In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Understanding atrial fibrillation: from molecules to treatment

Basic Sciences, Pharmacology, Genomics and Cardiovascular Pathology

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

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.