Correlation between obstructive sleep apnea-hypopnea syndrome and hypertension

Shichao Wang; Baojun Wang; Changchun Jiang; Xiue LI

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Correlation between obstructive sleep apnea-hypopnea syndrome and hypertension

VernacularTitle:阻塞性睡眠呼吸暂停低通气综合征与高血压的相关性
Author: Shichao WANG ; Baojun WANG ; Changchun JIANG ; Xiue LI
Publication Type:Journal Article
Keywords: Sleep apnea,obstructive; Hypertension
From: International Journal of Cerebrovascular Diseases 2010;18(2):91-96
CountryChina
Language:Chinese
Abstract: Objective To understand the incidence and the severity of hypertension in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and to analyze the impact of OSAHS on the circadian rhythm of blood pressure in patients with hypertension and to investigate the risk factors for the occurrence of hypertension from the aspects of nocturnal hypoxemia and sleep structure. Methods Polysomnography monitor was used for 7-hour sleep monitoring at night and 24-hour ambulatory blood pressure monitoring in 77 patients with OSAHS (severe, n = 33; moderate, n = 23; mild, n = 23). The sleep-related indicators and blood pressure at different times were analyzed, and they were compared to the patients with hypertension without OSAHS (n = 15) and normal controls (n = 15). Results (1) The body mass index (BMI) in the severe, moderate, and mild OSAHS groups was 29.1±2.8, 25.0±2.5, and 23.2±3.0 kg/m~2 respectively, and they were all significantly higher than 20.3±4.1 kg/m~2 in the control group (all P <0.05); sleep apnea-hypopnea index (AHI) was 56.2±14.7, 19.1± 4.4, and 11.2±4.3/h respectively, and they were significantly higher than 2.9±1.0/h in the control group (all P <0. 05); oxygen saturation index (ODI) was 62.5±20.4, 19.6±8.8, and 24.8±22.7/h respectively, and they were significantly higher than 2.7±2.0/h in the control group (all P <0.05); microarousal index (MI) was 47.5±20.9, 12.8±4.6, and 9.8±4.6/h respectively, arid they were significantly higher than 1.3±1.1/h in the control group (all P < 0.05); 24-hour mean systolic blood pressure was 133±14.5, 126±6.5, and 118± 9.9 mm Hg respectively, and the severe and moderate OSAHS groups were significantly higher than 117±9. 6 mm Hg (all P <0.05); 24-hour mean diastolic blood pressure was 92.8±9.6, 86.3±7.5, and 81.9±3.9 mm Hg respectively, and the severe and moderate OSAHS groups were significantly higher than 78.5±5.6 mm Hg in the control group (all P <0.05); and the lowest oxygen saturation was 65.5%±10.4%, 78.5%±5.1%, and 79.7%±9.6% respectively, and the severe and moderate OSAHS groups were significantly lower than 84.7% ±8.2% (P <0.05). (2) There was no significant difference in blood pressure before going to bed and waking up between the hypertension group and the control group. The blood pressure after waking up in the OSAHS combined with hypertension group was significantly higher than before going to bed (142.0±12.4/110.0±10.2 mm Hg vs. 127.4±9.8/84.2± 6.0 mm Hg, P <0.05). (3) ODI and MI in the OSAHS combined with hypertension group were 43.5±26.2/h and 31.6±21.2/h respectively, and they were significantly higher than 26.7± 13.2/h and 27.5±20.6/h in the non-hypertension OSAHS group (all P <0.05), and the non-rapid eye movement sleep period S3 +4 and the sleep efficiency of the former were 5.1%± 3.5% and 62.2±15.4% respectively, and they were all significantly lower than 8.8%± 5.2% and 69.92%±14.8% of the latter (P <0.05 and 0.01, respectively). (4) component ratio of non-dipper blood pressure curve was 56.1% in the OSAHS combined with hypertension group, and it was significantly higher than 13.1% in the control group and 16.7% in the simple hypertension group (all P <0.01 ). (5) Multivariate logistic regression analysis showed that ODI (OR = 1.29, 95% CI 1.57-1.07; P = 0.01 ), MI (OR = 0.925, 95% CI 0.874-0.980; P =0.008) and the time of period S3 +4 (OR = 1.087, 95% CI 1.034-1.142; P =0.001 ) were significantly correlated with hypertension alter adjusting for BMI, sex and age. Conclusions Systolic and diastolic blood pressures in the OSAHS group were significantly high-er than those in the normal control group, and the blood pressure increased with the aggravation of OSAHS. 1he circadian rhythm of blood pressure disappeared, and the blood pressure variabili-ty showed a non-dipper-shaped curve. The major risk factor for causing patients with OSAHS combined with hypertension was nocturnal hypoxemia and then severe sleep disorders and in-creased MI.