CONGESTIVE HEART FAILURE--NUCLEAR STUDIES

有证据表明过度的神经体液激活可能起到一定的作用。 在左心室(LV)衰竭的进展中。它已经被证明了 β-受体阻滞剂改善左心功能和充血性心力衰竭 扩张型和缺血性心肌病患者的症状。 然而，β-受体阻滞剂改善心力衰竭的机制是 不是很好理解。 我们假设β受体阻滞剂通过以下途径改善左心功能 提高心肌葡萄糖利用率。因此，我们比较了LV 射血分数(通过放射性核素血管造影术测量)和 氟脱氧葡萄糖(FDG)摄取(正电子发射测量 10例缺血性和非缺血性心肌病患者的体层摄影术 美托洛尔治疗6个月后。所有患者均为NYHA级 大于或等于II和标准充血性心力衰竭 在服用β-受体阻滞剂之前用药。左心室功能的改善 预定义为LVEF增加&gt；7%。FDG摄取量归一化为 应激状态下左室血流量最高的部位 测试。 基线时，平均左心室射血分数为19%加/减8%，平均血浆去甲肾上腺素 为455正负205 pg/ml，平均收缩压为116 正负23毫米汞柱。在6个月的β-受体阻滞剂治疗后，5 3名患者(3名缺血组，2名非缺血组)的左心室射血分数有所改善(从22 治疗前加/减10%到治疗后加/减13%)。LVEF中的 其余患者保持不变(从之前的14%加/减6%降至 16%加/减6%)。有一个显著的增长， 左心功能改善患者的FDG摄取(0.87+/-.23至 0.96加/减0.34，p&lt；0.01)。相比之下，没有改善的患者 左心功能显示FDG摄取显著下降(0.84 正负0.27至0.77正负0.23，p&lt；0.01)。 这些初步的发现表明，在左心功能的改善 心力衰竭患者接受β-受体阻滞剂治疗与 提高葡萄糖利用率。缺血型和非缺血型 心肌病患者表现出部分可逆性 β受体阻滞剂的功能障碍可能是通过改善来调节的 在葡萄糖代谢方面。

There is evidence that excessive neurohumoral activation may play a role in the progression of left ventricular (LV) failure. It has been shown that beta-blockers improve LV function and congestive heart failure symptoms in patients with dilated and ischemic cardiomyopathies. However, the mechanism by which beta-blockers improve heart failure is not well-understood. We hypothesized that beta blockers lead to improvement in LV function by increasing myocardial glucose utilization. Therefore, we compared LV ejection fraction (measured by radionuclide angiography) and fluorodeoxyglucose (FDG) uptake (measured by positron emission tomography) in 10 ischemic and nonischemic cardiomyopathy patients before and after 6 months of metoprolol therapy. All patients were NYHA class greater than or equal to II and on standard congestive heart failure medications prior to beta blockers. Improvement in LV function was pre-defined as an increase in LVEF of >7%. FDG uptake was normalized to the left ventricular sector with the highest blood flow on stress testing. At baseline, mean LVEF was 19% plus/minus 8%, mean plasma norepinephrine was 455 plus/minus 205 pg/ml and mean systolic blood pressure was 116 plus/minus 23 mmHg. After 6 months of beta blocker therapy, five patients (3 ischemic, 2 non-ischemic) had improved LVEF (from 22 plus/minus 10% before to 34 plus/minus 13% after therapy). LVEF in the remaining patients remained unchanged (from 14 plus/minus 6% before to 16% plus/minus 6% after therapy). There was a significant increase in FDG uptake in patients with improved LV function (0.87 plus/minus .23 to 0.96 plus/minus 0.34, p<0.01). In contrast, patients without improvement in LV function exhibited a significant decrease in FDG uptake (0.84 plus/minus 0.27 to 0.77 plus/minus 0.23, p<0.01). These preliminary findings indicate that improvement in LV function in heart failure patients treated with beta blockers is associated with increased glucose utilization. Both ischemic and non-ischemic cardiomyopathy patients demonstrate partial reversibility of LV dysfunction with beta blockers which may be mediated by an improvement in glucose metabolism.