厄贝沙坦氢氯噻嗪对高血压病患者血清C-反应蛋白浓度影响

目的：探讨厄贝沙坦氢氯噻嗪对高血压患者血清C-反应蛋白（CRP）浓度影响。方法：选择高血压患者50例,于用药前测定其CRP浓度;在厄贝沙坦氢氯噻嗪口服6周后再测定其血清CRP浓度。根据治疗后血压达标与否,分为血压达标组（28例）与非达标组（22例）,比较各组患者治疗前后血清CRP的变化。结果：与治疗前比较,治疗后血压达标组和非达标组患者血清CRP浓度均明显降低[（6．62±3．73）mg／L比（4．63±2．01）mg／L,（6．51±3．15）mg／L比（4．85±2．25）mg／L,P均〈0．05];血压达标组的血清CRP浓度低于非达标组的,但未达显著水平,P均〉0．05。结论：高血压患者服用厄贝沙坦氢氯噻嗪后血清C-反应蛋白浓度下降,提示厄贝沙坦可降低高血压患者的炎症反应。     

厄贝沙坦氢氯噻嗪片对老年高血压患者血管内皮功能的短期影响

目的 评价厄贝沙坦氢氯噻嗪片对老年高血压患者血管内皮功能的短期影响.方法 选择轻、中度原发性高血压患者106例,分为氢氯噻嗪组50例及厄贝沙坦氢氯噻嗪组56例,两组患者每日晨起分别口服氢氯噻嗪片25 mg及厄贝沙坦氢氯噻嗪片1片,连续12周,检测治疗前后患者的血压、血生化、高敏C反应蛋白（hs-CRP）、血管性血友病因子（vWF）等指标,以及肱动脉内皮依赖性舒张功能（EDD）和颈动脉内膜中层厚度（IMT）的变化.结果 与治疗前比较,氢氯噻嗪组患者治疗后收缩压、舒张压、血钾明显降低（P ＜0.05或P＜0.01）,尿酸明显升高（P＜0.01）,治疗前后vWF、EDD、IMT比较差异无统计学意义（P＞0.05）;厄贝沙坦氢氯噻嗪组患者治疗后收缩压、舒张压、hs-CRP及vWF均明显降低（P＜0.05或P＜0.01）,EDD明显提高（P＜0.05）,治疗前后IMT比较差异无统计学意义（P＞0.05）.两组患者治疗后比较,vWF、EDD比较差异有统计学意义（P＜0.05）.结论 老年轻、中度原发性高血压患者的血管内皮功能的损伤可以逆转,厄贝沙坦氢氯噻嗪片在降压同时可以改善受损的血管内皮功能.     

厄贝沙坦氢氯噻嗪对老年高血压患者不同水平尿白蛋白的影响

目的观察厄贝沙坦氢氯噻嗪对老年高血压患者不同水平尿白蛋白的影响。方法选择2013年4月~2015年10月在我院老年医学科接受治疗的老年1级、2级高血压患者138例,根据24h尿白蛋白水平分为对照组35例、轻度升高组33例、重度升高组40例及临床蛋白尿组30例,皆给予口服厄贝沙坦150mg/d、氢氯噻嗪12.5mg/d连续治疗6个月,比较4组患者治疗前后尿白蛋白的变化。结果轻度升高组[(93.51±30.17)mg/24hvs(119.38±35.76)mg/24h,P0.01]和重度升高组[(199.63±21.85)mg/24hvs(237.64±17.09)mg/24h,P0.05]患者治疗后尿白蛋白水平较治疗前明显下降,差异有统计学意义;对照组[(19.89±5.26)mg/24hvs(20.35±4.52)mg/24h,P0.05]和临床蛋白尿组[(319.16±15.71)mg/24hvs(334.24±17.05)mg/24h,P0.05]患者治疗后尿白蛋白无显著差异。治疗后,轻度升高组患者的尿白蛋白变化率较重度升高组明显下降,差异有统计学意义[(-21.35±4.78)%vs(-15.63±2.63)%,P0.05]。结论厄贝沙坦氢氯噻嗪可有效减少老年轻、中度高血压患者的尿白蛋白,对较低程度蛋白尿及临床蛋白尿短期内无明显影响。     

厄贝沙坦和氢氯噻嗪的长期抗高血压活性和耐受性

利尿剂氢氯噻嗪(HCTZ)虽然常被用作高血压的初始单药治疗，但它有多种剂量相关性不良代谢作用，包括血糖、胆固醇、尿酸和钙的升高以及镁和钾的降低。厄贝沙坦是一种强效的血管紧张素Ⅱ受体阻滞剂，与AT1受体亚型具有很高的亲和力。由于厄贝沙坦与HCTZ有互补的作用     

厄贝沙坦氢氯噻嗪对肱动脉内皮功能及颈动脉内膜中层厚度的影响

目的观察厄贝沙坦氢氯噻嗪对高血压患者肱动脉内皮功能及颈动脉内膜中层厚度的影响。方法选择2010年6月~2013年2月在徐州医学院附属医院老年科就诊的1级、2级原发性高血压患者137例,完成本研究127例,随机分为氢氯噻嗪组60例及厄贝沙坦氢氯噻嗪67例。2组患者每日晨起分别口服氢氯噻嗪25 mg及厄贝沙坦氢氯噻嗪1片,连续12个月。检测2组患者治疗前后血压、血脂、高敏C反应蛋白(hs-CRP)等指标,以及肱动脉内皮依赖性舒张功能(EDD)和颈动脉内膜中层厚度(IMT)的变化。结果与治疗前比较,氢氯噻嗪组和厄贝沙坦氢氯噻嗪组治疗后收缩压[(156.49±9.10)mm Hg vs.(126.37±8.12)mm Hg,(157.26±8.91)mm Hg vs.(124.46±8.07)mm Hg]、舒张压[(98.73±5.54)mm Hg vs.(77.65±5.42)mm Hg,(99.54±5.38)mm Hg vs.(76.36±5.71)mm Hg]均降低,差异具有显著统计学意义(P均0.01)。与治疗前比较,厄贝沙坦氢氯噻嗪组患者治疗后内皮依赖性舒张功能[(5.37±0.91)%vs.(6.79±1.08)%,P0.01]提高,颈动脉内膜中层厚度[(1.16±0.25)mm vs.(1.03±0.20)mm,P0.05]降低。与氢氯噻嗪组患者治疗后比较,厄贝沙坦氢氯噻嗪组患者治疗后内皮依赖性舒张功能[(5.56±0.99)%vs.(6.79±1.08)%,P0.01]提高,颈动脉内膜中层厚度[(1.15±0.19)mm vs.(1.03±0.20)mm,P0.05]下降。结论厄贝沙坦氢氯噻嗪降压的同时可以改善肱动脉内皮功能、减少颈动脉内膜中层厚度。     

厄贝沙坦联合氢氯噻嗪治疗老年原发性高血压86例

目的 探讨厄贝沙坦联合氢氯噻嗪(依伦平)治疗老年原发性高血压的临床疗效.方法 将86例老年原发性高血压患者随机分为观察组和对照组,各43例.观察组服用厄贝沙坦150 mg,氢氯噻嗪12.5 mg;对照组给予缬沙坦(平欣)40 mg联合左旋氨氯地平(施慧达)2.5 mg 口服,1次/日.结果 观察组显效35例,有效5例,总有效率为93.0%;对照组显效27例,有效6例,总有效率为76.8%(P<0.05).结论 厄贝沙坦联合氢氯噻嗪治疗老年原发性高血压疗效可靠.     

厄贝沙坦联合氢氯噻嗪治疗原发性高血压临床疗效观察

高血压是心脑血管疾病最常见、且可控制的危险因素，努力提高血压控制率，降低心血管疾病致死率和致残率已经成为各国指南所推荐的高血压治疗的主要目标。降压药物联合治疗是改善血压控制达标率的重要途径。20世纪90年代人们开始认识到大多数高血压患者（约70％）需要2种或2种以上降压药物联合治疗，才能控制血压达到目标值。因此，为了能使血压控制达标，近年来几乎所有的降压临床试验都采用了联合治疗方案。本研究采用厄贝沙坦和氢氯噻嗪（HCTZ）联合治疗原发性高血压患者，疗效满意，现报道如下。     

厄贝沙坦和氢氯噻嗪治疗原发性高血压33例临床观察

目的观察厄贝沙坦联合氢氯噻嗪治疗原发性高血压的疗效及安全性。方法65例轻中度原发性高血压患者,停药1～2周后,随机分为两组,治疗组33例,予厄贝沙坦150mg／d晨服,氢氯噻嗪12．5mg/d晨服。对照组32例仅予厄贝沙坦150mg／d晨服。疗程8周。观察两组治疗前后的血压、心率及不良反应。结果治疗组总有效率90．9％,对照组总有效率71．9％,两组比较差异有统计学意义（χ^2=3．910,P=0．048）;两组收缩压、舒张压均明显下降,但治疗组优于对照组（t’=7．0367。P〈0．05;t=3．6552,P=0．0005）。结论厄贝沙坦和氢氯噻嗪联用能有效控制血压,且耐受性好。     

无症状心肌缺血与高敏C反应蛋白和内皮功能失调

目的 探讨无症状心肌缺血（SMI）的发生是否与炎症因子和内皮功能失调有密切的关系。方法 对148例稳定性冠心病患者采用24h动态心电图监测,分为SMI组和非SMI组。并行血脂、血糖、高敏C反应蛋白（hsCRP）等测定,高分辨率超声评估肱动脉内皮功能。结果 60例患者（40．5％）动态心电图记录SMI,非SMI组与SMI组相比,hsCRP浓度明显降低（0．91±0．36：1．86±0．52,P〈0．05）,血流介导性舒张（FMD）功能有明显改善（3．02±1．46：6．36±3．79,P〈0．05）。多因素分析发现SMI仅与FMD（β=-0．452,P=0．046,OR=1．572）和hsCRP（β=1．233,P=0．036,OR=1．632）有独立相关性。结论 无症状冠心病患者仍有较高的SMI发生率;FMD、hsCRP与SMI之间有较强的相关性,提示炎症和内皮功能失调可能是SMI发生的机制之一,hsCRP和FMD有可能作为筛选SMI的替代指标。     

厄贝沙坦与氢氯噻嗪联合治疗原发性高血压疗效观察

高血压是我国最常见的心血管疾病,其发病率高,治疗率和控制率低。血压升高后,心血管疾病发病的危险性将随之增高,减少心血管疾病发生的关键在于降压治疗。中国高血压防治指南提倡高血压联合治疗,为尽早控制血压,大多数高血压患者从初始治疗阶段起就选择了联合用药,有利于及早控制血压。本研究观察厄贝沙坦片与氢氯噻嗪片联合治疗轻、中度原发性高血压的疗效和安全性,现报告如下。     

厄贝沙坦氢氯噻嗪片联合硝苯地平片对老年患者全身麻醉血流动力学的影响

目的 分析长期口服厄贝沙坦氢氯噻嗪片老年患者行全身麻醉的血流动力学变化.方法 选择2018年12月-2019年12月上海交通大学医学院附属第九人民医院ASAⅡ级老年择期手术患者68例,年龄65～75岁.按平时口服降压药分成A组(硝苯地平片组)和B组(硝苯地平片联合厄贝沙坦氢氯噻嗪片组),每组34例.手术日早晨停用厄贝沙...     

厄贝沙坦氢氯噻嗪复方片治疗轻中度高血压疗效观察

目的探讨厄贝沙坦氢氯噻嗪复方片治疗轻中度高血压的临床疗效。方法分析2008年1月至2013年1月我院收治的180例轻中度高血压患者的临床资料,将患者分为2组,比较2组患者的疗效差异。结果对照组患者经厄贝沙坦治疗,降压总有效率为68．89％,治疗组患者经厄贝沙坦氢氯噻嗪片治疗,降压总有效率为87．78％,明显高于对照组,经比较,P〈0．05,差异具有统计学意义。结论厄贝沙坦氢氯噻嗪复方片治疗轻中度高血压疗效确切,值得推广使用。     

依那普利和伊贝沙坦对糖尿病合并动脉粥样硬化患者血管内皮功能的影响

目的比较血管紧张素转换酶抑制剂（ACEI）依那普利5mg和血管紧张素受体拮抗剂（ARB）伊贝沙坦150mg治疗2型糖尿病合并动脉粥样硬化（AS）患者肱动脉内皮功能的变化。方法确诊的2型糖尿病合并AS患者用完全随机设计，将患者分为ACEI组47例，依那普利开始剂量2．5mg／d，逐渐加至5mg／d；ARB组49例，用伊贝沙坦逐渐加量至150mg／d；对照组48例，不用以上药物。疗程3个月以上。血管B超检查患者治疗前、后肱动脉内皮功能的变化。随访3个月。结果ACEI组患者治疗后肱动脉内皮依赖性舒张功能（EDV）从（3.3±2．7）％提高至（5．6±4．2）％（P=0．001），肱动脉非内皮依赖性舒张功能（EIV）从（12．6±7．4）％提高至（12．8±7．1）％（P=0．835）；ARB组患者治疗后EDV从（4．4±2．9）％提高到（6．2±3．2）％（P=0．038），EIV从（10．6±5．8）％下降到（9．5±4．7）％（P=0．230）；而对照组患者治疗前、后EDV、EIV改变差异元统计学意义（P〉0．05）。治疗前、后EDV、EIV变化值比较，ACEI组和ARB组相比差异元统计学意义（P〉0．05）。结论依那普利和伊贝沙坦均可改善2型糖尿病合并动脉粥样硬化患者的肱动脉内皮功能。     

Comparison of the effects of omapatrilat and irbesartan/hydrochlorothiazide on endothelial function and cardiac hypertrophy in the stroke-prone spontaneously hypertensive rat: sex differences

OBJECTIVE: The novel antihypertensive agent, omapatrilat, is both an inhibitor of neutral endopeptidase and angiotensin-converting enzyme. This study investigated the effects of omapatrilat in comparison with an angiotensin I-receptor antagonist/diuretic combination on blood pressure, endothelial function and cardiac hypertrophy in stroke-prone spontaneously hypertensive rats (SHRSP). METHODS: Male and female SHRSP were treated orally with omapatrilat or irbesartan plus hydrochlorothiazide (I + H) or vehicle for 8 weeks. Systolic blood pressure was measured weekly by tail-cuff. Cardiac hypertrophy was monitored by echocardiography at 8, 12 and 16 weeks of age. Endothelial function [basal nitric oxide (NO) bioavailability and stimulated NO release] was examined in carotid arteries using organ bath pharmacology and in mesenteric resistance arteries using wire myography. RESULTS: Compared with untreated controls, omapatrilat and I + H significantly attenuated hypertension [male control, 198.3 +/- 6.9 mmHg versus omapatrilat, 149.6 +/- 3.8 mmHg (F = 8.63 P < 0.0001), versus I + H, 145.6 +/- 5.1 mmHg (F = 7.38 P < 0.0001); female control, 170.3 +/-8.3 mmHg versus omapatrilat, 120.0 +/- 4.6 mmHg (F = 8.36, P < 0.0001), versus I + H, 112.2 +/- 2.9 mmHg (F = 9.08, P < 0.0001)] and left ventricular hypertrophy [male + female controls, 3.02 +/- 0.38 mg/g versus omapatrilat, 2.47 +/- 0.26 mg/g (P < 0.0001; 95% confidence interval, 0.27, 0.83), versus I + H, 2.49 +/- 0.21 mg/g (P < 0.0001; 95% confidence interval, 0.25, 0.83)]. Both treatments also significantly increased male carotid artery basal NO bioavailability relative to control [control, 0.62 +/- 0.17 g/g versus omapatrilat, 1.95 +/- 0.17 g/g (P < 0.0001; 95% confidence interval, -1.83, -0.36), versus I + H, 1.57 +/- 0.21 g/g (P < 0.026; 95% confidence interval, -1.31, -0.12)]. However, stimulated NO (EC50) was only improved in omapatrilat-treated males [controls, 0.19 +/- 0.06 micromol/l versus omapatrilat, 0.05 +/- 0.01 micromol/l (P = 0.05; 95% confidence interval, -1.16, -0.03)]. CONCLUSIONS: Omapatrilat treatment significantly reduced left ventricular hypertrophy and improved endothelial function in carotid arteries from male SHRSP by NO-dependent mechanisms. Despite equivalent antihypertensive and antihypertrophic actions, a similar improvement in endothelial function, specifically stimulated NO release, was not observed after treatment with I + H.     

心可舒联合尼可地尔对X综合征患者疗效及血管内皮功能的影响

目的观察心可舒联合尼可地尔对X综合征患者疗效及血管内皮功能的影响。方法选取90例临床诊断为X综合征的患者,随机分为对照组45例,给予常规药物治疗;治疗组45例,在常规治疗基础上加用心可舒和尼可地尔联合治疗。治疗6个月后,评价2组患者胸痛症状改善程度、中医症状积分及内皮功能指标肱动脉内皮依据性血管合性功能(FMD)、NO和内皮素1水平的变化。结果与对照组比较,治疗组治疗后胸痛症状改善有效(66.67%vs 56.67%)和总有效率(84.44%vs 63.33%)及中医症状积分、肱动脉FMD[(8.6±2.2)%vs(6.0±2.4)%]、NO[(35.1±3.7)μmol/Lvs(25.1±4.0)μmol/L]、内皮素1[(30.4±12.9)ng/Lvs(58.8±8.8)ng/L]水平均有明显改善,差异有统计学意义(P0.05)。结论心可舒联合尼可地尔治疗能改善心脏X综合征患者临床症状及血管内皮功能。     

Matrix study of irbesartan with hydrochlorothiazide in mild-to-moderate hypertension

The purpose of this study was to assess the safety and antihypertensive dose-response effects of irbesartan and hydrochlorothiazide (HCTZ) in patients with mild-to-moderate hypertension. After a 4- to 5-week single-blind placebo lead-in period, 683 patients with seated diastolic blood pressure (SeDBP) between 95 and110 mm Hg were randomized to receive once-daily dosing with one of 16 different double-blind, fixed combinations of irbesartan (0, 37.5, 100, and 300 mg irbesartan) and HCTZ (0, 6.25, 12.5, and 25 mg HCTZ) for 8 weeks. The primary efficacy variable was the change from baseline in trough SeDBP after 8 weeks of therapy. Data were analyzed by response surface modeling. At Week 8, mean changes from baseline in trough SeDBP (mm Hg) ranged from −3.5 for placebo, −7.1 to −10.2 for the irbesartan monotherapy groups, −5.1 to −8.3 for the HCTZ monotherapy groups, and −8.1 to −15.0 for the combination groups. Irbesartan plus HCTZ produced additive reductions in both SeDBP and seated systolic BP, with at least one combination producing greater BP reduction than either drug alone (P < .001). All treatments were well tolerated; there were no treatment-related serious adverse events. Irbesartan tended to ameliorate the dose-related biochemical abnormalities associated with HCTZ alone. In conclusion, the combination of HCTZ in doses up to 25 mg with irbesartan, in doses up to 300 mg, is safe and produces dose-dependent reductions in BP.     

The long-term antihypertensive activity and tolerability of irbesartan with hydrochlorothiazide.

The long-term safety, tolerability, and antihypertensive effects of irbesartan/hydrochlorothiazide (HCTZ) were assessed in hypertensive patients (seated diastolic blood pressure [SeDBP] 95-110 mm Hg). Patients (n = 1098) completing two randomised, double-blind trials of irbesartan alone, HCTZ alone, irbesartan/HCTZ combinations, or placebo, took 1 year of open-label therapy starting with irbesartan 75 mg/HCTZ 12.5 mg once daily. If target blood pressure (BP) (<140/<90 mm Hg) was not achieved, the dose was titrated sequentially at 2- to 4-week intervals to irbesartan 150 mg/HCTZ 12. 5 mg, then to irbesartan 300 mg/HCTZ 25 mg. If necessary, adjunctive therapies were added. Mean changes in trough seated systolic BP/SeDBP at months 2, 6, and 12 were -19.1/-14.2 mm Hg (n = 941), -20.7/ -15.7 mm Hg (n = 948), and -20.6/-15.6 mm Hg (n = 898), respectively. From months 2 to 12, normalisation rates (trough SeDBP <90 mm Hg) ranged from 75-85% and total responder rates (normalised or >/=10 mm Hg trough SeDBP reduction) ranged from 81-91%, while target BP was achieved in 65-75% of patients. At all time-points, most patients (>/=87%) were receiving irbesartan/HCTZ alone. Eighty-two patients (7.5%) discontinued the study due to adverse events, with half of these events considered unrelated to study medication. There were no reports of serious adverse events related to study medication. Long-term therapy with irbesartan/HCTZ is safe, well tolerated, and maintains normalised BP in >80% of patients.     

Treatment with irbesartan or atenolol improves endothelial function in essential hypertension

OBJECTIVES: To investigate if antihypertensive treatment could improve endothelium-dependent vasodilatation in hypertensive patients, and whether the angiotensin II subtype-1 (AT1)-receptor antagonist irbesartan and the beta1-receptor antagonist atenolol would differ in this respect. SUBJECTS AND METHODS: Thirty-four patients (28 men and six women) with mild-to-moderate essential hypertension (diastolic blood pressure 90-120 mmHg) were randomized to once daily 150-300 mg irbesartan or 50-100 mg atenolol in a double-blind fashion, preceded by a placebo run-in period. Forearm blood flow (FBF) was assessed by venous occlusion plethysmography during local intra-arterial infusions of methacholine and sodium nitroprusside, to evaluate endothelium-dependent and endothelium-independent vasodilatation, respectively. Measurements of FBF were undertaken at the end of the run-in placebo period and repeated after 3 months of active antihypertensive treatment. RESULTS: Irbesartan and atenolol induced a similar decline in blood pressure (from 171/107 to 158/98 mmHg, P < 0.05), and improved endothelium-dependent vasodilatation (e.g. an increase in FBF response to 4 microg/min methacholine from 325 +/- 29% to 411 +/- 41%, P < 0.05), with no difference between the two study drugs. No significant changes in endothelium-independent vasodilatation were induced by irbesartan or by atenolol. CONCLUSIONS: The present study shows that 3 months of antihypertensive therapy with irbesartan or atenolol improves endothelium-dependent vasodilatation.