It has long been known that structural and electrical remodeling are associated with progression of atrial fibrillation from its intermittent to persistent form. Our research aimed to better understand the underlying disease process and answer the question of whether the observed changes are the cause of the progression or the result of advancing disease.
Over the past five years we conducted a comprehensive preclinical and in-vitro research program at the University of Michigan. In particular, the paced sheep model of atrial fibrillation, the most advanced preclinical model available, has provided invaluable insights. We developed a theory of how atrial fibrillation progresses from its early form with an occasional episode to its most serious form of treatment-resistant persistent atrial fibrillation. Recently, we began testing the theory and initial results indicate that pharmacological disruption halts or slows structural and electrical remodeling.
Over the past several years great progress has been made in the prevention of complications of atrial fibrillation. Although very important, their significance would be dwarfed by an ability to prevent progression of atrial fibrillation after its initial clinical manifestation.
Our research may form the foundation of a new paradigm in atrial fibrillation – pharmacological prevention of persistent atrial fibrillation. If successful, it would address one of the most important unmet needs in cardiovascular disease and create a large new pharmaceutical opportunity.
We are proposing an unconventional path forward to accelerate the translation from our basic research finding to initiation of pharmaceutical development. We are establishing a collaborative pre-competitive industry program where biopharmaceutical companies jointly support and guide the research aiming at exploration and validation of the pathway and drug targets. Read more about how we plan to do this on the avertAF Initiative page.