Why do patients with congestive heart failure tolerate the initiation of beta-blocker therapy?
Why do patients with congestive heart failure tolerate the initiation of beta-blocker therapy?
复制标题
为什么充血性心力衰竭患者能够耐受β受体阻滞剂治疗？
DOI：
10.1161/01.cir.88.4.1610
复制
发表时间：
1993
期刊：
影响因子：
37.8
通讯作者：
Feldman,MD
中科院分区：
文献类型：
--
作者：
Haber,HL;Simek,CL;Gimple,LW;Bergin,JD;Subbiah,K;Jayaweera,AR;Powers,ER;Feldman,MD
背景：充血性心力衰竭(CHF)患者可以耐受β-肾上腺素能受体阻滞剂，尽管它具有负性肌力作用。因此，我们研究了β-肾上腺素能受体阻滞剂对左心室收缩和舒张期功能及室-动脉偶联的急性血流动力学影响。此外，CHF患者的分离心肌显示出选择性的β1受体下调，这意味着β2受体在维持体内左心室收缩能力方面发挥了更大的作用。作为第二个目的，我们假设非选择性β-肾上腺素能受体阻滞剂对CHF患者的负性肌力作用大于β1受体阻滞剂。方法和结果临床CHF患者(n=24)和对照组(n=24)分别给予非选择性β受体阻滞剂心得安或β1选择性阻滞剂美托洛尔。测定静脉注射β-受体阻滞剂前后的左心室压力-容量关系，并检测左心室收缩和舒张期功能。CHF患者左心室收缩功能恶化，左心室收缩压(139±-6~125+/-6 mm Hg)、心指数(2.56±0.11~2.20±0.11ml.min-1×M-1)、dp/dtmax(1173±/-63~897+/-50 mm Hg/S)、收缩末期弹性(0.88±/-0.10~0.64±0.10 mm Hg/mL)均下降，P<0.05。虽然主动左室舒张功能恶化(等容松弛63+/-2~73+/-3毫秒，峰值充盈率543+/-33~464+/-28毫升/S，P<0.05)，但被动左室舒张功能无明显变化(肺毛细血管楔形，24+/-2~24+/-1毫米汞柱；室壁硬度从0.0154+/-0.0005降至0.0163+/-0.0005毫升(P=NS)，后负荷下降(动脉弹性3.85+/-0.31至3.38+/-0.24毫米汞/毫升，P<；0.05)。对照组患者除等容松弛时间延长(48+/-1至55+/-2毫秒，P<；0.05)外，其他参数无明显变化。心得安(n=12)和美托洛尔(n=12)对CHF患者上述参数的影响相似。结论这些数据不支持心肌β2受体在CHF中发挥更大的生理作用。被动舒张期功能的保留和室-动脉耦合为心力衰竭患者耐受β-肾上腺素能受体阻滞剂提供了可能的解释。
BACKGROUNDDespite its negative inotropic effects, the initiation of beta-adrenergic blockade is tolerated by patients with congestive heart failure (CHF). Accordingly, we examined the acute hemodynamic effects of beta-adrenergic blockade on systolic and diastolic left ventricular (LV) function and ventriculo-arterial coupling. In addition, isolated myocardium from patients with CHF shows selective beta 1-receptor downregulation, implying a greater role for the beta 2-receptor in maintaining in vivo LV contractility. As a secondary aim, we hypothesized that nonselective beta-adrenergic blockade would have greater negative inotropic effect than beta 1-blockade in patients with CHF.METHODS AND RESULTSPatients with clinical CHF (n = 24) and control patients without CHF (n = 24) were given either the nonselective beta-blocker propranolol or the beta 1-selective blocker metoprolol. LV pressure-volume relations were obtained before and after the administration of intravenous beta-blocker, and measures of LV systolic and diastolic function were examined. Patients with CHF had a deterioration in LV systolic function with a fall in LV systolic pressure (139 +/- 6 to 125 +/- 6 mm Hg), cardiac index (2.56 +/- 0.11 to 2.20 +/- 0.11 mL.min-1 x M-1), dP/dtmax (1173 +/- 63 to 897 +/- 50 mm Hg/s), and end-systolic elastance (0.88 +/- 0.10 to 0.64 +/- 0.10 mm Hg/mL), P < .05 for all. Although there was deterioration of active LV relaxation (isovolumetric relaxation 63 +/- 2 to 73 +/- 3 milliseconds, peak filling rate 543 +/- 33 to 464 +/- 28 mL/s, P < .05 for both), there was no change in passive LV diastolic function (pulmonary capillary wedge, 24 +/- 2 to 24 +/- 1 mm Hg; chamber stiffness, 0.0154 +/- 0.0005 to 0.0163 +/- 0.0005 mL-1, P = NS for both), and a decrease in afterload (arterial elastance 3.85 +/- 0.31 to 3.38 +/- 0.24 mm Hg/mL, P < .05). Control patients had no change in these parameters other than a prolongation of isovolumetric relaxation (48 +/- 1 to 55 +/- 2 milliseconds, P < .05). The effects of propranolol (n = 12) versus metoprolol (n = 12) on these parameters in patients with CHF were similar.CONCLUSIONSThese data do not support a greater in vivo physiological role of the myocardial beta 2-receptor in CHF. The preservation of passive diastolic function and ventriculo-arterial coupling provide possible explanations of why beta-adrenergic blockade is tolerated by patients with CHF.