Background
Enhanced beat-to-beat variability of repolarization is strongly linked to arrhythmogenesis
and is largely due to variation in ventricular action potential duration (APD). Previous
studies in humans have relied on QT interval measurements; however, a direct relationship
between beat-to-beat variability of APD and arrhythmogenesis in humans has yet to
be demonstrated.
Objective
This study aimed to explore the beat-to-beat repolarization dynamics in patients with
heart failure at the level of ventricular APD.
Methods
Forty-three patients with heart failure and implanted cardiac resynchronization therapy
– defibrillator devices were studied. Activation-recovery intervals as a surrogate
for APD were recorded from the left ventricular epicardial lead while pacing from
the right ventricular lead to maintain a constant cycle length.
Results
During a mean follow-up of 23.6±13.6 months, 11 patients sustained ventricular fibrillation/ventricular
tachycardia (VT/VF) and received appropriate implantable cardioverter-defibrillator
therapies (antitachycardia pacing or shock therapy). Activation-recovery interval
variability (ARIV) was significantly greater in patients with subsequent VT/VF than
in those without VT/VF (3.55±1.3 ms vs 2.77±1.09 ms; P=.047). Receiver operating characteristic curve analysis (area under the curve 0.71;
P=.046) suggested high- and low-risk ARIV groups for VT/VF. Kaplan-Meier survival analysis
demonstrated that the time until first appropriate therapy for VT/VF was significantly
shorter in the high-risk ARIV group (P=.028). ARIV was a predictor for VT/VF in the multivariate Cox model (hazard ratio
1.623; 95% confidence interval 1.1–2.393; P=.015).
Conclusion
Increased left ventricular ARIV is associated with an increased risk of VT/VF in patients
with heart failure.
Keywords
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Article info
Publication history
Published online: December 04, 2018
Footnotes
This work was supported by the Wellcome/EPSRC Centre for Medical Engineering (WT 203148/Z/16/Z). The research was funded/supported by the National Institute for Health Research (NIHR) Biomedical Research Centre at Guy’s and St Thomas’ NHS Foundation Trust and King’s College London. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health.
Dr Porter is funded by an Abbott educational grant. Dr Bishop acknowledges support from the UK Medical Research Council (New Investigator Research Grant).
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