Intracoronary ethanol ablation in swine: characterization of myocardial injury in target and remote vascular beds.

INTRODUCTION: Physical or chemical ablation of arrhythmogenic tissue has been shown to be an effective modality of arrhythmia therapy. Chemical ablation by intracoronary infusion of ethanol into a specific coronary artery bed has been demonstrated, but the characteristics and distribution of necrosis relative to the coronary blood supply have not been delineated. METHODS AND RESULTS: A total of 40 myocardial lesions were created in 21 pigs by infusion of 1.6 +/- 0.6 mL of 50% ethanol and 50% iohexol contrast solution through a 2.7 French infusion catheter advanced into a branch of the left anterior descending or circumflex coronary artery. Prior to ethanol infusion, 5.3 +/- 1.2 mCi technetium-99m (Tc-99m) methoxyisobutyl isonitrile (sestamibi) was infused into the coronary branch in order to delineate the perfusion bed. After completion of the lesions, each heart was removed, sliced transversely in 5-mm slices, and stained with nitro blue tetrazolium in order to define the ablation bed. The slices were then imaged with a gamma camera and the area of Tc-99m sestamibi uptake was defined as the perfusion bed. These respective areas were planimetered for each slice and compared. No difference was observed in hemodynamic parameters between preablation and postablation measures except mean arterial pressure, which fell from 122 +/- 22 mmHg to 116 +/- 24 mmHg (P = 0.02). Significant ventricular arrhythmias were observed after 60% of the ablations. The mean left ventricular ejection fraction fell from 55% +/- 9% to 45% +/- 15% after completion of all ablations. The areas of the ablation beds were related to the areas of the perfusion beds but the correlation was poor (r = 0.41, P = 0.0001). Generally, the ablation bed was smaller than the perfusion bed, but evidence of ethanol reflux was observed in 29% of the lesions resulting in injury beyond the targeted perfusion bed. CONCLUSIONS: Intracoronary ethanol ablation is a promising technique for the treatment of arrhythmias. Significant arrhythmias and a decrease in left ventricular ejection fraction are associated with this technique. Lesions are generally produced within the distribution of the targeted coronary bed, but are also frequently associated with reflux to a second vascular distribution.

Observations on electrode-tissue interface temperature and effect on electrical impedance during radiofrequency ablation of ventricular myocardium.

The purpose of this study was to correlate changes in electrical impedance with the electrode-tissue interface temperature and to characterize the associated events occurring at the catheter tip electrode. In a canine model, lesions were created in vitro (n = 49) and in vivo (n = 31) and radiofrequency power settings were varied. Electrode-tissue interface temperature, delivered current, and voltage were recorded, and impedance was calculated. A sudden rise in electrical impedance was seen in only two of 17 ablations in vitro and in one of 16 ablations in vivo with a peak electrode-tissue interface temperature of less than 100 degrees C compared with 29 of 32 ablations in vitro (p = 0.0001) and 12 of 15 ablations in vivo with a temperature of more than 100 degrees C (p = 0.0001). This phenomenon was associated with the observation of boiling and popping at the tip in in vitro preparations and tissue avulsion and thrombus formation on the catheter tip in in vivo studies. The lesion size was directly proportional to the peak temperature for all ablations but not to the peak power, current, or voltage during radiofrequency catheter ablation in the heart. Maintaining electrode-tissue interface temperature at less than 100 degrees C during radiofrequency catheter ablation in the heart may avoid the complications associated with the sudden rise in electrical impedance.

Electrode radius predicts lesion radius during radiofrequency energy heating. Validation of a proposed thermodynamic model.

Myocardial heating by transcatheter delivery of radiofrequency (RF) energy has been proposed as an effective means of arrhythmia ablation. A thermodynamic model describing the radial temperature gradient at steady state during RF-induced heating is proposed. If one assumes that RF power output is adjusted to maintain a constant electrode-tissue interface temperature at all times, then this thermodynamic model predicts that the radius of the RF-induced lesion will be directly proportional to the electrode radius. A total of 76 RF-induced lesions were created in a model of isolated canine right ventricular free wall perfused and superfused with oxygenated Krebs-Henseleit buffer. Electrode radius was varied between 0.75 and 2.25 mm. RF energy (500 kHz) was delivered for 90 seconds, and the power output was adjusted to maintain a constant electrode-tissue interface temperature of 60 degrees C. A strong linear correlation was observed between electrode radius and lesion radius in two dimensions: transverse (p = 0.0001, r = 0.85) and transmural (p = 0.0001, r = 0.89). With these data, the temperature correlation with irreversible myocardial injury in this model was calculated at 46.6-48.8 degrees C. Therefore, the proposed thermodynamic model closely predicts the observed relation between electrode radius and lesion size during RF myocardial heating.