Atrial fibrillation (AF) is the most frequent arrhythmia in clinical practice. However, its pathogenesis is still not fully understood. The goal of research in this field is to identify new treatment targets, but also to prevent the occurrence of AF.
Atria have a complex anatomy and heterogeneous histological structure that could favour the formation of triggers and substrate for the arrhythmia. Dr M Mommersteeg (Amsterdam) showed impressive data on the role played by transcription factors Nkx2.5 and PITx2 in the organisation of the sinus node area and of the pulmonary myocardium observed in the pulmonary vein. A reduction during embryogenesis of theses transcription factors results in the spreading out of the pacemaker channel in the atrial wall or in the disorganisation of the pulmonary myocardium, an important source of focal electrical activity and AF trigger. The occurrence and perpetuation of AF is favoured by alteration of atrial electrical properties, including the shortening of refractory periods, which enhances the risk of formation of micro-reentries of the electrical impulse.
Dr Dobrev from Dresden reported that alterations in ionic currents involved in this electrical remodeling are mainly the result of changes in the phosphorylation status of several channels. Phophatases, PP2A and PP1 are key actors of these post translational modifications.
Dr B Casadei from Oxford, UK reported that oxidative stress is an important determinant of the pathogenesis of AF and is characterized by an upregulation of NADPH oxydase and the NOs uncoupling. With time during AF, mitochondria can become also a source of oxidative stress. These new actors of AF help to understand the efficacy of non classical antiarrhythmic agents to reduce the incidence of AF.
Dr I Saveleiva (London) presented evidence for the use of renin angiotensin aldosterone inhibitors when AF is associated with heart failure or hypertension. Cholesterol-lowering drugs also have demonstrated anti-fibrillatory properties, while controversial data exist for polyunsaturated fatty acids.
Notes to editor
This congress report accompanies a presentation given at the ESC Congress 2008. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.