Original Article
Obstructive Sleep Apnea Syndrome Is Associated With Higher Diastolic Blood Pressure in Men but Not in Women Yu-Jin G. Lee1 and Do-Un Jeong1 background Obstructive sleep apnea syndrome (OSAS) and poor sleep quality both increase blood pressure (BP). This study aimed to find the sex effects and the role of poor sleep quality on systolic BP (SBP) and diastolic BP (DBP) in OSAS patients.
results In male subjects, AHI predicted the high BP and high DBP groups but not the high SBP group. In female subjects, AHI did not predict any of
conclusions In male subjects only, OSAS was associated with DBP but not SBP. The significant association between OSAS and DBP may be responsible for the BP elevations in OSAS. It could be speculated that the stronger association between poor sleep quality and OSAS in male subjects compared with females may have partly contributed to the sex effect on BP. Keywords: blood pressure; hypertension; male; obstructive sleep apnea; sex; sleep apnea syndromes. doi:10.1093/ajh/hpt280
Obstructive sleep apnea syndrome (OSAS) is associated with hypertension (HT) and cardiovascular risk.1–4 Observational studies, including 24-hour ambulatory blood pressure (BP) monitoring, demonstrated a linear relationship between OSAS and HT prevalence/severity.1,4–6 Epidemiological studies, such as the Wisconsin Sleep Cohort Study of normotensive subjects, have shown that subjects with moderate to severe OSAS were more than 3 times as likely as subjects without OSAS to develop HT.2 The prevalence for OSAS and HT varies according to sex and age. OSAS is known to be more common in men than in women,2 but this sex difference declines in the elderly population.7 HT prevalence is higher in men than in women, but in the postmenopausal period, women have a sharp increase in BP to a comparable level with men.8 In the OSAS population, whether the male preponderance of HT still exists has not been established because of differences in OSAS severity and inclusion criteria of HT in past studies.9–13 Systolic and diastolic HT are manifested by different pathophysiological processes; sympathetic activation influences diastolic BP (DBP), whereas age-dependent arterial stiffness affects systolic BP (SBP).14 Several studies have looked into OSAS-induced BP elevations in regard to SBP and/or DBP elevations.4,9,15–19 The characteristically overactivated sympathetic
nervous system in OSAS may partly explain the predominance of diastolic HT in OSAS;9,15–18 however, a few studies have shown SBP elevations in association with OSAS.1,19 Intermittent hypoxemia and poor sleep quality, the cardinal features of OSAS, are both considered to be responsible for overactivating the sympathetic nervous system.20 Past reports have shown intermittent hypoxemia inducing sustained daytime BP elevations.21–23 A few studies24,25 have demonstrated that poor sleep quality,26 represented by frequent arousals, sleep fragmentation, and decreased slow wave sleep (SWS), elevated nocturnal BP and resulted in the loss of the normal nocturnal drop in BP (called dipping). However, to what extent poor sleep quality or hypoxemia is responsible for BP elevations has not been elucidated.27–29 Thus, in this study, we aimed to investigate the sex effects of OSAS severity on each of DBP and SBP, as well as the role of poor sleep quality in OSAS-associated high BP.
Correspondence: Do-Un Jeong ([email protected]).
1Department of Psychiatry and Center for Sleep and Chronobiology, Seoul National University College of Medicine and Hospital, Seoul, Republic of Korea.
Initially submitted July 10, 2013; date of first revision July 30, 2013; accepted for publication December 11, 2013; online publication January 16, 2014.
METHODS Subjects
We retrospectively examined 1,552 subjects diagnosed with OSAS with nocturnal polysomnography (NPSG) at
© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: [email protected]
American Journal of Hypertension 27(3) March 2014 325
Downloaded from http://ajh.oxfordjournals.org/ at University of Bath on June 22, 2015
methods Polysomnographic findings, morning BP values, and clinical data of 460 subjects (348 men; 112 women) diagnosed with OSAS were analyzed. Analyses were performed separately in each sex to examine the association of the apnea–hypopnea index (AHI) with BP, SBP, DBP, and sleep quality.
the high BP, DBP, or SBP groups. Poor sleep quality, in the absence of AHI effect, weakly correlated with BP in both sexes, but the association between poor sleep quality and high AHI was stronger in male subjects than in females.
Lee and Jeong
Sleep parameters
Grass model 15 or 78 (Grass Instrument, Middleton, WI) was used for NPSG. Sleep was scored using standard criteria,31 primarily by trained sleep technicians and secondarily by sleep physicians. Apnea was defined as complete or near-complete (≥90%) cessation of airflow lasting at least 10 seconds. Hypopnea was defined as a reduction of respiratory signal by >30% lasting at least 10 seconds and being associated with oxygen desaturation of at least 4%. AHI was defined as the average number of apneas and hypopneas per hour of sleep. The quantity and relative distributions of sleep stages (stages N1, N2, N3 (SWS), REM, and wake) and sleep efficiency were calculated. Sleep fragmentation index (SFI),32 defined as the total number of awakenings and shifts to stage N1 sleep divided by total sleep time per hour, was modified to add any other sleep-stage shifts.33 Poor sleep quality was represented as reduced sleep efficiency, SWS, and REM sleep and increased stage N1 sleep, arousals, and sleep fragmentation.26,34 Clinical data
Medical and surgical histories, Epworth Sleepiness Scale, Beck’s Depression Inventory scores, height, and weight were included in the data. BP was measured according to standard protocol by trained technicians30 with YM1000 (Mediana, Wonju, Korea) after a 5-minute rest in a seated position twice before and once after NPSG. The morning BP values were used in the analyses. Smoking status was classified into current smoker or nonsmoker/past smoker, and drinking status was classified into regular drinker or nonregular drinker. Informed consent of the subjects was obtained, and the study was approved by the Institutional Review Board of Seoul National University Hospital. 326 American Journal of Hypertension 27(3) March 2014
Statistical analyses
Statistical analyses were performed using SPSS for Windows version 17.0 (SPSS, Chicago, IL). For comparisons, 2-tailed t tests or χ2 tests were used. For correlations, Pearson correlations were used. For each sex, multiple logistic regression analyses in a stepwise method for the high BP, SBP, and DBP groups were performed. For comparisons among OSAS severity-stratified groups, multiple logistic regression analyses in a stepwise method were performed in each stratified group, and trend analyses were performed using the Jonckheere–Terpstra test. Multiple linear regression analyses were performed for AHI and sleep quality parameters. All multiple linear regression and multiple logistic regression analyses were adjusted for age, body mass index (BMI), drinking, and smoking. Results are presented as mean ± SD, with P
Obstructive Sleep Apnea Syndrome Is Associated With Higher Diastolic Blood Pressure in Men but Not in Women Yu-Jin G. Lee1 and Do-Un Jeong1 background Obstructive sleep apnea syndrome (OSAS) and poor sleep quality both increase blood pressure (BP). This study aimed to find the sex effects and the role of poor sleep quality on systolic BP (SBP) and diastolic BP (DBP) in OSAS patients.
results In male subjects, AHI predicted the high BP and high DBP groups but not the high SBP group. In female subjects, AHI did not predict any of
conclusions In male subjects only, OSAS was associated with DBP but not SBP. The significant association between OSAS and DBP may be responsible for the BP elevations in OSAS. It could be speculated that the stronger association between poor sleep quality and OSAS in male subjects compared with females may have partly contributed to the sex effect on BP. Keywords: blood pressure; hypertension; male; obstructive sleep apnea; sex; sleep apnea syndromes. doi:10.1093/ajh/hpt280
Obstructive sleep apnea syndrome (OSAS) is associated with hypertension (HT) and cardiovascular risk.1–4 Observational studies, including 24-hour ambulatory blood pressure (BP) monitoring, demonstrated a linear relationship between OSAS and HT prevalence/severity.1,4–6 Epidemiological studies, such as the Wisconsin Sleep Cohort Study of normotensive subjects, have shown that subjects with moderate to severe OSAS were more than 3 times as likely as subjects without OSAS to develop HT.2 The prevalence for OSAS and HT varies according to sex and age. OSAS is known to be more common in men than in women,2 but this sex difference declines in the elderly population.7 HT prevalence is higher in men than in women, but in the postmenopausal period, women have a sharp increase in BP to a comparable level with men.8 In the OSAS population, whether the male preponderance of HT still exists has not been established because of differences in OSAS severity and inclusion criteria of HT in past studies.9–13 Systolic and diastolic HT are manifested by different pathophysiological processes; sympathetic activation influences diastolic BP (DBP), whereas age-dependent arterial stiffness affects systolic BP (SBP).14 Several studies have looked into OSAS-induced BP elevations in regard to SBP and/or DBP elevations.4,9,15–19 The characteristically overactivated sympathetic
nervous system in OSAS may partly explain the predominance of diastolic HT in OSAS;9,15–18 however, a few studies have shown SBP elevations in association with OSAS.1,19 Intermittent hypoxemia and poor sleep quality, the cardinal features of OSAS, are both considered to be responsible for overactivating the sympathetic nervous system.20 Past reports have shown intermittent hypoxemia inducing sustained daytime BP elevations.21–23 A few studies24,25 have demonstrated that poor sleep quality,26 represented by frequent arousals, sleep fragmentation, and decreased slow wave sleep (SWS), elevated nocturnal BP and resulted in the loss of the normal nocturnal drop in BP (called dipping). However, to what extent poor sleep quality or hypoxemia is responsible for BP elevations has not been elucidated.27–29 Thus, in this study, we aimed to investigate the sex effects of OSAS severity on each of DBP and SBP, as well as the role of poor sleep quality in OSAS-associated high BP.
Correspondence: Do-Un Jeong ([email protected]).
1Department of Psychiatry and Center for Sleep and Chronobiology, Seoul National University College of Medicine and Hospital, Seoul, Republic of Korea.
Initially submitted July 10, 2013; date of first revision July 30, 2013; accepted for publication December 11, 2013; online publication January 16, 2014.
METHODS Subjects
We retrospectively examined 1,552 subjects diagnosed with OSAS with nocturnal polysomnography (NPSG) at
© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: [email protected]
American Journal of Hypertension 27(3) March 2014 325
Downloaded from http://ajh.oxfordjournals.org/ at University of Bath on June 22, 2015
methods Polysomnographic findings, morning BP values, and clinical data of 460 subjects (348 men; 112 women) diagnosed with OSAS were analyzed. Analyses were performed separately in each sex to examine the association of the apnea–hypopnea index (AHI) with BP, SBP, DBP, and sleep quality.
the high BP, DBP, or SBP groups. Poor sleep quality, in the absence of AHI effect, weakly correlated with BP in both sexes, but the association between poor sleep quality and high AHI was stronger in male subjects than in females.
Lee and Jeong
Sleep parameters
Grass model 15 or 78 (Grass Instrument, Middleton, WI) was used for NPSG. Sleep was scored using standard criteria,31 primarily by trained sleep technicians and secondarily by sleep physicians. Apnea was defined as complete or near-complete (≥90%) cessation of airflow lasting at least 10 seconds. Hypopnea was defined as a reduction of respiratory signal by >30% lasting at least 10 seconds and being associated with oxygen desaturation of at least 4%. AHI was defined as the average number of apneas and hypopneas per hour of sleep. The quantity and relative distributions of sleep stages (stages N1, N2, N3 (SWS), REM, and wake) and sleep efficiency were calculated. Sleep fragmentation index (SFI),32 defined as the total number of awakenings and shifts to stage N1 sleep divided by total sleep time per hour, was modified to add any other sleep-stage shifts.33 Poor sleep quality was represented as reduced sleep efficiency, SWS, and REM sleep and increased stage N1 sleep, arousals, and sleep fragmentation.26,34 Clinical data
Medical and surgical histories, Epworth Sleepiness Scale, Beck’s Depression Inventory scores, height, and weight were included in the data. BP was measured according to standard protocol by trained technicians30 with YM1000 (Mediana, Wonju, Korea) after a 5-minute rest in a seated position twice before and once after NPSG. The morning BP values were used in the analyses. Smoking status was classified into current smoker or nonsmoker/past smoker, and drinking status was classified into regular drinker or nonregular drinker. Informed consent of the subjects was obtained, and the study was approved by the Institutional Review Board of Seoul National University Hospital. 326 American Journal of Hypertension 27(3) March 2014
Statistical analyses
Statistical analyses were performed using SPSS for Windows version 17.0 (SPSS, Chicago, IL). For comparisons, 2-tailed t tests or χ2 tests were used. For correlations, Pearson correlations were used. For each sex, multiple logistic regression analyses in a stepwise method for the high BP, SBP, and DBP groups were performed. For comparisons among OSAS severity-stratified groups, multiple logistic regression analyses in a stepwise method were performed in each stratified group, and trend analyses were performed using the Jonckheere–Terpstra test. Multiple linear regression analyses were performed for AHI and sleep quality parameters. All multiple linear regression and multiple logistic regression analyses were adjusted for age, body mass index (BMI), drinking, and smoking. Results are presented as mean ± SD, with P
