title: Effect of Loss of Heart Rate Variability on T-Wave Heterogeneity and QT Variability in Heart Failure Patients: Implications in Ventricular Arrhythmogenesis.
abstract: Heart rate variability (HRV) modulates dynamics of ventricular repolarization. A diminishing value of HRV is associated with increased vulnerability to life-threatening ventricular arrhythmias, however the causal relationship is not well-defined. We evaluated if fixed-rate atrial pacing that abolishes the effect of physiological HRV, will alter ventricular repolarization wavefronts and is relevant to ventricular arrhythmogenesis. The study was performed in 16 subjects: 8 heart failure patients with 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-min records of 12-lead surface ECG at baseline and during atrial pacing at 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. Baseline T-wave morphology dispersion and QTV were higher in HFVT compared to HNormsubjects (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 HNormsubjects (interaction p value = 0.086). Atrial pacing failed to reduce QTV in both groups, however group differences were augmented (p < 0.0001). 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. This may partly explain the concerning relation between poorer HRV and the risk of ventricular arrhythmias.
authors.affiliation: Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Sachin
authors.initials: S
authors.lastname: Nayyar
authors.affiliation: School of Electrical & Electronic Engineering, University of Adelaide, Adelaide, Australia. muhammad.hasan@uhn.ca.|Division of Cardiology, University Health Network, Toronto, Canada. muhammad.hasan@uhn.ca.
authors.forename: Muhammad A
authors.initials: MA
authors.lastname: Hasan
authors.affiliation: Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Kurt C
authors.initials: KC
authors.lastname: Roberts-Thomson
authors.affiliation: School of Public Health, University of Adelaide, Adelaide, Australia.
authors.forename: Thomas
authors.initials: T
authors.lastname: Sullivan
authors.affiliation: School of Electrical & Electronic Engineering, University of Adelaide, Adelaide, Australia.
authors.forename: Mathias
authors.initials: M
authors.lastname: Baumert
mesh_terms: D000465:Algorithms; D001145:Arrhythmias, Cardiac; D017115:Catheter Ablation / Q000379:methods*; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology*; D006333:Heart Failure / Q000503:physiopathology / Q000601:surgery*; D006339:Heart Rate; D006801:Humans
keywords: Atrial pacing; Autonomic modulation; Cardiomyopathy; QT variability; T-Wave heterogeneity