Simons G R, Newby K H, Kearney M M, Brandon M J, Natale A
Department of Medicine, Duke University Medical Center, North Carolina, USA.
Pacing Clin Electrophysiol. 1998 Feb;21(2):430-7. doi: 10.1111/j.1540-8159.1998.tb00068.x.
The objective of this study was to assess the safety and efficacy of transvenous low energy cardioversion of atrial fibrillation in patients with ventricular tachycardia and atrial fibrillation and to study the mechanisms of proarrhythmia. Previous studies have demonstrated that cardioversion of atrial fibrillation using low energy, R wave synchronized, direct current shocks applied between catheters in the coronary sinus and right atrium is feasible. However, few data are available regarding the risk of ventricular proarrhythmia posed by internal atrial defibrillation shocks among patients with ventricular arrhythmias or structural heart disease. Atrial defibrillation was performed on 32 patients with monomorphic ventricular tachycardia and left ventricular dysfunction. Shocks were administered during atrial fibrillation (baseline shocks), isoproterenol infusion, ventricular pacing, ventricular tachycardia, and atrial pacing. Baseline shocks were also administered to 29 patients with a history of atrial fibrillation but no ventricular arrhythmias. A total of 932 baseline shocks were administered. No ventricular proarrhythmia was observed after well-synchronized baseline shocks, although rare inductions of ventricular fibrillation occurred after inappropriate T wave sensing. Shocks administered during wide-complex rhythms (ventricular pacing or ventricular tachycardia) frequently induced ventricular arrhythmias, but shocks administered during atrial pacing at identical ventricular rates did not cause proarrhythmia. The risk of ventricular proarrhythmia after well-synchronized atrial defibrillation shocks administered during narrow-complex rhythms is low, even in patients with a history of ventricular tachycardia. The mechanism of proarrhythmia during wide-complex rhythms appears not to be related to ventricular rate per se, but rather to the temporal relationship between shock delivery and the repolarization time of the previous QRS complex.
本研究的目的是评估经静脉低能量房颤复律对合并室性心动过速和房颤患者的安全性和有效性,并研究促心律失常的机制。既往研究表明,利用低能量、R波同步、在冠状窦和右心房导管之间施加直流电电击进行房颤复律是可行的。然而,关于室性心律失常或结构性心脏病患者心房内除颤电击导致室性心律失常风险的数据很少。对32例单形性室性心动过速和左心室功能不全患者进行了心房除颤。在房颤期间(基线电击)、静脉输注异丙肾上腺素、心室起搏、室性心动过速和心房起搏时给予电击。也对29例有房颤病史但无室性心律失常的患者给予基线电击。共进行了932次基线电击。在同步良好的基线电击后未观察到室性心律失常,尽管在不适当的T波感知后罕见地诱发了室颤。在宽QRS波节律(心室起搏或室性心动过速)期间给予的电击频繁诱发室性心律失常,但在相同心室率的心房起搏期间给予的电击未引起心律失常。即使在有室性心动过速病史的患者中,在窄QRS波节律期间同步良好的心房除颤电击后发生室性心律失常的风险也很低。宽QRS波节律期间促心律失常的机制似乎与心室率本身无关,而是与电击发放与前一个QRS波群复极时间的时间关系有关。