缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性的影响

目的 比较缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性及一氧化氮、内皮素的影响.方法选取61例2、3级老年高血压患者,随机分为两组,分别给予缬沙坦+氨氯地平或缬沙坦+氢氯噻嗪行降压治疗,观察入选时、治疗第8周和第16周各种相关指示的变化.人选时检测血脂、空腹血糖、血尿酸,试验各个阶段监测24 h动态血压,检测血浆一氧化氮、内皮素水平.结果在患者入选时、治疗第8周和第16周三个时间点,缬沙坦+氨氯地平组和缬沙坦+氢氯噻嗪组24 h血压及白昼血压比较差异无统计学意义.治疗第16周,缬沙坦+氨氯地平组晨峰收缩压较缬沙坦+氢氯嚷嗪组明显降低[(22.6±8.8)mm Hg(1 mm Hg=0.133 kPa)比(26.3±13.7)mm Hg,P＜0.05];缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组24 h收缩压变异性(SBPV)进行性降低[缬沙坦+氨氯地平组:(12.5±2.8)mm Hg比(10.2 ±2.2)mm Hg比(8.8±1.6)mm Hg,P＜0.01;缬沙坦±氢氯噻嗪组:(12.5±2.5)mmHg比(10.7±2.2)mm Hg比(9.6±2.0)mmHg,P＜0.01],缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组白昼SBPV明显降低[缬沙坦+氨氯地平组:(12.2±3.0)mm Hg比(10.1±2.3)mm Hg比(8.4±1.9)mm Hg,P＜0.01;缬沙坦+氢氯噻嗪组:(11.8±2.7)mm Hg比(10.4±1.9)mm Hg比(9.6±2.2)mm Hg,P＜0.01],缬沙坦+氨氯地平组24 h舒张压变异性(DBPV)显著降低[(15.5±3.4)mm Hg比(13.0±3.5)mm Hg比(12.3±2.5)mm Hg,P＜0.01],缬沙坦+氢氯噻嗪组24 h DBPV无显著性变化;缬沙坦+氨氯地平组第16周白昼SBPV低于缬沙坦+氢氯噻嗪组[(8.4±1.9)mm Hg比(9.6 ±2.2)mm Hg,p＜0.05],缬沙坦+氨氯地平第8周、第16周的24 h DBPV、白昼DBPV低于缬沙坦+氢氯噻嗪组(P ＜0.01～0.05);缬沙坦+氨氯地平组一氧化氮进行性升高[(27.3±13.6)μmol/L比(47.2±16.3)μmol/L比(69.5±18.9)μmol/L,P＜0.01]、内皮素进行性降低[(45.3±8.0)ng/L比(37.4±3.9)ng/L比(34.2±4.4)ng/L,P＜0.01];缬沙坦+氢氯噻嗪组一氧化氮进行性升高[(33.5±13.9)μmol/L 比(49.7±21.9)μmol/L比(66.7 ±24.7)μmol/L,P＜0.01]、内皮素显著降低[(46.6±10.4)ng/L比(37.0±5.4)ng/L比(36.1±8.2)ng/L,P＜0.01].治疗第8周,缬沙坦+氨氯地平组收缩压变异性的降幅与一氧化氮的升幅有相关性(r =0.401,P=0.025).结论缬沙坦联合氨氯地平或氢氯噻嗪均能降低老年高血压患者血压变异性、改善血管内皮功能,缬沙坦联合氨氯地平可能更适合于老年高血压患者.     

老年原发性高血压患者血压晨峰现象与靶器官损害的相关性研究

目的:探讨老年原发性高血压患者血压晨峰(MBPS)与靶器官损害的相关性。方法:老年原发性高血压患者292例,据24h动态血压分晨峰组(MBPS组,128例)与非晨峰组(非MBPS组,164例),检查血脂、空腹血糖、肌酐,计算人体质量指数(BMI)、行心脏和颈动脉超声检查,计算左室质量指数(LVMI)、颈动脉内膜中层厚度(IMT)。结果:与非MBPS组比较,MBPS组24h收缩压(SBP)[(138.2±13.2)mmHg比(153.1±12.1)mmHg]、白昼SBP[(143.3±12.7)mmHg比(158.2±9.1)mmHg]以及夜间SBP[(136.6±9.4)mmHg比(150.7±10.1)mmHg]均明显升高(P<0.05),LVMI[(101.76±34.45)g/m2比(138.13±37.6)g/m2]、颈动脉IMT[(0.84±0.11)mm比(1.35±0.35)mm]均明显增大(P<0.05);Pearson相关分析显示,血压晨峰与LVMI、IMT呈正相关(r分别=0.688,0.524,P均<0.05)。结论:老年原发性高血压患者血压晨峰现象加重靶器官损害。     

老年高血压患者动态血压监测分析

目的 分析老年原发性高血压患者24h动态血压波动规律.方法 对113例原发性高血压患者与90例血压正常者分别进行24 h动态血压监测.观察血压水平、血压负荷值、血压变异性指标及晨峰数值,并进一步分析具有晨峰现象的老年高血压患者昼夜节律变化.结果 (1)高血压患者24 h及日间、夜间血压监测数值均高于对照组(P＜0.05).(2)高血压患者24 h收缩压及舒张压负荷均高于对照组,血压变异系数升高(P＜0.05).(3)老年高血压患者血压晨峰数值明显高于对照组(P＜0.05).(4)高血压组昼夜节律异常者比例较对照组明显升高(P＜0.05).其中晨峰高血压组、非晨峰高血压组与对照组相比,差异均具有统计学意义(P＜0.05).(5)昼夜节律异常(非杓型)者在高血压组内具有晨峰现象者与不具有晨峰现象者之间相比,差异依然具有统计学意义(P＜0.05).结论 老年高血压患者血压升高明显,收缩压尤其突出,血压负荷增高,变异性增高,晨峰现象更为普遍.具有晨峰现象的高血压患者昼夜节律异常比例更明显增高.     

老年患者血压变异性影响因素分析

探讨年龄,高血压、平均动脉压和晨峰血压等因素对老年患者血压变异性的影响。方法:325例老年患者根据血压水平分为:高血压组(225例)和非高血压组(100例),对两组患者行动态血压监测,并进行统计分析。结果:与非高血压组相比,老年高血压患者收缩压变异[(10.82±2.72)mmHg比(14.18±2.98)mmHg]和舒张压变异[(8.12±1.83)mmHg比(9.05±1.94)mmHg]明显增加(P均<0.01);但其收缩压的变异性不随年龄增加而增加(t=1.277,P=0.215)。直线相关分析表明晨峰收缩压和收缩压变异呈明显正相关(r=0.342,P<0.05),平均舒张压和舒张压变异呈明显的正相关(r=0.323,P<0.05)。结论:老年高血压患者血压变异是增加的,晨峰血压和平均舒张压是老年收缩压变异的重要影响因素。     

老年原发性高血压患者血压变异性对新发心房颤动的影响

目的探讨老年原发性高血压患者血压变异性对新发心房颤动(房颤)的影响。方法回顾性研究2010年1月~2011年12月在我院住院治疗不伴房颤的老年原发性高血压患者683例,根据随访期间是否新发房颤分为房颤组69例及非房颤组614例。记录基线特征、超声心动图参数。进行动态血压监测,按收缩压变异性中位数9.89mm Hg(1mm Hg=0.133kPa)将入选患者分为高变异性342例和低变异性341例。应用Cox回归方程分析血压变异性对新发房颤的影响。结果房颤组24h收缩压变异性明显高于非房颤组[(11.13±3.50)mm Hg vs(10.21±3.41)mm Hg,P=0.034],24h舒张压明显低于非房颤组[(67.19±8.16)mm Hg vs(69.33±8.39)mm Hg,P=0.045]。多因素Cox回归分析显示,24h收缩压变异性、脑出血及心脏永久性起搏器置入是老年原发性高血压患者新发房颤的独立危险因素(HR=1.949,95%CI:1.175~3.233,P=0.010;HR=2.983,95%CI:1.075~8.277,P=0.036;HR=2.567,95%CI:1.370~4.810,P=0.003)。结论收缩压变异性升高是老年原发性高血压患者新发房颤的独立危险因素。     

高龄老年人血压变异性与踝臂指数关系探讨

目的评价高龄老年人群血压变异性(BPV)与踝臂指数(ABI)的关系。方法入选年龄≥80岁高龄老人111例,按照ABI分为异常ABI组(ABI≤0.9或ABI>1.3)56例和正常ABI组(ABI>0.9)55例,比较2组24h动态血压参数和BPV参数;另根据血压将患者分为高血压组48例和非高血压组63例,观察2组BPV及ABI差异。logistic回归分析ABI独立危险因素。结果异常ABI组较正常ABI组24h舒张压、昼间舒张压和夜间舒张压明显降低(P<0.05),24h收缩压变异性[(12.80±2.66)mm Hg(1mm Hg=0.133kPa)vs(14.14±3.64)mm Hg]明显降低、夜间收缩压变异性[(11.99±4.19)mm Hg vs(9.97±4.05)mm Hg]明显增高(P<0.05)。高血压组24h收缩压变异性[(14.87±3.91)mm Hg vs(13.20±3.41)mm Hg]、夜间收缩压变异性[(12.27±5.50)mm Hg vs(10.33±3.93)mm Hg]明显增高,ABI[(0.98±0.21)vs(1.07±0.20)]明显降低(P<0.05)。logistic回归分析提示,夜间舒张压和夜间收缩压变异性为ABI的独立危险因素(P<0.05)。结论高龄老年人群24h舒张压、昼间及夜间舒张压、24h收缩压变异性、夜间收缩压变异性可能是异常ABI的危险因素。     

老年原发性高血压患者血压晨峰与左心室肥厚的关系

目的探讨老年原发性高血压患者血压晨峰与左心室肥厚的关系。方法选择老年原发性高血压患者80例,根据24 h动态血压监测分为2组:血压晨峰值≥55 mm Hg(1 mm Hg=0.133 kPa)为晨峰组,血压晨峰值<55mm Hg为非晨峰组,每组40例,均常规行超声心动图检查,计算左心室重量指数(LVMI)。结果晨峰组24h、昼间、夜间收缩压及血压晨峰均明显高于非晨峰组(P<0.05),晨峰组LVMI明显高于非晨峰组;左心室肥厚比例明显高于非晨峰组(P<0.05)。结论老年原发性高血压患者血压晨峰与左心室肥厚密切相关。     

高龄高血压患者血压变异性与认知功能损害

目的探讨高龄高血压患者血压变异性与认知功能损害的关系。方法入选2017年3月至2017年12月北京积水潭医院干部保健科高龄高血压住院患者177例,根据认知功能评估结果分为轻度认知障碍(MCI)组114例和认知正常组63例,比较2组患者的一般情况、实验室检查、平均血压、血压变异系数、昼夜节律和晨峰血压。采用SPSS 17.0统计软件对数据进行处理。组间比较采用t检验或χ~2检验。结果 2组患者一般情况差异无统计学意义(P0.05)。与MCI组患者相比,认知正常组患者收缩压变异系数[(0.11±0.02)%vs(0.08±0.03)%]、舒张压变异系数[(0.12±0.02)%vs(0.11±0.03)%]水平明显增高,差异具有统计学意义(P0.05)。2组患者收缩压下降率、舒张压下降率和舒张压晨峰差异无统计学意义(P0.05)。MCI组患者收缩压晨峰明显高于认知正常组患者[(17.37±5.36)vs(13.60±3.57)mm Hg],差异有统计学意义(P0.05)。2组患者非杓型、杓型、反杓型和超杓型血压比例差异无统计学意义(P0.05)。结论控制血压变异性及收缩压晨峰有利于改善高龄高血压患者的认知功能。     

血脂康在老年高血压患者降压治疗中对血压和脉压的影响

目的 观察血脂康在老年高血压患者降压治疗中对血压和脉压的影响.方法 将经氨氯地平(5 mg,1次/d)降血压治疗后达到轻度高血压标准的老年高血压患者58例随机分为两组,血脂康组30例和对照组28例.对照组采用低脂、低盐饮食及按原剂量服用氨氯地平;血脂康组在此基础上加用血脂康600 mg,2次/d,连续服用12周,比较两组治疗前与治疗12周时血压和脉压的变化.结果 与治疗前比较,血脂康组治疗12周收缩压降低,分别为(149±9)mm Hg与(130±8)mm Hg;脉压缩小,分别为(64±11)mm Hg与(48±7)mm Hg(均为P＜0.05);12周时组间比较,血脂康组优于对照组,收缩压分别为(130±8)mm Hg与(144±9)mm Hg,脉压为(48±7)mm Hg与(60±10)mm Hg(均为P＜0.05).结论 老年高血压患者降压治疗中,应用常规剂量血脂康治疗可以起到降低血压的作用效应.     

血压变异性对老年女性高血压患者颈动脉硬化的影响

目的探讨血压变异性对老年女性高血压患者颈动脉硬化的影响。方法选择198例诊室血压正常的女性高血压患者作为高血压组,同时选择女性正常血压者200例作为对照组。2组均行颈动脉超声检查,测颈动脉内膜中层厚度(IMT),测定24h动态血压和生化指标。结果高血压组冠心病(48.5%vs 39.5%)、脑血管病(51.0%vs 40.5%)和肾病(15.2%vs 8.5%)及颈动脉硬化(65.7%vs 26.0%)比例明显高于对照组(P<0.05,P<0.01),高血压组IMT明显高于对照组[(1.18±0.31)mmvs(0.81±0.24)mm,P=0.003]。高血压组夜间平均收缩压[(159.1±13.2)mm Hg)vs(141.3±11.3)mm Hg,1mm Hg=0.133kPa],夜间收缩压标准差[(15.9±3.1)mm Hg vs(9.5±1.2)mm Hg]及夜间收缩压血压负荷[(41.4±2.2)%vs(21.3±2.6)%]明显增高,夜间舒张压标准差[(9.1±4.1)mm Hg vs(6.2±2.3)mm Hg]及夜间舒张压血压负荷[(34.7±11.2)%vs(22.6±11.5)%]明显增高,差异有统计学意义(P<0.05,P<0.01)。结论血压变异性增大,夜间血压增高及血压负荷的增加是女性颈动脉硬化的危险因素。     

老年男性原发性高血压患者动态血压及血压变异性与踝臂指数的关系探讨

目的评价老年男性原发性高血压患者动态血压及血压变异性(BPV)与踝臂指数(ABI)的关系。方法入选老年男性原发性高血压患者160例,按照ABI分为正常ABI组(ABI>0.90)104例和低ABI组(ABI≤0.90)56例,比较并分析其24 h动态血压参数和BPV参数。结果低ABI组较正常ABI组24 h平均脉压[(62.4±13.8)mm Hg比(53.0±13.0)mm Hg]、日间平均脉压[(67.3±17.0)mm Hg比(55.4±20.0)mm Hg]和夜间平均脉压[(63.0±16.0)mm Hg比(52.9±13.6)mm Hg]均高(P<0.01),同时夜间收缩压最大值[(146.5±17.4)mm Hg比(135.5±17.1)mm Hg]、夜间收缩压标准差[(12.4±4.0)mm Hg比(10.1±4.2)mm Hg]均大(P<0.05)。结论老年男性原发性高血压患者夜间收缩压最大值、夜间收缩压标准差、日间平均脉压、夜间平均脉压和24 h平均脉压升高可能是低ABI的危险因素。     

比较不同时间服用缬沙坦对高血压患者血压变异性的影响

目的比较不同时间服用缬沙坦及苯磺酸氨氯地平片对原发性高血压（高血压）患者血压变异性（bloodpressurevariability,BPV）的影响。方法采用随机数字法将120例轻一中度高血压患者分成3组,分别为日间口服缬沙坦组、夜间口服缬沙坦组、日间口服苯磺酸氨氯地平组,治疗前、后进行24h动态血压监测。以动态血压变异标准差作为血压变异性指标,比较3个月后3种治疗方案对血压及血压变异性的影响。结果3种治疗方案均能有效降低血压,与治疗前比较差异有统计学意义（P〈0．05）。在控制BPV方面,日间口服缬沙坦组的BPV改善不明显,与治疗前比较差异无统计学意义（P〉0．05）;与治疗前比较,夜间口服缬沙坦组[收缩压变异性：（11±3）mmHg眠（15±4）nlmHg（1mmHg=0．133kPa）,P〈0．05;舒张压变异性：（7±2）mmHgVS．（10±4）mmHg,P〈0．05]和苯磺酸氨氯地平组[收缩压变异性：（10±3）mmHgIJS．（16±3）mmHg,P〈0．05;舒张压变异性：（6±2）mmHgVS．（11±2）mmHg,P〈0．05]的24h动态血压变异性降低,差异有统计学意义;苯磺酸氨氯地平组在改善BPV方面仍优于夜间口服缬沙坦组,差异有统计学意义（P〈0．01）。结论与日间服药相比,夜间服用缬沙坦能更有效改善血压变异性。     

老年高血压患者血压变异性与左室肥厚的关系

目的 探讨老年高血原病患者血压变异性（BPV）与左室肥厚的关系。方法 选择216例高血压患者进行24h动态血压监测（ABPM）和超声心动图检查，分析血压变异性与左室肥厚的关系。结果 老年高血压患者合并左室肥厚组与无左室肥厚组比较，年龄、性别、24h平均血压和血糖、血脂水平无显著差异，但左室肥厚组的24h收缩压变异性（16．8±1．9VS14．3±2．3），白昼（14．9±2．5VS13．8±2．4）和夜间（10．8±3．7VS9．7±2．9）收缩压变异性均显著大于无左室肥厚组（P〈0．05）。结论 老年高血斥患者收缩斥波动与左室肥厚密切相关，可能预测高血压靶器官损害和不良心血管事件。     

原发性高血压患者血压变异性与早期肾损害

目的探讨血压变异性(BPV)和原发性高血压患者早期肾损害的关系。方法根据尿白蛋白与尿肌酐比值(UACR)把181例原发性高血压患者分为两组,UACR≤30mg/g为单纯高血压组(A组,120例),UACR>30mg/g为合并早期肾损害组(B组,61例),行24h动态血压监测,BPV以血压标准差和变异系数表示,用Pearson相关分析和多元线性回归分析比较两组患者BPV和早期肾损害之间的关系。结果两组患者各个时段的血压均值差异无统计学意义(P>0.05);除白昼收缩压变异性外,A组和B组24h收缩压变异性[标准差(13.6±3.0)比(15.3±4.1)mmHg;变异系数(0.11±0.02)比(0.12±0.03)]、24h舒张压变异性[标准差(9.6±2.6)比(11.8±4.2)mmHg;变异系数(0.13±0.04)比(0.15±0.05)]、白昼舒张压变异性[标准差(9.5±3.0)比(11.3±4.6)mmHg;变异系数(0.12±0.04)比(0.14±0.06)]、夜间收缩压变异性[标准差(10.0±3.9)比(13.2±4.7)mmHg;变异系数(0.08±0.03)比(0.11±0.04)]和夜间舒张压变异性[标准差(7.7±3.7)比(10.0±3.8)mmHg;变异系数(0.11±0.05)比(0.14±0.05)]差异均有统计学意义(均P<0.05)。Pearson相关分析显示UACR与24h收缩压变异性、24h舒张压变异性、白昼舒张压变异性、夜间收缩压变异性及夜间舒张压变异性呈正相关(均P<0.01)。多元线性回归分析显示UACR与夜间收缩压变异性、24h舒张压变异性、夜间舒张压水平和三酰甘油呈正相关(均P<0.05)。结论原发性高血压患者夜间收缩压变异性、24h舒张压变异性、夜间舒张压水平和三酰甘油与早期肾损害相关。     

中老年男性肥胖者阻塞性睡眠呼吸暂停低通气综合征与代谢综合征相关性研究

目的 探讨中老年男性肥胖者阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)与代谢综合征(metabolic syndrome,MS)及其组分之间的关系.方法 选择中老年男性肥胖患者154例,根据多导睡眠呼吸监测仪监测结果诊断OSAHS及病情严重程度,测定MS相关指标,应用统计学方法对OSAHS各组相关指标及OSAHS与MS之间的关系进行比较分析.结果 与对照组比较,重度OSAHS组高密度脂蛋白胆固醇明显降低[(1.03±0.29)mmol/L对(1.31±0.38)mmol/L,P＜0.05],血糖[(6.61±1.76)mmol/L对(5.47±0.64)mmol/L]、收缩压[(133±13)mm Hg对(125±12)mm Hg]及舒张压[(99±10)mm Hg对(80±5)mm Hg]明显升高(均P＜0.05);MS患病率轻度OSAHS组25.7%,中度OSAHS组46.5%,重度OSAHS组84.4%,均明显高于对照组16.1%(均P＜0.01);在OSAHS患者中,MS患病率是对照组的6.16倍.结论 中老年男性肥胖患者OSAHS是MS发病的独立危险因素.

Abstract：

Objective To explore the relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and metabolic syndrome (MS) in obese middle-aged and older men. Methods We selectively recruited 154 obese middle-aged and older men matched for body mass index (BMI) and age. The polysomnography was performed for diagnosing OSAHS and for discriminating disease severity. The BMI, waist circumference, blood pressure, plasma glucose and lipid profiles were measured and analyzed in all subjects. Appropriate statistical methods were used to compare the components of MS in each group. Logistic regression was taken to elucidate the relationship between OSAHS and MS. Results Compared to control group, severe OSAHS group had significantly lower high density lipoprotein cholesterol level [( 1.03 ± 0.29 ) mmol/L vs. ( 1.31 ± 0. 38) mmol/L,P＜0. 05] and higher fasting glucose [(6.61±1.76) mmol/L vs. (5.47±0.64) mmol/L, P＜0. 05]as well as higher systolic blood pressure [( 133 ± 13) mm Hg vs. ( 125 ± 12) mm Hg, P＜0. 05] and diastolic blood pressure [(99±10) mm Hg vs. (80±5) mm Hg, P＜0. 05]. The prevalence of MS was significantly higher in OSAHS group than in control group (mild OSAHS group: 25.7%,moderate OSAHS group: 46. 5%, severe OSAHS group: 84.4%, control group: 16. 1 %, all P＜0. 01). OSAHS was independently associated with an increased prevalence of MS Odds ratio, 6.16).Conclusions OSAHS is independently associated with MS in obese middle-aged and older men.     

Blood pressure variability and silent cerebral damage in essential hypertension

BACKGROUND: It is recognized that blood pressure (BP) variability has prognostic significance in determining target organ damage and cardiovascular mortality and morbidity. The aim of this study was to analyze the association between blood pressure variability and the presence of silent cerebral white matter lesions in middle-aged asymptomatic essential hypertensives. METHODS: We studied 43 middle-aged untreated hypertensive patients. Blood pressure variabilities (short-term and long-term) were evaluated by using both non-invasive, beat-to-beat, continuous finger 24-hour monitoring (Portapres) and oscillometric automated discontinuous ambulatory blood pressure monitoring. All patients underwent cerebral magnetic resonance imaging to detect the presence or not of white matter lesions. RESULTS: Hypertensive patients with cerebral white matter lesions exhibited significantly higher values of long-term systolic blood pressure variability (standard deviation of 24-hour blood pressure) measured both by continuous beat-to-beat monitoring (16.2 +/- 3.7 v 13.7 +/- 3.6 mm Hg; P = 0.047) and by ambulatory blood pressure monitoring (15.2 +/- 3.8 v 12.8 +/- 2.7 mm Hg; P = 0.022). However, these differences were not independent on blood pressure elevation and did not maintain their significance after adjusting for 24-hour systolic blood pressure. Neither short-term systolic blood pressure variability, nor short-term or long-term diastolic blood pressure variabilities showed differences between patients with and without white matter lesions. CONCLUSION: The present study indicates that long-term systolic blood pressure variability is significantly related to the presence of silent cerebral white matter lesions in essential hypertensive patients, although this relationship is partially dependent on absolute blood pressure elevation.     

小剂量左旋氨氯地平、替米沙坦及氢氯噻嗪同时和不同时给药对血压晨峰的影响

目的 探讨小剂量左旋氨氯地平、替米沙坦及氢氯噻嗪同时与不同时给药对轻中度高血压患者血压晨峰（MBPS）的影响.方法 选择我院2011年5月至2014年5月门诊及住院的高血压患者138例,男性86例,女性52例.入选者收缩压（SBP）＜180 mm Hg,舒张压（DBP）91～109 mm Hg,年龄＞45岁,24 h动态血压监测（ABDM）具有MBPS现象.随机分为2组：Ⅰ组（不同时给药组,70例）晨服替米沙坦40 mg和氢氯噻嗪10 mg,晚服左旋氨氯地平2.5 mg;Ⅱ组（同时给药组,68例）以上三种药物均晨服.所有病例治疗前及治疗8周后进行ABPM监测.结果 治疗8周后,Ⅰ组和Ⅱ组的24h SBP/DBP均较治疗前分别降低17.34/10.26 mm Hg和16.64/10.42 mm Hg,日间SBP/DBP分别降低15.48/9.86 mm Hg和17.36/10.28 mm Hg,均较治疗前明显降低（P＜0.01）,两组间降低幅度未见统计学差异（P＞0.05）.两组夜间SBP/DBP分别降低21.52/11.22 mm Hg和15.82/10.14 mm Hg,均较治疗前明显降低（P＜0.01）;Ⅰ组治疗后降低幅度较Ⅱ组明显,两组比较差异有统计学意义（P＜0.05）.治疗前与治疗8周后清晨收缩压差值（MSBPD）Ⅰ组分别为（37.26±10.34）mm Hg和（23.14±7.82）mm Hg,治疗后显著降低（P＜0.01）;Ⅱ组分别为（37.48±10.32）mm Hg和（29.34±8.46）mmHg,治疗后明显降低（P＜0.05）,两组治疗后比较,差异有统计学意义（P＜0.05）.结论 对于晨峰高血压患者,小剂量左旋氨氯地平、替米沙坦及氢氯噻嗪无论同时还是不同时给药均能有效控制24h、日间和夜间血压;而不同时给药治疗夜间血压优于同时给药,尤其控制MBPS现象更明显.     

Morning blood pressure surge and hypertensive cerebrovascular disease: role of the alpha adrenergic sympathetic nervous system

BACKGROUND: The morning surge of blood pressure (BP) is associated with alpha-adrenergic activity. We studied the association between the alpha-adrenergic morning surge in BP and silent cerebrovascular disease in elderly patients with hypertension. METHODS: We conducted ambulatory BP monitoring three times (twice at baseline and after nighttime dosing of the alpha1-blocker doxazosin) in 98 elderly hypertensive patients in whom the presence of silent cerebral infarcts (SCI) was assessed by brain magnetic resonance imaging. The morning BP surge (MBPS) was calculated as the mean systolic BP during the 2 h after waking minus the mean systolic BP during 1 h that included the lowest sleep BP. The alpha-adrenergic MBPS was calculated as the reduction of MBPS by doxazosin. RESULTS: The prevalence of multiple SCI was higher in the Surge group (top quartile: MBPS > or = 45 mm Hg, n = 24) than in the Nonsurge group (MBPS < 45 mm Hg, n = 74) (54% v 31%, P = .04), and in the higher alpha-adrenergic surge group (top quartile: alpha-adrenergic MBPS > or = 28 mm Hg, n = 25) than in the lower alpha-adrenergic surge group (< 28 mm Hg, n = 73) (68% v 26%, P < .0001). In the Surge group, subjects with higher alpha-adrenergic surge (n = 17) had a markedly higher frequency of multiple SCI, whereas none in the lower alpha-adrenergic surge group had multiple SCI (n = 7) (77% v 0%, P = .001). The alpha-adrenergic MBPS was closely associated with multiple SCI (10 mm Hg increase: OR = 1.96, P = .006), independently of age, MBPS, 24-h systolic BP, and other confounding factors. CONCLUSION: The morning BP surge, particularly that dependent on alpha-adrenergic activity, is closely associated with advanced silent hypertensive cerebrovascular disease in elderly individuals.