Noncontact mapping of ventricular tachycardia in a closed-chest animal model of chronic myocardial infarction.

Treatment of ventricular tachyarrhythmias in the setting of chronic myocardial infarction requires accurate characterization of the arrhythmia substrate. New mapping technologies have been developed that facilitate identification and ablation of critical areas even in rapid, hemodynamically unstable ventricular tachycardia. A noncontact mapping system was used to analyze induced ventricular tachycardia in a closed-chest sheep model of chronic myocardial infarction. Twelve sheep were studied 96 +/- 10 days after experimental myocardial infarction. During programmed stimulation, 15 different ventricular tachycardias were induced in nine animals. Induced ventricular tachycardia had a mean cycle length of 190 +/- 30 ms. In 12 ventricular tachycardias, earliest endocardial activity was recorded from virtual electrodes, preceding the surface QRS onset by 30 +/- 7 ms. Noncontact mapping identified diastolic activity in ten ventricular tachycardias. Diastolic potentials were recorded over a variable zone, spanning more than 30 mm. Timing of diastolic potentials varied from early to late diastole and could be traced back to the endocardial exit site. Entrainment with overdrive pacing was attempted in nine ventricular tachycardias, with concealed entrainment observed in seven. Abnormal endocardium in the area of chronic myocardial infarction identified by unipolar peak voltage mapping was confirmed by magnetic resonance imaging. These data suggest that induced ventricular tachycardia in the late phase of myocardial infarction in the sheep model is due to macroreentry involving the infarct borderzone. The combination of this animal model with noncontact mapping technology will allow testing of new strategies to cure and prevent ventricular tachycardia in the setting of chronic myocardial infarction.