Lyon Alexander R, Rees Paul S C, Prasad Sanjay, Poole-Wilson Philip A, Harding Sian E
Department of Cardiac Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, UK.
Nat Clin Pract Cardiovasc Med. 2008 Jan;5(1):22-9. doi: 10.1038/ncpcardio1066.
Stress cardiomyopathy, also referred to as Takotsubo cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. We hypothesize that stress cardiomyopathy is a form of myocardial stunning, but with different cellular mechanisms to those seen during transient episodes of ischemia secondary to coronary stenoses. In this syndrome, we believe that high levels of circulating epinephrine trigger a switch in intracellular signal trafficking in ventricular cardiomyocytes, from G(s) protein to G(i) protein signaling via the beta(2)-adrenoceptor. Although this switch to beta(2)-adrenoceptor-G(i) protein signaling protects against the proapoptotic effects of intense activation of beta(1)-adrenoceptors, it is also negatively inotropic. This effect is greatest at the apical myocardium, in which the beta-adrenoceptor density is greatest. Our hypothesis has implications for the use of drugs or devices in the treatment of patients with stress cardiomyopathy.
应激性心肌病，也称为Takotsubo心肌病，是一种越来越被认可的临床综合征，其特征为急性可逆性心尖部心室功能障碍。我们推测应激性心肌病是心肌顿抑的一种形式，但细胞机制与冠状动脉狭窄继发短暂缺血时所见不同。在该综合征中，我们认为高水平循环肾上腺素会触发心室心肌细胞内信号转导途径的转换，从G(s)蛋白信号转导转变为通过β(2)-肾上腺素能受体的G(i)蛋白信号转导。尽管这种向β(2)-肾上腺素能受体-G(i)蛋白信号转导的转换可对抗β(1)-肾上腺素能受体强烈激活的促凋亡作用，但它也具有负性肌力作用。这种效应在心尖部心肌最为明显，因为此处β-肾上腺素能受体密度最高。我们的假说对应用药物或装置治疗应激性心肌病患者具有指导意义。
