TY - JOUR
T1 - Physiological consequences of bipolar radiofrequency energy on the atria and pulmonary veins
T2 - A chronic animal study
AU - Prasad, Sunil M.
AU - Maniar, Hersh S.
AU - Diodato, Michael D.
AU - Schuessler, Richard B.
AU - Damiano, Ralph J.
AU - Nitta, Takashi
AU - Disesa, Verdi J.
N1 - Funding Information:
This study was funded by an unrestricted research grant from Enable, Inc, NIH 5 R01 HL32257 and NIH T32 HL07275. The authors would like to thank Diane Toeniskoetter, Kathy Fore, and Dennis Gordon for their technical assistance.
PY - 2003/9/1
Y1 - 2003/9/1
N2 - Background. Alternative energy sources have been proposed for the transvenous and surgical treatment of atrial fibrillation. This study examined the physiologic consequences of a novel energy source, bipolar radiofrequency energy, in a chronic animal model in order to determine its ability to produce transmural lesions on the beating heart. Methods. Five dogs underwent baseline pacing from the following target areas: right and left atrial appendage, superior and inferior vena cavae, and right and left pulmonary veins. A cuff of atrial myocardium, proximal to the target tissue was clamped and ablated between the arms of the bipolar radiofrequency energy device. Tissue conductance was used as a transmural indicator. After ablation, the pacing protocol was repeated. Baseline and postablation pulmonary vein flows were measured. Animals were survived for 30 days, and permanent electrical isolation was evaluated by pacing, epicardial mapping, and histology. Results. Mean ablation time was 5.0 ± 1.8 seconds and mean peak tissue temperature was 46.7°C ± 2.8°C. All lesions (30/30) acutely and permanently isolated atrial tissue. There was no change in pulmonary vein flow. Mapping studies with pacing of atrial tissue on both sides of the lesion confirmed isolation. Histology demonstrated that all lesions were linear, continuous, and transmural with no thrombus formation or stenosis. Conclusions. Bipolar radiofrequency energy rapidly produced permanent transmural linear lesions on the beating heart. Measurement of tissue conductance reliably predicted transmural lesions. This new technology may enable the development of a less invasive, surgical approach to atrial fibrillation.
AB - Background. Alternative energy sources have been proposed for the transvenous and surgical treatment of atrial fibrillation. This study examined the physiologic consequences of a novel energy source, bipolar radiofrequency energy, in a chronic animal model in order to determine its ability to produce transmural lesions on the beating heart. Methods. Five dogs underwent baseline pacing from the following target areas: right and left atrial appendage, superior and inferior vena cavae, and right and left pulmonary veins. A cuff of atrial myocardium, proximal to the target tissue was clamped and ablated between the arms of the bipolar radiofrequency energy device. Tissue conductance was used as a transmural indicator. After ablation, the pacing protocol was repeated. Baseline and postablation pulmonary vein flows were measured. Animals were survived for 30 days, and permanent electrical isolation was evaluated by pacing, epicardial mapping, and histology. Results. Mean ablation time was 5.0 ± 1.8 seconds and mean peak tissue temperature was 46.7°C ± 2.8°C. All lesions (30/30) acutely and permanently isolated atrial tissue. There was no change in pulmonary vein flow. Mapping studies with pacing of atrial tissue on both sides of the lesion confirmed isolation. Histology demonstrated that all lesions were linear, continuous, and transmural with no thrombus formation or stenosis. Conclusions. Bipolar radiofrequency energy rapidly produced permanent transmural linear lesions on the beating heart. Measurement of tissue conductance reliably predicted transmural lesions. This new technology may enable the development of a less invasive, surgical approach to atrial fibrillation.
UR - http://www.scopus.com/inward/record.url?scp=0041330009&partnerID=8YFLogxK
U2 - 10.1016/S0003-4975(03)00716-1
DO - 10.1016/S0003-4975(03)00716-1
M3 - Article
C2 - 12963212
AN - SCOPUS:0041330009
VL - 76
SP - 836
EP - 842
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
SN - 0003-4975
IS - 3
ER -