Habbab M A, el-Sherif N
Department of Medicine, State University of New York 11203.
Pacing Clin Electrophysiol. 1992 Jun;15(6):916-31. doi: 10.1111/j.1540-8159.1992.tb03082.x.
T or U wave alternans in association with long QTU and torsade de pointes (TdP) is uncommon and its mechanism(s) is unknown. We studied three patients with TU alternans, long QTU, and TdP: patient 1 was a newborn with congenital long QTU; patient 2 had marked hypokalemia and hypomagnesemia; and patient 3 was receiving procainamide. In the three patients, TU alternans was tachycardia dependent and preceded the onset of TdP. In the patient on procainamide, TU alternans and TdP occurred at long cardiac cycles. In this patient, endocardial monophasic action potential (MAP) recordings showed that TU alternans was associated with alternation of the duration of the plateau. A deflection consistent with early afterdepolarization (EAD) arose at a constant time interval from phase 0 but alternated from high and low levels of phase 3. The first ectopic beat of TdP arose on the descending limb of the EAD. TU alternans was investigated by MAP recordings in six normal dogs, following the administration of anthopleurin-A (AP-A), a drug shown to delay sodium inactivation and to induce bradycardia dependent long QTU, EADs, and TdP. In two dogs TU alternans was associated with 2:1 recordings of EAD and nearly constant plateau duration. In three dogs, TU alternans was associated with EAD that occurred in consecutive beats at constant time intervals from phase 0, but alternated from high and low phase 3 because of alternation of the duration of the plateau. In one dog, alternation of EAD and plateau duration occurred. In 36 separate episodes of TdP that were analyzed in the six dogs, 32 were bradycardia dependent but four developed on abrupt shortening of the cardiac cycle associated with alternation of action potential duration. Our results suggest: (1) TU alternans may be due to 2:1 propagation of an EAD or to alternation of the recovery kinetics of a repolarization current; (2) The constant occurrence of EAD in relation to phase 0 in spite of alternation of plateau duration suggests an ionic mechanism synchronized to depolarization; (3) Tachycardia dependent TdP in clinical and experimental examples of long QTU seems to be characteristically associated with TU alternans. Dispersion of repolarization may underlie the increased ventricular electrical instability in these cases.
T波或U波交替伴QTU间期延长及尖端扭转型室性心动过速（TdP）并不常见，其机制尚不清楚。我们研究了3例伴有TU波交替、QTU间期延长及TdP的患者：患者1为先天性QTU间期延长的新生儿；患者2有明显的低钾血症和低镁血症；患者3正在接受普鲁卡因胺治疗。在这3例患者中，TU波交替与心动过速相关，并先于TdP发作。在接受普鲁卡因胺治疗的患者中，TU波交替和TdP发生于长心动周期。在该患者中，心内膜单相动作电位（MAP）记录显示，TU波交替与平台期持续时间的交替有关。一个与早期后除极（EAD）一致的偏转在距0期恒定的时间间隔出现，但在3期高低水平交替。TdP的第一个异位搏动出现在EAD的下降支。在6只正常犬中，在给予海葵毒素-A（AP-A）后，通过MAP记录研究TU波交替，AP-A是一种已被证明可延迟钠失活并诱发心动过缓依赖性QTU间期延长、EAD及TdP的药物。在2只犬中，TU波交替与EAD的2:1记录及几乎恒定的平台期持续时间有关。在3只犬中，TU波交替与EAD有关，EAD在距0期恒定的时间间隔连续搏动时出现，但由于平台期持续时间交替，在3期高低水平交替。在1只犬中，出现了EAD和平台期持续时间的交替。在对6只犬分析的36次单独的TdP发作中，32次是心动过缓依赖性的，但有4次在心动周期突然缩短并伴有动作电位持续时间交替时发生。我们的结果提示：（1）TU波交替可能是由于EAD的2:1传导或复极电流恢复动力学的交替；（2）尽管平台期持续时间交替，但EAD与0期的恒定关系提示存在与去极化同步的离子机制；（3）在临床和实验性QTU间期延长的例子中，心动过速依赖性TdP似乎与TU波交替有特征性关联。复极离散可能是这些病例中心室电不稳定性增加的基础。
