ADENOSINE IN ATRIAL FIBRILLATION ABLATION: DOES IT IMPROVE THE OUTCOME?

P. Carmo, F. Moscoso Costa, N. Lopes, D. Cavaco, P. Santos, S. Carvalho, T. Teixeira, A. Soares, M. Marques, L. Parreira, P. Adragao

1. Hospital Luz, Heart Rythm Center, Lisbon, Portugal; 2. Hospital Santa Cruz, Department of Cardiology, Lisbon, Portugal

Abstract

Background: Pulmonary vein isolation is an essential part of the standard ablative treatment for atrial fibrillation. Vein reconnection has been referred as one of the main causes of recurrence after ablation. Adenosine testing at the end of the procedure allows to check for dormant conduction and to further deliver radiofrequency energy at the sites of reconnection aiming to achieve better efficacy and long lasting pulmonary vein isolation. The impact of this strategy during follow up after ablation is not well established.
Methods : We evaluated 305 consecutive patients submitted to pulmonary vein isolation since 1st January 2013, 60±11 years old, 47.5% hypertensive, 80.3% paroxysmal atrial fibrillation. The average left atrium volume was 101±28ml. At the end of the procedure, adenosine iv bolus was used in 162 pts (64.5%). Reconnection in at least one vein was observed in 43 pts (26.5%) and further radiofrequency energy was applied. During 173±128 days of follow up recurrence free was present in 90.5% of patients in adenosine group vs 95.3% in the control group (p=0.76, multivariate, adjusted for difference between groups). Having reconnection and further radiofrequency energy applied in the adenosine group didn’t correlate with better prognosis, 93% free of recurrence in reconnection subgroup vs 89.6% in non-reconnection subgroup (p=0.5).
Conclusions: In our registry of patients submitted to pulmonary vein isolation, further radiofrequency delivery in areas of adenosine inducible reconnection did not improve success rates during follow up. These results do not support the routine use of adenosine during atrial fibrillation ablation.

Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992;20:1391–1396. Bayés de Luna A, Brugada J, Baranchuk A, Borggrefe M, Breithardt G, Goldwasser D, Lambiase P, Riera AP, Garcia-Niebla J, Pastore C, Oreto G, McKenna W, Zareba W, Brugada R, Brugada P. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report. Journal of Electrocardiology. 2012; 45:433–442 Crea P., Picciolo G., Luzza F. and Oreto G. (2014), ST Segment Depression in the Inferior Leads in Brugada Pattern: A New Sign. Annals of Noninvasive Electrocardiology. doi: 10.1111/anec.12247 S. Nagase, S. Hiramatsu, H. Morita, N. Nishii, M. Murakami, K. Nakamura, K.F. Kusano, H. Ito, T. Ohe Electroanatomical correlation of repolarization abnormalities in Brugada syndrome: detection of type 1 electrocardiogram in the right ventricular outflow tract J Am Coll Cardiol, 56 (2010), pp. 2143–2145 C. Veltmann, T. Papavassiliu, T. Konrad, C. Doesch, J. Kuschyk, F. Streitner, D. Haghi, H.J. Michaely, S.O. Schoenberg, M. Borggrefe, C. Wolpert, R. Schimpf Insights into the location of type I ECG in patients with Brugada syndrome: correlation of ECG and cardiovascular magnetic resonance imaging Heart Rhythm, 9 (2012), pp. 414–421 van Oosterom A, Oostendorp T. ECGSIM; an interactive tool for studying the genesis of QRST waveforms. Heart 2004;90:16 van Oosterom A, Oostendorp TF, van Dam PM. Potential applications of the new ECGSIM. J Electrocardiol. 2011 Sep-Oct;44(5):577-83 Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation. 1999 Oct 12;100(15):1660-6.