阻塞性睡眠呼吸暂停低通气综合征与高血压的相关性

Correlation between obstructive sleep apnea-hypopnea syndrome and hypertension

目的了解阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea-hypopnea syndrome，OSAHS）患者高血压发病情况及其程度，分析OSAHS对高血压患者血压昼夜节律的影响，从夜间低氧血症和睡眠结构方面探讨高血压发生的危险因素。方法采用多导睡眠监测仪对77例OSAHS患者（重度33例，中度23例，轻度23例）进行夜间7h睡眠监测和24h动态血压监测，对睡眠相关指标及不同时段血压进行分析，并与不伴OSAHS的高血压患者（15例）和正常对照者（15例）进行比较。结果（1）重度、中度和轻度OSAHS组体质指数（boay mass index,BMI）分别为（29．1±2．8）、（25．0±2．5）和（23．2±3．0）kg/m^2，均显著高于对照组的（20．3±4．1）kg/m^2（P均〈0．05）；睡眠呼吸暂停低通气指数（apnea hypopnea index，AHI）分别为（56．2±14．7）、（19．1±4．4）和（11．2±4．3）次／h，显著高于对照组的（2．9±1．0）次／h（P均〈0．05）；氧减指数（oxygen desaturation index，ODI）分别为（62．5±20．4）、（19．6±8．8）和（24．8±22．7）次／h，显著高于对照组的（2．7±2．0）次／h（（P均〈0．05））；微觉醒指数（microarousal index，MI）分别为（47．5±20．9）、（12．8±4．6）和（9．8±4．6）次／h，显著高于对照组的（1．3±1．1）次／h（P均〈0．05）；24h平均收缩压分别为（133±14．5）、（126±6．5）和（118±9．9）mmHg，重度和中度OSAHS组显著高于对照组的（117±9．6）mmHg（P均〈0．05）；24h舒张压分别为（92．8±9．6）、（86．3±7．5）和（81．9±3．9）mmHg，重度和中度OSAHS组显著高于对照组的（78．5±5．6）mmHg（P均〈0．05）；最低血氧饱和度分别为（65．5±10．4）％、（78．5±5．1）％和（79．7±9．6）％，重度和中度OSAHS组显著低于对照组的（84．7±8．2）％（P〈0．05）。（2）高血雎组与对照组睡前和醒后血压无显著差异，OSAHS合并高血压组醒后血压显著高于睡前[（142．0±12．4）／（110．0±10．2）mmHg对（127．4±9．8）／（84．2±6．0）mmHg，P〈0．05]；（3）OSAHS合并高血压组ODI和MI分别为（43．5±26．2）次/h和（31．6±21．2）次/h，均显著高于无高血压OSAHS组的（26．7±13．2）次／h和（27．5±20．6）次／h（P均〈0．05），而且前者非快速动眼睡眠S3＋4期和睡眠效率分别为（5．1±3．5）％和（62．2±15．4）％，均显著低于后者[分别为（8．8±5．2）％和（69．92±14．8）％，P分别〈0．05和0．01）。（4）OSAHS合并高血压组非杓型血压曲线构成比为56．1％，显著高于对照组的13．1％和单纯高血压组的16．7％（P均〈0．01）。（5）多变量logistic叫归分析显示，校正BMI、性别和年龄因素后，ODI（OR=1．129，95％CI 1．057～1．207；P=0．001）、MI（OR=0．925，95％CI0．874～0．980；P=0．008）和S3＋4期时间（OR=1．087，95％CI1．034～1．142；P=0．001）与高血压发生显著相关。结论OSAHS组收缩压和舒张压均显著高于正常对照组，且血压随OSAHS病情的加重而增高，昼夜血压节律消失，血压波动呈非杓状曲线。导致OSAHS患者合并高血压的主要危险因素为夜间低氧血症，其次为睡眠结构严重紊乱和MI增高。

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 （u = 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 ±.6/h respectively, and 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 OSAFIS 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 ±26.2/11 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 nonrapid 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） The 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 after adjusting for BMI, sex and age. Conclusions Systolic and diastolic blood pressures in the OSAHS group were significantly higher 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 variability showed a non-dipper-shaped curve. 3-he major risk factor for causing patients with OSAHS combined with hypertension was nocturnal hypoxemia and then severe sleep disorders and increased MI.