Shimizu W, Tanaka K, Suenaga K, Wakamoto A
Department of Internal Medicine, Futami Central Hospital, Miyoshi, Hiroshima, Japan.
Pacing Clin Electrophysiol. 1991 Jul;14(7):1105-11. doi: 10.1111/j.1540-8159.1991.tb02841.x.
Endocardial monophasic action potentials (MAPs) were recorded at the right ventricular apex in a patient with QTU prolongation and torsade de pointes (TdP) in association with marked bradycardia and hypokalemia. There was a distinct hump on phase 3 repolarization of the MAPs characteristic of early afterdepolarizations (EADs), which was associated with marked prolongation of the QTU interval on the surface electrocardiogram. EAD amplitude was bradycardia dependent, and there was a strong correlation (r = 0.91) between the preceding RR interval and the amplitude of the EAD (percent of MAP amplitude). Intravenous administration of lidocaine or right ventricular pacing suppressed the ventricular premature complexes and TdP in association with the suppression of the EADs on the MAPs. Furthermore, these EADs were not recorded on the MAPs 1 month later when the QTU prolongation and TdP had disappeared. These findings suggest that the TU abnormality and QTU prolongation responsible for TdP were due to bradycardia-dependent EADs.
在一名QTU间期延长并伴有尖端扭转型室性心动过速（TdP）、显著心动过缓和低钾血症的患者中，于右心室心尖处记录心内膜单相动作电位（MAPs）。MAPs的复极3期存在一个明显的波峰，这是早期后除极（EADs）的特征，并且与体表心电图上QTU间期的显著延长相关。EAD幅度依赖于心动过缓，且在前RR间期与EAD幅度（占MAP幅度的百分比）之间存在强相关性（r = 0.91）。静脉注射利多卡因或右心室起搏在抑制MAPs上的EADs的同时，抑制了室性早搏复合波和TdP。此外，1个月后当QTU延长和TdP消失时，MAPs上未记录到这些EADs。这些发现提示，导致TdP的TU异常和QTU延长是由心动过缓依赖性EADs引起的。
