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Dr. Jean-Yves Le Heuzey,
The session devoted to new insights in atrial fibrillation showed that a great number of mechanisms may be involved in atrial fibrillation. The presenters demonstrated that there are many directions of research that it will be necessary to explore in the future. Most of them could lead to therapeutic innovations.
X.H.T. Wherens from Houston, USA, made a brilliant presentation about the role of intracellular calcium release. The regulation of Ryanodine receptors by phosphorylation is a key point. In atrial fibrillation, there is an increase in phosphorylation due to a decrease in the activity of the phosphatases. In knock-out mice, it has been possible to demonstrate the pro-arrhythmic effect of Ca MK II, as its inhibition prevents atrial fibrillation in these mice. Compounds like S2814A prevent atrial fibrillation by preventing the occurrence of Delayed After Depolarizations. J.W. Schrikel from Bonn, Germany, discussed the role of cytoskeleton reorganization. Cytoskeleton is involved in many cardiac disorders, mainly actin and desmin, which play a role in membrane fixation of proteins and channels. There is a modulation by continuous reorganization. Gelsolin may be considered as a possible proarrhythmic factor, able to induce atrial fibrillation in mice. Annexin 7 also plays a role in regulation and formation of channels. Desmin is expressed in conductive tissue. Disturbed actin modulation may promote atrial fibrillation and desmin deficiency increases atrial fibrillation inducibility. C. Veltmann from Mannheim, Germany, presented the state of the art concerning inherited atrial fibrillation, a syndrome known since 1943 and the first publication by Wolf. A first loci was described in 1997. The mutations known to be possibly involved in atrial fibrillation concern KCNQ1 with gain of function in IKs, KCNE2, KCNA5 and SCN5A for which there is a missence mutation leading to the occurrence of Early After Depolarisations. There are also some associations with other inherited diseases and arrhythmias such as Brugada syndrome or LQT3 syndrome, pointing out the complexity of these abnormalities. Finally, connexin 40 may be observed, implying a reduced number of gap junctions. U. Schotten (Maastricht, The Netherlands), presented a communication about the role of calcineurin/nuclear factor of activated T-cells signalling (NFAT). There is an activation of the calcineurin/NFAT pathway in atrial fibrillation. In the remodelling process occurring in the atria, it may in fact concern electrical, trigger, structural and hemodynamic loops. For the electrical loop, there is a NFAT signaling induced ICaL downregulation in tachycardia induced remodellng. NFAT signaling promotes stretch induced metalloproteinases activation.
Atrial fibrillation - new insights
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