阻塞性睡眠呼吸暂停综合征与高血压靶器官损害的相关性研究
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摘要
【目的】探讨睡眠呼吸暂停综合征(OSAS)合并高血压病患者靶器官损害程度,分析相关危险因素对高血压靶器官损害的影响,进而为睡眠呼吸暂停综合征合并高血压患者的靶器官损害预防和治疗提供有价值的临床信息。
【方法】以2006年6月至2008年11月我院门诊和住院75例高血压患者为研究对象,对所有患者进行一般情况,睡眠呼吸和靶器官功能监测。入选患者经病史、体检、超声心动图和血生化检查,排除瓣膜性心脏病、先天性心脏病、中枢型睡眠呼吸暂停综合征、长期严重酗酒、有严重肺部疾病、肾脏、脑部疾病,且近期无服用辅助睡眠的药物。据多导睡眠监测,将受试者分为睡眠呼吸暂停综合征合并高血压组(实验组)和单纯高血压组(对照组)两组,其中实验组46例,男39例,女7例,年龄39-71(61.5±5.6)岁。对照组29例,男22例,女7例,年龄41-79,平均(62.8±5.8)岁。对两组人群分别进行靶器官功能指标监测(包括超声心动图监测心脏结构指标,颈部血管超声监测血管指标,头颅CT监测脑血管意外等等),所有实验数据采用SPSS13.0软件包处理分析,计量资料以均值±标准差((?)±s),表示组间定量资料比较采用t检验,组间定性资料比较采用X~2检验,p＜0.05为差异有统计学意义。自变量和因变量之间相关分析,双变量为计量资料,成正态分布,行线性相关分析。因变量为计量资料,自变量为等级资料,行等级相关分析.在存在相关关系时,r＞0.7,两变量有高度相关关系;0.7＞r＞0.4,两变量有中度相关关系;r＜0.4,两变量有低度相关关系。实验组内因变量与自变量成正态分布,进入水准为a=0.05,剔除水准为β=0.10,逐步进入多重线性回归分析(前进法),得出回归方程,确定危险因素。因变量为概率估算,自变量成正态分布,进入Logistic回归分析(后退法),进入水准为a=0.05,剔除水准为β=0.10,得出回归方程,确定危险因素。
【结果】总体比较实验组与对照组在性别、年龄、吸烟、饮酒、血压(收缩压/舒张压)、患高血压年限、体重指数(BMI)、腰臀比(WHR)、肾功能指标、总胆固醇(TC)、LDL-C、高密度脂蛋白HDL-C、甘油三酯(TG)、空腹血糖(FPG)、餐后血糖(PPBS)相比较均无统计学差异。而实验组患者颈围(Nc)、心脏结构指标,包括室间隔厚度(IVST)、左心室舒张末期内径(LVPWT)、左室肌重量(LVM)、左室肌重量指数(LVMI);血管结构指标:颈总动脉内径(CCAId)、颈总动脉内膜中层厚度(CCA-IMT)均高于对照组(p＜0.05);实验组患者的颈动脉内斑块(CAPS)人数、心律失常(Arrhythmia)人数及脑血管意外(CVA)人数显著高于对照组。相关分析提示:心脏结构指标与缺氧时间指标成中高度相关,与缺氧程度指标成中高度相关,与缺氧综合指标成中度相关;血管结构指标与缺氧时间指标、缺氧程度指标及缺氧综合指标皆成中度以上相关;脑血管意外与缺氧时间成高度相关,与缺氧程度成中度相关;心律失常发生率与缺氧时间及缺氧程度均成低度相关。经多重线性回归分析和Logistic回归分析示:OSAS合并高血压患者心脏结构的变化、心律失常的发生、外周血管的损害、脑血管意外的发生是综合因素作用的结果,而缺氧的程度和缺氧时间对OSAS合并高血压患者上述靶器官的损害有直接的相关性,是靶器官损害的危险因素。
【结论】睡眠呼吸暂停综合征合并高血压患者的靶器官损害较单纯高血压患者更为严重。且与患者长期间歇性缺氧和再氧合障碍紧密相关。亟需采取多种有效的干预措施加以控制,以减少高血压靶器官损害对人类的危害。本研究较全面报道了睡眠呼吸暂停综合症与高血压靶器官损害相关性,并确定缺氧时间和缺氧程度是睡眠呼吸暂停综合征合并高血压靶器官损害的危险因素。这些研究结果将为今后进一步研究高血压靶器官损害的相关因素提供有价值的信息。
【[Objective】The aim of this study is to investigate the degree of target organs' damages in patients with hypertension suffering obstructive sleep apnea syndrome (OSAS) and analyze the impact of risk factors on target organ damages so as to provide the valuable clinical information for prevention and treatment of these patients.
【Methods】75 outpatients and inpatients with hypertension were enrolled to investigate.The contents monitored included the general condition,sleep apnea and target organ function.The disease history,physical examination,echocardiography and biochemical examination were performed in all patients.The exclusion criteria were as follow:valvular heart diseases,congenital heart diseases,central sleep apnea syndrome,a serious long-term alcohol drunk,serious lung diseases,kidney diseases, brain diseases and the recent use of drugs for sleep.According to polysomnography monitoring,the patients were divided into 2 groups.One is experimental group,i.e., sleep apnea syndrome with hypertension including 46 cases,males 39 cases,females 7,age(61.5±5.6) years,and the other is control group,i.e.,with hypertension including 29 cases,males 22,females 7,age(62.8±5.8) years.The target organ functions were monitored in all patients.All quantitative data were expressed as x±s and analyzed by SPSS13.0 statistical package.Student t-test was applied in inter-group comparison of quantitative data and chi-square test was employed in inter-group comparison of qualitative data.P＜0.05 is considered statistically significant.The correlation analysis was performed between independent variable and dependent ariable.Linear correlation analysis was used when data were normal distribution and orderly variance,on the contrary,the rank correlation analysis were performed.When correlational coefficient r＞0.7,highly correlational relation between two variables was considered;when 0.7＞r＞0.4,moderate correlational relation between two variables,when r＜0.4,low correlation relation between two variables was.When the internal variables of experimental group were the normal distribution, we used the multiple linear regression analysis step by step(forward) and produced a regression equation,and then the risk factors were determined,with the entering standard a = 0.05 and the-excluded standardβ= 0.10.When the dependent variable was probability estimates and the independent variable was normal distribution,we applied the Logistic regression analysis(backward),and produced a regression equation,then the risk factors were determined,with the entering standard a = 0.05 and the excluded standardβ=0.10.
【Result】Generally in terms of gender,age,smoking,drinking,blood press (SBP / DBP),duration of suffering from high blood pressure,body mass index(BMI), waist-hip ratio(WHR),renal function,total cholesterol(TC),LDL-C,HDL-cholestorol (HDL-C),triglyceride(TG ),fast plasma glucose(FPG),postprandial blood sugar (PPBS),comparisons between the experimental group and control group were not statistically difference.But,neck circumference,patients' the heart structure index, including interventricular septal thickness(IVST),left ventricular posterior wall thickness(LVPWT),left ventricle myocardium(LVM),left ventricle myocardium index(LVMI);Blood vessel structure index:common carotid artery internal dimension(CCAId),common carotid artery intima-media thickness(CCA-IMT) in experimental group were higher than those in control group(p＜0.05),patients' carotid artery plaque score(CAPS) number,arrhythmia cordis number and cerebral vascular accident(CVA) number in experimental group were notably higher than those in control group.By correlation analysis,it was showed that the heart of the structure indicators were correlated with indicators of hypoxic-time moderately and highly,they were also correlated with indicators of degree of hypoxia moderately and highly and correlated with comprehensive indicators of hypoxia moderately,the indicators of vascular structural indicators of hypoxia beyond moderate.Cerebral vascular accident was a highly correlated with time indicators of hypoxia and was a moderately correlated with the degree indicators of hypoxia,arrhythmia incidence was correlated with time indicators and degree indicators of hypoxia with low-grade. By multiple linear regression analysis and Logistic regression analysis,it was showed that the changes in the structure of the heart,arrhythmia,peripheral vascular damage, CVA of OSAS patients with hypertension was the result of a combination of factors, and the degree and time of hypoxia have a direct correlation with the target organ damage in patients who were OSAS with hypertension and they were risk factors of the target organ damage of patients who were OSAS with hypertension and correlated with time indicators,degree indicators and comprehensive of hypoxia.
【Conclusion】The sleep apnea syndrome patients with hypertension had more serious damage degree on target organ damage than the only hypertension ones,and the damage degree is closely related to long-term hypoxia and disturbance of re-oxygenation.So.there is a urgent need to adopt a variety of effective interventions to control and reduce the hazards brought by target organ damages due to hypertension. This is the allround report about the relevance between sleep apnea syndrome and hypertension target organ damage.The results of these studies will provide valuable information for further study on target organ damage in patients with hypertension.
【方法】以2006年6月至2008年11月我院门诊和住院75例高血压患者为研究对象,对所有患者进行一般情况,睡眠呼吸和靶器官功能监测。入选患者经病史、体检、超声心动图和血生化检查,排除瓣膜性心脏病、先天性心脏病、中枢型睡眠呼吸暂停综合征、长期严重酗酒、有严重肺部疾病、肾脏、脑部疾病,且近期无服用辅助睡眠的药物。据多导睡眠监测,将受试者分为睡眠呼吸暂停综合征合并高血压组(实验组)和单纯高血压组(对照组)两组,其中实验组46例,男39例,女7例,年龄39-71(61.5±5.6)岁。对照组29例,男22例,女7例,年龄41-79,平均(62.8±5.8)岁。对两组人群分别进行靶器官功能指标监测(包括超声心动图监测心脏结构指标,颈部血管超声监测血管指标,头颅CT监测脑血管意外等等),所有实验数据采用SPSS13.0软件包处理分析,计量资料以均值±标准差((?)±s),表示组间定量资料比较采用t检验,组间定性资料比较采用X~2检验,p＜0.05为差异有统计学意义。自变量和因变量之间相关分析,双变量为计量资料,成正态分布,行线性相关分析。因变量为计量资料,自变量为等级资料,行等级相关分析.在存在相关关系时,r＞0.7,两变量有高度相关关系;0.7＞r＞0.4,两变量有中度相关关系;r＜0.4,两变量有低度相关关系。实验组内因变量与自变量成正态分布,进入水准为a=0.05,剔除水准为β=0.10,逐步进入多重线性回归分析(前进法),得出回归方程,确定危险因素。因变量为概率估算,自变量成正态分布,进入Logistic回归分析(后退法),进入水准为a=0.05,剔除水准为β=0.10,得出回归方程,确定危险因素。
【结果】总体比较实验组与对照组在性别、年龄、吸烟、饮酒、血压(收缩压/舒张压)、患高血压年限、体重指数(BMI)、腰臀比(WHR)、肾功能指标、总胆固醇(TC)、LDL-C、高密度脂蛋白HDL-C、甘油三酯(TG)、空腹血糖(FPG)、餐后血糖(PPBS)相比较均无统计学差异。而实验组患者颈围(Nc)、心脏结构指标,包括室间隔厚度(IVST)、左心室舒张末期内径(LVPWT)、左室肌重量(LVM)、左室肌重量指数(LVMI);血管结构指标:颈总动脉内径(CCAId)、颈总动脉内膜中层厚度(CCA-IMT)均高于对照组(p＜0.05);实验组患者的颈动脉内斑块(CAPS)人数、心律失常(Arrhythmia)人数及脑血管意外(CVA)人数显著高于对照组。相关分析提示:心脏结构指标与缺氧时间指标成中高度相关,与缺氧程度指标成中高度相关,与缺氧综合指标成中度相关;血管结构指标与缺氧时间指标、缺氧程度指标及缺氧综合指标皆成中度以上相关;脑血管意外与缺氧时间成高度相关,与缺氧程度成中度相关;心律失常发生率与缺氧时间及缺氧程度均成低度相关。经多重线性回归分析和Logistic回归分析示:OSAS合并高血压患者心脏结构的变化、心律失常的发生、外周血管的损害、脑血管意外的发生是综合因素作用的结果,而缺氧的程度和缺氧时间对OSAS合并高血压患者上述靶器官的损害有直接的相关性,是靶器官损害的危险因素。
【结论】睡眠呼吸暂停综合征合并高血压患者的靶器官损害较单纯高血压患者更为严重。且与患者长期间歇性缺氧和再氧合障碍紧密相关。亟需采取多种有效的干预措施加以控制,以减少高血压靶器官损害对人类的危害。本研究较全面报道了睡眠呼吸暂停综合症与高血压靶器官损害相关性,并确定缺氧时间和缺氧程度是睡眠呼吸暂停综合征合并高血压靶器官损害的危险因素。这些研究结果将为今后进一步研究高血压靶器官损害的相关因素提供有价值的信息。
【[Objective】The aim of this study is to investigate the degree of target organs' damages in patients with hypertension suffering obstructive sleep apnea syndrome (OSAS) and analyze the impact of risk factors on target organ damages so as to provide the valuable clinical information for prevention and treatment of these patients.
【Methods】75 outpatients and inpatients with hypertension were enrolled to investigate.The contents monitored included the general condition,sleep apnea and target organ function.The disease history,physical examination,echocardiography and biochemical examination were performed in all patients.The exclusion criteria were as follow:valvular heart diseases,congenital heart diseases,central sleep apnea syndrome,a serious long-term alcohol drunk,serious lung diseases,kidney diseases, brain diseases and the recent use of drugs for sleep.According to polysomnography monitoring,the patients were divided into 2 groups.One is experimental group,i.e., sleep apnea syndrome with hypertension including 46 cases,males 39 cases,females 7,age(61.5±5.6) years,and the other is control group,i.e.,with hypertension including 29 cases,males 22,females 7,age(62.8±5.8) years.The target organ functions were monitored in all patients.All quantitative data were expressed as x±s and analyzed by SPSS13.0 statistical package.Student t-test was applied in inter-group comparison of quantitative data and chi-square test was employed in inter-group comparison of qualitative data.P＜0.05 is considered statistically significant.The correlation analysis was performed between independent variable and dependent ariable.Linear correlation analysis was used when data were normal distribution and orderly variance,on the contrary,the rank correlation analysis were performed.When correlational coefficient r＞0.7,highly correlational relation between two variables was considered;when 0.7＞r＞0.4,moderate correlational relation between two variables,when r＜0.4,low correlation relation between two variables was.When the internal variables of experimental group were the normal distribution, we used the multiple linear regression analysis step by step(forward) and produced a regression equation,and then the risk factors were determined,with the entering standard a = 0.05 and the-excluded standardβ= 0.10.When the dependent variable was probability estimates and the independent variable was normal distribution,we applied the Logistic regression analysis(backward),and produced a regression equation,then the risk factors were determined,with the entering standard a = 0.05 and the excluded standardβ=0.10.
【Result】Generally in terms of gender,age,smoking,drinking,blood press (SBP / DBP),duration of suffering from high blood pressure,body mass index(BMI), waist-hip ratio(WHR),renal function,total cholesterol(TC),LDL-C,HDL-cholestorol (HDL-C),triglyceride(TG ),fast plasma glucose(FPG),postprandial blood sugar (PPBS),comparisons between the experimental group and control group were not statistically difference.But,neck circumference,patients' the heart structure index, including interventricular septal thickness(IVST),left ventricular posterior wall thickness(LVPWT),left ventricle myocardium(LVM),left ventricle myocardium index(LVMI);Blood vessel structure index:common carotid artery internal dimension(CCAId),common carotid artery intima-media thickness(CCA-IMT) in experimental group were higher than those in control group(p＜0.05),patients' carotid artery plaque score(CAPS) number,arrhythmia cordis number and cerebral vascular accident(CVA) number in experimental group were notably higher than those in control group.By correlation analysis,it was showed that the heart of the structure indicators were correlated with indicators of hypoxic-time moderately and highly,they were also correlated with indicators of degree of hypoxia moderately and highly and correlated with comprehensive indicators of hypoxia moderately,the indicators of vascular structural indicators of hypoxia beyond moderate.Cerebral vascular accident was a highly correlated with time indicators of hypoxia and was a moderately correlated with the degree indicators of hypoxia,arrhythmia incidence was correlated with time indicators and degree indicators of hypoxia with low-grade. By multiple linear regression analysis and Logistic regression analysis,it was showed that the changes in the structure of the heart,arrhythmia,peripheral vascular damage, CVA of OSAS patients with hypertension was the result of a combination of factors, and the degree and time of hypoxia have a direct correlation with the target organ damage in patients who were OSAS with hypertension and they were risk factors of the target organ damage of patients who were OSAS with hypertension and correlated with time indicators,degree indicators and comprehensive of hypoxia.
【Conclusion】The sleep apnea syndrome patients with hypertension had more serious damage degree on target organ damage than the only hypertension ones,and the damage degree is closely related to long-term hypoxia and disturbance of re-oxygenation.So.there is a urgent need to adopt a variety of effective interventions to control and reduce the hazards brought by target organ damages due to hypertension. This is the allround report about the relevance between sleep apnea syndrome and hypertension target organ damage.The results of these studies will provide valuable information for further study on target organ damage in patients with hypertension.
引文
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34.R.C.Basner,Continuous positive airway pressure for obstructive sleep apnea,N Engl J Med 356(2007),pp.862-865
35.V.K.Somers,M.E.Dyken,A.L.Mark and F.M.Abboud,Sympathetic-nerve activity during sleep in normal subjects,N Engl J Med 328(1993),pp.303-307
36.V.K.Somers,M.E.Dyken,M.P.Clary and F.M.Abboud,Sympathetic neural mechanisms in obstructive sleep apnea.J Clin Invest 96(1995),pp.1897-1904
37.D.Levy,M.G.Larson,R.S.Vasan,W.B.Kannel and K.K.Ho,The progression from hypertension to congestive heart failure,JAMA 275(1996),pp.1557-1562
38.Gami AS,Friedman PA,ChungMK,et al.Therapy Insight:interactions between atrial fibrillation and obstructive sleep apnea.Nat Clin Pract CardiovascMed,2005,2:14514-14519.
39.陈宝元.阻塞性睡眠呼吸暂停低通气综合征与心血管疾病.临床内科杂志 2006.4:228-230
40.Tilkian AG,Goilleminault Schroder JS,et al.Sleep-induce apnea syndrome.Prevalence of cardiac arrhythmias and their reversal after tracheostomy.Am J Med,1977,63:348-358
41.Becker HF,Koehler U,Stammitz A,et al.Heart block in patient with sleep apnea.Thorx,1998.53 suppl 3:S29-S32
42.Ohayon MM,Guileminault C,Prist RC et al,Is sleep-disordred breathing an independent risk factor for hypertension in the general population? J Psychosom Res,2000,48:593
43.J.Harbison,G.J.Gibson,D.Birchall,et,al,White matter disease and sleep-disordered breathing after acute stroke,Neurology 14(2003),pp,959-963
44.A.S.Gami,D.O.Hodge,R.M.Herges,E.J.Olson/et,al.Obstruction sleep apnea,obesity,and the risk of incident atrial fibrillationJ.Am.Coll Cardiol 49(2007),pp565-571
45.Venugopal SK,Devaraj S,Yuhanna I,et al.Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells[J].Circulation,2002,106:1439-41.
46.Garcia RF,Racionero MA,Pino JM,et al.Sleep apnea and hypertension.Chest,2000,117:1417-1425
47.Duchna HW,Goilleminault C.stoohs RA,et al,Obstructive sleep apnea syndrome;a cardiovascular risk factor?Z Kardiol,2001,90:568-575
48.P.Hanly,Sleep apnea and daytime sleepiness in end-stage renal disease,Semin Dial 17(2004),pp.109-144
49.P.J.Hanly,T.W.Millar,D.G.Steljec,R.Baert,et al.The effect of oxygen on respiration and sleep in patient with congestive heart failure,Ann intern Med 111(1989),pp.777-782
1.The sixth report of Jolt National Committee on prevention,detection,evaluation,and treatment of high blood pressure[R].Arch.Intern.Med 1997,157:2413-2446
2.Chobanian AV,Bakris GL,Black HR,et al.The seventh report of Joit National Committee on prevention,detection,evaluation,and treatment of high blood pressure:the JNC7report[R].JAMA,2003,289:2560-2572
3.Bixler EO,Vgontzas AN,Lin HM et al.Association of hypertension and sleep-disordered breathing[J].Arch.Intern.Med.2000,160(15):2289-2295
4.Ohayon MM,Guileminault C,Prist RC et al,Is sleep-disordred breathing an independent risk factor for hypertension in the general population[J]? J Psychosom Res,2000,48:593
5.Franciso Garcia-Rio,Miguel A,Jose M,et al.Sleep apnea and hypertension[J].Chest,2000,117:1417-25
6.Loredo JS,Ancoli-lsrael S,Dimsdale JE.Sleep quality and blood pressure dipping in obstructive sleep apnea[J].Am J Hypertension,2001,14:887-892
7.何权瀛.重视阻塞性睡眠呼吸暂停低通气综合症靶器官损害的防治研究.中华结核和呼吸杂志[J].2005,28(6):362-363
8.Alonso-fernandez A,Garcia-Rio F,Racionero MA,et al.Cardiac rhythm disturbances and ST-segment depression episodes in patients with obstructive sleep apnea-hypopnea syndrome and its mechanisms[J].Chest,2005,127:15-22.
9.J.P.Baguet,K Narkiewicz,J.M Mailion.European society of hypertension scientific newsletter[J].Jourmal of Hypertension,2006,24:205-210
10.Roberto.Munoz,MD.Joaquin,Duran-Cantolla,MD;et al.Severe sleep apnea and risk of ischemic stroke in the elderly[J].Stroke,2006,37:2317-2321
11.Moller DS,Lind P,Strunge B,Pedersen EB.Abnormalvasoactive hormones and 24-hour blood pressure in ob-structive sleep apnea[J].Am J Hypertens,2003,16:274-80
12.Aldosterone excretion among subjects with resistant hypertension and symptoms of sleep apnea[J].Chest,2004,125:112-7
13.Krieger J,Benxoni D,Sforza E et al.Urinary excretion of prostanoids during sleep in obstructive sleep apnea patients[J].Clin Exp Pharmacol physiol,1991,18(8):551
14.Ohkita M,Takaoka M,Sugii M et al.The role of nuclear factor-nB in the regulation of endothelin-1 production by nitric oxideEuropean[J].Journal of Pharmacology,2003,472:159-164
15.Palma BD,Gabriel A J,Bignotto M,et al.Paradoxical sleep deprivation increases plasma endothelin levels[J].Braz J Med Biol Res,2002,35:75-79.
16.Shamsuzzaman AS,Winnicki M,Lanfranchi P et al.Elevated C-reactive protein in patient with obstructive sleep apnea[J].circulation,2002,105:2462-2464
17.Libby P,Ridker PM,Maseri A.Inflammation and atherosclerosis[J].Circulation,2002,105:1135-1143
18.Venugopal SK,Devaraj S,Yuhanna I,et al.Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells[J].Circulation,2002,106:1439-41.
19.Kisilevsky R,Tarn SP.Acute phase serum amyloid A,cholesterol metabolism,and cardiovascular disease[J].Pediatr Pathol Mol Med,2002,21:291-305.
20.Svatikova A,Wolk R,Shamsuzzaman AS,et al.Serum amyloid A in obstructive sleep apnea[J].Circulation,2003;108:1451-4.
21.Higashi Y,Sasaki S,Nakagawa K,et al.Effect of obesity on endothelium-dependent,nitric oxide-mediated vasodilation in nor-motensive individuals and patients with essential hypertension[J].Am J Hypertens 2001,14:103 8-45.
22.Kato M,Roberts-Thomson P,Phillips BG,et al.Impairment of endothe lium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea[J].Circulation,2000,102:2607-10.
23.Kraiczi H,Hedner J,Peker Y,Carlson J.Increased vaso-constrictor sensitivity in obstructive sleep apnea[J].J Appl Physiol,2000,89:493-8
24.Kathleen A.Ferguson,John A Fleetham.Consequences of sleep disordered breathing[J].Thorax,1995,50:998-1004
25.Ringler J,Baxner R,Shannon R,et al.Hypoxemia alone dose not explain blood pressure elevatins after obstructive apneas[J].J Appl Physiol,1990,69:2143-48
26.Glesson K,Zwillich CW,White DP.The influence of increasing ventilatory sffort in sleep apnea on arousal from sleep[J].Am Rev Respir Dis,1990,142:295-300
27.Svatikova A,Wolk R,Gami AS,et al.Interaction between obstructive sleep apnea.and the metabolic syndrome[J].Curr Diab Rep,2005,5:53-58
2.Coccagna G,Montovani M,Brignani F,et al.Continuous recording of the pulmonary and systemic arterial pressure during sleep in syndrome of hypertension with periodic breathing.Bull Eur Physiopathol Respir 1972;8:1159-72
3.Williams A.D,Houston D,Finberg C,et al.sleep apnea syndrome and essential hyprtension.Am J Cardiol 1985;551019-1022
4.The sixth report of Joit National Committee on prevention,detection,evaluation,and treatment of high blood pressure.Arch.Intern.Med 1997,157:2413-2446
5.Chobanian AV,Bakris GL,Black HR,et al.The seventh report of Joit National Committee on prevention,detection,evaluation,and treatment of high blood pressure:the JNC7 report.JAMA,2003,289:2560-2572
6.Bixler EO,Vgontzas AN,Lin HM et al.Association of hypertension and sleep-disordered breathing.Arch.Intern.Med.160(15),2289-2295(2000)
7.Ohayon MM,Guileminault C,Prist RC et al,ls sleep-disordred breathing an independent risk factor for hypertension in the general population? J Psychosom Res,2000,48:593
8.Franciso Garcia-Rio,Miguel A,Jose M,et al。Sleep apnea and hypertension。Chest 2000;117:1417-25
9.Robert J O Davies,Cardiovascular aspects of obstructive sleep apnea and their relevance to the assessment of the efficacy of nasal continuous positive airway pressure therepy.Thorax,1998,53:416-418
10.Loredo JS,Ancoli-lsrael S,Dimsdale JE.Sleep quality and blood pressure dipping in obstructive sleep apnea..Am J Hypertension 2001;14:887-892
11.Yehonatan Sharbi,Yaron Dagan,Ehud Grossman.Sleep apnea as a risk factor for hypertension Current opinion in Nephrology and Hypertension.2004;13:359-364
12.J.P.Baguet,K Narkiewicz,J.M Mallion.European society of hypertension scientific newsletter.Jourmal of Hypertension 2006,24:205-210
13.Roberto.Munoz,MD:Joaquin Duran-Cantolla,MD;et al.Severe sleep apnea and risk of ischemic stroke in the elderly.Stroke.2006,37:2317-2321
14.Morgan BG,Crabtree DC,Palta M,et al.Combined hypoxia and hypetcapnia evokes longlasting sympathetic activation in humans.J Appl Physiol 1995;79;205-213
15.Ferrario CM,Richmond RS,Smith R et al.Renirr angiotensin system as a therapeutic target in managing atherosclerosis.AmJ Ther,2004,11(1):44
16.Moiler DS,Lind P,Strunge B,Pedersen EB.Abnormalvasoactive hormones and 24-hour blood pressure in ob-structive sleep apnea.Am J Hypertens 2003;16:274-80
17.Krieger J,Benxoni D,Sforza E et al.Urinary excretion of prostanoids during sleep in obstructive sleep apnea patients.Clin Exp Pharmacol physiol,1991,18(8):551
18.Khraibi AA,Heublein DM,Knox FG,et al.Increase Plasma level of endothelin-1 in the Okamoto spontaneously hypertensive rat.Mayo Clin Proc 1993;68:42-46
19.李延忠 张万荣,王延础等.黏附分子在阻塞性睡眠呼吸暂停低通气综合症合并高血压发病中的作用.中华结核和呼吸杂志,2004,27(8):511
20.Hartmann G,Tschop M,Fischer R,Bidlingmaier C,Riepl R,Tschop K et al.High altitude increases circulating interleukin-6,interleukin-1 receptor antagonist and C-reactive protein.Cytokine 2000;12:246-52.
21.Vgontzas AN,Papanicolaou DA,Bixler EO,Lotsikas A,Zachman K,Kales Aet al.Circadian interleukin-6 secretion and quantity and depth of sleep.J Clin Endocrinol Metab 1999;84:2603-7.
22.Shamsuzzaman AS,Winnicki M,Lanfranchi P et al.Elevated C-reactive protein in patient with obstructive sleep apnea.circulation 2002;105:2462-2464
23.Libby P,Ridker PM,Maseri A.Inflammation and atherosclerosis Circulation,2002,105:1135-1143
24.Kisilevsky R,Tam SP.Acute phase serum amyloid A,cholesterol metabolism,and cardiovascular disease Pediatr Pathol Mol Med 2002;21:291-305.
25.Svatikova A,Wolk R,Shamsuzzaman AS,Kara T,Olson E J,Somers VK.Serum amyloid A in obstructive sleep apnea.Circulation 2003;108:1451-4.
26.Parrinello G,Scaglione R,Pinto A,Corrao S,Cecala M,Di Silvestre G et al.Central obesity and hypertension:the role of plasma endothelin.Am J Hypertens 1996;9:1186-91.
27.Higashi Y,Sasaki S,Nakagawa K,Matsuura H,Chayama K,Oshima T.Effect of obesity on endothelium-dependent,nitric oxide-mediated vasodilation in nor-motensive individuals and patients with essential hypertension.Am J Hypertens 2001;14:1038-45.
28.Kato M,Roberts-Thomson P,Phillips BG,Haynes WG,Winnicki M,Accurso Ⅴ et al.Impairment of endothe lium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea.Circulation2000;102:2607-10.
29.Kathleen A.Ferguson,John A Fleetham.Consequences of sleep disordered breathing Thorax 1995;50:998-1004
30.Ringler J,Baxner R,Shannon R,et al.Hypoxemia alone dose not explain blood pressure elevatins after obstructive apneas.J Appl Physiol 1990;69:2143-48
31.Glesson K,Zwillich CW,White DP.The influence of increasing ventilatory sffort in sleep apnea on arousal from sleep.Am Rev Respir Dis 1990;142:295-300
32.Svatikova A,Wolk,R,Gami AS,et al.Interaction between obstructive sleep apnea.and the metabolic syndrome.Curr Diab Rep,2005,5:53-58
33.R.J.Schwab,M.Pasirstein,R.Pierson,A.Mackley,R.Hachadoorian,R.Arens,G.Maislin and A.I.Pack,Identification of upper airway anatomic risk factors for obstructive sleep apnea with volumetric magnetc resonance imaging,Am J Respir Crit Care Med 168(2003),pp522-530
34.R.C.Basner,Continuous positive airway pressure for obstructive sleep apnea,N Engl J Med 356(2007),pp.862-865
35.V.K.Somers,M.E.Dyken,A.L.Mark and F.M.Abboud,Sympathetic-nerve activity during sleep in normal subjects,N Engl J Med 328(1993),pp.303-307
36.V.K.Somers,M.E.Dyken,M.P.Clary and F.M.Abboud,Sympathetic neural mechanisms in obstructive sleep apnea.J Clin Invest 96(1995),pp.1897-1904
37.D.Levy,M.G.Larson,R.S.Vasan,W.B.Kannel and K.K.Ho,The progression from hypertension to congestive heart failure,JAMA 275(1996),pp.1557-1562
38.Gami AS,Friedman PA,ChungMK,et al.Therapy Insight:interactions between atrial fibrillation and obstructive sleep apnea.Nat Clin Pract CardiovascMed,2005,2:14514-14519.
39.陈宝元.阻塞性睡眠呼吸暂停低通气综合征与心血管疾病.临床内科杂志 2006.4:228-230
40.Tilkian AG,Goilleminault Schroder JS,et al.Sleep-induce apnea syndrome.Prevalence of cardiac arrhythmias and their reversal after tracheostomy.Am J Med,1977,63:348-358
41.Becker HF,Koehler U,Stammitz A,et al.Heart block in patient with sleep apnea.Thorx,1998.53 suppl 3:S29-S32
42.Ohayon MM,Guileminault C,Prist RC et al,Is sleep-disordred breathing an independent risk factor for hypertension in the general population? J Psychosom Res,2000,48:593
43.J.Harbison,G.J.Gibson,D.Birchall,et,al,White matter disease and sleep-disordered breathing after acute stroke,Neurology 14(2003),pp,959-963
44.A.S.Gami,D.O.Hodge,R.M.Herges,E.J.Olson/et,al.Obstruction sleep apnea,obesity,and the risk of incident atrial fibrillationJ.Am.Coll Cardiol 49(2007),pp565-571
45.Venugopal SK,Devaraj S,Yuhanna I,et al.Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells[J].Circulation,2002,106:1439-41.
46.Garcia RF,Racionero MA,Pino JM,et al.Sleep apnea and hypertension.Chest,2000,117:1417-1425
47.Duchna HW,Goilleminault C.stoohs RA,et al,Obstructive sleep apnea syndrome;a cardiovascular risk factor?Z Kardiol,2001,90:568-575
48.P.Hanly,Sleep apnea and daytime sleepiness in end-stage renal disease,Semin Dial 17(2004),pp.109-144
49.P.J.Hanly,T.W.Millar,D.G.Steljec,R.Baert,et al.The effect of oxygen on respiration and sleep in patient with congestive heart failure,Ann intern Med 111(1989),pp.777-782
1.The sixth report of Jolt National Committee on prevention,detection,evaluation,and treatment of high blood pressure[R].Arch.Intern.Med 1997,157:2413-2446
2.Chobanian AV,Bakris GL,Black HR,et al.The seventh report of Joit National Committee on prevention,detection,evaluation,and treatment of high blood pressure:the JNC7report[R].JAMA,2003,289:2560-2572
3.Bixler EO,Vgontzas AN,Lin HM et al.Association of hypertension and sleep-disordered breathing[J].Arch.Intern.Med.2000,160(15):2289-2295
4.Ohayon MM,Guileminault C,Prist RC et al,Is sleep-disordred breathing an independent risk factor for hypertension in the general population[J]? J Psychosom Res,2000,48:593
5.Franciso Garcia-Rio,Miguel A,Jose M,et al.Sleep apnea and hypertension[J].Chest,2000,117:1417-25
6.Loredo JS,Ancoli-lsrael S,Dimsdale JE.Sleep quality and blood pressure dipping in obstructive sleep apnea[J].Am J Hypertension,2001,14:887-892
7.何权瀛.重视阻塞性睡眠呼吸暂停低通气综合症靶器官损害的防治研究.中华结核和呼吸杂志[J].2005,28(6):362-363
8.Alonso-fernandez A,Garcia-Rio F,Racionero MA,et al.Cardiac rhythm disturbances and ST-segment depression episodes in patients with obstructive sleep apnea-hypopnea syndrome and its mechanisms[J].Chest,2005,127:15-22.
9.J.P.Baguet,K Narkiewicz,J.M Mailion.European society of hypertension scientific newsletter[J].Jourmal of Hypertension,2006,24:205-210
10.Roberto.Munoz,MD.Joaquin,Duran-Cantolla,MD;et al.Severe sleep apnea and risk of ischemic stroke in the elderly[J].Stroke,2006,37:2317-2321
11.Moller DS,Lind P,Strunge B,Pedersen EB.Abnormalvasoactive hormones and 24-hour blood pressure in ob-structive sleep apnea[J].Am J Hypertens,2003,16:274-80
12.Aldosterone excretion among subjects with resistant hypertension and symptoms of sleep apnea[J].Chest,2004,125:112-7
13.Krieger J,Benxoni D,Sforza E et al.Urinary excretion of prostanoids during sleep in obstructive sleep apnea patients[J].Clin Exp Pharmacol physiol,1991,18(8):551
14.Ohkita M,Takaoka M,Sugii M et al.The role of nuclear factor-nB in the regulation of endothelin-1 production by nitric oxideEuropean[J].Journal of Pharmacology,2003,472:159-164
15.Palma BD,Gabriel A J,Bignotto M,et al.Paradoxical sleep deprivation increases plasma endothelin levels[J].Braz J Med Biol Res,2002,35:75-79.
16.Shamsuzzaman AS,Winnicki M,Lanfranchi P et al.Elevated C-reactive protein in patient with obstructive sleep apnea[J].circulation,2002,105:2462-2464
17.Libby P,Ridker PM,Maseri A.Inflammation and atherosclerosis[J].Circulation,2002,105:1135-1143
18.Venugopal SK,Devaraj S,Yuhanna I,et al.Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells[J].Circulation,2002,106:1439-41.
19.Kisilevsky R,Tarn SP.Acute phase serum amyloid A,cholesterol metabolism,and cardiovascular disease[J].Pediatr Pathol Mol Med,2002,21:291-305.
20.Svatikova A,Wolk R,Shamsuzzaman AS,et al.Serum amyloid A in obstructive sleep apnea[J].Circulation,2003;108:1451-4.
21.Higashi Y,Sasaki S,Nakagawa K,et al.Effect of obesity on endothelium-dependent,nitric oxide-mediated vasodilation in nor-motensive individuals and patients with essential hypertension[J].Am J Hypertens 2001,14:103 8-45.
22.Kato M,Roberts-Thomson P,Phillips BG,et al.Impairment of endothe lium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea[J].Circulation,2000,102:2607-10.
23.Kraiczi H,Hedner J,Peker Y,Carlson J.Increased vaso-constrictor sensitivity in obstructive sleep apnea[J].J Appl Physiol,2000,89:493-8
24.Kathleen A.Ferguson,John A Fleetham.Consequences of sleep disordered breathing[J].Thorax,1995,50:998-1004
25.Ringler J,Baxner R,Shannon R,et al.Hypoxemia alone dose not explain blood pressure elevatins after obstructive apneas[J].J Appl Physiol,1990,69:2143-48
26.Glesson K,Zwillich CW,White DP.The influence of increasing ventilatory sffort in sleep apnea on arousal from sleep[J].Am Rev Respir Dis,1990,142:295-300
27.Svatikova A,Wolk R,Gami AS,et al.Interaction between obstructive sleep apnea.and the metabolic syndrome[J].Curr Diab Rep,2005,5:53-58