Ventricular pacing inhibition by oversensing due to diaphragmatic myopotential during deep inspiration

AbstractAn 80-year-old man, who had dilated cardiomyopathy with right ventricular (RV) dilatation, underwent implantable cardioverter defibrillator (ICD) implantation for advanced atrioventricular block and primary prevention of sudden cardiac death. Tined and screw-in leads were placed on the right atrial appendage and RV apex, respectively. Ventricular pacing inhibition was detected after surgery due to oversensing by diaphragmatic myopotential occurring only during deep inspiration. We performed re-surgery and switched the screw-in lead for a tined lead. The diaphragmatic myopotential decreased, thereby improving oversensing by diaphragmatic myopotential and ventricular pacing inhibition. It might be beneficial to use a tined lead when placing the ventricular lead at the RV apex for implantation of a pacemaker or ICD if oversensing of diaphragmatic myopotential is observed using a screw-in lead.<Learning objective: Oversensing due to diaphragmatic myopotential is rarely observed. However if it occurs, it becomes a critical problem, which causes pacemaker inhibition or inappropriate ICD shock. However, the method of preventing this problem is unknown. In this case, we demonstrated that a tined-lead may be useful for the prevention of oversensing by diaphragmatic myopotential.

Atrial electrical abnormality in patients with Brugada syndrome assessed by signal-averaged electrocardiography

Background: Ventricular fibrillation and atrial fibrillation are well-known arrhythmias in patients with Brugada syndrome. This study evaluated the characteristics of the atrial arrhythmogenic substrate using the signal-averaged electrogram (SAECG) in patients with Brugada syndrome. Methods: SAECGs were performed during normal sinus rhythm in 23 normal volunteers (control group), 21 patients with paroxysmal atrial fibrillation (PAF; PAF group), and 21 with Brugada syndrome (Brugada group). Results: The filtered P wave duration (fPd) in the control, Brugada, and PAF groups was 113.9 ± 12.9 ms, 125.3 ± 15.0 ms, and 137.1 ± 16.3 ms, respectively. The fPd in the PAF group was significantly longer compared to that in the control and Brugada groups (p < 0.05). The fPd in the Brugada group was significantly longer than that in the control group (p < 0.05) and significantly shorter than that in the PAF group (p < 0.05). Conclusion: Patients with Brugada syndrome had abnormal P waves on the SAECG. The abnormal P waves on the SAECG in Brugada syndrome patients may have intermediate characteristics between control and PAF patients