Revista Española de Cardiología (English Edition) Revista Española de Cardiología (English Edition)
Rev Esp Cardiol. 2017;70:1024 - Vol. 70 Num.11 DOI: 10.1016/j.rec.2017.06.013

Ivabradine as an Atrioventricular Node Modulator. Promise or Reality? Response

Adolfo Fontenla a,, Lola Villagraz a, Álvaro Lozano a, María López-Gil a

a Unidad de Arritmias, Servicio de Cardiología, Hospital Universitario 12 de Octubre, Madrid, Spain

Refers to

Ivabradine as an Atrioventricular Node Modulator. Promise or Reality?
Luis Álvarez-Acosta, Marcos Pedro Farráis-Villalba, Julio Hernández-Afonso
Rev Esp Cardiol. 2017;70:1023
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Article

To the Editor,

First, we would like thank Dr Álvarez-Acosta et al. for their comments, which we will try to address here.

In accordance with the relevant guidelines,1 we routinely implant cardiac resynchronization devices to treat heart failure in optimally treated and nondecompensated patients. Our patient2 was stable at the time of implantation and his heart rate, although controlled, was insufficient to guarantee an adequate pacing percentage. Nevertheless, simply implanting a resynchronization device in a patient with heart failure rarely confers a clinical improvement in subsequent weeks if the biventricular pacing percentage is only about 70%. It would be as incredible as a drug left untouched by a patient in a bedside drawer exerting a clinically relevant effect. Because we can rule out an “inherent improvement” from a resynchronization device unable to achieve adequate pacing and there were no changes in any other treatment between the 2 consecutive revisions, we must delve into the eventual role of ivabradine in our patient's heart rate control.

The criteria of causation include temporality, biological plausibility (there is a high-density If current in the atrioventricular node), analogy (ivabradine reduces heart rate during atrial fibrillation in animals), and experiment (ivabradine decreased heart rate in atrial fibrillation vs placebo in a human trial). If the pacing percentage were to decrease after ivabradine withdrawal, our hypothesis would be strengthened but such an approach would be ethically questionable. The possible effects of ivabradine on heart rate are in no way ruled out by the publications on ivabradine, which make no mention of this mechanism of action. However, it is not necessary to turn to rare genetic mutations to explain the inhibitory effect of ivabradine on node conduction because the United States prescribing information for this drug states that first-degree atrioventricular block is a frequent adverse reaction.

We would also like to take this opportunity to report that the same effect on percentage of pacing was seen in another patient administered ivabradine in the same clinical setting.

Promises can become reality if we are proactive in the search for therapeutic options by not only researching new molecules, but also by exploring new indications for existing ones.

Corresponding author: drfontenla@gmail.com

Bibliography

1. Sionis Green A, Manito Lorite N, Bueno H, et al. Comentarios a la guía ESC 2016 sobre el diagnóstico y tratamiento de la insuficiencia cardiaca aguda y crónica. Rev Esp Cardiol. 2016;69:1119-25.
2. Fontenla A, Villagraz L, De Juan J, Lozano A, Giacoman S, López-Gil M. Ivabradine as an alternative to AV node ablation in a patient with permanent atrial fibrillation. Rev Esp Cardiol. 2017;70:1019-20.

1885-5857/© 2017 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved

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