Ikram H
Br Med J. 1977 Jun 11;1(6075):1505-7. doi: 10.1136/bmj.1.6075.1505.
Haemodynamic studies were performed in 10 patients with uncomplicated thyrotoxicosis and seven with thyrotoxic cardiac failure. The cardiac output of those with uncomplicated hyperthyroidism was higher than normal at rest. After 2 mg of intravenous propranolol there was a 13% fall but the level was still higher than normal. In patients with thyrotoxic cardiac failure the resting cardiac output was normal, but it fell after propranolol by 30% to subnormal levels. In both groups there was an increase in right heart pressures and fall in the rate of increase in arterial pressure, which indicated a decrease in myocardial contractility. These results indicate that increased autonomic activity is a compensatory phenomenon in hyperthyroid heart failure and that its abolition by beta-blocking drugs has a deleterious effect on cardiac function. They are therefore contraindicated in patients with thyrotoxic heart failure.
对10例无并发症的甲状腺毒症患者和7例甲状腺毒症性心力衰竭患者进行了血流动力学研究。无并发症甲亢患者的静息心输出量高于正常。静脉注射2mg普萘洛尔后，心输出量下降了13%，但仍高于正常水平。甲状腺毒症性心力衰竭患者的静息心输出量正常，但注射普萘洛尔后下降了30%，降至正常水平以下。两组患者右心压力均升高，动脉压上升速率下降，这表明心肌收缩力降低。这些结果表明，自主神经活动增加是甲状腺功能亢进性心力衰竭中的一种代偿现象，β受体阻滞剂消除这种活动对心脏功能有有害影响。因此，甲状腺毒症性心力衰竭患者禁用β受体阻滞剂。
