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阻塞性睡眠呼吸暂停与原发性醛固酮增多症共病的临床特征分析

沈阳阳, 朱婕, 时媛, 谭璐, 李桃美, 雷飞, 唐向东

沈阳阳, 朱婕, 时媛, 等. 阻塞性睡眠呼吸暂停与原发性醛固酮增多症共病的临床特征分析[J]. 四川大学学报(医学版), 2023, 54(2): 304-309. DOI: 10.12182/20230360213
引用本文: 沈阳阳, 朱婕, 时媛, 等. 阻塞性睡眠呼吸暂停与原发性醛固酮增多症共病的临床特征分析[J]. 四川大学学报(医学版), 2023, 54(2): 304-309. DOI: 10.12182/20230360213
SHEN Yang-yang, ZHU Jie, SHI Yuan, et al. Clinical Characteristics of Obstructive Sleep Apnea and Comorbid Primary Aldosteronism[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(2): 304-309. DOI: 10.12182/20230360213
Citation: SHEN Yang-yang, ZHU Jie, SHI Yuan, et al. Clinical Characteristics of Obstructive Sleep Apnea and Comorbid Primary Aldosteronism[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(2): 304-309. DOI: 10.12182/20230360213

阻塞性睡眠呼吸暂停与原发性醛固酮增多症共病的临床特征分析

基金项目: 科技部科技创新2030-“脑科学与类脑研究”重大项目(No. 2021ZD0201900)和国家自然科学基金(No. 82120108002、No.U21A20335)资助
详细信息
    通讯作者:

    唐向东: E-mail:2372564613@qq.com

Clinical Characteristics of Obstructive Sleep Apnea and Comorbid Primary Aldosteronism

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  • 摘要:
      目的  探讨阻塞性睡眠呼吸暂停(obstructive sleep apnea, OSA)与原发性醛固酮增多症(primary aldosteronism, PA)共病的疾病特征,并进一步探索影响血浆醛固酮浓度的相关因素。
      方法  回顾性分析2016年1月–2021年12月于四川大学华西医院确诊PA的住院患者105例,根据多导睡眠图(polysomnography, PSG)结果分为PA共病单纯性打鼾组(20例)、PA共病OSA组(85例),后者以呼吸暂停低通气指数(apnea-hypopnea index, AHI)分轻(31例)、中(24例)、重(30例)亚组。并纳入诊断单纯OSA的门诊患者85例作为对照组。分别比较组间的人口学、临床特征、生化指标和PSG参数等资料。
      结果  与单纯OSA患者相比:OSA共病PA患者的高血压占比增高,其收缩压、舒张压水平亦增高(P<0.05);OSA共病PA患者的AHI增加,平均血氧饱和度和睡眠效率降低(P<0.05)。随OSA严重程度的加重,PA患者的体质量指数、胆固醇、低密度脂蛋白、血尿酸水平升高。线性回归分析提示,最低血氧饱和度与血浆醛固酮浓度呈负相关(β=−0.222,P=0.045)。
      结论  与PA共病可加重OSA表现。OSA会加重PA患者的脂代谢及尿酸代谢指标异常。共病患者的血浆醛固酮浓度受最低血氧饱和度水平的影响。

     

    Abstract:
      Objective  To explore the characteristics of patients with obstructive sleep apnea (OSA) and comorbid primary aldosteronism (PA) and to explore the relevant factors affecting plasma aldosterone concentration.
      Methods  A total of 105 patients diagnosed with PA and admitted at West China Hospital, Sichuan University between January 2016 and December 2021 were retrospectively analyzed. The subjects were divided into a PA with comorbid snoring group (n=20) and a PA with comorbid OSA group (n=85) based on the results of polysomnography (PSG). The PA with comorbid OSA group was further divided into mild, moderate, and severe subgroups according to the apnea-hypopnea index (AHI). A total of 85 outpatients diagnosed with OSA were included as the control group. Demographic, clinical, biochemical, and PSG data were compared between the groups.
      Results  Compared with patients with only OSA, a significantly higher proportion of patients with OSA and comorbid PA had hypertension and elevated levels of systolic and diastolic blood pressure (P<0.05). In addition, patients with OSA and comorbid PA had significantly increased AHI and significantly decreased mean oxygen saturation and sleep efficiency (P<0.05). The more severe the OSA was, the higher levels of BMI, cholesterol, low-density lipoprotein, and uric acid the PA patients had. Linear regression analysis showed that the lowest oxygen saturation (β=−0.222, P=0.045) was negatively correlated with plasma aldosterone concentration.
      Conclusion  Comorbidity with PA can aggravate the clinical manifestations of OSA, while OSA further disrupted the metabolism of lipids and uric acid in PA patients. Plasma aldosterone concentrations in patients with comorbid OSA and PA were affected by the lowest oxygen saturation level.

     

  • 阻塞性睡眠呼吸暂停(obstructive sleep apnea, OSA)是一种常见的睡眠呼吸疾病,以睡眠中反复发生的上气道部分或全部塌陷所致的呼吸暂停、间歇性缺氧和睡眠片段化为特征。OSA的人群患病率为9%~38%[1],其诊断主要依靠多导睡眠图(polysomnography, PSG)。

    OSA引起的间歇性缺氧导致交感神经兴奋性增加,使得肾素-血管紧张素-醛固酮系统(renin-angiotensin-aldosterone system, RAAS)被激活,增加高血压的发生风险[2]。原发性醛固酮增多症(primary aldosteronism, PA)是一种肾上腺皮质球状带异常分泌醛固酮激素,导致血浆醛固酮浓度升高和血浆肾素活性下降,以高血压和低血钾为特征的疾病。PA的人群患病率为3%~13%[3-4]。既往研究提示,OSA和PA共病可相互影响和加重[5-6]。OSA人群中PA的患病率高达34%[7],PA人群中OSA的患病率更高达78.1%[8]。一方面,PA患者分泌过多的醛固酮会导致水钠潴留,引起咽壁水肿加重OSA的严重程度[9]。另一方面,OSA患者夜间间歇性缺氧可能增加RAAS的活性,从而导致PA的发生和发展[5]。有研究提示在白种人中,PA患者血浆醛固酮浓度与呼吸暂停低通气指数(apnea-hypopnea index, AHI)呈正相关[10-11],但亚洲人群研究未提示这种相关关系。目前国内对于OSA与PA共病的研究较少,且并未发现影响血浆醛固酮浓度的相关因素。

    本研究将通过比较OSA共病或不共病PA患者在人口学、临床特征、生化指标以及PSG参数指标的差异,探讨OSA与PA的共病特征,并进一步探索影响血浆醛固酮浓度的相关因素。

    回顾性纳入2016年1月–2021年12月在四川大学华西医院确诊为PA的住院患者,且因合并打鼾、嗜睡、睡眠中憋醒等症状疑诊OSA完善整夜睡眠呼吸监测。并纳入在四川大学华西医院睡眠医学中心行整夜睡眠呼吸监测确诊为单纯OSA的门诊患者。

    住院患者:①符合2016年美国内分泌学会原发性醛固酮增多症的诊断标准,以血浆醛固酮与肾素活性比值(aldosterone-renin ratio, ARR)>30 (ng/dL)/〔ng/(mL·h)〕为初筛阳性,以卡托普利试验后血浆醛固酮浓度(plasma aldosterone concentration, PAC)下降在30%以内,或生理盐水试验后PAC>10 ng/dL为确诊试验阳性[12],满足初筛试验阳性和一项确诊试验阳性即可确诊PA;②于四川大学华西医院行整夜睡眠呼吸监测;③年龄大于18岁。

    门诊患者:①与PA共病OSA患者以性别、年龄(±1岁)、体质量指数(body mass index, BMI)(±3 kg/m2)为配对因素,按1∶1匹配;②于四川大学华西医院行整夜睡眠呼吸监测,AHI≥5 h−1;③年龄大于18岁。

    ①排除合并慢性肾脏病,肾动脉狭窄,晚期恶性肿瘤,肝硬化,严重心脏病,慢性阻塞性肺疾病,妊娠的患者;②整夜睡眠呼吸监测所得的总睡眠时间<4 h的患者。

    四川大学华西医院伦理委员会已审核批准本研究方案,批准号:2022年审125号。

    PA患者根据整夜睡眠呼吸监测中的PSG结果(见1.2.3),分为PA合并单纯性打鼾、PA合并OSA组,并以AHI分轻、中、重亚组。诊断为单纯OSA的门诊患者作为对照组。对所有纳入研究的患者完成基本资料收集,包括年龄、身高、体质量、Epworth嗜睡量表(Epworth Sleepiness Scale, ESS)评分、收缩压、舒张压、吸烟史、饮酒史及共病史,如高血压病,糖尿病等。

    测定住院PA患者三酰甘油、胆固醇、低密度脂蛋白、血尿酸、血钾等生化指标。上述生化指标均采用我院实验医学科全自动生化分析仪测定。

    所有患者保持正常钠盐摄入和血钾浓度,停用显著影响ARR的药物4周以上。期间对确有必要控制血压的患者使用对ARR影响较小的药物,如维拉帕米。血浆肾素活性(plasma renin activity, PRA)与PAC的测定采用放射免疫法测定(北方生物技术研究所提供放射免疫试剂),其中部分患者血浆肾素与醛固酮的测定采用Liaison全自动化学发光免疫分析法测定(意大利Diasorin公司)。

    所有研究对象均完成一次整夜睡眠呼吸监测,输出PSG,睡眠呼吸相关参数的记录技术和评估方法都遵循美国睡眠医学会的标准(2.3版本)[13]。通过睡眠监测仪somte(澳大利亚Compumedics公司)或grael(澳大利亚Compumedics公司)收集数据,使用ProFusionPSG4分析和评价数据。监测参数包括脑电图(F3-M2、F4-M1、C3-M2、C4-M1、O1-M2、O2-M1)、心电图、肌电图(颏下和胫骨前肌)、双侧眼电图、口鼻热敏与气流、外周动脉氧饱和度和胸腹运动。低通气定义为气流下降30%或以上,持续至少10 s,伴有至少3%的氧饱和度降低或觉醒。呼吸暂停定义为气流下降超过90%,持续至少10 s。氧减事件定义为氧饱和度至少下降3%。氧减指数(oxygen desaturation index, ODI)定义为每小时氧减事件的次数。AHI定义为每小时呼吸暂停和低通气的次数。微觉醒指数定义为每小时微觉醒的次数。

    AHI≥5 h−1且合并相关症状(嗜睡、疲劳、打鼾、呼吸暂停等)诊断为OSA,AHI<5 h−1并伴有鼾症的患者诊断为单纯性打鼾。根据AHI区分OSA严重程度,分为轻度(AHI: 5~14.9 h−1)、中度(AHI: 15~29.9 h−1)及重度(AHI≥30 h−1[14]

    定性资料用例数和百分率表示,组间比较使用χ2检验。定量资料中符合正态分布用$ \bar x \pm s$表示,符合偏态分布用中位数(P25, P75)表示,组间比较使用t检验,多组间比较使用方差分析,偏态分布或未通过方差齐性检验的组间比较使用Mann-Whitney U检验。使用线性回归分析确定影响PAC的因素。P<0.05为差异有统计学意义。

    研究共纳入OSA共病PA患者85例、单纯OSA患者85例。如表1所示,在人口学和临床资料方面,OSA共病PA患者和单纯OSA患者在年龄、性别、BMI、ESS评分、吸烟等方面差异无统计学意义。OSA共病PA患者中的高血压占比增高,收缩压、舒张压水平也升高(P<0.05)。在PSG参数方面,两组患者在总睡眠时间上无差异,但是OSA共病PA患者的睡眠效率与2期睡眠百分比降低。在OSA严重程度方面,OSA共病PA患者平均血氧饱和度降低,AHI、ODI、血氧饱和度<90%的时间百分比升高(P<0.05)。两组间心率差异虽有统计学意义,但中位值差异较小。

    表  1  OSA共病PA与单纯OSA的人口学特征、临床和PSG特征比较
    Table  1.  Demographic, clinical, and polysomnography characteristics of study sample
    CharacteristicOSA with comorbid PA (n=85)OSA (n=85)P
    Demographic and clinical characteristics
     Age/yr. 48.5±9.7 48.5±9.9 0.963
     Male/case (%) 57 (67.1) 57 (67.1) 1.000
     BMI/(kg/m2) 26.7±3.9 27.4±3.0 0.231
     ESS* 5 (3, 8) 6 (3,10) 0.095
     Smoking/case (%) 39 (45.9) 31 (36.5) 0.429
     Alcohol drinking/case (%) 26 (30.6) 38 (44.7) 0.018
     SBP/mmHg 149±20 130±14 <0.001
     DBP*/mmHg 95 (87, 104) 84 (78, 91) <0.001
     Hypertension/case (%) 82 (96.5) 24 (28.2) <0.001
     Diabetes/case (%) 17 (20.0) 10 (11.8) 0.161
    Polysomnography parameters
     TST*/min 443.5 (398.3, 484.0) 436.0 (393.0, 474.0) 0.508
     SE*/% 80.7 (74.6, 86.8) 87.3 (81.1, 93.1) <0.001
     N1*/% 19.4 (14.9, 29.7) 18.6 (13.3, 23.9) 0.198
     N2/% 49.7±11.9 55.2±10.3 0.002
     N3*/% 6.2 (0.9, 14.5) 3.9 (0.0, 10.6) 0.109
     REM/% 18.5±5.8 17.7±5.5 0.372
     Arousal index*/h−1 12.2 (8.0, 18.1) 14.5 (10.0, 19.3) 0.084
     AHI*/h−1 23.4 (10.5, 37.6) 15.1 (8.0, 23.6) 0.002
     T90*/% 4.0 (0.6, 9.9) 1.0 (0.1, 4.0) <0.001
     Mean SpO2*/% 95 (93, 96) 95 (95, 96) <0.001
     Lowest SpO2*/% 80 (73, 85) 84 (74, 88) 0.064
     ODI*/h−1 20.4 (12.0, 36.3) 11.8 (7.1, 18.6) <0.001
     HR*/min−1 64 (57, 68) 67 (61, 75) 0.001
     * median (P25, P75). PA: primary aldosteronism; OSA: obstructive sleep apnea; BMI: body mass index; ESS: Epworth Sleepiness Scale; SBP: systolic blood pressure; DBP: diastolic blood pressure; TST: total sleep time; SE: sleep efficiency; N1–3: non–rapid eye movement sleep 1–3; REM: rapid eye movement sleep; AHI: apnea-hypopnea index; T90: percentage of time spent in sleep below 90% oxygen saturation; SpO2: peripheral capillary oxygen saturation; ODI: oxygen desaturation index; HR: heart rate. 1 mmHg=0.133 kPa.
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    共纳入PA共病单纯性打鼾20例,共病轻、中、重OSA各31例、24例、30例。本研究纳入的住院PA患者中,OSA患病率为81.0%,其中轻度29.5%、中度22.9%、重度28.6%。

    表2所示,在人口学和临床资料方面,4组年龄差异无统计学意义。在中、重度OSA中,男性比例更高、BMI更高。在生化指标方面,4组在PRA、PAC、ARR方面差异无统计学意义,但随着OSA加重,胆固醇、低密度脂蛋白、血尿酸浓度呈上升趋势。在PSG参数方面,4组患者在睡眠效率上差异无统计学意义。PA合并中、重度OSA的患者总睡眠时间增加,其中1期睡眠百分比增加,2期睡眠百分比降低,提示睡眠结构紊乱。

    表  2  PA共病不同严重程度OSA之间人口学特征、临床和PSG特征比较
    Table  2.  Comparison of the demographic, clinical, and polysomnography characteristics of patients with PA and comorbid OSA of different levels of severity
    CharacteristicPS (n=20)Obstructive sleep apneaP
    Mild OSA (n=31)Moderate OSA (n=24)Severe OSA (n=30)
    General demographic and clinical characteristics
     Age/yr. 48.2±7.7 48.1±9.8 45.8±7.7 51.1±10.6 0.215
     Male/case (%) 6 (30.0) 21 (67.7) 13 (54.2) 23 (76.7) 0.007
     BMI/(kg/m2) 23.9±3.6 25.6±3.8 26.5±3.4 28.1±4.2 0.002
     ESS* 6 (2, 9) 6 (4, 8) 4.5 (1, 6) 4 (3, 8) 0.527
     Smoking/case (%) 5 (20.0) 15 (48.9) 12 (50.0) 12 (40) 0.16
     Alcohol drinking/case (%) 6 (30.0) 8 (25.8) 5 (20.1) 13 (43.3) 0.294
     SBP*/mmHg 145 (135, 166) 142 (132, 163) 153 (143, 161) 146 (133, 162) 0.313
     DBP*/mmHg 92 (82, 103) 94 (83, 104) 97 (91, 107) 96 (85, 103) 0.553
     Hypertension/case (%) 19 (95.0) 29 (93.5) 24 (100.0) 29 (96.7) 0.485
     Diabetes/case (%) 2 (10.0) 5 (16.1) 4 (16.7) 8 (26.7) 0.479
    Biochemical parameters
     Total cholesterol/(mmol/L) 4.1±0.8 4.2±1.0 4.6±0.7 4.7±0.9 0.041
     LDL cholesterol/(mmol/L) 2.4±0.8 2.4±0.8 2.9±0.6 2.9±0.8 0.032
     Uric acid/(mmol/L) 308.2±79.8 360.8±85.7 346.7±71.5 382.9±99.8 0.029
     Serum patassium*/(mmol/L) 3.6 (3.3, 4.1) 3.6 (3.1, 3.9) 3.8 (3.2, 4.1) 3.6 (3.4, 3.7) 0.775
     PRA*/(ng/[mL·h]) 0.3 (0.1, 0.5) 0.3 (0.2, 0.8) 0.3 (0.1, 0.7) 0.3 (0.2, 0.7) 0.775
     PAC*/(ng/L) 30.0 (22.7, 40.9) 26.1 (21.5, 33.6) 27.0 (21.0, 37.0) 27.0 (21.7, 39.2) 0.331
     ARR*/([ng/L]/[ng/{mL·h}]) 84.3 (51.3, 250.5) 60.5 (37.1, 118.0) 106.3 (55.3, 274.2) 84.7 (40.4, 172.9) 0.26
    Polysomnography parameters
     TST/min 424.8±58.3 415.7±61.6 439.2±50.0 460.7±62.0 0.02
     SE/% 79.3±9.3 77.6±10.1 81.9±6.9 81.6±10.0 0.259
     N1*/% 11.5 (9.6, 16.0) 16.3 (12.5, 21.0) 19.6 (14.7, 24.7) 29.6 (18.6, 44.0) <0.001
     N2/% 57.4±9.6 53.7±8.8 52.3±9.8 43.4±13.6 <0.001
     N3/% 9.5±7.7 9.8±9.0 9.1±7.7 6.6±6.9 0.408
     REM/% 20.5±6.3 19.1±5.7 19.0±6.6 17.4±5.3 0.341
     Arousal index*/h−1 8.1 (6.7, 10.5) 8.8 (5.9, 12.6) 11.0 (8.1, 18.4) 17.2 (12.2, 36.8) <0.001
     AHI/h−1 3.0±1.4 9.5±2.5 22.7±3.8 53.5±22.4 <0.001
     T90*/% 0.0 (0.0, 0.1) 0.6 (0.1, 1.2) 3.4 (1.3, 6.7) 9.9 (6.9, 17.7) <0.001
     Mean SpO2*/% 96 (96, 97) 95 (94, 96) 95 (94, 96) 94 (92, 94) <0.001
     Lowest SpO2*/% 91 (87, 93) 85 (80, 89) 80 (74, 82) 73 (63, 79) <0.001
     ODI/h−1 2.5±1.8 9.8±4.1 20.8±5.6 50.7±22.0 <0.001
     HR/min−1 62±6 63±11 61±9 65±7 0.365
     * median (P25, P75). PS: primary snoring; LDL: low-density lipoprotein; PRA: plasma renin activity; PAC: plasma aldosterone concentration; ARR: aldosterone to renin activity ratio. The other abbreviations are explained in the note to Table 1. 1 mmHg=0.133 kPa.
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    表3所示,Model 1纳入最低血氧饱和度、睡眠效率、微觉醒指数、AHI、平均血氧饱和度、平均心率、血氧饱和度<90%时间百分比、ODI,最终发现最低血氧饱和度(β=−0.222,P=0.045)与PAC呈负相关。Model 2在增加控制性别、年龄、BMI、胆固醇、低密度脂蛋白、血尿酸、随机血糖、高血压、吸烟、饮酒之后,这种相关性依然存在。

    表  3  影响PAC的PSG参数的线性回归
    Table  3.  Linear regression of the effect of polysomnography parameters on PAC
    CharacteristicPlasma aldosterone concentration
    Model 1Model 2
    βPβP
    Lowest SpO2 −0.222 0.045 −0.222 0.046
    SE 0.019 0.865 0.018 0.873
    Arousal index −0.050 0.724 −0.066 0.647
    AHI −0.125 0.390 −0.145 0.323
    Mean SpO2 0.066 0.652 0.071 0.626
    HR −0.022 0.850 −0.036 0.775
    T90 −0.203 0.183 −0.209 0.173
    ODI −0.146 0.294 −0.168 0.234
      The abbreviations are explained in the note to Table 1. Model 1 includes lowest SpO2, SE, arousal index, AHI, mean SpO2, HR, T90, and ODI. Model 2 corrects for gender, age, BMI, total cholesterol, LDL cholesterol, uric acid, random blood sugar, hypertension, smoking, and alcohol drinking.
    下载: 导出CSV 
    | 显示表格

    本研究中发现住院PA患者中OSA患病率高达81.0%,远超过文献报道的一般人群9%~38%的患病率[1],此结果虽然存在基于住院人群研究的纳入偏倚,但是仍可以反映PA人群中需关注OSA共病的可能。

    本研究发现OSA共病PA患者中PAC与最低血氧饱和度呈负相关,在校正可能的混杂因素后这种关系依然存在。而既往研究中提示白人中PAC与AHI呈正相关[11]。上述不同结论的原因可能是由纳入检验的人群差异所造成的,本研究纳入OSA共病PA的人群,BUFFOLO等[11]纳入PA人群。OSA共病PA患者中PAC与最低血氧饱和度呈负相关可能与间歇性缺氧导致的RAAS激活有关[15]。在动物模型中,上气道反复塌陷导致的间歇性缺氧,使PRA和PAC升高[16],并促进大鼠颈动脉体血管紧张素1型受体的表达和血管紧张素Ⅱ对受体的刺激[17]。相反,持续气道正压通气治疗(continuous positive airway pressure therapy, CPAP)治疗OSA可以下调RAAS并降低血压[18]

    本研究发现与PA共病可加重OSA表现,其AHI、ODI、缺氧水平、缺氧时间等均显著上升。可能的机制是PA患者的水钠潴留和体液再分配使得咽部软组织水肿,加之醛固酮降低咽部肌群的质量和功能,使得OSA共病PA患者的上气道更容易闭塞,加重病情[19]。OSA共病PA的患者其高血压患病可能及高血压水平较单纯OSA显著升高。这是由于PA显著加重OSA表现,其缺氧程度、缺氧时间均显著提高。而OSA患者缺氧程度加重可导致其血压水平的升高和心血管事件发生风险的增加[20-21]。故而OSA共病PA可导致高血压进一步恶化。

    本研究还发现随着OSA严重程度的增高,共病患者的BMI 更高。重度OSA共病PA的患者,其BMI超过28 kg/m2,达到中国人群的肥胖标准[22]。这种现象的原因之一是重度OSA更常见于肥胖人群[23]。其次,RAAS系统可被脂肪细胞及其相关因子激活[24],肥胖会导致交感神经系统活性升高、RAAS活性升高、内皮功能障碍、炎症和代谢失调[25],故PA也更容易在肥胖人群中发生。在此基础上,本研究结果显示随着OSA的加重,PA患者的脂代谢及尿酸代谢指标明显异常。该异常改变跟OSA人群的BMI上升同步[26-27]

    本研究优势在于:所有的研究对象都进行整夜睡眠呼吸监测,除了设计了PA组间的比较,还设置了单纯OSA患者作为对照。不足之处在于:第一,基于医院数据的回顾性研究,数据缺失难以避免;第二,PA患者中醛固酮瘤与特发性醛固酮增多症的样本数量较小,故并未进行两组间的分析,后期可进一步扩大样本进行比较;第三,本研究主要是为了探讨OSA与PA之间的相互影响,因此未单独设立一组原发性高血压患者作为对照组,可在未来研究中进一步完善。

    综上所述,OSA与PA之间可以相互影响、加重病情。OSA共病PA患者的最低血氧饱和度与血浆醛固酮浓度呈负相关,提示临床医生要重视二者共病的发生,应常规筛查PA患者中OSA的可能,尤其是肥胖、血压控制较差的患者。

    *    *    *

    利益冲突 所有作者均声明不存在利益冲突

  • 表  1   OSA共病PA与单纯OSA的人口学特征、临床和PSG特征比较

    Table  1   Demographic, clinical, and polysomnography characteristics of study sample

    CharacteristicOSA with comorbid PA (n=85)OSA (n=85)P
    Demographic and clinical characteristics
     Age/yr. 48.5±9.7 48.5±9.9 0.963
     Male/case (%) 57 (67.1) 57 (67.1) 1.000
     BMI/(kg/m2) 26.7±3.9 27.4±3.0 0.231
     ESS* 5 (3, 8) 6 (3,10) 0.095
     Smoking/case (%) 39 (45.9) 31 (36.5) 0.429
     Alcohol drinking/case (%) 26 (30.6) 38 (44.7) 0.018
     SBP/mmHg 149±20 130±14 <0.001
     DBP*/mmHg 95 (87, 104) 84 (78, 91) <0.001
     Hypertension/case (%) 82 (96.5) 24 (28.2) <0.001
     Diabetes/case (%) 17 (20.0) 10 (11.8) 0.161
    Polysomnography parameters
     TST*/min 443.5 (398.3, 484.0) 436.0 (393.0, 474.0) 0.508
     SE*/% 80.7 (74.6, 86.8) 87.3 (81.1, 93.1) <0.001
     N1*/% 19.4 (14.9, 29.7) 18.6 (13.3, 23.9) 0.198
     N2/% 49.7±11.9 55.2±10.3 0.002
     N3*/% 6.2 (0.9, 14.5) 3.9 (0.0, 10.6) 0.109
     REM/% 18.5±5.8 17.7±5.5 0.372
     Arousal index*/h−1 12.2 (8.0, 18.1) 14.5 (10.0, 19.3) 0.084
     AHI*/h−1 23.4 (10.5, 37.6) 15.1 (8.0, 23.6) 0.002
     T90*/% 4.0 (0.6, 9.9) 1.0 (0.1, 4.0) <0.001
     Mean SpO2*/% 95 (93, 96) 95 (95, 96) <0.001
     Lowest SpO2*/% 80 (73, 85) 84 (74, 88) 0.064
     ODI*/h−1 20.4 (12.0, 36.3) 11.8 (7.1, 18.6) <0.001
     HR*/min−1 64 (57, 68) 67 (61, 75) 0.001
     * median (P25, P75). PA: primary aldosteronism; OSA: obstructive sleep apnea; BMI: body mass index; ESS: Epworth Sleepiness Scale; SBP: systolic blood pressure; DBP: diastolic blood pressure; TST: total sleep time; SE: sleep efficiency; N1–3: non–rapid eye movement sleep 1–3; REM: rapid eye movement sleep; AHI: apnea-hypopnea index; T90: percentage of time spent in sleep below 90% oxygen saturation; SpO2: peripheral capillary oxygen saturation; ODI: oxygen desaturation index; HR: heart rate. 1 mmHg=0.133 kPa.
    下载: 导出CSV

    表  2   PA共病不同严重程度OSA之间人口学特征、临床和PSG特征比较

    Table  2   Comparison of the demographic, clinical, and polysomnography characteristics of patients with PA and comorbid OSA of different levels of severity

    CharacteristicPS (n=20)Obstructive sleep apneaP
    Mild OSA (n=31)Moderate OSA (n=24)Severe OSA (n=30)
    General demographic and clinical characteristics
     Age/yr. 48.2±7.7 48.1±9.8 45.8±7.7 51.1±10.6 0.215
     Male/case (%) 6 (30.0) 21 (67.7) 13 (54.2) 23 (76.7) 0.007
     BMI/(kg/m2) 23.9±3.6 25.6±3.8 26.5±3.4 28.1±4.2 0.002
     ESS* 6 (2, 9) 6 (4, 8) 4.5 (1, 6) 4 (3, 8) 0.527
     Smoking/case (%) 5 (20.0) 15 (48.9) 12 (50.0) 12 (40) 0.16
     Alcohol drinking/case (%) 6 (30.0) 8 (25.8) 5 (20.1) 13 (43.3) 0.294
     SBP*/mmHg 145 (135, 166) 142 (132, 163) 153 (143, 161) 146 (133, 162) 0.313
     DBP*/mmHg 92 (82, 103) 94 (83, 104) 97 (91, 107) 96 (85, 103) 0.553
     Hypertension/case (%) 19 (95.0) 29 (93.5) 24 (100.0) 29 (96.7) 0.485
     Diabetes/case (%) 2 (10.0) 5 (16.1) 4 (16.7) 8 (26.7) 0.479
    Biochemical parameters
     Total cholesterol/(mmol/L) 4.1±0.8 4.2±1.0 4.6±0.7 4.7±0.9 0.041
     LDL cholesterol/(mmol/L) 2.4±0.8 2.4±0.8 2.9±0.6 2.9±0.8 0.032
     Uric acid/(mmol/L) 308.2±79.8 360.8±85.7 346.7±71.5 382.9±99.8 0.029
     Serum patassium*/(mmol/L) 3.6 (3.3, 4.1) 3.6 (3.1, 3.9) 3.8 (3.2, 4.1) 3.6 (3.4, 3.7) 0.775
     PRA*/(ng/[mL·h]) 0.3 (0.1, 0.5) 0.3 (0.2, 0.8) 0.3 (0.1, 0.7) 0.3 (0.2, 0.7) 0.775
     PAC*/(ng/L) 30.0 (22.7, 40.9) 26.1 (21.5, 33.6) 27.0 (21.0, 37.0) 27.0 (21.7, 39.2) 0.331
     ARR*/([ng/L]/[ng/{mL·h}]) 84.3 (51.3, 250.5) 60.5 (37.1, 118.0) 106.3 (55.3, 274.2) 84.7 (40.4, 172.9) 0.26
    Polysomnography parameters
     TST/min 424.8±58.3 415.7±61.6 439.2±50.0 460.7±62.0 0.02
     SE/% 79.3±9.3 77.6±10.1 81.9±6.9 81.6±10.0 0.259
     N1*/% 11.5 (9.6, 16.0) 16.3 (12.5, 21.0) 19.6 (14.7, 24.7) 29.6 (18.6, 44.0) <0.001
     N2/% 57.4±9.6 53.7±8.8 52.3±9.8 43.4±13.6 <0.001
     N3/% 9.5±7.7 9.8±9.0 9.1±7.7 6.6±6.9 0.408
     REM/% 20.5±6.3 19.1±5.7 19.0±6.6 17.4±5.3 0.341
     Arousal index*/h−1 8.1 (6.7, 10.5) 8.8 (5.9, 12.6) 11.0 (8.1, 18.4) 17.2 (12.2, 36.8) <0.001
     AHI/h−1 3.0±1.4 9.5±2.5 22.7±3.8 53.5±22.4 <0.001
     T90*/% 0.0 (0.0, 0.1) 0.6 (0.1, 1.2) 3.4 (1.3, 6.7) 9.9 (6.9, 17.7) <0.001
     Mean SpO2*/% 96 (96, 97) 95 (94, 96) 95 (94, 96) 94 (92, 94) <0.001
     Lowest SpO2*/% 91 (87, 93) 85 (80, 89) 80 (74, 82) 73 (63, 79) <0.001
     ODI/h−1 2.5±1.8 9.8±4.1 20.8±5.6 50.7±22.0 <0.001
     HR/min−1 62±6 63±11 61±9 65±7 0.365
     * median (P25, P75). PS: primary snoring; LDL: low-density lipoprotein; PRA: plasma renin activity; PAC: plasma aldosterone concentration; ARR: aldosterone to renin activity ratio. The other abbreviations are explained in the note to Table 1. 1 mmHg=0.133 kPa.
    下载: 导出CSV

    表  3   影响PAC的PSG参数的线性回归

    Table  3   Linear regression of the effect of polysomnography parameters on PAC

    CharacteristicPlasma aldosterone concentration
    Model 1Model 2
    βPβP
    Lowest SpO2 −0.222 0.045 −0.222 0.046
    SE 0.019 0.865 0.018 0.873
    Arousal index −0.050 0.724 −0.066 0.647
    AHI −0.125 0.390 −0.145 0.323
    Mean SpO2 0.066 0.652 0.071 0.626
    HR −0.022 0.850 −0.036 0.775
    T90 −0.203 0.183 −0.209 0.173
    ODI −0.146 0.294 −0.168 0.234
      The abbreviations are explained in the note to Table 1. Model 1 includes lowest SpO2, SE, arousal index, AHI, mean SpO2, HR, T90, and ODI. Model 2 corrects for gender, age, BMI, total cholesterol, LDL cholesterol, uric acid, random blood sugar, hypertension, smoking, and alcohol drinking.
    下载: 导出CSV
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  • 期刊类型引用(1)

    1. 段莉莉,杨莉,何燕. 原发性醛固酮增多症与阻塞性睡眠呼吸暂停低通气综合征相互作用机制研究进展. 实用心脑肺血管病杂志. 2023(11): 114-118 . 百度学术

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  • 收稿日期:  2022-12-07
  • 修回日期:  2023-02-17
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  • 发布日期:  2023-03-19

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