The acute effects of flecainide in the swine heart failing from incessant supraventricular tachycardia.

The acute hemodynamic and electrophysiologic effects of flecainide in tachycardia-induced ventricular dysfunction were investigated using an animal model. Seven swine were initially (CON) evaluated by echocardiography and then by right heart catheterization and provocative electrical ventricular stimulation both before and after treatment with intravenous flecainide. Rapid atrial pacing at 210 to 240 beats/min (SVT) was then employed for 2 to 4 weeks until echocardiographic evidence of left ventricular dysfunction developed. Immediately upon termination of pacing, the above studies were repeated both before and after treatment with flecainide. Significant (p less than 0.0001) pacing-related hemodynamic effects on the cardiac output (CON:3.0 L/min versus SVT:1.6 L/min), right ventricular ejection fraction (CON:55% versus SVT:17%), and pulmonary wedge pressure (CON:8 mm Hg versus SVT:22 mm Hg) were observed. Pacing-related electrophysiologic effects included increases in the PR interval (CON:94 msec versus SVT:119 msec, p less than 0.001) and QTc interval (CON:418 msec versus SVT:450 msec, p = 0.016). With serum flecainide concentrations in the human therapeutic range, no significant effect on hemodynamic or electrophysiologic parameters in either the normal or failing heart were detected. Nonsustained ventricular tachycardia induced prior to pacing in one animal and after pacing in another animal was seen before but not following use of flecainide. No acute proarrhythmic effects were observed. In summary, intravenous flecainide had no significant acute adverse hemodynamic, electrophysiologic, or proarrhythmic effects in an animal model of tachycardia-induced ventricular dysfunction.