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The creation of linear contiguous lesions in the atria with an expandable loop catheter

Boaz Avitall, MD, PhD, FACC^*, Ray W. Helms, BSE^*, Joseph B. Koblish, BS, Wayne Sieben, BSE, Alexey V. Kotov, MD^* and Gopal N. Gupta, BS^*

^* Section of Cardiology, University of Illinois at Chicago, Chicago, Illinois, USA
Boston Scientific Corporation/EP Technologies, San Jose, California, USA

View larger version (120K): [in a new window]   Figure 1 The two versions of the adjustable loop catheter. The fixed-tip (A, B) and monorail (C, D) systems are shown. The size of the loop can be adjusted by retracting the catheter into or pushing it further out of the guiding sheath.

View larger version (106K): [in a new window]   Figure 2 Fluoroscopic views of the catheter within the atria. The five locations where linear lesions were created are shown. Each lesion’s relationship to cardiac anatomic landmarks is described in the text. LAH = left atrial horizontal lesion; LAV = left atrial vertical lesion; RA = right atrial; RAI = RA isthmus lesion.

View larger version (22K): [in a new window]   Figure 3 Distribution of individual (4-mm electrode) lesions. Seven linear lesions were created with the 70°C power protocol (white bars), and four linear lesions were generated with the 70% local electrogram recording reduction protocol (black bars). The majority of lesions were type 3, which are contiguous and transmural and exhibit no char.

View larger version (19K): [in a new window]   Figure 4 Temperature and individual (4-mm electrode) lesion types. The figure shows the distribution of the average maximum temperatures for type 0–5 individual lesions. Eleven linear lesions were created in eight dogs using a catheter with a thermistor on each individual electrode. Seven linear lesions were created with the 70°C power protocol, and four were generated with the 70% local electrogram recording reduction protocol. Type 3 lesions, which were created with an average temperature of 71 ± 7°C, exhibited no charring or impedance rises. Contiguous and transmural lesions were not formed at lower temperatures (types 0–2). Desiccation (type 4) and charring (type 5) occurred at higher temperatures.

View larger version (109K): [in a new window]   Figure 5 Left atrial horizontal (LAH) and vertical (LAV) positions: gross lesions with charring and corresponding fluoroscopic images. The tissue specimen illustrates an encircling lesion around the pulmonary veins (PV) and a vertical lateral lesion connecting the mitral ring to the encircling lesion. The lesions were generated with radiofrequency power titration without temperature control. The heavy char formation is a potential source for embolic stroke. LAA = left atrial appendage; MV = mitral valve.

View larger version (48K): [in a new window]   Figure 6 Right atrial (RA) loop position: preablation and postablation recordings, gross lesions and fluoroscopic image. Electrode 1 is located at the inferior vena cava (IVC) atrial junction (note the low amplitude recording at electrode pair 1–2). The recordings from electrodes 1 to 9 are from the IVC–superior vena cava (SVC) region of the atrium. Electrode pair 9–10 traverses the SVC as depicted by the low electrogram amplitude. Electrodes 10 to 12 display the earliest electrograms, from the sinus node region at the anterior junction of the SVC and right atrial appendage (RAA). The recordings 13 to 22 are from across the RAA, and the remaining recordings traverse the tricuspid ring into the right ventricle. In regions progressively closer to the atrioventricular junction, the amplitude of the ventricular wave increases. Postablation, the propagation of the right atrial depolarization sequence still initiates from the region recorded by electrodes 9 to 11. However, the creation of the lesion resulted in a marked decrease in the electrograms’ amplitude and fragmentation of the local recordings. These double potentials coincide with the creation of contiguous linear lesions. TV = tricuspid valve.

View larger version (56K): [in a new window]   Figure 7 Left atrial horizontal position: pre-/postablation recordings, gross lesions and fluoroscopic image. The catheter was placed in a horizontal position superior to the mitral ring under the pulmonary veins (PV). Note the location of the coronary sinus catheter in relation to the ablation catheter. The distal and most proximal electrodes, 1 and 24, are both near the transeptal insertion site at the foramen ovale. The portion of the catheter positioned closer to the mitral ring (electrodes 7 to 13) recorded larger ventricular electrograms. The depolarization wavefront propagates from the septal region to the most distal recording within the left atrial appendage (LAA) in 50 ms. After radiofrequency ablation, the local electrogram amplitude decreased significantly. In addition, the recordings from electrodes 8 to 24 became fragmented, and the conduction time from the earliest to the latest electrode increased to 90 ms, 40 ms longer than preablation. These observations correspond to the linear contiguous lesions in the gross pathological photograph. MV = mitral valve.

View larger version (89K): [in a new window]   Figure 8 Left atrial horizontal position: gross lesions with charring and fluoroscopic image. This linear and contiguous encircling subpulmonary lesion was created with radiofrequency power titration of up to 20 W with no temperature control. Char was formed near the periphery of the electrode–tissue contact areas. The lesions are bridged with desiccated, blushed tissues between most of the individual burns. Abbreviations as in Figure 7.

View larger version (63K): [in a new window]   Figure 9 Epicardial electrical activity maps: before and after linear lesion creation. (A) An isochronal map of the left atrium (LA) during right atrial appendage (RAA) pacing at 400-ms cycle length. The mapping plaque was placed from the left atrial appendage (LAA) to the mitral valve ring around the atria with the pulmonary veins on the top of the plaque and mitral ring on the bottom extending to the atrial septum. The atrial activation progressed around the LA from two directions, anteriorly and posteriorly. The total LA activation lasted 28 ms. (B) A map obtained after creating a LA lesion bisecting the LAA circumferentially and vertically. The LA was activated from the atrial septum and reached the LAA in 109 ms. (C) An isochronal map of the right atrium (RA), paced from the RAA at 400-ms cycle length. The mapping plaque extended from the RAA (top) and superior vena cava (SVC) (bottom) to the tricuspid ring (top right) and inferior vena cava (IVC) (right bottom). The atrium was progressively depolarized starting at the RAA and ending at the tricuspid ring with total activation time of 40 ms. (D) An isochronal map following the RA linear lesion, which bisects across the RAA. The atrial activation started at the RAA and progressed to the lateral wall. The white area represents the territory of recording electrodes on the plaque where no electrical activity could be detected. The lateral wall tissues closer to the tricuspid valve were activated after 158 ms.