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  • br Case report A year

    2019-06-06


    Case report A 56-year-old man with a history of prior myocardial infarction and severe left ventricular dysfunction underwent an implantable cardioverter defibrillator (ICD) buy adenosine triphosphate for primary prevention of sudden cardiac death. Since the patient had normal sinus rhythm and normal atrio-ventricular conduction, a single lead, Biotronik, Lumax 640 VR-T DX ICD was selected. A DX system consists of a single lead, which provides atrial as well as ventricular electrograms, and enhances atrial arrhythmia detection [1]. The patient was followed-up in the clinic and via the home monitoring service. The procedure and the 1-month follow-up visit were uneventful. Three months later, several atrial monitoring episodes, classified as atrial tachycardia (Fig. 1), were recorded by the device and the home monitoring system. Unusual high frequency artifacts were seen on the far field (RV coil to can) and the atrial channels, whereas the bipolar right ventricular channel was unaffected. Due to the unusual combination of the far field and atrial channel artifacts, normal lead parameters (P=2.0mV, R=11.4mV, RV threshold=0.6V, and impedance=464Ω), and due to the unique high frequent “crescendo–decrescendo” artifacts pattern lead fracture was very unlikely. The patient was telephoned immediately; he confirmed using an electrical disk saw (Fig. 2) at the time that coincided with the abnormal ICD recordings. These recordings disappeared after he stopped using the saw. However, it was unclear why the artifacts were seen on the atrial channel but not on the right ventricular. The probable explanation was that the floating atrial dipole sensor was amplified 4-times, and the programming of the atrial sensitivity was higher than the ventricular sensitivity [2]. The relatively novel Lumax DX system consists of a single lead which provides both atrial and ventricular signals. The atrial signals are sensed by a floating atrial pole, and are amplified by the Lumax 640 VR-T DX device. This system along with the home monitoring was developed to decrease the risk of inappropriate ICD shocks by appropriately detecting atrial arrhythmias and enabling physicians to intervene earlier. However, in the present case, electromagnetic interference was detected by the atrial lead and falsely classified as atrial arrhythmia. Physicians should thus be aware of the unique DX atrial sensing mechanism, and carefully assess each of the intra-cardiac electrogram recorded by the device in order to avoid an inacurate diagnosis of a lead fracture or atrial arrhythmia.
    Conflict of interest
    Acknowledgements
    Introduction Current guidelines recommend implantable cardioverter–defibrillator (ICD) implantation for Brugada syndrome (BrS) patients with a history of ventricular fibrillation (VF). However; patients whose first presentation is VF are at high risk of recurrent VF episodes and/or electrical storm [1]. Here we report a case of BrS whose first presentation was electrical storm, for which, primary ablation (i.e. before ICD implantation) resulted in VF-free survival during a 48-month follow up.
    Case A 32-year-old cardiologist suddenly collapsed at midnight while bathing. After resuscitation, he was admitted to buy adenosine triphosphate a nearby hospital, where Brugada-type electrocardiographic readings (ECGs) were recorded. These findings were associated with frequent monomorphic premature ventricular contractions (PVCs) that degenerated to ventricular fibrillation (VF) 3 times during the night (Fig. 1). Telemetry revealed that the QRS morphology of the first beat in all VF episodes was identical (left bundle branch block and inferior axis configuration). The patient was then transferred to our hospital, where he was stable, with repetitive PVCs (>10PVCs/min) of the same initial morphology. Urgent cardiac magnetic resonance imaging and coronary angiography ruled out structural heart disease. Because these PVCs had led to an electrical storm and continued with similar frequency the next day, emergency catheter ablation (CA) was performed 4 hours after admission. Endocardial mapping revealed normal right ventricular (RV) voltage (Fig. 2) with late potentials (LP), scattered at the free wall of the RV outflow tract (RVOT) with only few LP points at its posterior aspect. An optimal pacemap and early activation were observed at the RVOT free wall, where CA completely eliminated the PVCs and rendered VF non-inducible. LP ablation and further energy applications in a broad area around the earliest activation site were performed. An ICD was then implanted. Pilsicainide provocation and treadmill exercise tests were performed; however, no triggering PVCs or VF occurred. The patient has been event free during a 48-month medication-free follow-up.