Abstract

Aim We aim to evaluate the efficacy and safety of determining the presence of true biventricular pacing by administration of intravenous adenosine. This aims to determine whether non-response to biventricular pacing therapy is partially explained by over-counting of the percentage of pacing therapy by the presence of fusion beats. We compared the proportion of patients with fusion beats in non-responders compared to responders Methods This will be a single centre, prospective, cohort study. 71 consecutive patients with implanted cardiac resynchronisation devices between July 2006 and November 2015 were identified. Patients underwent the adenosine trial at least 12 months post CRT device implantation to detect the presence of potentially ineffective biventricular pacing. This was compared with the recorded percentage of biventricular pacing reported during device interrogation. Correlation was made between response to CRT therapy and presence of effective biventricular pacing. Results Preliminary results from 24 patients demonstrate that symptomatic adenosine administration was successful in identifying true effective biventricular paced beats. This has allowed us to identify patients with fusion beats. 8 patients were non-responders to CRT, whereas 16 patients were responders. 50% (n=4) of non-responders and 12.5% (n=2) of responders had definite electrocardiography (ECG) changes through the symptomatic adenosine administration, showing that a percentage of the paced beats counted by the CRT device may in fact be fusion beats. Figure 1 shows the clear change in the morphology of the QRS complex in one of the non-responders. Figure 1 Electrocardiogram of a non-responder during symptomatic adenosine administration Conclusion Preliminary results suggest that symptomatic adenosine administration is successful in identifying true effective biventricular paced beats which may be overestimated by CRT device interrogation. Correlation with response to CRT is yet to be established, but in 50% of the non-responders we identified a definite change in the morphology of the paced rhythm during the symptomatic response to adenosine. This raises a question of whether the poor response to CRT for these patients is actually due to the insufficient percentage of effective biventricular pacing (

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