Mechanisms of ventricular tachycardia termination and acceleration during transvenous cardioversion as determined by cardiac mapping in man.

We examined the EP mechanisms underlying efficacy and inefficacy of transvenous cardioversion shocks in 13 patients with coronary artery disease and sustained VT during preoperative and intraoperative cardiac mapping procedures. Shocks were delivered at the right ventricular apex with a Medtronic 6880 catheter and a Model 5350 external cardioverter/defibrillator with two or three electrode configurations, resulting in unidirectional or bidirectional shocks, respectively. Single transvenous shocks with incremental energies ranging from 0.03 to 25 J were delivered in sinus rhythm and VT, and simultaneous right and left ventricular electrograms were obtained. Transvenous cardioversion shocks of 0.03 J in sinus rhythm and VT produced immediate local right ventricular depolarization and subsequently conducted to distant right ventricular and left ventricular sites after 30 to 100 msec. Shocks of 0.05 to 0.5 J produced immediate depolarization of progressively larger right ventricular and left ventricular regions, with shocks greater than or equal to 0.5 J producing immediate depolarization of distant left ventricular sites in sinus rhythm. High energy (greater than 5 J) shocks produced instantaneous depolarization of multiple right ventricular and left ventricular sites in VT. VT termination occurred due to either delay or interruption of conduction in the tachycardia circuit, despite prior depolarization of the early sites of ventricular activation during the QRS complex. This could be due to instantaneous or paced depolarization of critical "excitable" components of the VT circuit, resulting either in immediate conduction block or in instability followed by termination. VT acceleration with transvenous cardioversion was due to modification of the "excitable," slowly conducting components of the VT circuit with the development of new areas of conduction block, along with altered intraventricular conduction. Similar EP mechanisms were observed with unidirectional and bidirectional transvenous shock patterns. We conclude that transvenous shocks alter conduction in human ventricle, and clinical effects of QRS synchronized shocks are related to conduction changes induced in the excitable components of the VT circuit.