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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
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