ArticlemedRxiv : the preprint server for health sciences2024
Kir2.1 mutations differentially increase the risk of flecainide proarrhythmia in Andersen Tawil Syndrome.
Article in medRxiv : the preprint server for health sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Flecainide and other class-Ic antiarrhythmic drugs (AADs) are widely used in Andersen-Tawil syndrome type 1 (ATS1) patients. However, class-Ic drugs might be proarrhythmic in some cases. We investigated the molecular mechanisms of class-I AADs proarrhythmia and whether they might increase the risk of death in ATS1 patients with structurally normal hearts. Methods and Results: Of 53 ATS1 patients reviewed from the literature, 54% responded partially to flecainide, with ventricular arrhythmia (VA) reduction in only 23%. Of the latter patients, VA persisted in 20-50%. Flecainide was ineffective in 23%, and surprisingly, 13.5% suffered a non-fatal cardiac arrest. In five cardiac-specific ATS1 mouse models (Kir2.1 Conclusions: Class-Ic AADs are only partially effective and might be proarrhythmic in some ATS1 patients. Kir2.1 mutations impacting the resting membrane potential and cellular excitability create a substrate for life-threatening arrhythmias, raising significant concern about using these drugs in some ATS1 patients.
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