DeLacey W A, Nath S, Haines D E, Barber M J, DiMarco J P
Division of Cardiology, University of Virginia Health Sciences Center, Charlottesville 22908.
Pacing Clin Electrophysiol. 1992 Dec;15(12):2240-4. doi: 10.1111/j.1540-8159.1992.tb04166.x.
A ventricular tachycardia (VT) with right bundle branch block (RBBB) QRS morphology and left axis originating from the inferoapical segment of the left ventricle is described in a 49-year-old man without structural heart disease. This VT could be initiated during isoproterenol infusion and was terminated with intravenous administration of adenosine and verapamil. Radiofrequency ablation eliminated the tachycardia. Previous reports have suggested reentry as the mechanism for a verapamil-sensitive VT with this ECG morphology, while cAMP-mediated triggered activity has been proposed as a mechanism for VTs sensitive to adenosine. The latter more typically arise in the right ventricular outflow tract. The electrophysiological and electropharmacological characteristics of the tachycardia in this patient suggest that this VT morphology is not specific for a mechanism but rather for the location of the site of origin.
一名49岁无结构性心脏病的男性患者出现了起源于左心室下尖段、具有右束支传导阻滞(RBBB)QRS形态及电轴左偏的室性心动过速(VT)。该室性心动过速可在输注异丙肾上腺素期间诱发,并通过静脉注射腺苷和维拉帕米终止。射频消融消除了心动过速。既往报道提示折返是具有这种心电图形态的维拉帕米敏感性室性心动过速的机制,而cAMP介导的触发活动被认为是对腺苷敏感的室性心动过速的机制。后者更常见于右心室流出道。该患者室性心动过速的电生理和电药理学特征表明,这种室性心动过速形态并非特定机制所特有,而是起源部位的特征。