London G M, Pannier B, Guerin A P, Marchais S J, Safar M E, Cuche J L
Centre Hospitalier F.H. Manhes, Fleury-Mérogis, France.
Circulation. 1994 Dec;90(6):2786-96. doi: 10.1161/01.cir.90.6.2786.
We wished to assess the respective roles of the antihypertensive and blood pressure (BP)-independent effects of antihypertensive drugs on arterial hemodynamics and left ventricular hypertrophy (LVH) in end-stage renal disease (ESRD) patients.
In a double-blind study, 24 ESRD patients with LVH were randomized to 12 months' administration of either the angiotensin-converting enzyme (ACE) inhibitor perindopril (n = 14) or the calcium channel blocker nitrendipine (n = 10). Repeated measurements of the following parameters were performed: BP (mercury sphygmomanometry), left ventricular mass (LVM, echocardiography), cardiac output (aortic cross-section and velocity integral), total peripheral resistance (cardiac output and mean BP), aortic and large-artery compliance (pulse wave velocity, Doppler flowmeter), and arterial wave reflections (augmentation index, applanation tonometry). Radioimmunoassay was used to determine plasma renin activity, aldosterone, and plasma catecholamine levels. Two-way (time-treatment) ANOVA for repeated measures was used for statistical analysis. Perindopril and nitrendipine induced significant and similar decreases in BP, total peripheral resistance (P < .001), aortic and arterial pulse wave velocities (P < .001), and arterial wave reflections (P < .01). At baseline, the two groups had LVH mostly due to increased LV end-diastolic diameter (LVEDD) (perindopril, 54.3 +/- 1.4 and nitrendipine, 54.3 +/ 2.4 mm) with near-normal mean LV wall thickness (perindopril, 11.4 +/- 0.3 and nitrendipine, 11.2 +/- 0.4 mm). A decrease in LVM was observed only in patients receiving perindopril (from 317 +/- 18 to 247 +/- 21 g) (time-treatment interaction, P = .036). Nitrendipine had no significant effect on LVM (314 +/- 29 versus 286 +/- 32 g). The decrease in LVM observed with perindopril was associated with a reduction in LVEDD (49.9 +/- 1.6 versus 54.3 +/- 1.4 mm after 12 months) (time-treatment interaction, P = .04), while the mean LV wall thickness was unchanged (11.4 +/- 0.3 versus 10.5 +/- 0.5 mm). Cardiac alterations were not correlated with changes in BP or with alterations in plasma renin activity or aldosterone or catecholamine levels.
In ESRD patients with LVH, ACE inhibition decreases LVM independently of its antihypertensive effect and of associated alterations in arterial hemodynamics. The decrease in LVM was due primarily to a decrease in LV volume, which may have resulted in these patients from chronic volume overload.
我们希望评估降压药物的降压作用和非血压（BP）依赖性作用对终末期肾病（ESRD）患者动脉血流动力学和左心室肥厚（LVH）的各自影响。
在一项双盲研究中，24例患有LVH的ESRD患者被随机分为两组，分别接受12个月的血管紧张素转换酶（ACE）抑制剂培哚普利（n = 14）或钙通道阻滞剂尼群地平（n = 10）治疗。对以下参数进行重复测量：血压（汞柱式血压计）、左心室质量（LVM，超声心动图）、心输出量（主动脉横截面积和速度积分）、总外周阻力（心输出量和平均血压）、主动脉和大动脉顺应性（脉搏波速度，多普勒流量计）以及动脉波反射（增强指数，压平式眼压计）。采用放射免疫分析法测定血浆肾素活性、醛固酮和血浆儿茶酚胺水平。使用重复测量的双向（时间 - 治疗）方差分析进行统计分析。培哚普利和尼群地平均显著且相似地降低了血压、总外周阻力（P <.001）、主动脉和动脉脉搏波速度（P <.001）以及动脉波反射（P <.01）。基线时，两组患者的LVH主要归因于左心室舒张末期直径（LVEDD）增加（培哚普利组为54.3±1.4，尼群地平组为54.3±2.4 mm），平均左心室壁厚度接近正常（培哚普利组为11.4±0.3，尼群地平组为11.2±0.4 mm）。仅在接受培哚普利治疗的患者中观察到LVM降低（从317±18降至247±21 g）（时间 - 治疗交互作用，P =.036）。尼群地平对LVM无显著影响（314±29对286±32 g）。培哚普利治疗后观察到的LVM降低与LVEDD减小有关（12个月后为49.9±1.6对54.3±1.4 mm）（时间 - 治疗交互作用，P =.04），而平均左心室壁厚度未改变（11.4±0.3对10.5±0.5 mm）。心脏改变与血压变化、血浆肾素活性、醛固酮或儿茶酚胺水平的改变无关。
在患有LVH的ESRD患者中，ACE抑制作用可独立于其降压作用以及动脉血流动力学的相关改变而降低LVM。LVM降低主要归因于左心室容积减小，这可能是由于这些患者存在慢性容量负荷过重所致。
