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1.
目的评价坎地沙坦酯片治疗轻中度原发性高血压的疗效和安全性.方法随机、双盲、双模拟、阳性药物(氯沙坦)平行对照.61例轻、中度原发性高血压服用坎地沙坦酯片或氯沙坦片各1片,1次/d,必要时增加剂量1次.总疗程8周.结果氯沙坦组治疗前的血压为(146.2±11.6)/(100.3±3.3)mm Hg,治疗后的血压为(130.3±9.8)/(85.7±8.0)mm Hg,血压下降幅度为(16.0±11.8)/(14.6±6.8)mm Hg;坎地沙坦酯组治疗前的血压为(143.4±11.2)/(100.6±4.1)mm Hg,治疗后的血压为(130.4±11.2)/(86.3±8.0)mm Hg,血压下降幅度为(13.0±8.7)/(14.3±6.5) mm Hg.两组治疗后血压降低幅度均有统计学意义,主要降幅均在前2周.组间无差异.治疗前后心率无明显变化.坎地沙坦酯和氯沙坦降压显效率分别为60.7%和60.0%,总有效率分别为82.1%和76.7%,组间无差别.不良事件坎地沙坦酯和氯沙坦组为头晕各2例和1例,血生化等实验室指标无异常改变.结论国产坎地沙坦酯片治疗轻中度原发性高血压不良反应发生率很低,本文无1例出现咳嗽,耐受性良好,适用于长期治疗.  相似文献   

2.
目的研究老年综合评估在老年高血压患者综合治疗中的应用。方法选取122例老年原发性高血压患者,随机分为试验组61例和对照组61例。试验组在口服降压药物治疗的同时进行老年综合评估,并依据评估结果实施相应干预措施。观察2组治疗前和治疗后的血压变化情况,并进行分析。结果试验组和对照组治疗后偶侧收缩压/舒张压均较治疗前降低[(132. 72±10. 53)/(69. 28±6. 49) mm Hg(1 mm Hg=0. 133 k Pa) vs (165. 54±9. 28)/(82. 46±8. 87) mm Hg,(147. 21±8. 85)/(69. 61±4. 63) mm Hg vs (164. 26±8. 99)/(81. 92±9. 74) mm Hg,P 0. 01];试验组偶测收缩压较对照组下降更明显(P 0. 01)。试验组和对照组治疗后24 h收缩压/舒张压较治疗前降低[(131. 57±10. 14)/(69. 05±6. 04) mm Hg vs (161. 33±10. 10)/(80. 84±7. 86) mm Hg,(144. 30±8. 69)/(70. 51±4. 88) mm Hg vs (161. 28±8. 92)/(80. 10±7. 73) mm Hg,P 0. 01];试验组24 h收缩压较对照组下降更明显(P 0. 01)。2组治疗后的血压变异性均较治疗前明显降低,且试验组降低更为明显(P 0. 05,P 0. 01)。结论高血压患者进行老年综合评估,能够提高或维持其生活质量,使降压治疗效果更优化。  相似文献   

3.
目的:评价奥美沙坦治疗高血压晨峰血压(MBPS)的疗效。方法:103例原发性高血压MBPS患者随机分为2组,分别接受奥美沙坦(53例,20 mg/d)和苯磺酸氨氯地平(50例,5 mg/d)治疗8周,于治疗前和治疗后4、8周做24 h动态血压监测,调整药物剂量和观测服药前后清晨血压变化。结果:2组药物治疗8周,24 h、白天、夜间及最后2~4 h平均血压均降至正常范围。奥美沙坦组最后2~4 h舒张压(DBP)的降低幅度大于氨氯地平组(19.3±11.8 vs 9.0±6.6 mmHg,P=0.031)。2组降晨峰血压(MBPS)的幅度相近,△收缩压(15.8±6.7 vs 17.0±6.8 mmHg,P0.05);△舒张压(12.8±5.9 vs 9.3±2.1 mmHg,P0.05)。2组治疗后脉率均稍有上升(3.4±1.8 vs 4.2±1.3次/min,P0.05)。2组治疗后收缩压和舒张压的平滑指数(SI)无统计学差异。结论:奥美沙坦酯能有效平稳的控制原发性高血压MBPS,奥美沙坦能强效抑制清晨舒张压的波动。  相似文献   

4.
坎地沙坦加氢氯噻嗪对轻中度高血压的疗效和安全性   总被引:1,自引:0,他引:1  
目的 评价坎地沙坦加氢氯噻嗪(复方坎地沙坦酯片)对原发性高血压的降压疗效和安全性.方法 对原发性高血压患者经过2周清洗期后,进入坎地沙坦酯片8 mg单药治疗期,对4周后血压未达标者(达标血压为<140/90 mm Hg),以随机、双盲双模拟、平行对照、多中心试验方法 ,分别服复方坎地沙坦酯片(坎地沙坦酯16.0mg/氢氯噻嗪12.5 mg)或坎地沙坦酯片16 mg单药治疗8周.结果 经过2周清洗期,共有392例进入单药治疗期,坎地沙坦酯8 mg单药治疗(n=353)2周后,血压下降值(10.2±0.6)/(6.5±5.7)mm Hg;4周的下降值为(10.8±10.9)/(6.6±6.1)mm Hg,4周血压达标率为15.3%(54/353例),组内比较,差异有非常显著意义(P<0.01).在以后8周随机双盲对照期,复方坎地沙坦酯组(134例)与坎地沙坦酯单药组(142例)4周时的血压分别下降为(9.3±11.7)/(8.7±6.2)和(5.4±10.8)/(5.4±6.1)mm Hg;8周时为(11.1±11.2)/(10.7±6.6)和(7.8±11.1)/(7.8±6.3)mm Hg(组内及组间比较P<0.01).随机期4周时联合治疗组血压达标率分别为64.9%(87/134),单药组为39.4%(56/142),8周时分别为79.9%(107/134)和51.4%(73/142)(组间比较P<0.01).不良反应事件,在单药治疗期为6.2%(22/353),复方坎地沙坦组为2.9%(4/134),坎地沙坦酯组2.8%(4/142),组间比较差异无统计学意义(P>0.05).结论 复方坎地沙坦酯片较之单用坎地沙坦对原发性高血压患者有较好的降压效果和耐受性.  相似文献   

5.
目的:评价奥美沙坦酯治疗轻度及中度原发性高血压的疗效和安全性。方法:80例轻度及中度原发性高血压患者随机接受奥美沙坦酯20 mg或缬沙坦80 mg治疗,每日1次,总疗程8周。结果:奥美沙坦酯组治疗前的收缩压(SBP)/舒张压(DBP)为(155.2±11.4)/(96.1±5.2)mmHg(1 mmHg=0.133 kPa),治疗后的血压为(138.8±10.2)/(86.5±4.8)mmHg,血压下降幅度为(16.4±8.1/9.6±5.1)mmHg。缬沙坦组治疗前的SBP/DBP为(156.1±12.2)/(97.2±5.1)mmHg,治疗后的血压为(139.5±10.4)/(88.0±5.5)mmHg,血压下降幅度为(15.6±7.8/9.1±4.9)mmHg。2组治疗前后血压下降幅度差异均有统计学意义(P<0.01),2组间差异无统计学意义(P>0.05)。奥美沙坦酯组和缬沙坦组降压显效率分别为59.0%和60.5%,总有效率分别为87.2%和86.8%,2组间差异无统计学意义。本实验中奥美沙坦酯组出现不良反应者少。结论:奥美沙坦酯治疗轻度及中度原发性高血压疗效确切,且安全可靠。  相似文献   

6.
目的 评价奥美沙坦酯20 mg/氢氯噻嗪12.5 mg用于奥美沙坦酯20 mg单药治疗血压未达标的原发性轻中度高血压患者的疗效和安全性.方法 采用多中心、随机、双盲双模拟、活性药物对照设计.438例轻中度高血压患者人选.经过2周安慰剂导入期,380例进入4周奥美沙坦酯20 mg/d单药治疗期,最后304例血压未达标者(...  相似文献   

7.
《中华高血压杂志》2021,29(5):420-427
目的评价我国自主研发的一种新型的选择性非肽类血管紧张素受体阻滞药(ARB)1.1类口服降压药阿利沙坦酯联合氨氯地平或联合吲达帕胺,在单药治疗未达标的轻中度原发性高血压(EH)患者中的临床疗效及安全性。方法 2016年9月9日至2018年12月7日,在全国44家研究中心选择年龄18~75岁、体质量指数(BMI)18.5~30.0 kg/m~2、血压140/90~180/110 mm Hg的EH患者。给予阿利沙坦酯片240 mg/d,用药4周后评估血压是否达标,达标者继续用药8周,未达标者1∶1随机分配到阿利沙坦酯片240 mg+吲达帕胺缓释片1.5 mg组(A+D)或阿利沙坦酯片+苯磺酸氨氯地平片5 mg组(A+C)治疗8周。主要观察治疗12周坐位血压降低幅度和达标率(坐位血压140/90 mm Hg)以及安全性指标。结果共入选2 212例患者,其中纳入疗效分析共2 126例,平均年龄(55.1±10.2)岁。疗效结果显示,1 463例阿利沙坦酯单药治疗4周有效(68.8%),坐位收缩压/舒张压较基线降低(14.7±12.2)/(8.0±8.4)mm Hg(P0.001)。不达标者在阿利沙坦酯基础上联合氨氯地平或联合吲达帕胺治疗8周后,联合氨氯地平组相较于单药治疗4周时的收缩压和舒张压分别降低(14.0±12.2)/(8.3±9.2)mm Hg,达标率为57.7%(169/293);联合吲达帕胺组与单药治疗4周时相比,收缩压/舒张压下降(14.4±12.1)/(8.2±8.2)mm Hg,达标率为62.8%(181/288)。联合吲达帕胺组与联合氨氯地平组相比,血压降幅和达标率均相当,差异无统计学意义。不良反应发生率联合氨氯地平组为8.7%,联合吲达帕胺组为11.7%。结论阿利沙坦酯单药治疗未达标联合吲达帕胺或联合氨氯地平,可进一步提高达标率,2组间达标及疗效相同,安全性相当。  相似文献   

8.
目的探讨有氧运动对轻中度原发性高血压患者血压的影响。方法选择2010年10月—2011年12月我院收治的轻中度原发性高血压患者20例,均进行12周的有氧运动,观察有氧运动前后患者血压、睡眠不足所占比例及焦虑自评量表(SAS)评分的变化。结果有氧运动12周后,患者收缩压为(138±7)mm Hg,舒张压为(83±7)mm Hg,低于有氧运动前的(149±8)mm Hg、(95±7)mm Hg(P0.05);治疗后睡眠不足者所占比例和SAS评分均低于治疗前(P0.05)。结论有氧运动对轻中度原发性高血压患者血压具有调节作用,且能改善患者生活质量,可以作为部分轻中度原发性高血压患者尤其是早期患者单独选用的干预方法。  相似文献   

9.
目的比较奥美沙坦酯和缬沙坦治疗高血压患者血压晨峰的疗效。方法选择我院76例原发性高血压患者随机分为2组,分别接受奥美沙坦酯20-40mg/d或缬沙坦80-160mg/d治疗,共8周,观察服药前及服药后清晨血压变化。结果奥美沙坦酯组和缬沙坦组治疗后晨峰血压均有明显下降,与治疗前比较差异有统计学意义(P〈0.05)。奥美沙坦酯组和缬沙坦组晨峰血压下降的幅度分别为:/kSBP(10.22±0.35)mmHg、(5.63±0.21)mmHg;△DBP(7.71±0.29)mmHg、(3.55±0.14)mmHg,奥美沙坦酯组血压晨峰下降幅度高于缬沙坦组,差异有统计学意义(P〈0.05)。结论奥美沙坦酯和缬沙坦均可以有效地控制原发性高血压患者血压晨蜂现象,奥美沙坦酯优于缬沙坦。  相似文献   

10.
目的比较奥美沙坦酯加氨氯地平与奥美沙坦酯加氢氯噻嗪治疗原发性高血压的降压疗效。方法将原发性高血压患者(收缩压≥160 mmHg和/或舒张压≥100 mmHg)60例,分别给予奥美沙坦酯加氨氯地平(A组)与奥美沙坦酯加氢氯噻嗪(B组)治疗,每组各30例,共治疗8周。监测两组治疗前后24 h动态血压、血糖、血脂、肝肾功能,观察治疗期间药物不良反应及心血管事件(脑卒中、冠心病、心功能不全、肾衰等)。结果治疗后两组患者与治疗前比较24 h平均收缩压、24 h平均舒张压、白昼平均收缩压、白昼平均舒张压、夜间平均收缩压、夜间平均舒张压,白昼和夜间血压变异性均下降(P<0.05)。两组间相比奥美沙坦酯加氨氯地平组可更有效地降低患者白昼和夜间血压变异性(P<0.05),两组间相比奥美沙坦酯加氨氯地平组可更好地改善患者血压昼夜节律(P<0.01);两组患者在观察期间内均无不良反应及心血管事件发生。结论对于2级以上原发性高血压患者,奥美沙坦酯加氨氯地平组与奥美沙坦酯加氢氯噻嗪组的降压疗效相当;奥美沙坦酯加氨氯地平组在改善血压昼夜节律,降低血压变异性方面优于奥美沙坦酯加氢氯噻嗪治疗。  相似文献   

11.
目的探讨老年高血压伴发抑郁焦虑情绪患者的24h动态血压变化规律。方法选择老年高血压患者120例,进行抑郁自评量表和焦虑自评量表的心理问卷调查及汉密尔顿抑郁量表和汉密尔顿焦虑量表的评定,根据评分结果分为抑郁焦虑组75例和无抑郁焦虑组45例,对所有研究对象进行24h动态血压监测,并对结果进行比较分析。结果抑郁焦虑组24h收缩压、昼间收缩压、夜间收缩压明显高于无抑郁焦虑组[(136.0±14.6)mm Hg(1mm Hg=0.133kPa)vs(126.0±13.4)mm Hg,(139.0±15.2)mm Hg vs(130.0±13.6)mm Hg,(132.0±13.6)mm Hg vs(123.0±12.5)mm Hg,P<0.01]。抑郁焦虑组24h收缩压标准差、昼间收缩压标准差及24h收缩压加权标准差显著高于无抑郁焦虑组[(14.78±1.62)mm Hg vs(14.07±1.80)mm Hg,(13.25±2.94)mm Hg vs(12.28±3.05)mm Hg,(14.07±1.37)mm Hg vs(10.81±1.91)mm Hg,P<0.05,P<0.01]。结论有抑郁焦虑情绪的老年高血压患者血压变异性显著高于无抑郁焦虑高血压患者。  相似文献   

12.
Zhu JR  Cai NS  Fan WH  Zhu DL  He B  Wu ZG  Ke YN  Guo JX  Ma H  Huang J  Li XL  Chen YZ 《中华心血管病杂志》2006,34(10):877-881
目的 通过与氯沙坦钾比较评价奥美沙坦酯治疗轻、中度原发性高血压患者的疗效和安全性。方法采用随机、双盲、双模拟、阳性对照、平行分组、多中心临床试验方法。共入选287例轻、中度原发性高血压患者,按照1:1的比例随机分组,分别接受奥美沙坦酯20mg或氯沙坦钾50mg,每天1次口服治疗。在用药4周后对患者进行血压评价,如果患者舒张压(DBP)仍≥90mmHg(1mmHg=0.133kPa),则试验药物剂量加倍,直至8周试验结束;治疗4周后DBP〈90mmHg的患者则维持原剂量继续治疗至第8周。结果(1)治疗4周后,奥美沙坦酯组坐位DBP谷值平均下降11.72mmHg,氯沙坦钾组平均下降9.23mmHg,两组间比较P=0.004。(2)治疗8周后,奥美沙坦酯组坐位DBP谷值平均下降12.94mmHg,氯沙坦钾组平均下降11.01mmHg,两组间比较P=0.035。(3)治疗4周后,奥美沙坦酯组有效数为81例(65.3%),氯沙坦钾组有效数为68例(52.7%),两组间比较P=0.028;治疗8周后,两组有效病例数和有效率相当,P〉0.05。(4)治疗8周后,24h动态血压监测显示,奥美沙坦酯组DBP和SBP的个体和总体谷/峰比值均高于氯沙坦钾组,奥美沙坦酯在24h内的作用持续时间比氯沙坦钾组长。(5)奥美沙坦酯组和氯沙坦钾组发生的与试验药物有关的不良事件的发生率分别为10.5%和13.9%,P〉0.05。结论奥美沙坦酯每日口服20~40mg能够有效、安全地治疗高血压。与氯沙坦钾每日口服50-100mg相比,奥美沙坦酯的降压效果优于氯沙坦钾。  相似文献   

13.
Olmesartan medoxomil is a new angiotensin II receptor blocker. In this randomized, double-blind, placebo-controlled study, the efficacy and safety of olmesartan medoxomil was assessed in 334 patients with moderate to severe essential hypertension. Patients were randomized to receive placebo; 5, 20, or 80 mg olmesartan medoxomil q.d.; or 2.5, 10, or 40 mg olmesartan medoxomil b.i.d. Ambulatory and cuff blood pressure were measured prior to and after 8 weeks of treatment. Treatment with olmesartan medoxomil resulted in a significant placebo-adjusted reduction of mean 24-hour ambulatory diastolic blood pressure of 9.6 mm Hg, 12.2 mm Hg, and 10.6 mm Hg in the 5-, 20-, and 80-mg q.d. groups, respectively. Corresponding reductions in mean ambulatory systolic blood pressure were 14.5 mm Hg, 16.5 mm Hg, and 15.4 mm Hg. Similar reductions of diastolic and systolic blood pressure were seen with b.i.d. dosing. The diastolic trough-to-peak ratios of the q.d. doses of olmesartan medoxomil ranged from 57%–70%, indicating 24-hour effectiveness. The safety profile of olmesartan medoxomil was similar to that of placebo. Olmesartan medoxomil appears to be a safe and effective once-a-day treatment for hypertension.  相似文献   

14.
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。  相似文献   

15.
Olmesartan medoxomil is a new angiotensin II receptor blocker. In this randomized, double-blind, placebo-controlled study, the efficacy and safety of olmesartan medoxomil was assessed in 334 patients with moderate to severe essential hypertension. Patients were randomized to receive placebo; 5, 20, or 80 mg olmesartan medoxomil q.d.; or 2.5, 10, or 40 mg olmesartan medoxomil b.i.d. Ambulatory and cuff blood pressure were measured prior to and after 8 weeks of treatment. Treatment with olmesartan medoxomil resulted in a significant placebo-adjusted reduction of mean 24-hour ambulatory diastolic blood pressure of 9.6 mm Hg, 12.2 mm Hg, and 10.6 mm Hg in the 5-, 20-, and 80-mg q.d. groups, respectively. Corresponding reductions in mean ambulatory systolic blood pressure were 14.5 mm Hg, 16.5 mm Hg, and 15.4 mm Hg. Similar reductions of diastolic and systolic blood pressure were seen with b.i.d. dosing. The diastolic trough-to-peak ratios of the q.d. doses of olmesartan medoxomil ranged from 57%-70%, indicating 24-hour effectiveness. The safety profile of olmesartan medoxomil was similar to that of placebo. Olmesartan medoxomil appears to be a safe and effective once-a-day treatment for hypertension.  相似文献   

16.
目的探讨高血压患者血压昼夜节律异常对不同亚型急性缺血性脑卒中的影响。方法参照改良TOAST分型标准,将97例伴高血压的急性缺血性脑卒中患者分为动脉粥样硬化血栓形成(arterothrombosis,AT)组66例和小动脉病变(small artery disease,SAD)组31例,并进行24h动态血压监测。比较2组间24h、昼间和夜间的血压水平、晨峰血压及血压昼夜节律的变化。结果 AT组夜间收缩压明显高于SAD组[(133.86±18.17)mm Hg vs(124.42±16.06)mm Hg,1mm Hg=0.133kPa,P<0.05];AT组血压昼夜节律消失比例明显高于SAD组(84.8%vs 64.5%,P<0.05);2组晨峰血压发生率比较,差异无统计学意义(37.9%vs 19.4%,P>0.05)。结论血压昼夜节律消失和夜间血压水平升高与AT型缺血性脑卒中的发生有关。  相似文献   

17.
OBJECTIVE: The prevalence of isolated systolic hypertension (ISH) is high in the elderly, and the objective of this study was to compare the antihypertensive efficacy of olmesartan medoxomil with that of nitrendipine in elderly (65-74 years) and very elderly (>/= 75 years) male and female patients with ISH. METHODS: Patients were randomized to 24 weeks of treatment with either olmesartan medoxomil 20 mg daily (n = 256) or nitrendipine 20 mg (n = 126) twice daily, with possible dose increase (to 40 mg daily) and addition of hydrochlorothiazide (HCTZ) 12.5 or 25 mg daily if required. RESULTS: On the primary endpoint [reduction in mean sitting systolic blood pressure (SBP) after 12 weeks of treatment], the two treatments were similar (olmesartan medoxomil, -30.0 mmHg; nitrendipine, -31.4 mmHg). No significant difference between the treatment groups was observed, and non-inferiority of olmesartan medoxomil to nitrendipine was demonstrated using an analysis of covariance (ANCOVA) model. Reductions in mean sitting and standing SBP and diastolic blood pressure (DBP) up to week 24 were also similar with both treatments. Blood pressure (BP) goal attainment rates (sitting SBP 相似文献   

18.
急性脑卒中患者血压特点的分析   总被引:2,自引:0,他引:2  
目的研究急性脑卒中患者血压影响因素及动态血压特点。方法82例发病在7天内的急性脑卒中患者。记录患者住院诊室血压及24 h动态血压。血压≥140/90 mm Hg(1 mm Hg=0.133 kPa)为诊室血压升高;24 h动态血压平均值≥130/80 mm Hg、日间平均值≥135/85 mm Hg、夜间平均值≥125/75 mm Hg为动态血压升高。结果既往高血压病史对急性脑卒中患者诊室血压升高有影响(P<0.05)。有高血压病史者平均诊室血压(146.02±18.89)/(86.36±11.52)mm Hg,无高血压病史者平均诊室血压(136.22±14.63)/(82.61±11.86)mm Hg,二者收缩压水平差异有显著性意义(P<0.05)。急性脑卒中患者动态血压表现为夜间血压负荷增加,24 h平均血压于发病后4~5天明显升高,6~7天降低。诊室血压升高与诊室血压正常比较,血压形态均以非杓形和反杓形为主,2组差异无显著性意义(P>0.05)。结论急性脑卒中诊室血压升高与高血压病史有关,急性脑卒中随发病时间延长,血压呈下降趋势。  相似文献   

19.
Azilsartan medoxomil is an angiotensin receptor blocker (ARB) being developed for hypertension treatment. To compare this ARB with others in the class, we studied the effects of 2 doses of azilsartan medoxomil, with valsartan 320 mg and olmesartan medoxomil (olmesartan) 40 mg, in a randomized, double-blind, placebo-controlled trial using ambulatory blood pressure (BP) monitoring and clinic BP measurements. The primary efficacy end point was the change from baseline in 24-hour mean systolic BP. Hierarchical analysis testing for superiority over placebo was followed by noninferiority analysis and then superiority testing of azilsartan medoxomil (80 mg and then 40 mg) versus the comparator ARBs. For 1291 randomized patients, mean age was 56 years, 54% were men, and baseline 24-hour mean systolic BP was 145 mm Hg. Azilsartan medoxomil at 80 mg had superior efficacy to both valsartan at 320 mg and olmesartan at 40 mg: placebo-adjusted 24-hour systolic BP was lowered (-14.3 mm Hg) more than 320 mg of valsartan (-10.0 mm Hg; P<0.001) and 40 mg of olmesartan (-11.7 mm Hg; P=0.009). Azilsartan medoxomil at 40 mg was noninferior to 40 mg of olmesartan (difference: -1.4 mm Hg [95% CI: -3.3 to 0.5]). For clinic systolic BP, both doses of azilsartan medoxomil were superior to the comparator ARBs. Safety and tolerability were similar among the placebo and 4 active treatments. These data demonstrate that azilsartan medoxomil at its maximal dose has superior efficacy to both olmesartan and valsartan at their maximal, approved doses without increasing adverse events. Azilsartan medoxomil could provide higher rates of hypertension control within the ARB class.  相似文献   

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