Attwell D, Lee J A
Department of Physiology, University College London.
Lancet. 1988 May 21;1(8595):1136-9. doi: 10.1016/s0140-6736(88)91953-8.
In several syndromes sudden death is associated with a long Q-T interval on the electrocardiogram. Current treatment is aimed at correcting a notional imbalance of cardiac sympathetic drive. Although this approach can be effective, the primary disorder may be a defect in the cellular mechanism that alters the length of the ventricular action potential, and hence the Q-T interval, in response to a change of heart rate. Such defects may be underdiagnosed because the long Q-T syndromes are defined simply in terms of a prolonged Q-T interval, without consideration of the fact that susceptibility to arrhythmias is likely to be due, not to a lengthened Q-T per se, but to an absence or alteration of the normal Q-T shortening in response to an increase of heart rate. People susceptible to R-on-T related arrhythmias could be identified by measurement of the dependence of the Q-T interval on heart rate and how quickly the Q-T interval adapts to a change in rate.
在几种综合征中，猝死与心电图上的长QT间期相关。目前的治疗旨在纠正心脏交感神经驱动的一种假想失衡。尽管这种方法可能有效，但原发性疾病可能是细胞机制的缺陷，该机制会改变心室动作电位的长度，从而响应心率变化而改变QT间期。此类缺陷可能未得到充分诊断，因为长QT综合征仅仅根据延长的QT间期来定义，而没有考虑到心律失常易感性可能并非源于QT本身延长，而是由于心率增加时正常QT缩短的缺失或改变。可以通过测量QT间期对心率的依赖性以及QT间期适应心率变化的速度来识别易发生R-on-T相关心律失常的人群。
