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Gene‐Specific Therapy for Long QT Syndrome

Background: One form of the hereditary long QT syndrome (LQT‐3) has recently been shown to be caused by the SCN5A mutation of the human cardiac sodium channel. Cellular studies have suggested that type lb antiarrhythmics may be potentially therapeutic via preferential blockade of the resulting abnormal late inward sodium current. To test this hypothesis, we implemented a pilot study to evaluate the potential for long‐term, gene‐specific therapy in patients with this disease.