Arne van Hunnik

Arne van Hunnik, Postdoctoral fellow at the Department of Physiology at Maastricht University / Maastricht University Medical Centre (MUMC+)

I have a long track record in research with large animal models to investigate atrial fibrillation (AF) and hemodynamics. Early 2019 I obtained my PhD degree at the Maastricht University. My research focus was oriented on atrial fibrillation (AF), mechanisms of various anti-arrhythmic drugs (AAD) and the dynamics of conduction properties during atrial fibrillation. AAD’s reduce the complexity of conduction patterns towards AF termination. AF is often approached as being in the level of complexity or the type of pattern. However, conduction patterns during sustained AF may alternate in complexity and stability. Actually, switches between stable and unstable AF patterns become more apparent towards AF cardioversion. These finding stimulates us to understand how these switches between pattern are formed as a better understanding may contributed to more successful AF termination strategies in the future.

My RACE V YTP-funded project is aimed at identifying AF stabilizing processes in the early stage of AF. In this context I work on two projects.

In the first project we explore a new treatment modality to prevent AF stabilization by targeting miRNA’s that are involved electrical remodelling. Antagomirs are a novel class of chemically engineered oligonucleotides that prevent other molecules from binding to a desired site on a mRNA. They are used to inhibit the action of endogenous miRNA and thus, increase expression of one or more proteins that are regulated by miRNA’s. We believe that neural NO synthase regulating miRNA’s may be targets with high potential to inhibit electrical remodelling. We are currently in the pilot phase to test if early atrial electrophysiological changes induced by AF can be inhibited by targeted miRNA inhibition.

The second project we are working on is to setup a heart failure model in the goat. Heart failure is strongly associated with AF, and vice versa, and both are associated with hypercoagulability. The goat model will allow us to link remodelling at different levels to hypercoagulability and atrial properties and AF stability. Moreover, we will be able to investigate the interaction heart failure and AF in relation hyper coagulability and remodelling.