Isobe M, Kashida M, Isshiki T, Koizumi K, Kuwako K, Umeda T, Yamaguchi T, Machii K, Suzuki K, Tohda E
J Cardiogr. 1982 Dec;12(4):939-52.
Left ventricular (LV) relaxation was studied in patients with hypertensive heart disease with LV hypertrophy (HHD, n = 25) and hypertrophic cardiomyopathy (HCM, n = 9), and these data were compared with that of normal controls (n = 20). The effects of oral administration of propranolol (n = 11), pindolol (n = 3), nifedipine (n = 6) and diltiazem (n = 5) in patients with HHD and that of propranolol (n = 9) in patients with HCM were also studied. Isovolumic relaxation time (IRT) was measured using dual M-mode echocardiography and peak normalized rate of change of the LV cavity in early diastole (peak dD/dt/D) was calculated by M-mode echocardiography using a digitizer and microcomputer system. IRT was significantly longer in HHD (112 +/- 24 msec, p less than 0.001) and in HCM (85 +/- 40 msec, p less than 0.05) compared with that of normal subjects (64 +/- 24 msec). The normal value of peak dD/dt/D was 3.8 +/- 0.7 sec-1, and it was significantly lower in HHD (2.7 +/- 0.8 sec-1, p less than 0.001). It was also lower in HCM (3.2 +/- 0.8 sec-1), but without a statistical significance. In HHD there was a significant relationship (r = -0.611, p less than 0.01) between peak dD/dt/D and wall thickness of the LV (interventricular septum + LV posterior wall). There was no significant change in IRT before and after the administration of beta-blockers and calcium antagonists except nifedipine in HHD (before: 116 +/- 28 msec, after: 80 +/- 14 msec, p less than 0.005). It was probably due to the effect of an accompanied decrease in heart rate. However, peak dD/dt/D was significantly increased in both HHD and HCM groups after the administration of propranolol, pindolol, nifedipine and diltiazem. These data show that LV relaxation is abnormal in the hypertrophied LV. Although the genesis of this abnormality is not clear, there seems to be a close relationship between the relaxation abnormality and increased LV mass in HHD. Oral administration of propranolol, pindolol and diltiazem for patients with HHD and propranolol for patients with HCM seems to improve the abnormal LV relaxation of each disease.
对患有左心室肥厚的高血压心脏病患者(HHD,n = 25)和肥厚型心肌病患者(HCM,n = 9)的左心室(LV)舒张功能进行了研究,并将这些数据与正常对照组(n = 20)的数据进行了比较。还研究了口服普萘洛尔(n = 11)、吲哚洛尔(n = 3)、硝苯地平(n = 6)和地尔硫䓬(n = 5)对HHD患者的影响以及普萘洛尔(n = 9)对HCM患者的影响。使用双M型超声心动图测量等容舒张时间(IRT),并通过使用数字转换器和微机系统的M型超声心动图计算舒张早期左心室腔内径变化的峰值标准化速率(峰值dD/dt/D)。与正常受试者(64±24毫秒)相比,HHD患者(112±24毫秒,p<0.001)和HCM患者(85±40毫秒,p<0.05)的IRT明显更长。峰值dD/dt/D的正常值为3.8±0.7秒-1,在HHD患者中显著降低(2.7±0.8秒-1,p<0.001)。在HCM患者中也较低(3.2±0.8秒-1),但无统计学意义。在HHD患者中,峰值dD/dt/D与左心室壁厚度(室间隔+左心室后壁)之间存在显著相关性(r = -0.611,p<0.01)。除HHD患者服用硝苯地平外,服用β受体阻滞剂和钙拮抗剂前后IRT无显著变化(服药前:116±28毫秒,服药后:80±14毫秒,p<0.005)。这可能是由于伴随的心率下降的影响。然而,服用普萘洛尔、吲哚洛尔、硝苯地平和地尔硫䓬后,HHD和HCM组的峰值dD/dt/D均显著增加。这些数据表明,肥厚的左心室舒张功能异常。虽然这种异常的发生机制尚不清楚,但在HHD中,舒张功能异常与左心室质量增加之间似乎存在密切关系。对HHD患者口服普萘洛尔、吲哚洛尔和地尔硫䓬,对HCM患者口服普萘洛尔似乎可改善各疾病的左心室舒张功能异常。