Mapping of atrial activation during sustained atrial fibrillation in dogs with rapid ventricular pacing induced heart failure: evidence for a role of driver regions

K Ryu, SC Shroff, J Sahadevan… - Journal of …, 2005 - Wiley Online Library
K Ryu, SC Shroff, J Sahadevan, NL Martovitz, CM Khrestian, BS Stambler
Journal of Cardiovascular Electrophysiology, 2005Wiley Online Library
Introduction: Dogs with rapid ventricular pacing (RVP)‐induced congestive heart failure
(CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis
that rapid atrial activation in multiple regions and at different rates is responsible for
sustained AF in this CHF model. Methods and Results: We studied 12 episodes of sustained
(> 10 minutes) AF induced in 12 dogs with CHF produced by 3–6 weeks of RVP at 230
beats/minute. High‐density mapping of AF was performed using 382 unipolar atrial …
Introduction: Dogs with rapid ventricular pacing (RVP)‐induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model.
Methods and Results: We studied 12 episodes of sustained (>10 minutes) AF induced in 12 dogs with CHF produced by 3–6 weeks of RVP at 230 beats/minute. High‐density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 ± 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 ± 0.8 Hz) near the PVs (8.4 ± 0.3 Hz) and high RA (8.5 ± 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1–11.4 Hz; RA: 5.9–7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs.
Conclusions: In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.
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