EFFECT OF BETA-ADRENERGIC-BLOCKADE ON MYOCARDIAL-FUNCTION AND ENERGETICS IN CONGESTIVE HEART-FAILURE - IMPROVEMENTS IN HEMODYNAMIC, CONTRACTILE, AND DIASTOLIC PERFORMANCE WITH BUCINDOLOL
EFFECT OF BETA-ADRENERGIC-BLOCKADE ON MYOCARDIAL-FUNCTION AND ENERGETICS IN CONGESTIVE HEART-FAILURE - IMPROVEMENTS IN HEMODYNAMIC, CONTRACTILE, AND DIASTOLIC PERFORMANCE WITH BUCINDOLOL
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DOI：
10.1161/01.cir.82.2.473
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发表时间：
1990-08-01
期刊：
影响因子：
37.8
通讯作者：
GRAYBURN, PA
中科院分区：
文献类型：
--
作者：
EICHHORN, EJ;BEDOTTO, JB;GRAYBURN, PA
本文研究了非选择性β-受体阻滞剂布比妥洛尔对充血性心力衰竭患者的血流动力学影响。15名患者(纽约心脏协会I-IV级)在口服布汀多洛尔3个月前和3个月后接受了心导管术。左心室射血分数由治疗前的0.23±-增加。0.12至0.29+-。0.14(p=0.007)，而收缩末期弹性，一个相对负荷无关的收缩能力决定因素，从0.60.+-增加。0.40至1.11。+-。0.45 mm Hg/ml(p<；0.0049)。两组左心室每搏功指数(34.+-)。13至47。+-。19 g-m/m~2，p=0.0059)和微小功(5.5±-)。2.2至7.0。+-。2.6kg.m/min，p=0.0096)，尽管左室舒张末压力降低(19.0±-)。8至15。+-。5 mm Hg，p=0.021)。峰值+dp/dtmax-舒张末容量关系上移(p=0.0005)。这些数据表明，在β-肾上腺素能受体阻滞剂布地奈德后，心肌的收缩能力得到了改善。配对的心率为98。+-。15min-1，布比洛尔治疗后左室等容松弛时间常数显著降低(92.5±-1)。17比73。+-。11毫秒，p=0.0013)，治疗后收缩末压的时间常数下移(p=0.014)。治疗后左室舒张末压-舒张期容量对数斜率无明显变化(p=0.51)。这些数据表明，慢性β-肾上腺素能受体阻滞剂布比妥洛尔可改善舒张期松弛，但不改变心肌腔僵硬。尽管收缩功能和机械功有所改善，但心肌氧摄取、消耗和效率没有变化。因此，在充血性心力衰竭患者中，慢性β-肾上腺素受体阻滞剂布比妥洛尔显著改善心肌收缩能力和微小做功，但这并不是以牺牲心肌耗氧为代价的。此外，布汀多洛可改善心肌松弛，但不影响心腔僵硬。
The hemodynamic effects of .beta.-aderenergic blockade with bucindolol, a nonselective .beta.-antagonist with mild vasodilatory properties, were studied in patients with congestive heart failure. Fifteen patients (New York Heart Association class I-IV) underwent cardiac catheterization before and after 3 months of oral therapy with bucindolol. The left ventricular ejection fraction increased from 0.23 .+-. 0.12 to 0.29 .+-. 0.14 (p = 0.007), and end-systolic elastance, a relatively load-independent determinant of contractility, increased from 0.60 .+-. 0.40 to 1.11 .+-. 0.45 mm Hg/ml (p < 0.0049). Both left ventricular stroke work index (34 .+-. 13 to 47 .+-. 19 g-m/m2, p = 0.0059) and minute work (5.5 .+-. 2.2 to 7.0 .+-. 2.6 kg-m/min, p = 0.0096) increased despite reductions in left ventricular end-diasolic pressure (19 .+-. 8 to 15 .+-. 5 mm Hg, p = 0.021). There was an upward shift in the peak + dP/dtmax-end-diastolic volume relation (p = 0.0005). These data demonstrate improvements in myocardial contractility after .beta.-adrenergic blockade with bucindolol. At a matched paced heart rate of 98 .+-. 15 min-1, the time constant of left ventricular isovolumic relaxation was significantly reduced by bucinolol therapy (92 .+-. 17 versus 73 .+-. 11 msec, p = 0.0013), and the relaxation of the time constant to end-systolic pressure was shifted downward (p = 0.014) with therapy. The slope of the logarithm left ventricular end-diastolic pressure-end-diastolic volume relation was unchanged (p = 0.51) after bucindolol. These data suggest that chronic .beta.-adrenergic blockade with bucindolol improves diastolic relaxation but does not alter myocardial chamber stiffness. Myocardial oxygen extraction, consumption, and efficiency were unchanged despite improvement in contractile function and mechanical work. Thus, in patients with congestive heart failure, chronic .beta.-adrenergic blockade with bucindolol significantly improves myocardial contractility and minute work, yet it does not do so at the expense of myocardial oxygen consumption. Additionally, bucindolol improves myocardial relaxation but does not affect chamber stiffness.