To the Editor,
We thank Drs Rivas-Gándara and Francisco-Pascual for their interest shown in the BRAKE-AF project.1
There is indeed evidence to suggest that ivabradine could be effective for rate control in permanent atrial fibrillation (AF). Following publication of its efficacy in a patient with poorly-controlled AF,2 we were aware that to “make this hypothesis a reality” we would need to conduct a clinical trial.3
Permanent AF is the most common form of AF yet, surprisingly, new drugs for rate control have not been developed in the past 30 years. The industrial development of antiarrhythmic drugs is increasingly uncommon, probably because it involves investment that is risky and/or with small profit margins; this means that clinicians must assess the antiarrhythmic effect of drugs that are marketed for other indications, as is the case with ranolazine.4 We would like to point out that the BRAKE-AF project was undertaken with public funding only and thanks to the generous effort of independent investigators: cardiologists from several hospitals and pharmacologists from the Universidad Complutense de Madrid.
Our trial is currently in the recruitment phase, and bears the difficulties inherent to any clinical trial with the added impact of the recent COVID-19 outbreak. Like Rivas-Gándara and other authers,5 we hope that the BRAKE-AF trial will answer the question of whether there is a new drug for rate control in AF. If so, the next question will be, “Could ivabradine improve prognosis in patients with permanent AF?”
References
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