Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Promoting excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
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