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CATHETER ABLATION OF VENTRICULAR MYOCARDIUM


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Radiofrequency catheter ablation is proving to be a safe and effective method of treatment in patients with many forms of supraventricular tachycardia, including atrio-ventricular reentrant tachycardia using an accessory pathway. Attempts to extend this technique to the treatment of patients with ventricular tachycardia have met with only modest success to date. Unlike accessory pathways, which are essentially remnants of normal myocardial tissue, the substrate for ventricular tachycardia consists of areas of scarred and fibrotic tissue which may be located under a heavily fibrotic endocardium. These characteristics suggest that larger and deeper lesions may be needed for ablation of ventricular tachycardia than for supraventricular tachycardia. Unfortunately this requires higher power delivery than can be generated using current catheter electrodes and radiofrequency energy devices. The purpose of this experiment is to examine the use of alternate energy sources for ventricular tachycardia ablation in normal and infarcted myocardium. The two energy sources to be tested are "pulsed" radiofrequency energy and microwave energy. The two energy sources will be tested in an open chest, closed heart canine model. Serial ablations with incremental changes in power and duration (for microwave energy) and voltage and duration (for pulsed radiofrequency) will be carried out. Voltage, current, impedance, change in impedance over time, contact pressure, and temperature will be continuously monitored during ablation. The size and depth of each lesion and its relationship to the above variables will be examined. In particular the relationship between changes in temperatures and impedance over time will be examined. Based on these results, a series of dogs with experimentally created chronic infarcts will undergo catheter ablation in the area of scar. Animals will be sacrificed either acutely or at three months for pathologic examination of the heart. The size of the lesions created in normal and infarcted myocardium at similar delivered power will be compared.
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R01HL039670

Collapse Time 
Collapse start date
1988-07-01
Collapse end date
1995-06-30