Verrier Richard L, Malik Marek
Beth Israel Deaconess Medical Center, Division of Cardiovascular Medicine, Boston, MA, USA.
J Electrocardiol. 2013 Nov-Dec;46(6):580-4. doi: 10.1016/j.jelectrocard.2013.07.003. Epub 2013 Aug 12.
Extensive experimental evidence indicates a fundamental link between T-wave alternans (TWA) and arrhythmogenesis. Diverse physiologic and pathophysiologic influences alter TWA magnitude in parallel with their effects on vulnerability to ventricular tachyarrhythmias. Specifically, interventions that impede intracellular calcium handling, such as elevated heart rate, heightened adrenergic activity, myocardial ischemia, and heart failure, predispose to greater levels of TWA, reflecting heightened risk for arrhythmias. Conversely, vagus nerve stimulation, blockade of beta-adrenergic receptors and late sodium and L-type calcium channels, and sympathetic denervation decrease TWA magnitude, reflecting the potential of these interventions to reduce risk for ventricular tachycardia and fibrillation. TWA thus appears able to detect the influence of pathophysiologically relevant triggers as well as the efficacy of antiarrhythmic drugs without reducing the predictive capacity of the phenomenon.
大量实验证据表明T波交替（TWA）与心律失常发生之间存在根本联系。多种生理和病理生理影响会改变TWA幅度，且与它们对室性快速心律失常易感性的影响平行。具体而言，妨碍细胞内钙处理的干预措施，如心率升高、肾上腺素能活性增强、心肌缺血和心力衰竭，会导致更高水平的TWA，反映出心律失常风险增加。相反，迷走神经刺激、β-肾上腺素能受体及晚钠和L型钙通道阻滞剂，以及交感神经去神经支配会降低TWA幅度，反映出这些干预措施降低室性心动过速和颤动风险的潜力。因此，TWA似乎能够检测病理生理相关触发因素的影响以及抗心律失常药物的疗效，而不会降低该现象的预测能力。
