Morgan J M, Cunningham D, Rowland E
Royal Brompton National Heart and Lung Hospital, London, England.
J Am Coll Cardiol. 1992 May;19(6):1244-53. doi: 10.1016/0735-1097(92)90331-g.
Abnormal dispersion of repolarization may contribute to the arrhythmogenic physiologic substrate of ventricular arrhythmia. Geographic dispersion of monophasic action potential duration was determined in steady state (drive cycle lengths 600 and 430 ms) between widely spaced right ventricular endocardial sites (geographic dispersion) in 10 control patients with right ventricular disease and complicating ventricular tachycardia (n = 9), 6 patients with right and left ventricular disease and complicating ventricular tachycardia and 7 patients with ischemic heart disease and complicating ventricular tachycardia. No significant difference in geographic dispersion could be demonstrated among the groups. Difference of monophasic action potential duration at adjacent right ventricular endocardial sites (adjacent dispersion) was determined after ventricular extrastimulation during construction of simultaneous electrical restitution curves in the same patient groups. Maximal adjacent dispersion over the electrical restitution curve was compared between disease and control groups. There was a significant difference in observations of maximal adjacent dispersion in patients with right ventricular disease and complicating ventricular tachycardia (range 5 to 85 ms, median 22.5; 14 pairs of sites; p less than 0.05) and patients with right and left ventricular disease and complicating ventricular tachycardia (range 5 to 50 ms, median 17.5; 14 pairs of sites; p less than 0.05) compared with control patients (range 5 to 20 ms, median 10; 15 pairs of sites). This difference was not evident when patients with ischemic heart disease and complicating ventricular tachycardia (range 5 to 25 ms, median 12.5; 12 pairs of sites) were compared with control patients. Maximal percent monophasic action potential shortening from steady state was significantly greater (p less than 0.001) in both groups with greater adjacent dispersions, and prolongation of activation time at monophasic action potential recording sites after premature extrastimulation tended to be greater in patients with right or right and left ventricular disease and complicating ventricular tachycardia. It is concluded that in disease, exaggeration of monophasic action potential shortening after premature ventricular extrastimulation may contribute to the electrophysiologic arrhythmogenic substrate.
复极化异常离散可能是室性心律失常发生的生理基础。在10例患有右心室疾病并合并室性心动过速的对照患者（n = 9）、6例患有左右心室疾病并合并室性心动过速的患者以及7例患有缺血性心脏病并合并室性心动过速的患者中，测定了稳态下（驱动周期长度分别为600和430毫秒）右心室广泛间隔的心内膜位点之间的单相动作电位持续时间的地理离散情况。各组之间地理离散无显著差异。在同一患者组构建同步电恢复曲线期间，通过心室额外刺激后测定相邻右心室心内膜位点之间的单相动作电位持续时间差异（相邻离散）。比较疾病组和对照组电恢复曲线上的最大相邻离散情况。患有右心室疾病并合并室性心动过速的患者（范围为5至85毫秒，中位数为22.5；14对位点；p < 0.05）以及患有左右心室疾病并合并室性心动过速的患者（范围为5至50毫秒，中位数为17.5；14对位点；p < 0.05）与对照患者（范围为5至20毫秒，中位数为10；15对位点）相比，最大相邻离散的观察结果存在显著差异。当将患有缺血性心脏病并合并室性心动过速的患者（范围为5至25毫秒，中位数为12.5；12对位点）与对照患者进行比较时，这种差异并不明显。在两个相邻离散较大的组中，从稳态开始的最大单相动作电位缩短百分比显著更大（p < 0.001），并且在患有右心室或左右心室疾病并合并室性心动过速的患者中，过早额外刺激后单相动作电位记录位点的激活时间延长往往更大。结论是，在疾病状态下，过早心室额外刺激后单相动作电位缩短的夸大可能是电生理致心律失常基础的原因。
