Author + information
- Received December 28, 2016
- Revision received January 31, 2017
- Accepted February 9, 2017
- Published online December 4, 2017.
- Kunihiko Kiuchi, MDa,∗ (, )
- Koji Fukuzawa, MDa,
- Shumpei Mori, MDb,
- Yoshiaki Watanabe, MDc and
- Ken-ichi Hirata, MDa,b
- aSection of Arrhythmia, Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
- bDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
- cDepartment of Radiology, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
- ↵∗Address for correspondence:
Dr. Kunihiko Kiuchi, Section of Arrhythmia, Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-2 Kusunoki-chou chuou-ku, Kobe, Hyogo, Japan.
- atrial fibrillation
- cryoballoon ablation
- positron emission tomography
- radiofrequency hot balloon ablation
Acute lesion formation following isolation of the pulmonary vein(s) is known to occur after cryoballoon ablation (CBA) and radiofrequency hot balloon ablation (RHA) in an animal model. In this report, we describe for the first time the use of positron emission tomography (PET) to visualize the regional inflammation pattern occurring after CBA and RHA in the human left atrium (LA).
A 70-year-old man with palpitations was referred to our center for catheter ablation of paroxysmal atrial fibrillation. The pulmonary veins were completely isolated after CBA. Another 72-year-old man with palpitations was referred to our center for catheter ablation of paroxysmal atrial fibrillation. In this patient, the pulmonary veins were completely isolated after RHA. Fluorodeoxyglucose F 18 PET imaging of the LA was performed 48 h after the ablation in both cases and was fused with a simultaneously obtained 3-dimensional reconstructed magnetic resonance image (Figures 1A and 1B). As demonstrated in the images, we were able to visualize the acute regional inflammation following both CBA and RHA. Of interest, FDG uptake was localized primarily around the pulmonary veins and was comparable between the 2 technologies. The histological change after RHA in the animal model was reported to be mainly necrosis including contraction band necrosis and coagulation necrosis. The degree of the necrotic lesion could depend on the maximal balloon temperature (1,2). The cryothermal lesion could be created by 2 additional factors—direct cellular damage and immunological effects (3,4). The degree of the lesions produced by CBA and RHA are likely dependent on freezing time, maximal or minimal balloon temperature, application time, and balloon size. Although the energy sources were different, inflammation was induced by both types of balloons where there was adequate contact between the balloon surface and the myocardial tissue. It might be hypothesized that the durability of the ablation lesion might be less in an area demonstrating less inflammation compared with an area with extensive inflammation. Therefore, acute PET imaging of the LA could be helpful in detecting possible future reconnection sites and helping to evaluate the optimal application time, target temperature setting, and balloon size while developing new balloon-based ablation devices.
The authors greatly thank Mr. John Martin for his linguistic assistance.
The Section of Arrhythmia is financially supported by an endowment from Medtronic Japan and St. Jude Medical Japan. Drs. Kuichi and Fukuzawa belong to the Section. Dr. Hirata chairs the Section. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received December 28, 2016.
- Revision received January 31, 2017.
- Accepted February 9, 2017.
- 2017 American College of Cardiology Foundation
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