During the generation of radiofrequency (RF) lesions in the ventricular myocardium, the maintenance of adequate electrode-tissue contact is critically important. In this study, lesion dimensions and temperature and impedance changes were evaluated while controlling electrode-tissue contact levels (-5, 0, +1, and +3 mm) and power levels (10, 20, and 30 W). This data was used to assess the ability of impedance and temperature monitoring to provide useful information about the quality of electrode-tissue contact. The results show that as the electrode-tissue contact increases, so does the amount of temperature rise. With the electrode floating in blood (-5 contact), the average maximum temperature increase with 20 and 30 W was only 7 +/- 1 and 11 +/- 2 degrees C, respectively. At 20 and 30 W the temperature plateaued shortly after the initiation of power application. With good electrode-tissue contact (+1 mm or +3 mm), the temperature increase within the first 10 seconds was significantly greater than the temperature increase from baseline with poor contact (0 mm or -5 mm) and reached a maximum of 60 +/- 1 degrees C after 60 seconds of power application. As the electrode-tissue contact increased, so did the rate and level of impedance decrease. However, the rate of impedance decrease was slower compared to the rate of temperature rise. With the electrode floating in blood, the maximum impedance decreases with 20 and 30 W were 6 +/- 6 omega and 9 +/- 5 omega, respectively. The impedances plateaued after a few seconds of power application. With the electrode in good contact, the maximum impedance decreases with 20 and 30 W were 25 +/- 2 omega and 20 +/- 6 omega, respectively. In these cases the rate of the impedance decrease plateaued after 40 seconds of power application. The increase in lesion diameter and depth correlate well with decreasing impedance and increasing temperature. However, lesion depth appears to correlate better with impedance than temperature. We conclude that, since the electrode-tissue contact is not known prior to the application of power to the endocardium, in the absence of a temperature control system, the power should initially be set at a low level. The power should be increased slowly over 20-30 seconds, and then maintained at its final level for at least 90 seconds to allow for maximal lesion depth maturation. The power level should be lowered if the impedance drop exceeds 15 omega.

Ablation guided by automated detection of CFAE proved feasible, and was associated with a high AF termination rate in paroxysmal, but not persistent AF. As an adjunct to conventional techniques, it was associated with excellent long-term single procedure outcomes in both groups. Criteria for identifying optimal CFAE sites for ablation, and selection of patients most likely to benefit, require additional study.

Introduction: Creation of radiofrequency lesions to isolate the pulmonary veins (PV) and ablate atrial fibrillation (AF) has been complicated by stenosis of the PVs. We tested a cryoballoon technology that can create electrical isolation of the PVs, with the hypothesis that cryoenergy will not result in PV stenosis. Methods and Results: Lesions were created in 9 dogs (weight 31–37 kg). Cryoenergy was applied to the PV‐left atrial (LA) interface. Data collected before and after ablation included PV orifice size, arrhythmia inducibility, electrogram activity, and pacing threshold in the PVs. Tissue examination was performed immediately after ablation in 3 dogs and after 3 months (4.8 ± 1.0) in 6 dogs. After ablation there was no localized P wave activity in the ablation zone and no LA‐PV conduction. Before ablation, the pacing threshold was 1.9 ± 1.1 mA in each PV. After ablation, the pacing threshold increased significantly to 7.2 ± 1.8 mA , or capture was not possible. Burst pacing did not induce any sustained arrhythmias. Most dogs had hemoptysis during the first 24 to 48 hours. Acute tissue examination revealed hemorrhagic injury of the atrial‐PV junction that extended into the lung parenchyma. After recovery, the lesions were circumferential and soft with no PV stenosis. Histologic examination revealed fibrous tissue with no PV‐LA interface thickening. Conclusion: This new cryoballoon technology effectively isolates the PVs from LA tissue. No PV stenosis was noted. Acute tissue hemorrhage and hemoptysis are short‐term complications of this procedure. After 3 months of recovery, cryoablated tissue exhibits no collagen or cartilage formation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 281‐286, March 2003)

This adjustable loop catheter forces the atrial tissue to conform around the catheter and is capable of producing linear, contiguous lesions up to 16 cm long with minimal effort and radiation exposure. Pacing thresholds and electrogram amplitude and character are markers of effective lesion formation. Although Afib could not be induced after lesion set completion, sustained atrial flutter could be induced in 25% of the hearts.