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    • Our two groups of patients were similar in all but

    2019-06-20

    Our two groups of patients were similar in all, but two, parameters: the non-inducible group had a significantly higher prevalence of atrial fibrillation (Table 1) and a significantly lower use of β-blockers at the time of enrollment into the study (discharge time after PES only or ICD implantation). The latter difference may be related to the lack of back-up pacing, because some these patients had bradycardia.
    Study limitations
    Conflict of interest
    Introduction Pulmonary vein isolation (PVI) is the cornerstone of ablation for atrial fibrillation (AF) [1,2]. We have previously reported that the radiofrequency (RF) lesion can be visualized with delayed enhancement magnetic resonance imaging (DE-MRI) [3]. However, visualization of the RF lesion gap, especially that located at the anterior ridge or carina, was difficult in some patients for the following reasons: (1) The anatomy of the anterior ridge between the left pulmonary vein (LPV) and left atrial appendage (LAA) and the carina between the superior PV and inferior PV is complex and varied among patients. (2) The spatial resolution of DE-MRI is not adequate for visualization of complex anatomy. Recently, magnetic resonance angiography (MRA) was reported to provide similar information on the left atrium (LA) and PV anatomy as contrast-enhanced computed tomography angiography (CTA) [4]. Thus, we hypothesized that DE-MRI fused with MRA compensates for the inadequate quality of the anatomical information provided by DE-MRI alone.
    Material and methods
    Results
    Discussion
    Conclusion
    Disclosures
    Conflicts of interest
    Acknowledgments
    Introduction
    Case report A 65-year-old woman with a history of syncope and diastolic dysfunction was diagnosed with hypertrophic cardiomyopathy, as evaluated by echocardiography and myocardial biopsy. Although she had no family history of sudden death or cardiomyopathy, she had experienced syncope at the age of 42 years, which had not been fully examined. She had previously undergone a mastectomy of the left breast due to breast cancer. An electrocardiogram (ECG) indicated unstable sinus node function and Holter ECG recording revealed sinus arrest lasting up to 2.6s (Fig. 1). Furthermore, non-sustained ventricular tachycardia with a cycle length of 400ms lasting for a maximum of 3s was observed several times. Transthoracic echocardiography showed asymmetric mural thickening from the AZD0156 of the mid-interventricular septum. The left ventricular ejection fraction was recorded as 65%, and the left ventricular end-diastolic and end-systolic diameters measured 48mm and 23mm, respectively. There were no findings indicative of left ventricular dyssynchrony, while a thoracic MRI revealed delayed enhancement within the hypertrophied interventricular septum. The left ventricular outflow tract was observed to be free of obstruction. During the electrophysiological study, ventricular tachycardia induced by bursting stimuli from the right ventricular apex degraded to ventricular fibrillation and was terminated by an external defibrillator. Although the indication of ICD therapy seemed to be controversial, the patient consented to receive ICD for fear of sudden death. She was eligible for dual chamber ICD treatment to prevent sudden cardiac death and to create atrial pacing for brachycardia. Lack of the R-SVC was indicated by venography, and a CT scan revealed a right brachiocephalic vein running into the left superior vena cava (L-SVC) (Fig. 2). Lead insertion from the left subclavian vein was possible but there was a risk of lymphedema owing to the patient׳s mastectomy history. Although the greater pectoral muscle and subcutaneous fat were preserved during mastectomy, the left breast was surgically removed and the axillary lymph nodes were dissected. Therefore, we elected to use a transthoracic transatrial approach for surgical lead placement for ICD treatment. Thoracotomy was performed during median sternotomy and leads were placed on the beating heart. A scalpel was used to cut the center of a small purse-string suture on the right auricle, and a defibrillation lead was positioned in the right ventricle via the tricuspid valve. Bleeding around the lead was well controlled and diminished by the purse-string suture. An epicardial atrial lead was sutured to the atrial wall (Fig. 3) to overcome sinus bradycardia. Oversensing was avoided owing to the small size of the far-field R wave. A subcutaneous pocket was created in the left precordial area, and the leads were passed from the pericardial cavity through the intercostal space to the pocket and connected to a dual chamber ICD device designed to deliver a maximum of 35J (Fig. 4). We performed single defibrillation threshold testing (DFT) during the operation, and a 25-J shock successfully terminated ventricular fibrillation (VF). We did not perform DFT repeatedly in order to minimize the damage to the heart under thoracotomy. The postoperative course and 12-month follow-up assessment were unremarkable.