厄贝沙坦联合硝苯地平控释片对原发性高血压患者的治疗效果分析

目的 分析厄贝沙坦联合硝苯地平控释片对原发性高血压患者的治疗效果.方法 选取我院收治的原发性高血压患者100例,按照随机数字表法分为观察组和对照组,对照组给予口服硝苯地平控释片治疗高血压,观察组采用厄贝沙坦联合硝苯地平控释片治疗,比较两组患者的治疗效果.结果 经过3个月的治疗,观察组患者收缩压与舒张压水平均低于对照组,观察组治疗的总有效率高于对照组(P<0.05).结论 厄贝沙坦联合硝苯地平控释片对原发性高血压患者的治疗效果优于单纯使用硝苯地平控释片,作用时间长、安全、可靠、能提高治疗效果,使患者家属满意,值得在临床推广使用.     

厄贝沙坦联合硝苯地平控释片治疗高血压的效果

目的：探讨厄贝沙坦联合硝苯地平控释片治疗高血压的效果。方法选择原发性高血压患者80例,随机分为两组,观察组采用厄贝沙坦联合硝苯地平控释片治疗,对照组采用美托洛尔联合硝苯地平控释片治疗,比较两组治疗后肾功能、平均动脉压及超声心动图的改变。结果治疗后观察组尿素氮、肌酐水平及平均动脉压显著低于对照组,差异有统计学意义（P〈0.05）;治疗后观察组室间隔厚度和左室舒张末期内径均显著小于对照组,左室射血分数高于对照组,差异有统计学意义（P〈0.05）。结论厄贝沙坦联合硝苯地平控释片对高血压左心室肥厚具有明显的逆转作用,同时能够更好地控制患者血压及保护其肾功能。     

厄贝沙坦联合硝苯地平控释片治疗社区高血压的效果观察

目的探讨厄贝沙坦联合硝苯地平控释片治疗社区高血压的效果。方法420例高血压患者,采用随机法分为厄贝沙坦组、硝苯地平组、联合组,各140例。厄贝沙坦组采用厄贝沙坦片口服治疗,硝苯地平组采用硝苯地平控释片口服治疗,联合组采用厄贝沙坦片联合硝苯地平控释片口服治疗。比较三组患者血压控制效果、不良反应发生情况以及治疗前后的血压、心率、血管内皮生长因子(VEGF)、血清同型半胱氨酸(Hcy)水平。结果联合组血压控制总有效率97.86%均高于厄贝沙坦组的89.29%、硝苯地平组的88.57%,差异均具有统计学意义(P<0.05)。治疗后,三组患者收缩压(SBP)、舒张压(DBP)、心率(HR)水平均显著降低,且联合组患者SBP、DBP、HR水平均显著低于厄贝沙坦组、硝苯地平组,差异均具有统计学意义(P<0.05)。治疗后,联合组患者VEGF(90.24±6.33)pg/ml均低于厄贝沙坦组的(110.36±11.33)pg/ml、硝苯地平组的(110.25±11.29)pg/ml,Hcy(12.07±1.33)μmol/L均低于厄贝沙坦组的(17.51±1.26)μmol/L、硝苯地平组的(17.56±1.17)μmol/L,差异均具有统计学意义(P<0.05)。厄贝沙坦组与硝苯地平组血压控制效果、SBP、DBP、HR、VEGF、Hcy比较,差异均无统计学意义(P>0.05)。结论厄贝沙坦联合硝苯地平控释片治疗社区高血压控制血压及心率效果优于单种药物治疗,安全性高,值得在临床推广应用。     

探讨硝苯地平缓释片联合厄贝沙坦治疗原发性高血压的临床效果

目的研究硝苯地平缓释片联合厄贝沙坦片治疗原发性高血压的临床疗效。方法将原发性高血压患者106例的病例资料作为对象,均为2015年1月至2017年2月收治,依据治疗药物的不同分为对照组(硝苯地平缓释片)和观察组(硝苯地平缓释片与厄贝沙坦片联用)。连续治疗3个月后,观察两组患者的临床治疗效果和血压改善情况。结果观察组显效率49.06%,有效率43.40%,对照组显效率41.51%,有效率32.08%;两组总有效率比较χ2=11.523,P=0.001;两组患者治疗后血压均有显著下降,其中观察组患者的血压改善情况更为明显,对比差异具有显著性(P<0.05)。结论对于原发性高血压患者的临床治疗,采用硝苯地平缓释片联合厄贝沙坦具有显著的临床效果。     

厄贝沙坦联合硝苯地平缓释片治疗高血压疗效观察

目的观察厄贝沙坦联合硝苯地平缓释片治疗中、高度高血压疗效。方法选取中、高度原发性高血压患者76例随机分为二组,治疗组36例应用厄贝沙坦联合硝苯地平缓释片治疗4周,对照组40例仅用硝苯地平缓释片治疗,治疗4周后进行疗效分析。结果厄贝沙坦联合硝苯地平缓释片组有效率94.4%,对照组有效率70.0%,两组相比差异显著,有统计学意义(χ2=7.534,P<0.01)。结论厄贝沙坦联合硝苯地平缓释片治疗中、高度高血压疗效显著。     

厄贝沙坦联合硝苯地平缓释片治疗老年性高血压的疗效观察

目的:观察老年性高血压应用厄贝沙坦、硝苯地平缓释片联合治疗的疗效。方法:随机抽取本院110例老年性高血压患者,观察组与对照组各纳入55例,观察组采用厄贝沙坦、硝苯地平缓释片联合治疗,对照组采用硝苯地平缓释片单一治疗,观察治疗效果。结果:观察组治疗前血压与对照组无明显差异(P0.05);治疗后总有效率高于对照组,血压低于对照组,差异显著(P0.05)。结论:老年性高血压患者治疗时,联合应用厄贝沙坦与硝苯地平缓释片可有效提高治疗效果。     

厄贝沙坦、硝苯地平控释片及美托洛尔对高血压左心室肥厚的作用

目的比较厄贝沙坦,硝苯地平控释片及美托洛尔对高血压合并左心室肥厚(LVH)的逆转作用。方法92例高血压LVH患者随机分为厄贝沙坦组(31例),硝苯地平控释片组(31例)和美托洛尔组(30例),分别使用厄贝沙坦150～300mg,1次/d,硝苯地平控释片30～60mg,1次/d,美托洛尔25～50mg,2次/d,疗程6个月,治疗前后进行偶测血压(CBP)、动态血压(ABPM)及超声心动图检查。结果三组患者的血压均显著下降,舒张期左室后壁厚度(LVPWT)、舒张期室间隔厚度(IVST)、左室舒张末期内径(LVDd)、左室重量指数(LVMI)均有显著改善(P<0.05～0.01),LVH得到逆转,而厄贝沙坦组的逆转程度大于硝苯地平控释组及美托洛尔组(P<0.05)。结论三种药物均能有效降压,对LVH有不同程度的逆转作用,但厄贝沙坦的逆转作用相对较强。     

硝苯地平联合厄贝沙坦治疗老年原发性高血压的效果分析

目的 探讨硝苯地平联合厄贝沙坦治疗老年原发性高血压的疗效.方法 选择2014年10月至2016年6月我院收治的老年原发性高血压患者116例,采用随机双盲法分为观察组和对照组各58例,对照组给予硝苯地平联合美托洛尔治疗,观察组给予硝苯地平联合厄贝沙坦治疗.两组患者治疗3个月后,对比两组患者的临床疗效.结果 经3个月的治疗后,两组患者的舒张压、收缩压较治疗前均明显下降,差异具有统计学意义(P<0.05).治疗后比较,观察组患者的舒张压与收缩压明显低于对照组,差异显著(P<0.05).观察组患者总有效率高达93.10％,明显高于对照组的74.14％,差异具有统计学意义(P<0.05).治疗前后两组患者心率差异无统计学意义(P>0.05).结论 硝苯地平联合厄贝沙坦治疗老年原发性高血压效果较好,临床治疗效果优于硝苯地平联合美托洛尔,安全有效、作用时间长,值得临床中推广使用.     

硝苯地平控释片与非洛地平缓释片治疗难治性高血压的疗效比较

目的：评价硝苯地平控释片与非洛地平缓释片治疗难治性高血压的效果。方法：60例难治性高血压,经氢氯噻嗪、美托洛尔、厄贝沙坦联合治疗8周后仍未达标者随机分为两组,分别加用硝苯地平控释片30mg/d或者非洛地平缓释片5mg/d,4周后若仍未达标则剂量加倍继续服用4周,分别于服药后0,2,4,6,8周测量坐位血压。结果：治疗8周后,硝苯地平控释片组血压下降16.3/11.2±12.6/7.7mmhg,非洛地平缓释片组血压下降15.1/9.8±12.2/7.8mmhg,硝苯地平控释片组达标率83.3%,非洛地平缓释片组达标率80%。结论：硝苯地平控释片与非洛地平缓释片均能有效控制难治性高血压的血压水平,但降压效果比较无统计学意义。两组降压达标率比较无统计学意义。     

硝苯地平控释片对原发性高血压病患者血压变异性的影响

目的:观察硝苯地平控释片对原发性高血压病患者血压变异性的影响. 方法:临床观察原发性高血压患者99例,用硝苯地平控释片治疗4 wk前后分别采用无创性携带式动态血压监测仪监测动态血压及血压变异性,同时选取49例健康人作对照组观察血压及血压变异性. 结果:99例原发性高血压患者中85例完成观察,治疗前原发性高血压组血压及血压变异性明显比对照明组高(P<0.01),服用硝苯地平控释片后,原发性高血压患者的血压及血压变异性与用药前比较均明显降低(P<0.01).结论:原发性高血压患者血压变异性增高,硝苯地平控释片在稳定降压的同时可降低血压变异性.     

Management of essential hypertension

Hypertension, in spite of a very high prevalence, remains undertreated. This is not due to a lack of effective therapeutic modalities. Non-pharmacological treatments can be effective in many patients. If those treatments fail to reduce blood pressure sufficiently, the physician can choose between numerous classes of antihypertensive agents. However, interpatient variability in response to these agents is high, and use of multiple agents is frequently necessary. Thus, no single class has proven to be superior for the majority of patients. This article will review the different non-pharmacological and pharmacological methods available to treat hypertension, as well as the guidelines that are available to aid in proper selection of a treatment regimen.     

Management of essential hypertension

Hypertension, in spite of a very high prevalence, remains undertreated. This is not due to a lack of effective therapeutic modalities. Non-pharmacological treatments can be effective in many patients. If those treatments fail to reduce blood pressure sufficiently, the physician can choose between numerous classes of antihypertensive agents. However, interpatient variability in response to these agents is high, and use of multiple agents is frequently necessary. Thus, no single class has proven to be superior for the majority of patients. This article will review the different non-pharmacological and pharmacological methods available to treat hypertension, as well as the guidelines that are available to aid in proper selection of a treatment regimen.     

Homocysteine and essential hypertension

The authors examine the available clinical and experimental data supporting the view that homocysteine, an alternative risk factor of cardiovascular disease, may play a role in the pathogenesis of essential hypertension. The mechanism of this disease has not been elucidated, but it may be related to impairment of vascular endothelial and smooth muscle cell function. Therefore, the occurrence of endothelial dysfunction could contribute to alterations of the endothelium-dependent vasomotor regulation. Elevated homocysteinemia diminishes the vasodilation by nitric oxide, increases oxidative stress, stimulates the proliferation of vascular smooth muscle cells, and alters the elastic properties of the vascular wall. Thus, homocysteine contributes to elevate the blood pressure. Also it is known that elevated plasma levels of homocysteine could lead to oxidant injury to the endothelium. The correction of elevated homocysteinemia by administration of vitamins B12 and B6 plus folic acid, could be a useful adjuvant therapy of hypertension. However, further controlled randomized trials are necessary to establish the efficacy and tolerability of these potentially therapeutic agents.     

Labetalol in essential hypertension

Labetalol is an orally active adrenoreceptor-blocking drug which is a competitive antagonist of both alpha- and beta-adrenoreceptor sites. Thirty patients with essential hypertension were admitted to the study. The mean of initial systolic and diastolic blood pressures of these patients was 160/101 +/- 3/1 supine and 155/104 +/- 3/1 mm Hg standing, and the mean blood pressures at the end of the 16 week trial was 142/90 +/- 4/2 supine and 131/91 +/- 3/2 mm Hg standing. The average dose of labetalol was 546 mg: eight patients received a dose of 300 mg, seven a dose of 600 mg, six a dose f 900 mg, and two a dose of 1,200 mg. The patients who needed the highest doses of labetalol had an initial lowering of their blood pressures followed by a gradual increase despite the higher doses of labetalol. There was no significant change in the mean peripheral renin activity value. Side effects were reported by 18 of the 30 patients, but only 1 patient withdrew for this reason. Two patients were considered to be treatment failures. Overall, labetalol was found to be an effective antihypertensive agent in 15 patients.     

阿罗洛尔治疗原发性高血压

目的 :观察阿罗洛尔对轻、中度高血压的治疗效果。方法 :治疗对象 6 0例 (男性 38例 ,女性 2 2例 ,年龄 55a±s11a) ,给阿罗洛尔 10mg ,qd× 6wk。结果 :服用阿罗洛尔后 1～ 3wk血压、心率逐渐下降 ,血压从治疗前的 2 2 .3/ 12 .7kPa下降到wk4的 16 .9/ 10kPa ,wk 6的 16 .4 / 9.8kPa ,心率从治疗前的 80次·min- 1下降到wk 4的 6 8次·min- 1,wk6的 6 7次·min- 1,差异均有非常显著性意义 (P <0 .0 1) ,降低血压的总有效率为 85% ,对肝、肾功能及血常规无明显影响。结论 :阿罗洛尔是一种满意的降压药。     

Bucindolol in essential hypertension

The effects of bucindolol a new nonselective beta blocker were studied after short-term dosing and for up to six months in eight patients with essential hypertension. Bucindolol 100 mg acutely lowered supine and erect systolic and diastolic pressure without orthostatic features and without increases or decreases in heart rate. Plasma noradrenaline increased, but plasma renin activity fell. Long-term dosing of 100-400 mg/day led to modest decreases in blood pressure. The duration of the hypotensive effect after multiple dosing ranged from six to ten hours. After long-term dosing there was evidence of marked nonselective beta blockade but not of alpha 1 blockade from the responses to intravenous isoprenaline and phenylephrine respectively. In six out of eight patients the plasma creatinine phosphokinase rose transiently above the normal range. The increase appeared to be of muscle origin and was associated with myalgia in one patient. Bucindolol is a nonselective beta blocker, possibly with other vasodilator properties. These do not appear to be mediated by alpha blockade.     

The causes of essential hypertension

1 Confusion between the criteria for defining and diagnosing hypertension may have misled the search for the causes of hypertension.
2 The systematic approach of molecular genetics appears to offer the best chance of explaining hypertension, but the attractions are partly offset by the large numbers required, and unproven record of the genetic techniques in finding functional mutations in complex human disorders.
3 Part of the evidence for the polygenic nature of essential hypertension derives from the variable response to a large number of different anti-hypertensive agents. Systematic investigation of this variability may provide a basis for dividing patients into genetically more homogeneous sub-groups, within which smaller numbers will be required to detect the genes responsible for the susceptibility to hypertension.
4 The proportion of hypertensive patients with affected siblings has been studied in 6000 patients from Addenbrookes Hospital and local general practices. A recurrence risk for hypertension of∼3.5 was found.
5 Approximately two-thirds of patients have no known affected siblings. The next largest group, about one third, is patients whose siblings are all hypertensive. In a small group, <10% of all patients, half the siblings are hypertensive.
6 We conclude from these surprising findings that hypertension is not a continuous, multifactorial part of the normal blood pressure distribution. They suggest that several more single-gene disorders causing hypertension will be found. The sibships where all members are hypertensive are inconsistent with the segregation of Mendelian genetics and suggest the selection of some genes linked to hypertension at the time of gamete maturation.     

Pharmacotherapy of essential hypertension.

Practical clinical aspects of the evaluation and treatment of essential hypertension are reviewed. Drug therapy discussed includes diuretics, and as adjunctive therapy, sympathoplegic agents, peripheral vasodilators and beta blockers. Also covered are treatment of less common forms of essential hypertension, other forms of antihypertensive therapy, and the use of fixed combinations of antihypertensive drugs.     

The genetics of essential hypertension

Essential hypertension is an escalating problem for industrialized populations. It is currently seen as a 'complex' genetic trait caused by multiple susceptibility genes the effects of which are modulated by gene-environment and gene-gene interactions. Nevertheless, the success to date in identifying these susceptibility genes has been very limited. A number of candidates has been proposed, but demonstrating consistently the linkage or association with hypertension has been problematic. The data for angiotensinogen is undoubtedly the most extensive and meta-analysis has confirmed a significant association overall, although the risk contributed by this gene appears to be modest (odds ratio of 1.2). Identifying further genes - probably conferring even smaller attributable risks - represents a major challenge for future developments in this area. This contrasts markedly with the success that has been achieved in the past 5 years in solving the molecular genetics of a number of rare familial hypertension syndromes. The true incidences of some of these disorders may be higher than first appreciated, but it is still unclear if the genes for these syndromes also play a part in essential hypertension. A more complete understanding of the genetic basis of essential hypertension should be possible in the coming years using new strategies that take advantage of the information provided by the human genome project. This knowledge will irrevocably change the way we approach this disease in terms of its diagnosis, risk assessment for end-points such as stroke and heart disease, and the customised treatment that might be offered in the future.