阻塞性睡眠呼吸暂停对血压、内皮功能及左室质量的影响

目的探讨阻塞性睡眠呼吸暂停综合征(OSAS)对动态血压、血管内皮功能、肾素血管紧张素醛固酮系统(RAAS)及左室质量的影响。方法将130例有或无OSAS的高血压患者和血压正常者分为4组:对照组(NS组)、单纯高血压组(EH组)、单纯OSAS组及OSAS高血压组(OSAS EH组),进行了动态血压、超声心动图、血一氧化氮(NO)、内皮素(ET)、肾素(PRA)、血管紧张素Ⅱ(AngⅡ)和醛固酮(Ald)测定。结果(1)不论有无高血压的OSAS患者,夜间血压下降率<10%,比无OSAS组较多见(P<0.001);且OSAS EH组血压较EH组高(P<0.05～0.001)。(2)OSAS EH组和OSAS组ET(83.0±5.8,44.0±5.0)ng/L升高,与NS组比较差异有显著性(P<0.001)。而OSAS EH组与OSAS组NO(31.1±4.4,45.7±4.4)μmol/L下降,与NS组比较差异有显著性(P<0.001)。(3)血PRA、AngⅡ、Ald含量在OSAS EH组及OSAS组升高,与NS组比较差异有显著性(P<0.001)。(4)OSAS EH组、OSAS组左室质量指数(LVMI)(159.8±8.4,135.3±6.0)g/m2与NS组(121.2±6.5)g/m2比较,差异有显著性(P<0.001),且OSAS EH组与EH组(134.9±5.7)g/m2比较,差异有显著性(P<0.001)。结论OSAS患者血压昼夜节律消失,且伴有血管内皮功能紊乱、RAAS激活,由此进一步加重对心脏等靶器官的损害。     

肥胖和阻塞性睡眠呼吸暂停综合征对左室质量及左室几何构型的影响

目的评估阻塞性睡眠呼吸暂停综合征(OSAS)和肥胖对左室质量以及左室几何构型的影响。方法选取2018年1月—2019年7月因打鼾疑为OSAS来山西医科大学第一医院行多导睡眠呼吸监测(PSG)的病人193例,根据体质指数(BMI)和呼吸暂停低通气指数(AHI)将研究对象分为4组:正常体重非阻塞性睡眠呼吸暂停组(NW-NO)、肥胖非阻塞性睡眠呼吸暂停组(O-NO)、正常体重阻塞性睡眠呼吸暂停组(NW-O)、肥胖阻塞性睡眠呼吸暂停组(O-O)。比较4组超声心动图参数及异常左室几何构型分布情况。结果与NW-NO组相比,O-NO组、NW-O组与O-O组左室质量(LVM)、左室质量指数(LVMI)与相对室壁厚度(RWT)均增加,差异均有统计学意义(P<0.05);NW-NO组、O-NO组、NW-O组和O-O组异常左室几何构型发生率分别为7.1%、11.1%、39.1%和41.7%,NW-O组、O-O组异常左室几何构型发生率高于NW-NO组、O-NO组,差异均有统计学意义(P<0.05)。逐步线性回归分析显示,LVMI的影响因素包括AHI、收缩压、BMI(P<0.05)。结论OSAS与肥胖单独或合并存在时均使LVM、LVMI增加,且LVMI与AHI、收缩压和BMI有关。OSAS是否合并肥胖对异常左室几何构型的分布无明显影响。     

首乌降压胶囊对高血压病病人血压及RAAS的影响

目的 观察首乌降压胶囊对高血压病病人血压、血浆肾素-血管紧张素-醛固酮系统（RAAS）的影响，探讨其临床疗效及作用机制。方法 选取符合入选标准的病例68例，随机分为对照组34例与治疗组34例。对照组采用卡托普利片，每片25mg，每日3次，每次1片；治疗组服用首乌降压胶囊。每日3次，每次4粒。均以1个月为1个疗程。观察两组病人的血压、血浆RAAS指标的变化。结果 两组治疗后血压较治疗前均明显下降（P〈0．05），治疗组总有效率（94．1％）与对照组总有效率无差异（85．3％，P〉0．05）。两组治疗后血浆肾素（PRA）、血管紧张素（AngⅡ）、醛固酮（ALD）水平较治疗前均下降（P〈0．05）。结论 首乌降压胶囊能降低和控制高血压病病人的血压。其降压机制可能与其降低血浆及肾脏组织PRA、AngⅡ、ALD水平有关。     

阻塞性睡眠呼吸暂停综合征合并原发性高血压肾素-血管紧张素-醛固酮系统的变化研究

目的探讨肾素-血管紧张素-醛固酮系统(RAAS)在阻塞性睡眠呼吸暂停综合征(OSAS)合并高血压发病机制中的作用。方法 2006年3月至2008年6月根据整夜多导睡眠监测(PSG)、血压测量和病史采集收治的天津医科大学总医院93例受试者分为OSAS血压正常组、OSAS高血压组、非OSAS高血压组、正常对照组。测定PSG当晚睡眠前后血压、血浆肾素活性(PRA)、血管紧张素Ⅱ(ATⅡ)、醛固酮(ALD)。结果 OSAS组不论有无高血压,晨起血浆PRA和ATⅡ均显著高于睡前,OSAS高血压组升高更明显;醒后PRA、ATⅡ与醒后平均动脉压(MAP)、睡眠呼吸暂停低通气指数(AH I)、最长呼吸暂停时间、呼吸暂停总时间、氧减饱和指数、睡眠期间血氧饱和度低于90%的时间占总睡眠时间的百分比(T90)呈显著正相关,与夜间最低血氧饱和度(m inSaO2)和平均血氧饱和度(MSaO2)呈负相关。结论 OSAS可引起肾素、血管紧张素分泌增多,提示RAAS在OSAS患者夜间一过性血压升高和持续性高血压形成方面可能起重要作用。     

苯那普利对高血压血浆肾素、血管紧张素Ⅱ、醛固酮及左室舒张功能的影响

（ＡｎｇⅡ）ａｎｄｔｈｅａｌｄｏｓｔｅｒｏｎｅ（Ａｌｄ）ａｆｔｅｒｔｒｅａｔｍｅｎｔｗｉｔｈｂｅｎａｐｒｉｌ（５～２０ｍｇ１／ｄ）ｉｎｈｙｐｅｒｔｅｎｓｉｏｎｃｏｍｐｌｉ－ｃａｔｅｄｗｉｔｈｄｉａｓｔｏｌｉｃｆｕｎｃｔｉｏｎｉｎｓｕｆｉｃｉａｎｃｙ．ＭｅｔｈｏｄｓＴｈｅｓｅｒｕｍＰＲＡ，ＡｎｇⅡａｎｄＡＬＤｗｅｒｅｍｏｎｉｔｏｒｅｄ     

缬沙坦对老年高血压病患者肾素-血管紧张素系统和血管内皮功能的影响

目的 探讨缬沙坦对老年高血压病患者的降压疗效及对肾素－血管紧张素系统（RAS）和血管内皮功能的影响。方法 36例老年高血压患者，给予缬沙坦80－160mg/d口服，共8w，监测治疗前后血压。用放射免疫法测定治疗前后血浆肾素活性（PRA）、血管紧张素Ⅱ（AngⅡ）、醛固酮（ALD）及内皮素（ET）、一氧化氮（NO）水平。结果 （1）治疗后血压下降总有效率为86．6％（P＜0．01）；（2）治疗后血浆PRA、AngⅡ水平增高，ALD水平降低，治疗前后有显著差异（P＜0．01）；（3）治疗后血浆ET水平降低，而NO水平增高，治疗前后有显著性差异（P＜0．01）。结论 缬沙坦治疗老年高血压降压疗效明显，对RAS阻断更完全，并可以改善内皮功能。     

血管紧张素Ⅱ对内皮依赖性血管舒张功能的影响

目的 :探讨血浆中血管紧张素Ⅱ (AngⅡ )水平与肱动脉内皮依赖性舒张功能的关系。 方法 :测定冠心病 (CHD)组 30例、原发性高血压 (EH)组 2 8例、EH并发CHD(EH加CHD)组 39例和正常对照组 2 0例的血脂、AngⅡ、vWF、内皮素 1(ET 1)、一氧化氮 (NO)水平以及反应性充血时和含服硝酸甘油后肱动脉内径的变化。结果 :EH组、CHD组和EH加CHD组血流介导的肱动脉舒张 (FMD)和硝酸甘油所致的肱动脉舒张均低于对照组 [分别为 (7.32± 4 .36 )、(5 .6 2± 3.0 9)和 (3.72± 3.0 6 ) %∶(14 .2 1± 7.71) %以及 (17.82± 6 .0 0 )、(12 .6 1±4 .2 9)和 (9.5 2± 4 .85 ) %∶(19.33± 9.6 2 ) % ,均P <0 .0 5 ]。多因素线性逐步回归分析显示 :在CHD组和EH加CHD组与血清高密度脂蛋白胆固醇 (HDL C)水平呈正相关 [分别为 (r =0 .317,P <0 .0 1)和 (r =0 .2 98,P <0 .0 1) ],EH加CHD组与血浆AngⅡ水平呈负相关 (r =- 0 .4 71,P <0 .0 1) ;剔除HDL C影响因素后仍呈负相关 (r =- 0 .2 84 ,P >0 .0 1) ,硝酸甘油所致的肱动脉舒张与上述各因素无关。根据FMD程度将 4组受试者合并后再分为A、B两组 ,A组FMD≤ 5 % ,B组FMD >5 % ,结果显示 ,A组的AngⅡ和ET 1明显高于B组 [分别为(10 1.4 5± 13.4 2 )∶(35 .6 4± 9.6 2 )ng/L和     

血管紧张素Ⅱ及其受体与血管内皮功能的关系

血管紧张素Ⅱ (AngⅡ )作为肾素 血管紧张素系统 (RAS)最后的递质 ,是该系统中最为重要的血管活性物质。它行使着循环内分泌系统和组织旁分泌 /自分泌系统的功能。目前已认识到 ,它不仅是一种血管活性物质 ,可引起机体血流动力学改变 ,导致高血压的发生 ,更为重要的是它是一种生长因子 ,在慢性心血管、肾脏疾病的进展中也起着非常重要的作用。该生物学作用需通过其受体介导 ,AngⅡ及其受体在心血管系统中的作用越来越受到重视 ,而血管内皮功能与心脏病尤其是冠心病的发病机制之间的关系也日显密切 ,为此 ,本文旨在对AngⅡ及其受体、血管…     

高血压患者氯沙坦治疗前后血管内皮功能与血管紧张素Ⅱ的变化

目的探讨氯沙坦治疗前后高血压患者血管内皮功能和血浆血管紧张素Ⅱ的变化.方法50例高血压患者氯沙坦治疗4～6周,根据达目标血压(以舒张压<90mmHg为标准调整降压药每天剂量50～100mg,部分患者加双氢氯噻嗪25mg),观察氯沙坦治疗前后肱动脉超声检测血管内皮功能和血浆血管紧张素Ⅱ浓度的变化.结果肱动脉内径基础值及含服硝酸甘油后肱动脉内径变化差异均无显著性[(3.78±0.57)mm对(3.82±0.63)mm,(18.7±4.5)%对(20.1±7.2)%,P>0.05],反应性血管充血引起肱动脉内径的变化治疗前后差异有显著性[(4.32±0.71)%对(9.38±4.1)%,P<0.01)].氯沙坦治疗前后血浆血管紧张素Ⅱ浓度变化显著[(38.6±6.8)pmol/L对(76.9±15.3)pmol/L,P<0.01].结论氯沙坦在有效降压的同时,能改善血管内皮舒张功能.     

氯沙坦对糖尿病大鼠血浆血管紧张素Ⅱ及胸主动脉内皮功能的影响

为探讨血管紧张素Ⅱ特异性受体 1阻滞剂氯沙坦对血浆血管紧张素Ⅱ及胸主动脉内皮功能的影响 ,腹腔注射链脲佐菌素复制大鼠糖尿病模型 ,分别于第 4、8、16周处死动物 ,取胸主动脉环测定乙酰胆碱引起的内皮依赖性舒张反应 ,并测定血浆血管紧张素Ⅱ浓度。结果发现 ,糖尿病大鼠随病程进展 ,其胸主动脉环乙酰胆碱引起的内皮依赖性舒张反应渐进性下降 ,血浆中血管紧张素Ⅱ浓度升高。提示 ,氯沙坦可明显改善内皮依赖性舒张反应 ,但对血浆血管紧张素Ⅱ浓度无降低作用。     

阻塞性睡眠呼吸暂停对血压的影响

目的:探讨阻塞性睡眠呼吸暂停(OSA)对血压的复杂调节作用.方法:对2008-05至2009-05在本中心就诊的患者行整夜多导睡眠监测和晨起血压测量,根据呼吸暂停低通气指数(AHI)和最低血氧饱和度筛选共277例患者入选.对照组26例(AHI<5),单纯OSA组115例分为轻度亚组(5≤AHI<20)37例、中度亚组(20≤AHI<40)29例、重Ⅰ度亚组(40≤AHI<60)24例、重Ⅱ度亚组(AHI≥60)25例共4个亚组;OSA合并高血压病组136例,按单纯OSA组AHI标准分为轻度亚组27例、中度亚组20例、重Ⅰ度亚组33例、重Ⅱ度亚组56例共4个亚组.结果:与对照组比较,单纯OSA组和OSA合并高血压病组体重指数、AHI、最长呼吸暂停时间、氧饱和度低于90%的时间百分比、微觉醒指数、舒张压和平均动脉压均增加,最低血氧饱和度、平均血氧饱和度均降低,差异均有统计学意义(P均<0.05).单纯OSA组中度、重Ⅰ度、重Ⅱ度三亚组舒张压较轻度亚组升高,差异均有统计学意义(P均<0.05).OSA合并高血压病组中度、重Ⅱ度二亚组较轻度亚组收缩压和舒张压升高,差异均有统计学意义(P均<0.05);OSA合并高血压病组平均动脉压中度亚组较轻度亚组升高,重Ⅰ度、重Ⅱ度二亚组较中度亚组降低,差异均有统计学意义(P均<0.05).单纯OSA组轻度亚组舒张压与AHI呈正相关(r=0.69,P＜0.05);重Ⅱ度亚组平均动脉压与最低血氧饱和度呈负相关(r=-0.60,P＜0.05).OSA合并高血压病组轻度亚组收缩压与最长呼吸暂停时间呈正相关(r=0.60,P＜0.05);中度亚组收缩压与最长呼吸暂停时间呈正相关(r=0.73,P＜0.05),舒张压、平均动脉压与AHI呈正相关(r分别为0.88和0.86,P＜0.05);重Ⅰ度亚组舒张压、平均动脉压与AHI呈负相关(r分别为-0.58和-0.70,P＜0.05),舒张压与最低血氧饱和度呈正相关(r=0.47,P＜0.05).结论:OSA对血压的影响情况因病情程度不同而异.     

伴及不伴OSA高血压患者的血压变异性和OSA相关性研究

目的研究伴或不伴睡眠呼吸暂停(obstructive sleep apnea,OSA)高血压患者的血压变异性和OSA的相关性。方法纳入阴虚阳亢型轻中度高血压患者90例,对患者行便携式睡眠仪监测、24h动态血压(ABPM)监测。观察患者血压的均值、变异性,及昼夜节律和OSA的关系;采用多元逐步回归法分析OSA和血压的关系。结果与不伴OSA的高血压患者相比,伴OSA患者的血压变异性和非杓型血压发生率明显增高,夜间血压下降率明显降低(P<0.05);其中夜间平均收缩压、24h收缩压血压标准差与睡眠呼吸暂停低通气指数(apnea hypopnea index,AHI)呈正相关,夜间收缩压下降率和AHI呈负相关(P<0.05)。结论伴OSA患者的血压变异性增高,昼夜节律紊乱。     

原发性高血压伴阻塞性睡眠呼吸暂停低通气综合征对左心室结构的影响

目的研究原发性高血压(EH)伴阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与左心室结构改变的关系并分析其影响因素。方法对2004-07-2007-07住院的EH患者进行睡眠监测,并对其一般资料、生化指标、超声心动图检查结果进行分析,比较EH+OSAHS与EH患者间左心室构型的差异,观察其影响因素。结果EH+OSAHS组年龄、男性比例、体质量指数、收缩压、空腹及餐后2 h血糖均高于EH组(均P<0.01);EH+OSAHS组的左室舒张期内径、室间隔厚度、左室后壁厚度、左室质量指数、相对室壁厚度均高于EH组(均P<0.01);与左心室肥厚发生相关的危险因素为OSAHS、高血压病程、血压分级、糖尿病、肾功能不全。结论与EH相比,EH+OSAHS左心室构型改变更严重。     

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Increased circulating endothelial cells (CECs) have been observed in patients with vascular injury associated with acute myocardial infarction, pulmonary hypertension, and congestive heart failure. Decreased circulating endothelial progenitor cells (EPCs) have been observed in patients with risk factors for cardiovascular disease. Obstructive sleep apnea (OSA) is associated with increased risk of cardiovascular disease and endothelial dysfunction. Subjects were recruited from patients referred for overnight polysomnograms; 17 subjects had OSA and 10 control subjects did not have OSA. All subjects lacked vascular disease and risk factors for vascular disease. Peripheral blood was obtained from fasting subjects in the morning, following sleep studies. CECs and EPCs were quantified using magnetic bead separation with UV epifluorescence microscopy and flow cytometry immunophenotyping, respectively. Cell counts and demographic variables were compared using unpaired t tests. Regression analysis was performed comparing cell counts with the apnea-hypopnea index (AHI) and nadir SaO(2). Subjects with OSA and controls did not differ significantly in terms of age and body mass index. Subjects with OSA had higher AHI, lower nadir SaO(2), and greater sleepiness (Epworth Sleepiness Scale scores). There were no significant differences in CEC (7.0+/-1.5 vs. 4.9+/-0.9, p>0.05) or EPC (1077+/-318 vs. 853+/-176, p>0.05) between controls and OSA cases, respectively. In this small study, we found no differences in CECs or circulating EPCs between patients with OSA and controls. OSA may not be associated with these markers of vascular endothelial cell injury in patients with no concomitant vascular disease.     

The Impact of Obstructive Sleep Apnea on Chronic Kidney Disease

Obstructive sleep apnea (OSA) is an important clinical problem in the chronic kidney disease (CKD) population. OSA is associated with hypoxemia and sleep fragmentation, which activates the sympathetic nervous system, the renin-angiotensin-aldosterone system, alters cardiovascular hemodynamics, and results in free radical generation. In turn, a variety of deleterious processes such as endothelial dysfunction, inflammation, platelet aggregation, atherosclerosis, and fibrosis are triggered, predisposing individuals to adverse cardiovascular events and likely renal damage. Independent of obesity, OSA is associated with glomerular hyperfiltration and may be an independent predictor of proteinuria, a risk factor for CKD progression. OSA is also associated with hypertension, another important risk factor for CKD progression, particularly proteinuric CKD. OSA may mediate renal damage via several mechanisms, and there is a need to better elucidate the impact of OSA on incident renal disease and CKD progression.     

Obstructive Sleep Apnea and Blood Pressure Elevation: What is the Relationship?

Sleep disordered breathing has increasingly been recognised as a frequent cause of ill-health in the community. Moderate or severe forms of the most common condition, obstructive sleep apnea (OSA), occur in up to 12% of the adult male population. A substantial body of literature has been published on the potential relationship between OSA and cardiovascular disease. In particular, OSA has been associated with cardiac failure, stroke, myocardial infarction and hypertension. Part of this association may be explained by other confounders, mainly obesity, which is common in OSA patients. The present review was prepared following a workshop aimed to critically review available scientific evidence suggesting that hypertension is a direct consequence of OSA. In addition, pathophysiologic mechanisms that may be involved in the relationship between OSA and cardiovascular disease, particularly brief intermittent elevation of blood pressure and sustained systemic hypertension, are discussed.     

Effect of Continuous Positive Airway Pressure on Blood Pressure Variability in Patients With Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a common risk factor for cardiovascular disease. Continuous positive airway pressure (CPAP) improves OSA symptoms and blood pressure (BP) control. The effect of CPAP on BP variability (BPV) in patients with and without hypertension treated with autotitrating CPAP (APAP) for 2 weeks was studied. A total of 78 participants (76.9% men, 49% hypertensive, mean body mass index 36.2 [6.9] kg/m², age 49.0 [12.9] years) underwent 2 weeks of APAP therapy. Office BP, BPV (standard deviation of three BP measurements), and pulse rate were measured before and after treatment. Systolic BPV (5.3±4.9 vs 4.2±3.4 mm Hg, P=.047) and pulse rate (78.0±14.5 vs 75.5±15.8 beats per minute, P=.032) decreased after treatment, particularly in hypertensive participants. Mask leak was independently associated with reduced changes in systolic BPV (r=−0.237, P=.048). Short‐term APAP treatment reduced BPV and pulse rate, particularly in hypertensive patients with OSA.

Obstructive sleep apnea (OSA) is a well‐recognized risk factor for cardiovascular (CV) disease.¹ Its prevalence is rising as a result of the current obesity epidemic.² OSA is caused by recurrent obstructions of the upper airway when asleep. These obstructions result in apneas and hypopneas, which lead to repeated oxygen desaturations and arousals from sleep, and hence activation of the sympathetic nervous system.³ Increased sympathetic tone impacts on blood pressure (BP), heart rate,⁴ and importantly on the risk of CV morbidity.Continuous positive airway pressure (CPAP) maintains upper airway patency and abolishes or reduces obstructive events in patients with OSA,⁵ also reducing BP.⁶ Recent studies have revealed that optimal CPAP control reduces BP, with more marked effects in patients with resistant hypertension,⁷ implying a role of the autonom ous nervous system in relation to changes in BP.BP variability (BPV) is a marker of autonomic nervous system output and an independent predictor of CV morbidity and mortality.⁸ It is defined as the fluctuation of BP between different measurements over a defined time interval.⁹ Visit‐to‐visit BPV comparison is related to an increased risk of CV events.¹⁰, ¹¹ Patients with OSA are known to have an increased sympathetic tone, which causes increased BPV¹², ¹³ and leads to raised levels of absolute BP and increased risk of CV morbidity and mortality. Patients with hypertension exhibit higher BPV when compared with normotensives as expression of an enhanced sympathetic tone.⁹ We aimed to investigate how CPAP treatment modifies the risk of increased sympathetic activation, through its impact on BPV, in patients with obstructive sleep apnea.     

Blood Pressure Variability and Left Ventricular Mass Index in Children

Clinical implications of blood pressure variability (BPV) on subclinical organ damage in children are unknown. The authors sought to explore the potential utility of two newly derived BPV indices: weighted standard deviation (wBPSD) and real average variability (ARV), as well as two standard ambulatory blood pressure indices: average 24‐hour systolic blood pressure (SBP) and 24‐hour SBP load, to identify children at high risk for left ventricular (LV) hypertrophy (LVH). The study group consisted of 67 consecutive children who were referred to our institution for evaluation of suspected hypertension. LV mass was estimated by M‐mode echocardiography using Devereux's formula according to the Penn convention and indexed for height^2.7. We found a statistically significant, positive correlation between 24‐hour wBPSD and LV mass index (LVMI) (ρ=0.389; P=.002) and no correlation between 24‐hour ARV and LVMI (P>.05). However, partial correlation analysis of 24‐hour wBPSD adjusted for body mass index (BMI) and LVMI showed only a weak correlation (ρ=0.3; P=.022). By using multiple linear regression analysis in a model with LVMI as a dependent variable and 24‐hour wBPSD, 24‐hour ARV, and BMI as independent variables, only BMI showed statistically significant independent positive associations with LVMI (P=.028). Results of our study showed that currently used BPV indices (24‐hour wBPSD and 24‐hour ARV) are not clinically reliable parameters to identify children at risk for LVH. Apparent contribution of the 24‐hour wBPSD parameter to LVMI is negligible and is secondary to its close correlation with BMI (ρ=0.335 P=.009).