The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy.
The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy.
复制标题
正性肌力药物和血管扩张剂治疗对充血性心肌病患者舒张特性的不同影响。
DOI：
10.1161/01.cir.74.4.815
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发表时间：
1986
期刊：
影响因子：
37.8
通讯作者：
Rajfer,SI
中科院分区：
文献类型：
--
作者：
Carroll,JD;Lang,RM;Neumann,AL;Borow,KM;Rajfer,SI
充血性心力衰竭的症状通常反映收缩和舒张功能的异常。虽然关于正性肌力药物和血管扩张剂治疗影响收缩功能的机制已经报道了很多工作，但关于它们对舒张功能的影响却知之甚少。在12例弥漫性充血性心肌病患者中，用微压计同时记录左心室和主动脉压、二维靶向M型超声心动图和热稀释法测定心输出量。每名患者接受多巴胺（2、4和6微克/千克/分钟）和多巴酚丁胺（2、6和10微克/千克/分钟），10名患者接受硝普钠（0.125至2.0微克/千克/分钟）。基线血流动力学特征为低心脏指数（2.1 +/- 0.7 liter/min/m2，平均值+/- SD）、高左心室舒张末期压（24 +/- 10 mm Hg）、舒张末期（6.8 +/- 1.0 cm）和收缩末期（6.0 +/- 1.0 cm）增大。所有患者均出现异常左心室压力下降，时间常数延长（67 +/- 20毫秒），峰值舒张期延长率降低。多巴胺和多巴酚丁胺降低舒张时间常数，增加峰值延长率。多巴酚丁胺也将最低舒张压从14 +/- 7降至10 +/- 9 mm Hg（p <0.01）;两种药物均未降低舒张末期压。事实上，多巴胺升高了7名患者的舒张末期压，尽管压力衰减更快。多巴胺和多巴酚丁胺治疗后舒张压-尺寸关系显示随收缩末期心室尺寸减小而显著改变，但被动室僵硬度无显著变化。硝普钠使左心室最低舒张压降低4 ± 2 mm Hg，舒张末期压降低7 ± 4 mm Hg（p <0.01）。在测试剂量下，它并没有持续加速左心室压力衰减。硝普钠降低舒张末期压是由于5例患者舒张末期尺寸减小。在其他患者中，所有患者的右心房压力均升高，硝普钠治疗后舒张压-尺寸关系显示出平行的下移。因此，用β 1-肾上腺素受体激动剂的正性肌力治疗通过加速舒张、增加充盈和减小收缩末期室大小来增强舒张早期扩张性。血管扩张剂治疗在降低舒张压方面更有效。（400字处截断摘要）
Symptoms of congestive heart failure frequently reflect abnormalities in both systolic and diastolic performance. While much work has been reported regarding the mechanisms by which positive inotropic and vasodilator therapy affect systolic performance, little is known about their effect on diastolic function. In 12 patients with diffuse congestive cardiomyopathy micromanometer left ventricular and aortic pressure measurements were recorded simultaneously with two-dimensionally targeted M mode echocardiograms and thermodilution-determined cardiac output. Each patient received dopamine (2, 4, and 6 micrograms/kg/min), and dobutamine (2, 6, and 10 micrograms/kg/min), and 10 received nitroprusside (0.125 to 2.0 micrograms/kg/min). Baseline hemodynamics were characterized by low cardiac index (2.1 +/- 0.7 liter/min/m2, mean +/- SD), high left ventricular end-diastolic pressure (24 +/- 10 mm Hg), and increased end-diastolic (6.8 +/- 1.0 cm) and end-systolic dimensions (6.0 +/- 1.0 cm). All patients had abnormal left ventricular pressure decay with a prolonged time constant (67 +/- 20 msec) and reduced peak diastolic lengthening rates. Dopamine and dobutamine decreased the time constant of relaxation and increased the peak lengthening rate. Dobutamine also reduced the minimum diastolic pressure from 14 +/- 7 to 10 +/- 9 mm Hg (p less than .01); neither drug reduced end-diastolic pressure. In fact, dopamine elevated end-diastolic pressures in seven patients, despite more rapid pressure decay. Diastolic pressure-dimension relations after dopamine and dobutamine showed a leftward shift with a reduced end-systolic chamber size, but no significant changes in passive chamber stiffness. Nitroprusside decreased left ventricular minimum diastolic pressure by 4 +/- 2 mm Hg and end-diastolic pressure by 7 +/- 4 mm Hg (p less than .01). It did not consistently accelerate left ventricular pressure decay at the doses tested. The decreased end-diastolic pressure with nitroprusside was due to a reduced end-diastolic dimension in five patients. In the other patients, all of whom had elevated right atrial pressures, diastolic pressure-dimension relations showed a parallel downward shift after nitroprusside. Thus, positive inotropic therapy with beta 1-adrenoceptor agonists enhances early diastolic distensibility by accelerating relaxation, augmenting filling, and reducing end-systolic chamber size. Vasodilator therapy is much more effective in lowering diastolic pressures.(ABSTRACT TRUNCATED AT 400 WORDS)