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 mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
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. Niels Voigt
Reentry and ectopic activity are accepted pathomechanisms of atrial fibrillation (AF). In this symposium, the speakers highlighted novel molecular mechanisms contributing to reentry and/or ectopic activity.
Dr. Karin Sipido (Leuven) explained that AF is associated with increased incidence of spontaneous Ca2+-release events from the sarcoplasmic reticulum (SR) via “leaky” RyR2-channels. This may cause spontaneous depolarizations (DADs) and promote ectopic activity. In addition, she showed that a higher fragmentation of RyR-clusters in AF facilitates Ca2+-wave propagation, thereby further contributing to the development of ectopic activity.
Dr. Hatem (Paris) suggested that increased membrane trafficking of Kv1.5 channel subunits in AF may explain the apparent discrepancy between higher IKur-current density, which shortens the action-potential duration, and reduced expression of the underlying channel subunit Kv1.5. Since IKur is not present in the ventricle, it provides an interesting target for AF therapy without ventricular proarrhythmia.
Dr. Kirchhof (Birmingham) showed that AF is associated with genetic variations near the Pitx2 transcription factor gene. Pitx2 is highly expressed in the left atrium (LA) and promotes typical LA gene profile expression. Although Pitx2 seems to be important for normal LA function, its role in the initiation and maintenance of AF remains unclear.
In the final presentation, Dr. Casadei (Oxford) called attention to inflammation as a biomarker for development of postoperative AF in patients undergoing open-heart surgery. Inflammation causes oxidative stress, altering ion channel function in the sarcolemma and sarcoplasmic reticulum. It may thereby promote both a reentry-maintaining substrate and ectopic activity.
Understanding atrial fibrillation: from molecules to treatment