Focal initiation of sustained and nonsustained ventricular tachycardia in a canine model of ischemic cardiomyopathy.

INTRODUCTION

To define the role of focal and reentrant mechanisms underlying nonsustained (NSVT) and sustained ventricular tachycardia (SuVT) induced by programmed stimulation, 3-dimensional cardiac mapping was performed in 8 dogs with heart failure (HF) created by multiple intracoronary microsphere embolizations.

METHODS AND RESULTS

Continuous recording from 232 intramural sites throughout the left and right ventricles and the interventricular septum was performed during programmed stimulation in the absence and presence of isoproterenol (Iso, 0.1 μg/kg/min). Sinus beats and the last extrastimuli preceding induced VT conducted with total activation times (TA) of 51 ± 10 and 111 ± 8 milliseconds, respectively, that did not change during Iso infusion (47 ± 4 and 109 ± 5 milliseconds, P = NS). NSVT was induced in 75% of HF dogs; SuVT was induced in 38%. In all cases, initiation and maintenance of SuVT and NSVT arose by a focal mechanism. Compared to NSVT, SuVT had a shorter coupling interval (CI; 150 ± 7 vs 186 ± 16, P < 0.05) and a predilection for certain critical subendocardial initiation sites (that were initiation sites for only 29% of NSVT beats). After 21-30 beats, acceleration of SuVT by a focal mechanism to a CI less than 120 milliseconds led to functional conduction delay (TA increasing from 111 ± 3 to 137 ± 3 milliseconds, P < 0.0001), intramural reentry, and transition to ventricular fibrillation.

CONCLUSIONS

Thus, initiation of SuVT in a model of ischemic HF is due to a focal mechanism. However, subsequent acceleration of this focal mechanism can ultimately lead to functional conduction delay and development of intramural reentry.