 18, 1996;
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