Erasmus MC : Project number 38

Atrial fibrillation (AF) is associated with significant morbidity and mortality. The prevalence of AF will continue to rise and AF will persist to pose a major burden on public health costs.
Anti-arrhythmic drugs are often not effective in eliminating AF episodes and ablative therapy is also not so successful as first assumed. The expected epidemic of AF necessitates research in order to develop preventive strategies, to improve existing treatment modalities and design novel therapies.
After the discovery that paroxysms of AF can be triggered by pulmonary vein foci, isolation of the pulmonary veins was introduced as a potential curative treatment modality. It is in general assumed that in patients with persistent AF, AF has progressed from a trigger-driven to a substrate mediated arrhythmia. In these patients, persistence of AF no longer depends on the presence of a trigger (‘true fibrillation’) but is maintained by an arrhythmogenic substrate. Although animal studies have provided extensive insights into the various mechanisms that can explain perpetuation of AF, it is unknown which specific electropathological changes are relevant for the development of a substrate of persistent AF in humans. Also, it is unknown whether different cardiac diseases result in different electro-pathological alterations. Clinical mapping data of AF are scarce and the available studies are often limited to parts of the atria or a small number of beats.
Theoretically, multi-site high density mapping can be used to localize sources generating AF in patients with trigger-driven AF and to identify areas perpetuating AF in patients with substrate mediated-AF. Based on the premise that AF can be eliminated by ablation of either the trigger or the substrate perpetuating AF it is expected that multi-site high density mapping is a suitable tool to diagnose AF thereby allowing individualization of AF treatment.