INTRODUCTION: Direct injection of ethanol into myocardium has been shown to create large, well-demarcated lesions with transmural necrosis in normal ventricular myocardium and in regions of healed myocardial infarction. The aim of this study was to investigate the effects of direct ethanol injection on the inducibility of ventricular tachycardia (VT) in an animal model of chronic myocardial infarction. METHODS AND RESULTS: Eight sheep with reproducibly inducible VT underwent an electrophysiologic study 139 +/- 65 days after myocardial infarction. Noncontact mapping was used to analyze induced VT. Fifteen different VTs were targeted for catheter ablation. Ablation was achieved by catheter-based intramyocardial injection of a mixture of 96% ethanol, glycerine, and iopromide (ratio 3:1:1). Direct intramyocardial ethanol injection resulted in noninducibility of any VT 20 minutes after ablation in 7 of 8 animals. Four of 5 animals with initially successful ablation remained noninducible for any VT at follow-up study at least 2 days after the ablation procedure. Microscopic examination revealed homogeneous lesions with interstitial edema, intramural hemorrhage, and myofibrillar degeneration at the lesion border. The lesions were well demarcated from the surrounding tissue by a border zone of neutrophilic infiltration. CONCLUSION: Catheter ablation of VT by direct intramyocardial injection of ethanol during the chronic phase of myocardial infarction is feasible. It may be a useful tool for catheter ablation when the area of interest is located deep intramyocardially or subepicardially or when a more regional approach requires ablation of larger amounts of tissue.
INTRODUCTION: Direct injection of ethanol into myocardium has been shown to create large, well-demarcated lesions with transmural necrosis in normal ventricular myocardium and in regions of healed myocardial infarction. The aim of this study was to investigate the effects of direct ethanol injection on the inducibility of ventricular tachycardia (VT) in an animal model of chronic myocardial infarction. METHODS AND RESULTS: Eight sheep with reproducibly inducible VT underwent an electrophysiologic study 139 +/- 65 days after myocardial infarction. Noncontact mapping was used to analyze induced VT. Fifteen different VTs were targeted for catheter ablation. Ablation was achieved by catheter-based intramyocardial injection of a mixture of 96% ethanol, glycerine, and iopromide (ratio 3:1:1). Direct intramyocardial ethanol injection resulted in noninducibility of any VT 20 minutes after ablation in 7 of 8 animals. Four of 5 animals with initially successful ablation remained noninducible for any VT at follow-up study at least 2 days after the ablation procedure. Microscopic examination revealed homogeneous lesions with interstitial edema, intramural hemorrhage, and myofibrillar degeneration at the lesion border. The lesions were well demarcated from the surrounding tissue by a border zone of neutrophilic infiltration. CONCLUSION: Catheter ablation of VT by direct intramyocardial injection of ethanol during the chronic phase of myocardial infarction is feasible. It may be a useful tool for catheter ablation when the area of interest is located deep intramyocardially or subepicardially or when a more regional approach requires ablation of larger amounts of tissue.