老年高血压病并发阻塞性睡眠呼吸暂停综合征患者血压特点及与炎症因子的关系

目的研究并发中重度阻塞性睡眠呼吸暂停综合征（obstructive sleep apnea syndrome,OSAS）的老年高血压患者血压的变化情况及炎症因子的水平,从而揭示此类患者的疾病特点。方法将60例年龄大于60岁的研究对象根据诊所血压、24 h动态血压和多导睡眠图监测结果分为单纯高血压病组（n=30）和并发OSAS组（高血压病并发中重度睡眠呼吸暂停综合征,n=30）。用ELISA法测定白介素-6（IL-6）、sCD40L、超敏C反应蛋白（hs-CRP）、可溶性细胞间黏附分子1（ICAM-1）及血管细胞黏附分子1（VCAM-1）的浓度。结果①并发OSAS组中非杓型血压的发生率为67%,明显高于单纯高血压组的发生率37%（P<0.05）。②并发OSAS组24 h、白天、夜间平均脉压（mean arterial blood pressure,MAP）分别为（51±13）mmHg（1 mmHg=0.133 kPa）,（50±13）mmHg和（51±17）mmHg均明显高于单纯高血压组（45±7）mmHg,（46±8）mmHg和（44±6）mmHg,并有统计学意义（P<0.05）。③并发OSAS组的IL-6、sCD40L、hs-CRP、ICAM-1、VCAM-1浓度明显高于单纯高血压组。④并发OSAS组的hs-CRP、ICAM-1、VCAM-1浓度变化与呼吸紊乱指数、睡眠血氧下降程度正相关（r=0.852,P<0.05）。hs-CRP与MAP呈正相关（P<0.01）,ICAM-1与夜间血压下降率呈负相关（P<0.05）。结论中重度睡眠呼吸暂停影响老年人血压昼夜节律的变化,同时对脉压产生明显影响,炎症反应也明显加重。     

阻塞性睡眠呼吸暂停对高血压患者血管内皮影响研究

目的 回顾性分析高血压合并阻塞性睡眠呼吸暂停综合征(OSAS)患者的预后及影响因素.方法 对2004年1月至2007年10月江苏省省级机关医院确诊的高血压病患者共168例,通过电话和门诊随访,随访时间中位数35个月.根据多导睡眠仪监测结果 分为:高血压合并OSAS(OSAS+)组和高血压不合并OSAS(OSAS-)组.所有患者均通过彩色多普勒超声测定肱动脉血流介导的舒张功能(FMD),并测定与高血压预后相关的血清生化指标.随访患者心血管死亡、心绞痛或心肌梗死、脑卒中等事件.结果 OSAS+组患者血清超敏C反应蛋白(hsCRP)水平高于OSAS-组,(2.49±2.65)mmol/Lvs(1.73±1.76)mmol/L(P<0.05),FMD值低于OSAS-组,(6.20±3.40)%vs(8.39±3.86)0A(P<0.05).OSAS+组患者总事件发生率高于OSAS-组(28.8%A vs 13.7%,P=0.016).Logistic多因素回归分析显示:FMD主要损伤因素排名首位是OSAS(OR=2.89,P=0.003),其次是血清hsCRP(OR=1.23,P=0.044);FMD、血清hsCRP及尿酸成为高血压患者预后的影响因子(OR=1.7,1.7,3.5,P=0.03,0.00,0.01).结论 OSAS影响高血压患者血管内皮功能,使总的事件(心脑血管原因导致的死亡、心绞痛或心肌梗死和脑卒中)发生率增加.OSAS可能主要通过损伤血管内皮功能间接影响高血压患者的预后.     

男性高血压合并阻塞性睡眠暂停综合征患者动脉弹性与血浆肾素-血管紧张素-醛固酮活性改变的研究

目的:了解合并阻塞性睡眠呼吸暂停综合征的中年男性高血压病患者,动脉弹性改变和血浆肾素-血管紧张素-醛固酮活性改变,探讨两者的相互关系,从而对合并睡眠暂停的高血压病患者的针对性治疗提供理论依据。方法:选择中年男性高血压病住院患者276例,进行多导睡眠监测,根据睡眠呼吸暂停低通气指数(AHI)分为原发性高血压(EH)组(n=101)和原发性高血压合并阻塞性睡眠呼吸暂停综合征(EH+OSAS)组(n=175),两组分别测定晨起卧位肾素活性、血管紧张素Ⅱ(AngⅡ)、血浆醛固酮(Ald)、肱-踝动脉脉搏波传导速度(BaPWV),以及24h动态血压监测,观察两组患者血压、心率、肾素-血管紧张素-醛固酮活性及BaPWV的变化。结果:1EH+OSAS组患者血浆肾素活性[EH+OSAS:1.44(0.51,3.27)比EH:1.83(0.32,4.56)μg/L]和血管紧张素Ⅱ[EH+OSAS:54.99(45.07,71.61)比EH:58.89(50.16,65.52)ng/L]均低于EH组(P0.05),差异有统计学意义;EH+OSAS组患者血浆醛固酮[EH+OSAS:0.115(0.096,0.147)比EH:0.106(0.094,0.140)μg/L]高于EH组,差异有统计学意义(P0.05)。2EH+OSAS组患者左右BaPWV均高于EH组[左BaPWV:EH+OSAS:1 520(1 341,1 667)比EH:1 426(1 284,1 614)cm/s,P0.05;右BaPWV:EH+OSAS:1 537(1 375,1 690)比EH:1 479(1 304,1 621)cm/s,P0.05]。3患者睡眠呼吸暂停低通气指数(AHI)与血浆醛固酮浓度及左右BaPWV呈显著正相关。4患者左右BaPWV与醛固酮浓度呈显著正相关,与睡眠监测中最低血氧饱和度和平均血氧饱和度呈显著负相关。结论:1合并阻塞性睡眠呼吸暂停的男性高血压病患者的血浆醛固酮浓度明显升高,其血浆肾素、血管紧张素Ⅱ及醛固酮浓度较单纯高血压组具有明显差异性。2合并阻塞性睡眠呼吸暂停的男性高血压病患者的动脉弹性损害比单纯高血压组更加严重,可能与血浆醛固酮的升高有关。     

中青年高血压病患者动脉弹性功能与血清脂肪酸

目的观察中青年高血压病患者和健康对照者基线空腹血清游离脂肪酸(FFA)的差异和大、小动脉弹性功能2年的变化。方法社区筛选高血压病患者103例(33～60岁),并筛选128例健康非高血压者(年龄匹配),随访2年。采用CVProfilorDO-2020型动脉弹性功能测定仪检测两组2年前后大、小动脉弹性指数(C1和C2),测定基线空腹血FFA、血脂、血糖、胰岛素等。高血压组91例,非高血压组97例得到随访。结果1)高血压病患者(n=91)的C1、C2均显著低于非高血压病患者[n=97;C1,11.9±3.9比非高血压组:(14.0±4.2)mL/mmHg×10,P=0.001;C2,4.9±2.2比非高血压病组:(6.1±2.6)mL/mmHg×100,P=0.001]。2)高血压病患者2年的小动脉弹性指数变化值(ΔC2)显著低于非高血压病患者[-0.24±0.25比非高血压组:(0.75±0.31)mL/mmHg×100,P=0.014],其大动脉弹性指数变化值(ΔC1)也降低,但差异无统计学意义(P=0.458)。3)与非高血压病患者相比,高血压病患者基线空腹血清饱和脂肪酸、单不饱和脂肪酸水平均显著增高(P均<0.05),而n-3脂肪酸水平[(96.0±38.9)比非高血压病组:(123.0±36.0)μmol/L,P=0.001]、多不饱和与饱和脂肪酸比值(P/S)(1.60±0.37比非高血压病组:1.90±0.46,P=0.009)显著降低。4)logistic回归分析显示高血压病患者基线空腹血清亚麻酸(18:3n3)优势比(OR值)和95%可信区间为2.483(1.480～4.166,P=0.001),而DHA(22:6n3)的为0.329(0.195～0.554,P=0.001)。结论原发性高血压患者动脉弹性年龄相关降低过程加速,空腹血清FFA组成异常(如亚麻酸增高,DHA下降),可能是其高血压发病的危险因素之一。     

中青年高血压病患者动脉弹性功能与血清脂肪酸

目的 观察中青年高血压病患者和健康对照者基线空腹血清游离脂肪酸(FFA)的差异和大、小动脉弹性功能2年的变化.方法 社区筛选高血压病患者103例(33～60岁),并筛选128例健康非高血压者(年龄匹配),随访2年.采用CVProfilor DO-2020型动脉弹性功能测定仪检测两组2年前后大、小动脉弹性指数(C1和C2),测定基线空腹血FFA、血脂、血糖、胰岛素等.高血压组91例,非高血压组97例得到随访.结果 1)高血压病患者(n=91)的C1、C2均显著低于非高血压病患者[n=97;C1,11.9±3.9比非高血压组:(14.0±4.2)mL/mm Hg×10,P=0.001;C2,4.9±2.2比非高血压病组:(6.1±2.6)mL/mm Hg×100,P=0.001].2)高血压病患者2年的小动脉弹性指数变化值(△C2)显著低于非高血压病患者[-0.24±0.25比非高血压组:(0.75±0.31)mL/mm Hg×100,P=0.014],其大动脉弹性指数变化值(△C1)也降低,但差异无统计学意义(P=0.458).3)与非高血压病患者相比,高血压病患者基线空腹血清饱和脂肪酸、单不饱和脂肪酸水平均显著增高(P均＜0.05),而n-3脂肪酸水平[(96.0±38.9)比非高血压病组:(123.0±36.0)μmol/L,P=0.001]、多不饱和与饱和脂肪酸比值(P/S)(1.60±0.37比非高血压病组:1.90±0.46,P=0.009)显著降低.4)logistic回归分析显示高血压病患者基线空腹血清亚麻酸(18:3 n3)优势比(OR值)和95%可信区间为2.483(1.480～4.166,P=0.001),而DHA(22:6 n3)的为0.329(0.195～0.554,P=0.001).结论 原发性高血压患者动脉弹性年龄相关降低过程加速,空腹血清FFA组成异常(如亚麻酸增高,DHA下降),可能是其高血压发病的危险因素之一.     

夜间持续气道正压通气有助于降低中重度阻塞性睡眠呼吸暂停综合征伴高血压患者的收缩压

背景阻塞性睡眠呼吸暂停综合征(OSAS)与高血压相关,持续气道正压通气(CPAP)可有效改善OSAS患者的睡眠情况,但在血压控制方面的效果尚存争议。目的探究CPAP在中重度OSAS合并高血压患者血压控制中的作用。方法选取阜外心血管病医院高血压诊治中心2010年9月至2014年9月诊断为中重度OSAS合并高血压患者117例进行回顾性分析(失访31例),其中对照组65例,只给予常规降压药物治疗;CPAP治疗组52例,除常规药物治疗外加用CPAP治疗。每3月随访1次,2014年10月1日截止,对照组随访(41.95±22.18)月,CPAP组随访(39.43±24.74)月(P0.05)。比较两组患者血压变化情况,分析CPAP对OSAS合并高血压患者血压的影响。结果除糖尿病比例外,两组患者基本情况的差异无统计学意义,CPAP组呼吸暂停低通气指数、氧减饱和度指数更高。经过治疗后,CPAP组收缩压下降较对照组更明显[(12.6±18.1)比(4.5±16.8)mm Hg,P=0.02],但两组舒张压下降的差异无统计学意义[(10.0±12.4)比(6.9±15.0)mm Hg,P=0.23],并且治疗组增加降压药种类的患者明显少于对照组(2.0%比20.3%,P0.01)。结论 CPAP可在药物治疗基础上进一步降低中重度OSAS合并高血压患者的收缩压。     

高血压病患者动态血压参数与左心室舒张功能相关

目的:探讨高血压病患者动态血压参数与左心室舒张功能的相关性。方法: 入选原发性高血压患者137例,询问病史、体检并采用超声心动图测收缩末期左、右心房内径、左心室舒张末期内径（LVEDD）、左心室射血分数（LVEF）。左心室舒张功能测定用二尖瓣舒张早期血流峰值速度/舒张晚期血流峰值速度（E/A）值,以评价左室舒张功能。根据E/A值的大小将原发性高血压患者分为两组,E/A≥1组视为左心室舒张功能正常组（n=54例）,E/A<1为左心室舒张功能不全组（n=83例）。患者均行24h动态血压及血生化检测。结果: (1)左心室舒张功能不全组的24h平均收缩压(24hSBP)、LVEDD明显高于功能正常组,差异有统计学意义(P<0.05)。（2）偏相关性分析显示左室舒张功能与LVEDD、24hSBP呈显著正相关（r值分别为0.70,0.40,P<0.01）。结论: 高血压病患者动态血压参数与左心室舒张功能相关。     

高血压合并阻塞性睡眠呼吸暂停低通气综合征患者短时血压变异性的影响因素研究

目的:探讨高血压合并阻塞性睡眠呼吸暂停低通气综合征(OSAS)患者短时血压变异性(BPV)的影响因素。方法:选择2017年6月至2019年5月在宁波市第一医院心血管科诊治的153例高血压患者,给予多导睡眠呼吸监测及动态血压监测,根据睡眠呼吸暂停低通气指数(AHI)将患者分四组:单纯高血压作为对照组(41例)、高血压合并轻度OSAS组(36例)、高血压合并中度OSAS组(36例)、高血压合并重度OSAS组(40例)。采用因子分析方法提取影响高血压合并OSAS患者短时血压变异性的公因子,进行多元线性回归分析影响高血压合并OSAS患者短时血压变异性的因素。结果:因子分析纳入可能影响高血压合并OSAS患者短时血压变异性的因素,共提取4个公因子:体重指数、OSAS严重程度相关参数、生活行为习惯、年龄及高血压病程;多元线性回归分析显示OSAS严重程度与高血压合并OSAS患者夜间收缩压短时血压变异性(nSBPARV)及夜间舒张压短时血压变异性(nDBPARV)均存在相关性(β=0.277,P<0.05;β=0.360,P<0.05),对于高血压合并OSAS患者nSBPARV的影响因素依次为OSAS严重程度>年龄及高血压病程(分别为β=0.277,P<0.05;β=0.225,P<0.05),对于nDBPARV的影响因素依次为OSAS严重程度>体重指数(分别为β=0.360,P<0.05;β=0.187,P<0.05)。高血压合并轻度、中度、重度OSAS组的nSBPARV、nDBPARV均较对照组大;且高血压合并重度OSAS组的nSBPARV、nDBPARV、日间收缩压短时血压变异性均大于对照组、高血压合并轻度、中度OSAS组,差异均具有统计学意义(P<0.05)。结论:高血压患者合并OSAS时容易出现夜间短时血压变异性增加,OSAS严重程度是高血压合并OSAS患者夜间血压短时变异性增加的主要因素,肥胖、年龄及高血压病程也是重要影响因素。     

高血压主动脉夹层与OSAS相关性研究

目的探讨高血压并主动脉夹层(AD)与阻塞性睡眠呼吸暂停综合征(OSAS)之间的关系。方法选择83例高血压并AD作为试验组,另选80例高血压病病人作为对照组。通过多导睡眠图检查,分析发生OSAS的比例,及OSAS组与非OSAS组间的发病特征。结果高血压并AD组中患OSAS的比例明显高于对照组(42.17%vs 20.00%,P0.01)。高血压并AD病人中OSAS组与非OSAS组比较显示,OSAS组病人平均年龄较非OSAS组更小(P0.05),OSAS组男女比例明显比非OSAS组高(P0.01),OSAS组BMI指数较非OSAS组更高(P0.05)。结论高血压并AD病人更易合并OSAS;合并OSAS的AD病人较非OSAS的AD病人年龄更小且肥胖,以男性为主;高血压并OSAS可能是相对年轻男性AD病人的重要危险因素。     

老年阻塞性睡眠呼吸暂停患者血管内皮功能和心脑血管事件的相关性

目的 回顾性分析老年阻塞性睡眠呼吸暂停综合征(OSAS)患者的血管内皮功能和心脑血管事件的相关性及对预后的影响. 方法 OSAS患者79例(OSAS组),老年OSAS组和非老年OSAS组分别为39例和40例;排除OSAS诊断的老年患者60例(老年非OSAS组).通过电话和门诊进行随访,随访时间中位数25个月.所有患者均接受:(1)彩色多普勒超声测定肱动脉血流介导的血管舒张功能(FMD);(2)检查和测定睡眠呼吸事件、血清生化指标;(3)随访心脑血管事件. 结果 (1)老年OSAS组FMD低于老年非OSAS组(P<0.05).(2)老年OSAS组体质指数高于老年非OSAS组(P<0.01),最低血氧饱和度、平均血氧饱和度低于老年非OSAS组(P<0.01,P<0.05).多因素Logistic回归分析结果显示,空腹血糖升高是FMD主要危险因素(OR=1.83,95%CI:1.11～3.03),其次是最低血氧饱和度(OR=0.92,95% CI:0.85～1.00).(3)老年OSAS组心脑血管事件发生率高于非老年OSAS组和老年非OSAS组(χ~2=7.339,P<0.05).多因素Logistic回归分析结果显示,FMD与患者预后密切相关(OR=1.33,95%CI:1.06～1.66),其次是超敏C反应蛋白(OR=0.51,95% CI:0.34～0.76). 结论 老年OSAS患者血管内皮功能受损更为严重,心脑血管事件发生率增加.OSAS可能通过间歇低氧和炎性反应等多种机制损伤血管内皮功能,参与影响患者预后.     

阻塞性睡眠呼吸暂停综合征与脑血管病关系20年随访研究

目的 调查随访阻塞性睡眠呼吸暂停综合征(OSAS)与脑血管病的关系.方法 对1989年11月至2009年11月南京军区所属3市及地区军队和地方离退休干部休养所进行体检的人群进行随访调查,随访期间每年进行1次体检,检查血压、血脂、血糖、心电图及X线胸片等,发现存在脑血管病表现时行头颅CT检查,以发生脑血管病为随访终点,随访时间为20年.结果 共纳入患者1868例,年龄53～82岁,平均(63±6)岁,其中男956例,平均(65±7)岁,女912例,平均(60±6)岁.其中确诊OSAS者598例(32.0%),纳入OSAS组,其中男496例(82.9%),女102例(17.1%);其余为对照组.随访终点比较结果显示,OSAS组白天嗜睡、头痛、记忆力减退、痴呆及语言障碍等发生率明显高于对照组(P＜0.05).OSAS组276例(46.2%)发生脑血管病,对照组发生150例(11.8%)(P＜0.01).随访期间死亡患者817例,其中OSAS组396/598例(66.2%),对照组421/1270例(33.1%,P＜0.01).随访结束时OSAS组脑血管病患病率为276/598例(46.2%),对照组170/1270例(13.4%,P＜0.01).结论 OSAS患者发生脑血管病可能性较一般人群高,考虑OSAS与发生脑血管病存在相关性,提示OSAS可能是脑血管病的独立危险因素.

Abstract：

Objective To explore the correlation between obstructive sleep apnea syndrome (OSAS) and cerebrovascular disease(CVD). Methods A cohort of 1868 people was screened for OSAS,and followed from November 1989 to November 2009. Annual medical examinations including blood pressure,blood fat, serum glucose, electrocardiogram and chest x-ray were performed. Computer tomography was carried out when CVD, the endpoint of the study, was manifested. Results Among the 1868 elderly people, 598 ( 32.0% ) were confirmed to have OSAS, including 496 ( 82.9% ) males and 102 ( 17. 1% )females. Compared with the non-OSAS group, patients with OSAS had more symptoms including daytime somnolence, headache, decreased ability of memory, aphronesia and allolalia( P ＜ 0. 05 ). CVD occurred in 276(46. 2% )patients of the OSAS group, but in 150( 11.8% , P ＜ 0. 01 )subjects of the non-OSAS group.During the 20-year follow-up, 817 people died, 66. 2% (396/598) in the OSAS group, but 33. 1% (421/1270) in the non-OSAS group ( P ＜0. 01 ). Conclusion Patients with OSAS are more likely to suffer from CVD. OSAS may be an independent risk factor for CVD.     

高血压合并阻塞性睡眠呼吸暂停综合征的动态血压变化

目的：观察分析高血压合并阻塞性睡眠呼吸暂停综合征（OSAS）患者的动态血压（ABP）变化。方法：选择2008～2010年我科住院诊治的高血压患者80例,对其进行多导睡眠仪及动态血压监测。据结果分为高血压病（EH）组（15例）,EH合并OSAS组（40例）,单纯OSAS组（25例）。结果：与EH组相比,OSAS组及EH合并OSAS组血压昼夜节律消失比例明显升高（40.2%比60.6%比80.4%,P〈0.05）,睡眠呼吸紊乱指数（AHI）[（4.0±0.4）比（13.3±4.6）比（18.0±8.0）]、血氧饱和度减少时间[（80.6±12.8）s比（116.1±9.8）s比（131.0±16.8）s]明显增加,最低血氧饱和度[（0.83±0.09）%比（0.74±0.08）%比（0.73±0.09）%]明显降低（P均〈0.05）,而OSAS组及EH合并OSAS组两组间这些指标无显著差异（P〉0.05）。EH合并OSAS组血压[收缩压（159.5±15.1）mmHg,舒张压（105±9.3）mmHg]显著高于EH组的血压[收缩压（147±10.3）mmHg,舒张压（91.8±5.4）mmHg],P〈0.05。结论：患睡眠呼吸暂停综合征后,血氧饱和度明显降低,血压昼夜节律消失增加。高血压合并阻塞性睡眠呼吸暂停综合征组的血压显著高于高血压组,说明睡眠呼吸紊乱可加重高血压。     

阻塞性睡眠呼吸暂停综合征与 2 型糖尿病的相关性分析简

目的 探讨阻塞性睡眠呼吸暂停综合征（OSAS）与2型糖尿病的相关性分析.方法 选择218例2型糖尿病患者,其中合并OSAS者56例,未合并OSAS者162例,比较两组临床资料、检测血糖、糖化血红蛋白、血脂、体重指数（BMI）及腰围.结果 OSAS组患者高血压发生率显著高于非OSAS组;与非OSAS组相比,未见显著差别（P〉0.05）.结论 糖化血红蛋白是OSAS患病的独立风险因素,加强血糖控制有利于减少OSAS发生率.     

阻塞性睡眠呼吸暂停综合征与心血管病关系的随访研究

目的调查随访阻塞性睡眠呼吸暂停综合征（OSAS）与心血管病（CVD）的关系。方法自1989年1aY]起入组1868例,其中OSAS患者598例,无OSAS1270例作为对照组,对入组人群每年进行一次体检,以发生CVD为随访终点,如未发生CvD则随访至2009年结束。结果随访期间,OSAS组发生CVD者占83．9％（502／598例）,对照组发生CVD者占28．6％（363／1270例）,两组CVD发生率存在显著统计学差异（P〈0．01）。随访期间死亡率为43．7％（817／1868例）,其中OSAS组死亡率66．2％（396／598例）,对照组死亡率为33．1％（421／1270例）,两组死亡率存在显著统计学差异（P〈0．01）。结论与一般健康人群相比,OSAS患者发生CVD的比例和死亡率均较高。     

Endothelial function in patients with obstructive sleep apnea syndrome but without hypertension

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension. OBJECTIVES: Our aim was to evaluate the role of endothelial dysfunction in the pathogenesis of hypertension in OSAS. METHODS: Twenty-three patients with OSAS but without hypertension and 15 healthy normotensive subjects were investigated. The presence or absence of OSAS was evaluated with a sleep study. Endothelial function was investigated with brachial artery ultrasound examination. RESULTS: Baseline characteristics were equivalent between the two groups. Minimal oxygen saturation and apnea-hypopnea indexes in the OSAS and control groups were 62.9 +/- 16.5 versus 94.9 +/- 1.1% (p < 0.0001) and 53.1 +/- 20.3 versus 3.8 +/- 0.9 (p < 0.0001), respectively. There was not statistically significant difference between basal brachial artery diameters measured in the morning and in the evening in all groups. Flow-mediated dilation (FMD) values measured in the morning were lower than those measured in the evening in both OSAS patients and the control group: FMD of OSAS patients was 6.04 +/- 3.18% in the morning and 10.38 +/- 4.23% in the evening hours (p = 0.001), and FMD of control subjects was 10.9 +/- 2.6% in the morning and 13.9 +/- 2.32 in the evening hours (p = 0.002). Differences in FMD values measured both in the morning and evening hours in OSAS patients were lower compared with those in control subjects (p < 0.0001 in the morning hours and p = 0.003 in the evening hours). CONCLUSIONS: We detected a prominent diurnal deterioration in endothelial function in normotensive OSAS patients compared with healthy subjects. This deterioration may occur due to ongoing hypoxemia during the night and it may be a possible cause of hypertension and atherosclerotic cardiovascular diseases in patients with OSAS.     

QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension.

QT interval dispersion (QT(d)) reflects inhomogeneity of repolarisation. Delayed cardiac repolarisation leading to the prolongation of the QT interval is a well-characterised precursor of arrhythmias. Obstructive sleep apnoea syndrome (OSAS) can cause cardiovascular complications, such as arrhythmias, myocardial infarction, and systemic and pulmonary hypertension. The aim of this study was to assess QT(d) in OSAS patients without hypertension. A total of 49 subjects without hypertension, diabetes mellitus, any cardiac or pulmonary diseases, or any hormonal, hepatic, renal or electrolyte disorders were referred for evaluation of OSAS. An overnight polysomnography and a standard 12-lead ECG were performed in each subject. According to the apnoea-hypopnoea index (AHI), subjects were divided into control subjects (AHI <5, n = 20) and moderate-severe OSAS patients (AHI > or =15, n = 29). QT(d) (defined as the difference between the maximum and minimum QT interval) and QT-corrected interval dispersion (QT(cd)) were calculated using Bazzet's formula. In conclusion, the QT(cd) was significantly higher in OSAS patients (56.1+/-9.3 ms) than in controls (36.3+/-4.5 ms). A strong positive correlation was shown between QT(cd) and AHI. In addition, a significantly positive correlation was shown between QT(cd) and the desaturation index (DI). The AHI and DI were significantly related to QT(cd) as an independent variable using stepwise regression analysis. The QT-corrected interval dispersion is increased in obstructive sleep apnoea syndrome patients without hypertension, and it may reflect obstructive sleep apnoea syndrome severity.     

Obstructive Sleep Apnea Syndrome in Male Hypertensives,Refractory to Drug Therapy. Nocturnal Automatic Blood Pressure Measurements — an Aid to Diagnosis?

Sixteen therapy resistant hypertensive males and 16 responders to antihypertensive drug treatment, matched for age, gender and body mass index, were examined by means of Static Charge Sensitive Bed (SCSB) and oximetry for the presence of obstructive sleep apnea syndrome (OSAS). In borderline cases, polysomnography was performed. The prevalence of OSAS among therapy resistant patients was 56%, as compared to 19% in the control group (p < 0.05). This higher prevalence of OSAS in a weight-matched group of subjects with severe hypertension supports the notion of a causal connexion between hypertension and OSAS.

In 10 OSAS patients and 10 hypertensives with normal respiration during sleep, ambulatory noninvasive monitoring (ABPM) of arterial pressure (AP) and heart rate (HR) was also performed. The OSAS patients had a higher nocturnal variability of HR, systolic blood pressure (both p < 0.05), and diastolic blood pressure (p < 0.01) in 8 halfhourly single ABPM measurements. Contrary to the non-OSAS subjects they also had a higher HR variability during sleep than they had in the waking state.     

2型糖尿病患者阻塞性睡眠呼吸暂停综合征患病状况及相关因素分析

目的调查2型糖尿病患者阻塞性睡眠呼吸暂停综合征(OSAS)患病情况,并分析其相关特点。方法选择2型糖尿病患者213例,使用便携式睡眠呼吸监测仪调查睡眠呼吸情况。分析OSAS患病状况、严重程度,并分析其相关因素。最终完成睡眠呼吸监测共145例。根据诊断分为OSAS组114例和非OSAS组31例。结果与非OSAS组比较,OSAS组患者体重指数、腰围、糖化血红蛋白、高血压及冠心病患病率明显升高(P<0.01)。糖化血红蛋白与OSAS患病风险独立相关(OR=6.24,95%CI:2.21～9.23,P<0.01)。糖化血红蛋白、体重指数、高血压、年龄、糖尿病病程与呼吸暂停低通气指数独立相关,糖化血红蛋白是主要的独立危险因素。结论 2型糖尿病患者OSAS患病率较高,血糖控制差者OSAS发病风险高,且病情更为严重,肥胖、年龄大、病程长或合并高血压者OSAS较为严重。     

Does angiotensin‐converting enzyme gene polymorphism affect blood pressure? Findings after 6 years of follow‐up in healthy subjects

BACKGROUND: There has been an increase in research into the association between angiotensin-converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease, with conflicting results. The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects, over 6 years of follow-up. METHODS: Population: 684 healthy volunteers (aged, 25-55 years): normotensive and free of cardiovascular diseases, with acceptable echocardiographic window. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry. STUDY PROTOCOL: All subjects underwent a complete physical examination, 12-lead ECG and ECHO, and venous blood samples were drawn for DNA analysis and cholesterol. All subjects had a clinical evaluation each year for the 6 year duration of the study. RESULTS: All 684 subjects completed 6 years of follow-up. We identified three genetically distinct groups. The ACE-DD group (n=225, 80F/145M, mean age 43.4+/-7.6 years) had 42 hypertensive subjects (18.3%), 5 heart failure (HF) subjects and 6 subjects with acute coronary syndromes (ACS). There was no association between family history, smoking habit, hypercholesterolemia and events. The ACE-ID group (n=335, 116F/219M, mean age 43.6+/-7 years) had 16 hypertensive subjects (4.7%) and 3 subjects with ACS. The ACE-II group (n=124, 45F/79M, mean age 42.5+/-6.9 years) had 2 hypertensive subjects (1.6%) and 1 HF subject. The incidence of hypertension and cardiovascular events was significantly higher in the ACE-DD group (53 cases, 23%) than in the ACE-ID and ACE-II groups (20 and 3 cases, 5.9 and 2.4%, respectively), P=0.0001. The higher incidence of hypertension was observed in the older age groups (36-45 and 46-55 years) with ACE-DD and ACE-ID genotypes. CONCLUSION: Our data suggest that ACE-DD polymorphism is associated with a higher incidence of hypertension in baseline healthy subjects, irrespective of other risk factors. The higher incidence of hypertension was apparent predominantly in the older age groups.