Comparison of conventional and biventricular antitachycardia pacing in a geometrically realistic model of the rabbit ventricle.
BACKGROUND
ICDs often are programmed with antitachycardia pacing (ATP) as the first response to ventricular tachycardia (VT). Many ICDs have an additional lead available for ventricular pacing. We hypothesized that using the additional lead for ATP would improve therapy by advancing the orthodromic wavefront, thereby reducing the size of the excitable gap and inducing block of all reentrant activity.


RESULTS
Monomorphic VT was initiated in a thin-walled model of rabbit ventricular myocardium that included an apical infarct and anatomically realistic dimensions. ATP with up to eight pulses was delivered at 90% of VT cycle length to one (conventional) or two (biventricular) stimulation areas. Stimulation areas were adjusted from 0.017 cm2 to 0.169 cm2 to modulate interactions between the antidromic and VT wavefronts, and between the orthodromic wavefront and the VT's refractory region. During conventional ATP, we found that larger stimulation areas terminated the VT in three pulses. Continued pacing after termination caused VT reinitiation in the reversed direction in some instances. With smaller stimulation areas, conventional ATP simply reset the circuit. During biventricular ATP, larger stimulation areas terminated VT in one pulse. There were no instances of reinitiation with reversal. However, with smaller stimulation areas, prolongation of refractoriness near the additional stimulation area facilitated induction of functional reentry with pathways modified by continued pacing.


CONCLUSIONS
Our modeling suggests that biventricular ATP is superior to conventional ATP under conditions where the additional ventricular lead effectively advances the orthodromic wavefront. Failure to achieve this advancement poses a risk of VT acceleration.
Byrd
Israel A
IA
Department of Biomedical Engineering, Cardiac Rhythm Management Laboratory, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Rogers
Jack M
JM
Smith
William M
WM
Pollard
Andrew E
AE
D000818:Animals; D002304:Cardiac Pacing, Artificial; D017147:Defibrillators, Implantable; D006329:Heart Conduction System / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology*; D023421:Models, Animal; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D011817:Rabbits; D017180:Tachycardia, Ventricular / Q000628:therapy*