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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 总被引:2,自引:0,他引:2
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。 相似文献
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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 总被引:3,自引:0,他引:3
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。 相似文献
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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。 相似文献
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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 总被引:1,自引:0,他引:1
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)。 相似文献
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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。 相似文献
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左室肥厚与单纯收缩,舒张或双期血压增高的关系 总被引:2,自引:0,他引:2
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。 相似文献
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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。 相似文献
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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。 相似文献
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老年人不同体质对心脏结构、血流、功能及血压的影响 总被引:3,自引:0,他引:3
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。 相似文献
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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. 相似文献
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Olajide Williams John C. M. Brust 《Current treatment options in cardiovascular medicine》1996,6(3):209-216
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. 相似文献
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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. 相似文献
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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. 相似文献
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