Chest ACCP Career Connection
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ancoli-Israel, S.
Right arrow Articles by Johnson, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ancoli-Israel, S.
Right arrow Articles by Johnson, S.
(Chest. 2002;122:1148-1155.)
© 2002 American College of Chest Physicians

The Effect of Race and Sleep-Disordered Breathing on Nocturnal BP "Dipping"*

Analysis in an Older Population

Sonia Ancoli-Israel, PhD; Carl Stepnowsky, PhD; Joel Dimsdale, MD; Matthew Marler, PhD; Mairav Cohen-Zion, MA and Sherella Johnson, AA

* From the Department of Psychiatry, University of California, San Diego (Dr. Dimsdale), and Veterans Affairs San Diego Healthcare System (Drs. Ancoli-Israel, Stepnowsky, and Marler, and Ms. Johnson), San Diego; and San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology (Ms. Cohen-Zion), San Diego, CA.

Correspondence to: Sonia Ancoli-Israel, PhD, Department of Psychiatry, 116A, Veterans Affairs San Diego Healthcare System, 3350 La Jolla Village Dr, San Diego, CA 92161; e-mail: sancoliisrael{at}ucsd.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: BP normally drops (or "dips") by approximately 10% at nighttime; however, in a number of illnesses there is an increased amount of "nondipping" of nocturnal BP. This study examined whether nondipping in older African Americans and older white subjects is related to the presence of sleep-disordered breathing (SDB) and hypertension.

Design: Prospective study with a convenience sample.

Setting: All data were collected in the subjects’ homes.

Participants: Seventy self-defined African Americans with complaints of snoring or excessive daytime sleepiness, and 70 age-matched and gender-matched white subjects.

Measurements and results: Sleep was recorded for 2 nights, with 1 night of oximetry. BP was recorded on a separate 24-h period. African Americans had higher dipping ratios than white subjects even after accounting for covariates such as respiratory disturbance index (RDI), oxygen desaturation index (ODI), body mass index, and average 24-h mean arterial pressure (p = 0.025). Higher values of RDI (R2 = 0.0686, p = 0.021) and ODI (R2 = 0.042, p < 0.03) were correlated with higher dipping ratios in both African Americans and white subjects. However, there was a three-way interaction such that higher RDIs were correlated primarily with nondipping in African Americans receiving antihypertensive medication (R2 = 0.0373, p = 0.022).

Conclusions: These results demonstrated that African Americans tend to be "nondippers," while white subjects tended to be "dippers." This nondipping was not a result of weight, gender, or of having SDB. The analyses also confirmed that, in both races, the dipping ratio was greatest in those with SDB and hypertension. The third hypothesis, that RDI would be greatest in the nondipping hypertensive subjects, was true only for the African Americans.

Key Words: BP • dipping • hypertension • obstructive sleep apnea • race


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
In a study of randomly selected white and African-American elderly subjects, Ancoli-Israel et al,1 found that African Americans, when compared to white subjects, had twice the relative risk of severe sleep-disordered breathing (SDB) [defined as the presence of >= 30 respiratory events per hour of sleep] independent of age, gender, or body mass index (BMI). In a study of African-American families, Redline et al2 observed that the apnea index differed by race and age, finding a threefold risk for SDB in African Americans < 25 years old and a twofold greater risk in middle-aged African Americans (age range, 25 to 55 years). These data suggest that there may be a high rate of undiagnosed SDB among African Americans.

There is also a high rate of undiagnosed SDB among patients with hypertension.3 Approximately one third of all hypertensive subjects have SDB, and approximately one third of all patients with SDB have hypertension.4 5 Peppard et al6 found a dose-response association between SDB at baseline and hypertension 4 years later, suggesting that SDB may be a risk factor of hypertension and, consequently, of cardiac morbidity. Nieto et al,7 in one of the largest cross-sectional studies, found that the prevalence of hypertension increased with increasing levels of SDB. In addition, patients with severe SDB, defined as >= 30 respiratory events per hour of sleep, were one and a half times more likely to have hypertension than those with no or mild SDB. This association was significant in younger and older men and women, and in all ethnic groups.

With each episode of apnea during the night, there is an accompanying transient elevation of systemic BP, suggesting a causal relationship between SDB and sustained systemic hypertension.8 Dyken et al9 proposed that severe obstructive sleep apnea may predispose patients for hemorrhagic stroke as a result of prolonged obstructive events that produce a hypertensive effect due to sympathetic excitation. Noda et al10 hypothesized that the desaturations caused by apneas stimulate sympathetic nervous system activation, which plays a significant role in the development of nocturnal hypertension in these patients. The relationship between SDB and hypertension is often confounded by age and obesity. While some studies have failed to adequately control for these factors, studies that did control for obesity, age, and gender have concluded that SDB is independently and significantly associated with hypertension.11 12 13 14 15

The prevalence of hypertension is almost twice as high in African-American men and women than in white men and women.16 This higher prevalence has been shown to be related to genetic, dietary, social, and psychological factors.17 Although African Americans have more severe SDB and an increased prevalence of hypertension, and hypertension is strongly associated with SDB, very few studies have examined the relationship between hypertension and SDB in this population. In one study, Bartel et al18 studied 20 hypertensive black South Africans matched with a control group of African-American subjects and found that the hypertensive group had significantly more severe SDB.

One approach to examining the relationship between BP and SDB is to examine the circadian rhythm of BP. In normal individuals, BP fluctuates in a circadian rhythm with pressures falling during sleep.19 20 However, in patients with hypertension and in patients with SDB, this rhythm is altered.21 22 23 24 When studied with 24-h noninvasive ambulatory BP monitors, hypertensive patients with obstructive sleep apnea do not show the expected drop in BP levels during sleep, whereas normotensive patients with obstructive sleep apnea and healthy individuals with no obstructive sleep apnea do show a drop in pressures during sleep.10 The fall in BP, called "dipping," may be clinically relevant. For instance, hypertensive women who were "nondippers" (ie, blunted nocturnal fall or a rise in nocturnal BP) were more likely to have morbid cardiovascular events.25 Trenkwalder26 also found that nondippers showed a significant increase in cardiovascular complications. The severity of obstructive sleep apnea syndrome has been shown to play an important role in nocturnal BP elevation and, thus, in the circadian variation of BP.10

Reports from data gathered with ambulatory BP monitors suggest that there may be racial differences in BP chronobiology. Some studies have reported that African Americans tend to be nondippers (ie, BP in African Americans decreases less during the night than in white subjects).27 28 29 30 31 32 It is unclear if these differences are a result of different life circumstances, altered sleep patterns, or both, since social situations have a substantial impact on ambulatory BP.33 One hypothesis would be that undiagnosed SDB may be responsible for these differences, since SDB is associated with increased BP levels during sleep.

This study examined whether nondipping in older African Americans and older white subjects was independent of, or related to, the presence of SDB. We hypothesized the following: (1) nondipping would be related to SDB, rather than being a phenomenon of race; (2) that nondipping would be greatest in those with SDB and hypertension; and (3) that the respiratory disturbance index (RDI) would be highest in the nondipping hypertensive subjects.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Subjects
Seventy self-defined African-American men (n = 30) and women (n = 40), and 70 age-matched and gender-matched white subjects with complaints of snoring and/or excessive daytime sleepiness independent of their health status were recruited through newspaper advertisements, newspaper articles, and word of mouth. Mean age of the African-American group was 73.6 years (SD, 6.4 years; range, 65 to 88 years). Mean age of the white group was 73.3 years (SD, 5.7 years; range, 65 to 93 years). There were 46% of African Americans and 45% of white subjects with hypertension. Of the 70 African-American volunteers, 10% completed college and 67% completed high school; 49% were married, 33% were widowed, and 16% were divorced. Of the 70 white volunteers, 30% completed college and 95% completed high school; 54% were married, 19% were widowed, and 7% were divorced.

Procedure
The study was approved by the University of California, San Diego Institutional Review Board in accordance with the recommendations found in the 1975 Helsinki Declaration. All subjects were studied in their homes after signing informed consent.

Sleep was recorded for 2 nights in the subjects’ homes with the modified Respitrace/Medilog portable system (Ambulatory Monitoring; Ardsley, NY),34 which records two channels of respiration (thoracic and abdominal), one channel of wrist activity (used to distinguish wake from sleep), and one channel of tibialis electromyogram. This recording system has been validated against standard polysomnography in older adults and found to be highly reliable.35 Blood oxygen saturation levels were recorded on 1 of those 2 nights with a portable finger-pulse oximeter (Ohmeda 3700; Respironics; Morrisville, PA), which recorded saturation levels every 2 s throughout the night. Data were stored in memory and then scored using the PROFOX oximetry program (PROFOX Associates; Escondido, CA).36

At least 4 hours of recording had to be available for sleep data to be included in the analysis. Sleep records were scored for the number of apneas (defined as at least a 90% reduction in respiratory effort for a minimum of 10 s), number of hypopneas (defined as a 50 to 90% reduction in effort for a minimum of 10 s), total sleep time, and wake after sleep onset. Sleep apnea index (the number of apneas per hour of sleep) and RDI (number of apneas and hypopneas per hour of sleep) were computed. The mean of the 2 nights was used in all data analysis. Oximetry records were scored for number of desaturations and the oxygen desaturation index (ODI) [number of desaturations >= 4% divided by the total sleep time] was computed.

Since it is known that ambulatory BP monitoring can disrupt sleep,37 BP was recorded during a separate, nonsleep monitoring, 24-h period with the ambulatory BP monitor (ABPM) [Accutracker II Ambulatory BP Monitor; Suntech Medical Instruments; Raleigh, NC]. The BP cuff was placed on the arm and checked with a Y-tube connector with readings within 5 mm of those on a mercury gauge. BP was recorded every 15 min during the day (defined as 6 AM to 10 PM) and every 30 min during the night (defined as 10 PM to 6 AM). ABPM data were reviewed and artifactual readings were edited using standard defaults (Suntech Medical Instruments). For a record to be included in the analysis, there had to be at least 30 usable data points with at least 5 nighttime data points. The "dipping ratio" was defined as the mean nighttime mean arterial pressure divided by the mean daytime mean arterial pressure. "Dippers" were defined as those subjects having a dipping ratio < 0.9 (ie, mean arterial pressure dropped during the night by at least 10%), while "nondippers" were defined as those whose dipping ratios were >= 0.9 (ie, mean arterial pressure either stayed the same or increased during sleep) [Fig 1 , top, a, and bottom, b]. Therefore, a higher dipping ratio is physiologically worse, as it refers to more nondipping (higher BP levels). For purposes of analysis, hypertension was defined as having a mean systolic BP >= 140 mm Hg, a mean diastolic BP >= 90, or presently receiving antihypertensive medication.



View larger version (24K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1. Plots of 24-h hour ambulatory BP monitoring showing dipping (top, a) vs nondipping (bottom, b). The smooth curves are a result of fitting a nonlinearly transformed cosine curve to the data of each subject, thus highlighting the trends of the data.

 
Data Analysis
To examine the data, the question of whether the covariates (ie, SDB, ODI, BMI, and mean arterial pressure) were different between the races and genders was examined. The next step examined whether there was a difference in the dipping ratio between the races and genders. The last step then tested whether any difference in dipping ratio was accounted for by the covariates. In other words, the data were analyzed in a series of analyses of variance and analyses of covariance with dipping ratio as the dependent variable, race and gender as class variables, and SDB (represented by the RDI and ODI) and BMI as continuous covariates. Sample sizes and degrees of freedom (df) varied somewhat from analysis to analysis depending on which covariates were missing. Hypertension was included in the analysis as a class variable (present vs absent), and average 24-h mean arterial pressure (the average of daytime and nighttime mean arterial pressure) was used as a continuous covariate in an analysis that included presence/absence of antihypertensive medication as a class variable. All analyses were performed in SAS Version 8.1 (SAS Institute; Cary, NC).38


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Descriptive Statistics
Complete 24-h BP data and sleep data were available on 61 of the African Americans (28 men and 33 women) and 63 of the white subjects (27 men and 36 women). In 14 subjects, ABPM data were incomplete. In one subject, overnight sleep data were incomplete; in one subject, both were incomplete. There were no significant differences in age between the African-American men (mean age, 74.9 years; SD, 7.7 years) and women (mean age, 73.1 years; SD, 5.8 years) or between the white men (mean age, 74.4 years; SD, 6.5 years) and women (mean age, 74.0 years; SD, 5.7 years). The distribution of RDI severity by race and gender is shown in Table 1 , and the ODI distribution by race and gender is shown in Table 2 . The mean sleep efficiency (defined as the amount of sleep given the amount of time in bed) was 77% (SD, 12%; median, 79%; range, 39 to 98%) in the African-American group and 80% (SD, 11%; median, 84%; range, 40 to 97%) in the white group.


View this table:
[in this window]
[in a new window]

  		Table 1. Distribution of RDI Severity for African-American and White Subjects

 

View this table:
[in this window]
[in a new window]

  		Table 2. Distribution of ODIs for African-American and White Subjects

 
SDB
For RDI, analysis of variance with gender, race, and BP medication as class variables resulted in a significant effect of gender (F = 19.19, df = 1,111; p < 0.0001) and a statistically significant interaction of antihypertensive medication with gender (F = 5.87, df = 1,111; p < 0.017) independent of race. Men had a higher RDI than women (Table 1) , and men receiving antihypertensive medication had a higher RDI (mean, 31.9; SD, 23.9) than men not receiving antihypertensive medication (mean, 20.5; SD, 19.5). Among women, however, those receiving antihypertensive medication had a lower RDI (mean, 10.1; SD, 6.7) than women not receiving antihypertensive medication (mean, 14.7; SD, 12.6) [Fig 2 ]. There was no significant race/gender interaction.



View larger version (14K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2. For RDI, there was an interaction between BP medication with gender independent of race, such that men receiving antihypertensive medication had higher RDIs, while women receiving antihypertensive medication had lower RDIs (p < 0.017) On Meds = receiving medication; Off Meds = not receiving medication.

 
Blood Oxygen Saturation Levels
The analysis of variance with ODI as the dependent variable showed a statistically significant effect of gender (F = 8.22, df = 1,102; p < 0.01) and a statistically significant interaction of gender with race (F = 4.28, df = 1,102; p < 0.05). Overall, ODI was higher in men than in women; however, as shown in Table 2 , this difference was most pronounced among African-American subjects, with African-American men and white men and women having nearly equal ODI distributions, but African-American women have a lower ODI.

BP
For the average 24-h mean arterial pressure, analysis of variance showed that there was a statistically significant effect for race (F = 10.48, df =1,112; p = 0.016), with African Americans having higher average 24-h mean arterial pressure (mean, 91.7 mm Hg; SD, 12.7 mm Hg) than whites subjects (mean, 85.0 mm Hg; SD, 7.7 mm Hg).

BMI
Mean BMI was 27.7 (SD, 5.2) in African-Americanmen, 31.4 (SD, 7.3) in African-American women, 27.1 (SD, 3.6) in white men, and 28.0 (SD, 6.1) in white women. The analysis of BMI with race, gender, and antihypertensive medication as predictor variables showed an interaction between race and gender (F = 5.77, df = 1,109; p = 0.018), with BMI highest among the African-American women. There was an interaction of race with BP medication (F = 5.25, df = 1,109; p = 0.024) with mean BMI higher among African Americans receiving medication (mean, 30.6; SD, 7.1) than among whites subjects receiving medication (mean, 27.0; SD, 3.3).

Dipping Ratio
In the analysis of variance of dipping ratio with race, gender, and antihypertensive medication as predictor variables, there was a statistically significant effect of race (F = 5.20, df = 1,112; p = 0.025) but no effect of gender or antihypertensive medication. As expected, the dipping ratio was higher in African Americans (mean dipping ratio, 0.94; SD, 0.10) than in white subjects (mean dipping ratio, 0.89; SD, 0.09).

Neither RDI, ODI, average 24-h mean arterial pressure, nor diagnosis of hypertension accounted for the difference in mean dipping ratio between African Americans and white subjects. The analysis of covariance with these terms in the model still resulted in a statistically significant effect of race (t = 1.99, p = 0.050), with overall higher dipping ratios in the African-American group compared to the white group.

The analysis of covariance of dipping ratio, with antihypertensive medication, race, and gender as categorical variables, and with RDI, ODI, BMI, and mean arterial pressure as covariates, indicated that a higher dipping ratio was associated with higher values of RDI (R2 = 0.069; F = 10.01, df = 1,100; p = 0.021), higher levels of ODI (R2 = 0.042; F = 6.05, df = 1,90; p < 0.03), and higher average 24-h mean arterial pressure (R2 = 0.081; F = 11.16, df = 1,110; p = 0.0012). However, the interaction terms (R2 = 0.0373; F = 5.44, df = 1,110; p =0.022) clarified that these associations between RDI and dipping occurred only among African Americans receiving antihypertensive medication, but not among those not receiving antihypertensive medication.

Two of the ODI higher-order interactions (gender/medication and race/medication) were also significant. The gender/medication higher-order interaction (t = 2.36, p < 0.03) indicated that dipping ratio was positively associated (higher with higher ODI) in women not receiving antihypertensive medication and in men receiving antihypertensive medication, but was slightly negatively associated with ODI in the other two groups (women receiving antihypertensive medication and men not receiving antihypertensive medication). The race/medication higher-order interaction (t = - 3.38, p < 0.03) indicated that there were very slight tendencies for the dipping ratio to be positively related to ODI in African Americans not receiving antihypertensive medication, but to be negatively related to ODI in white subjects receiving antihypertensive medication.

Analysis of the contingency tables with the categorical variables dipper/nondipper, normotensive/hypertensive, and SDB (ie, RDI >= 15/h)/no SDB (ie, RDI < 15/h) showed that the relationship between SDB and dipping depended on race and the presence of hypertension (Table 3 ). There was more nondipping among the hypertensive patients who also had SDB; however, nondipping was still more common among African Americans than white subjects with or without SDB. Without the presence of hypertension, there was more nondipping and more SDB among the African Americans than the white subjects, but the association of SDB with dipping was not statistically significant in either group. Because of the small samples involved, it was not meaningful to try to subdivide the ethnic groups by gender or to subdivide the hypertension groups according to antihypertensive medication and high BP.


View this table:
[in this window]
[in a new window]

  		Table 3. Percentage of Dippers vs Nondippers Among Hypertensive and Normotensive Subjects With and Without SDB*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
These analyses demonstrated a difference in BP dipping at night between groups, with African Americans having higher dipping ratios than white subjects. This relationship was true even when accounting for covariates such as RDI, ODI, BMI, and average 24-h mean arterial pressure.

The analyses also confirmed that dipping ratio was greatest in those with SDB and hypertension. Both African-American subjects and white subjects with SDB and hypertension tended to be nondippers. The third hypothesis, that RDI would be greatest in the nondipping hypertensive subjects, was true only for the African Americans.

These results confirmed the findings of others,27 28 29 30 31 that African Americans have higher dipping ratios, thus tending to be nondippers compared to white subjects. It has not been previously clarified how much of this nondipping might be secondary to other conditions. Our data suggest that the nondipping was not a result of weight, gender, or of having SDB. In this data set, just race (ie, being African American) accounted for the higher prevalence of nondipping. This study suggests that SDB may not be a cause of the excess amount of nondipping found in African Americans, but the data do not answer the question of what causes the nondipping. Studies need to be done to determine what other factors, such as diet, socioeconomic status, genetics, or psychosocial factors, might explain the differences.

The data also suggest, however, that regardless of race, those with SDB had more nondipping than those with no SDB, again supporting previous findings that nondipping is a characteristic of patients with SDB,21 22 23 24 in particular among hypertensive patients with SDB. With the presence of hypertension, the association between SDB and dipping was similar in both ethnic groups. Nevertheless, nondipping was still more common among African Americans than white subjects, whether with or without SDB. This suggests that having both hypertension and SDB and being African American puts one at greater risk of becoming a nondipper.

It was not surprising that men had higher RDIs than women. However, it was less expected to find that men receiving antihypertensive medication would have higher RDIs than men not receiving antihypertensive medication. It is possible that although the men were receiving antihypertensive medication, their hypertension was not well controlled, thus resulting in higher RDIs.

It was even more surprising to find that women receiving antihypertensive medication had lower RDIs than women not receiving these medications. The low RDIs in the women receiving antihypertensive medication may be a function of the women being more compliant with the medication regime, or that the women receiving antihypertensive medication have their hypertension under better control than the men receiving antihypertensive medication. The fact that the women not receiving antihypertensive medication had higher RDIs may be a reflection of their higher weight, or possibly that some of these women may have had hypertension underdiagnosed, thus resulting in no treatment and higher RDIs. In fact, Stoohs et al39 suggested untreated SDB may have an adverse effect on the efficacy of antihypertensive treatment in hypertensive older men. The same may hold true in older women. In their study, a relationship was found between RDIs and systolic BP in subjects with SDB and hypertension who were nondippers.40 In our data, dipping was related to the amount of SDB differentially in African Americans receiving antihypertensive medication, but not in the white subjects. If the medications are lowering BP during the day but not during the night, this would create an "artificially" high dipping ratio, indicating more nondipping. Research studies are needed to explore the effect of antihypertensive medication on daytime vs nighttime BP levels, particularly in African Americans with SDB.

African-American women also had lower ODIs, indicating less desaturation. Previous studies showed that measurements of blood oxygen saturation levels from ear oximetry were found to be slightly less accurate in darker-skinned patient groups.41 The same may be true of finger-pulse oximeters. However, if this was the main reason for the lower ODI, one would have expected lower ODIs in the African-American men as well.

It has been demonstrated that nondippers are more likely to have morbid cardiovascular events,25 and more cardiovascular complications.26 The question arises whether these effects are made worse by the presence of SDB or whether these nondippers might have had covert SDB and hypertension. Since RDI was highest in nondippers, our data suggest that the latter may well be a possibility.

This study based the dipping classification on one 24-h period of BP monitoring. This is the standard for its field, yet published data suggest that such classifications may be unstable and repeated monitoring is advisable.42 However, given the large number of subjects participating in this study, the one 24-h period is less likely to be a problem.

Our study was one of older adults. While this is the population most seen in internal medicine and primary care offices, our sample was older than those with SDB generally seen in sleep-disorders clinics. Although these results therefore may not generalize to younger populations, they should be taken into consideration in older patient samples. Replication of these findings in younger sleep-clinic samples would be of interest.

In summary, the results confirmed that the covariates (ie, SDB, ODI, BMI, and mean arterial pressure) differed between the races and genders as expected. The results also confirmed that dipping ratio was higher in African Americans than white subjects. However, the differences in the covariates did not account for the differences seen in the dipping ratio. Research has suggested that nondipping is a phenomenon common to African Americans.27 28 29 30 31 In our data, although nondipping was found in both African-American hypertensive subjects and normotensive subjects with SDB, the results confirmed that the nondipping was not specifically a result of SDB. Although those with SDB had higher dipping ratios, nondipping was also independently related to race.

These results have clinical implications. Physicians presented with African American patients who are nondippers may want to consider screening for SDB, since SDB is also associated with nondipping. Treatment of SDB with continuous positive airway pressure in hypertensive patients with sleep apnea has resulted in a decrease in BP both during the day and during the night.14 43 African-American patients who are prone to SDB and who are nondippers might particularly benefit from treatment with continuous positive airway pressure. Clinical trials are needed to determine the extent of therapeutic benefit in this population.


   Footnotes
 
Abbreviations: ABPM = ambulatory BP monitor; BMI = body mass index; df = degrees of freedom; ODI = oxygen desaturation index; RDI = respiratory disturbance index; SDB = sleep-disordered breathing

Parts of this article were presented at the Second Annual Meeting of the Israel Sleep Research Society, March 9–13, 1997, Zichron Ya’akov, Israel; and at the Association of Professional Sleep Societies, June 19–24, 1999, Orlando, FL, and June 11–15, San Francisco, CA.

Supported by National Institute on Aging grants AG02711 and AG08415, National Cancer Institute grant CA85264, and National Heart, Lung, and Blood Institute grants HL44915 and HL36005; the Department of Veterans Affairs, VISN-22 Mental Illness Research, Education and Clinical Center; the UCSD Cancer Center; and the Research Service of the Veterans Affairs San Diego Healthcare System.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Ancoli-Israel, S, Klauber, MR, Stepnowsky, C, et al (1995) Sleep-disordered breathing in African-American elderly. Am J Respir Crit Care Med 152,1946-1949[Abstract]
  2. Redline, SS, Tishler, PV, Hans, MG, et al Racial differences in sleep-disordered breathing in African-Americans and Caucasians. Am J Respir Crit Care Med 1997;155,186-192[Abstract]
  3. Jeong, DU, Dimsdale, JE Sleep apnea and essential hypertension: a critical review of the epidemiological evidence for co-morbidity. Clin Exp Hypertens 1989;11,1301-1323
  4. Millman, RP, Redline, S, Carlisle, CC, et al Daytime hypertension in obstructive sleep apnea: prevalence and contributing risk factors. Chest 1991;99,861-866[Abstract/Free Full Text]
  5. Shepard, JW, Jr Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992;13,437-458[ISI][Medline]
  6. Peppard, P, Young, T, Palta, M, et al Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342,1378-1384[Abstract/Free Full Text]
  7. Nieto, FJ, Young, T, Lind, B, et al Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study: Sleep Heart Health Study. JAMA 2000;283,1829-1836[Abstract/Free Full Text]
  8. Shepard, JW Hemodynamics in obstructive sleep apnea. Fletcher, EC eds. Abnormalities of respiration during sleep 1986,39-57 WB Saunders Philadelphia, PA.
  9. Dyken, ME, Somers, VK, Yamada, T Hemorrhagic stroke: part of the natural history of severe obstructive sleep apnea [abstract]? Sleep Res 1991;20,371
  10. Noda, A, Okada, T, Hayashi, H, et al Twenty-four hour ambulatory blood pressure variability in obstructive sleep apnea syndrome. Chest 1993;103,1343-1347[Abstract/Free Full Text]
  11. Hla, KM, Young, TB, Bidwell, T, et al Sleep apnea and hypertension: a population-based study. Ann Intern Med 1994;120,382-388[Abstract/Free Full Text]
  12. Coy, TV, Dimsdale, J, Ancoli-Israel, S, et al The role of sleep disordered breathing in essential hypertension. Chest 1996;109,890-895[Abstract/Free Full Text]
  13. Carlson, JT, Hedner, JA, Ejnell, H, et al High prevalence of hypertension in sleep apnea patients independent of obesity. Am J Respir Crit Care Med 1994;150,72-77[Abstract]
  14. Wilcox, I, Grunstein, RR, Hedner, JA, et al Effect of nasal continuous positive airway pressure during sleep on 24-h blood pressure in obstructive sleep apnea. Sleep 1993;16,539-544[ISI][Medline]
  15. Lavie, P, Yoffe, N, Berger, I, et al The relationship between the severity of sleep apnea syndrome and 24-h blood pressure values in patients with obstructive sleep apnea. Chest 1993;103,717-721[Abstract/Free Full Text]
  16. Gillum, RF Epidemiology of hypertension in African American women. Am Heart J 1996;131,385-395[CrossRef][ISI][Medline]
  17. Hall, WD, Saunders, E, Shulman, N Hypertension in blacks: epidemiology, pathophysiology, and treatment. 1985,1-263 Year Book Medical Publishers Chicago, IL.
  18. Bartel, PR, Loock, M, van der Meyden, C, et al Hypertension and sleep apnea in black South Africans: a case control study. Am J Hypertens 1995;8(12 pt 1),1200-1205[CrossRef][ISI][Medline]
  19. Baumgart, P Circadian rhythm of blood pressure: internal and external time triggers. Chronobiol Int 1991;8,444-450[ISI][Medline]
  20. Marler, MR, Jacob, R, Lehoczky, JP, et al Statistical analysis of treatment and activity effects in 24-h ambulatory blood pressure monitoring. Stat Med 1988;7,697-716[ISI][Medline]
  21. Morfis, L, Howes, LG Nocturnal fall in blood pressure in the elderly is related to presence of hypertension and not age. Blood Press 1997;6,274-278[Medline]
  22. Davies, CW, Crosby, JH, Mullins, RL, et al Case-control study of 24-h ambulatory blood pressure in patients with obstructive sleep apnoea and normal matched control subjects. Thorax 2000;55,736-740[Abstract/Free Full Text]
  23. Pankow, W, Nabe, B, Lies, A, et al Influence of sleep apnea on 24-h blood pressure. Chest 1997;112,1253-1258[Abstract/Free Full Text]
  24. Greenblatt, DJ, Shader, RI Pharmacokinetics of antianxiety agents. Meltzer, HY eds. Psychopharmacology: the third generation of progress 1987,1377-1386 Raven Press New York, NY.
  25. Coca, A Circadian rhythm and blood pressure control: physiological and pathophysiological factors. J Hypertens 1994;12,S13-S21
  26. Trenkwalder, P Ambulatory blood pressure monitoring (ABPM) in the elderly. Z Kardiol 1996;85,85-91
  27. James, G Race and perceived stress independently affect the diurnal variation of blood pressure in women. Am J Hypertens 1991;4,382-384[ISI][Medline]
  28. Harshfield, GA, Hwang, C, Grim, CE Circadian variation in blacks: influence of age, gender, and activity. J Hum Hypertens 1990;4,43-47[ISI][Medline]
  29. Gretler, DD, Fumo, MT, Nelson, KS, et al Ethnic differences in circadian hemodynamic profile. Am J Hypertens 1994;7,7-14[ISI][Medline]
  30. Harshfield, GA, Hwang, C, Edmundson, J, et al Circadian rhythm of blood pressure in blacks. Hypertension 1989;14,598-603[Abstract/Free Full Text]
  31. Hebert, LA, Agarwal, G, Ladson-Wofford, SE, et al Nocturnal blood pressure in treated hypertensive African Americans compared to treated hypertensive European Americans. J Am Soc Nephrol 1996;7,2130-2134[Abstract]
  32. Profant, J, Dimsdale, J Race and diurnal blood pressure patterns: a review and meta-analysis. Hypertension 1999;33,1099-1104[Abstract/Free Full Text]
  33. Spitzer, S, Llabre, M, Ironson, G, et al The influence of social situations on ambulatory blood pressure. Psychosom Med 1992;54,79-86[Abstract/Free Full Text]
  34. Ancoli-Israel, S The use of a modified Respitrace/Medilog portable system in the evaluation of sleep apnea. J Ambul Monit 1988;1,267-278
  35. Ancoli-Israel, S, Kripke, DF, Mason, W, et al Comparisons of home sleep recordings and polysomnograms in older adults with sleep disorders. Sleep 1981;4,283-291[ISI][Medline]
  36. Timms, RM, Dawson, A, Taft, R, et al Oxygen saturation by oximetry: analysis by microcomputer. J Polysom Tech 1988;Spring,13-21
  37. Ona, E, Dimsdale, JE, Ancoli-Israel, S, et al A technique for improved blood sampling during sleep studies. Psychophysiology 1994;31,609-610[ISI][Medline]
  38. SAS/STAT User’s Guide, Version 8. 1999,1-3884 SAS Institute Cary, NC.
  39. Stoohs, RA, Gingold, J, Cohrs, S, et al Sleep-disordered breathing and systemic hypertension in the older male. J Am Geriatr Soc 1996;44,1295-1300[ISI][Medline]
  40. Suzuki, M, Guilleminault, C, Otsuka, K, et al Blood pressure "dipping" and "non-dipping" in obstructive sleep apnea syndrome patients. Sleep 1996;19,382-387[ISI][Medline]
  41. Ries, AL, Prewitt, LM, Johnson, JJ Skin color and ear oximetry. Chest 1989;96,287-290[Abstract/Free Full Text]
  42. Dimsdale, J, Heeren, M How reliable is nighttime blood pressure dipping? Am J Hypertens 1998;11,606-609[CrossRef][ISI][Medline]
  43. Fletcher, EC Can the treatment of sleep apnea syndrome prevent the cardiovascular consequences? Sleep 1996;19(9 Suppl),S67-S70[ISI][Medline]



This article has been cited by other articles:


Home page
 Arch Intern MedHome page
M. L. Jehn, D. J. Brotman, and L. J. Appel
Racial Differences in Diurnal Blood Pressure and Heart Rate Patterns: Results From the Dietary Approaches to Stop Hypertension (DASH) Trial
Arch Intern Med, May 12, 2008; 168(9): 996 - 1002.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
M. Barnes, R. D. McEvoy, S. Banks, N. Tarquinio, C. G. Murray, N. Vowles, and R. J. Pierce
Efficacy of Positive Airway Pressure and Oral Appliance in Mild to Moderate Obstructive Sleep Apnea
Am. J. Respir. Crit. Care Med., September 15, 2004; 170(6): 656 - 664.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
C. J. Stepnowsky Jr., R. A. Nelesen, D. DeJardin, and J. E. Dimsdale
Socioeconomic Status Is Associated With Nocturnal Blood Pressure Dipping
Psychosom Med, September 1, 2004; 66(5): 651 - 655.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ancoli-Israel, S.
Right arrow Articles by Johnson, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ancoli-Israel, S.
Right arrow Articles by Johnson, S.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS