• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • br Discussion T wave oversensing is caused


    Discussion T-wave oversensing is caused by alternations or variations in intracardiac electrograms for reasons such as hyperglycemia, drugs, sympathetic tones, ventricular pacing, and hyperkalemia. Several similar cases of hyperkalemia-induced T-wave oversensing with inappropriate ICD therapies have been reported [1,2]. However, the relationship between 12-lead surface electrograms and internal ICD electrograms during hyperkalemia was not fully elucidated. A previous study reported that T-wave oversensing is more commonly observed after paced beats than spontaneous beats and this glucose assay was attributed to the polarization voltage [3]. In the present case, T-wave oversensing originated from normal atrio-ventricular conduction, resulting in an inappropriate ICD shock. The amplitudes of the intracardiac R-waves and T-waves were measured as approximately 7–8mV and 3mV, respectively. Thus, the oversensing of T-waves with large amplitudes could not be prevented by a simple algorithm in this model. However, device programming may allow for the discrimination of T-wave oversensing. Possible approaches include prolongation of the number of intervals for tachycardia detection, adjustment of the VT and VF zone ranges, elevation of the sensing threshold, change of sensing vector, and use of all-time V pacing to mask T-waves in the blanking period. However, these strategies run the risk of ignoring true ventricular tachyarrhythmias and exhausting the battery. If these strategies are ineffective, ventricular lead repositioning/replacement may also be considered in order to obtain a greater R-wave amplitude, making oversensing less likely. In recently published reports, patients with ICDs including the latest T-wave oversensing discriminator program have experienced a dramatically lower rate of inappropriate ICD shocks compared to previous studies. Furthermore, the incidence of T-wave oversensing causing inappropriate ICD shocks in this study was much smaller than previously reported [4]. Therefore, device replacement should be considered if needed. Interestingly, the T-wave amplitude on ICD electrograms corresponded with that on 12-lead surface electrograms, and the amplitude on ICD electrograms was dramatically changed compared to that on 12-lead surface electrograms. Differences between the action potential characteristics of ventricular endocardial and epicardial tissues were reported previously [5,6]. Of note, the Ik1 channel is distributed in the endocardial tissue, and is strongly associated with the repolarization process and extracellular potassium concentration. Furthermore, the differential characteristics of Ik1 may contribute to the differences in action potential configuration between endocardial and epicardial myocytes [5,6]. Thus, we speculated that the change in the repolarization process during hyperkalemia was evident on the ICD electrogram as compared to the surface 12-lead ECG. This speculation was consistent with a previous case report [7]. Hyperkalemia should be carefully monitored in ICD recipients, especially those with CKD, to prevent inappropriate ICD shocks due to T-wave oversensing.
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    Case report The procedure was performed under local anesthesia. Leads were inserted through the left subclavian vein: (a) an active fixation double catheter in the right ventricle, (b) a bipolar active fixation lead in the right auricle (Fig. 1), and (c) a bipolar lead introduced from the coronary sinus into the antero-lateral vein. The previously implanted pacemaker and one atrial lead were removed (the old unipolar lead was left in the right ventricle) and a CRT device was connected to the new implanted leads. The atrial lead removal was uneventful. After satisfactory R-wave sensing (>5mV) and pacing thresholds (<1.0V at 0.5-ms pulse width) had been demonstrated, the patient underwent defibrillation threshold testing (DFT) to ensure proper device function. Sustained ventricular tachycardia and ventricular fibrillation were induced to make certain that the device was able to constantly sense, detect, and terminate arrhythmias with a shock at 25J. During skin closure, the patient went into cardiac arrest with pulseless electrical activity. Cardiopulmonary resuscitation maneuvers were performed immediately and echocardiography showed intrapericardial effusion that was partially drained. After 1h, pulseless electrical activity persisted, the patient was declared dead, and resuscitation attempts were halted.