Peters R W, Gonzalez R, Scheinman M M
Pacing Clin Electrophysiol. 1981 Jan;4(1):17-22. doi: 10.1111/j.1540-8159.1981.tb03670.x.
An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter. The atrial and ventricular effective refractory periods were 180 ms and less than 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atrial or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal by-pass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.
对一名患有预激综合征且有自发房颤病史但无器质性心脏病证据的患者进行了电生理研究。单次诱发的室性早搏导致室性心动过速，随后发展为心室颤动。同样，心房起搏或房性早搏刺激导致频繁发作的房颤或房扑。在驱动周期长度为480毫秒时，心房和心室的有效不应期分别为180毫秒和小于160毫秒。静脉注射普鲁卡因酰胺导致不应期延长，起搏未能诱发房性或室性心律失常。在大多数房室结增强或存在房室旁道的患者中，室性心动过速的机制与室上性心律失常期间心室反应过度快速有关。在我们的患者中，一种独特的机制很明显：心房和心室对颤动的易感性与心肌有效不应期极短有关。这一发现与心脏性猝死的关系有待进一步研究。
