Bhandari A K, Hong R A, Rahimtoola S H
Department of Medicine, LAC-USC Medical Center, University of Southern California School of Medicine 90033.
Br Heart J. 1988 Apr;59(4):501-5. doi: 10.1136/hrt.59.4.501.
Triggered activity was shown to be the likely mechanism of recurrent tachycardia in a 28 year old Vietnamese man. During baseline electrophysiological testing the tachycardia was induced consistently by prolonged atrial or ventricular pacing but not by premature extrastimuli. Moreover, the tachycardia coupling intervals varied directly with the cycle length of the initiating drive. Procainamide and propranolol did not suppress tachycardia, but verapamil terminated it and prevented its reinitiation. The origin of the tachycardia was localised to the left ventricular inferoapical segment and four direct current countershocks of 200 J each delivered via an electrode catheter abolished the tachycardia. During 12 months of follow up the patient was not treated with antiarrhythmic agents and the tachycardia did not recur.
在一名28岁的越南男性中,触发活动被证明是反复性心动过速的可能机制。在基础电生理检查期间,通过延长心房或心室起搏可持续诱发心动过速,但早搏刺激不能诱发。此外,心动过速的联律间期与起始驱动的周期长度直接相关。普鲁卡因胺和普萘洛尔不能抑制心动过速,但维拉帕米可终止心动过速并防止其再次发作。心动过速的起源定位于左心室下尖段,通过电极导管每次给予200J的四次直流电电击消除了心动过速。在12个月的随访期间,患者未接受抗心律失常药物治疗,心动过速未复发。