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Gain-of-function K + channel mutations cause familial atrial fibrillation (AF) by shortening of the atrial action potential duration (APD). APD-prolonging K + channel blockers are an effective therapeutic option in AF. In vitro, the dominant negative Kv4.2W362F mutation (Kv4DN) eliminates Ito,f in murine atrial myocytes and markedly prolongs the APD, so whether this loss-of-function of Ito,f alters the atrial effective refractory period (AERP) in vivo and/or affects AF-inducibility wasdoi:10.1253/circj.cj-08-0840 pmid:19145035 fatcat:icvtr52zlrfbnisirvhkpq366a