培哚普利、卡托普利和硝苯地平对老年轻中度高血压患者肾功能的影响

目的：观察培哚普利、卡托普利和硝苯地平对老年轻中度高血压患者肾功能的影响。方法：９４例老年轻中度高血压心室肥厚患者随机分为培哚普利、卡托普利和硝苯地平３组，服用２周安慰剂后用药３个月，剂量逐月递增。用药前后测定血压、尿微白蛋白分泌率（ＭＡＥＲ）、尿素氮、肌酐、肌酐清除率和血钾、血钠。结果：３组用药后血压均明显下降达正常范围；尿ＭＡＥＲ在培哚普利组显著下降（Ｐ＜０．０１），另两组下降不显著；尿素氮、肌酐、肌酐清除率３组治疗前后无明显变化；血钾在卡托普利组和培哚普利组均有上升（Ｐ＜０．００５和Ｐ＜０．０５），血钠水平３组间均无变化。结论：培哚普利、卡托普利和硝苯地平均可有效控制血压，培哚普利同时可降低尿ＭＡＥＲ，改善肾功能，但培哚普利与卡托普利均可引起血钾升高，应引起注意。     

高血压病左室重量与血管紧张素Ⅱ、醛固酮的相互关系及培哚普利、美托洛尔对其影响

研究６２例高血压病（ＥＨ）血浆血管紧张素Ⅱ（ＡＴⅡ）、醛固酮（ＡＬＤ）水平及其与左室肥厚（ＬＶＨ）的关系，并与２０例正常人进行对照。根据左室重量指数（ＬＶＭＩ）将ＥＨ伴ＬＶＨ者４７例随机分为两组，投以培哚普利或美托洛尔治疗８周。结果显示，ＥＨ患者血浆ＡＴⅡ及ＡＬＤ浓度明显高于对照组（Ｐ＜０．００１），ＬＶＨ组高于非ＬＶＨ组（Ｐ＜０．００５），ＬＶＨ组的ＬＶＭＩ与ＡＴⅡ和ＡＬＤ正相关（ｒ分别为０．３４２和０．３５６，Ｐ＜０．０１），用药后两组ＬＶＭＩ、ＡＴⅡ和ＡＬＤ水平均显著降低，且８周后两组ＬＶＭＩ差异有显著性（Ｐ＜０．０５），ＬＶＭＩ下降值与血浆ＡＴⅡ、ＡＬＤ浓度下降值呈正相关（ｒ分别为０．６１２和０．６４７，Ｐ＜０．００１），提示ＡＴⅡ、ＡＬＤ是引起ＥＨ心肌肥厚重要的体液因素，培哚普利及美托洛尔短期治疗均可使ＬＶＨ逆转，培哚普利对ＬＶＨ的逆转可能优于美托洛尔。     

苯那普利对高血压左室肥厚与QTc离散度的影响

目的:探讨苯那普利对高血压左室肥厚（ＬＶＨ）与ＱＴｃ离散度（ＱＴｃｄ）的影响。方法原发性高血压６０例用苯那普利治疗６个月,测定治疗前后左室重量指数（ＬＶＭＩ）和ＱＴｃｄ。结果ＬＶＨ组患者治疗后ＬＶＭＩ明显减少（Ｐ＜０．００１）,ＬＶＨ逆转率７２％。ＬＶＨ组ＱＴｃｄ治疗前显著高于无ＬＶＨ组（６９．１±１７．３比４０．６±１１．６ｍＳ,Ｐ＜０．００１）,治疗后明显降低（６９．１(１７．３比４３．９(１２．６ｍｓ,Ｐ＜０．００１）,而无ＬＶＨ组治疗前后ＱＴｃｄ无明显变化（Ｐ＞０．０５）。ＬＶＨ组中ＬＶＨ逆转者ＱＴｃｄ明显小于未逆转者（３８．２±１０．４比６０．０±１６．１ｍｓ,Ｐ＜０．００１）。ＬＶＭＩ与ＱＴｃｄ之间呈正相关（ｒ＝０．６７８,Ｐ＜０．００１）。结论高血压ＬＶＨ时ＱＴｃｄ增大,苯那普利长期治疗使ＬＶＭＩ减少的同时ＱＴｃｄ也明显降低。     

培哚普利与卡托普利治疗老年原发性高血压的疗效比较

目的：比较培哚普利与卡托普利对老年原发性高血压的降压效应与安全性。方法：６０例老年原发性高血压患者随机分组接受培哚普利（４～８ｍｇ／ｄ）和卡托普利（３７．５～７５．０ｍｇ／ｄ）（各３０例）治疗４周。结果：培哚普利和卡托普利的降压总有效率偶测血压分别为９０．０％和８６．７％（Ｐ＞０．０５），动态血压监测分别为９５．０％和６５．０％（Ｐ＜０．０５）。结论：培哚普利治疗老年原发性高血压有效而安全，降低夜间舒张压优于卡托普利。     

早期应用卡托普利对急性心肌梗塞后左室容积和功能的影响

本文对６５例急性心肌梗塞（ＡＭＩ）患者随机分为卡托普利组３３例，服用卡托普利（１２．５ｍｇ，ｔｉｄ）；安慰剂组３２例，服用安慰剂。两组均在服药后第１周和第１、２、３个月各做一次二维超声心动图检查。结果：卡托普利组左室收缩末期容积指数（ＬＶＥＳＶＩ）降低（Ｐ＜０．０５），舒张末期容积指数（ＬＶＥＤＶＩ）无显著改变，每搏量指数（ＳＶＩ）和射血分数（ＥＦ）增加（均Ｐ＜０．０５）；安慰剂组ＬＶＥＤＶＩ和ＬＶＥＳＶＩ增加，ＥＦ降低（均Ｐ＜０．０５）。两组比较，至服药后第３个月，上述各指标差异均显著（Ｐ＜０．０５）。     

充血性心衰患者血浆内皮素和一氧化氮变化的临床意义及培哚普利的干预作用

为了解充血性心衰（ＣＨＦ）时心钠素（ＡＮＦ），内皮素（ＥＴ）和一氧化氮（ＮＯ）变化的临床意义及培哚普利的于预作用，我们选择４０例临床确诊为ＣＨＦ的患者，并随机分为培哚普利治疗组和常规治疗组，放免法测定血浆ＡＮＦ，ＥＴ含量，比色法测定血浆ＮＯ含量，与正常对照组比较，并观察治疗前后上述指标的变化情况。结果ＣＨＦ患者的血浆ＡＮＦ，ＥＴ水平均显著高于对照组（Ｐ＜０．０１），ＮＯ明显低于对照组（Ｐ＜０．０５）。常规治疗组治疗前后上述指标无明显改变（Ｐ＞０．０５），培哚普利平均治疗８周后ＡＮＦ，ＥＴ显著下降（Ｐ＜０．００１）而ＮＯ显著上升（Ｐ＜０．０５），提示ＡＮＦ，ＥＴ和ＮＯ参与了ＣＨＦ的病理生理过程。培哚普利可以降低ＣＨＦ的治疗有益。     

左室肥厚与单纯收缩,舒张或双期血压增高的关系

目的研究高血压病患者单纯收缩期（ＩＳＨ）、单纯舒张期（ＩＤＨ）或双相高血压（ＴＨ）上左室肥厚的关系。方法根据２４小时动态血压将病人分为４组：１．对照组（ｎ＝２７）平均收缩压＜１４０ｍｍＨｇ，平均舒张压＜９０ｍｍＨｇ；２．ＩＳＨ组（ｎ＝１６）平均收缩压＞１４０ｍｍＨｇ，平均舒张压＜９０ｍｍＨｇ；３．ＩＤＨ组（ｎ＝３１）平均收缩压＜１４０ｍｍＨｇ，平均舒张＞９０ｍｍＨｇ；４．ＴＨ组（ｎ＝１９）平均收缩压＞１４０ｍｍＨｇ和平均舒张压＞９０ｍｍＨｇ。超声心动图检测或计算舒张末期左室内径（ＥＤＤ）、室间隔及左室后壁厚度（ＬＶＳＴ，ＬＶＰＷＴ）、左室重量指数（ＬＶＭＩ）。结果ＩＳＨ、ＩＤＨ及ＴＨ组ＬＶＭＩ明显大于对照组Ｐ＜０．００１。ＩＳＨ和ＩＤＨ间、ＩＤＨ和ＴＨ组间无明显统计学差异。结论２４小时动态血压监测诊断为高血压病的患者ＬＶＭＩ明显大于偶测血压增高者。双期血压均高者左室肥厚最重。     

培哚普利治疗原发性高血压的临床观察

目的观察培哚普利对原发性高血压的降压作用及副反应。方法３７例轻中度原发性高血压患者予培哚普利共８周，评价对随诊血压及２４ｈ动态血压的影响。结果治疗４周收缩压（ＳＢＰ）无明显降低（Ｐ＞０．０５），舒张压（ＤＢＰ）明显降低（Ｐ＜０．００１），８周ＳＢＰ、ＤＢＰ均明显降低（Ｐ＜０．００１），随诊血压降压有效率分别为５４．１％（４周）及６７．６％（８周），２４ｈ动态血压曲线８周时呈明显下降，除咳嗽外未发现其他严重副反应。结论培哚普利对轻中度原发性高血压是安全有效的降压药物。     

急性心肌梗塞后左室重构变化的研究

应用二维多普勒超声心动图对６８例急性心肌梗塞（ＡＭＩ）患者的左室重构（ＬＶＲ）变化进行了观察。结果显示，心肌梗塞后ＬＶＲ早期（３～６周）左室舒张末内径（ＬＶＤｄ）、左室舒张末容积（ＥＤＶ）、左室收缩末容积（ＥＳＶ）、左室收缩期最大室壁应力（Ｅｄｂ）、左室收缩末期室壁应力（Ｅｓｂ）、平均室壁应力（ｍｅａｎｂ）、二尖瓣舒张晚期血流速度峰值（ＰＶＡ）、左房张力（ＬＡＴ）、左房射血力（ＬＡＦ）及峰值充盈速度（ＰＦＲ）显著增大（Ｐ＜０．０１－０．００１），射血分数（ＥＦ）、心输出量（ＣＯ）、左室收缩期圆周指数（ＬＶＳＣＩ）、平均周边纤维缩短速率（ＭＶＣＦ）、二尖瓣舒张早期血流速度峰值（ＰＶＥ）及ＰＶＡ／ＰＶＥ显著降低（Ｐ＜０．０１－０．００１）。ＬＶＲ晚期（６－１２个月），ＥＤＶ、ＥＳＶ增加，ＥＦ、ＣＯ及ＬＶＳＣＩ降低（Ｐ＜０．００１）；与ＬＶＲ早期比较，ＰＶＥ、ＰＶＡ及ＬＡＦ无显著性差异（Ｐ＞０．０５）。提示ＡＭＩ后ＬＶＲ的主要病因是梗塞区膨展、左室扩张、容量负荷及室壁应力增加，从而导致心肌梗塞并发症；ＥＳＶ、ＥＤＶ及ＥＦ可作为了解远期ＡＭＩ患者预后的最佳指标。     

老年人不同体质对心脏结构、血流、功能及血压的影响

目的观察体重对老年人心血管系统的影响。方法６２３例老年人根据体质指数（ＢＭＩ）分为肥胖、超重、正常及消瘦４组，检测血压、空腹血糖（ＢＳ）、胆固醇（ＴＣ）、甘油三酯（ＴＧ）及超声心动图。结果肥胖及超重组较正常体重及消瘦组收缩压（ＳＢＰ）及舒张压（ＤＢＰ）均增高（均为Ｐ＜０．０５），主动脉径（ＡｏＤ）、左房径（ＬＡＤ）、左室舒张及收缩末径（ＥＤＤ及ＥＳＤ）及心肌质量（ＬＶＭ）增加（均为Ｐ＜０．０５）。ＳＢＰ、ＤＢＰ均与体重、ＢＭＩ、ＴＣ、ＬＶＭ及心房收缩期与舒张早期充盈峰值流速（ＡＰＦＶ与ＥＰＦＶ）之比值（Ａ／Ｅ）呈明显正相关（Ｐ＜０．０５、０．０１或０．００１），ＤＢＰ与年龄呈明显负相关（Ｐ＜０．００１）。多元逐步回归分析证实ＬＶＭ、ＡＰＦＶ及ＬＡＤ均与ＢＭＩ呈正相关（均为Ｐ＜０．０１），ＥＰＦＶ与ＢＭＩ呈负相关（Ｐ＜０．０５）；射血分数（ＥＦ）、年龄、ＢＳ与ＳＢＰ呈正相关（Ｐ＜０．０５、０．００１及０．０１），与ＤＢＰ呈负相关（Ｐ＜０．０５或０．００１）。结论体重是影响心脏结构、血流、功能及血压的重要因素；ＥＦ、年龄、ＢＳ是分别影响ＳＢＰ及ＤＢＰ的独立因素。     

Hypertensive emergencies

Critical cases of high blood pressure are common clinical occurrences that may account for as many as 25% of all medical emergencies. About 75% of these increases in blood pressure can be judged as hypertensive urgencies, 25% are even hypertensive emergency situations. Nevertheless, only less than 1% of the hypertensive population experiences hypertensive urgency or emergency situations. Hypertensive emergencies are defined as acute cardiac, vascular or cerebral target organ damages. In these cases an acute lowering of blood pressure is inevitable. The rate and intensity of blood pressure depression is dependent on the localization of organ damages. For cardiac and vascular damages it is absolutely necessary to lower the blood pressure rapidly to near normal values. On the contrary, cerebral organ damages are better treated by a moderate lowering of blood pressure peaks to slightly increased blood pressure levels. In hypertensive urgencies no target organ damages occur. For these patients a slow lowering of blood pressure values to normal levels is adequate.     

Hypertensive encephalopathy

Opinion statement The term hypertensive encephalopathy should be reserved for patients with diffuse cerebral effects of precipitous and sustained rises in blood pressure that reverse when blood pressure is lowered and are not due to infarction or hemorrhage. The definitive diagnosis of this syndrome depends on accurate exclusion of other causes that may be associated with elevated blood pressure and neurologic deficits. Treatment is aimed at preventing or limiting target organ (brain) damage. Therapy should be individualized but centered on reducing the mean arterial blood pressure within a period of minutes to 2 hours, by no more than 20% to 25% or to a diastolic blood pressure of 100 to 110 mm Hg (whichever is higher), using short-acting intravenous agents. Oral or sublingual agents should generally be avoided in hypertensive encephalopathy because they are more likely to cause precipitous falls in blood pressure.     

Hypertensive crises

Despite the availability of effective antihypertensive agents, hypertensive crises still occur with relative frequency and remain an important therapeutic challenge. Hypertensive crises are defined as an abrupt elevation of blood pressure (BP) to a systolic BP reading of more than 210 mm Hg and a diastolic BP level of more than 120 mm Hg. The most important initial clinical decision is to differentiate between hypertensive urgency and hypertensive emergency. In both cases, therapy should be promptly initiated to prevent any permanent loss of organ function or life. The underlying pathophysiology and the intent to avoid adverse effects should guide the choice of antihypertensive agents. The most important principle to remember is to lower the blood pressure sufficiently to limit end-organ dysfunction, but without necessarily reaching normotensive levels. Additionally, it is always important to assess the fluid status of the patient and reestablish euvolemia as soon as feasible to avoid precipitous falls in blood pressure.     

Hypertensive encephalopathy

Opinion statement  The term hypertensive encephalopathy should be reserved for patients with diffuse cerebral effects of precipitous and sustained rises in blood pressure that reverse when blood pressure is lowered and are not due to infarction or hemorrhage. The definitive diagnosis of this syndrome depends on accurate exclusion of other causes that may be associated with elevated blood pressure and neurologic deficits. Treatment is aimed at preventing or limiting target organ (brain) damage. Therapy should be individualized but centered on reducing the mean arterial blood pressure within a period of minutes to 2 hours, by no more than 20% to 25% or to a diastolic blood pressure of 100 to 110 mm Hg (whichever is higher), using short-acting intravenous agents. Oral or sublingual agents should generally be avoided in hypertensive encephalopathy because they are more likely to cause precipitous falls in blood pressure.