Shiotani M, Arita M, Nakatsu C, Nakamura N, Ohshika H, Nakamura Y, Fujiwara S, Ueno Y, Nishio I, Masuyama Y
Department of Medicine, Wakayama Medical College.
J Cardiol. 1990;20(1):135-45.
This study was performed to assess the effect of a calcium channel blocker (nifedipine) and beta-blockade (atenolol) on left ventricular early diastolic function and filling in essential hypertension (WHO stage I, II; HT). Twenty-two untreated patients were randomly divided as nifedipine (11 patients) and atenolol (11 patients) treatment groups and both the groups had complete echocardiographic and Doppler studies. Twenty normotensive cases served as controls. Clinical and echo-Doppler data obtained at baseline and four weeks after initiation of each therapy showed no difference between the two HT groups as to mean blood pressure (before therapy, 119 +/- 3 vs 117 +/- 11 mmHg; after therapy, 106 +/- 3 vs 110 +/- 3 mmHg), left ventricular dimension, left atrial dimension, and wall thickness. To evaluate early diastolic function, the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and that from MVO to the O point of the apexcardiogram were measured. The IIA-O interval was also calculated. The peak velocities in the rapid filling (R) and atrial contraction phases (A) were measured using pulsed Doppler echocardiography at the center of the mitral orifice. The MVO-O/IIA-MVO and A/R ratios were also calculated. Compared with the controls, the IIA-O interval (143.9 +/- 6.8 msec) and the IIA-MVO interval (81.5 +/- 4.9 msec) were significantly prolonged in HT (p less than 0.01). There was no significant difference between the MVO-O interval and R. Velocity A (54.2 +/- 2.7 cm/sec) and the A/R ratio (1.01 +/- 0.11) increased significantly in HT (p less than 0.05). The IIA-O interval (before therapy, 153.3 +/- 7.6 vs after therapy, 134.3 +/- 6.2 msec) and IIA-MVO interval (87.3 +/- 6.3 vs 77.8 +/- 5.9 msec) decreased and R (43.7 +/- 3.8 vs 49.1 +/- 3.0 cm/sec) increased significantly with nifedipine. The IIA-O interval (135.7 +/- 11.3 vs 150.4 +/- 7.6 msec) and the MVO-O (58.4 +/- 3.9 vs 66.5 +/- 4.7 msec) interval were significantly prolonged with atenolol, however the IIA-MVO interval, R, and A/R did not change. A (57.5 +/- 4.0 vs 50.2 +/- 2.9 cm/sec) was also significantly decreased with atenolol. There was a significant correlation between reduction in velocity A and prolongation in the MVO-O interval (r = -0.62, p less than 0.05) with atenolol. These results suggested that the prolongation of the diastolic closure rate of the mitral valve by atenolol was related to increased ventricular filling and decreased atrial contraction.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究旨在评估钙通道阻滞剂（硝苯地平）和β受体阻滞剂（阿替洛尔）对原发性高血压（WHO I、II期；HT）患者左心室舒张早期功能及充盈的影响。22例未经治疗的患者被随机分为硝苯地平治疗组（11例）和阿替洛尔治疗组（11例），两组均进行了完整的超声心动图和多普勒检查。20例血压正常者作为对照。在基线及每种治疗开始后4周获得的临床及超声多普勒数据显示，两组高血压患者在平均血压（治疗前，119±3 vs 117±11 mmHg；治疗后，106±3 vs 110±3 mmHg）、左心室大小、左心房大小及室壁厚度方面无差异。为评估舒张早期功能，测量了从主动脉瓣关闭音（IIA，心音图）至二尖瓣开放（MVO，超声心动图）的间期以及从MVO至心尖搏动图O点的间期。还计算了IIA - O间期。使用脉冲多普勒超声心动图在二尖瓣口中心测量快速充盈期（R）和心房收缩期（A）的峰值速度。还计算了MVO - O/IIA - MVO及A/R比值。与对照组相比，高血压患者的IIA - O间期（143.9±6.8毫秒）和IIA - MVO间期（81.5±4.9毫秒）显著延长（p<0.01）。MVO - O间期与R无显著差异。高血压患者的A峰速度（54.2±2.7 cm/秒）及A/R比值（1.01±0.11）显著增加（p<0.05）。硝苯地平治疗后，IIA - O间期（治疗前，153.3±7.6 vs治疗后，134.3±6.2毫秒）和IIA - MVO间期（87.3±6.3 vs 77.8±5.9毫秒）缩短，R（43.7±3.8 vs 49.1±3.0 cm/秒）显著增加。阿替洛尔使IIA - O间期（135.7±11.3 vs 150.4±7.6毫秒）和MVO - O间期（58.4±3.9 vs 66.5±4.7毫秒）显著延长，然而IIA - MVO间期、R及A/R未改变。阿替洛尔治疗后A（57.5±4.0 vs 50.2±2.9 cm/秒）也显著降低。阿替洛尔治疗后，A峰速度降低与MVO - O间期延长之间存在显著相关性（r = -0.62，p<0.05）。这些结果提示，阿替洛尔使二尖瓣舒张期关闭速率延长与心室充盈增加及心房收缩减弱有关。（摘要截选至400字）
