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Congenital loss of function and drug-induced inhibition of the slowly-activating delayed-rectifier K + current (I Ks ) cause impaired cardiac repolarization. β-Adrenergic-receptor stimulation contributes to sympathetically-induced torsades de pointes (TdP). An in vivo model of long-QT1 (LQT1) syndrome and TdP in a species with I Ks characteristics relevant to man is lacking...
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