Subendocardial and intramural temperature response during radiofrequency catheter ablation in chronic myocardial infarction and normal myocardium.

Abstract

The ability of radiofrequency energy to extend across scar tissue is unknown. We investigated the effects of radiofrequency catheter ablation on intramural temperature in experimental chronic myocardial infarction. Myocardial infarction was induced in eight dogs by a transcatheter coronary artery occlusion-reperfusion technique. The dogs were reanesthetized after 15 to 24 days. Four additional dogs served as controls. The freshly excised preparations were cut and placed in a saline bath at 37 degrees C. Temperature-guided energy applications with a preselected catheter tip temperature of 80 degrees C were performed for 60 seconds with a 7F ablation catheter. Thermoelements were inserted into the ventricular muscle at depths of 2.5 to 3.0 mm ("subendocardial") and 5.5 to 6.0 mm ("intramural"). Surviving muscle fibers were interspersed among the transmural scar tissue. The maximal temperatures did not differ significantly between normal hearts and chronic infarctions at the subendocardial (64.5+/-6.4 degrees C versus 66.7+/-6.6 degrees C) or intramural thermo-element (51.9+/-5.7 degrees C versus 52.3+/-5.7 degrees C). The myocardial temperature rise was slow, and steady-state temperatures had not been reached after 60 seconds. The intramural temperatures in chronic infarctions measured 49.0+/-4.3 degrees C after 40 seconds of energy delivery and were still below the critical tissue temperature of 50 degrees C that is necessary to induce permanent myocardial damage. Temperature-guided radiofrequency ablation in a dog model of chronic myocardial infarction may induce tissue temperatures >50 degrees C at a depth of 5.5 to 6.0 mm. The intramural temperature rise was slow, indicating that long energy applications might be necessary if the arrhythmogenic substrate is subepicardial.