Pacing-Associated Left Ventricular Dysfunction?
Pacing-Associated Left Ventricular Dysfunction?
The present study is an important proof of concept analysis of data collected from a non-selected cohort of consecutive attendees to a clinic designed to assess patients prior to pacemaker generator replacement. The intervention was not applied in a randomised, double-blind fashion, and the results of the analysis must be interpreted in light of this. However, programming changes and data collection followed a robust standardised process, in consecutive attendees and the analysis of the echocardiographic images, exercise and NT-pro-BNP results, and pacing data presented in this report were performed on an intention-to-treat basis in a randomised, blinded fashion by a single experienced cardiac physiologist. We were careful to avoid altering medical therapy over the 6-month follow-up period, although the patients' usual doctors were free to do so. Hence, we are confident that the changes described are purely due to alterations in pacemaker therapy. A larger study would require randomisation to correct for non-device treatments.
Other limitations include that the study was carried out in a single centre and that the outcome variables are surrogates for hospitalisation and mortality. However, the disadvantages of surrogate endpoints are typical of proof of concept small-scale studies, and we recognise that in order to establish the benefits of reprogramming on heart failure events in an unselected population of patients with conventional pacemakers, a larger randomised, placebo-controlled study with longer follow-up would be required to provide robust efficacy and cost-effective data.
Limitations
The present study is an important proof of concept analysis of data collected from a non-selected cohort of consecutive attendees to a clinic designed to assess patients prior to pacemaker generator replacement. The intervention was not applied in a randomised, double-blind fashion, and the results of the analysis must be interpreted in light of this. However, programming changes and data collection followed a robust standardised process, in consecutive attendees and the analysis of the echocardiographic images, exercise and NT-pro-BNP results, and pacing data presented in this report were performed on an intention-to-treat basis in a randomised, blinded fashion by a single experienced cardiac physiologist. We were careful to avoid altering medical therapy over the 6-month follow-up period, although the patients' usual doctors were free to do so. Hence, we are confident that the changes described are purely due to alterations in pacemaker therapy. A larger study would require randomisation to correct for non-device treatments.
Other limitations include that the study was carried out in a single centre and that the outcome variables are surrogates for hospitalisation and mortality. However, the disadvantages of surrogate endpoints are typical of proof of concept small-scale studies, and we recognise that in order to establish the benefits of reprogramming on heart failure events in an unselected population of patients with conventional pacemakers, a larger randomised, placebo-controlled study with longer follow-up would be required to provide robust efficacy and cost-effective data.
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