136-02: Effect of Loss of Heart Rate Variability on T-wave Heterogeneity and QT Variability in Heart Failure Patients: Implications in Ventricular Arrhythmogenesis

Abstract

Background: A diminishing value of heart rate variability (HRV) robustly increases vulnerability to life-threatening ventricular arrhythmias, yet the electrophysiological mechanism of this dynamic relationship is still not well understood. We evaluated if fixed-rate atrial pacing, that abolishes the effect of physiological HRV, will modulate ventricular repolarization wavefronts and is relevant to ventricular arrhythmogenesis. Methods: The study was performed in 16 subjects: 8 heart failure patients with history of spontaneous ventricular tachycardia [HFVT], and 8 subjects with structurally normal hearts (HNorm). The T-wave heterogeneity descriptors [total cosine angle between QRS and T-wave loop vectors (TCRT, negative value corresponds to large difference in the 2 loops), T-wave morphology dispersion, T-wave loop dispersion] and QT intervals were analyzed in a beat-to-beat manner on 3-minutes records of 12-lead surface ECG at baseline and during atrial pacing at physically inert rates of 80 and 100 bpm. The global T-wave heterogeneity was expressed as mean values of each of the T-wave morphology descriptors and variability in QT intervals (QTV) as standard deviation of QT intervals. Results: Baseline T-wave morphology dispersion and QTV were higher in HFVT compared to HNorm subjects (p ≤ 0.02). While group differences in T-wave morphology dispersion and T-wave loop dispersion remained unaltered with atrial pacing, TCRT tended to fall more in HFVT patients compared to HNorm subjects (interaction p value = 0.086). Atrial pacing failed to reduce QTV in both groups, however group differences were augmented (p < 0.0001). Conclusions: Atrial pacing and consequent loss of HRV appears to introduce unfavorable changes in ventricular repolarization in HFVT subjects. It widens the spatial relationship between wavefronts of ventricular depolarization and repolarization (Figure). This may partly explain the concerning relation between poorer HRV and the risk of ventricular arrhythmias.