閆瑢玓,曹潔,馮靖△
臨床研究
阻塞性睡眠呼吸暫?;颊叩母哐獕夯疾∏闆r及其與呼吸功能的關(guān)系
閆瑢玓1,2,曹潔2,馮靖2△
目的分析阻塞性睡眠呼吸暫停(OSA)患者的高血壓患病率,并分析其血壓與呼吸通氣功能指標(biāo)的關(guān)系。方法選取3 607例OSA患者,根據(jù)呼吸暫停低通氣指數(shù)(AHI)將患者分為4組:對(duì)照組(AHI<5,354例)、OSA輕度組(5≤AHI<15,658例)、中度組(15≤AHI<30,753例)、重度組(AHI≥30,1 842例)。測(cè)量入組患者4個(gè)時(shí)間點(diǎn)(日間、睡前、夜間、晨起)的血壓值,計(jì)算夜間與日間平均血壓比值(RN/D)、晨起與睡前平均血壓比值(RM/E)。比較4組的一般指標(biāo)、高血壓患病率、4個(gè)時(shí)間點(diǎn)的平均血壓(MBP)值等,分析MBP與AHI、最低血氧飽和度(LSaO2)的相關(guān)性。結(jié)果OSA輕(34.65%)、中(39.04%)、重度組(55.37%)的高血壓患病率均高于對(duì)照組(22.32%),重度組的高血壓患病率高于輕、中度組(均P<0.05)。對(duì)于日間及睡前MBP,OSA輕、中、重度組均高于對(duì)照組,OSA重度組高于輕、中度組;對(duì)于夜間及晨起MBP,重度組>中度組>輕度組>對(duì)照組(均P<0.05)。日間、睡前、夜間、晨起的MBP值均隨AHI增加而升高。RN/D及RM/E均隨疾病嚴(yán)重度增加而升高。日間血壓與AHI、LSaO2顯著相關(guān)(收縮壓,r分別為0.195和-0.206;舒張壓,r分別為0.248和-0.251,P<0.01)。隨著AHI的增加,日間MBP值逐漸增高;當(dāng)AHI達(dá)到61~65區(qū)間之后,日間MBP值通常不再增高或略有降低。結(jié)論OSA患者夜間和晨起血壓明顯升高,失去正常的晝夜節(jié)律。OSA是高血壓的獨(dú)立危險(xiǎn)因素。
睡眠呼吸暫停,阻塞性;高血壓;血壓;晝夜模式;低通氣指數(shù);最低血氧飽和度
高血壓患者具有罹患心血管病的高危風(fēng)險(xiǎn),其死亡率顯著高于血壓正常的同齡人[1]。相當(dāng)一部分高血壓患者經(jīng)過(guò)足量含利尿劑的三聯(lián)藥物治療后,血壓仍難以良好控制,稱為頑固性高血壓;而睡眠呼吸暫停是頑固性高血壓患者的常見(jiàn)癥狀;睡眠呼吸暫停越嚴(yán)重,血壓越難以控制[2]。阻塞性睡眠呼吸暫停(obstructive sleep apnea,OSA)是一種常見(jiàn)的睡眠呼吸障礙,主要因睡眠時(shí)上呼吸道的阻塞或狹窄導(dǎo)致。OSA與高血壓之間有明確的相關(guān)性。Goodson等[3]研究表明,OSA與高血壓控制不佳均會(huì)損害心肺功能、降低生活質(zhì)量,并可誘發(fā)急性心血管病事件,甚至夜間猝死。因此,提高對(duì)OSA患者罹患高血壓的患病率及臨床特點(diǎn)的認(rèn)識(shí),有助于改善OSA的遠(yuǎn)期治療效果,但目前國(guó)內(nèi)鮮見(jiàn)此類研究。本研究通過(guò)大樣本的流行病學(xué)調(diào)查,探討OSA患者血壓的變化規(guī)律,從而為降低OSA患者睡眠時(shí)心腦血管事件的發(fā)生率提供臨床指導(dǎo)。
1.1 研究對(duì)象納入2010年4月—2013年6月在天津醫(yī)科大學(xué)總醫(yī)院睡眠中心就診的3 607例患者;其中男3 119例,女488例,年齡(46.4±23.2)歲,由同一位專科護(hù)士收集每位患者的詳細(xì)資料,計(jì)算體質(zhì)指數(shù)(body mass index,BMI)及Epworth嗜睡評(píng)分(Epworth sleepiness score,ESS)。本研究經(jīng)天津醫(yī)科大學(xué)總醫(yī)院醫(yī)學(xué)倫理委員會(huì)批準(zhǔn),所有受試者均簽署了知情同意書(shū)。
1.2 方法
1.2.1 血壓測(cè)量高血壓的診斷標(biāo)準(zhǔn)為收縮壓≥140 mmHg(1 mmHg=0.133 kPa)和(或)舒張壓≥90 mmHg,和(或)有高血壓病史[4]。在標(biāo)準(zhǔn)條件下測(cè)量4個(gè)時(shí)間點(diǎn)的血壓值,分別為日間(9:00—11:00)血壓、睡前(21:30—23:30)血壓、夜間(2:00—4:00)血壓及晨起(5:30—7:30)血壓。測(cè)量條件:患者平臥位,分別在以上4個(gè)時(shí)間點(diǎn),于患者右上臂連續(xù)測(cè)得3次血壓值,測(cè)量間隔時(shí)間為15 s。計(jì)算3次血壓的平均值。采用如下公式計(jì)算平均血壓(mean blood pressure,MBP):MBP=(收縮壓–舒張壓)/3+舒張壓(單位:mmHg)[5]。計(jì)算夜間與日間平均血壓比值(RN/D)、晨起與睡前平均血壓比值(RM/E)。
1.2.2 多導(dǎo)睡眠圖所有入組患者均以夜間多導(dǎo)睡眠圖監(jiān)測(cè)口鼻氣流、呼吸努力、打鼾情況、心率及最低血氧飽和度(LSaO2)。使用睡眠呼吸暫停低通氣指數(shù)(apnea-hypopnea in?dex,AHI)來(lái)評(píng)價(jià)OSA的嚴(yán)重程度。根據(jù)多導(dǎo)睡眠圖監(jiān)測(cè)結(jié)果,將受試者分為4組:對(duì)照組(AHI<5,354例)、OSA輕度組(5≤AHI<15,658例)、OSA中度組(15≤AHI<30,753例)、OSA重度組(AHI≥30,1 842例)。
1.3 統(tǒng)計(jì)學(xué)方法使用SPSS 18.0軟件進(jìn)行統(tǒng)計(jì)學(xué)分析。計(jì)量資料比較采用單因素方差分析,組間多重比較用Tam?hane's T2檢驗(yàn)。計(jì)數(shù)資料比較采用列聯(lián)表卡方檢驗(yàn),各組藥效比較采用Kruskal Wallis秩和檢驗(yàn)。為排除干擾因素的影響,將血壓分別與AHI和LSaO2進(jìn)行雙變量偏相關(guān)分析。以P<0.05為差異有統(tǒng)計(jì)學(xué)意義。
2.1 各組一般資料和高血壓發(fā)病率比較中、重度組的男性比例大于對(duì)照組;輕、中、重度組的年齡均大于對(duì)照組,且重度組的年齡大于輕、中度組(P<0.05)。重度組的吸煙率、飲酒率、BMI均高于另外3組,且中度組的BMI大于對(duì)照組(P<0.05)。對(duì)于AHI、LSaO2及ESS,均為重度組>中度組>輕度組>對(duì)照組(P<0.05)。輕、中、重度組的高血壓患病率均高于對(duì)照組,重度組高于輕、中度組(P<0.05)。輕、中、重度組規(guī)律服藥的比例高于對(duì)照組,且重度組高于輕、中度組(P<0.05),但對(duì)照組與輕度組的治療效果優(yōu)于中度與重度組(P<0.05),見(jiàn)表1。
2.2 各組MBP比較對(duì)于日間及睡前MBP輕、中、重度組均高于對(duì)照組,重度組高于輕、中度組;對(duì)于夜間及晨起MBP均重度組>中度組>輕度組>對(duì)照組;中、重度組的RN/D高于對(duì)照組,且重度組高于輕度組;重度組的RM/E高于輕、中度組及對(duì)照組(均P<0.05),見(jiàn)表2。
2.3 MBP與AHI、LSaO2的相關(guān)性分析在排除了相關(guān)混雜因素如年齡、性別、BMI等的影響后,進(jìn)行偏相關(guān)分析。結(jié)果顯示在4個(gè)時(shí)間點(diǎn),平均動(dòng)脈壓與AHI呈正相關(guān),與LSaO2呈負(fù)相關(guān);日間收縮壓、舒張壓與AHI呈正相關(guān),與LSaO2呈負(fù)相關(guān)(均P<0.05),見(jiàn)表3。
2.4 AHI對(duì)日間MBP的影響隨著AHI的增加,日間MBP值逐漸增高;當(dāng)AHI達(dá)到61~65區(qū)間之后,日間MBP值通常不再增高或略有降低,見(jiàn)圖1。
近年來(lái),OSA對(duì)高血壓的影響日益引起關(guān)注。
OSA與高血壓均是心血管疾病的危險(xiǎn)因素,并在后者的發(fā)生發(fā)展中起到同樣重要的作用。本研究表明,OSA組高血壓患病率為47.40%(1 542/3 253),顯著高于對(duì)照組的22.32%,高血壓的患病率基本隨著OSA的嚴(yán)重度增加而增高。
Tab.1 Demographic data and the prevalence of hypertension in all groups表1 各組一般資料和高血壓發(fā)病率比較
Tab.2The daytime,evening,midnight,and moning MBP in different groups表2 各組不同時(shí)點(diǎn)MBP比較
Tab.2The daytime,evening,midnight,and moning MBP in different groups表2 各組不同時(shí)點(diǎn)MBP比較
組別對(duì)照組輕度組中度組重度組F n 354 658 753 1 842日間MBP(mmHg)90.87±10.76 94.41±10.61a95.45±11.23a99.83±12.28abc84.54**睡前MBP(mmHg)90.07±11.82 94.10±10.87a95.46±11.31a99.43±11.98abc86.12**夜間MBP(mmHg)89.58±10.94 93.65±11.64a95.84±12.19ab100.78±13.81abc108.64**組別對(duì)照組輕度組中度組重度組F n RN/D RM/E 354 658 753 1 842晨起MBP(mmHg)91.73±11.82 95.14±12.78a97.45±12.58ab103.55±13.96abc127.32**9.82**0.989±0.091 0.994±0.086 1.007±0.089a1.014±0.109ab1.025±0.112 1.014±0.099 1.023±0.091 1.045±0.106abc18.96**
Tab.3Correlations between AHI and LSaO2with prevalence of hypertension and BP表3 AHI、LSaO2與高血壓發(fā)生率及血壓的相關(guān)性(r)
Fig.1Relationship between daytime MBP and AHI in different groups圖1 日間平均血壓與睡眠呼吸暫停低通氣指數(shù)(AHI)的關(guān)系
本研究中,各組的AHI及LSaO2均與血壓值密切相關(guān)。在對(duì)相關(guān)混雜因素進(jìn)行校正后,各組的AHI增加和LSaO2降低均與日間、睡前、夜間、晨起MBP值增高相關(guān)。OSA患者通常具有較高的交感神經(jīng)活性。Wolf等[6]曾指出,反復(fù)上氣道阻塞可導(dǎo)致缺氧、高碳酸血癥,并通過(guò)負(fù)反饋調(diào)節(jié)機(jī)制刺激化學(xué)感受器、使交感神經(jīng)活性增加,從而導(dǎo)致外周血管收縮、血壓上升。此外,全身炎性反應(yīng)與氧化應(yīng)激引起的內(nèi)皮素、血管緊張素Ⅱ釋放[7]以及內(nèi)皮功能障礙[8]均可使血壓升高。
本研究中OSA患者的血壓變化規(guī)律有助于理解為何高血壓亞組患者的夜間血壓不下降(即呈非杓形節(jié)律)。非杓形高血壓是一種常見(jiàn)的高血壓類型,可增加心血管意外的發(fā)生率[9]。我們的研究結(jié)果表明,重度OSA可導(dǎo)致夜間血壓與晨起血壓顯著升高,其機(jī)制可能與正常睡眠及晝夜節(jié)律的紊亂有關(guān)[6]。對(duì)于正常人而言,深度睡眠常伴隨血壓下降(杓形血壓)。然而,慢波睡眠百分比與微覺(jué)醒指數(shù)僅能分別獨(dú)立預(yù)測(cè)約10%的夜間舒張壓降低。在腎素-血管緊張素-醛固酮系統(tǒng)(renin-angiotensin-aldosterone system,RAAS)的調(diào)節(jié)下,血漿中去甲腎上腺素與腎上腺素水平以峰值出現(xiàn)在清晨、最低值出現(xiàn)在夜間睡眠中的晝夜節(jié)律為特征。腎素原與血管緊張素轉(zhuǎn)換酶也表現(xiàn)為相同的晝夜節(jié)律。Belaidi等[7]和Wang等[10]的研究表明,OSA可通過(guò)以下機(jī)制干擾原發(fā)性高血壓患者的RAAS:夜間頻繁發(fā)作的低氧血癥和高碳酸血癥,導(dǎo)致血清血管緊張素Ⅱ與內(nèi)皮素水平升高。此類患者更易進(jìn)展為非杓形高血壓,從
而具有較高的心血管意外、終末器官損害以及與血壓載荷無(wú)關(guān)的死亡風(fēng)險(xiǎn)[10]。與我們的結(jié)果相近,Stergiou等[11]也證實(shí)了高AHI可抑制夜間血壓下降,并可使尿兒茶酚胺水平顯著升高;此外,持續(xù)氣道正壓通氣(continuous positive airway pressure,CPAP)可有效預(yù)防一過(guò)性血壓升高。Pinto等[12]報(bào)道,CPAP可有效控制重度OSA患者的血壓,并可明顯改善其24 h尿中的去甲腎上腺素水平。
本課題前期研究表明,OSA不僅升高睡眠中的血壓,也可影響晨起和日間血壓。睡眠中的呼吸暫停和低通氣越頻繁,日間血壓值越高。此外,收縮壓和舒張壓水平均與AHI顯著相關(guān)[13]。在幾種具有相同致病途徑的神經(jīng)體液機(jī)制的共同作用下,OSA患者可表現(xiàn)為持續(xù)的高交感活性及日間高血壓。這些機(jī)制包括化學(xué)反射和壓力反射的功能障礙、RAAS系統(tǒng)的功能障礙以及交感神經(jīng)活性增加導(dǎo)致的心血管變異性改變。即使在受試者日間清醒正常呼吸時(shí)且沒(méi)有明顯的低氧或化學(xué)反射活動(dòng)存在的情況下,高交感刺激仍然存在。萬(wàn)南生等[14]研究表明,間歇性低氧可引起大鼠血壓增高和交感活性增強(qiáng),且存在明顯的低氧程度依賴性和時(shí)間過(guò)程規(guī)律性。血清中高水平的血管收縮劑、系統(tǒng)性炎癥反應(yīng)與氧化應(yīng)激導(dǎo)致的內(nèi)皮功能障礙、代謝調(diào)節(jié)紊亂和動(dòng)脈粥樣硬化均可導(dǎo)致晨起和日間血壓的升高。而有效的CPAP則可顯著降低夜間和日間血壓[15-16]。本研究發(fā)現(xiàn),一旦AHI達(dá)到61,日間血壓升高的趨勢(shì)就會(huì)趨于平穩(wěn);其機(jī)制可能是內(nèi)皮細(xì)胞的炎癥狀態(tài)達(dá)到峰值后隨著間歇性低氧/再氧合頻率的增加又降到最低水平。體外實(shí)驗(yàn)證實(shí),間歇低氧(特別是同時(shí)合并高碳酸血癥時(shí))可嚴(yán)重?fù)p害內(nèi)皮細(xì)胞[17]。馮靖等[18]指出,在間歇低氧/再氧合條件下,炎癥損害通常發(fā)生于再氧合階段而非間歇低氧階段。
通常,OSA不僅可使血壓升高,亦可改變血壓的晝夜節(jié)律。本研究結(jié)果表明,OSA患者失去了正常的血壓晝夜節(jié)律,血壓在睡眠中和清醒時(shí)均增高。最近一項(xiàng)研究證實(shí),如果血壓正常的成人具有非杓形血壓節(jié)律,其靶器官損害的風(fēng)險(xiǎn)會(huì)顯著升高[19]。筆者認(rèn)為,如果OSA可以治療,那么就可由此有效控制血壓、改善血壓的晝夜節(jié)律,從而有助于減輕高血壓相關(guān)的靶器官損害,并降低高血壓患者的發(fā)病率和死亡率。Parati等[20]認(rèn)為必須重視OSA患者的血壓晝夜變異,特別是對(duì)于那些日間血壓正常而夜間血壓異常且未診斷為高血壓的患者更是如此。動(dòng)態(tài)血壓監(jiān)測(cè)可以有效監(jiān)測(cè)OSA患者的血壓變化規(guī)律[4]。對(duì)于非杓形難治性高血壓患者,將降壓藥的給藥時(shí)間改為睡前更有利于血壓控制[21]。借助動(dòng)態(tài)血壓監(jiān)測(cè)亦可顯著改善CPAP對(duì)于OSA患者血壓暫時(shí)性升高的治療效果[11,22]。
本研究的局限性在于:本睡眠中心的多數(shù)患者合并鼾癥,因此對(duì)照組的鼾癥患病率略高于既往的其他研究[15,23],而鼾癥可引起血壓升高[24]。此外,本研究結(jié)果也未考慮“第一夜”效應(yīng)和失眠的影響[25],使研究結(jié)果存在一定偏倚。
[1]Oliveras A,Schmieder RE.Clinical situations associated with diffi?cult-to-control hypertension[J].J Hypertens,2013,31 Suppl 1:S3-8.doi:10.1097/HJH.0b013e32835d2af0.
[2]Calhoun DA,Jones D,Textor S,et al.Resistant hypertension:Diag?nosis,evaluation,and treatment,a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research[J].Circulation,2008, 117(25),e510-526.doi:10.1161/CIRCULATIONAHA.108.189141.
[3]Goodson BL,Wung SF,Archbold KH.Obstructive sleep apnea hy?popnea syndrome and metabolic syndrome:A synergistic cardiovas?cular risk factor[J].J Am Acad Nurse Pract,2012,24(12):695-703. doi:10.1111/j.1745-7599.2012.00771.x.
[4]Mancia G,Fagard R,Narkiewicz K,et al.2013 ESH/ESC Guide?lines for the management of arterial hypertension:the Task Force for themanagement of arterial hypertension of the European Society of Hypertension(ESH)and of the European Society of Cardiology(ESC)[J].J Hypertens,2013,31(7):1281-1357.doi:10.1097/01. hjh.0000431740.32696.cc.
[5]Weber SA,Santos VJ,Semenzati Gde O.Ambulatory blood pressure monitoring in children with obstructive sleep apnea and primary snoring[J].Int J Pediatr Otorhinolaryngol,2012,76(6):787-790.doi: 10.1016/j.ijporl.2012.02.041.
[6]Wolf J,Hering D,Narkiewicz K.Non-dipping pattern of hyperten?sion and obstructive sleep apnea syndrome[J].Hypertens Res, 2010,33(9):867-871.Review.doi:10.1038/hr.2010.153.
[7]Belaidi E,Joyeux-Faure M,Ribuot C,et al.Major role for hypoxia inducible factor-1 and the endothelin system in promoting myocar?dial infarction and hypertension in an animal model of obstructive sleep apnea[J].J Am Coll Cardiol,2009,53(15):1309-1317.doi: 10.1016/j.jacc.2008.12.050.
[8]Bosc LV,Resta T,Walker B,et al.Mechanisms of intermittent hy?poxia induced hypertension[J].J Cell Mol Med,2010,14(1-2):3-17.Review.doi:10.1111/j.1582-4934.2009.00929.x.
[9]Sarigianni M,Dimitrakopoulos K,Tsapas A.Non-dipping status in arterial hypertension:An overview[J].Curr Vasc Pharmacol,2014, 12(3):527-536.doi:10.2174/157016111203140518173019.
[10]Wang HL,Wang Y,Zhang Y,et al.Changes in plasma angiotensin II and circadian rhythm of blood pressure in hypertensive patients with sleep apnea syndrome before and after treatment[J].Chin Med Sci J,2011,26(1):9-13.doi:10.1111/j.1479-8425.2012.00561.x.
[11]Stergiou GS,Triantafyllidou E,Cholidou K,et al.Asleep home blood pressure monitoring in obstructive sleep apnea:A pilot study
[12]Pinto P,Bárbara C,Montserrat JM,et al.Effects of CPAP on nitrate and norepinephrine levels in severe and mild-moderate sleep apnea[J].BMC Pulm Med,2013,13:13.doi:10.1186/1471-2466-13-13.
[13]Han MM,He Q,Shi Y,et al.the Effects of IH from OSA on cardiovas?cular and cerebrovascular diseases[J].Tianjin Med J,2014,42(9): 946-948.[韓苗苗,何慶,施遙,等.睡眠呼吸暫停模式間歇低氧對(duì)心腦血管的影響[J].天津醫(yī)藥,2014,42(9):946-948].doi:10.3969/j. issn.0253-9896.2014.09.028.
[14]Wan NS,Chen BY,Feng J,et al.The effects of chronic intermittent hypoxia on blood pressure and sympathetic nerve activity in rats[J]. Zhonghua Jie He He Hu Xi Za Zhi,2012,35(1):29-32.[萬(wàn)南生,陳寶元,馮靖,等.慢性間歇低氧對(duì)大鼠血壓和交感神經(jīng)興奮性的影響[J].中華結(jié)核和呼吸雜志,2012,35(1):29-32].
[15]Litvin AY,Sukmarova ZN,Elfimova EM,et al.Effects of CPAP on "vascular"risk factors in patients with obstructive sleep apnea and arterial hypertension[J].Vasc Health Risk Manag,2013,9:229-235.doi:10.2147/VHRM.S40231.
[16]Yorgun H,Kabak?i G,Canpolat U,et al.Predictors of blood pressure reduction with nocturnal continuous positive airway pressure therapy in patients with obstructive sleep apnea and prehypertension[J].An?giology,2014,65(2):98-103.doi:10.1177/0003319713477908.
[17]Feng J,Chen BY,Guo MN,et al.Interleukin-6 and tumor necrosis factor-alpha levels of endothelial cells in different hypoxia modes: in vitro experiment[J].Zhonghua Yi Xue Za Zhi,2007,87(11),:774-777.[馮靖,陳寶元,郭美南,等.內(nèi)皮細(xì)胞在不同低氧模式下白細(xì)胞介素6和腫瘤壞死因子α的變化[J].中華醫(yī)學(xué)雜志,2007,87(11):774-777].
[18]Feng J,Chen BY,Guo MN,et al.Inflammatory injury of vascular en?dothelial cells by various hypoxia of intermittent frequency[J].Chi?nese Journal of Geriatrics.2007,26(2):124-125[馮靖,陳寶元,郭美南,等.不同間歇低氧頻率對(duì)血管內(nèi)皮細(xì)胞的炎性損傷[J].中華老年醫(yī)學(xué)雜志,2007,26(2):124-125].
[19]Hermida RC,Ayala DE,Mojón A,et al.Blunted sleep-time relative blood pressure decline increases cardiovascular risk independent of blood pressure level-the"normotensive non-dipper"paradox[J]. Chronobiol Int,2013,30(1-2):87-98.doi:10.3109/07420528.2012.701 127.
[20]Parati G,Lombardi C,Hedner J,et al.Recommendations for the management of patients with obstructive sleep apnoea and hyperten?sion[J].Eur Respir J,2013,41(3):523-538.doi:10.1183/090319 36.00226711.
[21]Almirall J,Comas L,Martínez-Oca?a JC,et al.Effects of chrono?therapy on blood pressure control in non-dipper patients with re?fractory hypertension[J].Nephrol Dial Transplant,2012;27(5):1855-1859.doi:10.1093/ndt/gfr557.
[22]Deng T,Wang Y,Sun M,et al.Stage-matched intervention for ad?herence to CPAP in patients with obstructive sleep apnea:a random?ized controlled trial[J].Sleep Breath,2013,17(2):791-801.doi: 10.1007/s11325-012-0766-3.
[23]He QY,Feng J,Zhang XL,et al.Elevated nocturnal and morning blood pressure in patients with obstructive sleep apnea syndrome[J]. Chin Med J(Engl),2012,125(10):1740-1746.
[24]Nakano H,Hirayama K,Sadamitsu Y,et al.Mean tracheal sound energy during sleep is related to daytime blood pressure[J].Sleep, 2013,36(9):1361-1367.doi:10.5665/sleep.2966.
[25]Feng J,Chen BY.Prevalence and incidence of hypertension in ob?structive sleepapnea patients and the relationship between obstruc?tive sleep apnea and itsconfounders[J].Chin Med J(Engl),2009, 122(12):1464-1468.
(2015-06-05收稿 2015-07-06修回)
(本文編輯 閆娟)
The prevalence of hypertension in patients with obstructive sleep apnea hypopnea syndrome and their relationship
YAN Rongdi1,2,CAO Jie2,FENG Jing2△
1 Department of Occupational Disease,The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine,Jinan 250001,China;2 Department of Respiratory Medicine,General Hospital of Tianjin Medical University△
ObjectiveTo investigate the prevalence of hypertension in patients with obstructive sleep apnea hypopnea syndrome(OSA)and the relationship between blood pressure(BP)with respiratory ventilation function.MethodsPatients with OSA(n=3 607)were included in this study and divided into 4 groups based on their apnea-hypopnea index(AHI)scores:control group(control,n=354)with AHI<5;mild OSAHS(mild,n=658)with 5≤AHI<15;moderate OSAHS(moder?ate,n=753)with 15≤AHI<30;and severe OSA(severe,n=1 842)with AHI≥30.BP were measured at 4 time points(daytime, evening,midnight,and morning).The midnight/daytime average BP(RN/D)and morning/evening average BP(RM/E)ratios were calculated.Finally,the general profiles,prevalence of hypertension and average BP of 4 time points were compared among 4 groups.The correlations of MBP with AHI and LSaO2were also analyzed.ResultsThe prevalence of hypertension as well as MBP at daytime and in the morning in the mild group(34.65%),moderate group(39.04%)and severe group(55.37%)were all higher than that in control group(22.32%)(all P<0.05).The prevalence of hypertension as well as MBP at daytime and in the morning were both higher in severe group than those in mild and moderate groups.MPB in the evening and at midnight was higher in severe group than that in moderate group than that in mild group than in control group(P<0.05).Average MBP of all four time points rise with increasing AHI(all P<0.05).The ratios of nighttime to daytime MBP(RN/D)and of morning to evening MBP(RM/E)increased with the severity of the illness(F=9.821,18.957;P<0.001).The day?
sleep apnea,obstructive;hypertension;blood pressure;circadian variation;AHI;LSaO2
R54,R743
A DOI:10.11958/j.issn.0253-9896.2015.10.017
].Blood Press Monit,2013,18(1):21-26.
10.1097/MBP.0b013 e32835d3608.
國(guó)家自然科學(xué)基金資助項(xiàng)目(81270144,30800507,81170071);國(guó)家十二五科技支撐計(jì)劃(2012BAI05B02)
1山東中醫(yī)藥大學(xué)第二附屬醫(yī)院職業(yè)病科(郵編250001);2天津醫(yī)科大學(xué)總醫(yī)院呼吸科
閆瑢玓(1978),女,主治醫(yī)師,碩士,主要從事呼吸系統(tǒng)疾病與職業(yè)性呼吸疾病的診斷與治療研究
△通訊作者E-mail:zyyhxkfj@126.com
time BP correlated well with AHI and lowest oxygen saturation(LSaO2;systolic BP,r=0.195,-0.206;diastolic BP,r=0.248,-0.251,P<0.01).Daytime MBP increased gradually with increasing AHI until MPB reached 61-65,at which point it either plateaued or dropped slightly.ConclusionOSA patients have a significant increase in midnight and morning BP and lose normal BP nycterohemeral rhythm.OSA is an independent risk factor for hypertension.