Localization and mechanism of ventricular tachycardia by ice mapping 1 week after the onset of myocardial infarction in dogs.

Abstract

We developed a new technique of "ice mapping" to localize the site of termination of ventricular tachycardia in dogs 4 to 8 days after the onset of myocardial infarction. During programmed stimulation-induced ventricular tachycardia, the epicardium was mapped by moving an ice probe with a 1 cm tip over the infarct, lateral border, and normal areas. In 31 of 46 morphologically distinct sustained ventricular tachycardias, a specific area could be found that reproducibly terminated ventricular tachycardia. During ventricular tachycardia, bridging or late diastolic electrical activity was recorded from ice termination sites. In vitro microelectrode studies of 10 ice termination sites revealed slow conduction, but no spontaneous or triggered automaticity or delayed afterdepolarizations. Conduction slowed to complete block when the Tyrode perfusate was cooled from 37 degrees to 27 degrees C. We conclude that ice mapping can physiologically localize a site responsible for maintenance of ventricular tachycardia by termination of the arrhythmia, and that the presence of bridging or late diastolic electrical activity, slow conduction with cooling-induced block, and absence of spontaneous or triggered automaticity or delayed afterdepolarizations suggest that local cooling terminates ventricular tachycardia by slowing or blocking conduction in a reentrant loop.