Introduction: An implantable cardioverter defibrillator (ICD) is the most reliable therapeutic device for preventing sudden cardiac death in patients with sustained ventricular tachycardia (VT). Regarding the effectiveness of the ICD, targeted VT is defined based on the tachyarrhythmia cycle length. However, variation of the RR interval variability of VTs does occur. A few studies reported on VT characteristics and effects of ICD therapy according to RR interval variability. This study aimed to identify the clinical characteristics of VTs and effects of ICD therapy according to RR interval variability. Methods: We analyzed 821 VT episodes in 69 of 185 patients treated with ICDs or cardiac resynchronization therapy defibrillators. VTs were classified as regular or irregular based on RR interval variability. We evaluated successful termination using anti-tachycardia pacing (ATP)/shock therapy, spontaneous termination, and acceleration between regular and irregular VTs. Reproducibility of the RR interval variability in one VT episode and within an individual with recurrent VT episodes was evaluated. Results: Regular VT was significantly more successfully terminated than irregular VT by ATP therapy. There was no significant difference in shock therapy or VT acceleration, irrespective of the variability of the VT cycle length. Spontaneous termination of VT occurred significantly more often in irregular than in regular VT. Reproducibility of RR interval variability in an episode and individual was 89% and 73%, respectively. Conclusion: ATP therapy showed greater effectiveness for regular than for irregular VT. Spontaneous termination was more common in irregular than in regular VT. RR interval variability of VTs is reproducible.

An 82-year-old woman received pacemaker implantation for sick sinus syndrome. Two days after the implantation, electrocardiography showed 2:1 atrial pacing failure, followed by bradycardia-dependent increase in the atrial pacing threshold during a pacemaker examination. However, transient 1:1 atrial pacing capture recovered by adenosine triphosphate (ATP) administration, which was performed to evaluate the bradycardia-dependent pacing failure mechanism. We considered this phenomenon to be caused by phase 4 depolarization and avoided replacing this atrial lead. Three weeks later, the atrial pacing threshold had improved. We report the potential role of phase 4 depolarization in bradycardia-dependent increase in pacing threshold by using ATP.