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Israel A Byrd

Publications and source records attributed to Israel A Byrd.

2 recordsLinked to original sources

Interactions between paced wavefronts and monomorphic ventricular tachycardia: implications for antitachycardia pacing.

OBJECTIVES: Interactions between paced wavefronts and monomorphic ventricular tachycardia (VT) dictate antitachycardia pacing outcomes. We used optical mapping to assess those interactions during single and dual site pacing of rabbit ventricular epicardium. METHODS AND RESULTS: Monomorphic VTs were initiated in six isolated rabbit hearts that were endocardially cryoablated to limit viable tissue to visible epicardium and establish apical tissue as the anatomic anchor. Preparations were optically mapped during single (n = 39) and dual (n = 43) site pacing at 50%-90% of VT cycle length (CL) with eight pulses per trial. Overall, we found six pulses that abruptly terminated VT. This occurred because the VT wavefront collided with the antidromic portion of the paced wavefront and the orthodromic portion of paced wavefront blocked in the VT's refractory region. When effective, dual site pacing that captured tissue at both leads simultaneously terminated the VT immediately, while single site pacing or dual site pacing that captured tissue at only one lead terminated the VT after resetting advanced the orthodromic wavefront. We found 12 pulses that induced polymorphic VT, with 11 of those pulses occurring during capture at only one lead. Expansion of the combined antidromic-VT wavefront around one or both ends of the arc of conduction block formed by the interaction of the orthodromic wavefront with the VT's refractory region initiated functional reentry. Six of these polymorphic VTs were nonsustained because the underlying wavefronts self-terminated. The wavefronts did persist for 4.2 +/- 3.5 cycles before self-terminating in these trials, and the post-pacing cycles presented a 146% increase in CL variability, compared with the variability prior to pacing. These temporal characteristics are similar to those of delayed termination in patients with ICDs. CONCLUSIONS: The main difference between pulses that terminated abruptly and pulses that induced polymorphic VT was the effective separation of the antidromic and orthodromic portions of the paced wavefront from one another.

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Comparison of conventional and biventricular antitachycardia pacing in a geometrically realistic model of the rabbit ventricle.

INTRODUCTION: 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. METHODS AND 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. CONCLUSION: 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.

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