Intravenous adenosine shortened mean atrial fibrillation cycle length (mean difference 16.6 ms; P<0.0005) and increased localized rotational activation occurrences by 50%.
Observational (n=22)
Does intravenous adenosine alter wavefront propagation patterns in patients undergoing catheter ablation for persistent atrial fibrillation?
Adenosine accelerates atrial fibrillation and promotes rotational activation patterns, but these do not appear to represent stable arrhythmogenic sources for ablation targets.
Effect estimate: mean difference 16.6 (95% CI 11.3-21.9)
Absolute Event Rate: 165.1% vs 181.7%
p-value: p=<0.0005
Background Adenosine shortens action potential duration and refractoriness and provokes atrial fibrillation. This study aimed to evaluate the effect of adenosine on mechanisms of wavefront propagation during atrial fibrillation. Methods and Results The study included 22 patients undergoing catheter ablation for persistent atrial fibrillation. Left atrial mapping was performed using the AcQMap charge density system before and after administration of intravenous adenosine at 1 or more of 3 time points during the procedure (before pulmonary vein isolation, after pulmonary vein isolation, and after nonpulmonary vein isolation ablation). Wave‐front propagation patterns were evaluated allowing identification and quantification of localized rotational activation (LRA), localized irregular activation, and focal firing. Additional signal processing was performed to identify phase singularities and calculate global atrial fibrillation cycle length and dominant frequency. A total of 35 paired maps were analyzed. Adenosine shortened mean atrial fibrillation cycle length from 181.7±14.3 to 165.1±16.3, (mean difference 16.6 ms; 95% CI, 11.3–21.9, P <0.0005) and increased dominant frequency from 6.0±0.7 Hz to 6.6±0.8 Hz (95% CI, 0.4–0.9, P <0.0005). This was associated with a 50% increase in the number of LRA occurrences (16.1±7.6–24.2±8.1; mean difference 8.1, 95% CI, 4.1–12, P <0.0005) as well as a 20% increase in the number of phase singularities detected (30.1±7.8–36.6±9.3; mean difference 6.5; 95% CI, 2.6–10.0, P =0.002). The percentage of left atrial surface area with LRA increased with adenosine and 42 of 70 zones (60%) with highest density of LRA coincided with high density LRA zones at baseline with only 28% stable across multiple maps. Conclusions Adenosine accelerates atrial fibrillation and promotes rotational activation patterns with no impact on focal activation. There is little evidence that rotational activation seen with adenosine represents promising targets for ablation aimed at sites of stable arrhythmogenic sources in the left atrium.
Pope et al. (Fri,) conducted a observational in persistent atrial fibrillation (n=22). intravenous adenosine vs. baseline was evaluated on mean atrial fibrillation cycle length (ms) (mean difference 16.6, 95% CI 11.3-21.9, p=<0.0005). Intravenous adenosine shortened mean atrial fibrillation cycle length (mean difference 16.6 ms; P<0.0005) and increased localized rotational activation occurrences by 50%.