Sinus rhythm R-wave amplitude as a predictor of ventricular fibrillation undersensing in patients with implantable cardioverter-defibrillator.

BACKGROUND: Ventricular fibrillation (VF) is induced during implantable cardioverter-defibrillator (ICD) implantation to ensure that the ICD will sense, detect, and defibrillate VF. ICD implant guidelines state that the amplitude of the sinus rhythm R wave recorded from the ventricular electrogram should have amplitude ≥5 mV. No study has tested the relationship between sinus rhythm R-wave amplitude and VF sensing using modern, transvenous sensing electrodes. OBJECTIVE: The goal of this study was to determine whether there is a sinus rhythm R-wave amplitude cutoff that can be used to determine which patients are not at risk of VF undersensing. METHODS: A retrospective analysis of induced and spontaneous VF episodes from 2 clinical trials with 2022 patients was performed. Episodes with undersensing during the initial detection of VF were identified, and the distribution of sinus rhythm R-wave amplitudes for patients with and without VF undersensing was analyzed. RESULTS: Only 3% of analyzed induced VF episodes were considered to have VF undersensing, and none had clinically significant detection delays. There was no correlation between device-measured, rectified sinus rhythm R-wave amplitude and VF undersensing at the time of implantation or during follow-up, although <4% of patients had sinus rhythm R-waves with amplitude <3 mV. CONCLUSION: We analyzed true bipolar sensing of induced VF or spontaneous ventricular tachycardia/VF detected in the ICD VF zone. Sensing of VF was so reliable that clinically significant undersensing did not occur. Our findings do not support any recommended minimum sinus rhythm R wave to ensure reliable sensing of VF or the necessity of inducing VF to verify sensing for rectified sinus rhythm R-waves with amplitude ≥3 mV.

Automated vulnerability testing identifies patients with inadequate defibrillation safety margin.

BACKGROUND: Implantable cardioverter-defibrillator system efficacy is tested at implant by induction of ventricular fibrillation (VF). Defibrillation safety margin can be assessed without VF induction using upper limit of vulnerability methods, but these methods have required manual determination of T-wave timing. METHODS AND RESULTS: To test the feasibility of an inductionless system of implant testing, a multicenter prospective study of an automated vulnerability safety margin system was conducted, which measured T-wave timing using an intracardiac electrogram during a ventricular pacing train. The system delivered up to 4 T-wave shocks of 18 J. Lack of VF induction by all 4 shocks was considered evidence of defibrillation adequacy. Patients subsequently underwent conventional defibrillation testing to meet a standard implant criterion. The 95% lower CI for defibrillation success at 25 J for noninduced patients was found using Bayesian statistics. Sixty patients were enrolled at 6 centers. Vulnerability testing and defibrillation success results were obtained from 54 patients. Vulnerability testing induced VF in 10 (19%) patients, of whom 2 required system revision. All patients not induced by vulnerability testing were successfully defibrillated twice at ≤25 J. The Bayesian credible interval was 97% to 100% for the population success rate of defibrillation at 25 J for automated vulnerability safety margin noninduced patients. CONCLUSIONS: An automated system identified all patients who failed conventional safety margin testing, while inducing only 19% of patients. Although limited by sample size, this study suggests the feasibility of automated implant testing that substantially reduces the need for VF induction in patients receiving implantable cardioverter-defibrillators.

Bradycardia pacing-induced short-long-short sequences at the onset of ventricular tachyarrhythmias: a possible mechanism of proarrhythmia?

OBJECTIVES: The purpose of this study was to characterize interactions between normal pacing system operation and the initiating sequence of ventricular tachycardia (VT)/ventricular fibrillation (VF). BACKGROUND: Abrupt changes in ventricular cycle lengths (short-long-short, S-L-S) might initiate VT/VF. The S-L-S sequences might be passively permitted or actively facilitated by bradycardia pacing. METHODS: Initiating sequences of 1,356 VT/VF episodes in the PainFree Rx II (n = 634) and EnTrust Trial (n = 421) were analyzed with stored electrograms and by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]). Interactions between pacing and VT/VF initiation were classified as: non-pacing associated, pacing associated, pacing permitted, and pacing facilitated. RESULTS: Non-pacing associated (no pacing, no S-L-S) and pacing associated (ventricular pacing without S-L-S) onset accounted for 44.0% and 29.8% of all VT/VF, respectively. Pacing permitted (S-L-S sequences without ventricular pacing) episodes accounted for 6.4% (DDD/R), 20.0% (MVP), and 25.6% (VVI/R) of 1,356 VT/VF episodes. Pacing facilitated onset (S-L-S sequences actively facilitated by ventricular pacing including the terminal beat after a pause) accounted for 8.2% (MVP), 9.4% (VVI/R), and 14.8% (DDD/R) of 1,356 VT/VF episodes. Pacing facilitated S-L-S VT/VF occurred in 2.6% (MVP), 3.3% (VVI/R), and 5.2% (DDD/R) of patients with episodes and was the sole initiating sequence in approximately 1% of patients. Pause durations during pacing facilitated S-L-S differed between modes (DDD/R 793 +/- 172 ms vs. MVP 865 +/- 278 ms vs. VVI/R 1180 +/- 414 ms, p = 0.002). The majority of these episodes were monomorphic VT. CONCLUSIONS: Ventricular tachycardia/VF in some implantable cardioverter-defibrillator patients might be initiated by S-L-S sequences that are actively facilitated by bradycardia pacing operation and might constitute an important mechanism of ventricular proarrhythmia.